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Integrative Medicine Denver | Hormone Replacement Therapy

Aging is inevitable, but how you age is not! Americans are living longer, but are not necessarily healthier. We all want to be active and productive as long as possible. The good news is that our concept of aging is changing, and there are new medical approaches to living healthier as we age. Taking into account genetics, environmental influences, nutrition and lifestyle, hormonal balancing, digestive health, as well as minimizing markers of inflammation and oxidative stress are all vitally important to your overall health.

By combining both Functional Medicine and Age Management medicine, we can begin to bridge the gap between the traditional medical model and complimentary therapies. Functional Medicine and Age Management medicine both treat the whole person, and identifies the root cause of chronic diseases and symptoms of aging. It starts at the cellular level healthy cells lead to healthier bodies. Finding the right balance is the ultimate goal. It starts at the cellular level healthy cells lead to healthier bodies. Finding the right balance is the ultimate goal.

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Integrative Medicine Denver | Hormone Replacement Therapy

Recommendation and review posted by sam

Stem Cell Conferences | Cell and Stem Cell Congress | Stem …

On behalf of the organizing committee, it is my distinct pleasure to invite you to attend the Stem Cell Congress-2017. After the success of the Cell Science-2011, 2012, 2013, 2014, 2015, Conference series.LLC is proud to announce the 6th World Congress and expo on Cell & Stem Cell Research (Stem Cell Congress-2017) which is going to be held during March 20-22, 2017, Orlando, Florida, USA. The theme of Stem Cell Congress-2017 is Explore and Exploit the Novel Techniques in Cell and Stem Cell Research.

This annual Cell Science conference brings together domain experts, researchers, clinicians, industry representatives, postdoctoral fellows and students from around the world, providing them with the opportunity to report, share, and discuss scientific questions, achievements, and challenges in the field.

Examples of the diverse cell science and stem cell topics that will be covered in this comprehensive conference include Cell differentiation and development, Cell metabolism, Tissue engineering and regenerative medicine, Stem cell therapy, Cell and gene therapy, Novel stem cell technologies, Stem cell and cancer biology, Stem cell treatment, Tendency in cell biology of aging and Apoptosis and cancer disease, Drugs and clinical developments. The meeting will focus on basic cell mechanism studies, clinical research advances, and recent breakthroughs in cell and stem cell research. With the support of many emerging technologies, dramatic progress has been made in these areas. In Stem Cell Congress-2017, you will be able to share experiences and research results, discuss challenges encountered and solutions adopted and have opportunities to establish productive new academic and industry research collaborations.

In association with the Stem Cell Congress-2017 conference, we will invite those selected to present at the meeting to publish a manuscript from their talk in the journal Cell Science with a significantly discounted publication charge. Please join us in Philadelphia for an exciting all-encompassing annual Stem Cell get together with the theme of better understanding from basic cell mechanisms to latest Stem Cell breakthroughs!

Haval Shirwan, Ph.D. Executive Editor, Journal of Clinical & Cellular Immunology Dr. Michael and Joan Hamilton Endowed Chair in Autoimmune Disease Professor, Department of Microbiology and Immunology Director, Molecular Immunomodulation Program, Institute for Cellular Therapeutics, University of Louisville, Louisville, KY

Track01:Stem Cells

The most well-established and widely used stem cell treatment is thetransplantationof blood stem cells to treat diseases and conditions of the blood and immune system, or to restore the blood system after treatments for specific cancers. Since the 1970s,skin stem cellshave been used to grow skin grafts for patients with severe burns on very large areas of the body. Only a few clinical centers are able to carry out this treatment and it is usually reserved for patients with life-threatening burns. It is also not a perfect solution: the new skin has no hair follicles or sweat glands. Research aimed at improving the technique is ongoing.

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7thAnnual Conference on Stem Cell and Regenerative MedicineAug 4-5, 2016, Manchester, UK;2nd InternationalConference on AntibodiesJuly 14-15, 2016 Philadelphia, USA; 2nd InternationalConference on Innate ImmunityJuly 21-22, 2016 Berlin, Germany; 2ndInternational Congress on Neuroimmunology March 31-April 02, 2016 Atlanta, USA; InternationalConference on Cancer Immunology July 28-30, 2016 Melbourne, Australia; 5th InternationalConference on ImmunologyOctober 24-26, 2016 Chicago, USA;Cancer Vaccines: Targeting Cancer Genes for Immunotherapy, Mar 610 2016, Whistler, Canada;Systems Immunology: From Molecular Networks to Human Biology, Jan 1014 2016, Big Sky, USA;Novel Immunotherapeutics Summit, Jan 2526 2016, San Diego, USA;Stromal Cells in Immunity, Feb 711 2016, Keystone, USA; 26th European Congress ofClinical Microbiology, April 912 2016, Istanbul, Turkey

Track 02: Stem Cell Banking:

Stem Cell Banking is a facility that preserves stem cells derived from amniotic fluid for future use. Stem cell samples in private or family banks are preserved precisely for use by the individual person from whom such cells have been collected and the banking costs are paid by such person. The sample can later be retrieved only by that individual and for the use by such individual or, in many cases, by his or her first-degree blood relatives.

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8thWorld Congress on Stem Cell ResearchMarch 20-22, 2017 Orlando, USAInternationalConference on Cancer ImmunologyJuly 28-30, 2016 Melbourne, Australia; 5th InternationalConference on ImmunologyOctober 24-26, 2016 Chicago, USA;Cancer Vaccines: Targeting Cancer Genes for Immunotherapy, Mar 610 2016, Whistler, Canada;Systems Immunology: From Molecular Networks to Human Biology, Jan 1014 2016, Big Sky, USA;Novel Immunotherapeutics Summit, Jan 2526 2016, San Diego, USA;Stromal Cells in Immunity, Feb 711 2016, Keystone, USA; 26th European Congress ofClinical Microbiology, April 912 2016, Istanbul, Turkey

Track 03: Stem Cell Therapy:

Autologous cells are obtained from one’s own body, just as one may bank his or her own blood for elective surgical procedures. Adult stem cells are frequently used in medical therapies, for example in bone marrow transplantation. Human embryonic stem cells may be grown in vivo and stimulated to produce pancreatic -cells and later transplanted to the patient. Its success depends on response of the patients immune system and ability of the transplanted cells to proliferate, differentiate and integrate with the target tissue.

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4th InternationalConference on Plant GenomicsJuly 14-15, 2016 Brisbane, Australia; 8thWorld Congress on Stem Cell ResearchMarch 20-22, 2017 Orlando, USA; 7thAnnual Conference on Stem Cell and Regenerative MedicineAug 4-5, 2016, Manchester, UK; 2nd InternationalConference on Tissue preservation and BiobankingSeptember 12-13, 2016 Philadelphia, USA, USA;World Congress on Human GeneticsOctober 31- November 02, 2016 Valencia, Spain; 12thEuro Biotechnology CongressNovember 7-9, 2016 Alicante, Spain; 2nd InternationalConference on Germplasm of Ornamentals, Aug 8-12, 2016, Atlanta, USA; 7th Internationalconference on Crop Science, Aug 1419 2016, Beijing, China;Plant Epigenetics: From Genotype to Phenotype, Feb 1519 2016, Taos, USA;Germline Stem Cells Conference, June 1921 2016, San Francisco, USA;Conference on Water Stressin Plants, 29 May 3 June 2016, Ormont-Dessus, Switzerland

Track 04: Novel Stem Cell Technologies:

Stem cell technology is a rapidly developing field that combines the efforts of cell biologists, geneticists, and clinicians and offers hope of effective treatment for a variety of malignant and non-malignant diseases. Stem cells are defined as totipotent progenitor cells capable of self-renewal and multilineage differentiation. Stem cells survive well and show stable division in culture, making them ideal targets for in vitro manipulation. Although early research has focused on haematopoietic stem cells, stem cells have also been recognised in other sites. Research into solid tissue stem cells has not made the same progress as that on haematopoietic stem cells.

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InternationalConference on Next Generation SequencingJuly 21-22, 2016 Berlin, Germany; 5th InternationalConference on Computational Systems BiologyAugust 22-23, 2016 Philadelphia, USA; 7th InternationalConference on BioinformaticsOctober 27-28, 2016 Chicago, USA; InternationalConference on Synthetic BiologySeptember 28-30, 2015 Houston, USA; 4th InternationalConference on Integrative BiologyJuly 18-20, 2016 Berlin, Germany; 1st InternationalConference on Pharmaceutical BioinformaticsJan 2426 2016, Pattaya, Thailand; EMBL Conference: TheEpitranscriptome, Apr 2022 2016, Heidelberg, Germany; 2016Whole-Cell ModelingSummer School, Apr 38 2016, Barcelona, Spain; 3rd InternationalMolecular Pathological Epidemiology, May 1213 2016, Boston, USA; 5thDrug FormulationSummit, Jan 2527 2016, Philadelphia, USA

Track 05: Stem Cell Treatment:

Bone marrow transplant is the most extensively used stem-cell treatment, but some treatment derived from umbilical cord blood are also in use. Research is underway to develop various sources for stem cells, and to apply stem-cell treatments for neurodegenerative diseases and conditions, diabetes, heart disease, and other conditions.

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7th InternationalConference on BioinformaticsOctober 27-28, 2016 Chicago, USA; InternationalConference on Synthetic BiologySeptember 28-30, 2015 Houston, USA; 7thAnnual Conference on Stem Cell and Regenerative MedicineAug 4-5, 2016, Manchester, UK; 4th InternationalConference on Integrative BiologyJuly 18-20, 2016 Berlin, Germany; 1st InternationalConference on Pharmaceutical BioinformaticsJan 2426 2016, Pattaya, Thailand; EMBL Conference: TheEpitranscriptome, Apr 2022 2016, Heidelberg, Germany; 2016Whole-Cell ModelingSummer School, Apr 38 2016, Barcelona, Spain; 3rd InternationalMolecular Pathological Epidemiology, May 1213 2016, Boston, USA; 5thDrug FormulationSummit, Jan 2527 2016, Philadelphia, USA

Track 06: Stem cell apoptosis and signal transduction:

Apoptosis is the process of programmed cell death (PCD) that may occur in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global mRNA decay. Most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy.

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InternationalConference on Restorative MedicineOctober 24-26, 2016 Chicago, USA;; 3rdWorld Congress onHepatitis and Liver Diseases October 17-19, 2016 Dubai, UAE; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; 2nd InternationalConference on Tissue preservation and Biobanking September12-13, 2016 Philadelphia USA; 26thEuropean Congress ofClinical Microbiology, April 912 2016, Istanbul, Turkey;Conference onCell Growth and Regeneration, Jan 1014 2016, Breckenridge, USA ;

Track 07: Stem Cell Biomarkers:

Molecular biomarkers serve as valuable tools to classify and isolate embryonic stem cells (ESCs) and to monitor their differentiation state by antibody-based techniques. ESCs can give rise to any adult cell type and thus offer enormous potential for regenerative medicine and drug discovery. A number of biomarkers, such as certain cell surface antigens, are used to assign pluripotent ESCs; however, accumulating evidence suggests that ESCs are heterogeneous in morphology, phenotype and function, thereby classified into subpopulations characterized by multiple sets of molecular biomarkers.

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8thWorld Congress on Stem Cell ResearchMarch 20-22, 2017 Orlando, USA; 5th International Conference onCell and Gene TherapyMay 19-21, 2016 San Antonio, USA; 7thAnnual Conference on Stem Cell and Regenerative MedicineAug 4-5, 2016, Manchester, UK; InternationalConference on Restorative MedicineOctober 24-26, 2016 Chicago, USA; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; 2nd InternationalConference on Tissue preservation and Biobanking September12-13, 2016 Philadelphia USA;Conference on Cardiac Development, Regeneration and RepairApril 3 7, 2016 Snowbird, Utah, USA; Stem Cell DevelopmentMay 22-26, 2016 Hillerd, Denmark; Conference onHematopoietic Stem Cells, June 3-5, 2016 Heidelberg, Germany; ISSCR Pluripotency – March 22-24, 2016 Kyoto, Japan

Track 08: Cellular therapies:

Cellular therapy also called Cell therapy is therapy in which cellular material is injected into a patient, this generally means intact, living cells. For example, T cells capable of fighting cancer cells via cell-mediated immunity may be injected in the course of immunotherapy.

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InternationalConference on Genetic Counseling and Genomic MedicineAugust 11-12, 2016 Birmingham, UK;World Congress on Human GeneticsOctober 31- November 02, 2016 Valencia, Spain; InternationalConference on Molecular BiologyOctober 13-15, 2016 Dubai, UAE; 3rd InternationalConference on Genomics & PharmacogenomicsSeptember 21-23, 2015 San Antonio, USA; EuropeanConference on Genomics and Personalized MedicineApril 25-27, 2016 Valencia, Spain;Genomics and Personalized Medicine, Feb 711 2016, Banff, Canada; Drug Discovery for Parasitic Diseases, Jan 2428 2016, Tahoe City, USA; Heart Failure: Genetics,Genomics and Epigenetics, April 37 2016, Snowbird, USA; Understanding the Function ofHuman Genome Variation, May 31 June 4 2016, Uppsala, Sweden; 5thDrug Formulation SummitJan2527,2016,Philadelphia, USA

Track 09: Stem cells and cancer:

Cancer can be defined as a disease in which a group of abnormal cells grow uncontrollably by disregarding the normal rules of cell division. Normal cells are constantly subject to signals that dictate whether the cells should divide, differentiate into another cell or die. Cancer cells develop a degree of anatomy from these signals, resulting in uncontrolled growth and proliferation. If this proliferation is allowed to continue and spread, it can be fatal.

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2ndWorld Congress on Applied MicrobiologyOctober 31-November 02, 2016 Istanbul, Turkey; InternationalConference on Infectious Diseases & Diagnostic MicrobiologyOct 3-5, 2016 Vancouver, Canada;18th International conference on Neuroscience, April 26 2016, Sweden, Austria; 6th Annual Traumatic Brain Injury Conference, May 1112 2016, Washington, D.C., USA; Common Mechanisms of Neurodegeneration, June 1216 2016, Keystone, USA; Neurology Caribbean Cruise, Aug 2128 2016, Fort Lauderdale, USA; Annual Meeting of the German Society ofNeurosurgery(DGNC), June 1215 2016, Frankfurt am Main, Germany

Track 10: Embryonic stem cells:

Embryonic stem cells have a major potential for studying early steps of development and for use in cell therapy. In many situations, however, it will be necessary to genetically engineer these cells. A novel generation of lentivectors which permit easy genetic engineering of mouse and human embryonic stem cells.

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4thCongress on Bacteriology and Infectious DiseasesMay 16-18, 2016 San Antonio, USA; 2ndWorld Congress on Applied MicrobiologyOctober 31-November 02, 2016 Istanbul, Turkey; InternationalConference on Infectious Diseases & Diagnostic MicrobiologyOct 3-5, 2016 Vancouver, Canada; InternationalConference on Water MicrobiologyJuly 18-20, 2016 Chicago, USA; 5th InternationalConference on Clinical MicrobiologyOctober 24-26, 2016 Rome, Italy; Axons: FromCell Biologyto Pathology Conference, 2427 January 2016, Santa Fe, USA; 26th EuropeanCongress of Clinical MicrobiologyApril 912 2016, Istanbul, Turkey;Conference on Gut Microbiota, Metabolic Disorders and Beyond, April 1721 2016, Newport, USA; 7th EuropeanSpores Conference, April 1820 2016, Egham, UK; New Approaches to Vaccines forHuman and Veterinary Tropical Diseases, May 2226 2016, Cape Town, South Africa

Track 11: Cell differentiation and disease modeling:

Cellular differentiation is the progression, whereas a cell changes from one cell type to another. Variation occurs numerous times during the development of a multicellular organism as it changes from a simple zygote to a complex system of tissues and cell types. Differentiation continues in adulthood as adult stem cells divide and create fully differentiated daughter cells during tissue repair and during normal cell turnover. Some differentiation occurs in response to antigen exposure. Differentiation dramatically changes a cell’s size, shape, membrane potential, metabolic activity, and responsiveness to signals. These changes are largely due to highly controlled modifications in gene expression and are the study of epigenetics. With a few exceptions, cellular differentiationalmost never involves a change in the DNA sequence itself. Thus, different cells can have very different physical characteristics despite having the same genome.

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4thCongress on Bacteriology and Infectious DiseasesMay 16-18, 2016 San Antonio, USA; 2ndWorld Congress on Applied MicrobiologyOctober 31-November 02, 2016 Istanbul, Turkey; InternationalConference on Infectious Diseases & Diagnostic MicrobiologyOct 3-5, 2016 Vancouver, Canada; InternationalConference on Water MicrobiologyJuly 18-20, 2016 Chicago, USA; 5thInternationalConference on Clinical MicrobiologyOctober 24-26, 2016 Rome, Italy; Axons: FromCell Biologyto Pathology Conference, 2427 January 2016, Santa Fe, USA; 26thEuropeanCongress of Clinical MicrobiologyApril 912 2016, Istanbul, Turkey;Conference on Gut Microbiota, Metabolic Disorders and Beyond, April 1721 2016, Newport, USA; 7thEuropeanSpores Conference, April 1820 2016, Egham, UK; New Approaches toVaccines forHuman and Veterinary Tropical Diseases, May 2226 2016, Cape Town, South Africa

Track 12: Tissue engineering:

Tissue Engineering is the study of the growth of new connective tissues, or organs, from cells and a collagenous scaffold to produce a fully functional organ for implantation back into the donor host. Powerful developments in the multidisciplinary field of tissue engineering have produced a novel set of tissue replacement parts and implementation approaches. Scientific advances in biomaterials, stem cells, growth and differentiation factors, and biomimetic environments have created unique opportunities to fabricate tissues in the laboratory from combinations of engineered extracellular matrices cells, and biologically active molecules.

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4thCongress on Bacteriology and Infectious DiseasesMay 16-18, 2016 San Antonio, USA; 2ndWorld Congress on Applied MicrobiologyOctober 31-November 02, 2016 Istanbul, Turkey; InternationalConference on Infectious Diseases & Diagnostic MicrobiologyOct 3-5, 2016 Vancouver, Canada; InternationalConference on Water MicrobiologyJuly 18-20, 2016 Chicago, USA; 5thInternationalConference on Clinical MicrobiologyOctober 24-26, 2016 Rome, Italy; Axons: FromCell Biologyto Pathology Conference, 2427 January 2016, Santa Fe, USA; 26thEuropeanCongress of Clinical MicrobiologyApril 912 2016, Istanbul, Turkey;Conference on Gut Microbiota, Metabolic Disorders and Beyond, April 1721 2016, Newport, USA; 7thEuropeanSpores Conference, April 1820 2016, Egham, UK; New Approaches toVaccines forHuman and Veterinary Tropical Diseases, May 2226 2016, Cape Town, South Africa

Track 13: Stem cell plasticity and reprogramming:

Stem cell plasticity denotes to the potential of stem cells to give rise to cell types, previously considered outside their normal repertoire of differentiation for the location where they are found. Included under this umbrella title is often the process of transdifferentiation the conversion of one differentiated cell type into another, and metaplasia the conversion of one tissue type into another. From the point of view of this entry, some metaplasias have a clinical significance because they predispose individuals to the development of cancer.

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InternationalConference on Case ReportsMarch 31-April 02, 2016 Valencia, Spain; 2nd International Meeting onClinical Case ReportsApril 18-20, 2016 Dubai, UAE; 3rd Experts Meeting onMedical Case ReportsMay 09-11, 2016 New Orleans, Louisiana, USA; 12thEuro BiotechnologyCongress November 7-9, 2016 Alicante, Spain; 2nd International Conference onTissue preservation and BiobankingSeptember 12-13, 2016 Philadelphia, USA; 11thWorld Conference BioethicsOctober 20-22, 2015 Naples, Italy;Annual Conference Health Law and Bioethics, May 6-7 2016 Cambridge, MA, USA; 27th Maclean Conference on Clinical Medical Ethics, Nov 13-14, 2015, Chicago, USA; CFP: Global Forum on Bioethics in Research, Nov 3-4, 2015, Annecy, France

Track 14: Gene therapy and stem cells

Gene therapy is the therapeutic delivery of nucleic acid polymers into a patient’s cells as a drug to treat disease. Gene therapy could be a way to fix a genetic problem at its source. The polymers are either expressed as proteins, interfere with protein expression, or possibly correct genetic mutations. In the future, this technique may allow doctors to treat a disorder by inserting a gene into a patient’s cells instead of using drugs or surgery.

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Track 15: Tumour cell science:

An abnormal mass of tissue. Tumors are a classic sign of inflammation, and can be benign or malignant. Tomour usually reflect the kind of tissue they arise in. Treatment is also specific to the location and type of the tumor. Benign tumors can sometimes simply be ignored, cancerous tumors; options include chemotherapy, radiation, and surgery.

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Track 16: Reprogramming stem cells: computational biology

Computational Biology, sometimes referred to as bioinformatics, is the science of using biological data to develop algorithms and relations among various biological systems. Bioinformatics groups use computational methods to explore the molecular mechanisms underpinning stem cells. To accomplish this bioinformaticsdevelop and apply advanced analysis techniques that make it possible to dissect complex collections of data from a wide range of technologies and sources.

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The fields of stem cell biology and regenerative medicine research are fundamentally about understanding dynamic cellular processes such as development, reprogramming, repair, differentiation and the loss, acquisition or maintenance of pluripotency. In order to precisely decipher these processes at a molecular level, it is critical to identify and study key regulatory genes and transcriptional circuits. Modern high-throughput molecular profiling technologies provide a powerful approach to addressing these questions as they allow the profiling of tens of thousands of gene products in a single experiment. Whereas bioinformatics is used to interpret the information produced by such technologies.

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8th World Congress on Cell & Stem Cell Research

The success of the 7 Cell Science conferences series has given us the prospect to bring the gathering one more time for our 8thWorld Congress 2017 meet in Orlando, USA. Since its commencement in 2011 cell science series has perceived around 750 researchers of great potentials and outstanding research presentations around the globe. The awareness of stem cells and its application is increasing among the general population that also in parallel offers hope and add woes to the researchers of cell science due to the potential limitations experienced in the real-time.

Stem Cell Research-2017has the goal to fill the prevailing gaps in the transformation of this science of hope to promptly serve solutions to all in the need.World Congress 2017 will have an anticipated participation of 100-120 delegates from around the world to discuss the conference goal.

History of Stem cells Research

Stem cells have an interesting history, in the mid-1800s it was revealed that cells were basically the building blocks of life and that some cells had the ability to produce other cells. Efforts were made to fertilize mammalian eggs outside of the human body and in the early 1900s, it was discovered that some cells had the capacity to generate blood cells. In 1968, the first bone marrow transplant was achieved successfully to treat two siblings with severe combined immunodeficiency. Other significant events in stem cell research include:

1978: Stem cells were discovered in human cord blood 1981: First in vitro stem cell line developed from mice 1988: Embryonic stem cell lines created from a hamster 1995: First embryonic stem cell line derived from a primate 1997: Cloned lamb from stem cells 1997: Leukaemia origin found as haematopoietic stem cell, indicating possible proof of cancer stem cells

Funding in USA:

No federal law forever did embargo stem cell research in the United States, but only placed restrictions on funding and use, under Congress’s power to spend. By executive order on March 9, 2009, President Barack Obama removed certain restrictions on federal funding for research involving new lines of humanembryonic stem cells. Prior to President Obama’s executive order, federal funding was limited to non-embryonic stem cell research and embryonic stem cell research based uponembryonic stem celllines in existence prior to August 9, 2001. In 2011, a United States District Court “threw out a lawsuit that challenged the use of federal funds for embryonic stem cell research.

Members Associated with Stem Cell Research:

Discussion on Development, Regeneration, and Stem Cell Biology takes an interdisciplinary approach to understanding the fundamental question of how a single cell, the fertilized egg, ultimately produces a complex fully patterned adult organism, as well as the intimately related question of how adult structures regenerate. Stem cells play critical roles both during embryonic development and in later renewal and repair. More than 65 faculties in Philadelphia from both basic science and clinical departments in the Division of Biological Sciences belong to Development, Regeneration, and Stem Cell Biology. Their research uses traditional model species including nematode worms, fruit-flies, Arabidopsis, zebrafish, amphibians, chick and mouse as well as non-traditional model systems such as lampreys and cephalopods. Areas of research focus include stem cell biology, regeneration, developmental genetics, and cellular basis of development, developmental neurobiology, and evo-devo (Evolutionary developmental biology).

Stem Cell Market Value:

Worldwide many companies are developing and marketing specialized cell culture media, cell separation products, instruments and other reagents for life sciences research. We are providing a unique platform for the discussions between academia and business.

Global Tissue Engineering & Cell Therapy Market, By Region, 2009 2018

$Million

Why to attend???

Stem Cell Research-2017 could be an outstanding event that brings along a novel and International mixture of researchers, doctors, leading universities and stem cell analysis establishments creating the conference an ideal platform to share knowledge, adoptive collaborations across trade and world, and assess rising technologies across the world. World-renowned speakers, the most recent techniques, tactics, and the newest updates in cell science fields are assurances of this conference.

A Unique Opportunity for Advertisers and Sponsors at this International event:

http://stemcell.omicsgroup.com/sponsors.php

UAS Major Universities which deals with Stem Cell Research

University of Washington/Hutchinson Cancer Center

Oregon Stem Cell Center

University of California Davis

University of California San Francisco

University of California Berkeley

Stanford University

Mayo Clinic

Major Stem Cell Organization Worldwide:

Norwegian Center for Stem Cell Research

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Stem Cell Conferences | Cell and Stem Cell Congress | Stem …

Recommendation and review posted by Bethany Smith

Breast Cancer Risk Factors: Genetics

About 5% to 10% of breast cancers are thought to be hereditary, caused by abnormal genes passed from parent to child.

Genes are particles in cells, contained in chromosomes, and made of DNA (deoxyribonucleic acid). DNA contains the instructions for building proteins. And proteins control the structure and function of all the cells that make up your body.

Think of your genes as an instruction manual for cell growth and function. Abnormalities in the DNA are like typographical errors. They may provide the wrong set of instructions, leading to faulty cell growth or function. In any one person, if there is an error in a gene, that same mistake will appear in all the cells that contain the same gene. This is like having an instruction manual in which all the copies have the same typographical error.

Most inherited cases of breast cancer are associated with two abnormal genes: BRCA1 (BReast CAncer gene one) and BRCA2 (BReast CAncer gene two).

Everyone has BRCA1 and BRCA2 genes. The function of the BRCA genes is to repair cell damage and keep breast, ovarian, and other cells growing normally. But when these genes contain abnormalities or mutations that are passed from generation to generation, the genes don’t function normally and breast, ovarian, and other cancer risk increases. Abnormal BRCA1 and BRCA2 genes may account for up to 10% of all breast cancers, or 1 out of every 10 cases.

Having an abnormal BRCA1 or BRCA2 gene doesn’t mean you will be diagnosed with breast cancer. Researchers are learning that other mutations in pieces of chromosomes — called SNPs (single nucleotide polymorphisms) — may be linked to higher breast cancer risk in women with an abnormal BRCA1 gene as well as women who didn’t inherit an abnormal breast cancer gene.

Women who are diagnosed with breast cancer and have an abnormal BRCA1 or BRCA2 gene often have a family history of breast cancer, ovarian cancer, and other cancers. Still, most people who develop breast cancer did not inherit an abnormal breast cancer gene and have no family history of the disease.

You are substantially more likely to have an abnormal breast cancer gene if:

If one family member has an abnormal breast cancer gene, it does not mean that all family members will have it.

The average woman in the United States has about a 1 in 8, or about 12%, risk of developing breast cancer in her lifetime. Women who have an abnormal BRCA1 or BRCA2 gene (or both) can have up to an 80% risk of being diagnosed with breast cancer during their lifetimes. Breast cancers associated with an abnormal BRCA1 or BRCA2 gene tend to develop in younger women and occur more often in both breasts than cancers in women without these abnormal genes.

Women with an abnormal BRCA1 or BRCA2 gene also have an increased risk of developing ovarian, colon, and pancreatic cancers, as well as melanoma.

Men who have an abnormal BRCA2 gene have a higher risk of breast cancer than men who don’t — about 8% by the time they’re 80 years old. This is about 80 times greater than average.

Men with an abnormal BRCA1 gene have a slightly higher risk of prostate cancer. Men with an abnormal BRCA2 gene are 7 times more likely than men without the abnormal gene to develop prostate cancer. Other cancer risks, such as cancer of the skin or digestive tract, also may be slightly higher in men with abnormal BRCA1 or BRCA2 genes.

Changes in other genes are also associated with breast cancer. These abnormal genes are much less common and don’t seem to increase risk as much as abnormal BRCA1 and BRCA2 genes, which are considered rare. Still, because these genetic mutations are rarer, they haven’t been studied as much as the BRCA genes.

In 2015, an abnormal version of the SEC23B gene also was linked to Cowden syndrome. The SEC23B gene also helps regulate cell growth. Because this discovery is so new, there is not a clinical test available for an abnormal SEC23B gene.

Inheriting two abnormal copies of the BRCA2, BRIP1, MRE11A, NBN, PALB2, RAD50, or RAD51C genes causes the disease Fanconi anema, which suppresses bone marrow function and leads to extremely low levels of red blood cells, white blood cells, and platelets. People with Fanconi anemia also have a higher risk of several other types of cancer, including kidney cancer and brain cancer.

There are genetic tests available to determine if someone has an abnormal BRCA1 or BRCA2 gene. A genetic counselor also may order testing for an abnormal ATM, CDH1, CHEK2, MRE11A, NBN, PALB2, PTEN, RAD50, RAD51C, or TP53 gene, individually or as part of a larger gene panel that includes BRCA1 and BRCA2 if it’s determined from your personal or family history that these tests are an option. Right now, there is not a clinical test for an abnormal SEC23B gene.

For more information, visit the Breastcancer.org Genetic Testing pages.

If you know you have an abnormal gene linked to breast cancer, there are lifestyle choices you can make to keep your risk as low it can be:

These are just a few steps you can take. Review the links on the left side of this page for more options.

Along with these lifestyle choices, there are other risk-reduction options for women at high risk because of abnormal genetics.

Hormonal therapy medicines: Two SERMs (selective estrogen receptor modulators) and two aromatase inhibitors have been shown to reduce the risk of developing hormone-receptor-positive breast cancer in women at high risk.

Hormonal therapy medicines do not reduce the risk of hormone-receptor-negative breast cancer.

More frequent screening: If you’re at high risk because of an abnormal breast cancer gene, you and your doctor will develop a screening plan tailored to your unique situation. You may start being screened when you’re younger than 40. In addition to the recommended screening guidelines for women at average risk, a screening plan for a woman at high risk may include:

Women with an abnormal breast cancer gene need to be screened twice a year because they have a much higher risk of cancer developing in the time between yearly screenings. For example, the Memorial Sloan-Kettering Cancer Center in New York, NY recommends that women with an abnormal BRCA1 or BRCA2 gene have both a digital mammogram and an MRI scan each year, about 6 months apart (for example, a mammogram in December and an MRI in June).

A breast ultrasound is another powerful tool that can help detect breast cancer in women with an abnormal breast cancer gene. This test does not take the place of digital mammography and MRI scanning.

Talk to your doctor, radiologist, and genetic counselor about developing a specialized program for early detection that addresses your breast cancer risk, meets your individual needs, and gives you peace of mind.

Protective surgery: Removing the healthy breasts and ovaries — called prophylactic surgery (“prophylactic” means “protective”) — are very aggressive, irreversible risk-reduction options that some women with an abnormal BRCA1 or BRCA2 gene choose.

Prophylactic breast surgery may be able to reduce a woman’s risk of developing breast cancer by as much as 97%. The surgery removes nearly all of the breast tissue, so there are very few breast cells left behind that could develop into a cancer.

Women with an abnormal BRCA1 or BRCA2 gene may reduce their risk of breast cancer by about 50% by having prophylactic ovary and fallopian tube removal (salpingo-oophorectomy) before menopause. Removing the ovaries lowers the risk of breast cancer because the ovaries are the main source of estrogen in a premenopausal womans body. Removing the ovaries doesnt reduce the risk of breast cancer in postmenopausal women because fat and muscle tissue are the main producers of estrogen in these women. Prophylactic removal of both ovaries and fallopian tubes reduces the risk of ovarian cancer in women at any age, before or after menopause.

Research also has shown that women with an abnormal BRCA1 or BRCA2 gene who have prophylactic ovary removal have better survival if they eventually are diagnosed with breast or ovarian cancer.

The benefit of prophylactic surgeries is usually counted one year at a time. Thats why the younger you are at the time of surgery, the larger the potential benefit, and the older you are, the lower the benefit. Also, as you get older youre more likely to develop other medical conditions that affect how long you live, such as diabetes and heart disease.

Of course, each woman’s situation is unique. Talk to your doctor about your personal level of risk and how best to manage it.

It’s important to remember that no procedure — not even removing both healthy breasts and ovaries at a young age — totally eliminates the risk of cancer. There is still a small risk that cancer can develop in the areas where the breasts used to be. Close follow-up is necessary, even after prophylactic surgery.

Prophylactic surgery decisions require a great deal of thought, patience, and discussion with your doctors, genetic counselor, and family over time — together with a tremendous amount of courage. Take the time you need to consider these options and make decisions that feel comfortable to you.

For more information, visit the Breastcancer.org Prophylactic Mastectomy and Prophylactic Ovary Removal pages.

Think Pink, Live Green: A Step-by-Step Guide to Reducing Your Risk of Breast Cancer teaches you the biology of breast development and how modern life affects breast cancer risk. Order a free booklet by mail or download the PDF of the booklet to learn 31 risk-reducing steps you can take today.

See the article here:
Breast Cancer Risk Factors: Genetics

Recommendation and review posted by Bethany Smith

Cat coat genetics – Wikipedia, the free encyclopedia

The genetics of cat coat coloration, pattern, length, and texture is a complex subject, and many different genes are involved.

Cat coat genetics can produce a variety of colors and coat patterns. These are physical properties and should not be confused with a breed of cat. Furthermore, cats may show the color and/or pattern particular to a certain breed without actually being of that breed. For example, cats may have point coloration, but not be Siamese.

A cat with Oo and white spotting genes is commonly called a calico. The reason for the patchwork effect in female cats heterozygous for the O gene (Oo) is X-inactivation one or the other X chromosome in every cell in the embryo is randomly inactivated (see Barr body), and the gene in the other X chromosome is expressed.

For a cat to be tortoiseshell, calico, or one of the variants such as blue-cream or chocolate tortoiseshell, the cat must simultaneously express two alleles, O and o, which are located on the X chromosome. Males normally cannot do this, as they have only one X chromosome, and therefore only one allele, and so calico cats are normally only female. Male tortoiseshell or calico cats occur only if they have chromosomal abnormalities such as the genotype XXY (in which case they are sterile), chromosomal mosaicism (only portions of their cells have the genotype XXY, so these cats may be fertile), or chimerism (a single individual formed from two fused embryos, at least one of which was male). Approximately 1 in 3,000 calico/tortoiseshell cats are male.[4] Chimericism (which may result in fertile male cats) appears to be the most common mechanism.

One can deduce that a grey male cat with a white bib and paws, but showing no tabby pattern:

Tabby cats (AA or Aa), normally have:

Most or all striping disappears in the chinchilla or shaded cat, but it is still possible to identify the cat as a tabby from these other features.

The genetics involved in producing the ideal tabby, tipped, shaded, or smoke cat is complex. Not only are there many interacting genes, but genes sometimes do not express themselves fully, or conflict with one another. For example, the melanin inhibitor gene sometimes does a poor job blocking pigment, resulting in an excessively gray undercoat, or in tarnishing (yellowish or rusty fur).

Likewise, poorly-expressed non-agouti or over-expression of melanin inhibitor will cause a pale, washed out black smoke. Various polygenes (sets of related genes), epigenetic factors, or modifier genes, as yet unidentified, are believed to result in different phenotypes of coloration, some deemed more desirable than others by fanciers.

Here are the genetic influences on tipped or shaded cats:

Cat fur length is governed by the Long hair gene in which the dominant form, L, codes for short hair, and the recessive l codes for long hair. In the longhaired cat, the transition from anagen (hair growth) to catagen (cessation of hair growth) is delayed due to this mutation. A rare recessive shorthair gene has been observed in some lines of Persian cat (silvers) where two longhaired parents have produced shorthaired offspring.

There have been many genes identified that result in unusual cat fur. These genes were discovered in random-bred cats and selected for. Some of the genes are in danger of going extinct because the cats are not sold beyond the region where the mutation originated or there is simply not enough demand for cats expressing the mutation.

In many breeds, coat gene mutations are unwelcome. An example is the rex allele which appeared in Maine Coons in the early 1990s. Rexes appeared in America, Germany and the UK, where one breeder caused consternation by calling them “Maine Waves”. Two UK breeders did test mating which indicated that this was probably a new rex mutation and that it was recessive. The density of the hair was similar to normally coated Maine Coons, but consisted only of down type hairs with a normal down type helical curl, which varied as in normal down hairs. Whiskers were more curved, but not curly. Maine Coons do not have awn hairs, and after moulting, the rexes had a very thin coat.

There are various genes producing curly coated or “rex” cats. New types of rex pop up spontaneously in random-bred cats now and then. Here are some of the rex genes that breeders have selected for:

There are also genes for hairlessness:

Some rex cats are prone to temporary hairlessness, known as baldness, during moulting.

Here are a few other genes resulting in unusual fur:

More:
Cat coat genetics – Wikipedia, the free encyclopedia

Recommendation and review posted by Bethany Smith

Cloning – Learn Genetics

About Cloning

What is Cloning?

Learn the basics about cloning and see how its done.

Why Clone?

Evaluate the reasons for using cloning technologies.

The History of Cloning

Explore the history of cloning technologies.

Cloning Myths

Here we help you separate the facts from the fiction.

Click and Clone

Try it yourself in the mouse cloning laboratory.

Is it Cloning? Or Not?

Test your cloning savvy with this interactive quiz.

APA format:

Genetic Science Learning Center. (2014, July 10) Cloning. Retrieved August 24, 2016, from http://learn.genetics.utah.edu/content/cloning/

CSE format:

Cloning [Internet]. Salt Lake City (UT): Genetic Science Learning Center; 2014 [cited 2016 Aug 24] Available from http://learn.genetics.utah.edu/content/cloning/

Chicago format:

Genetic Science Learning Center. “Cloning.” Learn.Genetics.July 10, 2014. Accessed August 24, 2016. http://learn.genetics.utah.edu/content/cloning/.

The rest is here:
Cloning – Learn Genetics

Recommendation and review posted by Bethany Smith

Genetics of human male infertility.

Infertility is defined as a failure to conceive in a couple trying to reproduce for a period of two years without conception. Approximately 15 percent of couples are infertile, and among these couples, male factor infertility accounts for approximately 50 percent of causes. Male infertility is a multifactorial syndrome encompassing a wide variety of disorders. In more than half of infertile men, the cause of their infertility is unknown (idiopathic) and could be congenital or acquired. Infertility in men can be diagnosed initially by semen analysis. Seminograms of infertile men may reveal many abnormal conditions, which include azoospermia, oligozoospermia, teratozoospermia, asthenozoospermia, necrospermia and pyospermia. The current estimate is that about 30 percent of men seeking help at the infertility clinic are found to have oligozoospermia or azoospermia of unknown aetiology. Therefore, there is a need to find the cause of infertility. The causes are known in less than half of these cases, out of which genetic or inherited disease and specific abnormalities in the Y chromosome are major factors. About 10-20 percent of males presenting without sperm in the ejaculate carry a deletion of the Y chromosome. This deleted region includes the Azoospermia Factor (AZF) locus, located in the Yq11, which is divided into four recurrently deleted non-overlapping subregions designated as AZFa, AZFb, AZFc and AZFd. Each of these regions may be associated with a particular testicular histology, and several candidate genes have been found within these regions. The Deleted in Azoospermia (DAZ) gene family is reported to be the most frequently deleted AZF candidate gene and is located in the AZFc region. Recently, a partial, novel Y chromosome 1.6-Mb deletion, designated “gr/gr” deletion, has been described specifically in infertile men with varying degrees of spermatogenic failure. The DAZ gene has an autosomal homologue, DAZL (DAZ-Like), on the short arm of the chromosome 3 (3p24) and it is possible that a defective autosomal DAZL may be responsible for the spermatogenic defect. The genetic complexity of the AZF locus on the long arm of the Y chromosome could be revealed only with the development of sequence tagged sites. Random attacks on the naked mitochondrial DNA (mtDNA) of sperm by reactive oxygen species or free radicals will inevitably cause oxidative damage or mutation to the mitochondrial genome with pathological consequences and lead to infertility in males. The key nuclear enzyme involved in the elongation and repair of mtDNA strands is DNA polymerase gamma, mapped to the long arm of chromosome 15 (15q25), and includes a CAG repeat region. Its mutation affects the adenosine triphosphate production. The introduction of molecular techniques has provided great insight into the genetics of infertility. Yet, our understanding of the genetic causes of male infertility remains limited.

Visit link:
Genetics of human male infertility.

Recommendation and review posted by sam

Definitions for Terms in Genetics Problems

Definitions for terms in genetics problems

All the different forms of the same gene.

All genes on chromosomes other than the sex chromosomes (X and Y).

One strand of a replicated chromosome as illustrated in the image of a chromosome at the right. A single strand by itself with it’s own centromere is a chromosome and not a chromatid.

A single (before replication) or double (after replication) strand of DNA with only a single centromere. Chromosomes contain the loci for alleles of different genes. The illustration below shows a chromosome with the parts labeled before (on the left) and after (on the right) replication.

A process that occurs during prophase I of meiosis in which genetic material from the chromatid of one chromosome exchanges places with the material from the same area of a chromatid on it’s homolog. This process increases the variation in gametes produced by an individual. The images below illustrate a homologous pair of chromosomes before (on the left) and after (on the right) crossing over has occurred.

Cells which have two copies of a gene, on a pair of homologous chromosomes.

An allele which, if present, masks the effect of any recessive allele paired with it. Indicated by a capital letter.

first-generation offspring (children).

second-generation offspring (grand children).

The haploid cells produced by meiosis which later fuse to form the diploid zygote. In humans, these are the eggs and sperm.

Units of information about specific traits, passed from parents to offspring. Each gene has a specific location (locus) on a chromosome and may come in several forms (alleles).

The actual genes for a trait present in an individual.

The expected numbers of different genotypes produced by a particular cross. Example: 1 RR, 2 Rr, and 1 rr individuals could result from a cross of two Rr individuals. The genotypic ration is 1:2:1.

Cells which have only one allele from the originally homologous pair. In humans, gametes are the only haploid cells.

The two alleles of a pair are not identical (for example: one dominant and one recessive allele for the color trait in roses).

A pair of chromosomes in the same individual that carry the same type of information (eye color) but not necessarily the same alleles (blue or brown). One of these “homologs” comes from the individual’s mother and one from the father.

Both alleles of a gene in a homologous pair are identical.

Genes that appear on the same chromosome and that do not sort independently during meiosis.

The physical location of the alleles of a gene on it’s chromosome (See the definition for chromosome for an image).

A type of cell division that produces haploid gametes. The image below shows the very basic steps of meiosis and it’s products.

A change in a gene’s molecular structure and thus it’s information about a trait.

parental generation

An individual’s observable traits (how the organism looks, behaves, etc.).

The expected numbers of different phenotypes produced by a particular cross. Example: 3 red flowered plants and 1 white flowered plant result from a cross of two red flowered plants. The phenotypic ratio is 3:1.

A graphical representation of a cross between two individuals and the possible genotypes of the offspring produced. The gametes of one individual are placed across the top of the square and the gametes of the other individual are placed down the left side. The gametes are then combined in the cells of the square. Below is an example of a dihybrid cross between two individuals worked in the punnett square.

An allele which must be homozygous for it’s effect to be observed. Indicated by a lowercase letter.

sex-linked genes are those that are carried on the X chromosome. In humans, females carry 2 X chromosomes while males carry only one.

See the article here:
Definitions for Terms in Genetics Problems

Recommendation and review posted by Bethany Smith

5th International Conference and Exhibition on

Track-1 Cell Therapy:

Cell therapyas performed by alternativemedicinepractitioners is very different from the controlled research done by conventionalstem cellmedical researchers. Alternative practitioners refer to their form of cell therapy by several other different names includingxenotransplanttherapy,glandular therapy, and fresh cell therapy. Proponents ofcell therapyclaim that it has been used successfully to rebuild damaged cartilage in joints, repair spinal cord injuries,strengthen a weakenedimmune system, treat autoimmune diseases such as AIDS, and help patients withneurological disorderssuch as Alzheimers disease,Parkinson’s diseaseand epilepsy.

Related Conferences:

6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017,8th World Congress and Expo onCell & Stem Cell Research,Orlando, USA, March 20-22, 2017,15thWorld Congress on Biotechnology and Biotech Industries Meet,Rome, Italy,March 20-21,2017 ,2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017, International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017.

Track-2 Gene therapy:

Gene therapyand cell therapy are overlapping fields of biomedical research with the goals of repairing the direct cause of genetic diseases in the DNA orcellularpopulation, respectively. The development of suitablegene therapytreatments for manygenetic diseasesand some acquired diseases has encountered many challenges and uncovered new insights into gene interactions and regulation. Further development often involves uncovering basic scientific knowledge of the affected tissues, cells, and genes, as well as redesigning vectors, formulations, and regulatory cassettes for the genes.Cell therapyis expanding its repertoire of cell types for administration.Cell therapytreatment strategies include isolation and transfer of specific stem cell populations, administration of effector cells, and induction of mature cells to becomepluripotent cells, and reprogramming of mature cells.

Related Conferences:

2nd International Conference onMolecular Biology,London, UK,June 22-24, 2017,3rd World Bio Summit & Expo, Abu Dhabi, UAE, June 19-21, 2017,5th International Conference onIntegrative Biology, London, UK, June 19-21,2017,2nd World Congress on Human Genetics, Chicago, USA, July 24-26, 2017,9th International Conference onGenomics and Pharmacogenomics, Chicago, USA, July 13-14, 2017.

Track-3 Cell and gene therapy products:

Articles containing or consisting ofhuman cellsor tissues that are intended for implantation,transplantation, infusion, or transfer to a human recipient.Gene therapiesare novel and complex products that can offer unique challenges in product development. Hence, ongoing communication between the FDA and stakeholders is essential to meet these challenges.Gene therapy productsare being developed around the world, the FDA is engaged in a number of international harmonization activities in this area.

Examples:Musculoskeletal tissue, skin, ocular tissue, human heart valves;vascular graft, dura mater, reproductive tissue/cells, Stem/progenitor cells,somatic cells, Cells transduced withgene therapyvectors , Combination products (e.g., cells or tissue + device)

Related Conferences:

Track-4 Cellular therapy:

Cellular therapy, also calledlive cell therapy, cellular suspensions, glandular therapy, fresh cell therapy, sick cell therapy,embryonic cell therapy, andorgan therapy- refers to various procedures in which processed tissue from animal embryos, foetuses or organs, is injected or taken orally. Products are obtained from specific organs or tissues said to correspond with the unhealthy organs or tissues of the recipient. Proponents claim that the recipient’s body automatically transports the injected cells to thetarget organs, where they supposedly strengthen them and regenerate their structure. The organs and glands used in cell treatment include brain, pituitary,thyroid, adrenals, thymus, liver,kidney, pancreas, spleen, heart,ovary, testis, and parotid. Several different types of cell or cell extract can be given simultaneously – some practitioners routinely give up to 20 or more at once.

Related Conferences:

3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017, 5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3,2017,International Conference onCell Signalling and Cancer Therapy, Aug 20-22, 2017, Paris, France,7th Annual Conference on Stem Cell and Regenerative Medicine, Aug 04-05, 2016, Paris, France,3rd International Conference & Exhibition onTissue Preservation and Bio banking, June 29-30, 2017, Baltimore, USA.

Track-5 Cancer gene therapy:

Cancer therapiesare drugs or other substances that block the growth and spread ofcancerby interfering with specific molecules (“molecular targets”) that are involved in the growth, progression, and spread ofcancer. Many cancer therapies have been approved by the Food and Drug Administration (FDA) to treat specific types of cancer. The development of targetedtherapiesrequires the identification of good targets that is, targets that play a key role in cancer cell growth and survival. One approach to identify potential targets is to compare the amounts of individualproteinsin cancer cells with those in normal cells.Proteinsthat are present in cancer cells but not normal cells or that are more abundant incancercells would be potential targets, especially if they are known to be involved incell growthor survival.

Related Conferences:

2nd Biotechnology World Convention,London, UK,May 25-27, 2017, ,International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017,9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017, 6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017,8th World Congress and Expo onCell & Stem Cell Research, Orlando, USA, March 20-22, 2017.

Track-6 Nano therapy:

Nano Therapymay be defined as the monitoring, repair, construction and control of human biological systems at themolecular level, using engineerednanodevicesand nanostructures. Basic nanostructured materials, engineeredenzymes, and the many products of biotechnology will be enormously useful in near-term medical applications. However, the full promise ofnanomedicineis unlikely to arrive until after the development of precisely controlled or programmable medical Nano machines andnanorobots.

Related Conferences:

15thWorld Congress on Biotechnology and Biotech Industries Meet March,Rome, Italy,20-21, 2017,2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017, , International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017, 15th Euro Biotechnology Congress, Valencia, Spain, June 05-07, 2017,International Conference onIntegrative Medicine & Nutrition, Dubai, UAE, May11-13, 2017.

Track-7 Skin cell therapy:

Stem cellshave newly become a huge catchphrase in theskincarebiosphere. Skincare specialists are not usingembryonic stem cells; it is impossible to integrate live materials into a skincare product. Instead, scientists are creating products with specialized peptides andenzymesor plantstem cellswhich, when applied topically on the surface, help to protect the human skinstem cellsfrom damage and deterioration or stimulate the skins own stem cells. Currently, the technique is mainly used to save the lives of patients who have third degree burns over very large areas of their bodies.

Related Conferences:

5th International Conference and Exhibition onCell and Gene Therapy,Madrid,Spain,Mar 2-3, 2017, ,International Conference onCell Signalling and Cancer Therapy,Paris, France,Aug 20-22, 2017,2nd Biotechnology World Convention,London, UK,May 25-27, 2017,International Conference on Animal and Human Cell Culture,Jackson Ville, USA, Sep 25-27, 2017,9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017.

Track-8 HIV gene therapy:

Highly activeantiretroviral therapydramatically improves survival inHIV-infected patients. However, persistence of HIV in reservoirs has necessitated lifelong treatment that can be complicated bycumulative toxicities, incomplete immune restoration, and the emergence of drug-resistant escapemutants. Cell and gene therapies offer the promise of preventing progressiveHIV infectionby interfering with HIV replication in the absence of chronicantiviral therapy.

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3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017, International Conference onIntegrative Medicine & Nutrition, Dubai, UAE, May 11-13, 2017, International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017, International Conference onCell Signalling and Cancer Therapy, Aug 20-22, 2017,Paris, France.

Track-9 Diabetes for gene therapy:

Cell therapyapproaches for this disease are focused on developing the most efficient methods for the isolation ofpancreasbeta cells or appropriatestem cells, appropriate location forcell transplant, and improvement of their survival upon infusion. Alternatively, gene andcell therapyscientists are developing methods to reprogram some of the other cells of the pancreas to secreteinsulin. Currently ongoingclinical trialsusing these gene andcell therapystrategies hold promise for improved treatments of type I diabetes in the future. The firstgene therapyapproach to diabetes was put forward shortly after the cloning of theinsulingene. It was proposed that non-insulin producing cells could be made into insulin-producingcells using a suitable promoter and insulin gene construct, and that these substitute cells could restore insulin production in type 1 and some type 2 diabetics.

Related Conferences:

15thWorld Congress on Biotechnology and Biotech Industries Meet,Rome, Italy,March 20-21, 2017, 6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017,8th World Congress and Expo onCell & Stem Cell Research, Orlando, USA, March 20-22, 2017, 14th Asia-Pacific Biotech Congress,Beijing, China,April 10-12, 2017,5th International Conference onIntegrative Biology, London, UK, June 19-21, 2017.

Track-10 Viral gene therapy:

Converting avirusinto a vector Theviral life cyclecan be divided into two temporally distinct phases: infection and replication. Forgene therapyto be successful, an appropriate amount of a therapeutic gene must be delivered into the target tissue without substantial toxicity. Eachviral vectorsystem is characterized by an inherent set of properties that affect its suitability for specific gene therapy applications. For some disorders, long-term expression from a relatively small proportion of cells would be sufficient (for example, genetic disorders), whereas otherpathologiesmight require high, but transient,gene expression. For example, gene therapies designed to interfere with a viral infectious process or inhibit the growth ofcancer cellsby reconstitution of inactivated tumour suppressor genes may require gene transfer into a large fraction of theabnormal cells.

Related Conferences:

Track-11 Stem cell therapies:

Stem cells have tremendous promise to help us understand and treat a range of diseases, injuries and other health-related conditions. Their potential is evident in the use ofblood stem cellsto treat diseases of the blood, a therapy that has saved the lives of thousands of children withleukaemia; and can be seen in the use ofstem cellsfor tissue grafts to treat diseases or injury to the bone, skin and surface of the eye. Some bone, skin andcorneal(eye) injuries and diseases can be treated bygraftingor implanting tissues, and the healing process relies on stem cells within thisimplanted tissue.

Related Conferences:

2nd World Congress on Human Genetics, Chicago, USA, July 24-26, 2017, 2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017, , International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017,2nd International Conference onMolecular Biology,London, UK,June 22-24, 2017, 15th Biotechnology Congress, Baltimore, USA, June 22-23, 2017.

Track-12 Stem cell preservation:

The ability to preserve the cells is critical to theirclinicalapplication. It improves patient access to therapies by increasing the genetic diversity of cells available. In addition, the ability to preserve cells improves the “manufacturability” of acell therapyproduct by permitting the cells to be stored until the patient is ready for administration of the therapy, permitting inventory control of products, and improving management of staffing atcell therapyfacilities. Finally, the ability to preservecell therapiesimproves the safety of cell therapy products by extending the shelf life of a product and permitting completion of safety and quality control testing before release of the product for use. preservation permits coordination between the manufacture of the therapy and patient care regimes.

Related Conferences:

7th Annual Conference on Stem Cell and Regenerative Medicine,Paris,France,Aug 04-05,2016,2nd Biotechnology World Convention,LONDON, UK,May 25-27, 2017, ,International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017,9th International Conference onCancer Genomics, Chicago, USA, May 29-31, 2017, 3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017.

Track-13 Stem cell products:

The globalstemcell,Stem cell productsmarket will grow from about $5.6 billion in 2013 to nearly $10.6 billion in 2018, registering a compound annual growth rate (CAGR) of 13.6% from 2013 through 2018.This trackdiscusses the implications ofstemcellresearchand commercial trends in the context of the current size and growth of thepharmaceutical market, both in global terms and analysed by the most important national markets.

Related Conferences:

6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017,8th World Congress and Expo onCell & Stem Cell Research, Orlando, USA, March 20-22, 2017,15thWorld Congress on Biotechnology and Biotech Industries Meet,Rome, Italy,March 20-21, 2017 ,2nd International Conference onGenetic Counselling and Genomic Medicine , Beijing, China,July 10-12, 2017, ,International Conference onClinical and Molecular Genetics, las vegas, USA, April 24-26, 2017.

Track-14 Genetically inherited diseases:

Related Conferences:

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Track-15 Plant stem cells:

Related Conferences:

9th International Conference onGenomics and Pharmacogenomics, Chicago, USA, July 13-14, 2017,7th International Conference onPlant Genomics, Bangkok, Thailand, July 03-05, 2017,15th Euro Biotechnology Congress, Valencia, Spain, June 05-07, 2017,5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3,2017,3rd International Conference & Exhibition onTissue Preservation and Bio banking,Baltimore, USA,June 29-30, 2017.

Track-16 Plant stem cell rejuvenation:

Asplantscannot escape from danger by running or taking flight, they need a special mechanism to withstandenvironmental stress. What empowers them to withstand harsh attacks and preserve life is the stem cell. According to Wikipedia, plantstem cellsnever undergo theagingprocess but constantly create new specialized and unspecialized cells, and they have the potential to grow into any organ, tissue, or cell in the body. The everlasting life is due to the hormones auxin andgibberellin. British scientists found that plant stem cells were much more sensitive toDNAdamage than other cells. And once they sense damage, they trigger death of these cells.

Rejuvenate with Plant Stem Cells.

Detoxifyand release toxins on a cellular level. Nourishyour body with vital nutrients. Regenerateyour cells and diminish the effects of aging.

Related Conferences:

International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017, 14th Asia-Pacific Biotech Congress,Beijing, China,April 10-12, 2017,15th Biotechnology Congress, Baltimore, USA, June 22-23, 2017,3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017,5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017.

Track-17 Clinical trials in cell and gene therapy:

Aclinical trialis a research study that seeks to determine if a treatment is safe and effective. Advancing new cell andgene therapies(CGTs) from the laboratory into early-phaseclinical trialshas proven to be a complex task even for experienced investigators. Due to the wide variety ofCGTproducts and their potential applications, a case-by-case assessment is warranted for the design of each clinical trial.

Objectives:Determine thepharmacokineticsof this regimen by the persistence of modified T cells in the blood of these patients, Evaluate theimmunogenicityof murine sequences in chimeric anti-CEA Ig TCR, Assess immunologic parameters which correlate with the efficacy of this regimen in these patients, Evaluate, in a preliminary manner, the efficacy of this regimen in patients with CEA bearingtumours.

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Track-18 Molecular epigenetics:

Epigeneticsis the study of heritable changes in thephenotypeof a cell or organism that are not caused by its genotype. The molecular basis of anepigeneticprofile arises from covalent modifications of protein andDNAcomponents ofchromatin. The epigenetic profile of a cell often dictates cell fate, as well as mammalian development,agingand disease. Epigenetics has evolved to become the science that explains how the differences in the patterns ofgene expressionin diverse cells or tissues are executed and inherited.

Related Confderences:

5th International Conference onIntegrative Biology, London, UK, June 19-21, 2017,2nd World Congress on Human Genetics, Chicago, USA, July 24-26, 2017,9th International Conference onGenomics and Pharmacogenomics, Chicago, USA, July 13-14, 2017, International Conference onIntegrative Medicine & Nutrition, Dubai, UAE, May11-13, 2017,14th Asia-Pacific Biotech Congress,Beijing, China,April 10-12, 2017.

Track-19 Bioengineering therapeutics:

The goals ofbioengineeringstrategies for targetedcancertherapies are (1) to deliver a high dose of an anticancer drug directly to a cancer tumour, (2) to enhance drug uptake by malignant cells, and (3) to minimize drug uptake by non-malignant cells. In ESRD micro electro mechanical systems andnanotechnologyto create components such as robust silicon Nano pore filters that mimic natural kidney structure for high-efficiency toxin clearance. It also usestissue engineeringto build a miniature bioreactor in which immune-isolated human-derived renal cells perform key functions, such as reabsorption of water and salts.In drug delivery for a leading cause ofblindness, photo-etching fabrication techniques from themicrochipindustry to create thin-film and planar micro devices (dimensions in millionths of meters) with protectivemedicationreservoirs andnanopores(measured in billionths of meters) for insertion in the back of the eye to deliver sustained doses of drug across protective retinalepithelial tissuesover the course of several months.

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6th International Conference onTissue Engineering & Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017,8th World Congress and Expo onCell & Stem Cell Research, Orlando, USA, March 20-22, 2017,15thWorld Congress on Biotechnology and Biotech Industries Meet,Rome, Italy,March 20-21, 2017 ,2nd International Conference onGenetic Counselling and Genomic Medicine ,Beijing, China,July 10-12, 2017, ,International Conference onClinical and Molecular Genetics, Las Vegas, USA, April 24-26, 2017.

Track-20 Advanced gene therapy:

Advanced therapiesare different fromconventional medicines, which are made from chemicals or proteins.Gene-therapymedicines:these contain genes that lead to atherapeuticeffect. They work by inserting ‘recombinant’ genes into cells, usually to treat a variety of diseases, including genetic disorders, cancer or long-term diseases.Somatic-cell therapymedicines:these contain cells or tissues that have been manipulated to change their biological characteristics.Advanced Cell &Gene Therapyprovides guidanceinprocess development, GMP/GTP manufacturing,regulatory affairs, due diligence and strategy, specializing in cell therapy,gene therapy, and tissue-engineeredregenerative medicineproducts.

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2nd Biotechnology World Convention,London, UK,May 25-27, 2017, ,15th Biotechnology Congress, Baltimore, USA, June 22-23, 2017,3rd International Conference onSynthetic Biology, Munich, Germany, July 20-21, 2017,5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017, ,International Conference onCell Signalling and Cancer Therapy,paris, France,Aug 20-22, 2017, International Conference on Animal and Human Cell Culture, Jackson Ville, USA, Sep 25-27, 2017.

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Recommendation and review posted by simmons

NATESTO (testosterone) Nasal Gel CIII | Prescriber Site

On each valid NATESTO prescription or refill, maximum savings is $150 per use, up to 13 uses. Patient is responsible for any balance remaining, and for reporting receipt of this coupon benefit to any insurer, health plan, or other third party who pays for or reimburses any part of the prescription filled using the coupon, as may be required. Patient, pharmacist, and prescriber agree not to seek reimbursement for all or any part of the benefit received by the patient through this offer.

Offer only valid for male patients over age 18 who have private health insurance. Offer not valid for uninsured patients or for patients eligible for Medicaid, Medicare, TRICARE, Veterans Affairs or any other state or federal healthcare program (including state prescription drug programs). Offer good only in USA and void where prohibited by law, taxed, or restricted. Aytu Pharmaceuticals reserves the right to rescind, revoke, or amend this offer without notice. Card is limited to one per person, is not transferable, and cannot be reproduced. This card is not health insurance.

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Recommendation and review posted by Bethany Smith

Deep imaging of bone marrow shows non-dividing stem cells …

a, Hindlimb bone marrow cellularity (n=9 mice for -catulin+/+,n=4 mice for -catulinGFP/+ and n=9 mice for -catulinGFP/GFP genotype) and spleen cellularity (n=6 mice for -catulin+/+,n=4 mice for -catulinGFP/+ and n=6 mice for -catulinGFP/GFP genotype), spleen mass (7 mice for -catulin+/+,n=4 mice for -catulinGFP/+ and n=7 mice for -catulinGFP/GFP genotype). b, White blood cell (WBC), red blood cell (RBC) and platelet (PLT) counts per microliter of peripheral blood from 812 week old -catulin+/+, -catulinGFP/+, and -catulinGFP/GFP mice (n=9 mice/genotype). c,d, Frequencies of mature hematopoietic cells and progenitors in the bone marrow of 812 week old -catulin+/+ and -catulinGFP/GFP mice (Pre-ProB cells were B220+sIgMCD43+CD24; ProB cells were B220+sIgMCD43+CD24+; Pre-B cells were B220+sIgMCD43; common lymphoid progenitors (CLPs) were Linc-kitlowSca1lowCD127+CD135+; common myeloid progenitors (CMPs) were Linc-kit+Sca1CD34+CD16/32; granulocyte-macrophage progenitors (GMPs) were Linc-kit+Sca1CD34+CD16/32+; and megakaryocyte-erythroid progenitors (MEPs) were Linc-kit+Sca1CD34CD16/32 (n=3 mice/genotype). e, Bone marrow CD150+CD48LSK HSC frequency, bone marrow CD150CD48LSK MPP frequency (n=12 mice/genotype in 12 independent experiments), and spleen HSC frequency (n=3 mice/genotype in 3 experiments). f, Percentage of HSCs and whole bone marrow cells that incorporated a 3 day pulse of BrdU in vivo (n=6 -catulin+/+, 9 -catulinGFP/+, and 7 -catulinGFP/GFP 812 week old mice in 3 independent experiments). g, Colony formation by HSCs in methylcellulose cultures (GM means granulocyte-macrophage colonies, GEMM means granulocyte-erythroid-macrophage-megakaryocyte colonies, Mk means megakaryocyte colonies; (n=5 mice/genotype in 5 independent experiments). h, Reconstitution of irradiated mice by 300,000 donor bone marrow cells from 812 week old -catulin+/+, -catulinGFP/+, or -catulinGFP/GFP mice competed against 300,000 recipient bone marrow cells (n=4 donor mice and 16 recipient mice for -catulin+/+, n=3 donor mice and 9 recipient mice for -catulinGFP/+, and n=4 donor mice and 18 recipients for -catulinGFP/GFP in 3 independent experiments). i, Serial transplantation of 3 million WBM cells from primary recipient mice shown in panel d into irradiated secondary recipient mice (n=4 primary -catulin+/+ recipients were transplanted into 17 secondary recipients and n=6 primary -catulinGFP/GFP recipients were transplanted into 20 secondary recipients). All data represent means.d. The statistical significance of differences between genotypes was assessed using Students t-tests or ANOVAs. None were significant.

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Deep imaging of bone marrow shows non-dividing stem cells …

Recommendation and review posted by simmons

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Recommendation and review posted by simmons

stem cells – The ALS Association

Quick links:

Stem cells are cells that have the ability to divide for indefinite periods in culture and give rise to multiple specialized cell types. They can develop into blood, bone, brain, muscle, skin and other organs.

Stem cells occur naturally, or they can be created from other kinds of cells. Stem cells form during development (embryonic stem cells). They are also present in small numbers in many different tissues (endogenous adult stem cells). Most significantly, stem cells can be created from skin cells (induced pluripotent stem cells, or iPS cells).

iPS cells have emerged in recent years as by far the most significant source of stem cells for ALS research. A simple skin biopsy provides the skin cells (fibroblasts). These cells are treated in a lab dish with a precise cocktail of naturally occurring growth factors that turns back the clock, transforming them back into cells much like those that gave rise to themstem cells.

Embryonic stem cells can be isolated from fertilized embryos less than a week old. Before the development of iPS cells, human embryos were the only source of human stem cells for research or therapeutic development. The ethical issues involved hindered development of this research. Most stem cell research in ALS is currently focused on iPS cells, which are not burdened with these issues.

Stem cells are being used in many laboratories today for research into the causes of and treatments for ALS. Most commonly, iPS cells are converted into motor neurons, the cells affected in ALS. These motor neurons can be grown in a dish and studied to determine how the disease develops. They can also be used to screen for drugs that can alter the disease process. The availability of large numbers of identical neurons, made possible by iPS cells, has dramatically expanded the ability to search for new treatments.

Because iPS cells can be made from skin samples of any person, researchers have begun to make individual cell lines derived from dozens of individuals with ALS. Comparing the motor neurons derived from these cells lines allows them to ask what is common, and what is unique, about each case of ALS, leading to further understanding of the disease process.

Stem cells may also have a role to play in treating the disease. The most likely application may be to use stem cells or cells derived from them to deliver growth factors or protective molecules to motor neurons in the spinal cord. Clinical trials of such stem cell transplants are in the early stages, but appear to be safe.

While the idea of replacing dying motor neurons with new ones derived from stem cells is appealing, there are multiple major hurdles that must be overcome before it is a possibility. Perhaps the most challenging is coaxing the implanted cells to grow the long distances from the spinal cord, where they would be implanted, out to the muscle, where they cause contraction. While work is ongoing to overcome these challenges, it is likely that providing support and protection to surviving neurons represents a more immediate possible form of stem cell therapy.

The presence of endogenous stem cells in the adult brain and spinal cord may provide an alternative to transplantation, eliminating the issues of tissue rejection. If there were a way to stimulate resident stem cells to replace dying cells the limitations of transplantation could be overcome. Small biotech companies are pursuing this direction in the hope of finding therapeutic compounds that will do this. Further research into molecules and genes that govern cell division, migration and specialization is needed, ultimately leading to new drug targets and therapies for ALS.

The mechanism of motor neuron death in ALS remains unclear. It is not certain that transplanted stem cells would be resistant to the same source(s) of damage that causes motor neurons to die and stem cells may need to be modified to protect against the toxic environment. There is also the potential that cultured stem cells used in transplant medicine could face rejection by the body’s immune system.

The NeuralStem trial demonstrated the safety of transplanting human embryonic stem cells into the spinal cord of people with ALS. As of late 2014, a larger trial of the same technique is underway, to determine whether treatment can improve function or slow decline. More information can be found here: http://www.alsconsortium.org/news_neuralstem_phaseII_first_patient.php

The BrainStorm trial is underway as of late 2014, examining the safety and efficacy of transplantation of autologous mesenchymal stem cells secreting neurotrophic factors. These stem cells are extracted from the patients own bone marrow, then treated to increase their production of protective factors, and then injected into muscle and the region surrounding the spinal cord. More information can be found here: http://www.alsconsortium.org/

Read The ALS Associations Statement on Stem Cell Research.

Last update: 08/26/14

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stem cells – The ALS Association

Recommendation and review posted by sam

Hypopituitarism.

Hypopituitarism is the partial or complete insufficiency of anterior pituitary hormone secretion and may result from pituitary or hypothalamic disease. The reported incidence (12-42 new cases per million per year) and prevalence (300-455 per million) is probably underestimated if its occurrence after brain injuries (30-70% of cases) is considered. Clinical manifestations depend on the extent of hormone deficiency and may be non specific, such as fatigue, hypotension, cold intolerance, or more indicative such as growth retardation or impotence and infertility in GH and gonadotropin deficiency, respectively.A number of inflammatory, granulomatous or neoplastic diseases as well as traumatic or radiation injuries involving the hypothalamic-pituitary region can lead to hypopituitarism. Several genetic defects are possible causes of syndromic and non syndromic isolated/multiple pituitary hormone deficiencies. Unexplained gonadal dysfunctions, developmental craniofacial abnormalities, newly discovered empty sella and previous pregnancy-associated hemorrhage or blood pressure changes may be associated with defective anterior pituitary function.The diagnosis of hypopituitarism relies on the measurement of basal and stimulated secretion of anterior pituitary hormones and of the hormones secreted by pituitary target glands. MR imaging of the hypothalamo-pituitary region may provide essential information. Genetic testing, when indicated, may be diagnostic.Secondary hypothyroidism is a rare disease. The biochemical diagnosis is suggested by low serum FT4 levels and inappropriately normal or low basal TSH levels that do not rise normally after TRH. L-thyroxine is the treatment of choice. Before starting replacement therapy, concomitant corticotropin deficiency should be excluded in order to avoid acute adrenal insufficiency. Prolactin deficiency is also very rare and generally occurs after global failure of pituitary function. Prolactin deficiency prevents lactation. Hypogonadotropic hypogonadism in males is characterized by low testosterone with low or normal LH and FSH serum concentrations and impaired spermatogenesis. Hyperprolactinemia as well as low sex hormone binding globulin concentrations enter the differential diagnosis. Irregular menses and amenorrhea with low serum estradiol concentration (

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Hypopituitarism.

Recommendation and review posted by simmons

Stem cells: What they are and what they do – Mayo Clinic

Stem cells: What they are and what they do Stem cells and derived products offer great promise for new medical treatments. Learn about stem cell types, current and possible uses, ethical issues, and the state of research and practice. By Mayo Clinic Staff

You’ve heard about stem cells in the news, and perhaps you’ve wondered if they might help you or a loved one with a serious disease. You may wonder what stem cells are, how they’re being used to treat disease and injury, and why they’re the subject of such vigorous debate.

Here are some answers to frequently asked questions about stem cells.

Researchers and doctors hope stem cell studies can help to:

Generate healthy cells to replace diseased cells (regenerative medicine). Stem cells can be guided into becoming specific cells that can be used to regenerate and repair diseased or damaged tissues in people.

People who might benefit from stem cell therapies include those with spinal cord injuries, type 1 diabetes, Parkinson’s disease, Alzheimer’s disease, heart disease, stroke, burns, cancer and osteoarthritis.

Stem cells may have the potential to be grown to become new tissue for use in transplant and regenerative medicine. Researchers continue to advance the knowledge on stem cells and their applications in transplant and regenerative medicine.

Test new drugs for safety and effectiveness. Before using new drugs in people, some types of stem cells are useful to test the safety and quality of investigational drugs. This type of testing will most likely first have a direct impact on drug development for cardiac toxicity testing.

New areas of study include the effectiveness of using human stem cells that have been programmed into tissue-specific cells to test new drugs. For testing of new drugs to be accurate, the cells must be programmed to acquire properties of the type of cells to be tested. Techniques to program cells into specific cells continue to be studied.

For instance, nerve cells could be generated to test a new drug for a nerve disease. Tests could show whether the new drug had any effect on the cells and whether the cells were harmed.

Stem cells are the body’s raw materials cells from which all other cells with specialized functions are generated. Under the right conditions in the body or a laboratory, stem cells divide to form more cells called daughter cells.

These daughter cells either become new stem cells (self-renewal) or become specialized cells (differentiation) with a more specific function, such as blood cells, brain cells, heart muscle or bone. No other cell in the body has the natural ability to generate new cell types.

Researchers have discovered several sources of stem cells:

Embryonic stem cells. These stem cells come from embryos that are three to five days old. At this stage, an embryo is called a blastocyst and has about 150 cells.

These are pluripotent (ploo-RIP-uh-tunt) stem cells, meaning they can divide into more stem cells or can become any type of cell in the body. This versatility allows embryonic stem cells to be used to regenerate or repair diseased tissue and organs, although their use in people has been to date limited to eye-related disorders such as macular degeneration.

Adult stem cells. These stem cells are found in small numbers in most adult tissues, such as bone marrow or fat. Compared with embryonic stem cells, adult stem cells have a more limited ability to give rise to various cells of the body.

Until recently, researchers thought adult stem cells could create only similar types of cells. For instance, researchers thought that stem cells residing in the bone marrow could give rise only to blood cells.

However, emerging evidence suggests that adult stem cells may be able to create unrelated types of cells. For instance, bone marrow stem cells may be able to create bone or heart muscle cells. This research has led to early-stage clinical trials to test usefulness and safety in people. For example, adult stem cells are currently being tested in people with neurological or heart disease.

This new technique may allow researchers to use these reprogrammed cells instead of embryonic stem cells and prevent immune system rejection of the new stem cells. However, scientists don’t yet know if altering adult cells will cause adverse effects in humans.

Researchers have been able to take regular connective tissue cells and reprogram them to become functional heart cells. In studies, animals with heart failure that were injected with new heart cells experienced improved heart function and survival time.

Perinatal stem cells. Researchers have discovered stem cells in amniotic fluid in addition to umbilical cord blood stem cells. These stem cells also have the ability to change into specialized cells.

Amniotic fluid fills the sac that surrounds and protects a developing fetus in the uterus. Researchers have identified stem cells in samples of amniotic fluid drawn from pregnant women during a procedure called amniocentesis, a test conducted to test for abnormalities.

More study of amniotic fluid stem cells is needed to understand their potential.

Embryonic stem cells are obtained from early-stage embryos a group of cells that forms when a woman’s egg is fertilized with a man’s sperm in an in vitro fertilization clinic. Because human embryonic stem cells are extracted from human embryos, several questions and issues have been raised about the ethics of embryonic stem cell research.

The National Institutes of Health created guidelines for human stem cell research in 2009. Guidelines included defining embryonic stem cells and how they may be used in research and donation guidelines for embryonic stem cells. Also, guidelines stated embryonic stem cells may only be used from embryos created by in vitro fertilization when the embryo is no longer needed.

The embryos being used in embryonic stem cell research come from eggs that were fertilized at in vitro fertilization clinics but never implanted in a woman’s uterus. The stem cells are donated with informed consent from donors. The stem cells can live and grow in special solutions in test tubes or petri dishes in laboratories.

Although research into adult stem cells is promising, adult stem cells may not be as versatile and durable as are embryonic stem cells. Adult stem cells may not be able to be manipulated to produce all cell types, which limits how adult stem cells can be used to treat diseases.

Adult stem cells also are more likely to contain abnormalities due to environmental hazards, such as toxins, or from errors acquired by the cells during replication. However, researchers have found that adult stem cells are more adaptable than was initially suspected.

.

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Stem cells: What they are and what they do – Mayo Clinic

Recommendation and review posted by simmons

Stripping donor hearts and repopulating them with …

Heart transplants have been around since 1967, but they’re still anything but routine. In an effort to ensure a steady supply of compatible organs, a team of scientists from Massachusetts General Hospital (MGH) is working on ways to create bioengineered human hearts by first stripping donor hearts of cells that could provoke an immune response in a potential recipient, and then using the recipient’s own induced pluripotent stem cells (iPSCs) to generate cardiac muscle cells that can be used to repopulate the heart in an automated bioreactor system.

Every year, 800,000 people worldwide have heart conditions that require a transplant. Unfortunately, there are only enough suitable donor hearts for around 3,500 operations. Part of the reason for this isn’t that there aren’t enough healthy hearts donated to go around, but that a heart needs to be biologically compatible with the recipient.

And even if there is an extremely close tissue match, the recipient’s body will treat still the new heart as alien and attack it. To prevent this tissue rejection, the recipient’s autoimmune system must be suppressed by a battery of pills for a lifetime, combined with another battery of pills to correct the damage caused by suppressing the immune system.

What the MGH team led by Dr Harald Ott is trying to achieve is a way of turning the alien heart into a not-alien one. In other words, to make it as much like the recipient’s original heart from a cellular point of view. This way, the body is less likely to reject it and the follow-up medical regime can be less aggressive.

The MGH approach to essentially take a donor heart, strip it down and rebuild it much as one might strip a house down to its frame and then rebuild it with all-new materials. The heart, like most organs, consists of living cells that are held in place by a connective matrix made of collagen fibers. It’s the living cells that allow the heart to pump blood, but they’re also what spark an immune reaction in the host body, so the idea is to remove the original cells, then replace them in the remaining collagen matrix with cells created from the recipient’s own. Since the new cells are genetically identical to those of the recipient, tissue rejection is less likely.

According to MGH, Dr Ott had already developed a procedure in 2008 that allowed him to remove living cells from organs using a detergent solution. The MGH team then used the leftover extracellular matrix as a scaffold that can then be repopulated with new cells. In this way, they could not only create working rat lungs and kidneys, but also decellularized large-animal hearts, lungs, and kidneys.

The next step was to scale up the method on a whole human heart. This was done by creating iPSCs. The iPSCs are made by using a new method to reprogram skin cells with messenger RNA factors so they revert to an embryonic state.

These all-purpose stem cells can then be induced to become any kind of cell in the human body. In this case, they were turned into cardiac muscle cells, or cardiomyocytes. According to MGH, this method not only is more efficient and allows for creating cells in large enough quantities for clinical use, but it also avoids many regulatory obstacles that more conventional methods come up against.

These cardiac cells were then introduced into 73 decellularized human hearts from donors who were brain dead or had suffered cardiac death. The hearts selected weren’t suitable for transplant, so were used with consent for research purposes. The cells were reseeded into the 3D matrix of the left ventricular wall of the decellularized hearts as thin slices, then as 15 mm fibers, which began to contract on their own within days.

The hearts were then placed for 14 days in an automated bioreactor system developed by the MGH team. This provided the tissues with nourishment in the form of a solution while ventricular pressure and other stressors were applied to exercise them. The researchers say the result was dense regions of iPSC-derived cells that resembled immature cardiac muscle tissue and contracted like heart tissue when subjected to electrical stimulation.

“Regenerating a whole heart is most certainly a long-term goal that is several years away, so we are currently working on engineering a functional myocardial patch that could replace cardiac tissue damaged due to a heart attack or heart failure,” says Jacques Guyette, PhD, of the MGH Center for Regenerative Medicine (CRM). “Among the next steps that we are pursuing are improving methods to generate even more cardiac cells recellularizing a whole heart would take tens of billions optimizing bioreactor-based culture techniques to improve the maturation and function of engineered cardiac tissue, and electronically integrating regenerated tissue to function within the recipient’s heart.”

The team’s results were was published in Circulation Research.

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Stripping donor hearts and repopulating them with …

Recommendation and review posted by simmons

Induction of Pluripotent Stem Cells from Adult Human …

Summary

Successful reprogramming of differentiated human somatic cells into a pluripotent state would allow creation of patient- and disease-specific stem cells. We previously reported generation of induced pluripotent stem (iPS) cells, capable of germline transmission, from mouse somatic cells by transduction of four defined transcription factors. Here, we demonstrate the generation of iPS cells from adult human dermal fibroblasts with the same four factors: Oct3/4, Sox2, Klf4, and c-Myc. Human iPS cells were similar to human embryonic stem (ES) cells in morphology, proliferation, surface antigens, gene expression, epigenetic status of pluripotent cell-specific genes, and telomerase activity. Furthermore, these cells could differentiate into cell types of the three germ layers in vitro and in teratomas. These findings demonstrate that iPS cells can be generated from adult human fibroblasts.

Embryonic stem (ES) cells, derived from the inner cell mass of mammalian blastocysts, have the ability to grow indefinitely while maintaining pluripotency (Evans and Kaufman, 1981andMartin, 1981). These properties have led to expectations that human ES cells might be useful to understand disease mechanisms, to screen effective and safe drugs, and to treat patients of various diseases and injuries, such as juvenile diabetes and spinal cord injury (Thomson etal., 1998). Use of human embryos, however, faces ethical controversies that hinder the applications of human ES cells. In addition, it is difficult to generate patient- or disease-specific ES cells, which are required for their effective application. One way to circumvent these issues is to induce pluripotent status in somatic cells by direct reprogramming (Yamanaka, 2007).

We showed that induced pluripotent stem (iPS) cells can be generated from mouse embryonic fibroblasts (MEF) and adult mouse tail-tip fibroblasts by the retrovirus-mediated transfection of four transcription factors, namely Oct3/4, Sox2, c-Myc, and Klf4 (Takahashi and Yamanaka, 2006). Mouse iPS cells are indistinguishable from ES cells in morphology, proliferation, gene expression, and teratoma formation. Furthermore, when transplanted into blastocysts, mouse iPS cells can give rise to adult chimeras, which are competent for germline transmission (Maherali etal., 2007, Okita etal., 2007andWernig etal., 2007). These results are proof of principle that pluripotent stem cells can be generated from somatic cells by the combination of a small number of factors.

In the current study, we sought to generate iPS cells from adult human somatic cells by optimizing retroviral transduction in human fibroblasts and subsequent culture conditions. These efforts have enabled us to generate iPS cells from adult human dermal fibroblasts and other human somatic cells, which are comparable to human ES cells in their differentiation potential in vitro and in teratomas.

Induction of iPS cells from mouse fibroblasts requires retroviruses with high transduction efficiencies (Takahashi and Yamanaka, 2006). We, therefore, optimized transduction methods in adult human dermal fibroblasts (HDF). We first introduced green fluorescent protein (GFP) into adult HDF with amphotropic retrovirus produced in PLAT-A packaging cells. As a control, we introduced GFP to mouse embryonic fibroblasts (MEF) with ecotropic retrovirus produced in PLAT-E packaging cells(Morita etal., 2000). In MEF, more than 80% of cells expressed GFP (FigureS1). In contrast, less than 20% of HDF expressed GFP with significantly lower intensity than in MEF. To improve the transduction efficiency, we introduced the mouse receptor for retroviruses, Slc7a1 (Verrey etal., 2004) (also known as mCAT1), into HDF with lentivirus. We then introduced GFP to HDF-Slc7a1 with ecotropic retrovirus. This strategy yielded a transduction efficiency of 60%, with a similar intensity to that in MEF.

The protocol for human iPS cell induction is summarized inFigure1A. We introduced the retroviruses containing human Oct3/4, Sox2, Klf4, and c-Myc into HDF-Slc7a1 (Figure1B; 8 105 cells per 100 mm dish). The HDF derived from facial dermis of 36-year-old Caucasian female. Six days after transduction, the cells were harvested by trypsinization and plated onto mitomycin C-treated SNL feeder cells (McMahon and Bradley, 1990) at 5 104 or 5 105 cells per 100 mm dish. The next day, the medium (DMEM containing 10% FBS) was replaced with a medium for primate ES cell culture supplemented with 4 ng/ml basic fibroblast growth factor (bFGF).

Induction of iPS Cells from Adult HDF

(A) Time schedule of iPS cell generation.

(B) Morphology of HDF.

(C) Typical image of non-ES cell-like colony.

(D) Typical image of hES cell-like colony.

(E) Morphology of established iPS cell line at passage number 6 (clone 201B7).

(F) Image of iPS cells with high magnification.

(G) Spontaneously differentiated cells in the center part of human iPS cell colonies.

(HN) Immunocytochemistry for SSEA-1 (H), SSEA-3 (I), SSEA-4 (J), TRA-1-60 (K), TRA-1-81 (L), TRA-2-49/6E (M), and Nanog (N). Nuclei were stained with Hoechst 33342 (blue). Bars = 200 m (BE, G), 20 m (F), and 100 m (HN).

Approximately two weeks later, some granulated colonies appeared that were not similar to hES cells in morphology (Figure1C). Around day 25, we observed distinct types of colonies that were flat and resembled hES cell colonies (Figure1D). From 5 104 fibroblasts, we observed 10 hES cell-like colonies and 100 granulated colonies (7/122, 8/84, 8/171, 5/73, 6/122, and 11/213 in six independent experiments, summarized in Table S1). At day 30, we picked hES cell-like colonies and mechanically disaggregated them into small clumps without enzymatic digestion. When starting with 5 105 fibroblasts, the dish was nearly covered with more than 300 granulated colonies. We occasionally observed some hES cell-like colonies in between the granulated cells, but it was difficult to isolate hES cell-like colonies because of the high density of granulated cells. The nature of the non-hES-like cells remains to be determined.

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Induction of Pluripotent Stem Cells from Adult Human …

Recommendation and review posted by sam

A gay Gene – Is Homosexuality Inherited Assault On Gay …

Historians of homosexuality will judge much twentieth-century “science” harshly when they come to reflect on the prejudice, myth, and downright dishonesty that litter modern academic research on sexuality. Take, for example, the lugubrious statements of-once respected investigators. Here is Sandor Feldman, a well-known psychotherapist, in 1956:

Or consider the remarks of the respected criminologist Herbert Hendin:

The notion of the homosexual as a deeply disturbed deviant in need of treatment was the orthodoxy until only recently. Bernard Oliver, Jr., a psychiatrist specializing in sexual medicine, wrote in 1967 that Dr. Edmond Bergler feels that the homosexual’s real enemy is not so much his perversion but [sic] ignorance of the possibility that he can be helped, plus his psychic masochism which leads him to shun treatment….

There is good reason to believe now, more than ever before, that many homosexuals can be successfully treated by psychotherapy, and we should encourage homosexuals to seek this help.[3]

Such views about the origin of homosexual preferences have become part of American political culture as well. When, in 1992, Vice-President Dan Quayle offered the view that homosexuality “is more of a choice than a biological situation…. It is a wrong choice,”[4] he merely reasserted the belief that homosexuality reflected psychological conditioning with little biological basis, and certainly without being influenced by a person’s biological inheritance.

And now we have the much publicized spectacle–Time magazine has taken up the story in a dramatic feature entitled “Search for a Gay Gene”[5] –of homosexuality’s origins being revealed in the lowly fruit fly, Drosophila.[6] Males and females of this, one has to admit, rather distant relation adopt courtship behavior that has led two researchers at the US National Institutes of Health to draw extravagant parallels with human beings.

Shang-Ding Zhang and Ward F. Odenwald found that what they took to be homosexual behavior among male fruit flies–touching male partners with forelegs, licking their genitalia, and curling their bodies to allow genital contact–could be induced by techniques that abnormally activated a gene called w (for “white,” so called because of its effect on eye color). Widespread activation (or “expression”) of the white gene in Drosophila produced male-to-male rituals that took place in chains or circles of five or more flies. If female fruit flies lurked nearby, male flies would only rarely be tempted away from their male companions. These findings, which have apparently been reproduced by others, have led the investigators to conclude that “w misexpression has a profound effect on male sexual behavior.”

Zhang and Odenwald go on to speculate that the expression of w could lead to severe shortages of serotonin, an important chemical signal that enables nerve cells to communicate with one another. The authors conjecture that mass activation of w diminishes brain serotonin by promoting its use elsewhere in the body. Indeed, cats, rabbits, and rats all show some elements of “gay” behavior when their brain serotonin concentrations fall. Intriguing and, you might think, convincing evidence.

Yet, although w is found in modified form in human beings, it is a huge (and, it seems to me, a dangerous) leap to extrapolate observations from fruit flies to humans. In truth, when the recent data are interpreted literally we find that (a) the w gene induces male group sex behavior in highly ritualized linear or circular configurations, and (b) while these tend more toward homosexual than straight preferences, they are truly bisexual (as pointed out by Larry Thompson in Time). Zhang and Odenwald force their experimental results with fruit flies to fit their preconceived notions of homosexuality. How simplistic it seems to equate genital licking in Drosophila with complex individual and social homosexual behavior patterns in humans. Can notions of homosexuality apply uniformly across the biological gulf that divides human beings and insects? Such arguments by analogy seem hopelessly inadequate.

By contrast, the work of Simon LeVay, Dean Hamer, and a small group of researchers concerned to distinguish biological and genetic influences on sexual behavior has discredited much of the loose rhetoric that has been used about homosexuality. In August 1991, LeVay, a neuroscientist who now directs the Institute of Gay and Lesbian Education in southern California, published in the magazine Science findings from autopsies of men and women of known sexual preference. He found that a tiny region in the center of the brain–the interstitial nucleus of the anterior hypothalamus (INAH) 3–was, on average, substantially smaller in nineteen gay men who died from AIDS than among sixteen heterosexual men.[7]

The observation that the male brain could take two different forms, depending on one’s sexual preference, was a stunning discovery. The hypothalamus-a small, intricate mass of cells lying at the base of the brain-was long believed to have a role in sexual behavior, but direct evidence that it did so was weak. Yet LeVay expressed caution. Although his data showed that human sexual preference “is amenable to study at the biological level,” he noted that it was impossible to be certain whether the anatomical differences between the brains of gay and straight men were a cause or a consequence of their preference.[8]

In the thirteen persuasive essays that make up The Sexual Brain, LeVay takes account of the current bio-behavioral controversy over the science of sex. From the union of wiry sperm and bloated ovum to the child-rearing practices of mammals and humans, for which mothers are largely responsible, he writes (metaphorically), the “male is little more than a parasite who takes advantage of [the female’s] dedication to reproduction.” He goes on to draw from a wide range of sources to support his contentious assertion that “there are separate centers within the hypothalamus for the generation of male-typical and female-typical sexual behavior and feelings.” He argues that a connection–the details of which remain mysterious–between brain and behavior exists through hormones such as testosterone.

The most convincing evidence he puts forward to support his view comes from women with congenital adrenal hyperplasia. This condition, in which masculine characteristics, such as androgenized genitalia, including clitoral enlargement and partially fused labia, become pronounced in women, is caused by excessive testosterone production and leads, in adulthood, to an increased frequency of lesbianism affecting up to half of all the women who have the condition. The theory, still unproven, that is proposed to explain these behavioral effects of hormones is that one or more chemical signals act during a brief early critical period in the development of most males to alter permanently both the brain and the pattern of their later adult behavior. Unless this hormonal influence is switched on, a female pattern of development will follow automatically.

What might be the origin of biological differences underlying male sexual preference? In 1993 Dean Hamer and his colleagues at the National Cancer Institute discovered a preliminary but nevertheless tantalizing clue.[9] Hamer began his painstaking search for a genetic contribution to sexual behavior by studying the rates of homosexuality among male relatives of seventy-six known gay men. He found that the incidence of homosexual preference in these family members was strikingly higher (13.5 percent) than the rate of homosexuality among the whole sample (2 percent). When he looked at the patterns of sexual orientation among these families, he discovered more gay relatives on the maternal side. Homosexuality seemed, at least, to be passed from generation to generation through women.

Maternal inheritance could be explained if there was a gene influencing sexual orientation on the X chromosome, one of the two human sex chromosomes that bear genes determining the sex of offspring.[10] Men have both X and Y chromosomes, while women have two X chromosomes. A male sex-determining gene, called SRY, is found on the Y chromosome. Indeed, the Y chromosome is the most obvious site for defining male sexuality since it is the only one of the forty-six human chromosomes to be found in men alone. The SRY gene is the most likely candidate both to turn on a gene that prevents female development and to trigger testosterone production. Since the female has no Y chromosome, she lacks this masculinizing gene. In forty pairs of homosexual brothers, Hamer and his team looked for associations between the DNA on the X chromosome and the homosexual trait. They found that thirty-three pairs of brothers shared the same five X chromosomal DNA “markers,” or genetic signatures, at a region near the end of the long arm of the X chromosome designated Xq28.[11] The possibility that this observation could have occurred by chance was only 1 in 10,000.

LeVay takes a broad philosophical perspective in his discussion of human sexuality by placing his research in the context of animal evolution. Hamer, on the other hand, has written, with the assistance of the journalist Peter Copeland, a more focused popular account of his research. He conceived his project after reflecting on a decade of laborious research on yeast genes. Although the project was approved by the National Institutes of Health after navigating a labyrinthine course through government agencies, it remained rather meagerly funded.

Taken together, the scientific papers of both LeVay and Hamer and the books that their first reports have now spawned[12] make a forceful but by no means definitive case for the view that biological and genetic influences have an important–perhaps even decisive–part in determining sexual preference among males. LeVay writes, for example, that “…the scientific evidence presently available points to a strong influence of nature, and only a modest influence of nurture.” But there is no broad scientific agreement on these findings. They have become mired in a quasi-scientific debate that threatens to let obscurantism triumph over inquiry. What happened?

To begin with, we must ask what LeVay and Hamer have not shown. LeVay has found no proof of any direct link between the size of INAH 3 and sexual behavior. Size differences alone prove nothing. He was also unable to exclude the possibility that AIDS has an influence on brain structure, although this seemed unlikely, since six of the heterosexual men he studied also had AIDS. Moreover, Hamer did not find a gene for homosexuality; what he discovered was data suggesting some influence of one or more genes on one particular type of sexual preference in one group of people. Seven pairs of brothers did not have the Xq28 genetic marker, yet these brothers were all gay. Xq28 is clearly not a sine qua non for homosexuality; it is neither a necessary nor a sufficient cause by itself.

And what about women? Although the genitalia of women as well as men are clearly biologically determined, no data exist to prove a genetic link, or a link based on brain structure, with female sexual preferences, whether heterosexual or homosexual. Finally, neither study has been replicated by other researchers, the necessary standard of scientific proof. Indeed, there is every reason to suppose that the INAH 3 data will be extremely difficult to confirm. Only a few years ago INAH 1 (located close to INAH 3) was also thought to be larger in men than in women. Two groups, including LeVay’s, have failed to reproduce this result.

Most of these limitations are clearly acknowledged by both LeVay and Hamer in their original scientific papers and are reinforced at length in their books. But reactions to their findings have nevertheless been harshly critical. For instance, after pointing out several potential weaknesses in Hamer’s study and criticizing his decision to publish in Science at a time when gay “lives are at stake,” two biologists, Anne Fausto-Sterling and Evan Balaban, asked “whether it might not have been prudent for the authors and the editors of Science to have waited until more of the holes in the study had been plugged….”[13] Fortunately, their somewhat hysterical reaction has been followed by more careful comment by other scientists.[14]

Lack of prudence also characterized the response in the press. In London, the conservative Daily Telegraph ran the clumsy headline, “Claim that homosexuality is inherited prompts fears that science could be used to eradicate it.” Another story began, “A lot of mothers are going to feel guilty,” while another was entitled “Genetic tyranny.”

These headlines are part of the popular rhetoric about DNA, which supposes that a gene represents an irreducible and immutable unit of the human self. The correlation between a potentially active gene and a behavior pattern is assumed to indicate cause and effect. Was Hamer himself guilty of over-interpretation? In his original paper, he went to extraordinary lengths to qualify his findings. He and his co-authors offer no fewer than ten statements advising a cautious reading of their data, and they note that “replication and confirmation of our results are essential.” Neither the hyperbolic press response with its relentless message of genetic determinism nor the ill-judged scientific criticism was appropriate.

Nevertheless, there are three conceptual issues raised by these reports –namely, heritability, sexual categorization, and the meaning of the phrase “biological basis of behavior” –which have been largely ignored in the scramble to publish instant analyses of the findings of LeVay and Hamer, among others.

Heritability is a measure of the resemblance between relatives; it is expressed as the proportion of variability in an observable characteristic that can be attributed to genetic factors. Eye color, for example, is 100 percent heritable, whereas we know that most behavioral traits have genetic contributions of well below 50 percent. Heritability is a quarrelsome issue among geneticists, and its proportional value is often quoted without the necessary qualifications. Variation in any trait is accounted for by the influence of genes (including, importantly, the interaction among genes), environment (the family and one’s wider life experience), and the interaction between one or more genes and one or more environmental variables. The standard measure of heritability is the sum of all genetic influences, and it ignores potentially complex interactions–for example, the influence of the family milieu on the behavioral expression of a gene influencing sexual preference. The most common error made by those who discuss genetic contributions to behavior is to forget that heritability is a property only of the population under study at one particular time. It cannot be generalized to characterize the behavior itself.

When we apply these considerations to Hamer’s data, we make a surprising discovery. If we accept his own hypothesis of the relation between the Xq28 marker and the behavioral trait, the maximum heritability of homosexuality in the group he studied is 67 percent, which may seem a remarkably high figure. Yet this group was a particularly selected one: the seventy-six study participants openly acknowledged being gay, and had volunteered for the study. What Hamer’s results do not tell us is what the influence of the Xq28 marker in the general population might be. He infers from various mathematical calculations “that Xq28 plays some role in about 5 to 30 percent of gay men.” But he admits that this is merely a preliminary estimate and that accurate measuring of Xq28 heritability in the general population remains to be done. In fact, a frequent criticism of Hamer’s Science paper was that he did not measure the incidence of Xq28 markers among heterosexual brothers of gay sibling pairs. Without this information, it is impossible to guess the influence of any genes that might be located at Xq28. Their effects will be unpredictable at best, and any interaction with the environment will assume critical importance.

At this point, science inches uneasily toward dogma and diatribe. Hamer cites Richard Lewontin’s Not in Our Genes[15] as one of his early inspirations to change the direction of his research. Hamer writes that he

knew that [Lewontin] had criticized the idea that behavior is genetic, arguing instead that it is a product of class-based social structures….Why was Lewontin, a formidable geneticist, so determined not to believe that behavior could be inherited? He couldn’t disprove the genetics of behavior in a lab, so he wrote a political polemic against it.

Indeed, Lewontin has frequently provided cogent arguments against the view that heritability can help delineate the effects of genes on human behavior.[16] He has described the separation of behavioral variation into genetic and environmental contributions and the interaction between the two as “illusory.”[17] For him and his co-writers, such a model “cannot produce information about causes of phenotypic difference,” i.e., differences in observable physical and mental traits. The precise meaning of heritability forces the inevitable conclusion, Lewontin has written, that whatever proportion is quoted, it “is nearly equivalent to no information at all for any serious problem in human genetics.”

Imagine Dean Hamer’s astonishment, therefore, when he received a letter from Richard Lewontin in 1992. A Harvard professor teaching genetics and behavior had invited Hamer to submit a pamphlet describing his research as an example of “conceptual advances” in “modern behavior genetic studies.” He had willingly complied, but only later discovered that it had been ruled “scientifically unacceptable” by Ruth Hubbard, an emeritus professor at the Harvard Biological Laboratories deeply skeptical about determinism. In his letter, Hamer writes, Lewontin

went on to theorize that human behaviors must be “very, very far from the genes” because “there are some at least that we know for sure are not influenced by genes as, for example, the particular language one speaks.” That made about as much sense as saying that since some people eat tacos and some eat hamburgers, there is no biological drive to eat.

Hamer, tongue firmly in cheek, offered to give Lewontin’s students a lecture on how good research into behavior genetics is done. Lewontin accepted. On the day of his scheduled talk, Hamer faced not only Lewontin but also Ruth Hubbard and Evan Balaban (a co-author of the hostile letter later published in Science). Hamer described his methods carefully and stressed that his research could identify only potential genetic influences and not isolate specific genetic causes of behavior. At the end of the lecture, Lewontin indicated that he had no dispute with Hamer after all, and left the classroom without further comment. One wonders from this if Lewontin has modified his views on studying genetic contributions to human behavior.

Although it is true that heritability is only a crude measure of genetic influence, it remains a valuable research tool if, as one scientist has said, the researchers realize that

genetic influence on behavior appears to involve multiple genes rather than one or two major genes, and nongenetic sources of variance are at least as important as genetic factors….This should not be interpreted to mean that genes do not affect human behavior; it only demonstrates that genetic influence on behavior is not due to major-gene effects.[18]

More importantly, one can move beyond the “lump sum” theory of genetic influences to study the way in which genes affect behavior over time, or to discover how a gene influences different but possibly related behaviors, for instance both sexual preference and aggression.

Lewontin also cited the “terrible mischief” that could result from a research program based on heritability as his reason to suggest stopping “the endless search for better methods of estimating useless quantities.”” Hamer agrees that precise genetic determinacy is an impossible goal; his 1993 article for Science on DNA markers also ended with an unusual admonition:

We believe that it would be fundamentally unethical to use [this] information to try to assess or alter a person’s current or future sexual orientation, either heterosexual or homosexual, or other normal attributes of human behavior. Rather, scientists, educators, policy-makers, and the public should work together to ensure that such research is used to benefit all members of society.

If scientists who have opposed research on heritability would accept that it can have, when it is carried out in this spirit, an important place in the study of behavior, that would add much-needed weight to calls to expand, and improve, research on human sexuality.

Although Hamer and LeVay have both expressed cautious confidence in their results, they are evidently uneasy about their own categorizations of men as either gay or straight. Hamer writes that,

In truth, I don’t think that there is such a thing as “the” rate of homosexuality in the population at large. It all depends on the definition, how it’s measured, and who is measured.

Classifying sexuality into homosexual and heterosexual categories may have benefits of simplicity for researchers, but how closely does this division fit the real world? Poorly is the answer. Sexual behavior and styles of life among men and women vary from day to day and year to year, and a conclusion about whether or not sexual experience is characterized as homosexual frequently depends on the definition one uses.[20] The slippery nature of our crude categories should alert us to beware of conclusions about groups labeled as “homosexual” or “heterosexual.”

Moreover, the concept of sexuality itself cannot easily be analyzed. It exists at several levels–chromosomal, genital, brain, preference, gender self-image, gender role, and a range of subtle influences on behavior (hair color, eye color, and many more). Each of these can be grouped together with the others to produce a single measurable component on a scale, devised by Alfred Kinsey in the 1940s, that allegedly shows a person’s degree of homosexual preference. Hamer used this scale somewhat uncritically to categorize his volunteers. Stephen Levine, a medical expert on sexual behavior, has noted that the conflated and crude Kinsey scale “does not do justice to the diversity among homosexual women and men.”[21]

One of Hamer’s severest critics, Anne Fausto-Sterling, a developmental geneticist at Brown University, has tried to extend sexual categories beyond the binary divisions of male and female[(22] She suggests adding three more groups based on “intersex” humans: herms (true hermaphrodites who possess one testis and one ovary), merms (individuals who have testes, no ovaries, but some female genitalia), and ferms (who have ovaries, no testes, but some male characteristics). This attempt to create multiple categories is, however, futile. It tries to systematize the un-systematizable by proposing a neatly divided-up continuum of sexuality, while, in fact, very different and mutually exclusive factors may be at work in particular cases. It is an impossible and intellectually misguided task.

Two major studies examining the historical origins of modern sexual categories show how social groupings that evolve over time can mislead one into supposing that inherent biological classes exist in some unchangeable sense. Michel Foucault chronicled the history of sexual norms by concentrating on the fluid notion of “homosexuality.”[23] He denounced what he called “Freud’s conformism” in taking heterosexuality to be the normal standard in psychoanalysis. He concluded:

We must not forget that the psychological, psychiatric, medical category of homosexuality was constituted from the moment it was characterized–Westphal’s famous article of 1870 on “contrary sexual sensations” can stand as its date of birth[24]–less by a type of sexual relations than by a certain quality of sexual sensibility…. The sodomite had been a temporary aberration; the homosexual was now a species.

This analysis, it seems to me, points to a critical error in the research of both Hamer and LeVay. Both, in spite of their qualifications, adopt the idea of the homosexual as a physical “species” different from the heterosexual. But there are no convincing historical grounds for this view. As Foucault points out, at the time of Plato,

People did not have the notion of two distinct appetites allotted to different individuals or at odds with each other in the same soul; rather, they saw two ways of enjoying one’s pleasure…

The cultural historian Jonathan Katz has recently attacked the naive partitioning of sexual orientation by tracing the dominance of the norm–heterosexuality –throughout history.[25] He provides a convincing argument that the “just-is hypothesis” of heterosexuality–i.e., that the word corresponds to a true behavioral norm–is an “invented tradition.” He shows that the categories of gay and straight are gradually dissolving as notions of the family become more various. Basing his view more on intuition than on sociological evidence, he predicts “the declining significance of sexual orientation.”

The final issue that has confused the interpretation of research into sexuality is the meaning of “biological influence.” Unfortunately, both LeVay and Hamer, in their effort to popularize their findings, ignore the subtlety of this question. As has been noted, LeVay is unambiguous about his own position on biological determinism,

The most promising area for exploration is the identification of genes that influence sexual behavior and the study of when, where, and how these genes exert their effects.

Both researchers ignore the central issue in the debate over nature and nurture. The question is: How do genes get you from a biochemical program that instructs cells to make proteins to an unpredictable interplay of behavioral impulses–fantasy, courtship, arousal, sexual selection–that constitutes “sexuality”? The question remains unresolved. The classic fall-back position is to claim that genes merely provide a basis, at most a predisposition, to a particular behavior. But such statements lack a precise or testable meaning.

Perhaps we are asking the wrong question when we set out to find whether there is a gene for sexual orientation. We know that genes are responsible for the development of our lungs, larynx, mouth, and the speech areas of our brain. And we understand that this complexity cannot be collapsed into the notion of a gene for “talking.” Similarly, what possible basis can there be for concluding that there is a single gene for sexuality, even though we accept that there are genes that direct the development of our penises, vaginas, and brains? This analogy is not to deny the importance of genes, but merely to recast their role in a different conceptual setting, one devoid of dualist prejudice.

The search for a single dominant gene–the “O-GOD” (one gene, one disorder) hypothesis–that would influence a behavioral variant is likely to be fruitless. Many different genes, together with many different environmental factors, will interact in unpredictable ways to guide behavioral preferences. Each component will contribute small quanta of influence. One result of such a quantum theory of behavior is that it makes irrelevant the overstretched speculations of both Hamer and LeVay about why a gene for homosexuality still exists when it apparently has little apparent survival value in evolutionary terms. The quest for a teleological explanation to identify a reason for the existence of a “gay gene” becomes pointless when one understands that there is not now, and never was, a single and final reason for being gay or straight, or having any other identity along the continuum of sexual preference.

Does this complexity, together with an adverse and polarized social milieu, preclude successful research efforts concerning human sexuality? In 1974, Lewontin wrote that reconstruction of man’s genetic past is “an activity of leisure rather than of necessity.”[26] Perhaps so. But, as Robert Plomin argues, the value of studying inheritance in behavior lies in its importance

per se rather than in its usefulness for revealing how genes work. Some of society’s most pressing problems, such as drug abuse, mental illness, and mental retardation, are behavioral problems. Behavior is also a key in health as well as illness, in abilities as well as disabilities, and in the personal pluses of life, such as sense of well-being and the ability to love and work.[27]

What research into human sexuality, then, lies ahead? Dean Hamer has repeated his initial work among male homosexuals in an entirely new group of families and has included a much-needed analysis of women. He has also compared the frequency of the Xq28 marker among pairs of gay siblings and their heterosexual brothers, important control data that he did not acquire the first time around. This work has been submitted to the journal Nature Genetics. Two other teams–one recently formed at the National Institutes of Health and a Canadian group that has reached some preliminary results–are attempting to replicate Hamer’s initial findings. All Hamer will say about his latest data is that they have not discouraged him from continuing with his project.

To track down and sequence the DNA from one or more relevant genes at Xq28, from a total of about two hundred candidates, seems an almost insuperable task. To read the molecular script of DNA involves deciphering millions of constituent elements. Moreover, each gene will have to be studied individually and many more pairs of gay brothers will be needed to achieve this goal. The work will be extremely difficult for a single laboratory to undertake on its own. Hamer’s request for a federally funded center for research into sexuality–a National Institute of Sexual Health–is therefore timely, for the study of differences between the sexes has reached a critical, though admittedly fragmented, stage and a coordinated research program would be valuable.

The concerns of such an institute should be broad. For example, it might have included the recent work reported from Yale which overturns the conventional view that language function is identical for both men and women.[28] By studying which brain areas were activated during various linguistic tasks, the Yale scientists found that women used regions in both their right and left brain cortices in certain instances, while men used only the left side of their brains. If functional brain differences for sophisticated behaviors exist between the sexes, the task for the future would be to link function to structure and to describe how both evolve from a background of genetic and environmental influence.

Inevitably, the idea of biological determinism carries with it the threat of manipulating the genes or the brain in order to adapt to the prevailing norm. As I have noted, Hamer was acutely aware of this possibility when he wrote his paper. But the prospects for pinpointing genetic risk have moved rapidly and worryingly forward with the recent availability of genetic screening techniques for, among other diseases, several cancers, including a small proportion of cancers of the breast, colon, and thyroid. Most such techniques are used without any current prospect for gene therapy or for any other effective treatment of the conditions identified. Geneticists such as Francis Collins, director of the Human Genome Project, have opposed unrestricted and unregulated screening techniques, describing their recent uses as “alarming”[29] because we are “treading into a territory which the genetics community has felt rather strongly is still [in the stage of] research.” Hamer’s fine words opposing genetic manipulation are likely to mean little in the marketplace if his work eventually leads to the isolation of a gene that has an effect on sexual preference, even if it has only a small effect that is present in only a limited number of people. US state legislatures are slowly responding to these issues. Colorado recently became the eleventh state to enact a law preventing information derived from genetic testing to be used in a discriminatory fashion.

In recognition of the emerging risks from dubious applications of preliminary discoveries, NIH launched a Task Force on Genetic Testing in April. The twenty-member committee includes representatives from industry, managed-care organizations, and patient-advocacy groups, and is chaired by Neil A. Holtzman, a professor of pediatrics and health policy at Johns Hopkins University. Far from being a friend to the hyperbolists, Holtzman has written that “physicians should be at the forefront of decrying florid genetic determinism and its dire implications for health and welfare reform.”[30] His committee is charged with performing a two-year study of genetic technologies, which will look specifically at the accuracy, safety, reliability, and social implications of new testing procedures. This move is not without self-interest on the part of the geneticists at the NIH. Members of the US Congressional House Appropriations Committee, which closely monitors NIH spending, have said that they may freeze the Human Genome Project’s $153 million grant if ethics issues are not given close attention.

But sex-based research has already run into political trouble. The Council for Citizens Against Government Waste has charged that some NIMH research is a misuse of taxpayer’s money. Tom Schatz, CCAGW’s president, has criticized twenty such studies, including one involving research into sex offenders. Rex Cowdry, acting director of the National Institute of Mental Health, argues that “for these grants, I think first you have to believe that the factors that motivate and control sexual behavior are worth knowing about…you have to believe that knowing more about how men and women are both similar and different is important.”[31]

With such partisan pressures dominating the future of the research agenda, the circulation of uninformed opinions couched in scholarly prose is a cause for anxiety. In an otherwise superb and iconoclastic critique of the history of heterosexuality, Jonathan Katz ends with a sweeping and badly informed declaration:

Biological determinism is misconceived intellectually, as well as politically loathsome…Contrary to today’s bio-belief, the heterosexual/homosexual binary is not in nature, but is socially constructed, therefore deconstructable.

LeVay and Hamer on the one hand, and Katz, on the other, evidently have taken completely antithetical positions. But Katz’s extreme intellectual reductionism makes him as guilty as the more simplistic biologists and journalists who inflate claims about every new genetic discovery. After convincingly undermining the distinction between gay and straight, he then accepts the naive dualism of nature vs. nurture. It is such attempts as Katz’s to put into opposition forces that are not in opposition which argue so strongly for planned research free from the ideological temptations that he succumbs to. Biological research into sexuality will indeed be misconceived if we assume that we already understand the differences between the sexes. In part the results of that research often contradict any such assumption. Katz demands that “we need to look less to oracles [presumably biological], and trust more in our desires, visions, and political organizing.” But to take this path risks perpetuating a debate based on ignorance rather than one based on evidence.

It is true that the research of Hamer and LeVay presents technical and conceptual difficulties and that their preliminary findings obviously need replication or refutation. Yet their work represents a genuine epistemological break away from the past’s rigid and withered conceptions of sexual preference. The pursuit of understanding about the origins of human sexuality –the quest to find an answer to the question, What does it mean to be gay and/or straight?–offers the possibility of eliminating what can be the most oppressive of cultural forces, the prejudiced social norm.

1 See Perversions: Psychodynamics and Therapy, edited by Sandor Lorand and Michael Balint (Ortolan Press, 1965; first edition, Random House, 1956), p. 75.

2 Quoted in Kenneth Lewes, The Psychoanalytic Theory of Male Homosexuality (Simon and Schuster, 1988), p. 188.

3 See Bernard J. Oliver, Jr., Sexual Deviation in American Society (College and University Press, 1967), p. 146.

4 See Karen de Witt, “Quayle Contends Homosexuality Is a Matter of Choice, Not Biology,” The New York Times, September 14, 1992, p. A17.

5 See Larry Thompson, “Search for a Gay Gene,” Time (June 12, 1995), pp. 60-61.

6 See Shang-Ding Zhang and Ward F. Odenwald, “Misexpression of the White (w) Gene Triggers Male-male Courtship in Drosophila,” Proceedings of the National Academy of Sciences, USA, Vol. 92 (June 6, 1995), pp. 5525-5529.

7 See Simon LeVay, “A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men,” Science (August 30, 1991), pp. 1034-1037.

8 The suprachiasmatic nucleus, also located in the hypothalamus, is larger in homosexual men than in either heterosexual men or women. The anterior commissure of the corpus callosum (a band of tissue that connects the right and left hemispheres of the brain) is also larger in gay men.

9 See Dean H. Hamer et al., “A Linkage Between DNA Markers on the X Chromosome and Male Sexual Orientation,” Science (July 16, 1993), pp. 321-327.

10. The normal complement of human chromosomes is forty-six per individual, two of which are designated sex chromosomes. In the male, the sex chromosomal makeup is XY, while in the female it is XX. If a gene for homosexuality (Xh) was transmitted through the maternal line, one can see how the subsequent offspring would be affected.

(Chart omitted)

Suppose the unaffected female carrier for homosexuality (XXh) produced offspring with a non-Xh male (XY). Half of all female children would be carriers of Xh (like their mothers), while half of all male offspring would carry Xh unopposed by another X. The Xh trait — homosexuality — would then be able to express itself.

11 By chance, one would expect each pair of brothers to share half their DNA. So, assuming that there was no gene for homosexuality, one would expect twenty of the forty pairs of brothers to share the X chromosome marker.

12 LeVay has recently completed a second book in collaboration with Elisabeth Nonas–City of Friends–that surveys gay and lesbian culture; it will be published by MIT Press in November. He is currently working on Queer Science, a study of how scientific research has affected the lives of gays and lesbians.

13 See Anne Fausto-Sterling and Evan Balaban, “Genetics and Male Sexual Orientation,” Science (September 3, 1993), p. 1257.

14 For example, see David Weatherall, Science and the Quiet Art (Norton, 1995) who notes that “these findings should not surprise us. Almost every condition…reveals a complex mixture of nature and nurture,” p. 287.

15 See R.C. Lewontin, S. Rose, and L. J. Kamin, Not in Our Genes (Pantheon, 1984).

16 Lewontin is not a total skeptic about the importance of molecular genetics research in medicine. For instance, he accepts “that some fraction of cancers arise on a background of genetic predisposition.” See R.C. Lewontin, “The Dream of the Human Genome,” The New York Review (May 28, 1992), pp. 31-40.

17 See M. W. Feldman and R. C. Lewontin, “The Heritability Hang-up,” Science (December 19, 1975), pp. 1163-1168.

18 See Robert Plomin, “The Role of Inheritance in Behavior,” Science (April 13, 1990), pp. 183-188.

19 See R.C. Lewontin, “The Analysis of Variance and the Analysis of Causes,” The American Journal of Human Genetics, Vol. 26 (1974), pp. 400-411.

20 For example, in a UK study (see Anne M. Johnson, “Sexual lifestyles and HIV risks,” Nature [December 3, 1992], pp. 410-412), although only 1.4 percent of men reported a male partner during the past five years, 6.1 percent of men reported having experienced some same-gender behavior.

21 See Stephen B Levine, Sexual Life: A Clinician’s Guide (Plenum, 1992). The Kinsey scale has seven levels ranging from exclusively heterosexual (0) to exclusively gay (6). Hamer applied this scale to four aspects of sexuality: self-identification, attraction, fantasy, and behavior.

22 See Anne Fausto-Sterling, “The Five Sexes: Why Male and Female Are Not Enough,” The Sciences (March/April, 1993), pp. 20-24.

23 See Michel Foucault, The History of Sexuality, Vols. One and Two (Vintage, 1990).

24 Dr. K.F.O. Westphal became the first modern author to publish an account of what he described as a “contrary sexual feeling” (Die contrare Sexualempfindung), although the word homosexual was first used in a private letter written by Karl Maria Kertbeny on May 6, 1868. This linguistic history is described in detail by Jonathan Katz (see note 25).

25 See Jonathan Ned Katz, The Invention of Heterosexuality (Dutton, 1995).

26 R.C. Lewontin, “The Analysis of Variance and the Analysis of Causes,” The American Journal of Human Genetics, Vol. 26 (1974), pp. 400-411.

27. Robert Plomin, “The Role of Inheritance in Behavior,” Science (April 13, 1990), pp. 183-188.

28. See Bennett A. Shaywitz et al., “Sex differences in the functional organization of the brain for language,” Nature (February 16, 1995), pp. 607-609.

29 See Gina Kolata, “Tests to Assess Risks for Cancer Raising Questions,” The New York Times (March 27, 1995), p. A1.

30 See Neil A. Holtzman, “Genetics,” Journal of the American Medical Association (April 26, 1995), pp. 1304-1306.

31 See “NIMH’s Cowdry Defends Institute’s Research Against Appropriations Committee, Watchdog Group Criticism,” The Blue Sheet (March 29, 1995), pp. 5-6.

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A gay Gene – Is Homosexuality Inherited Assault On Gay …

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Gene Therapy – Learn Genetics

What Is Gene Therapy?

Explore the what’s and why’s of gene therapy research, includingan in-depth look at the genetic disorder cystic fibrosis and how gene therapy could potentially be used to treat it.

Gene Delivery: Tools of the Trade

Explore the methods for delivering genes into cells.

Space Doctor

You are the doctor! Design and test gene therapy treatments with ailing aliens.

Challenges In Gene Therapy

Researchers hoping to bring gene therapy to the clinic face unique challenges.

Approaches To Gene Therapy

Beyond adding a working copy of a broken gene, gene therapy can also repair or eliminate broken genes.

Gene Therapy Successes

The future of gene therapy is bright. Learn about some of its most encouraging success stories.

Gene Therapy Case Study: Cystic Fibrosis

APA format:

Genetic Science Learning Center. (2012, December 1) Gene Therapy. Retrieved August 05, 2016, from http://learn.genetics.utah.edu/content/genetherapy/

CSE format:

Gene Therapy [Internet]. Salt Lake City (UT): Genetic Science Learning Center; 2012 [cited 2016 Aug 5] Available from http://learn.genetics.utah.edu/content/genetherapy/

Chicago format:

Genetic Science Learning Center. “Gene Therapy.” Learn.Genetics. December 1, 2012. Accessed August 5, 2016. http://learn.genetics.utah.edu/content/genetherapy/.

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Heart – Wikipedia, the free encyclopedia

The heart is a muscular organ in humans and other animals, which pumps blood through the blood vessels of the circulatory system.[1] Blood provides the body with oxygen and nutrients, and also assists in the removal of metabolic wastes. The heart is located in the middle compartment of the mediastinum in the chest.[3]

In humans, other mammals, and birds, the heart is divided into four chambers: upper left and right atria; and lower left and right ventricles.[4][5] Commonly the right atrium and ventricle are referred together as the right heart and their left counterparts as the left heart. Fish in contrast have two chambers, an atrium and a ventricle, while reptiles have three chambers.[5] In a healthy heart blood flows one way through the heart due to heart valves, which prevent backflow.[3] The heart is enclosed in a protective sac, the pericardium, which also contains a small amount of fluid. The wall of the heart is made up of three layers: epicardium, myocardium, and endocardium.[7]

The heart pumps blood through the body. Blood low in oxygen from the systemic circulation enters the right atrium from the superior and inferior venae cavae and passes to the right ventricle. From here it is pumped into the pulmonary circulation, through the lungs where it receives oxygen and gives off carbon dioxide. Oxygenated blood then returns to the left atrium, passes through the left ventricle and is pumped out through the aorta to the systemic circulationwhere the oxygen is used and metabolized to carbon dioxide. In addition the blood carries nutrients from the digestive tract to various organs of the body, while transporting waste to the liver and kidneys. Normally with each heartbeat the right ventricle pumps the same amount of blood into the lungs as the left ventricle pumps to the body. Veins transport blood to the heart and carry deoxygenated blood – except for the pulmonary and portal veins. Arteries transport blood away from the heart, and apart from the pulmonary artery hold oxygenated blood. Their increased distance from the heart cause veins to have lower pressures than arteries.[3] The heart contracts at a resting rate close to 72 beats per minute.Exercise temporarily increases the rate, but lowers resting heart rate in the long term, and is good for heart health.

Cardiovascular diseases (CVD) are the most common cause of death globally as of 2008, accounting for 30% of deaths.[11][12] Of these more than three quarters follow coronary artery disease and stroke.[11] Risk factors include: smoking, being overweight, little exercise, high cholesterol, high blood pressure, and poorly controlled diabetes, among others.[13] Diagnosis of CVD is often done by listening to the heart-sounds with a stethoscope, ECG or by ultrasound.[3] Specialists who focus on diseases of the heart are called cardiologists, although many specialties of medicine may be involved in treatment.[12]

The human heart is situated in the middle mediastinum, at the level of thoracic vertebrae T5-T8. A double-membraned sac called the pericardium surrounds the heart and attaches to the mediastinum.[15] The back surface of the heart lies near the vertebral column, and the front surface sits behind to the sternum and rib cartilages.[7] The upper part of the heart is the attachment point for several large blood vessels – the venae cavae, aorta and pulmonary trunk. The upper part of the heart is located at the level of the third costal cartilage.[7] The lower tip of the heart, the apex, lies to the left of the sternum (8 to 9cm from the midsternal line) between the junction of the fourth and fifth ribs near their articulation with the costal cartilages.[7]

The largest part of the heart is usually slightly offset to the left side of the chest (though occasionally it may be offset to the right) and is felt to be on the left because the left heart is stronger and larger, since it pumps to all body parts. Because the heart is between the lungs, the left lung is smaller than the right lung and has a cardiac notch in its border to accommodate the heart.[7] The heart is cone-shaped, with its base positioned upwards and tapering down to the apex.[7] An adult heart has a mass of 250350 grams (912oz).[16] The heart is typically the size of a fist: 12cm (5in) in length, 8cm (3.5in) wide, and 6cm (2.5in) in thickness.[7] Well-trained athletes can have much larger hearts due to the effects of exercise on the heart muscle, similar to the response of skeletal muscle.[7]

The heart has four chambers, two upper atria, the receiving chambers, and two lower ventricles, the discharging chambers. The atria open into the ventricles via the atrioventricular valves, present in the atrioventricular septum. This distinction is visible also on the surface of the heart as the coronary sulcus. There is an ear-shaped structure in the upper right atrium called the right atrial appendage, or auricle, and another in the upper left atrium, the left atrial appendage. The right atrium and the right ventricle together are sometimes referred to as the right heart. Similarly, the left atrium and the left ventricle together are sometimes referred to as the left heart. The ventricles are separated from each other by the interventricular septum, visible on the surface of the heart as the anterior longitudinal sulcus and the posterior interventricular sulcus.

The cardiac skeleton is made of dense connective tissue and this gives structure to the heart. It forms the atrioventricular septum which separates the atria from the ventricles, and the fibrous rings which serve as bases for the four heart valves.[19] The cardiac skeleton also provides an important boundary in the heart’s electrical conduction system since collagen cannot conduct electricity. The interatrial septum separates the atria and the interventricular septum separates the ventricles.[7] The interventricular septum is much thicker than the interatrial septum, since the ventricles need to generate greater pressure when they contract.[7]

The heart, showing valves, arteries and veins. The white arrows shows the normal direction of blood flow.

The heart has four valves, which separate its chambers.[7] The valves ensure blood flows in the correct direction through the heart and prevents backflow. Each valve consists of two to three cusps. The valves between the atria and ventricles connected to cartilaginous strings called chordae tendinae which in turn connect to muscles on the heart wall called papillary muscles.

The valves between the atria and ventricles are called the atrioventricular valves. Between the right atrium and the right ventricle is the tricuspid valve. The tricuspid valve has three cusps, which connect to chordae tendinae and three papillary muscles named the anterior, posterior, and septal muscles, after their relative positions. The mitral valve lies between the left atrium and left ventricle. It is also known as the bicuspid valve due to its having two cusps, an anterior and a posterior cusp. These cusps are also attached via chordae tendinae to two papillary muscles projecting from the ventricular wall.

The papillary muscles extends from the walls of the heart to the chordae tendinae of valves. These muscles prevent the valves from falling too far back when they close.[22]During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight. As the heart chambers contract, so do the papillary muscles. This creates tension on the chordae tendineae, helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria.[7][g]

Two additional semilunar valves sit at the exit of each of the ventricles. The pulmonary valve is located at the base of the pulmonary artery. This has three cusps which are not attached to any papillary muscles. When the ventricle relaxes blood flows back into the ventricle from the artery and this flow of blood fills the pocket-like valve, pressing against the cusps which close to seal the valve. The semilunar aortic valve is at the base of the aorta and also is not attached to papillary muscles. This too has three cusps which close with the pressure of the blood flowing back from the aorta.[7]

The right heart consists of two chambers, the right atrium and the right ventricle, separated by a valve, the tricuspid valve.[7]

The right atrium receives blood almost continuously from the body’s two major veins, the superior and inferior venae cavae. A small amount of blood from the coronary circulation also drains into the right atrium via the coronary sinus, which is immediately above and to the middle of the opening of the inferior vena cava.[7] In the wall of the right atrium is an oval-shaped depression known as the fossa ovalis, which is a remnant of an opening in the fetal heart known as the foramen ovale.[7] Most of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface has prominent ridges of pectinate muscles, which are also present in the right atrial appendage.[7]

The right atrium is connected to the right ventricle by the tricuspid valve.[7] The walls of the right ventricle are lined with trabeculae carneae, ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the lower part of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle.[7] The right ventricle tapers into the pulmonary trunk, into which it ejects blood when contracting. The pulmonary trunk branches into the left and right pulmonary arteries that carry the blood to each lung. The pulmonary valve lies between the right lung and the pulmonary trunk.[7]

The left heart has two chambers: the left atrium, and the left ventricle, separated by the mitral valve.[7]

The left atrium receives oxygenated blood back from the lungs via one of the four pulmonary veins. The left atrium has an outpouching called the left atrial appendage. Like the right atrium, the left atrium is lined by pectinate muscles.[23] The left atrium is connected to the left ventricle by the mitral valve.[7]

The left ventricle is much thicker as compared with the right, due to the greater force needed to pump blood to the entire body. Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The left ventricle pumps blood to the body through the aortic valve and into the aorta. Two small openings above the aortic valve carry blood to the heart itself, the left main coronary artery and the right coronary artery.[7]

The heart wall is made up of three layers: the inner endocardium, middle myocardium and outer epicardium. These are surrounded by a double-membraned sac called the pericardium.

The innermost layer of the heart is called the endocardium. It is made up of a lining of simple squamous epithelium, and covers heart chambers and valves. It is continuous with the endothelium of the veins and arteries of the heart, and is joined to the myocardium with a thin layer of connective tissue.[7] The endocardium, by secreting endothelins, may also play a role in regulating the contraction of the myocardium.[7]

The middle layer of the heart wall is the myocardium, which is the cardiac muscle a layer of involuntary striated muscle tissue surrounded by a framework of collagen. The cardiac muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart, with the outer muscles forming a figure 8 pattern around the atria and around the bases of the great vessels, and inner muscles formining a figure 8 around the two ventricles and proceed toward the apex. This complex swirling pattern allows the heart to pump blood more effectively.[7]

There are two types of cells in cardiac muscle: muscle cells which have the ability to contract easily, and pacemaker cells of the conducting system. The muscle cells make up the bulk (99%) of cells in the atria and ventricles. These contractile cells are connected by intercalated discs which allow a rapid response to impulses of action potential from the pacemaker cells. The intercalated discs allow the cells to act as a syncytium and enable the contractions that pump blood through the heart and into the major arteries.[7] The pacemaker cells make up 1% of cells and form the conduction system of the heart. They are generally much smaller than the contractile cells and have few myofibrils which gives them limited contractibility. Their function is similar in many respects to neurons.[7] Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed rate spreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart.[7]

The pericardium surrounds the heart. It consists of two membranes: an inner serous membrane called the epicardium, and an outer fibrous membrane. Blood vessels and nerves reach the cardiac muscle from the epicardium.[7] These help influence the heart rate.[7] These enclose the pericardial cavity which contains the pericardial fluid that lubricates the surface of the heart.

Heart tissue, like all cells in the body, need to be supplied with oxygen, nutrients and a way of removing metabolic wastes. This is achieved by the coronary circulation, which includes arteries, veins, and lymphatic vessels, Blood circulates through the coronary circulation cyclically, in peaks and troughs relating to the heart muscle’s relaxation or contraction.[7]

Heart tissue receives blood from two arteries which arise just above the aortic valve. These are the left main coronary artery and the right coronary artery. The left main coronary artery splits shortly after leaving the aorta into two vessels, the left anterior descending and the left circumflex artery. The left anterior descending artery supplies heart tissue and the front, outer side, and the septum of the left ventricle. It does this by smaller branching arteries – diagonal and septal branches. The left circumflex supplies the back and underneath of the left ventricle. The right coronary artery supplies the right atrium, right ventricle, and lower posterior sections of the left ventricle. The right coronary artery also supplies blood to the atrioventricular node (in about 90% of people) and the sinoatrial node (in about 60% of people). The right coronary artery runs in a groove at the back of the heart and the left anterior descending artery runs in a groove at the front. There is significant variation between people in the anatomy of the arteries that supply the heart The arteries divide at their furtherst reaches into smaller branches that join together at the edges of each arterial distribution.[7]

The coronary sinus is a large vein that drains into the right atrium, and receives most of the venous drainage of the heart. It receives blood from the great cardiac vein (receiving the left atrium and both ventricles), the posterior cardiac vein (draining the back of the left ventricle), the middle cardiac vein (draining the bottom of the left and right ventricles), and small cardiac veins. The anterior cardiac veins drain the front of the right ventricle and drain directly into the right atrium.[7]

Small lymphatic networks called plexuses exist beneath each of the three layers of the heart. These networks collect into a main left and a main right trunk, which travel up the groove between the ventricles that exists on the heart’s surface, receiving smaller vessels as they travel up. These vessels then travel into the atrioventricular groove, and receive a third vessel which drains the section of the left ventricle sitting on the diaphragm. The left vessel joins with this third vessel, and travels along the pulmonary artery and left atrium, ending in the inferior tracheobronchial node. The right vessel travels along the right atrium and the part of the right ventricle sitting on the diaphragm. It usually then travels in front of the ascending aorta and then ends in a brachiocephalic node.

The heart is the first functional organ to develop and starts to beat and pump blood at about three weeks into embryogenesis. This early start is crucial for subsequent embryonic and prenatal development.

The heart derives from splanchnopleuric mesenchyme in the neural plate which forms the cardiogenic region. Two endocardial tubes form here that fuse to form a primitive heart tube known as the tubular heart.[28] Between the third and fourth week, the heart tube lengthens, and begins to fold to form an S-shape within the pericardium. This places the chambers and major vessels into the correct alignment for the developed heart. Further development will include the septa and valves formation and remodelling of the heart chambers. By the end of the fifth week the septa are complete and the heart valves are completed by the ninth week.[7]

Before the fifth week, there is an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the lungs. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern. A depression in the surface of the right atrium remains where the foramen ovale once walls, called the fossa ovalis.[7]

The embryonic heart begins beating at around 22 days after conception (5 weeks after the last normal menstrual period, LMP). It starts to beat at a rate near to the mother’s which is about 7580 beats per minute (bpm). The embryonic heart rate then accelerates and reaches a peak rate of 165185 bpm early in the early 7th week (early 9th week after the LMP).[29][30] After 9 weeks (start of the fetal stage) it starts to decelerate, slowing to around 145 (25) bpm at birth. There is no difference in female and male heart rates before birth.[31]

The heart functions as a pump in the circulatory system to provide a continuous flow of blood throughout the body. This circulation consists of the systemic circulation to and from the body and the pulmonary circulation to and from the lungs. Blood in the pulmonary circulation exchanges carbon dioxide for oxygen in the lungs through the process of respiration. The systemic circulation then transports oxygen to the body and returns carbon dioxide and relatively deoxygenated blood to the heart for transfer to the lungs.[7]

The right heart collects deoxygenated blood from two large veins, the superior and inferior venae cavae. Blood collects in the right and left atrium continuously.[7] The superior vena cava drains blood from above the diaphragm and empties into the upper back part of the right atrium. The inferior vena cava drains the blood from below the diaphragm and empties into the back part of the atrium below the opening for the superior vena cava. Immediately above and to the middle of the opening of the inferior vena cava is the opening of the thin-walled coronary sinus.[7] Additionally, the coronary sinus returns deoxygenated blood from the myocardium to the right atrium. The blood collects in the right atrium. When the right atrium contracts, the blood is pumped through the tricuspid valve into the right ventricle. As the right ventricle contracts, the tricuspid valve closes and the blood is pumped into the pulmonary trunk through the pulmonary valve. The pulmonary trunk divides into pulmonary arteries and progressively smaller arteries throughout the lungs, until it reaches capillaries. As these pass by alveoli carbon dioxide is exchanged for oxygen. This happens through the passive process of diffusion.

In the left heart, oxygenated blood is returned to the left atrium via the pulmonary veins. It is then pumped into the left ventricle through the mitral valve and into the aorta through the aortic valve for systemic circulation. The aorta is a large artery that branches into many smaller arteries, arterioles, and ultimately capillaries. In the capillaries, oxygen and nutrients from blood are supplied to body cells for metabolism, and exchanged for carbon dioxide and waste products.[7] Capillary blood, now deoxygenated, travels into venules and veins that ultimately collect in the superior and inferior vena cavae, and into the right heart.

The cardiac cycle refers to a complete heartbeat which includes systole and diastole and the intervening pause. The cycle begins with contraction of the atria and ends with relaxation of the ventricles. Systole refers to contraction of the atria or ventricles of the heart contract. Diastole is when the atria or ventricles relax and fill with blood. The atria and ventricles work in concert, so in systole when the ventricles are contracting, the atria are relaxed and collecting blood. When the ventricles are relaxed in diastole, the atria contract to pump blood to the ventricles. This coordination ensures blood is pumped efficiently to the body.[7]

At the beginning of the cardiac cycle, in early diastole, both the atria and ventricles are relaxed. Since blood moves from areas of high pressure to areas of low pressure, when the chambers are relaxed, blood will flow into the atria (through the coronary sinus and the pulmonary veins). As the atria begin to fill, the pressure will rise so that the blood will move from the atria into the ventricles. In late diastole the atria contract, pumping more blood into the ventricles. This causes a rise in pressure in the ventricles. As the ventricles reach systole, blood will be pumped into the pulmonary artery (right ventricle) or aorta (left ventricle).

When the atrioventricular valves (tricuspid and mitral) are open, during blood flow to the ventricles, the aortic and pulmonary valves are closed to prevent backflow into the ventricles. When the ventricular pressure is greater than the atrial pressure the tricuspid and mitral valves will shut. When the ventricles contract the pressure forces the aortic and pulmonary valves open. As the ventricles relax, the aortic and pulmonary valves will close in response to decreased pressure.

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle (stroke volume) in one minute. This is calculated by multiplying the stroke volume (SV) by the beats per minute of the heart rate (HR). So that: CO = SV x HR.[7] The cardiac output is normalized to body size through body surface area and is called the cardiac index.

The average cardiac output, using an average stroke volume of about 70mL, is 5.25 L/min, with a normal range of 4.08.0 L/min.[7] The stroke volume is normally measured using an echocardiogram and can be influenced by the size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload and afterload.[7]

Preload refers to the filling pressure of the atria at the end of diastole, when they are at their fullest. A main factor is how long it takes the ventricles to fillif the ventricles contract faster, then there is less time to fill and the preload will be less.[7] Preload can also be affected by a person’s blood volume. The force of each contraction of the heart muscle is proportional to the preload, described as the Frank-Starling mechanism. This states that the force of contraction is directly proportional to the initial length of muscle fiber, meaning a ventricle will contract more forcefully, the more it is stretched.[7]

Afterload, or how much pressure the heart must generate to eject blood at systole, is influenced by vascular resistance. It can be influenced by narrowing of the heart valves (stenosis) or contraction or relaxation of the peripheral blood vessels.[7]

The strength of heart muscle contractions controls the stroke volume. This can be influenced positively or negatively by agents termed inotropes. These can be either conditions or drugs. Positive inotropes that cause stronger contractions include high blood calcium and drugs such as Digoxin, which will act to stimulate the sympathetic nerves in the fight-or-flight response. Negative inotropes causing weaker contractions include high blood potassium, hypoxia, acidosis, and drugs such as beta blockers and calcium channel blockers.

The normal rhythmical heart beat, called sinus rhythm, is established by the sinoatrial node, the heart’s pacemaker. Here an electrical signal is created that travels through the heart, causing the heart muscle to contract.

The sinoatrial node is found in the upper part of the right atrium near to the junction with the superior vena cava.[33] The electrical signal generated by the sinoatrial node travels through the right atrium in a radial way that is not completely understood. It travels to the left atrium via Bachmann’s bundle, such that both left and right atria contract together.[34][35][36] The signal then travels to the atrioventricular node. This is found at the bottom of the right atrium in the atrioventricular septumthe boundary between the right atrium and the left ventricle. The septum is part of the cardiac skeleton, tissue within the heart that the electrical signal cannot pass through, which forces the signal to pass through the atrioventricular node only.[7] The signal then travels along the bundle of His to left and right bundle branches through to the ventricles of the heart. In the ventricles the signal is carried by specialized tissue called the Purkinje fibers which then transmit the electric charge to the cardiac muscle.[37]

The normal resting heart rate is called the sinus rhythm, created and sustained by the sinoatrial node, a group of pacemaking cells found in the wall of the right atrium. Cells in the sinoatrial node do this by creating an action potential. The cardiac action potential is created by the movement of specific electrolytes into and out of the pacemaker cells. The action potential then spreads to nearby cells.

When the sinoatrial cells are resting, they have a negative charge on their membranes. However a rapid influx of sodium ions causes the membrane’s charge to become positive. This is called depolarisation and occurs spontaneously.[7] Once the cell has a sufficiently high charge, the sodium channels close and calcium ions then begin to enter the cell, shortly after which potassium begins to leave it. All the ions travel through ion channels in the membrane of the sinoatrial cells. The potassium and calcium only start to move out of and into the cell once it has a sufficiently high charge, and so are called voltage-gated. Shortly after this, the calcium channels close and potassium channels open, allowing potassium to leave the cell. This causes the cell to have a negative resting charge and is called repolarization. When the membrane potential reaches approximately 60 mV, the potassium channels close and the process may begin again.[7]

The ions move from areas where they are concentrated to where they are not. For this reason sodium moves into the cell from outside, and potassium moves from within the cell to outside the cell. Calcium also plays a critical role. Their influx through slow channels means that the sinoatrial cells have a prolonged “plateau” phase when they have a positive charge. A part of this is called the absolute refractory period. Calcium ions also combine with the regulatory protein troponin C in the troponin complex to enable contraction of the cardiac muscle, and separate from the protein to allow relaxation.[39]

The normal sinus rhythm of the heart, giving the resting heart rate, is influenced by the autonomic nervous system through sympathetic and parasympathetic nerves.[40] These arise from two paired cardiovascular centres in the medulla oblongata.The vagus nerve of the parasympathetic nervous system acts to decrease the heart rate, and nerves from the sympathetic trunk act to increase the heart rate. These come together in the cardiac plexus near the base of the heart. Without parasympathetic input which normally predominates, the sinoatrial node would generate a heart rate of about 100 bpm.[7]

The nerves from the sympathetic trunk emerge through the T1-T4 thoracic ganglia and travel to both the sinoatrial and atrioventricular nodes, as well as to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heart rate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.[7] Norepinephrine binds to the beta1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate.[7]

The cardiovascular centres receive input from a series of receptors including proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Through a series of reflexes these help regulate and sustain blood flow. For example, increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. With increased rates of firing, the parasympathetic stimulation may decrease or sympathetic stimulation may increase as needed in order to increase blood flow.[7]

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.[7]

There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase heart rate. The opposite is also true.[7]

In addition to the autonomic nervous system, other factors can impact on this. These include epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance. Factors that increase the heart rate can include release of norepinephrine, hypoxemia, low blood pressure and dehydration, a strong emotional response, a higher body temperature, and metabolic and hormonal factors such as a low potassium or sodium level or stimulus from thyroid hormones.[7] Decreased body temperature, relaxation, and metabolic factors can also contribute to a decrease in heart rate.[7]

The resting heart rate of a newborn can be 129 beats per minute (bpm) and this gradually decreases until maturity.[41] The adult resting heart rate ranges from 60 to 100 bpm. Exercise and fitness levels, age and basal metabolic rate can all affect the heart rate. An athlete’s heart rate can be lower than 60 bpm. During exercise the rate can be 150 bpm with maximum rates reaching from 200 to 220 bpm.[7]

One of the simplest methods of assessing the heart’s condition is to listen to it using a stethoscope.[7] Typically, healthy hearts have only two audible heart sounds, called S1 and S2. The first heart sound S1, is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as “lub”. The second heart sound, S2, is the sound of the semilunar valves closing during ventricular diastole and is described as “dub”.[7] Each sound consists of two components, reflecting the slight difference in time as the two valves close.[42] S2 may split into two distinct sounds, either as a result of inspiration or different valvular or cardiac problems.[42] Additional heart sounds may also be present and these give rise to gallop rhythms. A third heart sound, S3 usually indicates an increase in ventricular blood volume. A fourth heart sound S4 is referred to as an atrial gallop and is produced by the sound of blood being forced into a stiff ventricle. The combined presence of S3 and S4 give a quadruple gallop.[7]

Heart murmurs are abnormal heart sounds which can be either pathological or benign.[43] One example of a murmur is Still’s murmur, which presents a musical sound in children, has no symptoms and disappears in adolescence.[44]

A different type of sound, a pericardial friction rub can be heard in cases of pericarditis where the inflamed membranes can rub together.[45]

Cardiovascular diseases, which include diseases of the heart, are the leading cause of death worldwide.[46] The majority of cardiovascular disease is noncommunicable and related to lifestyle and other factors, becoming more prevalent with ageing.[46] Heart disease is a major cause of death, accounting for an average of 30% of all deaths in 2008, globally.[11] This rate varies from a lower 28% to a high 40% in high-income countries.[12] Doctors that specialise in the heart are called cardiologists. Many other medical professionals are involved in treating diseases of the heart, including doctors such as general practitioners, cardiothoracic surgeons and intensivists, and allied health practitioners including physiotherapists and dieticians.[47]

Coronary artery disease is also known as ischemic heart disease, is caused by atherosclerosis a build-up of plaque along the inner walls of the arteries which narrows them, reducing the blood flow to the heart.[48] A stable plaque may cause chest pain (angina) or breathlessness during exercise or at rest, or no symptoms at all. A ruptured plaque can block a blood vessel and lead to ischaemia of the heart muscle, causing unstable angina or a heart attack. In the worst case this may cause cardiac arrest, a sudden and utter loss of output from the heart.Obesity, high blood pressure, uncontrolled diabetes, smoking and high cholesterol can all increase the risk of developing atherosclerosis and coronary artery disease.[46][48]

Heart failure is where the heart can’t beat enough blood to meet the needs of the body.[48] It is generally a chronic condition, associated with age, that progresses gradually.Each side of the heart can fail independently of the other, resulting in heart failure of the right heart or the left heart. Left heart failure can also lead to right heart failure (cor pulmonale) by increasing strain on the right heart. If the heart is unable to pump sufficient blood, it may accumulate throughout the body, causing breathlessness in the lungs (pulmonary congestion; pulmonary edema), swelling (edema) of the feet or other gravity-dependent areas, decrease exercise tolerance, or cause other clinical signs such as an enlarged liver, cardiac murmurs, or a raised jugular venous pressure. Common causes of heart failure include coronary artery disease, valve disorders and diseases of cardiac muscle.

Cardiomyopathy is a noticeable deterioration of the heart muscle’s ability to contract, which can lead to heart failure. The causes of many types of cardiomyopathy are poorly understood; some identified causes include alcohol, toxins, systemic disease such as sarcoidosis, and congenital conditions such as HOCM. The types of cardiomyopathy are described according to how they affect heart muscle. Cardiomyopathy can cause the heart to become enlarged (hypertrophic cardiomyopathy), constrict the outflow tracts of the heart (restrictive cardiomyopathy), or cause the heart to dilate and impact on the effiency of its beating (dilated cardiomyopathy). HOCM is often undiagnosed and can cause sudden death in young athletes.[7]

Heart murmurs are abnormal heart sounds which can be either related to disease or benign, and there are several kinds. There are normally two heart sounds, and abnormal heart sounds can either be extra sounds, or “murmurs” related to the flow of blood between the sounds. Murmurs are graded by volume, from 1) the quietest, to 6) the loudest, and evaluated by their relationship to the heart sounds, position in the cardiac cycle, and additional features such as their radiation to other sites, changes with a person’s position, the frequency of the sound as determined by the side of the stethoscope by which they are heard, and site at which they are heard loudest.Phonocardiograms can record these sounds,[7] and echocardiograms are generally required for their diagnosis. Murmurs can result from valvular heart diseases due to narrowing (stenosis), or regurgitation of any of the main heart valves, such as aortic stenosis, mitral regurgitation or mitral valve prolapse. They can also result from a number of other disorders, including atrial and ventricular septal defects. Two common and infective causes of heart murmurs, are infective endocarditis and rheumatic fever, particularly in developing countries. Infective endocarditis involves colonisation of a heart valve, and rheumatic fever involves an initial bacterial infection by Group A streptococcus followed by a reaction against heart tissue that resembles the streptococcal antigen.

Abnormalities in the normal sinus rhythm of the heart can prevent the heart from effectively pumping blood, and are generally identified by ECG. These cardiac arrhythmias can cause an abnormal but regular heart rhythm, such as a rapid heart rate (tachycardia, classified as arising from above the ventricles or from the ventricles) or a slow heart rate (bradycardia); or may result in irregular rhythms. Tachycardia is generally defined as a heart rate faster than 100 beats per minute, and bradycardia as a heart rate slower than 60.Asystole is the cessation of heart rhythm. A random and varying rhythm is classified as atrial or ventricular fibrillation depending if the electrical activity originates in the atria or the ventricles. Abnormal conduction can cause a delay or unusual order of contraction of the heart muscle. This can be a result of a disease process, such as heart block, or congenital, such as Wolff-Parkinson-White syndrome.

Diseases may also affect the pericardium which surrounds the heart, which when inflammed is called pericarditis. This may result from infective causes (such as glandular fever, cytomegalovirus, coxsackievirus, tuberculosis or Q fever), systemic disorders such as amyloidosis or sarcoidosis, tumours, high uric acid levels, and other causes. This inflammation affects the ability of the heart to pump effectively. When fluid builds up in the pericardium this is called pericardial effusion, which when it causes acute heart failure is called cardiac tamponade. This may be blood from a traumatic injury or fluid from an effusion. This can compress the heart and adversely affect the function of the heart. The fluid can be removed from the pericardial sac using a syringe in a procedure called pericardiocentesis.

The heart can be affected by congenital diseases. These include failure of the developmental foramen ovale to close, present in up to 25% of people;[60]ventricular or atrial septal defects, congenital diseases of the heart valves (e.g. congenital aortic stenosis) or disease relating to blood vessels or blood flow from the heart (such as a patent ductus arteriosus or aortic coarctation).; Harrisons 14581465 These may cause symptoms at a variety of ages. If unoxygenated blood travels directly from the right to the left side of the heart, it may be noticed at birth, as it may cause a baby to become blue (cyanotic) such as Tetralogy of Fallot. A heart problem may impact a child’s ability to grow. Some causes rectify with time and are regarded as benign. Other causes may be incidentally detected on a cardiac examination. These disorders are often diagnosed on an echocardiogram.

Heart disease is diagnosed by the taking of a medical history, a cardiac examination, and further investigations, including blood tests, echocardiograms, ECGs and imaging. Other invasive procedures such as cardiac catheterisation can also play a role.

The cardiac examination includes inspection, feeling the chest with the hands (palpation) and listening with a stethoscope (auscultation).[64] It involves assessment of signs that may be visible on a person’s hands (such as splinter haemorrhages), joints and other areas. A person’s pulse is taken, usually at the radial artery near the wrist, in order to assess for the rhythm and strength of the pulse. The blood pressure is taken, using either a manual or automatic sphygmomanometer or using a more invasive measurement from within the artery. Any elevation of the jugular venous pulse is noted. A person’s chest is felt for any transmitted vibrations from the heart, and then listened to with a stethoscope. A normal heart has two hearts sounds – additional heart sounds or heart murmurs may also be able to be heard and may point to disease. Additional tests may be conducted to assess a person’s heart murmurs if they are present, and peripheral signs of heart disease such as swollen feet or fluid in the lungs may be assessed.

Using surface electrodes on the body, it is possible to record the electrical activity of the heart. This tracing of the electrical signal is the electrocardiogram (ECG) or (EKG). An ECG is a bedside test and usually requires the placement of ten leads on the body. This produces a “12 lead” ECG (three extra leads are calculated mathematically, and one lead is a ground).

There are five prominent features on the ECG: the P wave (atrial depolarisation), the QRS complex (atrial repolarisation and ventricular depolarisation) and the T wave (ventricular repolarisation).[7] These reflect the summed action potential of the heart’s muscle cells as they contract. A downward deflection on the ECG implies cells are becoming more negative in charge (“depolarising”), whereas an upward inflection implies cells are becoming more positive (“repolarising”). The ECG is a useful tool in detecting rhythm disturbances and in detecting insufficient blood supply to the heart.[64] Sometimes abnormalities are not immediately visible on the ECG. Testing when exercising can be used to provoke an abnormality, or an ECG can be worn for a longer period such as a 24-hour Holter monitor if a suspected rhythm abnormality is not present at the time of assessment.

Several imaging methods can be used to assess the anatomy and function of the heart, including ultrasound (echocardiography), angiography, CT scans, MRI and PET. An echocardiogram is an ultrasound of the heart used to measure the heart’s function, assess for valve disease, and look for any abnormalities. Echocardiography can be conducted by a probe on the chest (“transthoracic”) or by a probe in the esophagus (“transoesophageal”). A typical echocardiography report will include information about the width of the valves noting any stenosis, whether there is any backflow of blood (regurgitation) and information about the blood volumes at the end of systole and diastole, including an ejection fraction, which describes how much blood is ejected from the left and right ventricles after systole. Ejection fraction can then be obtained by dividing the volume ejected by the heart (stroke volume) by the volume of the filled heart (end-diastolic volume).[66] Echocardiograms can also be conducted under circumstances when the body is more stressed, in order to examine for signs of lack of blood supply. This cardiac stress test involves either direct exercise, or where this is not possible, injection of a drug such as dobutamine.

CT scans, chest X-rays and other forms of imaging can help evaluate the heart’s size, evaluate for signs of pulmonary oedema, and indicate whether there is fluid around the heart. They are also useful for evaluating the aorta, the major blood vessel which leaves the heart.

A number of medications are used to treat diseases of the heart, or ameliorate symptoms.

For diseases of the heart rate or rhythm, a number of different antiarrhythmic agents are used. These may interfere with electrolyte channels and thus the cardiac action potential (such as calcium channel blockers, sodium channel blockers), interfere with stimulation of the heart by the sympathetic nervous system (beta blockers), or interfere with the movement of sodium and potassium across the cell membrane, such as digoxin.[67] Other examples include atropine for slow rhythms, and amiodarone for irregular rhythms. Such medications are not the only way of treating diseases of heart rate or rhythm. In the context of a new-onset irregular heart rhythm (atrial fibrillation), immediate electrical cardioversion may be attempted. For a slow heartbeat or heart block, a pacemaker or defibrillator may be inserted. The acuity of onset often affects how a rhythm disturbance is managed, as does whether a rhythm causes hemodynamic instability, such as low blood pressure or symptoms. An instigating cause is investigated for, such as a heart attack, medication, or metabolic problem.

For ischaemic heart disease, treatment also includes amelioration of symptoms. This includes GTN, beta blockers and, in the context of an acute event, stronger pain relief such as morphine and other opiates. Many of these drugs have additional protective benefits, by decreasing the sympathetic tone on the heart that occurs with the pain, or by dilating blood vessels (GTN).

Treatment of heart disease includes primary and secondary prevention to prevent the occurrence or worsening of symptoms and atherosclerosis. This includes recommendations to cease smoking, decrease alcohol consumption, increase exercise, and make modifications to their diet to decrease the consumption of fats and sugars. Medications may also be given to help better control concurrent diabetes. Statins or other drugs such as fibrates may also be given to decrease a person’s cholesterol levels. Blood pressure medication may also be commenced or modified.

For many diseases of the heart, including atrial fibrillation and valvular disease, and after a heart operation, anticoagulation in the form of aspirin, warfarin, clopidogrel or novel oral anticoagulants is often given simultaneously, because of an increased risk of stroke or, in the context of a clotted heart vessel, rethrombosis.

Surgery, when considered necessary for diseases of the heart, can take place via an open operation or via small guidewires inserted via peripheral arteries (“percutaneous coronary intervention”). Percutaneous coronary intervention is usually used in the context of an acute coronary syndrome, and may be used to insert a stent.

Coronary artery bypass surgery is one such operation. In this operation, one or more arteries surrounding the heart that have become narrowed are bypassed. This is done by taking blood vessels harvested from another part of the body. Commonly harvested veins include the saphenous veins or the internal mammary artery. Because this operation involves the heart tissue, a machine is used so that blood can bypass the heart during the operation.

Heart valve repair or valve replacement are options for diseases of the heart valves.

Humans have known about the heart since ancient times, although its precise function and anatomy were not clearly understood.[71] From the primarily religious views of earlier societies towards the heart, ancient Greeks are considered to have been the primary seat of scientific understanding of the heart in the ancient world. [72][73][74]Aristotle considered the heart to be organ responsible for creating blood; Plato considered the heart as the source of circulating blood and Hippocrates noted blood circulating cyclically from the body through the heart to the lungs.[72][74]Erasistratos (304-250 BC) noted the heart as a pump, causing dilation of blood vessels, and noted that arteries and veins both radiate from the heart, becoming progressively smaller with distance, although he believed they were filled with air and not blood. He also discovered the heart valves.[72]

The Greek physician Galen (2nd century AD) knew blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions.[72] Galen, noting the heart as the hottest organ in the body, concluded that it provided heat to the body.[74] The heart did not pump blood around, the heart’s motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves. [74] Galen believed the arterial blood was created by venous blood passing from the left ventricle to the right through ‘pores’ between the ventricles.[71] Air from the lungs passed from the lungs via the pulmonary artery to the left side of the heart and created arterial blood. [74]

These ideas went unchallenged for almost a thousand years.[71][74]

The earliest descriptions of the coronary and pulmonary circulation systems can be found in the Commentary on Anatomy in Avicenna’s Canon, published in 1242 by Ibn al-Nafis.[75] In his manuscript, al-Nafis wrote that blood passes through the pulmonary circulation instead of moving from the right to the left ventricle as previously believed by Galen.[76] His work was later translated into Latin by Andrea Alpago.[77]

In Europe, the teachings of Galen continued to dominate the academic community and his doctrines were adopted as the official canon of the Church. Andreas Vesalius questioned some of Galen’s beliefs of the heart in De humani corporis fabrica (1543), but his magnum opus was interpreted as a challenge to the authorities and he was subjected to a number of attacks.[78]Michael Servetus wrote in Christianismi Restitutio (1553) that blood flows from one side of the heart to the other via the lungs.[78]

The breakthrough came with the publication of De Motu Cordis (1628) by the English physician William Harvey. Harvey’s book completely describes the systemic circulation and the mechanical force of the heart, leading to an overhaul of the Galenic doctrines.[79]Otto Frank (18651944) was a German physiologist; among his many published works are detailed studies of this important heart relationship. Ernest Starling (18661927) was an important English physiologist who also studied the heart. Although they worked largely independently, their combined efforts and similar conclusions have been recognized in the name “FrankStarling mechanism”.[7]

Although Purkinje fibers and the bundle of His were discovered as early as the 19th century, their specific role in the electrical conduction system of the heart remained unknown until Sunao Tawara published his monograph, titled Das Reizleitungssystem des Sugetierherzens, in 1906. Tawara’s discovery of the atrioventricular node prompted Arthur Keith and Martin Flack to look for similar structures in the heart, leading to their discovery of the sinoatrial node several months later. These structures form the anatomical basis of the electrocardiogram, whose inventor, Willem Einthoven, was awarded the Nobel Prize in Medicine or Physiology in 1924.[80]

The first successful heart transplantation was performed in 1967 by the South African surgeon Christiaan Barnard at Groote Schuur Hospital in Cape Town. This marked an important milestone in cardiac surgery, capturing the attention of both the medical profession and the world at large. However, long-term survival rates of patients were initially very low. Louis Washkansky, the first recipient of a donated heart, died 18 days after the operation while other patients did not survive for more than a few weeks.[81] The American surgeon Norman Shumway has been credited for his efforts to improve transplantation techniques, along with pioneers Richard Lower, Vladimir Demikhov and Adrian Kantrowitz. As of March 2000, more than 55,000 heart transplantations have been performed worldwide.[82]

By the middle of the 20th century, heart disease had surpassed infectious disease as the leading cause of death in the United States, and it is currently the leading cause of deaths worldwide. Since 1948, the ongoing Framingham Heart Study has shed light on the effects of various influences on the heart, including diet, exercise, and common medications such as aspirin. Although the introduction of ACE inhibitors and beta blockers has improved the management of chronic heart failure, the disease continues to be an enormous medical and societal burden, with 30 to 40% of patients dying within a year of receiving the diagnosis.[83]

As one of the vital organs, the heart was long identified as the center of the entire body, the seat of life, or emotion, or reason, will, intellect, purpose or the mind.[84] The heart is an emblematic symbol in many religions, signifying “truth, consience or moral courage in many religions – the temple or throne of God in Islamic and Judeo-Christian thought; the divine centre, or atman, and the third eye of transcendent wisdom in Hinduism; the diamond of purity and essence of the Buddha; the Taoist centre of understanding.”[84]

In the Hebrew Bible, the word for heart, lev, is used in these meanings, as the seat of emotion, the mind, and referring to the anatomical organ. It is also connected in function and symbolism to the stomach.[85]

An important part of the concept of the soul in Ancient Egyptian religion was thought to be the heart, or ib. The ib or metaphysical heart was believed to be formed from one drop of blood from the child’s mother’s heart, taken at conception.[86] To ancient Egyptians, the heart was the seat of emotion, thought, will, and intention. This is evidenced by Egyptian expressions which incorporate the word ib, such as Awi-ib for “happy” (literally, “long of heart”), Xak-ib for “estranged” (literally, “truncated of heart”).[87] In Egyptian religion, the heart was the key to the afterlife. It was conceived as surviving death in the nether world, where it gave evidence for, or against, its possessor. It was thought that the heart was examined by Anubis and a variety of deities during the Weighing of the Heart ceremony. If the heart weighed more than the feather of Maat, which symbolized the ideal standard of behavior. If the scales balanced, it meant the heart’s possessor had lived a just life and could enter the afterlife; if the heart was heavier, it would be devoured by the monster Ammit.[88]

The Chinese character for “heart”, , derives from a comparatively realistic depiction of a heart (indicating the heart chambers) in seal script.[89] The Chinese word xn also takes the metaphorical meanings of “mind”, “intention”, or “core”.[90]In Chinese medicine, the heart is seen as the center of shn “spirit, consciousness”.[91] The heart is associated with the small intestine, tongue, governs the six organs and five viscera, and belongs to fire in the five elements.[92]

The Sanskrit word for heart is hd or hdaya, found in the oldest surviving Sanskrit text, the Rigveda. In Sanskrit, it may mean both the anatomical object and “mind” or “soul”, representing the seat of emotion. Hrd may be a cognate of the word for heart in Greek, Latin, and English.[93][94]

Many classical philosophers and scientists, including Aristotle, considered the heart the seat of thought, reason, or emotion, often disregarding the brain as contributing to those functions.[95] The identification of the heart as the seat of emotions in particular is due to the Roman physician Galen, who also located the seat of the passions in the liver, and the seat of reason in the brain.[96]

The heart also played a role in the Aztec system of belief. The most common form of human sacrifice practiced by the Aztecs was heart-extraction. The Aztec believed that the heart (tona) was both the seat of the individual and a fragment of the Sun’s heat (istli). To this day, the Nahua consider the Sun to be a heart-soul (tona-tiuh): “round, hot, pulsating”.[97]

In Catholicism, there has been a long tradition of worship of the heart, stemming from worship of the wounds of Jesus Christ which gained prominence from the mid sixteenth century.[98] This tradition influenced the development of the medieval Christian devotion to the Sacred Heart of Jesus and the parallel worship of Immaculate Heart of Mary, made popular by John Eudes.[99]

The expression of a broken heart is a cross-cultural reference to grief for a lost one or to unfulfilled romantic love.

The notion of “Cupid’s arrows” is ancient, due to Ovid, but while Ovid describes Cupid as wounding his victims with his arrows, it is not made explicit that it is the heart that is wounded. The familiar iconography of Cupid shooting little heart symbols is a Renaissance theme that became tied to Valentine’s day.[84]

Animal hearts are widely consumed as food. As they are almost entirely muscle, they are high in protein. They are often included in dishes with other offal, for example in the pan-Ottoman kokoretsi.

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Heart – Wikipedia, the free encyclopedia

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Primary Cells Overview – stemcell.com

Unlike cell lines, primary cells are non-transformed, non-immortalized cells that are isolated directly from tissue. Closely mimicking a living model and yielding more biologically and physiologically relevant results, human primary cells have become an essential tool in the development of therapeutic treatments. Choose from an extensive range of fresh and cryopreserved peripheral blood products, as well as cryopreserved cord blood products, to incorporate into your research workflow.

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Human peripheral blood cells are isolated from adult whole blood or from a leukapheresis preparation produced using state-of-the-art apheresis systems. These apheresis collections, known as “Leuko Paks”, contain very high concentrations of mononuclear cells and are available in the following Pak sizes: full, half and quarter Pak. Specific cell subsets are purified using STEMCELL’s cell isolation products. Fresh whole blood products are collected directly into blood bags using acid-citrate-dextrose solution A (ACDA) or citrate-phosphate-dextrose (CPD) as the anticoagulant.

Human cord blood is collected using citrate-phosphate-dextrose (CPD) as the anticoagulant. Mononuclear cells are obtained by density gradient centrifugation. Specific cell subsets are obtained using STEMCELLs cell isolation products.

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Cryopreserved Leuko Pak and Whole Blood Products

Donor Screening: Donors are screened for HIV (1 & 2), Hepatitis B, and Hepatitis C. Cryopreserved products are shipped with negative test results from donor screening that is done within 90 days of collection.

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Donor Screening: Donors are screened for HIV (1 & 2), Hepatitis B, and Hepatitis C. If the donor was screened within 90 days of donation the product will be shipped with negative test results from donor screening. If the donor was not screened within 90 days of collection, a test sample will be taken at the time of donation and the product will be shipped before the screening results are available. In the unlikely event that a test result is positive, the customer will be contacted as soon as possible (usually within 24-72 hours from the time of shipment).

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Fresh Cord Blood Products

Donor Screening: Cord blood is only collected from mothers that have tested negative for HIV (1 & 2) and Hepatitis B during their pregnancy. Hepatitis C is tested for at the time of collection. Fresh cord blood products are shipped with negative test results for HIV (1 & 2) and Hepatitis B donor screening. Hepatitis C test results are not available at the time of shipment. In the unlikely event that the Hepatitis C test result is positive, the customer will be contacted as soon as possible (usually within 24-72 hours from the time of shipment).

Shipment date of fresh Leuko Pak or whole blood orders is subject to change based on the ability of donors to meet procedural requirements during collection or on changes in donor availability. Collections will be rescheduled as soon as possible according to customer requirements.

STEMCELL does not test for infectious diseases other than those listed above and the testing that is done cannot completely guarantee that the donor was virus-free. Therefore THESE PRODUCTS SHOULD BE TREATED AS POTENTIALLY INFECTIOUS and only used following appropriate handling precautions such as those described in biological safety level 2. When handling these products do not use sharps such as needles and syringes.

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Primary Cells Overview – stemcell.com

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Peripheral-blood stem cells versus bone marrow from …

See comment in PubMed Commons below N Engl J Med. 2012 Oct 18;367(16):1487-96. doi: 10.1056/NEJMoa1203517. Anasetti C, Logan BR, Lee SJ, Waller EK, Weisdorf DJ, Wingard JR, Cutler CS, Westervelt P, Woolfrey A, Couban S, Ehninger G, Johnston L, Maziarz RT, Pulsipher MA, Porter DL, Mineishi S, McCarty JM, Khan SP, Anderlini P, Bensinger WI, Leitman SF, Rowley SD, Bredeson C, Carter SL, Horowitz MM, Confer DL; Blood and Marrow Transplant Clinical Trials Network. Collaborators (182)

Horowitz MM, Carter SL, Confer DL, DiFronzo N, Wagner E, Merritt W, Wu R, Anasetti C, Logan BR, Lee SJ, Waller EK, Weisdorf DJ, Wingard JR, Couban S, Anderlini P, Bensinger WI, Leitman SF, Rowley SD, Carter SL, Karanes C, Horowitz MM, Confer DL, Allen C, Colby C, Gurgol C, Knust K, Foley A, King R, Mitchell P, Couban S, Pulsipher MA, Ehninger G, Johnston L, Khan SP, Maziarz RT, McCarty JM, Mineishi S, Porter DL, Bredeson C, Anasetti C, Lee S, Waller EK, Wingard JR, Cutler CS, Westervelt P, Woolfrey A, Logan BR, Carter SL, Lee SJ, Waller EK, Anasetti C, Logan BR, Lee SJ, Stadtmauer E, Wingard J, Vose J, Lazarus H, Cowan M, Wingard J, Westervelt P, Litzow M, Wu R, Geller N, Carter S, Confer D, Horowitz M, Poland N, Krance R, Carrum G, Agura E, Nademanee A, Sahdev I, Cutler C, Horwitz ME, Kurtzberg J, Waller EK, Woolfrey A, Rowley S, Brochstein J, Leber B, Wasi P, Roy J, Jansen J, Stiff PJ, Khan S, Devine S, Maziarz R, Nemecek E, Huebsch L, Couban S, McCarthy P, Johnston L, Shaughnessy P, Savoie L, Ball E, Vaughan W, Cowan M, Horn B, Wingard J, Silverman M, Abhyankar S, McGuirk J, Yanovich S, Ferrara J, Weisdorf D, Faber E Jr, Selby G, Rooms LM, Porter D, Agha M, Anderlini P, Lipton J, Pulsipher MA, Pulsipher MA, Shepherd J, Toze C, Kassim A, Frangoul H, McCarty J, Hurd D, DiPersio J, Westervelt P, Shenoy S, Agura E, Culler E, Axelrod F, Chambers L, Senaldi E, Nguyen KA, Engelman E, Hartzman R, Sutor L, Dickson L, Nademanee A, Khalife G, Lenes BA, Eames G, Sibley D, Gale P, Antin J, Ehninger G, Newberg NR, Gammon R, Montgomery M, Mair B, Rossmann S, Wada R, Waxman D, Ranlett R, Silverman M, Herzig G, Fried M, Atkinson E, Weitekamp L, Bigelow C, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Price T, Young C, Hilbert R, Oh D, Cable C, Smith JW, Kalmin ND, Schultheiss K, Beck T, Lankiewicz MW, Sharp D.

Randomized trials have shown that the transplantation of filgrastim-mobilized peripheral-blood stem cells from HLA-identical siblings accelerates engraftment but increases the risks of acute and chronic graft-versus-host disease (GVHD), as compared with the transplantation of bone marrow. Some studies have also shown that peripheral-blood stem cells are associated with a decreased rate of relapse and improved survival among recipients with high-risk leukemia.

We conducted a phase 3, multicenter, randomized trial of transplantation of peripheral-blood stem cells versus bone marrow from unrelated donors to compare 2-year survival probabilities with the use of an intention-to-treat analysis. Between March 2004 and September 2009, we enrolled 551 patients at 48 centers. Patients were randomly assigned in a 1:1 ratio to peripheral-blood stem-cell or bone marrow transplantation, stratified according to transplantation center and disease risk. The median follow-up of surviving patients was 36 months (interquartile range, 30 to 37).

The overall survival rate at 2 years in the peripheral-blood group was 51% (95% confidence interval [CI], 45 to 57), as compared with 46% (95% CI, 40 to 52) in the bone marrow group (P=0.29), with an absolute difference of 5 percentage points (95% CI, -3 to 14). The overall incidence of graft failure in the peripheral-blood group was 3% (95% CI, 1 to 5), versus 9% (95% CI, 6 to 13) in the bone marrow group (P=0.002). The incidence of chronic GVHD at 2 years in the peripheral-blood group was 53% (95% CI, 45 to 61), as compared with 41% (95% CI, 34 to 48) in the bone marrow group (P=0.01). There were no significant between-group differences in the incidence of acute GVHD or relapse.

We did not detect significant survival differences between peripheral-blood stem-cell and bone marrow transplantation from unrelated donors. Exploratory analyses of secondary end points indicated that peripheral-blood stem cells may reduce the risk of graft failure, whereas bone marrow may reduce the risk of chronic GVHD. (Funded by the National Heart, Lung, and Blood Institute-National Cancer Institute and others; ClinicalTrials.gov number, NCT00075816.).

Survival after Randomization in the Intention-to-Treat Analysis

The P value is from a stratified binomial comparison at the 2-year point. The P value from a stratified log-rank test was also not significant. A total of 75 patients in each group were still alive at 36 months.

N Engl J Med. ;367(16):10.1056/NEJMoa1203517.

Outcomes after Transplantation, According to Study Group

Panel A shows the rate of overall survival, and Panel B the rate of disease-free survival. Panel C shows the incidence of death unrelated to relapse. Panel D shows the incidence of relapse. Panel E shows the incidence of neutrophil engraftment (>500 neutrophils per cubic millimeter), and Panel F the incidence of platelet engraftment (>20,000 platelets per cubic millimeter, without platelet transfusion during the prior 7 days). Panel G shows the incidence of acute graft-versus-host disease (GVHD) of grades II to IV, and Panel H the incidence of chronic GVHD. P values for the between-group differences in overall survival (Panel A) and disease-free survival (Panel B) are from a stratified binomial comparison at the 2-year point; P values from stratified log-rank tests for survival and disease-free survival were also not significant. All other P values shown are from stratified log-rank tests.

N Engl J Med. ;367(16):10.1056/NEJMoa1203517.

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Peripheral-blood stem cells versus bone marrow from …

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Comparative Analysis of Mesenchymal Stem Cells from Bone …

Abstract

Mesenchymal stem cells (MSCs) represent a promising tool for new clinical concepts in supporting cellular therapy. Bone marrow (BM) was the first source reported to contain MSCs. However, for clinical use, BM may be detrimental due to the highly invasive donation procedure and the decline in MSC number and differentiation potential with increasing age. More recently, umbilical cord blood (UCB), attainable by a less invasive method, was introduced as an alternative source for MSCs. Another promising source is adipose tissue (AT). We compared MSCs derived from these sources regarding morphology, the success rate of isolating MSCs, colony frequency, expansion potential, multiple differentiation capacity, and immune phenotype. No significant differences concerning the morphology and immune phenotype of the MSCs derived from these sources were obvious. Differences could be observed concerning the success rate of isolating MSCs, which was 100% for BM and AT, but only 63% for UCB. The colony frequency was lowest in UCB, whereas it was highest in AT. However, UCB-MSCs could be cultured longest and showed the highest proliferation capacity, whereas BM-MSCs possessed the shortest culture period and the lowest proliferation capacity. Most strikingly, UCB-MSCs showed no adipogenic differentiation capacity, in contrast to BM- and AT-MSCs. Both UCB and AT are attractive alternatives to BM in isolating MSC: AT as it contains MSCs at the highest frequency and UCB as it seems to be expandable to higher numbers.

Mesenchymal stem cells (MSCs) found in many adult tissues are an attractive stem cell source for the regeneration of damaged tissues in clinical applications because they are characterized as undifferentiated cells, able to self-renew with a high proliferative capacity, and possess a mesodermal differentiation potential [1].

Although bone marrow (BM) has been the main source for the isolation of multipotent MSCs, the harvest of BM is a highly invasive procedure and the number, differentiation potential, and maximal life span of MSCs from BM decline with increasing age [24]. Therefore, alternative sources from which to isolate MSCs are subject to intensive investigation.

One alternative source is umbilical cord blood (UCB), which can be obtained by a less invasive method, without harm for the mother or the infant [5]. However, controversy still exists whether full-term UCB can serve as a source for isolating multipotent MSCs: although some groups did not succeed in isolating MSCs [6, 7], we and other groups succeeded in isolating MSCs from full-term UCB [812].

Adipose tissue (AT) is another alternative source that can be obtained by a less invasive method and in larger quantities than BM. It has been demonstrated that AT contains stem cells similar to BM-MSCs, which are termed processed lipoaspirate (PLA) cells [13]. These cells can be isolated from cosmetic liposuctions in large numbers and grown easily under standard tissue culture conditions [13]. The multilineage differentiation capacity of PLA cells has been confirmed [13].

As BM-MSCs are best characterized, we asked whether MSCs derived from other sources share the characteristics of BM-MSCs. The aim of our study was to compare MSCs isolated from the three sources under identical in vitro conditions with respect to their morphology, frequency of colonies, expansion characteristics, multilineage differentiation capacity, immunophenotype, and success rate of isolating the cells.

We compared MSCs from BM and two alternative sources, namely UCB and AT, concerning basic MSC characteristics. All cells isolated from these three sources exhibited typical MSC characteristics: a fibroblastoid morphology, the formation of CFU-F, a multipotential differentiation capability, and the expression of a typical set of surface proteins. Whereas MSCs derived from the three sources expressed classic MSC marker proteins, but lacked hematopoietic and endothelial markers, we observed significant differences concerning the expression of CD90, CD105, and CD106. These molecules are described to be associated with hematopoiesis and cell migration [18 20]. It needs to be further investigated whether these molecules are functionally important for stroma and homing capacities. In a first approach, we created a comprehensive protein expression profile of undifferentiated UCB-MSCs, which will be extended to BM- and AT-MSCs and then correlated to functional properties [21].

Since the relevance of the observed differences of marker expression has not been properly investigated yet, differences concerning differentiation capacity seem to be more relevant for MSC quality at present. We demonstrated a multilineage differentiation capacity for BM- and AT-MSCs. Interestingly, UCB-MSCs could not be differentiated toward the adipogenic lineage, which was not related to the CFU-F origin. Actually, there are conflicting data concerning the adipogenic differentiation capacity of UCB-MSCs [9 12, 22, 23]. Nevertheless, we assume that UCB-MSCs are less sensitive toward the adipogenic differentiation (supported by results of Chang et al. [22]) which might be related to the ontogenetic age of these cells. This is further supported by the fact that adipocytes reside in adult human BM and AT but are absent in fetal BM and by the observation of an increased adipogenesis correlated with age [24]. Further comparative genomic or proteomic approaches are needed to assess the susceptibility toward adipogenesis of MSCs.

None of our UCB-MSCs showed adipogenic differentiation capacity, but all differentiated into both the chondro- and osteogenic lineages. In contrast, a tripotential differentiation capacity was observed for most AT samples but only for a few BM samples. One sample each of BM and AT was observed to undergo only the chondrogenic pathway. In accordance with this, a hierarchical or even restricted differentiation potential of MSCs has been reported [1, 13, 25].

In our study, investigations were limited to the mesodermal differentiation capacity. Based on recent reports, however, the spectrum of differentiation of MSCs does not seem to be restricted to this lineage. MSCs derived from all three tissues have been shown to differentiate into further mesodermal lineages and into endo- and ectodermal lineages as well [10 13, 26 33]. Comparative experiments need to be performed to assess responsiveness toward cardiomyogenic, endothelial, hepatic, neuronal, and pancreatic differentiation.

A high impact on clinical exploitation might be related to the abundance and expansion capacity of MSCs. Based on our results, both BM and AT are reliable sources for isolating and expanding MSCs in autologous settings since all preparations gave rise to MSCs. UCB, in contrast, had an isolation efficacy of a maximum of 63% [8]. We attribute these differences to the fact that MSCs are circulating in the prenatal organism and are residing in tissues of the adult [9]. Despite the low frequency of UCB-MSCs, the expansion potential was highest compared with other cell sources. Considering clinical applications, the resulting cell numbers may be similar to both BM and AT, which can be obtained at higher frequencies. One argument against AT might be the limited availability in some patients. However, we believe that due to the high frequency of AT-MSCs, also small fat reservoirs might be sufficient for MSC isolation. BM has been the main source for clinical application of MSCs, such as the treatment of osteogenesis imperfecta, graft versus host disease, and acute myocardial infarction [3436]. As the number, frequency, and differentiation capacity of BM-MSCs correlate negatively with age, they could be clinically inefficient when derived from elderly patients. In that case, an allogeneic approach would be required. In case a matching donor is required, BM or AT from HLA identical siblings, haplo-identical relatives, or HLA-screened donors might be best choice. Speculating on a off-the-shelf product requiring mass production, AT might be a solid starting basis due to the abundance, relatively easy harvest, and high MSCs frequency.

Transplantation of MSCs is currently a highly experimental procedure, resembling the early beginnings of hematopoietic stem cell transplantation. In the latter, BM has been replaced gradually by peripheral blood progenitor cells and umbilical cord blood. Also, in the field of MSCs, alternative sources are intensely investigated, and one day these new sources may replace BM. Taking into account all the advantages and disadvantages of the three sources discussed above, depending on the therapeutic indication, the clinical applications may be based on differentiation capacity, but more likely on the abundance, frequency, and expansion potential of the cells.

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Stem cell trial suggests damaged heart tissue could be …

Embryonic stem cells seen through a microscope. The study saw a 40% reduction in the size of scarred tissue on the patients hearts. Photograph: Mauricio Lima/AFP/Getty Images

People suffering from heart disease have been offered hope by a new study that suggests damaged tissue could be regenerated through a stem cell treatment injected into the heart during surgery.

The small-scale study, published in the Journal of Cardiovascular Translational Research, followed 11 patients who during bypass surgery had stem cells injected into their hearts near the site of tissue scars caused by heart attacks.

One of the trials most dramatic results was a 40% reduction in the size of scarred tissue. Such scarring occurs during a cardiac event such as a heart attack, and can increase the chances of further heart failure. The scarring was previously thought to be permanent and irreversible.

At the time of treatment, the patients were suffering heart failure and had a very high (70%) annual mortality rate. But 36 months after receiving the stem cell treatment all are still alive, and none have suffered a further cardiac event such as a heart attack or stroke, or had any readmissions for cardiac-related reasons.

According to the British Heart Foundation, while there are several treatments to help people with heart failure, there is no known cure, and in some cases a heart transplant may be the only option.

Twenty-four months after participants were injected with the stem cell treatment there was a 30% improvement in heart function, 40% reduction in scar size, and 70% improvement in quality of life, as judged by the Minnesota living with heart failure (MLHF) score.

Related: Brain damage could be repaired by creating new nerve cells

Quite frankly it was a big surprise to find the area of scar in the damaged heart got smaller, said Prof Stephen Westaby from John Radcliffe hospital in Oxford, who undertook the research at AHEPA university hospital in Thessaloniki, Greece, with Kryiakos Anastasiadis and Polychronis Antonitsis.

Westaby began theorising about the impact of stem cells on regenerating heart tissue and reducing scarring after observing how scar tissue on the hearts of babies who have had heart attacks and undergone heart failure disappeared by the time they reached adolescence, suggesting that residual stem cells might be able to repair the damaged tissue.

Its an early study and its difficult to make large-scale predictions based on small studies, said Ajan Reginald, the founder of Celixir, the company that produces the treatment. But even in a small study you dont expect to see results this dramatic.

These are 11 patients who were in advanced heart failure, they had had a heart attack in the past, multiple heart attacks in many cases. The life expectancy for these patients is less than two years, were excited and honoured that these patients are still alive.

Related: Nearly 2m people may have undiagnosed killer disease

Jeremy Pearson, the associate medical director at the British Heart Foundation (BHF), said: This very small study suggests that targeted injection into the heart of carefully prepared cells from a healthy donor during bypass surgery, is safe. It is difficult to be sure that the cells had a beneficial effect because all patients were undergoing bypass surgery at the same time, which would usually improve heart function.

A controlled trial with substantially more patients is needed to determine whether injection of these types of cells proves any more effective than previous attempts to improve heart function in this way, which have so far largely failed.

Westaby conceded that the improvement in patients health was partly due to the heart bypass surgery those in the study were undergoing, and said the next study would include a control group who undergo bypass but do not receive stem cell treatment, to measure exactly what impact the treatment has.

These patients came out of heart failure partly due to the bypass grafts of course, but we think it was partly due to the fact that they had a smaller area of scar [as a result of the stem cell treatment]. Certainly this finding of scar being reduced is quite fascinating, he said.

Westaby will commence a large-scale controlled study later this year at the Royal Brompton hospital in London, and Celixir hopes to make the Heartcel treatment available to patients in 2018 or 2019.

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Stem cell trial suggests damaged heart tissue could be …

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Histogen – About Histogen – Latest news, upcoming events …

Multipotent Cell-Secreted Extracellular Matrix Supports Cartilage Formation Histogen to present at International Cartilage Repair Society 2015

CHICAGO, May 8, 2015 – Histogen, Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, will present new research on its human extracellular matrix (hECM) material in the promotion of cartilage regeneration during the International Cartilage Repair Society (ICRS) 2015 Meeting, taking place May 8-11, 2015 in Chicago, IL. The orthobiologic applications of all of Histogen’s products are being developed by its worldwide joint venture, PUR Biologics LLC.

Histogen has previously shown that hypoxia-induced multipotent cells produce soluble and insoluble materials that contain components associated with stem cell niches in the body and with scarless healing. These proteins include a variety of laminins, osteonectin, decorin, hyaluronic acid, collagen type IV, SPARC, CXCL12, NID1, NID2, NOTCH2, tenascin, thrombospondin, fibronectin, versican, and fibrillin-2. In vitro studies further demonstrated that the CCM and ECM promote the adhesion, proliferation and migration of bone marrow-derived human mesenchymal stem cells (MSCs).

In this latest research, in vivo studies with the hECM were undertaken to determine their potential as orthobiologics. Rabbit studies demonstrated the potential of the hECM to promote regeneration and repair of full-thickness articular cartilage defects. Eight weeks following hECM treatment of femoral osteochondral defects, mature bone and hyaline cartilage formation was seen, exemplified by the presence of a tide mark and integration into the adjacent cartilage. This work is currently being repeated in a goat cartilage defect model, with similar results to date.

“The efficacy we have seen with the multipotent cell-secreted ECM in bone and cartilage regeneration is unprecedented,” said Ryan Fernan, CEO of PUR Biologics. “The preclinical work overwhelmingly supports use of the material as an orthobiologic to reduce inflammation and promote cartilage regeneration in the articulating joint and intervertebral spinal disc. We look forward to entering human trials for these indications, as well as to continuing our research on utilizing the product for soft tissue repair in a variety of sports injuries.”

Histogen’s cell conditioned media (CCM) and hECM were also evaluated in an ex vivo rabbit intervertebral spinal disc model to study the effects of these materials in an environment where an extensive inflammatory response was induced by thrombin injection. Compared to untreated controls, both the CCM and ECM treatment significantly down regulated the expression of the inflammatory cytokine genes IL-1, IL-6, TNF-alpha, as well as the genes encoding the extracellular matrix degrading enzymes MMP3, and ADAMTS4, while upregulating aggrecan expression in the annulus fibrosus and nucleus pulposus tissue.

Dr. Gail Naughton, CEO of Histogen, will present “Human Cell Conditioned Media and Extracellular Matrix Reduce Inflammation and Support Hyaline Cartilage Formation” at the ICRS 2015 meeting in Chicago on May 9, 2015. Following the event, the presentation will be available upon request.

About PUR Biologics PUR Biologics is dedicated to providing regenerative biologic solutions to address musculoskeletal surgical needs, including spine, dental, ligament and medical device coating applications. In addition to distribution of approved allograft and biologic products, PUR is focused on development of next-generation orthopedic products based upon human protein and growth factor materials for bone and tissue regeneration. For more information visit http://www.purbiologics.com.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of multipotent human proteins that have been shown to support stem cell growth and differentiation. For more information, please visit http://www.histogen.com.

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Novel Immunomodulatory Treatment Induces Apoptosis in Melanoma Histogen to present data at 2015 Society of Investigative Dermatology Annual Meeting

ATLANTA, May 6, 2015 – Histogen, Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, will present new research on its 105F immunomodulatory treatment candidate for melanoma during the 2015 Society of Investigative Dermatology (SID) Annual Meeting, taking place May 6-9, 2015 in Atlanta, GA.

Histogen has previously shown that hypoxia-induced multipotent cells produce a soluble material with anti-oncologic properties, with potential benefit in the treatment of a wide range of cancers. Studies to characterize the active components of the material have identified a low molecular weight fraction (105F) which directly induces apoptosis, or controlled cell death, in 21 human cancer cell lines. In its latest research, Histogen sought to further examine the mechanism of action of 105F in melanoma through in vitro and in vivo studies.

After treatment with 105F, melanoma cells were shown to release Interleukin 6 (IL-6) and TNF a, pro-inflammatory cytokines acting as signals to the immune system. This induction of an immune “flare” in combination with tumor cell apoptosis could be critically important in recruiting immune cells to the tumor for cytotoxic attack.

“We were excited to see the dual activity of 105F, both directly inducing cancer cell death and activating an anti-tumorigenic immune response to reduce metastatic disease,” said Dr. Gail Naughton, CEO and Chairman of the Board of Histogen. “These results represent a potential treatment for melanoma and other solid tumors that works through multiple channels to eliminate cancer cells, but is not toxic to the body’s healthy cells.”

An in vivo model of lung metastasis in C57Bl/6 mice further showed the efficacy of 105F in the treatment of melanoma. Daily intravenous injections of 105F over 14 days resulted in a significant (p=0.0049) reduction in lesions and marked immune cell infiltration as compared to controls.

Dr. Naughton will present “105F is a novel immunoadaptive treatment candidate for melanoma that induces apoptosis and the secretion of pro-inflammatory IL-6” at the 2015 SID Annual Meeting in Atlanta beginning May 6, 2015. Following the event, the presentation will be available upon request.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of multipotent human proteins that have been shown to support stem cell growth and differentiation. For more information, please visit http://www.histogen.com.

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Histogen’s Composition for Oncology Treatments Receives US Patent

SAN DIEGO, October 8, 2014 – Histogen Oncology, a company developing innovative cancer therapies based on Histogen’s regenerative medicine technology, today announced that the United States Patent & Trademark Office has issued patent 12/363,479 entitled “Extracellular matrix compositions for the treatment of cancer” to Histogen.

The patent, which is the fifth U.S. patent issued to Histogen, covers the soluble and insoluble compositions of proteins and cofactors that are secreted by multipotent stem cells through Histogen’s technology process for use in the treatment of cancer. The patent claims support of the use of the compositions alone or as a delivery system for traditional chemotherapeutic agents.

Through the recent formation and funding of the Histogen Oncology joint venture, research and development of the unique, naturally secreted compositions is progressing toward a Phase I clinical trial for end stage pancreatic cancer.

“We are pleased about the timely issuance of our U.S. patent for the treatment of cancer,” said Dr. Gail K. Naughton, Histogen CEO and Chairman of the Board. “Our collaborations with top institutions continue to produce mounting evidence supporting the unique mechanism of action of our secreted material in preventing metastasis and reducing tumor load while having no toxic affect on normal cells.”

Histogen’s composition has shown effectiveness in inhibiting over 21 human cancer cell lines both in vitro as well as in animal models. The mechanism of action of the secreted material is through the induction of apoptosis (controlled cell death) primarily in malignant cells, so there is little to no toxicity to normal cells. Histogen Oncology is studying the efficacy of a small molecular weight fraction of the cell secreted composition as a stand alone treatment as well as in combination therapy to evaluate whether effectiveness can be demonstrated with less toxic drug doses.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of multipotent human proteins that have been shown to support stem cell growth and differentiation. For more information, please visit http://www.histogen.com.

Contacts Eileen Brandt, (858) 200-9520 ebrandt@histogeninc.com

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Histogen Oncology Created to Develop Novel Biologic Cancer Treatments Histogen, Inc. and Wylde, LLC Form Joint Venture

SAN DIEGO, July 8, 2014 – Histogen Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, has partnered with Southern California medical device group Wylde, LLC to create Histogen Oncology. This joint venture will focus on the development of unique cell-derived materials for cancer applications.

Under this joint venture, Histogen Oncology has acquired exclusive rights to Histogen’s human multipotent cell conditioned media (CCM) and extracellular matrix (ECM) materials, as well as their derivatives, for oncology applications throughout North America. Histogen Oncology’s initial clinical focus is pancreatic cancer, a highly treatment-resistant cancer in which a sub-fraction of the CCM has shown substantial preclinical promise.

“We have been very impressed with the results of Histogen’s preliminary oncology work, not only because of the significant survival benefit but also because it is a naturally-derived material that is showing no toxicity,” said Christopher Wiggins of Wylde, LLC. “There are so many patients out there who are not candidates for existing therapies due to the toxic nature of available drugs. This is particularly true in pancreatic cancer, where 80% of people diagnosed already have stage four disease.”

In post-resection nude mouse models, intravenous treatment with the CCM sub-fraction resulted in prolonged survival by more than three fold in a majority of treated animals. In non-resection models, more than 50% of treated mice lived twice as long as the control. These results point to a potentially significant outcome for pancreatic cancer patients, and Histogen Oncology intends to progress the material toward a Phase I clinical trial for no-option pancreatic cancer patients in the coming 18 months.

Research on the mechanism responsible for cancer cell inhibition by the CCM shows the upregulation of Caspase 9 and cleaved Caspase 3, which causes cancer cells to enter apoptosis, or programmed cell death.

“The activity of the CCM sub-fraction is unique in a number of ways. Whereas most cancer therapies target rapidly dividing cells but not cancer stem cells, the inhibitory effect of this material is seen in malignant cells and circulating tumor cells as well,” said Dr. Gail Naughton, CEO and Chairman of the Board of Histogen, Inc. “In addition, the activity is selective for malignant cells, supporting the proliferation of human dermal fibroblasts, embryonic stem cells and mesenchymal stem cells, while inhibiting tumor growth.”

Histogen Oncology will be supported by Histogen’s research group and funded by Wylde, LLC., made up of experts from the surgery and medical device industries. The creation of this joint venture allows for dedicated development of the CCM sub-fraction as a cancer treatment, as Histogen continues to allocate resources to the Company’s revenue-generating aesthetic and promising therapeutic programs.

“We are extremely excited to fuel and push the next stage of development for this innovative and potentially life-saving therapy,” said Wiggins. “The next generation of cancer treatment will have cell-signaling at its core, be beneficial in combination with existing therapies as well as stand alone, and provide an option to patients who currently have none. We believe Histogen’s material has all of those characteristics and more.”

About Histogen Aesthetics Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of multipotent human proteins that have been shown to support stem cell growth and differentiation. For more information, please visit http://www.histogen.com.

Contacts Eileen Brandt, (858) 200-9520 ebrandt@histogeninc.com

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Histogen Aesthetics Acquires CellCeuticals Biomedical Skin Treatments

SAN DIEGO, March 10, 2014 – Histogen Aesthetics, a subsidiary of regenerative medicine company Histogen, Inc. focused on skin care and cosmeceuticals, announced today that the Company has acquired the CellCeuticals Biomedical Skin Treatments line of skincare products.

Histogen Aesthetics will continue sales of the eleven existing CellCeuticals Biomedical Skin Treatments skincare products, while bringing new innovation to the line through the addition of a unique regenerative medicine technology, working to improve skin aging at a cellular level.

“We have long admired the science, clinical data and elegant formulas behind the CellCeuticals line, and see it as an ideal fit for our recently revitalized aesthetics subsidiary,” said Dr. Gail K. Naughton, CEO and Chairman of Histogen, Inc. “We are very excited to begin infusing unique cell-signaling factors into the CellCeuticals regimen, to truly transform skin one cell at a time.”

Dr. Naughton has spent more than 30 years in tissue engineering and regenerative medicine, and holds over 100 patents in the field. She founded Histogen in 2007, focused on developing therapies that work to stimulate the stem cells in the body to regenerate tissues and organs. Through this work, she has also seen how different compositions of human proteins can have cosmetic benefits, particularly in anti-aging and rejuvenation.

“I am pleased that the CellCeuticals Biomedical Skin Treatments will evolve, and see Histogen Aesthetics as an excellent home for this innovative product line,” said Paul Scott Premo, co-founder of CellCeuticals Skin Care, Inc. “I believe the addition of this regenerative medicine technology will be the opportunity to introduce a new generation of products that are the vanguard of regenerative skin care.”

The CellCeuticals system is made up of eleven distinctive products including the Extremely Gentle Skin Cleanser, CellGenesis Regenerative Skin Treatment, and PhotoDefense Color Radiance SPF55+ with proprietary and patented PhotoPlex technology. The line is currently available at retailers including QVC.com, Dermstore.com, and Nordstrom.com, as well as http://www.cellceuticalskincare.com.

About Histogen Aesthetics Histogen Aesthetics LLC, formed in 2008 as a subsidiary of Histogen, Inc., focuses on the development of innovative skin care products utilizing regenerative medicine technology. Histogen Aesthetics’ technology is based on the expertise of founder Dr. Gail K. Naughton, in which fibroblasts are grown under unique conditions, producing a complex of naturally-secreted proteins and synergistic bio-products known to stimulate skin cells to regenerate and rejuvenate tissues. In 2014, Histogen Aesthetics acquired CellCeuticals Biomedical Skin Treatments, a line of scientifically-proven products that reactivate cells to help aging skin perform and look healthier and younger. For more information, visit http://www.cellceuticalskincare.com.

About Suneva Medical, Inc. Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process is also being researched for oncology applications, and in orthopedics through joint venture PUR Biologics, LLC. For more information, please visit http://www.histogen.com.

Contacts Eileen Brandt, (858) 200-9520 ebrandt@histogeninc.com

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Histogen and Suneva Medical Expand License for Cell Conditioned Media-based Aesthetic Products Internationally

SAN DIEGO, CA, January 14, 2014 – Histogen, Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, today announced that they have entered into an international license agreement with Suneva Medical, Inc. for physician-dispensed aesthetic products containing Histogen’s proprietary multipotent cell conditioned media (CCM).

This agreement is an amendment to the existing license between Histogen and Suneva Medical, through which Suneva has exclusively licensed the Regenica skincare line within the United States since February 2012. Under the terms of the international agreement, Suneva Medical is now the exclusive licensee for the distribution of Regenica through the physician-dispensed channel in Europe, most of Asia, South America, Canada, Australia, and the Middle East.

“Not only has Suneva had sales success, but they have generated enthusiasm around the Regenica product line and our technology here in the US,” said Gail K. Naughton, Ph.D., CEO and Chairman of the Board of Histogen. “We are excited about expanding our skincare partnership internationally, and look forward to an exciting year for Regenica.”

Regenica contains Histogen’s proprietary Multipotent Cell Conditioned Media, made up of soluble cell-signaing proteins and growth factors which support the body’s epidermal stem cells and renew skin throughout life. Through Histogen’s technology process, which mimics the embryonic environment including conditions of low oxygen and suspension, cells are triggered to become multipotent, and naturally produce these proteins associated with skin renewal and scarless healing.

“We believe that Regenica truly is the next generation in growth factor technology, and we are extremely pleased that the products will now have a presence around the world,” said Nicholas L. Teti, Jr., Chairman and Chief Executive Officer of Suneva Medical. “Our relationship with Histogen in the US physician market has been a valuable asset to Suneva, and has laid the groundwork for international success.”

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process can be found in skincare products including ReGenica, which is distributed by Suneva Medical in partnership with Obagi Medical Products. For more information, please visit http://www.histogen.com.

About Suneva Medical, Inc. Suneva Medical, Inc. is a privately-held aesthetics company focused on developing, manufacturing and commercializing novel, differentiated products for the general dermatology and aesthetic markets. The company currently markets Artefill in the US, Korea, Singapore and Vietnam; Refissa and Regenica Skincare in the U.S.; and Bellafill in Canada. For more information, visit http://www.sunevamedical.com.

Regenica is a trademark of Suneva Medical, Inc. The Multipotent Cell Conditioned Media Complex is covered by U.S. patents #8,257,947 and #8,524,494.

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Multipotent Stem Cell Proteins Support Soft Tissue Regeneration Histogen to present data at TERMIS AM Annual Conference in Atlanta

ATLANTA, November 13, 2013 – Histogen, Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, announced that Dr. Michael Zimber will give a podium presentation entitled “Human Multipotent Stem Cell Proteins Support Soft Tissue Regeneration” today at the Tissue Engineering and Regenerative Medicine International Society (TERMIS) Americas Annual Meeting in Atlanta, GA.

Through its proprietary technology process that simulates the conditions of the embryonic environment, Histogen has developed a human extracellular matrix (hECM) material composed of stem cell-associated proteins including SPARC, decorin, collagens I,III,IV, V, fibronectin, fibrillin, laminins, and hyaluronic acid. The hECM’s distinctive composition of growth factors and other proteins are known to stimulate stem cells in the body, regenerate tissues, and promote scarless healing.

Histogen sought to examine whether the hECM may promote scarless healing in full thickness wounds, similar to that seen in fetal healing, using a variety of forms of the material, including hollow spheres to maximize void fill volume. In preclinical studies, all hECM-treated wounds healed rapidly with minimum contractions, and the hECM microspheres had a statistically significant improvement in healing as compared to the controls (p

“We are very pleased that our propriety materials produced by hypoxia-induced human multipotent stem cells have shown significant healing results in both soft and hard tissues,” said Dr. Gail Naughton, CEO and Chairman of the Board of Histogen. “These results open new therapeutic markets, show tremendous potential for our material in cutaneous wound care and orthopedics, as well as support the expansion of our aesthetic pipeline to include soft tissue fillers.”

In addition to “Human Multipotent Stem Cell Proteins Support Soft Tissue Regeneration”, Dr. Zimber will also be presenting “Human Multipotent Stem Cell Proteins Support Osteogenesis In Vitro” during the TERMIS AM Annual Meeting taking place November 10-13, 2013 in Atlanta. Following the event, these presentations will be available upon request.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process can be found in skincare products including ReGenica, which is distributed by Suneva Medical in partnership with Obagi Medical Products. For more information, please visit http://www.histogen.com.

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Multipotent Stem Cell Proteins Support Rejuvenation while Inhibiting Skin Cancer Histogen to present data at TERMIS AP Annual Conference in Shanghai

San Diego, October 24, 2013 – Histogen, Inc., a regenerative medicine company developing solutions based on the products of cells grown under simulated embryonic conditions, announced that the Company’s Chairman and CEO, Dr. Gail Naughton, will present today at the Tissue Engineering and Regenerative Medicine International Society (TERMIS) Asia Pacific Annual Meeting in Shanghai, China.

Through its proprietary technology process that simulates the conditions of the embryonic environment, Histogen is uniquely able to trigger the de-differentiation of skin cells into multipotent stem cells without genetic manipulation. The cells express key stem cell markers including Oct4, Sox2 and Nanog, and secrete a distinctive composition of growth factors and other proteins known to stimulate stem cells in the body, regenerate tissues, and promote scarless healing.

It is the soluble and insoluble compositions of multipotent proteins and growth factors resulting from this process that have been shown to both promote skin regeneration and induce controlled cell death in multiple skin cancers.

“The anti-aging and rejuvenation benefits of human multipotent stem cell proteins have been shown in several clinical studies, and have resulted in the material’s use as a thriving next-generation ingredient for skin care,” said Dr. Naughton. “In parallel, we have also been studying the anti-cancer activity of these proteins, and have shown that, just as in the embryonic environment, they support normal tissue growth while resulting in the controlled death of cancer cells”.

In vitro studies performed with Histogen’s material have shown reduction in Squamous Cell Carcinoma (SCC), Basal Cell Carcinoma, and Melanoma cell number through the mechanism of apoptosis, or controlled cell death, induced by the upregulation of Caspase in these cancer cells. In one in vivo model, melanoma load was reduced by up to 80% versus the control (p

“Human Multipotent Stem Cell Proteins Stimulate Skin Regeneration While Inducing Skin Cancer Cell Apotosis” will be presented by Dr. Naughton during the TERMIS AP Annual Meeting taking place October 23-26, 2013 in Shanghai. Further information and data on the ability of multipotent stem cell proteins to induce apoptosis in skin cancers can be found in the publication Journal of Cancer Therapy at file.scirp.org/Html/1-8901700_33923.htm.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process can be found in skincare products including ReGenica, which is distributed by Suneva Medical in partnership with Obagi Medical Products. For more information, please visit http://www.histogen.com.

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Histogen to present at 2013 STEM CELL MEETING ON THE MESA

San Diego, October 11, 2013 – Histogen, Inc., a regenerative medicine company developing therapies for conditions including hair loss and cancer, announced today that Histogen CEO Gail K. Naughton, Ph.D. will give a company presentation at the 3rd Annual Regen Med Partnering Forum, part of the Stem Cell Meeting on the Mesa to be held October 14-16 in La Jolla, CA.

Histogen’s solutions are based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. The technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of proteins that have been shown to support stem cell growth and differentiation.

“It is an exciting time for Histogen, as we continue to move the technology forward with expanded partnerships in skincare, compelling clinical data in both male and female hair loss, and early but exciting results in orthopedics,” said Dr. Naughton. “We look forward to sharing our story during the Stem Cell Meeting on the Mesa, and to progressing our products even further through growing relationships with industry leaders and through our potential merger with Stratus Media to form publicly-traded Restorgenex.”

Organized by the Alliance for Regenerative Medicine (ARM), the California Institute for Regenerative Medicine (CIRM) and the Sanford Consortium for Regenerative Medicine, the 2013 Stem Cell Meeting on the Mesa is a three-day conference aimed at bringing together senior members of the regenerative medicine industry with the scientific research community to advance stem cell science into cures. The Regen Med Partnering Forum, held October 14 &15 at the Estancia La Jolla Hotel, is the only partnering meeting organized specifically for the regenerative medicine and advanced therapies industry.

The following are specific details regarding Histogen’s presentation at the conference:

Event: Regen Med Partnering Forum – 2013 Stem Cell Meeting on the Mesa Date: October 14, 2013 Time: 3:15pm Location: Estancia La Jolla Hotel & Spa, 9700 North Torrey Pines Road, La Jolla

A live video webcast of all company presentations will be available at: stemcellmeetingonthemesa.com/webcast and will also be published on ARM’s website shortly after the event. Histogen will also make a copy of Dr. Naughton’s presentation available at http://www.histogen.com.

About Histogen Histogen is a regenerative medicine company developing solutions based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. Through this unique technology process, newborn cells are encouraged to naturally produce the vital proteins and growth factors from which the Company has developed its rich product portfolio. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process can be found in skincare products including ReGenica, which is distributed by Suneva Medical in partnership with Obagi Medical Products. For more information, please visit http://www.histogen.com.

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Stratus Media Group and Histogen Execute Letter of Intent for Biotechnology Merger

LOS ANGELES, October 07, 2013 – Stratus Media Group, Inc. (OTCQB:SMDI) announced today that it was planning to expand its entrance into the biotechnology industry with the execution of a letter of intent between the Company and Histogen, Inc., a regenerative medicine company developing innovative therapies for conditions including hair loss and cancer.

The non-binding letter of intent outlines the primary terms of a merger of San Diego-based Histogen into Stratus, to be renamed Restorgenex Corporation. The letter of intent has been approved by the board of directors of both companies, and the parties are engaged in completing a formal merger agreement.

Histogen’s solutions are based upon the products of cells grown under proprietary conditions that mimic the embryonic environment, including low oxygen and suspension. The technology focuses on stimulating a patient’s own stem cells by delivering a proprietary complex of proteins that have been shown to support stem cell growth and differentiation. Histogen’s lead product, Hair Stimulating Complex (HSC) has shown success in two Company-sponsored clinical trials as an injectable treatment for alopecia. In addition, the human multipotent cell conditioned media produced through Histogen’s process can be found in skincare products including ReGenica, which is distributed by Suneva Medical in partnership with Obagi Medical Products.

“Histogen’s technology platform opens a spectrum of potential product opportunities in both aesthetics and therapeutics, an ideal fit with our vision for Restorgenex,” said Sol J. Barer, Ph.D., who will assume the position of Chairman of the Board of Restorgenex effective November 1, 2013. “The expertise of the Histogen team in developing regenerative products from concept to market, along with the success Histogen has already found in skincare partnering, will add significant value to our Company.”

Following successful completion of this proposed merger, the company’s goal is to build Restorgenex into a world-class cosmeceutical and pharmaceutical company in the large and expanding fields of dermatology and hair restoration. The parties intend to move toward a formal merger agreement in which Histogen would become a wholly-owned subsidiary, Histogen founder Gail K. Naughton, Ph.D. would assume the position of Chief Executive Officer of Restorgenex, and the corporate headquarters of Restorgenex would be located in San Diego. The merger will require, among other things, the satisfaction of customary closing conditions including the approval of Histogen’s shareholders.

“I am very excited about the potential of a merger between Histogen and Restorgenex, and look forward to moving into the next stage,” said Dr. Naughton. “It is an honor to be working with biotechnology visionaries Dr. Sol Barer and Isaac Blech, and to have them recognize the promise of Histogen’s products is a true testament to the unique and exciting nature of our technology.”

Dr. Naughton has spent more than 25 years extensively researching the tissue engineering process, holds more than 95 U.S. and foreign patents, and has been honored for her pioneering work in the field by prestigious organizations including receiving the Intellectual Property Owners Association Inventor of the Year Award.

Prior to founding Histogen in 2007, Dr. Naughton oversaw the design and development of the world’s first up-scaled manufacturing facility for tissue engineered products, was pivotal in raising over $350M from the public market and corporate partnerships, and brought four human cell-based products from concept through FDA approval and market launch as President of Advanced Tissue Sciences.

“I believe the potential acquisition of Histogen, and the expertise and vision Dr. Naughton will bring as Chief Executive Officer will be a tremendous asset in ushering the Company into the biotechnology industry,” said Jerold Rubinstein, current Chairman and Chief Executive Officer of Stratus.

http://www.histogen.com http://www.stratusmediagroup.com

Forward-Looking Statements Statements in this press release relating to plans, strategies, projections of results, and other statements that are not descriptions of historical facts may be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and the Securities Acts of 1933 and 1934. Forward-looking information is inherently subject to risks and uncertainties, and actual results could differ materially from those currently anticipated due to a number of factors. Although the company’s management believes that the expectations reflected in the forward-looking statements are reasonable, it cannot guarantee future results, performance or achievements. The company has no obligation to update these forward-looking statements.

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