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TUESDAY, July 22, 2014 (HealthDay News) -- One of the largest studies ever conducted into the genetic origins of a psychiatric disorder has uncovered 83 new sites on chromosomes that harbor inherited genes tied to schizophrenia.

The findings, made by an international team of researchers, now bring the total number of common gene variants linked to the disorder to 108.

Although these schizophrenia-associated genes aren't specific enough to be used as a test to predict who will or will not develop the illness, researchers say they might someday be used as a screening tool for high-risk people who may benefit from preventative treatments.

Right now, the total group of schizophrenia-linked genes "only explains only about 3.5 percent of the risk for schizophrenia," Dr. Thomas Insel, director of the U.S. National Institute of Mental Health, said in an agency news release. However, "even based on these early predictors, people who score in the top 10 percent of risk may be up to 20-fold more prone to developing schizophrenia."

Prior research had only identified about 30 common gene variants linked to schizophrenia. In looking for more clues to the molecular basis of the disorder, an international team of more than 500 scientists at more than 80 research institutions in 25 countries re-examined all available schizophrenia gene samples from people with schizophrenia.

The combined data involved more than 37,000 people with schizophrenia and 113,000 people without the disorder.

The analysis looked at people's complete genomes -- the "map" of DNA that makes up a human. Out of a pool of roughly 9.5 million gene variants, the study authors found 108 sites on various chromosomes that appear to be linked to schizophrenia.

The newly discovered sites are grouped around pathways tied to certain processes associated with the disorder. These include communication between brain cells, as well as pathways involving learning, memory and immune function. One site was even focused on a specific target for schizophrenia medication, the study revealed.

One association was confirmed with a variation in a gene that codes for a receptor for dopamine -- a brain chemical messenger that is a known target for drugs used to treat schizophrenia.

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By Amy Norton HealthDay Reporter

WEDNESDAY, July 23, 2014 (HealthDay News) -- The timing of a girl's first menstrual period may be determined by hundreds, and possibly thousands, of gene variations, a new study suggests.

Researchers have identified over 100 regions of DNA that are connected to the timing of menarche -- a woman's first menstrual period. The researchers hope these findings will shed light on the biology of a number of diseases ranging from Type 2 diabetes to breast cancer.

"These findings will provide additional insights into how puberty timing is linked to the risk of disease in later life," said lead researcher John Perry, a senior scientist at the University of Cambridge MRC epidemiology unit, in the United Kingdom.

"We hope that with the help of future studies, this will in turn lead to better understanding of the underlying biology behind diseases such as Type 2 diabetes and breast cancer," Perry said.

Earlier puberty has been linked to increased risks of some of the most common health problems today, including obesity, Type 2 diabetes, heart disease and breast cancer. Although estrogen levels are thought to be involved, the full reasons for the connection between menarche and health conditions later in life aren't clear.

The new study found that some of the gene regions linked to menarche overlap with genes tied to hormone production, body weight, weight at birth, adulthood height and bone density -- among other things.

Perry and his colleagues report the findings in the July 23 online issue of Nature.

Combing through data on more than 180,000 women, the researchers found that girls vary widely in the age at which they start menstruating. Some start as early as age 8, while others start in high school. Exercise levels, nutrition and body weight are all influences, but there are probably many other factors involved, too, Perry pointed out.

"We identified over 100 regions of the genome that were associated with puberty timing," he said. "However, our analyses suggest there are likely to be thousands of gene variants -- and possibly genes -- involved."

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PUBLIC RELEASE DATE:

24-Jul-2014

Contact: Mary Beth O'Leary moleary@cell.com 617-397-2802 Cell Press

Autism spectrum disorder and intellectual disability often occur together and may even share similar genetic causes. Researchers reporting in the Cell Press journal Cell Reports have now linked mutations in a particular gene to the two disorders in humans. By revealing these genetic changes and their potential impact on common brain processes, researchers may uncover treatment approaches that could benefit a variety of patients.

In a study of four families with a total of 16 individuals affected by a spectrum of cognitive and social impairments, the research team, led by investigators from Boston Children's Hospital and Harvard Medical School, discovered two mutations in the CC2D1A gene that prevent the gene's expression. When inherited from both parents, the lack of gene expression can cause mild to severe intellectual disability, autism, and/or seizures. The scientists then explored the function of this gene through experiments in mice.

"A neuron must perform a very complex balancing act to respond to signals from other cells, and we found that CC2D1A is a key component in controlling this balance," says senior author Dr. Christopher Walsh. A critical part of that balance involves the control of a signaling pathway that relies on NF-kappaB, a protein necessary for the survival and function of neurons. Reducing CC2D1A expression in mice led to decreased complexity of neurons and to increased NF-kappaB activity. Furthermore, the effects of CC2D1A depletion in neurons could be reversed by treating the mice with compounds that inhibit NF-kappaB activity.

"We hope that in the future, by fully understanding how this gene affects signaling in the brain, we may be able to identify drugs to restore the normal signaling balance in neurons and improve cognitive and social function in patients," says lead author Dr. M. Chiara Manzini. "In addition, by studying how the same exact genetic change can cause either intellectual disability or autism, we can explore how these disorders originate and where they overlap."

The researchers plan to investigate what percentage of individuals individuals with intellectual disability and autism may carry CC2D1A mutations and to determine whether other genes affect neurons in a similar fashion.

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Cell Reports, Manzini et al.: "CC2D1A regulates human intellectual and social function, and NF-B signaling homeostasis."

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24-Jul-2014

Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 24, 2014Malcolm K. Brenner, MD, PhD, Baylor College of Medicine (Houston, TX) has devoted his career in basic and clinical research toward understanding how tumors are able to escape detection by the body's immune defense system, and developing genetically modified T cells that can effectively target tumors. In recognition of his scientific achievements and leadership in the field, Dr. Brenner is the recipient of a Pioneer Award from Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. Human Gene Therapy is commemorating its 25th anniversary by bestowing this honor on the leading 12 Pioneers in the field of cell and gene therapy selected by a blue ribbon panel* and publishing a Pioneer Perspective by each of the award recipients. The Perspective by Dr. Brenner is available on the Human Gene Therapy website.

In "Gene Modified Cells for Stem Cell Transplantation and Cancer Therapy", Dr. Brenner recounts the highlights of his career to date. He describes the evolution of his research, which has contributed significantly to advancing the field of gene transfer using retroviral vectors in the development of both autologous (AUTO) and allogeneic (ALLO) hematopoietic stem cell transplantation (HSCT) approaches to cancer immunotherapy, and the strategy of using chimeric antigen receptors (CARs) to modify T cells stimulating their activation, proliferation, and anti-tumor activity.

Dr. Brenner received a PhD in immunology and early in his career sought to understand how B cells interact with T cells to produce antibodies. After pursuing the development of cellular therapies to treat immune disorders, Dr. Brenner shifted the focus of his research to bone marrow transplantation, or what is now called HSCT. Together with colleagues he developed and tested an approach to improve patients' immune recovery after their T cells are depleted in preparation for a transplant. As Dr. Brenner explains, "This work was the forerunner of our later efforts to improve antiviral and antitumor immunity by adoptive transfer of T cells."

"Malcolm has been driving the field of cell-based gene therapy forward since its infancy. His contributions have been truly seminal," says James M. Wilson, MD, PhD, Editor-in-Chief of Human Gene Therapy and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

*The blue ribbon panel of leaders in cell and gene therapy, led by Chair Mary Collins, PhD, MRC Centre for Medical Molecular Virology, University College London selected the Pioneer Award recipients. The Award Selection Committee selected scientists that had devoted much of their careers to cell and gene therapy research and had made a seminal contribution to the field--defined as a basic science or clinical advance that greatly influenced progress in translational research.

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Malcolm K. Brenner receives Pioneer Award for advances in gene-modified T cells targeting cancer

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Cancer is a disease of the genome resulting from a combination of genetic modifications (or mutations). We inherit from our parents strong or weak predispositions to developing certain kinds of cancer; in addition, we also accumulate new mutations in our cells throughout our lifetime. Although the genetic origins of cancers have been studied for a long time, researchers were not able to measure the role of non-coding regions of the genome until now. A team of geneticists from the University of Geneva (UNIGE), by studying tissues from patients suffering from colorectal cancer, have succeeded in decoding this unexplored, but crucial, part of our genome. Their results can be found in Nature.

To better understand how cancer develops, scientists strive to identify genetic factors -- whether hereditary or acquired -- that could serve as the catalyst or trigger for tumor progression. Until now, the genetic basis of cancers had only been examined in the coding regions of the genome, which constitutes only 2% of it. However, as recent scientific advances have shown, the other 98% is far from inactive: it includes elements that serve to regulate gene expression, and therefore should play a major role in the development of cancer.

In order to better understand this role, Louis-Jeantet professor Emmanouil Dermitzakis and his team, from the Department of Genetic and Developmental Medicine in UNIGE's Faculty of Medicine, studied colorectal cancer, one of the most common and most deadly cancers. Indeed, each year, one million new cases are detected around the world, and for almost half of these patients, the disease will prove fatal. Using genome sequencing technology, the UNIGE geneticists compared the RNA between healthy tissue and tumor tissue from 103 patients, searching for regulatory elements present in the vast, non-coding portion of the genome that impact the development of colorectal cancer. The goal was to identify the effect, present only in cancerous tissue, of acquired mutations whose activation would have triggered the disease. This approach is totally new: it is the first study of this scale to examine the non-coding genome of cancer patients.

Unknown Mutations

The UNIGE team was able to identify two kinds of non-coding mutations that have an impact on the development of colorectal cancer. They found, on one hand, hereditary regulatory variants that are not active in healthy tissue, but are activated in tumors and seem to contribute to cancer progression. It shows that the genome we inherit not only affects our predisposition towards developing cancer, but also has an influence on its progression. On the other hand, the researchers identified effects of acquired mutations on the regulation of gene expression that affect the genesis and progression of colorectal tumors.

'The elements responsible for the development and progression of cancers located in the non-coding genome are as important as those found in the coding regions of the genome. Therefore, analyzing genetic factors in our whole genome, and not only in the coding regions as it was done before, gives us a much more comprehensive knowledge of the genetics behind colorectal cancer,' explains Halit Ongen, the lead author of this study. 'We applied this completely innovative methodology to colorectal cancer, but it can be applied to understand the genetic basis of all sorts of cancers,' underlines Professor Dermitzakis.

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The above story is based on materials provided by Universit de Genve. Note: Materials may be edited for content and length.

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge: Cowgirl and Horse Edition Episode 24
Come join me on my latest journey into the complex world of sims 3 genetics, as I try to get perfect foals and perfect children. Will I succeed in getting pe...

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Christian Enemark. Panel 3: Manipulated Microbes: Genetics, Genomics and Global Health Security
Annual Conference 2014: #39;Genetics, Genomics and Global Health -- Inequalities, Identities and Insecurities #39; 19th July 2014 University of Sussex Conference Ce...

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DeKalb Plant Genetics: Video Transfers From 16mm Films
This VHS tape contains a variety of films that were converted to VHS from film reels. Films contained in this tape include: XL 25-A, XL 55-A, Microwave Promotion (3 Parts), Food for America,...

By: DeKalb Area Agricultural Heritage Association (DAAHA)

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Dr. Kri Stefnsson on genetics - The New Yorker Conference
Dr. Kri Stefnsson, the founder of the biopharmaceutical company deCODE Genetics, talks with Michael Specter about his research into human genetics and its applications for drug development....

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Saving the Honeybee with Genetics and Beekeeping
The disappearance of honeybees continues to make headlines in the news and science journals, but are their numbers still dwindling, and if so, what are the causes? Dr. Jack Bishop, a researcher...

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Ashley Saulsberry: Speciation Genetics in Nasonia
(Note: Volume needs to be turned up) Vanderbilt University undergraduate and Littlejohn Summer Research Scholar Ashley Saulsberry discusses her thesis work on the origin of species. In the...

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge: Cowgirl and Horse Edition Episode 27
Come join me on my latest journey into the complex world of sims 3 genetics, as I try to get perfect foals and perfect children. Will I succeed in getting perfect genetics in both? Can I keep...

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Let's Play The Sims 3 - Perfect Genetics Challenge: Cowgirl and Horse Edition Episode 27 - Video

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New Gene Therapy Procedure Could Allow Own Cells To Act As Pacemakers
Implantable electronic pacemakers are some of the most common heart procedures done every year. But what if doctors could turn your own cells into pacemakers...

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PUBLIC RELEASE DATE:

24-Jul-2014

Contact: Byron Spice bspice@cs.cmu.edu 412-268-9068 Carnegie Mellon University

PITTSBURGHComputer scientists at Carnegie Mellon University, working with high-throughput data generated by breast cancer biologists at Lawrence Berkeley National Laboratory, have devised a computational method to determine how gene networks are rewired as normal breast cells turn malignant and as they respond to potential cancer therapy agents.

This method for analyzing how genes interact with each other in laboratory-grown cells is described in a report published today by the online journal PLOS Computational Biology.

The method could provide new insights into cancer and identify the most promising molecular targets for drug therapy. In their study, for instance, the researchers were able to show how changes in these gene networks led breast cancer cells to develop resistance to several different agents being evaluated as drugs for targeted therapy.

"With our system, pharmaceutical developers wouldn't need to go to expensive clinical trials to discover that a drug isn't going to work," said Wei Wu, associate research professor in CMU's Lane Center for Computational Biology. "It could save them a tremendous amount of money and a tremendous amount of time."

The approach also might be used to detect differences in gene regulation between individuals, helping physicians select which treatment will be most effective for each patient, she added.

Wu and Eric P. Xing, associate professor of machine learning, worked with Mina Bissell, a renowned breast cancer researcher at the Berkeley Lab, to investigate whether distinctly different gene regulatory networks could be identified within cells as normal cells become malignant and as the malignant cells respond to various drug treatments. The researchers studied these breast cancer cells using a 3D cell culturing technique developed by Bissell's laboratory.

These networks can be inferred based on microarrays, which measure the expression levels of tens of thousands of genes in a cell. But the number of microarrays that investigators can afford to run for each cell state normal cells, malignant cells and malignant cells that have reverted to normal-looking cells that also are organized normally is limited. So researchers often pool microarray data from several cell states in hopes of gaining enough samples to draw solid conclusions about networks, Wu said.

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Surgeons at the University Hospital Southampton have designed the new procedure to coat damaged cartilage with stem cells taken from the hip If successful, it will regenerate the remaining tissue, creating a permanent 'like-for-like' replacement for the first time Cartilage is a tough tissue covering the surface of joints and enables bones to slide over one another, reducing friction and acting as a shock absorber

By Lizzie Parry

Published: 07:05 EST, 23 July 2014 | Updated: 07:21 EST, 23 July 2014

Surgeons have designed a new operation which they hope could prevent the development of arthritis and extend sporting careers.

The procedure, which is currently being trialled at Southampton General Hospital, involves coating damaged cartilage with stem cells, taken from a patients own hip, and surgical glue.

If successful, it will regenerate the remaining tissue and create a permanent 'like-for-like' replacement for the first time.

Surgeons at University Hospital Southampton have pioneered a new operation to treat knee injuries, which they hope will extend sporting careers. Argentinian striker Luis Suarez had an operation to remove his damaged meniscus, part of the cartilage in the knee, prior to the World Cup

Cartilage is a tough, flexible tissue that covers the surface of joints and enables bones to slide over one another while reducing friction and acting as a shock absorber.

Damage to the tissue in the knee is common and occurs mainly following sudden twists or direct blows, such as falls or heavy tackles playing sports such as football and rugby, but can also develop over time through gradual wear and tear.

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New knee op using stem cells could stop arthritis and extend sporting careers

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Inference in Personalized Medicine Models
student seminar, April, 2014.

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21st Century Cures Roundtable on Personalized Medicine
Learn more here: http://1.usa.gov/1nRZvAb.

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Monthly financial statements
Paul describes what you need to be ware of when submitting your monthly reports.

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Hip Pain and Regenerative Medicine
Hip pain that won #39;t go away Dr. Lox | http://www.drlox.com | Call (844) 440-8503 Hip Pain that won #39;t go away often involves consultations with multiple specialists....

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Patients' virus levels became undetectable after a bone-marrow therapy with stem cells

Scanning electron microscope (SEM) image of a lymphocyte with HIV cluster. Credit: National Cancer Institute via Wikimedia Commons

Scientists have uncovered two new cases of HIV patients in whom the virus has become undetectable.

The two patients, both Australian men, became apparently HIV-free after receiving stem cells to treat cancer. They are still on antiretroviral therapy (ART) as a precaution, but those drugs alone could not be responsible for bringing the virus to such low levels, says David Cooper, director of the Kirby Institute at the University of New South Wales in Sydney, who led the discovery. A year ago, a different group of researchers had reported cases with a similar outcome.

Cooper presented details of the cases today at a press briefing in Melbourne, Australia, where delegates are convening for next week's 20th International AIDS Conference. The announcement came just a day after the news that at least six people heading to the conference died when aMalaysia Airlines flight was shot down in Ukraine.

Cooper began searching for patients who had been purged of the HIV virus after attending a presentation by a US team last year at a conference of the International AIDS Society in Kuala Lumpur. At that meeting, researchers from Brigham and Womens Hospital in Boston, Massachusetts, reported that two patients who had received stem-cell transplants were virus-free.

Cooper and his collaborators scanned the archives of St Vincents hospital in Sydney, one of the largest bone-marrow centres in Australia. We went back and looked whether we had transplanted [on] any HIV-positive patients, and found these two, says Cooper.

The first patient had received a bone-marrow transplant for non-Hodgkin's lymphoma in 2011. His replacement stem cells came from a donor who carried one copy of a gene thought to afford protection against the virus. The other had been treated for leukaemia in 2012.

Unfortunately, several months after the 'Boston' patients stopped taking ART,the virus returned. An infant born with HIV in Mississippi who received antiretroviral therapy soon after birth, then stopped it for more than three years,was thought to have been cured, buthas had the virus rebound, too.

Natural resistance At the moment, there is only one person in the world who is still considered cured of HIV:Timothy Ray Brown, the 'Berlin patient', who received a bone-marrow transplant and has had no signs of the virus in his blood for six years without ART. The bone marrow received by the Berlin patient came from a donor who happened to have a natural genetic resistance to his strain of HIV.

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HIV Cleared in 2 Patients via Cancer Treatment

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Surgeons have pioneered a new knee operation that could prevent the development of arthritis and extend sporting careers.

The procedure, which is currently being trialled at Southampton General Hospital, involves coating damaged cartilage with stem cells, taken from a patient's own hip, and surgical glue.

Known as Abicus (Autologous Bone Marrow Implantation of Cells University Hospital Southampton), the technique, if successful, will regenerate the remaining tissue and create a permanent "like-for-like" replacement for the first time.

Cartilage is a tough, flexible tissue that covers the surface of joints and enables bones to slide over one another while reducing friction and acting as a shock absorber.

Damage to the tissue in the knee is common and occurs mainly following sudden twists or direct blows, such as falls or heavy tackles playing sports such as football and rugby, but can also develop over time through gradual wear and tear.

Around 10,000 people a year in the UK suffer cartilage damage serious enough to require treatment due to pain, "locking" and reduced flexibility. If left untreated, it can progress to arthritis and severely impair leg movement.

Currently, the most commonly used procedure to repair the injury - microfracture - involves trimming any remaining damaged tissue and drilling holes in the bone beneath the defect via keyhole surgery to promote bleeding and scar tissue to work as a substitute.

However, the technique has variable results, with studies in the US suggesting the procedure offers only a short term benefit (the first 24 months after surgery), and does not lead to the formation of new cartilage.

Patients who undergo the Abicus operation have the cartilage cut and tidied and undergo microfracture, but their cartilage tissue is then coated with a substance made up of bone marrow cells, platelet gel and hyaluronic acid.

During the 30-minute procedure, the bone marrow sample is spun in a centrifuge in the operating theatre to give a concentrated amount of the patient's own stem cells.

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High hopes for new knee operation

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Scientists have discovered a new way to make human platelets, which could help patients worldwide who need blood transfusions.

Platelets are the cells we use to form blood clots. They're traditionally created in our bone marrow. But scientists are now using a machine called a platelet bioreactoralong with human stem cells to create platelets outside the human body.(ViaYouTube / ThrombosisAdviser,American Society of Hematology)

Essentially, this"next-generation"device asBoston Magazinecalls it features the same characteristics asbone marrow. The crucial difference: It's able to carry out a reaction on an industrial scale.

An author of the study said in a press release published byHealthDay,"The ability to generate an alternative source of functional human platelets with virtually no disease transmission represents a paradigm shift in how we collect platelets that may allow us to meet the growing need for blood transfusions."

Brigham and Women's Hospital reports more than 2 million donor platelet units are transfused each year in the U.S. to help patients in need.

That includestrauma patients and those undergoing chemotherapy, organ transplants and surgery. (Getty Images)

But platelet shortages are common due to increased demand, a short shelflife and the possibility of contamination, rejection and infection. (Getty Images)

The problem lab-created platelets have runinto in the past istime: Growing new platelets took too long.

A doctor not associated with this researchsaid,"This study addresses that gap, while contributing to our understanding of platelet biology at the same time."(ViaHealthDay /Brigham and Women's Hospital)

Butthe rules are tough on blood products, so the platelets will undergo safety tests over the next three years. Clinical human trials likely won't start until 2017. (Getty Images)

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Scientists have already successfully coaxed stem cells into becoming red blood cells, which could be used to create "man-made" blood for transfusion. Red blood cells, however, aren't the only component of human blood. Now, researchers at Harvard-affiliated Brigham and Womens Hospital have also created functional human platelets, using a bioreactor that simulates the medium in which blood cells are naturally produced bone marrow.

The main role of platelets (also known as thrombocytes) is to stop wounds from bleeding, by essentially "plugging the hole" in the skin with a clot. Without sufficient numbers of them in the blood, spontaneous and excessive bleeding can occur. Such shortages can be caused by diseases, as a result of undergoing chemotherapy, or by other factors. In these situations, transfusions of platelets harvested from donated blood are often necessary.

In previous studies, scientists have successfully gotten induced pluripotent stem cells to change into megakaryocytes these are the cells that ordinarily sit in the bone marrow and release platelets into the bloodstream. Unfortunately, it's proven difficult to get those lab-grown megakaryocytes to produce platelets outside of the body.

That's where Brigham and Womens new "bioreactor-on-a-chip" comes into the picture. By mimicking bone marrow's extracellular matrix composition, stiffness, micro-channel size and shear forces, it persuades the megakaryocytes to produce anywhere from 10 to 90 percent more platelets than was previously possible.

It is hoped that once the technology is scaled up, platelets made with it could be used to address shortages of donated natural platelets, and to minimize the risk of diseases being transmitted between donors and recipients. Human clinical trials are planned to begin in 2017.

The research was led by Dr. Jonathan Thon, and is described in a paper recently published in the journal Blood.

Source: Brigham and Womens Hospital

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ST. PETERSBURG, Fla. -

Cheri Kovacsev's face is dripping with blood, and she wouldn't have it any other way.

"I'm hoping to achieve smaller pores, [and] the fine lines around my lips to improve over this process," Kovacsev said.

Licensed paramedical aesthetician Amaris Centofanti performs rejuvapen micro-needling.

"After you are done with the treatment, collagen elastin kicks in to heal the skin, so in a few days, your skin starts to look more flawless," Centofanti said.

People like the professor of dermatology, Dr. James Spencer, however, aren't sold on micro-needling, which costs about $350 a pop.

"There was just a study in the Journal of the American Medical Association Dermatology, JAMA Dermatology, last month, of three cases of allergy to the medication to the serum that was put on after micro-needling," Spencer said.

Some other extreme beauty treatments include the bee venom facial. The theory is the venom tightens skin by pumping up collagen. It costs about $130.

Then there is the vampire face-lift, which costs about $600 to $800. For this treatment, plasma is taken from your blood and injected back into your skin.

The placenta facial uses stem cells from a sheeps placenta to boost collagen.

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PUBLIC RELEASE DATE:

23-Jul-2014

Contact: David McKeon dmckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation

NEW YORK, NY -- The New York Stem Cell Foundation (NYSCF) and Beyond Batten Disease Foundation (BBDF) have partnered to develop stem cell resources to investigate and explore new treatments and ultimately find a cure for juvenile Batten disease, a fatal illness affecting children.

NYSCF scientists will create induced pluripotent stem (iPS) cell lines from skin samples of young people affected by juvenile Batten disease as well as unaffected family members. IPS cell lines are produced by artificially "turning back the clock" on skin cells to a time when they were embryonic-like and capable of becoming any cell in the body. Reprogramming juvenile Batten iPS cells to become brain and heart cells will provide the infrastructure needed to investigate what is going wrong with the cells adversely affected by the disease. Thus far, efforts to study juvenile Batten disease have been done using rodent models or human skin cells, neither of which accurately mimic the disease in the brain, leaving researchers without proper tools to study the disease or a solid platform for testing drugs that prevent, halt, or reverse its progression. This will be the largest and first genetically diverse collection of human iPS cells for a pediatric brain disease.

In addition to working with BBDF to actively recruit patients and families to donate skin samples, Batten Disease Support and Research Association (BDSRA) is providing resources and technical support, spreading awareness among academic scientists, and notifying its Pharmaceutical partners. Together, BBDF and BDSRA will ensure that juvenile Batten disease and other researchers are aware of and utilize the 48 stem cell lines resulting from this collaboration to further juvenile Batten disease research worldwide.

"We know the genetic mutations associated with juvenile Batten disease. This partnership will result in stem cell models of juvenile Batten, giving researchers an unprecedented look at how the disease develops, speeding research towards a cure," said Susan L. Solomon, NYSCF Chief Executive Officer.

"Working with NYSCF to generate functional neuronal subtypes from patients and families is a stellar example of one of our key strategies in the fight against juvenile Batten disease: creating resource technology with the potential to transform juvenile Batten disease research and accelerate our timeline to a cure," said Danielle M. Kerkovich, PhD, BBDF Principal Scientist.

Juvenile Batten disease begins in early childhood between the ages of five and ten. Initial symptoms typically begin with progressive vision loss, followed by personality changes, behavioral problems, and slowed learning. These symptoms are followed by a progressive loss of motor functions, eventually resulting in wheelchair use and premature death. Seizures and psychiatric symptoms can develop at any point in the disease.

Juvenile Batten disease is one disorder in a group of rare, fatal, inherited disorders known as Batten disease. Over 40 different errors (mutations) in the CLN3 segment of DNA (gene) have been attributed to juvenile Batten disease. The pathological hallmark of juvenile Batten is a buildup of lipopigment in the body's tissues. It is not known why lipopigment accumulates or why brain and eventually, heart cells are selectively damaged. It is, however, clear that we need disease-specific tools that reflect human disease in order to figure this out and to build therapy.

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NYSCF partners with Beyond Batten Disease Foundation to fight juvenile Batten disease

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