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Stem Cells for Heart Cell Therapies – National Center for …

Abstract

Myocardial infarctioninduced heart failure is a prevailing cause of death in the United States and most developed countries. The cardiac tissue has extremely limited regenerative potential, and heart transplantation for reconstituting the function of damaged heart is severely hindered mainly due to the scarcity of donor organs. To that end, stem cells with their extensive proliferative capacity and their ability to differentiate toward functional cardiomyocytes may serve as a renewable cellular source for repairing the damaged myocardium. Here, we review recent studies regarding the cardiogenic potential of adult progenitor cells and embryonic stem cells. Although large strides have been made toward the engineering of cardiac tissues using stem cells, important issues remain to be addressed to enable the translation of such technologies to the clinical setting.

Heart disease is a significant cause of morbidity and mortality worldwide. In the United States, heart failure is ranked number one as a cause of death, affecting over 5 million people and with more than 500,000 new cases diagnosed each year.1 The health care expenditures associated with heart failure were $26.7 billion in 2004 and are estimated to $33.2 billion in 2007. Although significant progress has been made in mechanical devices and pharmacological interventions, more than half of the patients with heart failure die within 5 years of initial diagnosis. Wide application of heart transplantation is severely hindered by the limited availability of donor organs. To this end, cardiac cell therapy may be an appealing alternative to current treatments for heart failure.

Recent investigations focusing on engineering cells and tissues to repair or regenerate damaged hearts in animal models and in clinical trials have yielded promising results. Considering the limited regenerative capacity of the heart muscle, renewable sources of cardiomyocytes are highly sought. Cells suitable for myocardial engineering should be nonimmunogenic, should be easy to expand to large quantities, and should differentiate into mature, fully functional cardiomyocytes capable of integrating to the host tissue. Adult progenitor cells (APCs) and embryonic stem cells (ESCs) have extensive proliferative potential and can adopt different cell fates, including that of heart cells. The recent advances in the fields of stem cell biology and heart tissue engineering have intensified efforts toward the development of regenerative cardiac therapies. In this article, we review findings pertaining to the cardiogenic potential of major APC populations and of ESCs (). We also discuss significant challenges in the way of realizing stem cellbased therapies aiming to reconstitute the normal function of heart.

Potential sources of stem/progenitor cells for cardiac repair. ESCs derived from the inner cell mass of a blastocyst can be manipulated ex vivo to differentiate toward heart cells. APCs residing in various tissues such as the BM and skeletal muscle may …

Bone marrow (BM) is a heterogeneous tissue comprising of multiple cell types, including minute fractions of mesenchymal stem cells (MSCs; 0.0010.01% of total cells2) and hematopoietic stem cells (HSCs; 0.71.5cells/108 nucleated marrow cells3). The heterogeneity of BM makes challenging the identification of a subpopulation of cells capable of cardiogenesis, and studies of BM celltocardiac cell transdifferentiation should be examined through this prism.

The notion that BM-derived cells may contribute to the regeneration of the heart was first illustrated when dystrophic (mdx) female mice received BM cells from male wild-type mice.4 More than 2 months after the transplantation, tissues of the recipient mice were histologically examined for the presence of Y-chromosome+ donor cells. Besides the skeletal muscle, donor cells were identified in the cardiac region, suggesting that circulating BM cells contribute to the regeneration of cardiomyocytes.

Further supporting evidence was provided by Jackson et al.5 in studies using a side population (SP) of cells characterized by their intrinsic capacity to efflux Hoechst 33342 dye through the ATP-binding Bcrp1/ABCG2 transporter. The cells were isolated from the BM fraction of HSCs of Rosa26 mice constitutively expressing the -galactosidase reporter gene (LacZ). After SP cells were injected into mice with coronary occlusioninduced ischemia, cells coexpressing LacZ and cardiac -actinin were identified around the infarct region with a frequency of 0.02%. Endothelial engraftment was more prevalent (3.3%). The observed improvement in myocardial function may thus be attributed to the potential of BM cells to give rise to a rather endothelial progeny. This may be a parallel to cardiovascular progenitors from differentiating ESCs giving rise to cardiomyocytes, and endothelial and vascular smooth muscle lineages.6,7

Orlic et al.8 also reported the regeneration of infarcted myocardium after transplantation of lineage-negative (LIN)/C-KIT+ BM cells from transgenic mice constitutively expressing enhanced green fluorescent protein (eGFP). Cells were injected in the contracting wall close to the infarct area. Nine days after transplantation, an impressive 68% of the infarct was occupied by newly formed myocardium with eGFP+ cells displaying cardiomyocyte markers such as troponin, MEF2, NKX2.5, cardiac myosin, GATA-4, and -sarcomeric actin. Similar outcomes were reported by the same group9 when mouse C-KIT+ (but not screened for LIN) BM cells were transplanted.

Although these findings led to the conclusion that BM cells can repopulate a damaged heart, work by other investigators has casted doubt on this assertion. Balsam et al.10 noted that mice with infarcts receiving BM LIN/C-KIT+, C-KIT-enriched or THY1.1low/LIN/stem cell antigen-1 (SCA-1+) cells exhibited improved ventricular function. However, donor cells expressed granulocyte but not heart cell markers 1 month after injection. In another study,11 HSCs carrying a nuclear-localized LacZ gene flanked by the cardiac -myosin heavy chain promoter were delivered into the periinfarct zone of mice 5h after coronary artery occlusion. One to 4 weeks later, LacZ+ cells were absent in heart tissue sections from 117 mice that received HSCs. Similarly, no eGFP+ cells were detected in the infarcted hearts of mice infused with BM cells constitutively expressing eGFP. Finally, Nygren et al.12 in similar transplantation experiments observed only blood cells (mainly leukocytes) originating from BM HSCs in the infarcted myocardium without evidence of transdifferentiation of donor cells to cardiomyocytes.

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Stem Cells for Heart Cell Therapies – National Center for …

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Male Hair Loss All You Need To Know – The Belgravia Centre

Although there are a number of hair loss conditions that can affect men, the most common is Male Pattern Baldness (MPB). Other names for this condition are androgenetic alopecia and genetic hair loss. This page will concentrate primarily on this condition but will also make reference to the less widespread hair loss conditions that could be affecting you, with links to more informative pages.

Male Pattern Baldness is a genetic condition that can be passed down from either side of the family tree. So if your Father has a perfectly thick head of hair, dont think you are definitely safe (although you could be!). It is a condition caused by a bi-product of testosterone named Dihydrotestosterone, or DHT. DHT attaches to the hair follicles and causes them to shrink over time, which causes the hair to become thinner and thinner until some men become totally bald on the top of the head.

This is a very good question, and although the answer might seem obvious, many men do not identify their hair loss until it has become fairly advanced, which could be too late to achieve a full recovery. The reasons men do not identify their own hair loss are usually down to simple denial, or because the process is very slow and it is something that they simply might not notice. At the opposite end of the scale, many men worry about hair loss when they have no reason to worry.

The best ways to know if you are losing your hair are:

MPB is in fact easy to identify even for somebody with no clinical experience as it only affects hair on the top of the scalp and not the sides, causing a horseshoe-shaped pattern of hair loss. There are a number of different common patterns of hair loss a receding hairline, a thinning crown, or general thinning spread over the top area of the head. You can read more about these below. MPB never affects the sides or back of the hair.

There are a number of options available for treating Male Pattern Baldness, including clinically proven medications, laser devices and hair restoration surgery. There are also numerous products out there that have no clinical efficacy, so it is easy to waste time and money whilst your hair continues to shed. It is therefore very important that you carry out the necessary research before deciding how you are going to treat your hair loss. The good news is that unless you have lost all or most of your hair, there is a solution out there for you, whether it be a medical solution, a surgical one, or a combination of the two.

Our comprehensive hair loss treatment guide walks you through all the most effective options available for treating hair loss and also gives you an in-depth look at the products that may not be worth using.

hair loss treatment guide

This depends on a number of factors. Firstly, the condition causing your hair loss if you have a temporary hair loss condition (which is unusual in men) then the answer may be no. Please refer to our list of other hair loss conditions below if your problem doesnt appear to be MPB.

Assuming your condition is Male Pattern Baldness, the extent of your eventual hair loss really depends. Those men who have a very early or aggressive onset of MPB are more likely to lose their hair more extensively or at a faster rate, which could result in baldness at an early age. We see men who begin to lose their hair at 18 years old (or sometimes earlier). These men will of course be the ones most likely to reach eventual baldness, sometimes at a fairly early age (mid-twenties). Whereas some men only begin to see signs of thinning in their mid-to-late twenties, or even later. These men are much less likely to experience eventual baldness and may just have thin hair by the time they reach old age.

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Male Hair Loss All You Need To Know – The Belgravia Centre

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Cancer – Wikipedia, the free encyclopedia

Cancer i, also known as a malignant tumor or malignant neoplasm, is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] Not all tumors are cancerous; benign tumors do not spread to other parts of the body.[2] Possible signs and symptoms include: a new lump, abnormal bleeding, a prolonged cough, unexplained weight loss, and a change in bowel movements among others.[3] While these symptoms may indicate cancer, they may also occur due to other issues.[3] There are over 100 different known cancers that affect humans.[2]

Tobacco use is the cause of about 22% of cancer deaths.[1] Another 10% is due to obesity, a poor diet, lack of physical activity, and consumption of ethanol (alcohol).[1] Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants.[4] In the developing world nearly 20% of cancers are due to infections such as hepatitis B, hepatitis C, and human papillomavirus.[1] These factors act, at least partly, by changing the genes of a cell.[5] Typically many such genetic changes are required before cancer develops.[5] Approximately 510% of cancers are due to genetic defects inherited from a person’s parents.[6] Cancer can be detected by certain signs and symptoms or screening tests.[1] It is then typically further investigated by medical imaging and confirmed by biopsy.[7]

Many cancers can be prevented by not smoking, maintaining a healthy weight, not drinking too much alcohol, eating plenty of vegetables, fruits and whole grains, being vaccinated against certain infectious diseases, not eating too much red meat, and avoiding too much exposure to sunlight.[8][9] Early detection through screening is useful for cervical and colorectal cancer.[10] The benefits of screening in breast cancer are controversial.[10][11] Cancer is often treated with some combination of radiation therapy, surgery, chemotherapy, and targeted therapy.[1][12] Pain and symptom management are an important part of care. Palliative care is particularly important in those with advanced disease.[1] The chance of survival depends on the type of cancer and extent of disease at the start of treatment.[5] In children under 15 at diagnosis the five year survival rate in the developed world is on average 80%.[13] For cancer in the United States the average five year survival rate is 66%.[14]

In 2012 about 14.1 million new cases of cancer occurred globally (not including skin cancer other than melanoma).[5] It caused about 8.2 million deaths or 14.6% of all human deaths.[5][15] The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer, and stomach cancer, and in females, the most common types are breast cancer, colorectal cancer, lung cancer, and cervical cancer.[5] If skin cancer other than melanoma were included in total new cancers each year it would account for around 40% of cases.[16][17] In children, acute lymphoblastic leukaemia and brain tumors are most common except in Africa where non-Hodgkin lymphoma occurs more often.[13] In 2012, about 165,000 children under 15 years of age were diagnosed with cancer. The risk of cancer increases significantly with age and many cancers occur more commonly in developed countries.[5] Rates are increasing as more people live to an old age and as lifestyle changes occur in the developing world.[18] The financial costs of cancer have been estimated at $1.16 trillion US dollars per year as of 2010.[19]

Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth, and will often form a mass or lump, but may be distributed diffusely.[20][21]

Six characteristics of cancer have been proposed:

The progression from normal cells to cells that can form a discernible mass to outright cancer involves multiple steps known as malignant progression.[22][23]

When cancer begins, it invariably produces no symptoms. Signs and symptoms only appear as the mass continues to grow or ulcerates. The findings that result depend on the type and location of the cancer. Few symptoms are specific, with many of them also frequently occurring in individuals who have other conditions. Cancer is the new “great imitator”. Thus, it is not uncommon for people diagnosed with cancer to have been treated for other diseases, which were assumed to be causing their symptoms.[24]

Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can cause blockage of the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, resulting in changes in bowel habits. Masses in breasts or testicles may be easily felt. Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine, and in the uterus to vaginal bleeding. Although localized pain may occur in advanced cancer, the initial swelling is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen.[24]

General symptoms occur due to distant effects of the cancer that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, being excessively tired, and changes to the skin.[25]Hodgkin disease, leukemias, and cancers of the liver or kidney can cause a persistent fever of unknown origin.[24]

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Cancer – Wikipedia, the free encyclopedia

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Types of Genetic Testing – Genetics Home Reference

Genetic testing can provide information about a persons genes and chromosomes. Available types of testing include:

Newborn screening is used just after birth to identify genetic disorders that can be treated early in life. Millions of babies are tested each year in the United States. All states currently test infants for phenylketonuria (a genetic disorder that causes intellectual disability if left untreated) and congenital hypothyroidism (a disorder of the thyroid gland). Most states also test for other genetic disorders.

Diagnostic testing is used to identify or rule out a specific genetic or chromosomal condition. In many cases, genetic testing is used to confirm a diagnosis when a particular condition is suspected based on physical signs and symptoms. Diagnostic testing can be performed before birth or at any time during a persons life, but is not available for all genes or all genetic conditions. The results of a diagnostic test can influence a persons choices about health care and the management of the disorder.

Carrier testing is used to identify people who carry one copy of a gene mutation that, when present in two copies, causes a genetic disorder. This type of testing is offered to individuals who have a family history of a genetic disorder and to people in certain ethnic groups with an increased risk of specific genetic conditions. If both parents are tested, the test can provide information about a couples risk of having a child with a genetic condition.

Prenatal testing is used to detect changes in a fetuss genes or chromosomes before birth. This type of testing is offered during pregnancy if there is an increased risk that the baby will have a genetic or chromosomal disorder. In some cases, prenatal testing can lessen a couples uncertainty or help them make decisions about a pregnancy. It cannot identify all possible inherited disorders and birth defects, however.

Preimplantation testing, also called preimplantation genetic diagnosis (PGD), is a specialized technique that can reduce the risk of having a child with a particular genetic or chromosomal disorder. It is used to detect genetic changes in embryos that were created using assisted reproductive techniques such as in-vitro fertilization. In-vitro fertilization involves removing egg cells from a womans ovaries and fertilizing them with sperm cells outside the body. To perform preimplantation testing, a small number of cells are taken from these embryos and tested for certain genetic changes. Only embryos without these changes are implanted in the uterus to initiate a pregnancy.

Predictive and presymptomatic types of testing are used to detect gene mutations associated with disorders that appear after birth, often later in life. These tests can be helpful to people who have a family member with a genetic disorder, but who have no features of the disorder themselves at the time of testing. Predictive testing can identify mutations that increase a persons risk of developing disorders with a genetic basis, such as certain types of cancer. Presymptomatic testing can determine whether a person will develop a genetic disorder, such as hereditary hemochromatosis (an iron overload disorder), before any signs or symptoms appear. The results of predictive and presymptomatic testing can provide information about a persons risk of developing a specific disorder and help with making decisions about medical care.

Forensic testing uses DNA sequences to identify an individual for legal purposes. Unlike the tests described above, forensic testing is not used to detect gene mutations associated with disease. This type of testing can identify crime or catastrophe victims, rule out or implicate a crime suspect, or establish biological relationships between people (for example, paternity).

A Brief Primer on Genetic Testing, which outlines the different kinds of genetic tests, is available from the National Human Genome Research Institute.

Educational resources related to patient genetic testing/carrier screening are available from GeneEd. Johns Hopkins Medicine provides additional information about genetic carrier screening.

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Types of Genetic Testing – Genetics Home Reference

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hypopituitarism – definition of hypopituitarism by Medical …

Hypopituitarism Definition

Hypopituitarism is loss of function in an endocrine gland due to failure of the pituitary gland to secrete hormones which stimulate that gland’s function. The pituitary gland is located at the base of the brain. Patients diagnosed with hypopituitarism may be deficient in one single hormone, several hormones, or have complete pituitary failure.

The pituitary is a pea-sized gland located at the base of the brain, and surrounded by bone. The hypothalamus, another endocrine organ in the brain, controls the function of the pituitary gland by providing “hormonal orders.” In turn, the pituitary gland regulates the many hormones that control various functions and organs within the body. The posterior pituitary acts as a sort of storage area for the hypothalamus and passes on hormones that control function of the muscles and kidneys. The anterior pituitary produces its own hormones which help to regulate several endocrine functions.

In hypopituitarism, something interferes with the production and release of these hormones, thus affecting the function of the target gland. Commonly affected hormones may include:

Gonadotropin deficiency involves two distinct hormones affecting the reproductive system. Luteinizing hormone (LH) stimulates the testes in men and the ovaries in women. This deficiency can affect fertility in men and women and menstruation in women. Follicle-stimulating hormone (FSH) has similar effects to LH.

Also known as corticotropin, adrenocorticotopic hormone (ACTH) stimulates the adrenal gland to produce a hormone similar to cortisone, called cortisol. The loss of this hormone can lead to serious problems.

Growth hormone (GH) regulates the body’s growth. Patients who lose supply of this hormone before physical maturity will suffer impaired growth. Loss of the hormone can also affect adults.

Deficiency of a single pituitary hormone occurs less commonly than deficiency of more than one hormone. Sometimes referred to as progressive pituitary hormone deficiency or partial hypopituitarism, there is usually a predictable order of hormone loss. Generally, growth hormone is lost first, then luteinizing hormone deficiency follows. The loss of follicle-stimulating hormone, thyroid stimulating hormone and adrenocorticotopic hormones follow much later. The progressive loss of pituitary hormone secretion is usually a slow process, which can occur over a period of months or years. Hypopituitarism does occasionally start suddenly with rapid onset of symptoms.

This condition represents the loss of all hormones released by the anterior pituitary gland. Panhypopituitarism is also known as complete pituitary failure.

There are three major mechanisms which lead to the development of hypopituitarism. The first involves decreased release of hypothalamic hormones that stimulate pituitary function. The cause of decreased hypothalamic function may be congenital or acquired through interference such as tumors, inflammation, infection, mass lesions or interruption of blood supply. A second category of causes is any event or mass which interrupts the delivery of hormones from the hypothalamus. These may include particular tumors and aneurysms. Damage to the pituitary stalk from injury or surgery can also lead to hypopituitarism.

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hypopituitarism – definition of hypopituitarism by Medical …

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Stem Cell Basics: Introduction [Stem Cell Information]

Introduction: What are stem cells, and why are they important? What are the unique properties of all stem cells? What are embryonic stem cells? What are adult stem cells? What are the similarities and differences between embryonic and adult stem cells? What are induced pluripotent stem cells? What are the potential uses of human stem cells and the obstacles that must be overcome before these potential uses will be realized? Where can I get more information?

Stem cells have the remarkable potential to develop into many different cell types in the body during early life and growth. In addition, in many tissues they serve as a sort of internal repair system, dividing essentially without limit to replenish other cells as long as the person or animal is still alive. When a stem cell divides, each new cell has the potential either to remain a stem cell or become another type of cell with a more specialized function, such as a muscle cell, a red blood cell, or a brain cell.

Stem cells are distinguished from other cell types by two important characteristics. First, they are unspecialized cells capable of renewing themselves through cell division, sometimes after long periods of inactivity. Second, under certain physiologic or experimental conditions, they can be induced to become tissue- or organ-specific cells with special functions. In some organs, such as the gut and bone marrow, stem cells regularly divide to repair and replace worn out or damaged tissues. In other organs, however, such as the pancreas and the heart, stem cells only divide under special conditions.

Until recently, scientists primarily worked with two kinds of stem cells from animals and humans: embryonic stem cells and non-embryonic “somatic” or “adult” stem cells. The functions and characteristics of these cells will be explained in this document. Scientists discovered ways to derive embryonic stem cells from early mouse embryos more than 30 years ago, in 1981. The detailed study of the biology of mouse stem cells led to the discovery, in 1998, of a method to derive stem cells from human embryos and grow the cells in the laboratory. These cells are called human embryonic stem cells. The embryos used in these studies were created for reproductive purposes through in vitro fertilization procedures. When they were no longer needed for that purpose, they were donated for research with the informed consent of the donor. In 2006, researchers made another breakthrough by identifying conditions that would allow some specialized adult cells to be “reprogrammed” genetically to assume a stem cell-like state. This new type of stem cell, called induced pluripotent stem cells (iPSCs), will be discussed in a later section of this document.

Stem cells are important for living organisms for many reasons. In the 3- to 5-day-old embryo, called a blastocyst, the inner cells give rise to the entire body of the organism, including all of the many specialized cell types and organs such as the heart, lungs, skin, sperm, eggs and other tissues. In some adult tissues, such as bone marrow, muscle, and brain, discrete populations of adult stem cells generate replacements for cells that are lost through normal wear and tear, injury, or disease.

Given their unique regenerative abilities, stem cells offer new potentials for treating diseases such as diabetes, and heart disease. However, much work remains to be done in the laboratory and the clinic to understand how to use these cells for cell-based therapies to treat disease, which is also referred to as regenerative or reparative medicine.

Laboratory studies of stem cells enable scientists to learn about the cells essential properties and what makes them different from specialized cell types. Scientists are already using stem cells in the laboratory to screen new drugs and to develop model systems to study normal growth and identify the causes of birth defects.

Research on stem cells continues to advance knowledge about how an organism develops from a single cell and how healthy cells replace damaged cells in adult organisms. Stem cell research is one of the most fascinating areas of contemporary biology, but, as with many expanding fields of scientific inquiry, research on stem cells raises scientific questions as rapidly as it generates new discoveries.

I.Introduction|Next

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Stem Cell Basics: Introduction [Stem Cell Information]

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Hormone Replacement Therapy in NYC | NYC Hormone …

Sue Decotiis, MD

As we age, even as early as age 30, our internal production of hormones can start to decline. Initially the effects are subtle and vary between individuals. But as we head toward middle age most of us experience adverse symptoms.

Symptoms of low hormones vary with the actual hormone that is low. But many deficiencies overlap, for example weight gain can occur from hypoactive thyroid as well as in menopause and andropause. Men with low testosterone and women with low estrogen may also have low DHEA and need treatment for both.

Common Symptoms of Hormone Deficiency :

We used to accept any or all of the above as normal part of getting older. But if we treat the deficiencies that lead to all of the symptoms touched on above a person can feel their best. He or she can maintain a healthy body weight and have the energy and desire to lead an active life. Plus look great doing it.

Hormone Replacement Doctor is an evidence-based medical practice. In our practice we only prescribe Bioidentical Hormone Therapy.

Why Are Hormones Important to You? Hormones are intrinsic substances that provide a continuum of specific information to nurture and direct specific cells in target organs. Without optimal hormone levels your body function is off balance and you know it. Even after seeing your physician and being told you are okay, something just isnt right. Hormone replacement therapy can make such a difference for these individuals. Most of us are or will become these individuals.

Individual body organs and their systems heart; cardiovascular system, brain; neurological system are not isolated systems. They need communicating hormones to stay vital. Looking back, life expectancy in 1900 was late 40s; so many died before reaching menopause or andropause. Now that we expect to live so many decades more than our grandparents we will have to deal with the effects of low hormone levels.With modern medicine extending life in to the ninth and tenth decade we need to think about the quality of life that hormone replacement treatment produces. Prescription medications and sophisticated treatments are not enough by themselves to produce the level of health and well being that we deserve today.

If you have any questions for the NYC Doctor in regards to Hormone Replacement Therapyor to make a consultation with Sue Decotiis, MD please contact the Doctors NYC office.

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Hormone Replacement Therapy in NYC | NYC Hormone …

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Bone marrow or stem cell transplants for AML | Cancer …

Having someone elses marrow or stem cells is called a donor transplant, or an allogeneic transplant. This is pronounced al-lo-jen-ay-ik.

The donors bone marrow cells must match your own as closely as possible. The most suitable donor is usually a close relative, such as a brother or sister. It is sometimes possible to find a match in an unrelated donor. Doctors call this a matched unrelated donor (MUD). To find out if there is a suitable donor for you, your doctor will contact The Anthony Nolan Bone Marrow Register and other UK based and international bone marrow registers.

To make sure that your donors cells match, you and the donor will have blood tests. These are to see how many of the proteins on the surface of their blood cells match yours. This is called tissue typing or HLA matching. HLA stands for human leucocyte antigen.

Once you have a donor and are in remission, you have high dose chemotherapy either on its own or with radiotherapy. A week later the donor goes into hospital and their stem cells or marrow are collected. You then have the stem cells or bone marrow as a drip through your central line.

If you’ve had a transplant from a donor, there is a risk of graft versus host disease (GVHD). This happens because the transplanted stem cells or bone marrow contain cells from your donor’s immune system. These cells can sometimes recognise your own tissues as being foreign and attack them. This can be an advantage because the immune cells may also attack any leukaemia cells left after your treatment.

Acute GVHD starts within 100 days of the transplant and can cause

If you develop GVHD after your transplant, your doctor will prescribe medicines to damp down this immune reaction. These are called immunosuppressants.

Chronic GVHD starts more than 100 days after the transplant and you may have

Your doctor is likely to suggest that you stay out of the sun because GVHD skin rashes can often get worse in the sun.

There is detailed information about graft versus host disease in the section about coping physically with cancer.

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Bone marrow or stem cell transplants for AML | Cancer …

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Stem Cells Therapy

Charles A. Goldthwaite, Jr., PhD.

Data from 2007 suggest that approximately 1.4 million men and women in the U.S. population are likely to be diagnosed with cancer, and approximately 566,000 American adults are likely to die from cancer in 2008.1 Data collected between 1996 and 2004 indicate that the overall 5-year survival rate for cancers from all sites, relative to the expected survival from a comparable set of people without cancer, is 65.3%.1 However, survival and recurrence rates following diagnosis vary greatly as a function of cancer type and the stage of development at diagnosis. For example, in 2000, the relative survival rate five years following diagnosis of melanoma (skin cancer) was greater than 90%; that of cancers of the brain and nervous system was 35%. Once a cancer has metastasized (or spread to secondary sites via the blood or lymph system), however, the survival rate usually declines dramatically. For example, when melanoma is diagnosed at the localized stage, 99% of people will survive more than five years, compared to 65% of those diagnosed with melanoma that has metastasized regionally and 15% of those whose melanoma has spread to distant sites.2

The term cancer describes a group of diseases that are characterized by uncontrolled cellular growth, cellular invasion into adjacent tissues, and the potential to metastasize if not treated at a sufficiently early stage. These cellular aberrations arise from accumulated genetic modifications, either via changes in the underlying genetic sequence or from epigenetic alterations (e.g., modifications to gene activation- or DNA-related proteins that do not affect the genetic sequence itself).3,4 Cancers may form tumors in solid organs, such as the lung, brain, or liver, or be present as malignancies in tissues such as the blood or lymph. Tumors and other structures that result from aberrant cell growth, contain heterogeneous cell populations with diverse biological characteristics and potentials. As such, a researcher sequencing all of the genes from tumor specimens of two individuals diagnosed with the same type of lung cancer will identify some consistencies along with many differences. In fact, cancerous tissues are sufficiently heterogeneous that the researcher will likely identify differences in the genetic profiles between several tissue samples from the same specimen. While some groupings of genes allow scientists to classify organ-or tissue-specific cancers into subcategories that may ultimately inform treatment and provide predictive information, the remarkable complexity of cancer biology continues to confound treatment efforts.

Once a cancer has been diagnosed, treatments vary according to cancer type and severity. Surgery, radiation therapy, and systemic treatments such as chemotherapy or hormonal therapy represent traditional approaches designed to remove or kill rapidly-dividing cancer cells. These methods have limitations in clinical use. For example, cancer surgeons may be unable to remove all of the tumor tissue due to its location or extent of spreading. Radiation and chemotherapy, on the other hand, are non-specific strategieswhile targeting rapidly-dividing cells, these treatments often destroy healthy tissue as well. Recently, several agents that target specific proteins implicated in cancer-associated molecular pathways have been developed for clinical use. These include trastuzumab, a monoclonal antibody that targets the protein HER2 in breast cancer,5 gefitinib and erlotnib, which target epidermal growth factor receptor (EGFR) in lung cancer,6 imatinib, which targets the BCR-ABL tyrosine kinase in chronic myelogenous leukemia,7 the monoclonal antibodies bevacizumab, which targets vascular endothelial growth factor in colorectal and lung cancer,8 and cetuximab and panitumumab, which target EGFR in colorectal cancer.8 These agents have shown that a targeted approach can be successful, although they are effective only in patients who feature select subclasses of these respective cancers.

All of these treatments are most successful when a cancer is localized; most fail in the metastatic setting.911 This article will discuss the CSC hypothesis and its supporting evidence and provide some perspectives on how CSCs could impact the development of future cancer therapy.

A consensus panel convened by the American Association of Cancer Research has defined a CSC as a cell within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor.12 It should be noted that this definition does not indicate the source of these cellsthese tumor-forming cells could hypothetically originate from stem, progenitor, or differentiated cells.13 As such, the terms tumor-initiating cell or cancer-initiating cell are sometimes used instead of cancer stem cell to avoid confusion. Tumors originate from the transformation of normal cells through the accumulation of genetic modifications, but it has not been established unequivocally that stem cells are the origin of all CSCs. The CSC hypothesis therefore does not imply that cancer is always caused by stem cells or that the potential application of stem cells to treat conditions such as heart disease or diabetes, as discussed in other chapters of this report, will result in tumor formation. Rather, tumor-initiating cells possess stem-like characteristics to a degree sufficient to warrant the comparison with stem cells; the observed experimental and clinical behaviors of metastatic cancer cells are highly reminiscent of the classical properties of stem cells.9

The CSC hypothesis suggests that the malignancies associated with cancer originate from a small population of stem-like, tumor-initiating cells. Although cancer researchers first isolated CSCs in 1994,14 the concept dates to the mid-19th century. In 1855, German pathologist Rudolf Virchow proposed that cancers arise from the activation of dormant, embryonic-like cells present in mature tissue.15 Virchow argued that cancer does not simply appear spontaneously; rather, cancerous cells, like their non-cancerous counterparts, must originate from other living cells. One hundred and fifty years after Virchows observation, Lapidot and colleagues provided the first solid evidence to support the CSC hypothesis when they used cell-surface protein markers to identify a relatively rare population of stemlike cells in acute myeloid leukemia (AML).14 Present in the peripheral blood of persons with leukemia at approximately 1:250,000 cells, these cells could initiate human AML when transplanted into mice with compromised immune systems. Subsequent analysis of populations of leukemia-initiating cells from various AML subtypes indicated that the cells were relatively immature in terms of differentiation.16 In other words, the cells were stem-likemore closely related to primitive blood-forming (hematopoietic) stem cells than to more mature, committed blood cells.

The identification of leukemia-inducing cells has fostered an intense effort to isolate and characterize CSCs in solid tumors. Stem cell-like populations have since been characterized using cell-surface protein markers in tumors of the breast,17 colon,18 brain,19 pancreas,20,21 and prostate.22,23 However, identifying markers that unequivocally characterize a population of CSCs remains challenging, even when there is evidence that putative CSCs exist in a given solid tumor type. For example, in hepatocellular carcinoma, cellular analysis suggests the presence of stem-like cells.24 Definitive markers have yet to be identified to characterize these putative CSCs, although several potential candidates have been proposed recently.25,26 In other cancers in which CSCs have yet to be identified, researchers are beginning to link established stem-cell markers with malignant cancer cells. For instance, the proteins Nanog, nucleostemin, and musashi1, which are highly expressed in embryonic stem cells and are critical to maintaining those cells pluripotency, are also highly expressed in malignant cervical epithelial cells.27 While this finding does not indicate the existence of cervical cancer CSCs, it suggests that these proteins may play roles in cervical carcinogenesis and progression.

Given the similarities between tumor-initiating cells and stem cells, researchers have sought to determine whether CSCs arise from stem cells, progenitor cells, or differentiated cells present in adult tissue. Of course, different malignancies may present different answers to this question. The issue is currently under debate,9,12 and this section will review several theories about the cellular precursors of cancer cells (see Fig. 9.1).

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Stem Cells Therapy

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cardiovascular disease :: Cardiac stem cells | Britannica.com

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

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cardiovascular disease :: Cardiac stem cells | Britannica.com

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Low Testosterone in Men | Hypogonadism

In men 45 and older, most cases of hypogonadism or Low-T often go overlooked due to the fact that the symptoms may be more general in nature and slower in onset. Many men simply attribute their symptoms to aging and often dismiss them because they don’t think that there is anything that they can do about them. This is largely because the symptoms of hypogonadism are nearly identical to those experienced by men going through andropause (the male menopause): low libido, fatigue, depression, memory loss, difficulty concentrating and irritability. The difference between andropause and hypogonadism is simple. Andropause is a natural part of a man’s life where his hormones begin to decline right around the age of 35 and continue to decrease until they plateau in his late 60’s. Hypogonadism is a condition where testosterone is not being produced due to a physical abnormality of the testes or brain. It can also be due to an outside factor such as stress, poor diet or pre-existing health conditions. Both Hypogonadism and andropause however can be treated and corrected under the care of experienced hormonal specialists.

There are two basic forms of hypogonadism found in men. Primary hypogonadism is also known as ?testicular failure? and stems from a complication in the testicles. Some common causes of primary hypogonadism are:

The other type of hypogonadism is called secondary hypogonadism, and it describes a condition where the testicles are normal on a physiological level, but still don’t function properly due to a problem stemming from the pituitary gland or the hypothalamus. This creates a problem with the signal from the brain to the testicle. Although the testicles function well, they can’t get the information from the brain that testosterone needs to be produced. Some common causes of secondary hypogonadism are:

The most effective ways to treat hypogonadism are to enhance the body’s ability to make its own testosterone or to supplement the testosterone that your body would produce normally, using natural bioidentical testosterone replacement therapy. It is critical to combine bioidentical hormone therapy with appropriate diet, exercise, lifestyle and stress management. Although there are many different causes for the condition, hypogonadism always leads to hormonal imbalance and can lead to a wide range of symptoms and chronic health issues. Fortunately, under the proper care of a highly trained BodyLogicMD affiliated physician, the condition can be corrected.

Through comprehensive testing, your BodyLogicMD affiliated physician will determine your hormone levels to uncover potential hormone deficiencies. Based on cutting edge diagnostic technologies, BodyLogicMD affiliated physicians pinpoint the source of underlying hormonal imbalances and use all natural bioidentical hormone replacement therapy (BHRT) interlaced with customized nutrition and fitness regimens to help men find relief symptoms of hormonal imbalance. BodyLogicMD affiliated physicians have helped thousands of men get their edge back and overcome testosterone deficiencies such as andropause and hypogonadism.

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Low Testosterone in Men | Hypogonadism

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japanese | StemCell Therapy MD

SAN DIEGO(BUSINESS WIRE)Cytori Therapeutics, Inc. (NASDAQ: CYTX) today confirmed that two Japanese regenerative medicine laws, which went into effect on November 25, 2014, remove regulatory uncertainties and provide a clear path for the Company to commercialize and market Cytori Cell Therapy and its Celution System under the Companys existing and planned regulatory approvals.

Japans new regenerative medicine laws substantially clarify regulatory ambiguities of pre-existing guidelines and this news represents a significant event for Cytori, said Dr. Marc Hedrick, President & CEO of Cytori. We have a decade of operating experience in Japan and Cytori is nicely positioned to see an impact both on existing commercial efforts and on our longer-term efforts to obtain therapeutic claims and reimbursement for our products.

Under the two new laws, Cytori believes its Celution System and autologous adipose-derived regenerative cells (ADRCs) can be provided by physicians under current Class I device regulations and used under the lowest risk category (Tier 3) for many procedures with only the approval by accredited regenerative medicine committees and local agencies of the Ministry of Health, Labour and Welfare (MHLW). This regulatory framework is expected to streamline the approval and regulatory process and increase clinical use of Cytori Cell Therapy and the Celution System over the former regulations.

Before these new laws were enacted, the regulatory pathway for clinical use of regenerative cell therapy was one-size-fits-all, irrespective of the risk posed by certain cell types and approaches, said Dr. Hedrick. Now, Cytoris point-of-care Celution System can be transparently integrated into clinical use by providers under our Class I device status and the streamlined approval process granted to cell therapies that pose the lowest risk. Our technology is unique in that respect.

Cytoris Celution System Is in Lowest of Three Risk Categories

The Act on the Safety of Regenerative Medicines and an amendment of the 2013 Pharmaceutical Affairs Act (the PMD Act), collectively termed the Regenerative Medicine Laws, replace the Human Stem Cell Guidelines. Under the new laws, the cell types used in cell therapy and regenerative medicine are classified based on risk. Cell therapies using cells derived from embryonic, induced pluripotent, cultured, genetically altered, animal and allogeneic cells are considered higher risk (Tiers 1 and 2) and will undergo an approval pathway with greater and more stringent oversight due to the presumed higher risk to patients. Cytoris Celution System, which uses the patients own cells at the point-of-care, will be considered in the lowest risk category (Tier 3) for most cases, and will be considered in Tier 2 if used as a non-homologous therapy.

Streamlined Regulatory Approval for Certain Medical Devices

In the near future, Cytori intends to pursue disease-specific or therapeutic claims and reimbursement for Cytoris Celution System and the Company would, at that point, sponsor a clinical trial to obtain Class III device-based approval and reimbursement. The new laws include changes to streamline regulation of Class II and some Class III devices, which will now require the approval of certification bodies rather than the PMDA, similar to the European notified body model. To date, certification bodies have only been used for some Class II devices.

Conditional Regulatory Approval and Reimbursement Potential

As a supplementary benefit to Cytori, the Company may also choose to take advantage of the new conditional approval opportunities granted under the new laws. Once clinical safety and an indication of efficacy are shown, sponsors may apply for their cell product to receive conditional approval for up to seven years and may be eligible for reimbursement under Japans national insurance coverage. Under the conditional approval, the sponsor can then generate post-marketing data to demonstrate further efficacy and cost effectiveness.

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japanese | StemCell Therapy MD

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Life Extension Bio Pyrroloquinoline Quinone,10 mg, 30 …

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Life Extension Bio Pyrroloquinoline Quinone,10 mg, 30 …

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The Cell Cycle – CELLS alive

During development from stem to fully differentiated, cells in the body alternately divide (mitosis) and “appear” to be resting (interphase). This sequence of activities exhibited by cells is called the cell cycle. Follow the events in the entire cell cycle with the following animation.

Interphase: Interphase, which appears to the eye to be a resting stage between cell divisions, is actually a period of diverse activities. Those interphase activities are indispensible in making the next mitosis possible. Interphase generally lasts at least 12 to 24 hours in mammalian tissue. During this period, the cell is constantly synthesizing RNA, producing protein and growing in size. By studying molecular events in cells, scientists have determined that interphase can be divided into 4 steps: Gap 0 (G0), Gap 1 (G1), S (synthesis) phase, Gap 2 (G2).

Gap 0(G0): There are times when a cell will leave the cycle and quit dividing. This may be a temporary resting period or more permanent. An example of the latter is a cell that has reached an end stage of development and will no longer divide (e.g. neuron).

Gap 1(G1): Cells increase in size in Gap 1, produce RNA and synthesize protein. An important cell cycle control mechanism activated during this period (G1 Checkpoint) ensures that everything is ready for DNA synthesis. (Click on the Checkpoints animation, above.)

S Phase: To produce two similar daughter cells, the complete DNA instructions in the cell must be duplicated. DNA replication occurs during this S (synthesis) phase.

Gap 2(G2): During the gap between DNA synthesis and mitosis, the cell will continue to grow and produce new proteins. At the end of this gap is another control checkpoint (G2 Checkpoint) to determine if the cell can now proceed to enter M (mitosis) and divide.

MitosisorM Phase:Cell growth and protein production stop at this stage in the cell cycle. All of the cell’s energy is focused on the complex and orderly division into two similar daughter cells. Mitosis is much shorter than interphase, lasting perhaps only one to two hours. As in both G1 and G2, there is a Checkpoint in the middle of mitosis (Metaphase Checkpoint) that ensures the cell is ready to complete cell division. Actual stages of mitosis can be viewed atAnimal Cell Mitosis.

Cancer cells reproduce relatively quickly in culture. In theCancer Cell CAMcompare the length of time these cells spend in interphase to that formitosisto occur.

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The Cell Cycle – CELLS alive

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The Genetics of Male Infertility – The Turek Clinic

Your Expert in Male Fertility & Sexual Health

High technology approaches to fertility, including ICSI, are really a two edged sword: they allow us to treat severe male infertility, but they may alter natural selection in that decisions regarding sperm and eggs are made in the laboratory and not by nature.

Dr. Paul Turek

Among the 15% of couples who experience infertility, about 40% of the time the infertility is due to male factors. About half of male infertility cases are due to defined reasons, including varicocele, infection, hormone imbalances, exposures such as drugs or medications, x-rays, tobacco use and hot tubs, blockage of the reproductive tract ducts, and previous surgery that has left scarring. Another cause of male infertility that has been underestimated in the past, but is now gaining in importance is genetic infertility. The reason for its increased importance is that our knowledge about genetics is growing so quickly. Men who may have had unexplained infertility in the past may now be diagnosed with genetic causes of infertility through recently available testing. In fact, this field is progressing so quickly that genetic infertility has already become one of the most commonly diagnosed reasons for male infertility.

Developed in the early 1990s, assisted reproduction in the form of IVF and ICSI (intracytoplasmic sperm injection) is a revolutionary laboratory technique in which a single sperm is placed directly inside an egg for fertilization. This technique has opened the door to fertility for men who formerly had few available treatment options, as it allows men who were previously considered severely infertile or sterile the possibility of fatherhood. However, with ICSI sperm are chosen by laboratory technicians and not by nature and because of this, it is not clear what barriers to natural selection are altered. Thus, along with this technology comes the possibility of passing on to a child certain genetic issues that may have caused the fathers infertility, or even more severe conditions. Another reason to know whether male

Infertility is genetic or not is because classic treatments such as varicocele repair or medications given to improve male infertility. In fact, Dr Turek was one of the first to publish on this issue, showing that varicocele repair was not effective in improving fertility in men with genetic infertility. Because he recognized these issues early on, Dr. Turek, while at UCSF in 1997, founded the first formal genetic counseling and testing program for infertility in the U.S. Called the Program in the Genetics of Infertility (PROGENI), Dr. Tureks program has helped over 2000 patients at risk for genetic infertility to navigate the decision-making waters that surround this condition.

Men with infertility should be seen by a urologist for a thorough medical history, physical examination, and appropriate medical testing. If genetic infertility is a possibility, then a genetic counselor can help couples understand the possible reasons, offer appropriate genetic testing, and discuss the complex emotional and medical implications of the test results. The approach taken early on by Dr. Turek is outlined in Figure 1. Just like the medical diagnosis from a urologist or fertility specialist, information about family history plays a critical role in genetic risk assessment. This approach to genetic evaluation, termed non-prescriptive, has been the corner- stone of Dr. Tureks critically acclaimed clinical program that now has over a dozen publications contributing to our current knowledge in the field. It is important to note that a lack of family history of infertility or other medical problems does not eliminate or reduce the risk of genetic infertility. In fact, a family history review will often be unremarkable. However, family history can provide crucial supporting in- formation toward making a genetic diagnosis (such as a family history of recurrent miscarriages or babies born with problems). Dr. Turek has published that having a genetic counselor obtain family history information is much more accurate than simply giving patients a written questionnaire to fill out and bring to their visit. A genetic counselor can also discuss appropriate genetic testing options and review the test results in patients in a meaningful way.

When speaking to Dr. Tureks genetic counselor about genetic testing, keep in mind that he or she will not tell you what to do. Genetic counselors are trained to provide information, address questions and concerns, and support you in the decision making process. A genetic counselor does not assume which decisions are most appropriate for you.

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The Genetics of Male Infertility – The Turek Clinic

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How Are Hormones And Anxiety Related? – Calm Clinic

Anxiety is known as a psychological/mental health disorder, and at its core, it is. But scientists now know that your genetics and current physical health can play a very significant role in both the development of anxiety and how it manifests. For example, it’s known that low levels of serotonin – a common neurotransmitter – may lead to anxiety and depression, which is why drugs that improve the flow of serotonin are prescribed for anxiety.

Hormones also appear to play a significant role in anxiety development. Those that feel as though their anxieties appeared over time despite effective coping strategies and a high overall quality of life may be suffering from hormonal anxiety, caused by any number of problems with hormone balance.

When the body causes anxiety, treatment may seem more difficult. But powerful anxiety cures can stop anxiety forever. Want to learn more about your anxiety and how to cure it forever?

Take my free 7 minute anxiety test now.

The truth is that it’s almost impossible to know the exact cause of your anxiety. Your hormonal imbalance may have caused your anxiety, but your anxiety may also have caused your hormonal imbalance, and in some cases the imbalance may have no effect on anxiety whatsoever.

That’s why it’s best to start at the symptoms and move forward from there. If you haven’t yet, click here to take my free anxiety symptoms questionnaire.

Anxiety hormone imbalance has the potential to cause anxiety, because anxiety is often caused by those whose bodies are under stress trying to operate efficiently. It’s the reason that those that don’t exercise and those that eat an unhealthy diet often have anxiety as well – without exercise or nutrition, your body struggles to function. In addition, hormones are the messengers to the brain. Without hormones, your body may not produce the right amount of neurotransmitters, and anxiety may be the result.

That said, some examples of hormones that may contribute to anxiety include:

Again, nearly any type of hormonal dysfunction can contribute to anxiety, because the body often responds to poorly functioning hormones with stress. But the three examples above tend to be the most common hormones that cause anxiety.

What is perhaps most interesting about anxiety, however, is that even if your anxiety is caused by a change in hormones, it rarely requires any hormonal therapy. Those in natural medicine often talk about the mind/body connection, and many of those that support research-based treatments laugh at the idea that the mind can genuinely affect the body, and vice versa.

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How Are Hormones And Anxiety Related? – Calm Clinic

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Cell – Dragon Ball Wiki

Directory: Characters Villains DBZ villains Bio-Androids

Perfect Cell Super Perfect Cell Android 21 Artifical Human no. 21 The Ultimate Fighter Mr. Cell The Perfect Being Future Cell Super (Albanian dub) The Perfect Warrior Celula (Spanish dub) Komrczak (Polish dub) Selas (Lithuanian dub) Artificial Human Cell

Cell () is a major supervillain who comes from a future timeline in the Dragon Ball manga and the Dragon Ball Z anime, also making an appearance in Dragon Ball GT. He is the ultimate creation of Dr. Gero, designed to possess all the abilities of the greatest fighters to have ever inhabited or visited Earth; the result is a “perfect warrior”, possessing numerous favorable genetic traits and special abilities. Cell is one of the few Red Ribbon Androids not directly completed by Dr. Gero; the others are Android 15, Android 14, Android 13, and possibly Android 8. Cell, Android 13, Android 14, and Android 15’s completions involve Dr. Gero’s Super Computer.

Cell was named after the English word for “cell” because he absorbs humans and transforms.[8]Insects served as the model for Cell’s design. Besides his design, the way in which he hatches from an egg and sheds his skin as he grows was also based on insects.[8] Thus Cell very much resembles an insect in both in appearances and in the way he goes through different stages of metamorphosis.

“You fool! Don’t you realize yet you’re up against the perfect weapon?!” “Save the World”

Cell has as an original personality with various other characters’ personalities added in; Gero’s computer redesigned the weak parts of the original personality, adding in the personalities of various different characters to make him the perfect weapon.[8] Throughout the Androids Arc, Cell’s personality changes drastically with each transformation. At first, Cell’s desire to complete his evolution by absorbing both Android 17 and Android 18 is what fuels him in his imperfect form. Upon reaching his final form, his eagerness to test the limits of his newfound power is what defines his character. Cell is unique among most villains of the series in that he is quite sophisticated. Because of his genetic composition from other warriors, he is able to psychologically manipulate those warriors and exploit their weaknesses to his advantage. He also found the Dragon Balls’ reviving ability to be a nuisance, as evidenced by his relief when he learned that the Dragon Balls were rendered inert due to Piccolo and Kami’s fusion.

Some initial sketches of Cell (Daizenshuu 4)

Initially, Cell is completely single-minded in pursuit of his goals and is very cautious, sneaky, cunning and calculating in achieving his main goal of perfection. Upon reaching his first transformation, he becomes far more brash and impulsive in his actions, relying less on strategy and more on brute force, often becoming clouded and not thinking rationally when things do not go his way. Upon reaching perfection, Cell displays a number of traits shared by those whose cells he possesses; Piccolo’s cunning, Vegeta’s pride, Goku’s laid-back disposition, Frieza’s smugness, and the Saiyan lust for battle. He is also shown to be calm and genuinely polite in this Perfect form. Perhaps Cell’s most distinguishable trait in this form is his uninhibited vanity, which he shamelessly puts on display by launching the Cell Games, a tournament organized for the sole purpose of showing off his newfound power. It can also be seen during Cell’s confrontation with Gohan when he affirms his true purpose: the annihilation of anything he considers imperfect, a category in which he places everyone and everything but himself.

In the English manga, Cell is referred to as “it”, while in the anime (and the Japanese versions of both), he is referred to as “he.” He is likely described that way in the English manga to emphasize the fact that he is an artificial being.

First colored image of Cell, made for the anime staff (“Ginger Town Showdown”)

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Cell – Dragon Ball Wiki

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Male hypogonadism: Symptoms and treatment

Abstract

Male hypogonadism is a condition in which the body does not produce enough of the testosterone hormone; the hormone that plays a key role in masculine growth and development during puberty. There is a clear need to increase the awareness of hypogonadism throughout the medical profession, especially in primary care physicians who are usually the first port of call for the patient. Hypogonadism can significantly reduce the quality of life and has resulted in the loss of livelihood and separation of couples, leading to divorce. It is also important for doctors to recognize that testosterone is not just a sex hormone. There is an important research being published to demonstrate that testosterone may have key actions on metabolism, on the vasculature, and on brain function, in addition to its well-known effects on bone and body composition. This article has been used as an introduction for the need to develop sensitive and reliable assays for sex hormones and for symptoms and treatment of hypogonadism.

Keywords: Male hypogonadism, pituitary, sex hormone, testosterone, testis

Hypogonadism is a medical term for decreased functional activity of the gonads. The gonads (ovaries or testes) produce hormones (testosterone, estradiol, antimullerian hormone, progesterone, inhibin B, activin) and gametes (eggs or sperm).[1] Male hypogonadism is characterized by a deficiency in testosterone a critical hormone for sexual, cognitive, and body function and development. Clinically low testosterone levels can lead to the absence of secondary sex characteristics, infertility, muscle wasting, and other abnormalities. Low testosterone levels may be due to testicular, hypothalamic, or pituitary abnormalities. In individuals who also present with clinical signs and symptoms, clinical guidelines recommend treatment with testosterone replacement therapy.

There are two basic types of hypogonadism that exist:

Primary: This type of hypogonadism also known as primary testicular failure originates from a problem in the testicles.

Secondary: This type of hypogonadism indicates a problem in the hypothalamus or the pituitary gland parts of the brain that signal the testicles to produce testosterone. The hypothalamus produces the gonadotropin releasing hormone, which signals the pituitary gland to make the follicle-stimulating hormone (FSH) and luteinizing hormone. The luteinizing hormone then signals the testes to produce testosterone. Either type of hypogonadism may be caused by an inherited (congenital) trait or something that happens later in life (acquired), such as an injury or an infection.

Common causes of primary hypogonadism include:

Klinefelter’s Syndrome: This condition results from a congenital abnormality of the sex chromosomes, X and Y. A male normally has one X and one Y chromosome. In Klinefelter’s syndrome, two or more X chromosomes are present in addition to one Y chromosome. The Y chromosome contains the genetic material that determines the sex of a child and the related development. The extra X chromosome that occurs in Klinefelter’s syndrome causes abnormal development of the testicles, which in turn results in the underproduction of testosterone.

Before birth, the testicles develop inside the abdomen and normally move down into their permanent place in the scrotum. Sometimes, one or both of the testicles may not descend at birth. This condition often corrects itself within the first few years of life without treatment. If not corrected in early childhood, it may lead to malfunction of the testicles and reduced production of testosterone.

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Male hypogonadism: Symptoms and treatment

Recommendation and review posted by Bethany Smith

Galaxy Of Genetic Differences Between Men & Women

Scientists have found genetic evidence for what some men have long suspected: it is dangerous to make assumptions about women. The key is the X chromosome, the “female” sex chromosome that all men and women have in common. In a study published this week in the journal Nature, scientists said they had found an unexpectedly large genetic variation in the way parts of womens two X chromosomes are distributed among them. The findings were published in conjunction with the first comprehensive decoding of the chromosome. Females can differ from each other almost as much as they do from males in the way many genes at the heart of sexual identity behave, researchers say. “Literally every one of the females we looked at had a different genetic story,” says Duke University genetics expert Huntington Willard, who co-wrote the study. “It is not just a little bit of variation.” The analysis also found that the obsessively debated differences between men and women were, at least on the genetic level, even greater than previously thought. As many as 300 of the genes on the X chromosomes may be activated differently in women than in men, says the other author of the paper, Laura Carrel, molecular biologist at the Pennsylvania State University College of Medicine. The newly discovered genetic variation between women might help account for differing gender reactions to prescription drugs and the heightened vulnerability of women to some diseases, experts say. “The important question becomes how men and women actually vary and how much variability there is in females,” Carrel says. “We now might have new candidate genes that could explain differences between men and women.” All told, men and women may differ by as much as 2 per cent of their entire genetic inheritance, greater than the hereditary gap between humankind and its closest relative, the chimpanzee. “In essence,” Willard says, “there is not one human genome, but two: male and female.” SCIENTISTS estimate that there may be as many as 30,000 genes in the chemical DNA blueprint for human growth and development known as the human genome. The genes are parcelled in 23 pairs of rod-like structures called chromosomes, which are contained in every cell of the body. The most distinctive of the chromosomes are the mismatched pair of X and Y chromosomes that guide sexual development. Until now, researchers considered the shuffle of sex chromosomes at conception a simple matter of genetic roulette. The chromosomes that dictate sexual development are mixed and matched in predictable combinations: A female inherits one X chromosome from each parent; a male inherits an X chromosome from his mother and a Y chromosome from his father. To avoid any toxic effect from double sets of X genes, female cells randomly choose one copy of the X chromosome and “silence” it – or so scientists had believed. The new analysis found that the second X chromosome was not a silent partner. As many as 25 per cent of its genes are active, serving as blueprints to make necessary proteins. To investigate this variation, Carrel and Willard isolated cells from 40 women and measured the activity of hundreds of genes to see whether those on the second X chromosome were active or silent. Although those extra genes were supposed to be turned off, they found that about 15 per cent of them in all female cells were still active, or “expressed”. In some women, up to an additional 10 per cent of those X-linked genes showed varying patterns of activity. “This is 200 to 300 genes that are expressed up to twice as much as in a male or some other females,” Willard says. “This is a huge number.” Researchers were surprised that they found so many unexpected differences in the behaviour of the one sex chromosome that men and women share. Though there is dramatic variation in the activation of genes on the X chromosomes that women inherit, there is none among those in men, the researchers reported. Researchers have yet to understand the effect of so many different patterns of gene activation among women, or determine what controls them, but all the evidence suggests that they are not random. ILLUMINATING this complex palette was the work of an international team of 250 scientists, led by geneticist Mark Ross, at the Wellcome Trust Sanger Institute in Hinxton, Cambridge. The team produced the first complete sequence of the X chromosome about two years after the decoding of the male Y chromosome. The researchers found that the X chromosome, though relatively poor in genes, is rich in influence, deceptively subtle, and occasionally deadly to males. The international team identified 1,098 functional genes along the X chromosome, more than 14 times as many as scientists had located on the tiny Y chromosome. Even so, the researchers say, there are fewer genes to be found on the X chromosome than on any of the other 22 chromosomes sequenced so far. Most of the X genes are slightly smaller than average. But one is the largest known gene in the human genome, a segment of DNA linked to diseases such as muscular dystrophy, that is more than 2.2 million characters long. The X chromosome contains a larger share of genes linked to disease than any other chromosome. It is implicated in 300 hereditary disorders, including colour blindness, haemophilia and Duchenne muscular dystrophy. Nearly 10 per cent of the genes may belong to a group known to be more active in testicular cancers, melanomas and other cancers, the team reports. “The biggest surprise for us was just how many of these [cancer-related] genes there are on the X,” Ross says. The complete gene sequence provided some clues to the origins of the human sex chromosomes. The researchers found that most of the genes on the X chromosome also reside on chromosome 1 and chromosome 4 of chickens. That supports the theory that the human sex chromosomes evolved from a regular pair of chromosomes from a common ancestor of chickens and humans – about 300 million years ago. 2005 Scotsman.com http://news.scotsman.com/scitech.cfm?id=295472005

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Galaxy Of Genetic Differences Between Men & Women

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Gene Therapy | Doctor | Patient

In the 1990s there was great hope that this novel approach may provide an answer to many hitherto incurable diseases. The basic idea is to correct defective genes responsible for disease development. This can be achieved in a number of ways:

When a normal gene is inserted into the genome, a carrier molecule (a vector) is used. This will deliver the new gene to the target cells. The most commonly used vectors are viruses. The most commonly used viruses are:

These viruses are altered to carry normal human DNA. The patient’s target cells are infected with the vector, which deposits its genetic load including the gene to be replaced . The target cell is then able to produce a functioning protein. More recently, success has been seen by combining a tumour-specific adenovirus vector and several single therapy genes. Targeting gene-virotherapy has killed tumour cells with minimal damage to normal cells in mice.[1][2] There are also nonviral insertion options. The simplest method is direct introduction of new DNA into the target tissues. This is limited by the type of tissue and the amount of DNA required. An artificial lipid sphere with an aqueous core is created – a liposome – which can both carry the therapeutic DNA and pass it through the target cells membrane. The therapeutic DNA can also bind chemically to molecules that will attach to target cell receptor sites. These are then taken into the cell’s interior. This tends to be less effective than the other methods.

Human gene therapy is still largely in the experimental phase. There have been few big breakthroughs since the first trial started in 1990. There has also been at least one death attributed to therapy and two cases of leukaemia developing post-therapy. There are also technical problems involved:

In a bid to alleviate disease at the earliest possible stage, in utero fetal gene therapy has also been tried.[6] Prenatal screening for severe genetic disease such as Crigler-Najjar syndrome, Pompe’s disease and haemophilia B has been tested in mouse models. There have been issues with the development of liver tumours, insufficient target cells are reached and the therapy is not toxic enough to target cells. There are attempts underway to manufacture antitumour vaccines.In this technique Epstein-Barr virus vectors mediate gene transfer into human B lymphocytes.[7] Other areas of research include:

A recent trial, approved by the American Food and Drug Administration, is for the treatment of Parkinson’s disease. This is a phase 1 clinical trial with 11 patients already enrolled. They are aiming to produce the neuroprotective and restorative subthalamic glutamic decarboxylase. There have been no adverse events reported to date.[13]

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Gene Therapy | Doctor | Patient

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Regulation of Genetic Tests

Regulation of Genetic Tests Overview of Genetic Testing

As the science of genomics advances, genetic testing is becoming more commonplace in the clinic. Yet most genetic tests are not regulated, meaning that they go to market without any independent analysis to verify the claims of the seller. The Food and Drug Administration (FDA) has the authority to regulate genetic tests, but it has to date only regulated the relatively small number of genetic tests sold to laboratories as kits. Whereas the Centers for Medicare and Medicaid Services (CMS) does regulate clinical laboratories, it does not examine whether the tests performed are clinically meaningful. Since the 1990s, expert panels and members of Congress have expressed concern about this regulatory gap and the need for FDA to address it. In response, the FDA in 2010 announced plans to expand its regulation to all genetic tests; this expansion has yet to take place. In the interim, FDA continues to regulate test kits, and has begun to regulate genomics tools in clinical research.

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The term “genetic testing” covers an array of techniques including analysis of human DNA, RNA, or protein.Genetic testsare used as a health care tool to detect gene variants associated with a specific disease or condition, as well as for non-clinical uses such as paternity testing and forensics. In the clinical setting, genetic tests can be performed to determine the genetic cause of a disease, confirm a suspected diagnosis, predict future illness, detect when an individual might pass a genetic mutation to his or her children, and predict response to therapy. They are also performed to screen newborns, fetuses, or embryos used in in vitrofertilization for genetic defects.

The first genetic tests were for the detection of chromosomal abnormalities (seekaryotype) and mutations in single genes causing rare, inherited disorders likecystic fibrosis. In recent years, however, the variety of tests has greatly expanded. There are now tests involving complex analyses of a number of genes to, for example, identify one’s risk for chronic diseases such as heart disease and cancer, or to quantify a patient’s risk of cancer reoccurrence. There are also many tests to predict the effectiveness of therapeutics and guide their administration. Furthermore, NHGRI is pursuing research to enable the clinical use of multi-gene panels, whole exome sequencing (analysis of all a patient’s genes), and whole genome sequencing (analysis of a patient’s entire genetic code), to detect, for instance, the cause of an undiagnosed disease or a cancerous tumor.

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Three federal agencies play a role in the regulation of genetic tests: CMS, FDA, and the Federal Trade Commission (FTC). CMS is responsible for regulating all clinical laboratories performing genetic testing, ensuring their compliance with the Clinical Laboratory Improvement Amendments of 1988 (CLIA). The objective of CLIA is to certify the clinical testing quality, including verification of the procedures used and the qualifications of the technicians processing the tests. It also comprises proficiency testing for some tests. More details of CLIA are available in this factsheet

The FDA has the broadest authority in terms of regulating the safety and effectiveness of genetic tests as medical devices under the Federal Food, Drug, and Cosmetic Act. Whether FDA regulates a test is determined by how it comes to market. A test may be marketed as a commercial test “kit,” a group of reagents used in the processing of genetic samples that are packaged together and sold to multiple labs. More commonly, a test comes to market as a laboratory-developed test (LDT), where the test is developed and performed by a single laboratory, and where specimen samples are sent to that laboratory to be tested. The FDA regulates only tests sold as kits and, to date, has practiced “enforcement discretion” for LDTs.

The degree of FDA oversight of a genetic test is based on its intended use and the risks posed by an inaccurate test result. The FDA categorizes medical devices, including genetic tests, into three separate classes, ranging from class I, for relatively low risk products, to class III, where tests are subject to the greatest level of scrutiny.A complete list of approved human genetic tests is listed here.

FDA oversight also includes pharmacogenomics, which is the use of genomic information to help predict how an individual might respond to a particular drug, to identify individuals who might experience an adverse reaction to taking a drug, or to assist in selecting the optimal dosage of a drug. Part of the FDA’s oversight of marketed drugs is to ensure that manufacturers provide information on drug labels about genetic markers that is relevant for drug safety and effectiveness. A list of approved pharmacogenomic drugs is available here.

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Regulation of Genetic Tests

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Bone Marrow Transplantation – Recommendations on …

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Bone Marrow Transplantation – Recommendations on …

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Bone Marrow Transplantation – Haploidentical hematopoietic …

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A new role for zebrafish: Larger scale gene function …

IMAGE:NHGRI scientists are homing in on specific genes in zebrafish to help them better understand the function of genes in people. view more

Credit: Darryl Leja, NHGRI

A relatively new method of targeting specific DNA sequences in zebrafish could dramatically accelerate the discovery of gene function and the identification of disease genes in humans, according to scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health (NIH).

In a study posted online on June 5, 2015, and to be published in the July 2015 issue of Genome Research, the researchers reported that the gene-editing technology known as CRISPR/Cas9 is six times more effective than other techniques at homing in on target genes and inserting or deleting specific sequences. The study also demonstrated that the CRISPR/Cas9 method can be used in a “multiplexed” fashion – that is, targeting and mutating multiple genes at the same time to determine their functions.

“It was shown about a year ago that CRISPR can knock out a gene quickly,” said Shawn Burgess, Ph.D., a senior investigator with NHGRI’s Translational and Functional Genomics Branch and head of the Developmental Genomics Section. “What we have done is to establish an entire pipeline for knocking out many genes and testing their function quickly in a vertebrate model.” Researchers often try to determine the role of a gene by knocking it out – turning it off or removing it – and watching the potential effects on an organism lacking it.

Such larger scale – termed “high-throughput” – gene targeting in an animal model could be particularly useful for human genomic research. Only 10 to 20 percent of recognized human genes have been subjected to such rigorous testing, Dr. Burgess said. The functions of many other genes have been inferred based on analyzing proteins or have been identified as possible disease genes, but the functions of those genes have not been confirmed by knocking them out in animal models and seeing what happens.

“This is a way to do that on a more cost-efficient and large scale,” Dr. Burgess said.

“The study of zebrafish has already led to advances in our understanding of cancer and other human diseases,” said NHGRI Director Eric Green, M.D., Ph.D. “We anticipate that the techniques developed by NHGRI researchers will accelerate understanding the biological function of specific genes and the role they play in human genetic diseases.”

The CRISPR/Cas9 method of gene editing is one of the two essential components in the NHGRI team’s high-throughput method. Modeled on a defense mechanism evolved by bacteria against viruses, CRISPR/Cas9 activity was first described in 2012. Since then, its use has spread quickly – in other words, has gone “viral” – in genomic research labs in the United States and abroad.

The acronym CRISPR stands for “clustered, regularly interspaced, short palindromic repeat,” referring to a pattern of DNA sequences that appears frequently in bacterial DNA. Scientists believe the CRISPR sequences reflect evolutionary responses to past viral attacks.

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What Is a Hormone Doctor? | eHow StemCell Doctors

A hormone doctor, or an endocrinologist, is a physician who treats diseases related to the endocrine system. While primary care physicians (family practitioners and internal medicine physicians) can treat many hormonal disorders without a need for specialized training, a physician may also receive advanced training and specialize in endocrinology. A primary care physician can determine whether he or she can treat a patient or whether the patient should be referred to a specialist treating only disorders of the endocrine system.

The endocrine system is composed of many glands, including the pituitary, thyroid, parathyroids, adrenals, hypothalamus, pineal body, ovaries and testicles. The islet cells of the pancreas are also part of the endocrine system. These glands secrete hormones (chemical messengers) that regulate the bodys metabolism, growth, sexual development and sexual function, by complex feedback systems comparable to a thermostat regulating room temperature.

A hormone doctor can specialize in diseases of one or two glands or treat patients in all areas of endocrinology. A large part of a typical practice could involve treating diabetes and related complications. The physician may also treat thyroid disorders, inborn metabolic disorders, over- and underproduction of hormones, osteoporosis, menopause, cholesterol disorders, hypertension, and short or tall stature. Patients with endocrine cancer are usually referred to an oncologist.

To treat non-reproductive hormonal disorders, a physician generally completes four years of medical or osteopath school and a three-year residency in either family medicine or internal medicine. He or she must pass a board examination to become board certified in family or internal medicine. To become board certified as an endocrine specialist, the physician completes a three-year endocrinology fellowship program and passes a board certification examination.

Reproductive endocrinologists complete four years of residency training in obstetrics and gynecology, rather than training in family medicine or internal medicine. They must complete two or three years of fellowship training in reproductive endocrinology and infertility and pass the board certification examination. These specialists treat infertility by using in vitro fertilization, embryo and sperm freezing, assisted embryo hatching, pre-implantation genetic diagnosis and other emerging technologies. Reproductive endocrinologists also treat a wide range of reproductive disorders, including endometriosis, polycystic ovary syndrome, gonadal dysgenesis, galactorrhea, repeat pregnancy loss, ectopic pregnancy and excess hair in women, to name just a few.

A hormone doctor may work in academic medical centers, community hospitals, private group practices or private solo practices. Each situation can involve different work hours, a different patient base, and different lifestyles. Unlike surgical specialties, hormone doctors generally do not take call hours, but they may be called on an emergency basis to see a patient in a hospital when the physician on staff cannot appropriately treat the patient.

Problems Caused by Hormone Imbalance

Job Description for an Endocrinologist

What Is the Difference Between Family Medicine & Internal Medicine Physicians?

A doctor with special training that treats diseases and disorders of the endocrine system, a complex system in the human body that

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