If you or a loved one is struggling with hypogonadism, you may already know that it can be a devastating condition that reduces your quality of life and livelihood. People with hypogonadism can experience muscle loss, low libido, infertility and depressed mood. In fact, these symptoms can make talking about hypogonadism difficult. (1)

Thankfully, research shows that there are ways to balance your hormones, either using hormone replacement therapy, which is the conventional form of treatment for this condition, or natural estrogen and testosterone boosters like exercise, dietary and lifestyle changes, adaptogen herbs and essential oils. But if youve been struggling with the symptoms of hypogonadism, rest assured that there are natural remedies to help support your treatment and improve your quality of life.

Hypogonadism is a condition that occurs when the bodys sex glands, the testes for males and ovaries for females, produce little or no hormones. For males with hypogonadism, low testosterone can affect the development and maintenance of male reproductive organs, including the testes, penis and prostate. In fact, low testosterone levels can lead to issues like reduced muscle strength, hair loss and impotence.

For females, hypogonadism occurs when the ovaries arent producing enough estrogen. Estrogen is responsible for maintaining sex organs like the uterus, vagina, fallopian tubes and mammary glands. But low or little estrogen in the body can lead to infertility, loss of libido, mood swings, loss of menstruation and osteoporosis. (2)

There are two types of hypogonadism, primary or central, or secondary. The definition of these types of hypogonadism depends on the cause of the condition.

Primary hypogonadism: Primary hypothyroidism occurs when theres a problem in a persons testes or ovaries, which are the gonads. The gonads are receiving messages from the brain to produce hormones, but they arent functioning properly.

The symptoms of hypogonadism vary depending on the patients age, sex and type of condition.

Symptoms in Females: Women with hypogonadism may experience the following symptoms:

If a young girl has hypogonadism, she may not menstruate. Plus the condition can affect her height and breast development.

Boys with low testosterone may have growth problems, with a delay in muscle growth and beard development, impaired testicle and penis growth, and enlarged male breasts. Also, low testosterone levels may result in failure of normal pubertal progression.

The cause of hypogonadism depends on the type of condition, either primary or central.

Primary hypogonadism can be caused by any of the following health conditions or factors (5):

Central hypogonadism (also known as hypogonadotropic hypogonadism) occurs when theres an issue with the centers of the brain that control hormone production. The following issues can cause it:

Androgen deficiency of the aging male (known as ADAM) is a cause of secondary hypogonadism. ADAM occurs when a mans testosterone levels decline progressively after age 40, leading to sexual dysfunction and altered body composition, cognition and metabolism. (6) In fact, research published by the International Journal of Clinical Practice indicates that older men are more likely to have low testosterone levels, with the prevalence being 34 percent in men between the ages of 45 and 54, and 50 percent in men over 85 years. (7)

According to research published in the International Journal of Clinical Practice, hypogonadism is significantly associated with various health issues, including Type 2 diabetes, hypertension, obesity, osteoporosis and metabolic syndrome. (8)

Treatment for hypogonadism depends on the cause of the condition. But the most common form of treatment is hormone replacement therapy, which is used to restore hormone levels to the normal range.

For Females: Women with hypogonadism are usually given a combination of estrogen and progesterone. However, research shows that estrogen therapy can increase the risk of heart disease, blood clots and cancer. Progesterone is added to estrogen therapy because it may reduce the risk of endometrial cancer.

1. Reduce Stress

A study conducted at the University of Massachusetts Medical School investigated the association between testosterone levels and stress. Researchers measured the stress levels of participants by taking into account daily hassles, major life events and perceived stress. They found that testosterone levels were significantly associated with stress in both males and females. This study suggests that testosterone levels are reflective of a persons ability to respond to stressors and his or her emotional coping mechanisms. (14)

To support your treatment for hypogonadism, practice some simple stress relievers, like spending time outdoors, meditating, exercising, being social and keeping a journal. Pursuing some form of therapeutic practice, like cognitive behavioral therapy, may also be beneficial because it helps you to better react to stressful situations. Plus, vocalizing your fears and emotions about coping with hypogonadism can be extremely helpful.

2. Address your Weight and Diet

Being overweight and being underweight can both contribute to low sex hormone levels. For the majority of people, before they can maintain a normal body weight to help regulate their hormone levels, they need to change the way they eat. This may be the most important natural remedy to help treat hypogonadism. (15)

In fact, a 2014 study published in the Journal of Neuroinflammation found that low testosterone and diet-induced obesity can contribute to impairments in neural health, increasing the risk of serious disorders like type 2 diabetes and Alzheimers disease. (16) Theres also a childhood obesity epidemic that is causing serious health issues among children, including problems with growth and development.

So if you have low testosterone and youre struggling with weight loss, now is the time to make some serious changes to your diet in order to get well.

First, cut out all of the junk food, the processed, packaged and fast food, the refined carbohydrates and the artificial sweeteners. Focus on eating whole, real foods, including the following:

If you are having trouble staying on track with your diet and eating healthy, consider working with a health coach who can serve as a mentor and help you to reach your weight and health-related goals.

3. Exercise Regularly

Theres plenty of research that proves exercise can regulate or boost low testosterone levels. In fact, one study published in the Indian Journal of Physiology and Pharmacology found that even short-term exercise produces an elevation in serum testosterone levels in adults. (17)

Some of the best forms of exercise to boost testosterone and human growth hormone levels are weight training and high intensity interval training (HIIT workouts). Research shows that even moderate and light weightlifting can increase serum testosterone levels when compared to not doing any exercise at all. (18)

Try lifting weights for at least 30 minutes, three times a week. Doing this in combination with burst training can be even more beneficial in helping to elevate your testosterone levels. Burst training means that you are exercising at 90100 percent of your maximum effort for short, bursts of time (about 30 to 60 seconds), followed by a period of low impact exercise for recovery.

Exercise can also be helpful for women with hypogonadism because it helps to reduce stress and helps you to get to a normal weight. Weighing too little or being overweight are both factors that may cause low estrogen levels. Low-impact exercises like yoga and pilates can be very beneficial in helping to relieve symptoms and reduce some causes of hypogonadism.

4. Supplement with L-arginine

L-arginine is a type of amino acid that we obtain from our diets. It has multiple benefits, including its ability to stimulate the production of growth hormones, correct impotence, and improve erectile dysfunction and male infertility. A study published in The Journal of Endocrinology found that dietary arginine is actually required for the anabolic action of androgens, like testosterone. (19)

Research also shows that L-arginine ingestion enhances growth hormone response, increasing resting human growth hormone (HGH) levels by at least 100 percent. This is beneficial for men with hypogonadism because HGH is a natural testosterone booster. (20)

The best way to help your body make and use more L-arginine is by eating a diet based on whole, real foods, including organic grass-fed beef, wild-caught salmon, cage-free eggs, cultured yogurt, nuts and seeds, sea vegetables and coconut meat.

To supplement with L-arginine in order to improve hypogonadism symptoms, I recommend you take 36 grams per day, divided into two doses.

5. Try Ashwagandha

According to research published in Evidence-Based Complementary and Alternative Medicine, ashwagandha has been used in Ayurvedic medicine as an aphrodisiac that can treat male sexual dysfunction and infertility. Researchers involved in a pilot study found that patients with a low sperm count who were using ashwagandha had a 167 percent increase in sperm count, 53 percent increase in sperm volume and 57 percent increase in sperm motility. The ashwagandha group also showed improved serum hormone levels compared to the placebo group. (21)

To use ashwagandha to boost your libido, improve your hormone levels, increase your endurance and improve your mood, I recommend supplementing with 500 milligrams, one to two times daily. But do this in combination with eating a diet filled with healthy fats, fiber and clean protein.

6. Use Essential Oils

Two essential oils that can help to regulate hormone levels and improve hypogonadism symptoms are clary sage and sandalwood.

Clary sage contains natural phytoestrogens, so it helps to balance estrogen levels. According to a 2017 study published in Neuro Endocrinology Letters, clary sage can be used to alleviate menopausal symptoms caused by declining levels of estrogen secretion. In fact, researchers found that some essential oils, including clary sage, were able to increase estrogen concentration. (22) To use clary sage oil to support your hypogonadism treatment, combine 5 drops with a teaspoon of coconut oil and massage the mixture into your abdomen, wrists and bottoms of your feet.

Sandalwood essential oil can be used to relieve hypogonadism symptoms, like low sex drive, moodiness, stress and cognitive issues. A 2015 study conducted at South Dakota State University shows that sandalwood also has anticancer mechanisms because of its antioxidant and anti-inflammatory properties. Researchers found that sandalwood has anticancer effects against both breast and prostate cancer. (23) You can diffuse 5 drops of sandalwood at home, inhale it directly from the bottle or apply 23 drops to the bottoms of your feet.

Talk to your doctor about the risks and benefits of hormone replacement therapy. There are studies supporting the benefits of hormone replacement therapy, and evidence opposing its use for hypogonadism.

Use the natural remedies discussed in this article to support your treatment for hypogonadism or to naturally boost your low estrogen or testosterone levels. However, make sure that you discuss any supplements that you choose to take with your doctor.

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Hypogonadism Causes + 6 Ways to Help Balance ... - Dr. Axe

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We understand that you may have a lot of questions when your child is diagnosed with hypopituitarism. Is it dangerous? Will it affect my child long term? What do we do next? Weve tried to provide some answers to those questions on this site, and our experts can explain your childs condition fully.

Growth hormone is a protein produced by the pituitary gland, which is located near the base of the brain and attached to the hypothalamus (a part of the brain that helps to regulate the pituitary gland). If the pituitary gland or the hypothalamus is malformed or damaged, it may mean that the pituitary gland cant produce some or all of its hormones.

Hypopituitarism in children may be caused by:

Hypopituitarism can also be idiopathic, meaning that no exact cause can be determined.

The symptoms of hypopituitarism will vary depending on two things: which hormones are lacking, and your childs age. Symptoms that newborn babies may have include:

Older infants and children may have these symptoms:

Because the symptoms of hypopituitarism may resemble other conditions or medical problems, you should always consult your child's physician for a diagnosis.

Q: What is hypopituitarism?

A: Hypopituitarism occurs when the anterior (front) lobe of the pituitary gland loses its ability to make hormones, resulting in multiple pituitary hormone deficiencies. Physical symptoms depend on which hormones are no longer being produced by the gland.

Q: What causes hypopituitarism?

A: Hypopituitarism may be caused by many different conditions, including:

Hypopituitarism can also be idiopathic, meaning that no exact cause can be determined.

Q: Is hypopituitarism treatable?

A: Treating hypopituitarism depends both on its cause and on which hormones are missing. The goal of treatment is to restore normal levels of hormones. Treating the underlying condition thats causing your childs hypopituitarism often leads to a full recovery.

Since your childs body is unable to make some or all of these missing hormones, life-long hormone replacement therapy is necessary. Replacement therapy needs to be monitored and adjusted, but the extent of your childs pituitary deficiency will determine how often he will need to see his doctor.

Q: How safe is treatment?

A: While there are many potential side effects, researchers generally agree that hormone replacement therapy is safe and effective.

You and your family are key players in your childs medical care. Its important that you share your observations and ideas with your childs health care provider and that you understand your providers recommendations.

If your child is experiencing symptoms of hypopituitarism and youve set up an appointment, you probably already have some ideas and questions on your mind. But at the appointment, it can be easy to forget the questions you wanted to ask. Its often helpful to jot them down ahead of time so that you can leave the appointment feeling like you have the information you need.

If your child is old enough, you may want to suggest that she write down what she wants to ask her health care provider, too.

Some of the questions you may want to ask include:

Link:
Hypopituitarism Symptoms & Causes | Boston Children's Hospital

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The thyroid is a small butterfly-shaped gland inside the neck, located in front of the trachea (windpipe) and below the larynx (voicebox). It produces two thyroid hormonestriiodothyronine (T3) and thyroxine (T4)that travel through the blood to all tissues of the body.

Thyroid hormones regulate how the body breaks down food and either uses that energy immediately or stores it for the future. In other words, our thyroid hormones regulate our body's metabolism.

Another gland, called the pituitary gland, controls how well the thyroid works. The pituitary gland is located at the base of the brain and produces thyroid-stimulating hormone (TSH). The bloodstream carries TSH to the thyroid gland, where it tells the thyroid to produce more thyroid hormones, as needed.

Thyroid hormones influence virtually every organ system in the body. They tell organs how fast or slow they should work. Thyroid hormones also regulate the consumption of oxygen and the production of heat.

Endocrinologistsphysicians and scientists who study and care for patients with endocrine gland and hormone problemsstudy and treat several major disorders of the thyroid gland. The following is a list of some common thyroid disorders.

Too much thyroid hormone from an overactive thyroid gland is called hyperthyroidism, because it speeds up the body's metabolism. This hormone imbalance occurs in about 1 percent of all women, who get hyperthyroidism more often than men. One of the most common forms of hyperthyroidism is known as Graves' disease. This autoimmune disorder (when your bodys defense system attacks your own cells) tends to run in families. Because the thyroid gland is producing too much hormone in hyperthyroidism, the body develops an increased metabolic state, with many body systems developing abnormal function.

Too little thyroid hormone from an underactive thyroid gland is called hypothyroidism. In hypothyroidism, the body's metabolism is slowed. Several causes for this condition exist, most of which affect the thyroid gland directly, impairing its ability to make enough hormone. More rarely, there may be a pituitary gland tumor, which blocks the pituitary from producing TSH. Whether the problem is caused by the thyroid or by the pituitary gland, the result is that the thyroid is producing too few hormones, causing many physical and mental processes to become sluggish. The body consumes less oxygen and produces less body heat.

A thyroid nodule is a small lump in the thyroid gland. Thyroid nodules are common. These nodules can be either a growth of thyroid tissue or a fluid-filled cyst, which forms a lump in the thyroid gland. Almost half of the population will have tiny thyroid nodules at some point in their lives but, typically, these are not noticeable until they become large and affect normal thyroid size. About 5% of people develop large nodules, more than a half inch across (about 1 centimeter).

Although most nodules are not cancerous, people who have them should seek medical attention to rule out cancer. Also, some thyroid nodules may produce too much thyroid hormone and cause hyperthyroidism, or become too large, interfering with breathing or swallowing or causing neck discomfort.

Other thyroid problems include cancer, thyroiditis (swelling of the thyroid gland), or a goiter, which is an enlargement of the thyroid gland.

July 2018

Editors

Bryan Haugen, MD

Leonard Wartofsky, MD, MACP

Ramon Martinez, MD

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Thyroid Disorders | Hormone Health Network

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CANDU reactors can operate economically and reliably for up to 60 years. After about 30 years of operation, reactor components are replaced and refurbished, extending the life of a reactor for another 30 years. This process is called life extension.

During life extension, the reactors pressure tubes, calandria tubes and end fitters are removed and replaced. Our experts have designed and delivered multi-tonne, remotely controlled tooling systems to accomplish this in a safe and effective manner. The outage also allows operators to refurbish other key reactor components, and make system upgrades.

All utilities that operate CANDU reactors are currently undergoing or will at some point consider life extension work on their reactors.

One of the worlds top-performing CANDU stations, the Darlington Nuclear Generating Station supplies 20% of Ontarios energy needs. Its refurbishment is crucial to deliver the power required to serve the provinces residents. Refurbishment operations began in the fall of 2016; it is the largest clean energy project in Canada.

This life extension project will allow Argentinas Embalse Nuclear Station to continue producing safe, reliable, low-carbon power for up to another 30 years. The Embalse CANDU 6 reactor began commercial operation in January 1984 and the single-unit has a gross output of 648 Mwe. The station shut down for this project in December 2015; the outage is expected to last until December 2017.

Bruce Power is Ontarios lowest cost source of nuclear, currently generating over 30% of the provinces electricity. Extending the operational life of the Bruce Power Units 3-8 will ensure long-term price stability. We are currently working with Bruce Power to solidify our scope for the Bruce Power major component replacement(MCR) project and look forward to concluding negotiations in late 2016.

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Life Extension | SNC-Lavalin

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Bioidentical hormones offer an alternative to Hormone Replacement Therapy and are a way to relieve menopause symptoms. They are chemically identical to those the hormones your body produces. The body cant distinguish the bioidentical hormones from the ones produced by your ovaries. The hormone levels in our bodies decline as we age. By having hormone replacement therapy, your hormones are restored to more youthful levels resulting in more energy, a sharper memory, stronger bones, a healthier heart and an overall more youthful glow. The treatment comes in patch form, a cream form or pill form. Dr. Pavilonis has treated patients for years with bioidentical hormone replacement therapy in Chicago and has had outstanding results with it.

Almost all women over 40 start to experience hormone imbalance. In day to day living, we are exposed to many different toxins from our food to our environment. These toxins start to contribute to our hormone decline as we age. To balance your hormones, it is critical to be evaluated by a highly trained doctor and have the treatment of hormone replacement therapy in Chicago. You will also have comprehensive lab testing and answer an in-depth questionnaire before we create a personalized treatment plan can for you.

Having your hormones out of balance can contribute to many conditions and diseases such as:

As a result of your hormones being out of balance, you may be experiencing several of these classic symptoms of aging:

If you are experiencing any of these symptoms, you may be a candidate for bioidentical hormone therapy.

Estrogen is a womans most important hormone. Studies have shown, without hormone replacement therapy, the loss of estrogen puts her at increased risk for premature ovary failure, osteoporosis, heart disease, colon cancer, Alzheimers disease, tooth loss, impaired vision, Parkinsons disease and diabetes. The longer a woman is without the protection of estrogen, the greater the risk for serious health consequences of these conditions.

There are estrogen receptors in a variety of organs throughout the body. Thats why hormonal imbalance produces different symptoms such as loss of skin elasticity, bone shrinkage, moodiness and cognitive decline. On the other hand, when estrogen levels rise as they do in the first week of menses, their overall effect is to increase the amount of serotonin available in the spaces between the brains nerve cells. That improves mood. Within the brain, estrogen may in fact act as a natural antidepressant and mood stabilizer. It is therefore essential that a woman suffering from premature ovary failure or surgical menopause receive treatment from an HRT physician who understands the many ramifications of the disease and is willing and able to meet her endocrine and emotional needs. This is the reason why you need to look for hormone replacement therapy in Chicago.

Studies have shown, testosterone hormone therapy can provide a woman with mental clarity, increased libido and muscle tone and mass. When this hormone is at low levels, women often complain of mental confusion, weight gain and poor muscle tone, even with regular exercise.

The effect of hormone deficiency on the brain, muscle, bone, heart and metabolism can be significant without hormone replacement therapy for women, and it can be dangerous to long-term health. The brain needs normal amounts of testosterone in balance with estrogen to produce serotonin, which supports emotional balance. When lacking in these hormones, a woman will experience emotional instability that often results in increased anxiety, irritability, sleep disturbances, anger, sadness and depression.

The musculoskeletal system is also adversely affected by the loss of testosterone. By not having bio-identical hormone therapy, the deficiency or imbalance of testosterone can lead to muscle atrophy, osteopenia, osteoporosis, and pain in the muscles and joints. Think upon it once and search for testosterone clinic in Chicago.

Studies have shown, men begin losing testosterone at a rate of 3% to 10% per year beginning at age 30. Current medical research now defines a male equivalent to menopause asandropause. Because the testosterone used is totally natural, it is ideal for men who want s the benefits of a bio-identical hormone without the drawbacks of a synthetic.

Symptoms of testosterone deficiency in men include fatigue, lack of mental acuity, loss of libido, and difficulty achieving or sustaining an erection.Why bio-identical hormone pellet therapy for men? Hormonal needs for men have received national attention, but with marginal treatment options available. Hormonal treatments for men can be expensive, require daily consumption, and, in many cases, need to be carefully timed with their partners needs for normal sexual activities and pleasure.

Bio-identical hormone pellet therapy is the only delivery method of testosterone therapy that gives sustained and consistent testosterone levels throughout the day for four to six months without any roller coaster blood levels of testosterone, which can result in mood and energy fluctuations for the patient.BioTE Medical has had excellent results treating men with bio-identical hormone therapy. There have been only a few reported side effects, which are all minor and treatable.

Men find themselves lacking in sexual desire, gaining weight, losing muscle mass, and feeling sluggish, depressed and irritable. Yet, they believe they must endure these body and hormonal changes as part of aging. It is a high time when you need to consider testosterone clinic in Chicago and enhance your health.

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Hormone Replacement Therapy and Testosterone Clinic in Chicago

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Snow and ice cause cars to stall out on the road to their destination. In patients with CLL, its their stem cells that stall out and researchers want to know why.

For patients who have chronic lymphocytic leukemia, fighting off a serious infection can be difficult and often is just not possible. And a team of Mayo researchers is starting to find out why in a paper published recently in the journal Leukemia.

What is Chronic Lymphocytic Leukemia?

This disease is cancer of an immune cell called a B lymphocyte. These cells form in bone marrow and migrate out to patrol in the blood stream and lymphoid organs. But in chronic lymphocytic leukemia, the immune system is depleted, a state called immunodeficiency. Because of that, people with this type of leukemia are prone to serious infections and the diseases those may cause. They are also prone to developing other types of cancer.

And its those resulting problems that may ultimately contribute to death explains Kay Medina, Ph.D., a Mayo Clinic immunologist. Dr. Medina specializes in how immune cells develop from bone marrow stem cells.

In our bone marrow, stem cells convert to red blood cells, platelets or a variety of immune cells. Those are then sent into the blood stream where they do their job. Red blood cells replace cells that are worn out.

White blood cells patrol the byways of our circulation, chasing down everything from cellular debris to bacteria to virus particles.But not in patients with chronic lymphocytic leukemia.

Joining the Team

Research on chronic lymphocytic leukemia is going on in several labs at Mayo Clinic. Dr. Medina got involved after speaking with colleagues Wei Ding, M.B.B.S, Ph.D., and Neil Kay, M.D., both chronic lymphocytic leukemia physician researchers.

Mayo has a strong tradition of encouraging physician/basic research collaborations to advance knowledge of disease mechanisms, development, and assessment of new treatment approaches, says Dr. Medina.

The basic research helps us understand the cause of the disease, in this case the leukemia cell, but it also helps to understand what the disease does to other parts of the body, such as the lymph nodes, spleen, blood and bone marrow, she says.

Bone marrow is the organ that replenishes all cells in the immune system but has not been evaluated for functional proficiency in CLL patients, explains Dr. Medina.

Checking out the Cells and their Environment

Kay Medina, Ph.D.

Dr. Medinas team, with funding from Mayo Clinics Center for Biomedical Discovery, decided to look at bone marrow stem cells and their ability to generate all blood cell types. Some of the immune deficiency may be the result of treatment, but untreated patients have the same problem. The chronic nature of the disease itself may also dampen immune activity. But Dr. Medina explains that the leukemia cells may promote an environment that suppresses immune function.

Our research seeks to add to the discussion by identifying additional ways patients with CLL are unable to fight off tumors and other diseases, says Dr. Medina.

In a paper published late last year, Dr. Medina and her team, including first author Bryce Manso who is a student in the Mayo Clinic Graduate School of Biomedical Sciences, examined bone marrow and blood samples from chronic lymphocytic leukemia patients and healthy controls to determine the frequency of bone marrow stem cells in each sample and how well they did their job.

Bryce Manso, presenting a poster to a conference attendee.

The authors reported that, in general, samples from patients with chronic lymphocytic leukemia have fewer stem cells in their bone marrow, and those stem cells that remain work less well than stem cells from controls.

Stalled-Out Bone Marrow Stem Cells

As to why this happens, the authors found that it was linked to loosening controls for the on/off switches which regulate this process, proteins called transcription factors. These proteins regulate key functions in the cell, and are out of whack in samples from chronic lymphocytic leukemia patients. They may prevent bone marrow stem cells from pursuing a pathway for development; stalling-out their ability to differentiate, resulting in decreased production of important blood cells that provide the first line of defense against infectious agents.

But, Dr. Medina cautions, there is more to this story.

This is an emerging area of research in that its both a unique explanation for the clinical problem of immune deficiency and it has been minimally studied, says Dr. Medina. Future studies are planned to look at specific transcription factors that control stem cell differentiation as well as how the presence of leukemic cells in the bone marrow alter blood cell development. They will then relate this information to clinically relevant complications reported in chronic lymphocytic leukemia patients, she says.

Basic Research to Improve Patient Care

Dr. Medina, her team, and their clinical colleagues hope that by understanding how bone marrow function is impaired in chronic lymphocytic leukemia patients, they can develop unique strategies to boost bone marrow function or find alternate treatments that do not block or modify marrow function.

Through this work we hope to find ways to reduce infections and the incidence of second cancers in chronic lymphocytic leukemia patients. Our research has the potential to improve quality of life as well as extend the lives of these patients says Dr. Medina.

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Related Resources:

Tags: basic science, blood cancer, cancer, Center for Biomedical Discovery, chronic lymphocytic leukemia, Findings, immunology, Kay Medina, leukemia, Mayo Clinic Cancer Center, Neil Kay, News, Progress Updates, Wei Ding

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Bone Marrow Stem Cells Stall Out in Chronic Lymphocytic ...

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You might have a stem cell or bone marrow transplant as part of your treatment for non-Hodgkin lymphoma (NHL). Find out how a transplant works and why you might have it.

A transplant allows you to have high doses of chemotherapy and other treatments. The stem cellsare collected from the bloodstream or the bone marrow.

Stem cells are very earlycells made inthe bone marrow. Bone marrow is a spongy material that fills the bones.

These stem cells develop into red blood cells, white blood cells and platelets.

Red blood cells contain haemoglobin which carries oxygen around the body. White blood cells are part of your immune system and help to fight infection. Platelets help to clot the blood to prevent bleeding.

These stem cells develop into red blood cells, white blood cells and platelets.

You have a stem cell transplant after very high doses of chemotherapy. You might have targeted drugs with the chemotherapy. You may also have radiotherapy to your whole body. This is called total body irradiation or TBI.

The radiotherapy and chemotherapy has a good chance of killing the lymphomacells. But it also kills the stem cells in your bone marrow.Soyour team either collects:

After the treatment you have the stem cells into your bloodstreamthrough a drip. The cells find their way back to your bone marrow where theystart making blood cells again and your bone marrow slowly recovers.

The main difference between a stem cell and bone marrow transplant is whether stem cells are collected from the bloodstream or bone marrow.

A stem cell transplant uses stem cells from your bloodstream, or a donors bloodstream. This is also called a peripheral blood stem cell transplant.

A bone marrow transplant uses stem cells from your bone marrow, or a donors bone marrow.

Stem cell transplants are the most common type of transplant. Bone marrow transplants are not used as much. This is because:

You might have a bone marrow transplant if collecting stem cells has been difficult in your situation.

The aim of NHL treatment is usually to put it into remission. Remission means there is no sign of lymphoma.

Your doctor might suggest a transplant if your NHL:

High dose chemotherapy and a transplant aims to cure some types of NHL. Or it might control the lymphoma for longer if a cure is not possible.

Depending on your situation, you might have a transplant using:

See the article here:
What is a stem cell or bone marrow transplant? | non ...

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New 75,000 sq. ft. State of the Art Facility in uCity Square Adjacent to Penn Campus

Strengthens Amicus Capabilities as a Leading Global Rare Disease Biotechnology Company

CRANBURY, N.J. and PHILADELPHIA, Feb. 26, 2019 (GLOBE NEWSWIRE) -- Amicus Therapeutics (FOLD) today announced it is establishing a new Global Research and Gene Therapy Center of Excellence in uCity Square in Philadelphia, PA, to advance its commitment to world-class science that makes a meaningful difference in the lives of people living with rare metabolic diseases. Philadelphia is a well-regarded ecosystem for biotechnology and gene therapy research and offers an ideal environment for Amicus to advance its pipeline, attract and retain top talent and foster external collaborations within the rare diseases.

John F. Crowley, Chairman and Chief Executive Officer of Amicus Therapeutics, stated, This Amicus Global Research and Gene Therapy Center of Excellence is an important next step in the evolution of our science, research and gene therapy capabilities. In considering locations, Philadelphia became the clear choice as a burgeoning hub for medical breakthroughs. The proximity to our collaborators at the University of Pennsylvania and other major academic centers and hospitals in the area also provides a tremendous opportunity to advance our commitment to gene therapies. Philadelphia is easily accessible to New Jersey, which has been a strong contributor to our success and will remain the location of our global headquarters. As Amicus continues to expand globally, my hope is that the great science to come from our research in Philadelphia will one day soon lead to medicines with the potential to alleviate an enormous amount of suffering. This is our mission at Amicus and we are honored to be a part of the exciting Philadelphia research community.

Under the leadership of Jeff Castelli, PhD, Chief Portfolio Officer and newly appointed Head of Gene Therapy, and Hung Do, PhD, Chief Science Officer, the new facility will be located at 3675 Market Street in uCity Square, a 6.5 million square-foot, mixed-use knowledge community consisting of office, laboratory, clinical, residential and retail space designed to enable university and corporate research, entrepreneurial activity and community engagement.

An initial group of Amicus research employees has moved into temporary space in the building at BioLabs@CIC Philadelphia during construction of the permanent space. The new 75,000 sq. ft. Center will be completed in the second half of 2019 and will serve as the headquarters for the global Amicus science organization and the gene therapy leadership team. Amicus expects up to 200 employees to eventually be based at the new Philadelphia facility. The Company is maintaining global business operations in Cranbury, NJ, and international headquarters in Marlow, UK.

J. Larry Jameson, MD, PhD, Executive Vice President for the Health System and Dean of the Raymond and Ruth Perelman School of Medicine stated, On behalf of Penn Medicine, I would like to welcome Amicus Therapeutics to Philadelphia. Amicus is working to pioneer significant advancements in gene therapy, which includes a collaboration with Dr. James Wilson and his team at our Orphan Disease Center. This relationship reflects how the innovation ecosystem at Penn brings together researchers, innovators, and entrepreneurs to accelerate research discoveries to patients as quickly as possible. The close proximity between the Amicus Center of Excellence and our campus will further strengthen this relationship and create additional opportunities to work together.

Jim Kenney, Mayor of Philadelphia, commented, The City of Philadelphia is committed to fostering innovative companies, academic institutions, and hospitals that are focused on the latest advancements in research and development, while also elevating the patient experience within our healthcare systems. Amicus Therapeutics is an established leader in biotechnology with a unique and intense patient-dedicated mission. The Companys presence and investment in Philadelphia will create additional opportunities that will be highly influential as our city continues its transformation into a major global biotech hub.

About Amicus Therapeutics Amicus Therapeutics (FOLD) is a global, patient-dedicated biotechnology company focused on discovering, developing and delivering novel high-quality medicines for people living with rare metabolic diseases. With extraordinary patient focus, Amicus Therapeutics is committed to advancing and expanding a robust pipeline of cutting-edge, first- or best-in-class medicines for rare metabolic diseases. For more information please visit the companys website at http://www.amicusrx.com, and follow us on Twitter and LinkedIn.

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Forward-Looking StatementsThis press release contains "forward- looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 Words such as, but not limited to, look forward to, believe, expect, anticipate, estimate, intend, "confidence," "encouraged," potential, plan, targets, likely, may, will, would, should and could, and similar expressions or words identify forward-looking statements. The forward looking statements included in this press release are based on management's current expectations and belief's which are subject to a number of risks, uncertainties and factors. In addition, all forward looking statements are subject to the other risks and uncertainties detailed in our Annual Report on Form 10-K for the year ended December 31, 2017 and Quarterly Report on 10-Q for the Quarter ended September 30, 2018. As a consequence, actual results may differ materially from those set forth in this press release. You are cautioned not to place undue reliance on these forward looking statements, which speak only of the date hereof. All forward looking statements are qualified in their entirety by this cautionary statement and we undertake no obligation to revise this press release to reflect events or circumstances after the date hereof.

CONTACTS:

Investors/Media:Amicus TherapeuticsSara Pellegrino, IRCVice President, Investor Relations & Corporate Communicationsspellegrino@amicusrx.com (609) 662-5044

Media:Amicus TherapeuticsMarco WinklerDirector, Corporate Communicationsmwinkler@amicusrx.com(609) 662-2798

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Amicus Establishes Global Research and Gene Therapy Center ...

Recommendation and review posted by Bethany Smith

As a postdoctoral researcher at the University of California, Berkeley, Emilia Huerta-Snchez noticed something strange in the fine print of an old population genetics study. In the acknowledgements, the studys author, a well-known geneticist, wrote, I wish to thank Mrs. Jennifer Smith for ably programming and executing all the computations.

Huerta-Snchez showed the odd credit line to fellow postdoc Rori Rohlfs. Smiths level of computing, she remarked, would normally warrant authorship today. In all likelihood, the two scientists mused privately, other womens contributions to the burgeoning field of population genetics had also been relegated to the footnotes.

Years later, after watching the 2016 movie Hidden Figures, which depicts the black female mathematicians behind NASAs human spaceflight program, Huerta-Snchez and Rohlfsnow with university appointments of their owndiscussed the idea again. This time, they wanted to test the hypothesis. How many programmers had been left in the footnotes of their field, they wondered, and how many of those less-acknowledged contributors were women?

Huerta-Snchez and Rohlfs assembled a team of student researchers to flip through the archival pages of 20 years worth of articles in the programming-heavy journal Theoretical Population Biology, documenting the authors and the names in the acknowledgements and categorizing them by gender. After the group reviewed 800-plus articles by over 1,000 authors (about 93 percent of whom were men), Huerta-Snchezs initial suspicion proved correct. Women whod contributed to influential studies tended to receive a hat-tip in the acknowledgements rather than full authorship.

In a recent study published in the journal Genetics, the San Francisco State University and Brown University researchers found that just under half of the 46 acknowledged programmers they identified in theoretical population genetics studies were women, in contrast to only about seven percent of credited authors. Ezequiel Lopez Barragan, one of the San Francisco State University students who worked on (and got authorship) for the new study, says he felt the skewed acknowledgement of women as programmers was just not fair, not equitable.

By identifying the biases in old research conventions, the team hopes to draws attention to who doesand does notreceive acknowledgement in scientific papers today.

Population genetics, which sprouted up in the first half of the 20th century after the rediscovery of Gregor Mendels foundational work in genetics, is a computation-heavy field that looks at genetic variation to better understand how natural selection and population makeup influence evolution. By the 1970s, one of the decades reviewed in the new study, computer-generated models had become accessible tools for scientists, and technological advances made it possible to gather detailed protein variation data. The field of population genetics took off, Rohlfs says.

Some of the data couldnt be analyzed by hand, which is where the acknowledged programmers came in, computing on the new machines to conduct numerical analysis. These programming roles were often carried out by women, but the researchers crunching the numbers didnt receive the same acknowledgment in published research that they might expect today.

The practice of downplaying womens scientific contributions isnt anything new, says historian Marsha Richmond, who studies womens early contributions to academic biology. Instead, she says, it follows a long trend that was probably first established in astronomy. The Harvard computers, for example, who calculated the positions and characteristics of thousands of stars at Harvard Observatory at the turn of the 20th centuryand made many important discoveries in astronomy along the waymirrored the mathematical roles that women played at NASA more than half a century later.

Historically, women tended to enter emerging fields like ecology or radiation science, and as employees, they were cheaper to hire than their male counterparts. But once the field develops, they get rather marginalized and the men take over, Richmond says. Although the 1960s and 70s heralded increased visibility for some female scientists, like ecologist Rachel Carson and geneticist Charlotte Auerbach, both genetics and the initially pink-collar field of programming followed the pattern of sidelining women contributors. The proportion of female acknowledged programmers in the new study, for instance, decreased between the 1970s and 1980s as the field became more male-dominated and lucrative.

Richmond calls Huerta-Snchez and Rohlfs paper exciting. It was the first shed learned of women involved in this era of evolutionary biology. The lack of female scientists and programmers in the historic record, Richmond says, is not just a problem of science and society but also of historians. Historians have tended to gravitate towards the males who are considered geniuses.

Both Richmond and the studys principal investigators emphasized that uncovering the presence of women in population genetics could inspire future scientists and guard against the negative impact of gender stereotypes in science. Such work reveals paths to success in a field thats still relatively male-dominated. The more we see women doing science, the more its normal, Rohlfs says, and we hope that will lead to change.

Margaret Wu is an early contributor to population genetics and one of the acknowledged programmers whose name cropped up repeatedly in the new study. As the Atlantics Ed Yong explains, her work help develop a statistical toolstill used todaythat approximates the level of genetic diversity in a population.

But when the team behind the study finally reached Wu, she initially thought theyd contacted the wrong person. Wu, after working as a research assistant at Monash University in Australia, has gone on to specialize in educational statistics, not population genetics. She earned a PhD almost 30 years after the highly-cited study that she contributed numerical work to, and she is now on the faculty of the University of Melbourne.

I was in no way frustrated about the authorship. I didnt even think I should be acknowledged that was the norm in those days, Wu writes in an email. But she also says shes observed and experienced gender discrimination throughout her career in academia. My conclusion was that men are often mates (to use an Australian term), she says, and they unite and are unwilling to contradict each other even though someone is not doing the right thing.

Upon reading about Margaret Wu in the Atlantic, Jess Wade, a physics postdoc at Imperial College London whos created around 510 Wikipedia pages for female scientists, made Wu a Wikipedia page. Wade says via Twitter that her first reaction to the study was anger. I made [the Wikipedia page] because Im sick of these people being written out of history.

Rohlfs also pointed to norms, not individuals, as being responsible for the lack of acknowledgement for women. Because authorship, which is totally crucial for career advancement, can be distributed subjectively, its subject to all the biases we have, she says. Today, for instance, the contributions of technicians might be overlooked, and technicians, Rohlfs says, are more often women and people of color.

Everybody just thought it was okay that these women didnt get authorship, she says. I think that leads us directly then to think about what are our authorship norms today, and who are we excluding because we just tacitly agree that its right to exclude those people.

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In the early days of gene editing, biologists had a molecular tool kit that was somewhat akin to a printing press. Which is to say, altering DNA was a messy, labor-intensive process of loading genes onto viruses bound for target cells. It involved more than a fair amount of finger-crossing. Today, scientists have the genetic equivalent of Microsoft Word, and they are beginning to edit DNA almost as easily as software engineers modify code. The precipitating event? Call it the Great Crispr Quake of 2012.

If youre asking, whats Crispr? the short answer is that its a revolutionary new class of molecular tools that scientists can use to precisely target and cut any kind of genetic material. Crispr systems are the fastest, easiest, and cheapest methods scientists have ever had to manipulate the code of life in any organism on Earth, humans included.

The long answer is that Crispr stands for Clustered Regularly Interspaced Palindromic Repeats. Crispr systems consist of a protein with sequence-snipping capabilities and a genetic GPS guide. Such systems naturally evolved across the bacterial kingdom as a way to remember and defend against invading viruses. But researchers recently discovered they could repurpose that primordial immune system to precisely alter genomes, setting off a billion-dollar boom in DNA hacking.

Every industry is throwing mad money at Crisprpharma, agriculture, energy, materials manufacturing, you name it. Even the weed guys want in. Companies are using it to make cancer-curing medicines, climate-change-fighting crops, biofuel-oozing algae, and self-terminating mosquitoes. Academic researchers have almost universally adopted Crispr to more deeply understand the biology of their model organisms. Supporting this biohacking bonanza is an increasingly crowded Crispr backend supply chain; businesses building gene-editor design tools and shipping synthetic guide RNAs or pre-Crisprd cell lines to these companies doors. So far, though, very few Crispr-enhanced products have made it into the hands of actual consumers. In their place, hyperbolic headlines have bugled societys greatest hopes and fears for the technology, from saving near-extinct species to igniting a superbaby arms race.

Crispr isnt going to end disease or hunger or climate change any time soon. Maybe it never will. Nor is it about to deliver designer children or commit genetic genocide. (Though its never too early to start talking about the ethical dilemmas such a powerful technology could pose.) Crispr is, however, already beginning to reshape the physical world around us in much less radical ways, one base pair at a time.

It all started with yogurt. To make it, dairy producers have long employed the help of Streptococcus thermophilus, a bacteria that gobbles up the lactose in milk and poops out lactic acid. It wasnt until 2005, though, that a young microbiologist named Rodolphe Barrangou discovered that S. thermophilus contained odd chunks of repeating DNA sequencesCrisprsand that those sequences were keeping it safe from the viruses that attack it and result in spoilage. (If the thermophilus is gone, nastier bacteria can move in and feed off the lactose, ruining the product.)

Before long, DuPont bought the Danish company that Barrangou worked for and began using Crispr to protect all of its yogurt and cheese cultures. Since DuPont owns about 50 percent of the global dairy culture market, that means youve probably already eaten Crispr-optimized cheese on your pizza.

Viruses work by turning your cells into little factories for their DNA. A Crispr-based test could pick out that foreign DNA from just a drop of blood, spit, or urine and tell you in minutes if youve got the Zika virus, dengue, or yellow fever circulating in your body.

Every year, fungi wipe out a third of all crops. Crispr panels tuned to identify the worst offenders could help farmers save their harvests before the blight sets in.

Thanks to overuse, the worlds antibiotic arsenal is losing its effectiveness. New Crispr-based drugs that only target bad bugs would leave your microbiome intact and help fight antibiotic resistance.

All the while, gene sequencing costs were plummeting and research scientists around the world were assembling the genomes of bacteria. As they did, they found Crisprs everywheremore than half of the bacterial kingdom turned out to have them. Oftentimes those sequences were flanked by a set of genes coding for a class of strand-cutting enzymes called endonucleases. Scientists suspected they were involved in this primitive immune system, but how exactly?

The key insight came from a particularly nasty bugthe one that causes strep throat. Its Crispr system made two RNA sequences that attached to a clam-shaped endonuclease called Cas9. Like a genetic GPS, those sequences directed the enzyme to a strand of DNA complementary to the RNA sequences. When it got there, Cas9 changed shape, grabbing the DNA and slicing it in two. The molecular biologists who made this discoveryJennifer Doudna and Emmanuelle Charpentierpublished their work on bacteria in Science in 2012. But not before patenting the technology as a tool for genetic engineering. If you just switch out the RNA guide, you can send Cas9 anywhereto the gene that causes Huntingtons disease, say, and snip it out. Crispr, they realized, would be a molecular biologists warp drive.

Six months later, a molecular biologist at the Broad Institute of MIT and Harvard named Feng Zhang published a paper in Science showing how Crispr-Cas9 could edit human cells too. In fact, with the right genetic guides, you can Crispr pretty much anything. That meant it might be put to work on next-generation medicines that could do things like erase genetic defects and supercharge the bodys natural defenses against cancer. And that meant big money.

Perhaps predictably, a patent battle ensuedone that is still going on today. Crisprs early pioneers founded three companies with exclusive licenses to exploit Crispr/Cas9 to cure human diseases; the first clinical trials are expected to begin in the US in 2018. Uncertainty over who will ultimately own the technology has done little to slow the appetite for all things Crispr. If anything, it has unleashed a flood of interest in developing competing and adjacent tools that promise to further refine and expand Crisprs already ample potential.

For now, Crispr is still a biologist's buzzword. But just as computers evolved from a nerdy, niche tool for math geeks to a ubiquitous, invisible extension of our own bodies, so Crispr will one day weave seamlessly into the fabric of our physical reality. It will simply be the way to solve a problem, if that problem is remotely biological in nature.

Take industrial fermentation for example. With the help of old-school genetic engineering techniques, scientists have already reprogrammed microbes like E. Coli and brewers yeast into factories that can make everything from insulin to ethanol. Crispr will rapidly enlarge the catalog of designer chemicals, molecules, and materials that biorefineries can produce. Self-healing concrete? Fire-resistant, plant-based building materials lighter than aluminum? Fully biodegradable plastics? Crispr not only makes all these possible, it makes it possible to produce them at scale.

But we wont get there with the tools weve currently got. Which is why researchers are now racing to chart the full expanses of the Crispr universe. At this moment theyre scouring the globe for obscure bacteria to sequence, and theyre tinkering with the systems that have already been discovered. Theyre filing patents on every promising new nuclease they come across, adding to a list that is sure to expand in the coming decade. Each new enzyme will not only advance Crisprs gene editing powers, but extend its capabilities far beyond DNA manipulation. You see, slicing and dicing isnt the only interesting thing to do to DNA. Tricked out new Crispr systems could temporarily toggle genes on and off or surveil the genome to fix mutations as they happen in real time, no snipping required. The first would let scientists treat human diseases where theres too much or too little of a certain substancesay insulinwithout permanently altering a patients DNA. The second could one day prevent diseases like cancer from occurring altogether. The specificity of Crispr, perhaps more than its actual cutting mechanism, will inspire applications we cant yet imagine.

Good at cutting DNA, great for knockouts. Already being replaced by newer base pair editors with more fine-tuned control.

Like Cas9 but not as sloppy. It leaves sticky DNA ends, which are easier to work with when making edits.

Cuts RNA not DNA. Could knock down protein levels without permanently changing your genome. Pair it with a reporter signal and youve got a diagnostic.

Cas3 gives zero f***. It offers no repair mechanismonce it finds that target DNA sequence it just starts cutting till there aint no DNA left.

Just discovered in an abandoned silver mine, we dont know yet what these tiny enzymes superpowers will be.

Meanwhile, consumers can expect to see their first Crisprd products lining grocery store shelves very soon. Because Crispr doesnt use plant pathogens to manipulate DNA (the old GMO-generating method), the USDA has given a free regulatory pass to gene-edited crops, allowing drought-tolerant soybeans and extra-starchy corn to ease into your favorite processed foods. Specialty fruits and vegetables will likely follow the commodity crops; the reduced regulatory burden and the cheapness of Crispr will allow companies appealing to consumers senses rather than farmers bottom lines to enter the market. Already a dozen or so startups have popped up to challenge the Bayer/Monsanto, DowDupont/Pioneers of the world.

This democratizing aspect of Crispr-based tech, combined with its nearly limitless commercial possibilities, make today a great time to be a molecular biologist. Want to make antibiotics that only target bad bugs without wiping out the entire microbiome? There are companies doing that. Want to make paper-based diagnostics that doctors can take into the field to test for diseases like dengue and Zika? There are research labs and startups doing that too. And as more tools come online, the backend Crispr ecosystem will continually expand to support, supply, and optimize them.

Crispr applications are only going to become more powerful, and when they do they will rightly invite more scrutiny, and probably more regulation. Were going to have to figure out if its OK to wipe out an entire species in the name of conservation and bring other ones back from extinction. Well have to wrestle with the possibility that gene editing tools might be used to produce biological weapons of unfathomable destruction. And yes, well eventually have to talk about designer babies; when is it acceptable to fix a genetic mutation? Would we ever start adding features? Where do we draw the line? Crispr, and all the tools that will one day make up the Crispr universe will undoubtedly force societiesnot just scientiststo confront these questions and ponder the oldest one of all; what does it mean to be human?

Everything You Need To Know About Crispr Gene EditingOkay, you get it, Crisprs a big deal. But now, arent you curious to know exactly how it works? You dont have to be a microbiologist to understand this step-by-step look inside the molecular multitool of the century.

What Good Is Crispr If It Cant Get Where It Needs To Go?It doesnt matter how good Crispr gets, in order to actually snip away humanitys worst diseases, it first has to get to the right cells. And thats way harder said than done. Its time to talk about Crisprs delivery problem.

First Human-Pig Chimera Is a Step Toward Custom OrgansScientists have long been dreaming of xenotransplantationputting animal organs into peopleas a possible solution to the current human organ shortage. But almost all attempts to do so have failed. Heres how Crispr is bringing new hope to the dream of animal organ farms.

Read This Before You Freak Out Over Gene-Edited SuperbabiesIn the last few years, scientists in the US and China have used Crispr to fix genetic mutations in human embryos, prompting concerns over the imminent takeover of genetically superior designer children. Breathe, people: You dont need to worry about that for a long, long, long time.

America Needs To Figure Out the Ethics of Gene Editing NowStill. All that successful human embryo modification has scientists around the world calling for varying levels of caution against it. And while pretty much everyone agrees on avoiding a Gattaca-type situation, thats where the consensus ends.

Process of EliminationFor decades conservationists have used medieval methods for eradicating invasive island predators like rats. And all those traps and guns and poisons still havent gotten the job done. Local species are still under threat of extinction. Now some scientists are turning to Crispr gene drives, a particularly potent genetic tool that could forever transform our power over nature. Emma Marris went to the Galapagos to see how they might work in the wild.

The FDA Wants to Regulate Gene-Edited Animals as DrugsWe get it. Its hard to contort the USs 1938 patchwork of laws around 21st century technology. But companies making hornless cows and tailless pigs and all-male beef cattle are pissed at the FDAs new interpretation of the rules, and talking about taking their tech elsewhere.

Easy DNA Editing Will Remake the World. Buckle Up.Still havent had enough Crispr? Amy Maxmens 2015 cover story is the definitive survey of this gene-editing technology; from its humble bacterial beginnings, to the trenches of its ferocious patent battle, to inside the companies already churning toward our Crispr-created future.

Plus! Crispr uploads a galloping horse GIF into a living bacteria and more WIRED gene editing coverage.

This guide was last updated on April 26, 2018.

Enjoyed this deep dive? Check out more WIRED Guides.

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What is Crispr Gene Editing? The Complete WIRED Guide | WIRED

Recommendation and review posted by Bethany Smith

Leber congenital amaurosis is an inherited retinal disease that can cause blindness. This rare eye disorder can cause severe vision loss among infants, affecting two to three infants per 100,000 births. Fortunately, new medical treatment for this condition has recently been developed. In todays post, your glaucoma doctor from EyeSite of The Villages discusses how gene therapy can help treat inherited retinal problems.

Understanding Leber Congenital Amaurosis

The retina is a specialized tissue at the back of the eye that detects light and color. Leber congenital amaurosis attacks this part of the eye, causing severe visual impairment. Its considered an inherited degenerative disease, wherein both of the parents of the affected child carry a defective gene, including the RPE65 gene. Scientists have identified 14 genes with mutations that can cause this eye condition.

Patients diagnosed with Leber congenital amaurosis have reduced vision at birth. During infancy, parents may notice a lack of visual responsiveness and unusual eye movement. Typical eye exams conducted by a cataract doctor, however, may reveal normal retinas during eye exams. Electroretinography tests, however, may detect little if any activity in the retina.

Introduction to Gene Therapy

In 2009, Israeli researchers found a herd of Awassi sheep that suffered from day blindness. They began gene therapy trials for the sheep. The treatment included injecting a virus that carries a normal copy of the missing gene. The treated sheep regained their day vision, while the untreated remained visually impaired.

How Gene Therapy Can Help

After successful clinical trials, gene therapy has been approved by the Food and Drug Administration to treat Leber congenital amaurosis. This therapy doesnt restore normal eyesight; instead, it allows patients to see shapes and light. It involves injecting a healthy version of the affected gene in the retina, which helps detect light and convert it into visual signals for the brain to interpret.

Turn to the EyeSite of The Villages glaucoma doctor to help diagnose different eye conditions. We offer comprehensive eye exams to gauge your vision health. Call us today at (352) 504-4560 to schedule an appointment. We serve residents of Lady Lake and Fruitland Park, FL.

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Gene Therapy: The Future of Vision Treatment

Recommendation and review posted by Bethany Smith

The development of in vitro fertilitzation (IVF) has allowed many couples to have the families they might otherwise have been unable to create independently. At the same time, this technology has allowed researchers to study the genetic make-up of the earliest stages of embryos. These advances are providing insights into the link between genetics and infertility and how defects (mutations) in specific genes may result in male or female infertility. It is possible that many cases of unexplained infertility will one day be found to have a clear genetic basis.

What has been learned in the last two decades of assisted reproduction is that some cases of severe male factor infertility are clearly related to gene deletions, mutations or chromosomal abnormalities.

Some men with very severe male factor infertility will be found, upon testing their blood chromosomes (known as a "karyotype") to have an extra X chromosome. That is, instead of having a 46 XY karyotype, they have a 47 XXY karyotype. This condition is known as "Klinefelter Syndrome" and can result in failure to achieve puberty or even when puberty is achieved, these men often have male infertility. Some men with Klinefelter Syndrome can father pregnancies through the use of in vitro fertilitzation (IVF) with Intra-Cytoplasmic Sperm injection (ICSI). So far, we are not seeing an increased risk of Klinefelter Syndrome or other chromosome abnormalities in the offspring achieved in these cases.

Also discovered in recent years is that some men with very severe low sperm counts will be found to have deletions in a certain part of their Y chromosome, known as the DAZ gene. Their karyotype is normal (46 XY) but close inspection of the Y chromosome shows there are sections of the chromosome that are missing. A portion of these men will have no recoverable sperm in the ejaculate or on testicular surgery and donor sperm is the only option. With other deletions in the DAZ gene, there is a small amount of sperm present and conception with IVF-ICSI is possible. In these cases, the male offspring which will always inherit their father's Y chromosome, will also have this deletion, and will themselves be infertile.

A single gene mutation in the gene for Cystic Fibrosis (CF) is associated with absence of the part of the tube (the "vas deferens") that leads from the testicle to the urethra in the penis. These men are usually carriers for the CF gene mutation and do not themselves have the disease of Cystic Fibrosis. Sperm can be recovered from the testicles in these men to be used for IVF with ICSI but it is imperative that their wife (or egg provider) be fully tested for CF mutations as well, otherwise there is significant risk of having a child with Cystic Fibrosis.

For men with sperm counts routinely in the less than 5 million total motile sperm range, testing for genetic conditions is warranted so that these men or couples can be made aware of the genetic issues and how these issues might affect their offspring.

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Genetics and Male Infertility - pacificfertilitycenter.com

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The relationship between biology and sexual orientation is a subject of research. While scientists do not know the exact cause of sexual orientation, they theorize that a combination of genetic, hormonal, and social factors determine it.[1][2][3] Hypotheses for the impact of the post-natal social environment on sexual orientation, however, are weak, especially for males.[4]

Biological theories for explaining the causes of sexual orientation are favored by scientists[1] and involve a complex interplay of genetic factors, the early uterine environment and brain structure.[5] These factors, which may be related to the development of a heterosexual, homosexual, bisexual, or asexual orientation, include genes, prenatal hormones, and brain structure.

A number of twin studies have attempted to compare the relative importance of genetics and environment in the determination of sexual orientation. In a 1991 study, Bailey and Pillard conducted a study of male twins recruited from "homophile publications", and found that 52% of monozygotic (MZ) brothers (of whom 59 were questioned) and 22% of the dizygotic (DZ) twins were concordant for homosexuality.[6] 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In a study of 61 pairs of twins, researchers found among their mostly male subjects a concordance rate for homosexuality of 66% among monozygotic twins and a 30% one among dizygotic twins.[7] In 2000 Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance.[8] They found 20% concordance in the male identical or MZ twins and 24% concordance for the female identical or MZ twins. Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. Other researchers support biological causes for both men and women's sexual orientation.[9]

Bearman and Brckner (2002) criticized early studies concentrating on small, select samples[10] and non-representative selection of their subjects.[11] They studied 289 pairs of identical twins (monozygotic, or from one fertilized egg) and 495 pairs of fraternal twins (dizygotic, or from two fertilized eggs) and found concordance rates for same-sex attraction of only 7.7% for male identical twins and 5.3% for females, a pattern which they say "does not suggest genetic influence independent of social context".[10]

A 2010 study of all adult twins in Sweden (more than 7,600 twins)[12] found that same-sex behavior was explained by both heritable factors and individual-specific environmental sources (such as prenatal environment, experience with illness and trauma, as well as peer groups, and sexual experiences), while influences of shared-environment variables such as familial environment and social attitudes had a weaker, but significant effect. Women showed a statistically non-significant trend to weaker influence of hereditary effects, while men showed no effect of shared environmental effects. The use of all adult twins in Sweden was designed to address the criticism of volunteer studies, in which a potential bias towards participation by gay twins may influence the results;

Biometric modeling revealed that, in men, genetic effects explained .34.39 of the variance [of sexual orientation], the shared environment .00, and the individual-specific environment .61.66 of the variance. Corresponding estimates among women were .18.19 for genetic factors, .16.17 for shared environmental, and .64.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.[12]

Twin studies have received a number of criticisms including self-selection bias where homosexuals with gay siblings are more likely to volunteer for studies. Nonetheless, it is possible to conclude that, given the difference in sexuality in so many sets of identical twins, sexual orientation cannot be attributed solely to genetic factors.[13]

Another issue is the finding that even monozygotic twins can be different and there is a mechanism which might account for monozygotic twins being discordant for homosexuality. Gringas and Chen (2001) describe a number of mechanisms which can lead to differences between monozygotic twins, the most relevant here being chorionicity and amniocity.[14] Dichorionic twins potentially have different hormonal environments because they receive maternal blood from separate placenta, and this could result in different levels of brain masculinisation. Monoamniotic twins share a hormonal environment, but can suffer from the 'twin to twin transfusion syndrome' in which one twin is "relatively stuffed with blood and the other exsanguinated".[15]

Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993 Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families.[16] Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed the "gay gene" in the media, causing significant controversy. Sanders et al. in 1998 reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared with 6% on the paternal side.[17]

A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28.[18] Two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men.[17] One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[19] Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation.[20]

Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects. In the full sample they did not find linkage to Xq28.[21]

Results from the first large, comprehensive multi-center genetic linkage study of male sexual orientation were reported by an independent group of researchers at the American Society of Human Genetics in 2012.[22] The study population included 409 independent pairs of gay brothers, who were analyzed with over 300,000 single-nucleotide polymorphism markers. The data strongly replicated Hamer's Xq28 findings as determined by both two-point and multipoint (MERLIN) LOD score mapping. Significant linkage was also detected in the pericentromeric region of chromosome 8, overlapping with one of the regions detected in the Hamer lab's previous genomewide study. The authors concluded that "our findings, taken in context with previous work, suggest that genetic variation in each of these regions contributes to development of the important psychological trait of male sexual orientation". Female sexual orientation does not seem to be linked to Xq28,[18][23] though it does appear moderately heritable.[24]

In addition to sex chromosomal contribution, a potential autosomal genetic contribution to the development of homosexual orientation has also been suggested. In a study population composed of more than 7000 participants, Ellis et al. (2008) found a statistically significant difference in the frequency of blood type A between homosexuals and heterosexuals. They also found that "unusually high" proportions of homosexual males and homosexual females were Rh negative in comparison to heterosexuals. As both blood type and Rh factor are genetically inherited traits controlled by alleles located on chromosome 9 and chromosome 1 respectively, the study indicates a potential link between genes on autosomes and homosexuality.[25][26]

The biology of sexual orientation has been studied in detail in several animal model systems. In the common fruit fly Drosophila melanogaster, the complete pathway of sexual differentiation of the brain and the behaviors it controls is well established in both males and females, providing a concise model of biologically controlled courtship.[27] In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred a female mice specifically lacking a particular gene related to sexual behavior. Without the gene, the mice exhibited masculine sexual behavior and attraction toward urine of other female mice. Those mice who retained the gene fucose mutarotase (FucM) were attracted to male mice.[28]

In interviews to the press, researchers have pointed that the evidence of genetic influences should not be equated with genetic determinism. According to Dean Hamer and Michael Bailey, genetic aspects are only one of the multiple causes of homosexuality.[29][30]

In 2017, Nature published an article with a genome wide association study on male sexual orientation. The research consisted of 1,077 homosexual men and 1,231 heterosexual men. A gene named SLITRK6 on chromosome 13 was identified.[31] The research supports another study which had been done by Simon LeVay. LeVay's research suggested that the hypothalamus of gay men is different from straight men.[32] The SLITRK6 is active in the mid-brain where the hypothalamus is. The researchers found another gene, named "thyroid stimulating hormone receptor" (TSHR) on chromosome 14 which dna sequence is different also for gay men.[31] TSHR stimulates thyroid and grave disease interrupted the function of TSHR. The previous research also indicated that grave disease had been seen more in gay men than in straight men.[33] Research indicated that gay people have lower body weight than straight people. It had been presumed that the overactive TSHR hormone lowered body weight in gay people.[34][35]

In 2018, Ganna et al. performed another genome wide association study on sexual orientation of men and women with data from 26,890 people who had at least one same-sex partner and 450,939 controls. The data in the study was meta-analyzed and obtained from the UK Biobank study and 23andMe. The researchers identified four variants more common in people who reported at least one same-sex experience on chromosomes 7, 11, 12, and 15. The variants on chromosomes 11 and 15 were specific to men, with the variant on chromosome 11 located in an olfactory gene and the variant on chromosome 15 having previously been linked to male-pattern baldness. The four variants were also correlated with mood and mental health disorders; major depressive disorder and schizophrenia in men and women, and bipolar disorder in women. However, none of the four variants could reliably predict sexual orientation.[36]

A study suggests linkage between a mother's genetic make-up and homosexuality of her sons. Women have two X chromosomes, one of which is "switched off". The inactivation of the X chromosome occurs randomly throughout the embryo, resulting in cells that are mosaic with respect to which chromosome is active. In some cases though, it appears that this switching off can occur in a non-random fashion. Bocklandt et al. (2006) reported that, in mothers of homosexual men, the number of women with extreme skewing of X chromosome inactivation is significantly higher than in mothers without gay sons. 13% of mothers with one gay son, and 23% of mothers with two gay sons, showed extreme skewing, compared to 4% of mothers without gay sons.[37]

Blanchard and Klassen (1997) reported that each additional older brother increases the odds of a man being gay by 33%.[38][39] This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation".[40] To explain this finding, it has been proposed that male fetuses provoke a maternal immune reaction that becomes stronger with each successive male fetus.This maternal immunization hypothesis (MIH) begins when cells from a male fetus enter the mother's circulation during pregnancy or while giving birth.[41]Male fetuses produce H-Y antigens which are "almost certainly involved in the sexual differentiation of vertebrates".These Y-linked proteins would not be recognized in the mother's immune system because she is female, causing her to develop antibodies which would travel through the placental barrier into the fetal compartment. From here, the anti-male bodies would then cross the blood/brain barrier (BBB) of the developing fetal brain, altering sex-dimorphic brain structures relative to sexual orientation, increasing the likelihood that the exposed son will be more attracted to men than women.[41]It is this antigen which maternal H-Y antibodies are proposed to both react to and 'remember'. Successive male fetuses are then attacked by H-Y antibodies which somehow decrease the ability of H-Y antigens to perform their usual function in brain masculinisation.[38]

However, the maternal immune hypothesis has been criticized because the prevalence of the type of immune attack proposed is rare compared with the prevalence of homosexuality.[42]

The "fraternal birth order effect" however, cannot account for between 71-85% of male homosexual preference.[43] Additionally, it does not explain instances where a firstborn child displays male homosexual preference (MHP).[44]

In 2017, researchers discovered a biological mechanism of gay people who tend to have older brothers. They think Neuroligin 4 Y-linked protein is responsible for a later son being gay. They found that women had significantly higher anti-NLGN4Y levels than men. The result also indicates that number of pregnancies, mothers of gay sons, particularly those with older brothers, had significantly higher anti-NLGN4Y levels than did the control samples of women, including mothers of heterosexual sons.[45]

In 2004, Italian researchers conducted a study of about 4,600 people who were the relatives of 98 homosexual and 100 heterosexual men. Female relatives of the homosexual men tended to have more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. The researchers concluded that there was genetic material being passed down on the X chromosome which both promotes fertility in the mother and homosexuality in her male offspring. The connections discovered would explain about 20% of the cases studied, indicating that this is a highly significant but not the sole genetic factor determining sexual orientation.[46][47]

Research conducted in Sweden[48] has suggested that gay and straight men respond differently to two odors that are believed to be involved in sexual arousal. The research showed that when both heterosexual women and gay men are exposed to a testosterone derivative found in men's sweat, a region in the hypothalamus is activated. Heterosexual men, on the other hand, have a similar response to an estrogen-like compound found in women's urine.[49] The conclusion is that sexual attraction, whether same-sex or opposite-sex oriented, operates similarly on a biological level. Researchers have suggested that this possibility could be further explored by studying young subjects to see if similar responses in the hypothalamus are found and then correlating these data with adult sexual orientation.[citation needed]

A number of sections of the brain have been reported to be sexually dimorphic; that is, they vary between men and women. There have also been reports of variations in brain structure corresponding to sexual orientation. In 1990, Dick Swaab and Michel A. Hofman reported a difference in the size of the suprachiasmatic nucleus between homosexual and heterosexual men.[50] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure,[51] but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.[52][53][54]

Research on the physiologic differences between male and female brains are based on the idea that people have male or a female brain, and this mirrors the behavioral differences between the two sexes. Some researchers state that solid scientific support for this is lacking. Although consistent differences have been identified, including the size of the brain and of specific brain regions, male and female brains are very similar.[55][56]

Simon LeVay, too, conducted some of these early researches. He studied four groups of neurons in the hypothalamus called INAH1, INAH2, INAH3 and INAH4. This was a relevant area of the brain to study, because of evidence that it played a role in the regulation of sexual behaviour in animals, and because INAH2 and INAH3 had previously been reported to differ in size between men and women.[57]

He obtained brains from 41 deceased hospital patients. The subjects were classified into three groups. The first group comprised 19 gay men who had died of AIDS-related illnesses. The second group comprised 16 men whose sexual orientation was unknown, but whom the researchers presumed to be heterosexual. Six of these men had died of AIDS-related illnesses. The third group was of six women whom the researchers presumed to be heterosexual. One of the women had died of an AIDS-related illness.[57]

The HIV-positive people in the presumably heterosexual patient groups were all identified from medical records as either intravenous drug abusers or recipients of blood transfusions. Two of the men who identified as heterosexual specifically denied ever engaging in a homosexual sex act. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been primarily or exclusively heterosexual "on the basis of the numerical preponderance of heterosexual men in the population".[57]

LeVay found no evidence for a difference between the groups in the size of INAH1, INAH2 or INAH4. However, the INAH3 group appeared to be twice as big in the heterosexual male group as in the gay male group; the difference was highly significant, and remained significant when only the six AIDS patients were included in the heterosexual group. The size of INAH3 in the homosexual men's brains was comparable to the size of INAH3 in the heterosexual women's brains.

However, other studies have shown that the sexually dimorphic nucleus of the preoptic area, which include the INAH3, are of similar size in homosexual males who died of AIDS to heterosexual males, and therefore larger than female. This clearly contradicts the hypothesis that homosexual males have a female hypothalamus. Furthermore, the SCN of homosexual males is extremely large (both the volume and the number of neurons are twice as many as in heterosexual males). These areas of the hypothalamus have not yet been explored in homosexual females nor bisexual males nor females. Although the functional implications of such findings still haven't been examined in detail, they cast serious doubt over the widely accepted Drner hypothesis that homosexual males have a "female hypothalamus" and that the key mechanism of differentiating the "male brain from originally female brain" is the epigenetic influence of testosterone during prenatal development.[58][59]

William Byne and colleagues attempted to identify the size differences reported in INAH 14 by replicating the experiment using brain sample from other subjects: 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). The researchers found a significant difference in INAH3 size between heterosexual men and heterosexual women. The INAH3 size of the homosexual men was apparently smaller than that of the heterosexual men, and larger than that of the heterosexual women, though neither difference quite reached statistical significance.[60]

Byne and colleagues also weighed and counted numbers of neurons in INAH3 tests not carried out by LeVay. The results for INAH3 weight were similar to those for INAH3 size; that is, the INAH3 weight for the heterosexual male brains was significantly larger than for the heterosexual female brains, while the results for the gay male group were between those of the other two groups but not quite significantly different from either. The neuron count also found a male-female difference in INAH3, but found no trend related to sexual orientation.[60]

A 2010 study, Garcia-Falgueras and Swaab asserted that "the fetal brain develops during the intrauterine period in the male direction through a direct action of testosterone on the developing nerve cells, or in the female direction through the absence of this hormone surge. In this way, our gender identity (the conviction of belonging to the male or female gender) and sexual orientation are programmed or organized into our brain structures when we are still in the womb. There is no indication that social environment after birth has an effect on gender identity or sexual orientation."[61]

The domestic ram is used as an experimental model to study early programming of the neural mechanisms which underlie homosexuality, developing from the observation that approximately 8% of domestic rams are sexually attracted to other rams (male-oriented) when compared to the majority of rams which are female-oriented. In many species, a prominent feature of sexual differentiation is the presence of a sexually dimorphic nucleus (SDN) in the preoptic hypothalamus, which is larger in males than in females.

Roselli et al. discovered an ovine SDN (oSDN) in the preoptic hypothalamus that is smaller in male-oriented rams than in female-oriented rams, but similar in size to the oSDN of females. Neurons of the oSDN show aromatase expression which is also smaller in male-oriented rams versus female-oriented rams, suggesting that sexual orientation is neurologically hard-wired and may be influenced by hormones. However, results failed to associate the role of neural aromatase in the sexual differentiation of brain and behavior in the sheep, due to the lack of defeminization of adult sexual partner preference or oSDN volume as a result of aromatase activity in the brain of the fetuses during the critical period. Having said this, it is more likely that oSDN morphology and homosexuality may be programmed through an androgen receptor that does not involve aromatisation. Most of the data suggests that homosexual rams, like female-oriented rams, are masculinized and defeminized with respect to mounting, receptivity, and gonadotrophin secretion, but are not defeminized for sexual partner preferences, also suggesting that such behaviors may be programmed differently. Although the exact function of the oSDN is not fully known, its volume, length, and cell number seem to correlate with sexual orientation, and a dimorphism in its volume and of cells could bias the processing cues involved in partner selection. More research is needed in order to understand the requirements and timing of the development of the oSDN and how prenatal programming effects the expression of mate choice in adulthood.[62]

The early fixation hypothesis includes research into prenatal development and the environmental factors that control masculinization of the brain. Some studies have seen pre-natal hormone exposures as the primary factor involved in determining sexual orientation.[63][64][65] This hypothesis is supported by both the observed differences in brain structure and cognitive processing between homosexual and heterosexual men. One explanation for these differences is the idea that differential exposure to hormone levels in the womb during fetal development may change the masculinization of the brain in homosexual men. The concentrations of these chemicals is thought to be influenced by fetal and maternal immune systems, maternal consumption of certain drugs, maternal stress, and direct injection. This hypothesis is connected to the well-measured effect of fraternal birth order on sexual orientation.

Daryl Bem, a social psychologist at Cornell University, has theorized that the influence of biological factors on sexual orientation may be mediated by experiences in childhood. A child's temperament predisposes the child to prefer certain activities over others. Because of their temperament, which is influenced by biological variables such as genetic factors, some children will be attracted to activities that are commonly enjoyed by other children of the same gender. Others will prefer activities that are typical of another gender. This will make a gender-conforming child feel different from opposite-gender children, while gender-nonconforming children will feel different from children of their own gender. According to Bem, this feeling of difference will evoke psychological arousal when the child is near members of the gender which it considers as being 'different'. Bem theorizes that this psychological arousal will later be transformed into sexual arousal: children will become sexually attracted to the gender which they see as different ("exotic"). This proposal is known as the "exotic becomes erotic" theory.[66]

Bem sought support from published literature but did not present new data testing his theory.[67] Research cited by him as evidence of the "exotic becomes erotic" theory includes the study Sexual Preference by Bell et al. (1981)[67] and studies showing the frequent finding that a majority of gay men and lesbians report being gender-nonconforming during their childhood years. A meta-analysis of 48 studies showed childhood gender nonconformity to be the strongest predictor of a homosexual orientation for both men and women.[68] In six "prospective" studiesthat is, longitudinal studies that began with gender-nonconforming boys at about age 7 and followed them up into adolescence and adulthood 63% of the gender nonconforming boys had a homosexual or bisexual orientation as adults.[69]

Sexual practices that significantly reduce the frequency of heterosexual intercourse also significantly decrease the chances of successful reproduction, and for this reason, they would appear to be maladaptive in an evolutionary context following a simple Darwinian model (competition amongst individuals) of natural selectionon the assumption that homosexuality would reduce this frequency. Several theories have been advanced to explain this contradiction, and new experimental evidence has demonstrated their feasibility.[70]

Some scholars[70] have suggested that homosexuality is indirectly adaptive, by conferring a reproductive advantage in a non-obvious way on heterosexual siblings or their children. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia when two copies are present, also confers resistance to malaria with a lesser form of anemia when one copy is present (this is called heterozygous advantage).[71]

Scholars have also pointed out that Darwin himself described kin selection in The Origin of Species, so under a Darwinian model of evolution, not only individuals, but family groups (bloodlines) can compete for selection.

Brendan Zietsch of the Queensland Institute of Medical Research proposes the alternative theory that men exhibiting female traits become more attractive to females and are thus more likely to mate, provided the genes involved do not drive them to complete rejection of heterosexuality.[72]

In a 2008 study, its authors stated that "There is considerable evidence that human sexual orientation is genetically influenced, so it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency." They hypothesized that "while genes predisposing to homosexuality reduce homosexuals' reproductive success, they may confer some advantage in heterosexuals who carry them". Their results suggested that "genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could help explain the evolution and maintenance of homosexuality in the population".[73]

However, in the same study, the authors noted that "nongenetic alternative explanations cannot be ruled out" as a reason for the heterosexual in the homosexual-heterosexual twin pair having more partners, specifically citing "social pressure on the other twin to act in a more heterosexual way" (and thus seek out a greater number of sexual partners) as an example of one alternative explanation. Also, the authors of the study acknowledge that a large number of sexual partners may not lead to greater reproductive success, specifically noting there is an "absence of evidence relating the number of sexual partners and actual reproductive success, either in the present or in our evolutionary past".

The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men.[46][47] As originally pointed out by Hamer,[74] even a modest increase in reproductive capacity in females carrying a "gay gene" could easily account for its maintenance at high levels in the population.[47]

The "gay uncle hypothesis" posits that people who themselves do not have children may nonetheless increase the prevalence of their family's genes in future generations by providing resources (e.g., food, supervision, defense, shelter) to the offspring of their closest relatives.

This hypothesis is an extension of the theory of kin selection, which was originally developed to explain apparent altruistic acts which seemed to be maladaptive. The initial concept was suggested by J. B. S. Haldane in 1932 and later elaborated by many others including John Maynard Smith, W. D. Hamilton and Mary Jane West-Eberhard.[75] This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.

Vasey and VanderLaan (2010) tested the theory on the Pacific island of Samoa, where they studied women, straight men, and the fa'afafine, men who prefer other men as sexual partners and are accepted within the culture as a distinct third gender category. Vasey and VanderLaan found that the fa'afafine said they were significantly more willing to help kin, yet much less interested in helping children who aren't family, providing the first evidence to support the kin selection hypothesis.[76][77]

The hypothesis is consistent with other studies on homosexuality, which show that it is more prevalent amongst both siblings and twins.[76][77][78][bettersourceneeded] Since both twins and non-twin siblings share genes and therefore have a higher factor of genetic redundancy, there is less genetic familial risk if the strategy is expressed. It is speculated that environmental and hormonal stress factors (linked to resource feedbacks) may act as triggers.

Since the hypothesis solves the problem of why homosexuality has not been selected out over thousands of years, despite it being antithetical to reproduction, many scientists consider it the best explanatory model for non-heterosexual behaviour such as homosexuality and bisexuality. The natural bell curve variation that occurs in biology and sociology everywhere, explains the variable spectrum of expression.

Vasal and VanderLaan (2011) provides evidence that if an adaptively designed avuncular male androphilic phenotype exists and its development is contingent on a particular social environment, then a collectivistic cultural context is insufficient, in and of itself, for the expression of such a phenotype.[79]

Some studies have found correlations between physiology of people and their sexuality; these studies provide evidence which suggests that:

Whether genetic or other physiological determinants form the basis of sexual orientation is a highly politicized issue. The Advocate, a U.S. gay and lesbian newsmagazine, reported in 1996 that 61% of its readers believed that "it would mostly help gay and lesbian rights if homosexuality were found to be biologically determined".[106] A cross-national study in the United States, the Philippines, and Sweden found that those who believed that "homosexuals are born that way" held significantly more positive attitudes toward homosexuality than those who believed that "homosexuals choose to be that way" or "learn to be that way".[107][108]

Equal protection analysis in U.S. law determines when government requirements create a suspect classification" of groups and therefore eligible for heightened scrutiny based on several factors, one of which is immutability.

Evidence that sexual orientation is biologically determined (and therefore perhaps immutable in the legal sense) would strengthen the legal case for heightened scrutiny of laws discriminating on that basis.[109][110][111]

The perceived causes of sexual orientation have a significant bearing on the status of sexual minorities in the eyes of social conservatives. The Family Research Council, a conservative Christian think tank in Washington, D.C., argues in the book Getting It Straight that finding people are born gay "would advance the idea that sexual orientation is an innate characteristic, like race; that homosexuals, like African-Americans, should be legally protected against 'discrimination;' and that disapproval of homosexuality should be as socially stigmatized as racism. However, it is not true." On the other hand, some social conservatives such as Reverend Robert Schenck have argued that people can accept any scientific evidence while still morally opposing homosexuality.[112] National Organization for Marriage board member and fiction writer Orson Scott Card has supported biological research on homosexuality, writing that "our scientific efforts in regard to homosexuality should be to identify genetic and uterine causes... so that the incidence of this dysfunction can be minimized.... [However, this should not be seen] as an attack on homosexuals, a desire to 'commit genocide' against the homosexual community.... There is no 'cure' for homosexuality because it is not a disease. There are, however, different ways of living with homosexual desires."[113]

Some advocates for the rights of sexual minorities resist linking that cause with the concept that sexuality is biologically determined or fixed at birth. They argue that sexual orientation can shift over the course of a person's life.[114] At the same time, others resist any attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm.[112] Chandler Burr has stated that "[s]ome, recalling earlier psychiatric "treatments" for homosexuality, discern in the biological quest the seeds of genocide. They conjure up the specter of the surgical or chemical "rewiring" of gay people, or of abortions of fetal homosexuals who have been hunted down in the womb."[115] LeVay has said in response to letters from gays and lesbians making such criticisms that the research "has contributed to the status of gay people in society".[112]

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Biology and sexual orientation - Wikipedia

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The Japanese governments health ministry has given the go-ahead for a trial of human induced pluripotent stem cells to treat spinal cord injury, Reutersreports today (February 18).Researchers at Keio University plan to recruit four adults who have sustained recent nerve damage in sports or traffic accidents.

Its been 20 years since I started researching cell treatment. Finally we can start a clinical trial, Hideyuki Okano of Keio University School of Medicine told a press conference earlier today, The Japan Timesreports. We want to do our best to establish safety and provide the treatment to patients.

The teams intervention involves removing differentiated cells from patients and reprogramming them via human induced pluripotent stem cells (iPSCs) into neural cells. Clinicians will then inject about 2 million of these cells into each patients site of injury. The approach has been successfully tested in a monkey, which recovered the ability to walk after paralysis, according to the Times.

Its not the first time Japan has approved the use of iPSCs in clinical trials. Last year, researchers at Kyoto University launched a trial using the cells to treat Parkinsons disease. And in 2014, a team at the RIKEN Center for Developmental Biology led the first transplant of retina cells grown from iPSCs to treat a patients eye disease.

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Japan Approves iPS Cell Therapy Trial for Spinal Cord ...

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Stem Cell Therapy has been around for quite some time, but due to high cost it was primarily used for recovery in athletes and the financial elite. However, with the progression of science and knowledge, stem cell therapy has become much more widely used and financially attainable.

Tampa Rejuvenation is the first in Tampa Bay to utilize the benefits of stem cell therapy for the purpose of anti-aging and sexual performance. We realize as our patients age, their bodies no longer have the regenerative properties to attain the desired results from using their growth factors alone as with our PRP, or Plasma Rich Platelet, therapy. Although many patients will still yield improvement with the PRP alone, the magnitude of cytokines and growth factors in your blood as you age will deplete with age. By implementing stem cell therapy, the number of growth factors are exponential allowing our bodies to regenerate on a magnitude that is otherwise unattainable with some results lasting for 3-5 years.

Stem Cell Therapy can be used to restore vitality to the skin, encourage the growth of hair, and even restore sexual performance and pleasure.

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Stem Cell Therapy for Anti-Aging and Sexual Performance ...

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INTRODUCTION

Pregnancy is a unique clinical scenario in which several endocrine disorders may be more frequent and/or have specific considerations for diagnosis and treatment. In this review, anterior pituitary insufficiency, adrenal, parathyroid, and thyroid disorders of pregnancy are discussed.

Anterior pituitary insufficiency is an uncommon disease. The etiology includes destruction of the anterior pituitary gland by tumors, infarction (postpartum necrosis or Sheehan's syndrome), idiopathic disease (Simmonds' disease), surgery, and radiotherapy to the pituitary gland. There have also been reports of pituitary necrosis in patients with elevated intracerebral pressure.1 Disease of the hypothalamus affecting the secretion of releasing hormones may produce a similar clinical picture; some cases of Sheehan's syndrome and idiopathic hypopituitarism are due to hypothalamic diseases.2 Finally, congenital hypopituitarism is a rare diagnosis among newborn infants.3

Sheehans syndrome

The most common cause of panhypopituitarism in women of childbearing age is postpartum necrosis, or Sheehan's syndrome.4 The pathogenesis is not clear, although Sheehan in his original description did associate it with severe postpartum hemorrhage.5 Although the classic clinical etiology of Sheehan's syndrome in about 90% of patients is severe bleeding of the anterior pituitary during delivery or immediately postpartum, no catastrophic event can be detected in more than 10% of patients.

Lack of lactation after delivery, amenorrhea, loss of pubic and axillary hair or failure of pubic hair to grow back, anorexia and nausea, lethargy and weakness, and weight loss are typical presenting signs and symptoms. On physical examination, the findings depend on the severity and duration of the disease. Commonly, the skin has a waxy character with fine wrinkles about the eyes and mouth. There is some periorbital edema, and a decrease in pigmentation is often seen. Axillary and pubic hair becomes increasingly sparse. Atrophy of the breast tissue may be present. Even in those patients losing weight, cachexia is not a feature of the disease. Hypotension may be present, and normocytic anemia is common. However, this full constellation of symptoms does not occur in every patient, and it is not unusual for the full-blown picture to take 1020 years to develop. Occasionally, the diagnosis is made when the patient develops acute adrenal insufficiency secondary to a stressful situation (e.g. infection, trauma, surgery).

It was recognized by Sheehan that not all patients with pituitary apoplexy develop panhypopituitarism, and partial pituitary insufficiency is not uncommon. In one retrospective case series of 44 patients in France, only 88% had hypopituitarism, with adrenocorticotropic hormone (ACTH) deficiency most common (70%).6 A few patients with partial hypopituitarism may present with the classic syndrome of acute panhypopituitarism with deficiency of all pituitary hormones. However, after treatment with corticosteroids alone, there is a spontaneous normalization in the menstrual cycle, with a return of thyroid test results to normal limits.

Successful pregnancies following a diagnosis of Sheehan's syndrome have been reported.7, 8, 9 In a few patients, the diagnosis of partial hypopituitarism may occur upon the presentation of a pregnancy. Although several patients conceive after treatment with gonadotropin, others conceive spontaneously, an indication of partial pituitary failure. Placental function is not altered in patients with pituitary insufficiency.

Pituitary adenoma

During normal pregnancy, the pituitary enlarges by approximately one-third of its size.10 Pituitary insufficiency in women of childbearing age may result in the setting of a pituitary tumor, usually in association with increased production of prolactin. The most common symptom is secondary amenorrhea with galactorrhea, although cases of primary amenorrhea have been reported. When there is local expansion of the tumor, patients may have neurologic symptoms, such as headache or bilateral temporal hemianopia. In such cases, other pituitary hormones may become affected with growth hormone, ACTH, and thyrotropin-stimulating hormone (TSH) deficiencies.

The diagnosis is confirmed by the use of appropriate tests to investigate each of the pituitary hormones. Baseline or random determination of serum pituitary hormone concentrations is of no value in the diagnosis of the disease; dynamic tests to evaluate pituitary reserve must be used. The most practical tests are presented in Table 1. However, their use in pregnancy is limited because of the blunted response of many of these tests.

Table 1. Tests of anterior pituitary hormone reserve

Hormone

Test

Normal Response

Response in Pregnancy

GH

L-Dopa, 500 mg, GH levels at 0, 1, 2 hour

by 10 ng/dl

Blunted

Insulin hypoglycemia 0.1 U regular IV/kg, then draw GH at 0, 20, 60, 90 min

by 10 ng/dl

Blunted

ACTH

Insulin hypoglycemia (see above), then draw cortisol at 0, 20, 60, 90 min

by 10 g/dl

Blunted

Metyrapone 750 mg every 4 hour 6

Urinary 17-KGS

Blunted

TSH

Free thyroxine index

Normal

Serum TSH

Normal

Prolactin

Can no longer be tested, given the inavailability of TRH

LH-FSH

Assess by regularity/presence of menses

When anterior pituitary insufficiency develops in pregnancy, the clinical manifestations may be local signs, such as headaches and visual disturbances, which are the consequence of an acute enlargement of, or bleeding into, the pituitary gland.11 The initial manifestations also could be related to endocrine deficiency, mainly hypoglycemia, nausea, vomiting, and hypotension secondary to ACTH deficiency.

Isolated ACTH deficiency is rare and has been infrequently described.12, 13 Acute enlargement of the pituitary gland is characterized by severe, deep, midline headaches (lasting for 23 days) and visual field disturbances. Severe hypoglycemia with convulsions and coma, unresponsive to large doses of glucose, but rapidly reversible after the administration of hydrocortisone, can be seen.

Partial or total hypopituitarism developing in patients with diabetes mellitus has been reported.14 In a review of 31 cases (19 women), the episode was associated with pregnancy in 11 (during the postpartum period in seven and during the antepartum period in four, with three maternal deaths).15 The mean age of the patients in this case series was 27 years, and the mean duration of their diabetes mellitus was 6 years, which makes vascular complication an unlikely cause of pituitary insufficiency. Furthermore, no specific vascular changes were found in the examined pituitary glands. Characteristically, the patients developed severe headaches that lasted for a few days with or without visual field disturbances, and a decrease in insulin requirement was observed. There was a high proportion of women with fetal loss. Although the mechanism supporting the increased risk of hypopituitarism among individuals with diabetes mellitus remains unclear, an association between pituitary antibodies and type 1 diabetes mellitus has been described.16

Lymphocytic hypophysitis

Lymphocytic hypophysitis can be another cause of pituitary dysfunction,17 and in pregnant women, usually presents close to delivery or in the immediate postpartum period.18 Sheehan described lymphocytic infiltration of the pituitary gland in some women with postpartum pituitary insufficiency,19 and it is possible that many of the cases mentioned above were due to lymphocytic hypophysitis.

The clinical presentation may be characterized by headaches and visual disturbances related to pressure from the expanding lesion mimicking a pituitary tumor;20, 21 spontaneous regression of the lesion was seen in several cases.22 diabetes insipidus and galactorrhea. Report of a case and review of the literature) The differential diagnosis between pituitary tumor and hypophysitis can be made only by histologic examination.18 Conversely, the patient may present with signs and symptoms of hypopituitarism, such as protracted hypoglycemia responding to glucocorticoid therapy and hypotension. It can also present in the postpartum period as pituitary insufficiency, similar to Sheehan's syndrome without the history of profound bleeding.22, 23, 24, 25

Involvement of other endocrine glands has been recognized, consistent with the concept of an autoimmune disease,26 in addition to antibodies against pituitary cells.27 It is possible that these cases are typical of the autoimmune polyendocrine deficiency syndrome that may be exacerbated during pregnancy or in the immediate postpartum period.

Treatment

Patients with partial or total hypopituitarism who become pregnant spontaneously or after treatment with gonadotropins may carry a normal pregnancy with no increase in the dose of corticosteroid replacement therapy. The usual amount of hydrocortisone in patients with pituitary insufficiency is 2030 mg/day (two-thirds of the total amount in the morning and one-third in the evening). In some instances, the amount of hydrocortisone can be decreased by one-third of the total dose because the effect of hydrocortisone is potentiated during pregnancy by estrogen.28 However, this potentiation does not occur when synthetic corticosteroids (i.e. prednisone, dexamethasone) are used. The equivalent amounts of prednisone and dexamethasone, respectively, are 5.07.5 mg daily and 0.50.75 mg daily. Because these patients have ACTH deficiency, aldosterone secretion is normal and there is no need for mineralocorticoid replacement therapy. If thyroid deficiency is present, the amount of levothyroxine needed for replacement is usually 0.10.2 g daily.

Successful pregnancy in cases of isolated growth hormone deficiency has been reported.29, 30 In these patients, lactation was unimpaired and placental function studies and intrauterine growth were normal.

The most common pituitary tumor diagnosed in women of childbearing age is a prolactinoma.31 It can be accompanied by amenorrhea, oligohypomenorrhea, and anovulation, and with or without galactorrhea. Hyperprolactinemia decreases gonadotropin-releasing hormone (GnRH) secretion, accounting for the infertility observed in these patients. Pituitary tumors are divided, according to size, into microadenomas (less than 10 mm in diameter) and macroadenomas (greater than 10 mm in diameter); the latter are further classified according to suprasellar extension and invasion of adjacent structures. Serum prolactin concentrations correlate fairly well with the size of the tumor. Hyperprolactinemia in the absence of a pituitary adenoma (idiopathic hyperprolactinemia) is a common finding.

Complications

Serum prolactin levels in women with prepregnancy hyperprolactinemia, with a few exceptions, remained unchanged during pregnancy. It was shown that prolactin levels did not change significantly in most women with baseline prolactin levels of over 60 pg/dL.32 However, in those patients with prolactin levels of less than 60 pg/dL, the mean level doubled at the end of pregnancy and returned to pretreatment levels at the end of lactation. Therefore, serum prolactin determination during pregnancy is not a predictor of tumor growth and is of no value in monitoring tumor growth.

The incidence of complications during pregnancy in patients with pituitary tumors varies according to tumor size. Due to the stimulatory effect of estrogen on lactotrophs, the size of the tumor increases in 2.7% of microprolactinomas and 22.9% of macroprolactinomas during pregnancy.31 In one study of 56 pregnant women with microprolactinomas, one developed headaches and five showed mild tumor growth.33 In studies of pregnant women with macroprolactinomas, the proportion of women developing neurologic symptoms and visual disturbances is significantly decreased upon treatment.31

Complications can occur at any stage of pregnancy. In patients with microadenomas, visual field examinations are indicated only if there are signs and symptoms of tumor enlargement, in which case an MRI is also indicated. If there is any objective evidence of tumor enlargement, bromocriptine is resumed and continued throughout pregnancy at up to 20 mg/day. If after a few days there is no improvement, dexamethasone 4 mg every 6 hours can be added. Surgery is indicated in those complicated cases not responding to the above therapies, but the recurrence rate is high among those with invasive prolactinomas even after surgery.34

Breastfeeding is not contraindicated in mothers with a diagnosis of prolactinoma. There is no difference in the remission rates of women with prolactinomas managed with dopamine-receptor agonists who breastfeed following delivery versus those who do not.35 It is advisable in patients with microadenomas to measure prolactin levels a few months after delivery and to reinstate bromocriptine therapy in the presence of persistent hyperprolactinemia. A pituitary MRI should be repeated in cases of macroprolactinoma soon after delivery because of the potential for tumor size increase.

Treatment

Once the diagnosis of prolactinoma is made, several types of therapy are available. The choice of therapy depends on tumor size, radiologic classification, local symptoms, and the patient's age and desire for pregnancy or current pregnancy.36

Medical therapy with dopamine-receptor agonists has been very effective in producing ovulation among hyperprolactinemic women37 and restores ovulation in approximately 90% of cases.31 Bromocriptine has historically been the preferred option, and no significant adverse effects have been observed in over 6000 pregnancies managed with bromocriptine.38 Most patients respond to doses of 2.55 mg/day, although occasionally a dose of 7.5 mg/day or more is needed. Bromocriptine is effective not only in normalizing prolactin levels but also in reducing the size of the tumor.31 It is advisable to use mechanical contraception during the first few months of bromocriptine therapy until the rhythm of the menstrual period is established. In those patients who have side effects such as nausea and vomiting, the oral bromocriptine tablet can be administered vaginally.39

Cabergoline is another dopamine-receptor agonist which can be considered.40 Although only 800 pregnancies have been reported with its use, there similarly does not appear to be any increased risks of preterm delivery or congenital malformations associated with this medication.38 In one 10-year observational study of 143 women, carbergoline therapy during pregnancy resulted in the ability of nearly 98% of the women to breastfeed following delivery.41 Once conception takes place, the dopamine-receptor agonist should be discontinued and the patient followed closely. For women in whom the macroprolactinoma is likely to increase, or in whom pressure symptoms occur, therapy during pregnancy should be continued.42

Radiation therapy as the initial and only therapy is seldom indicated, as medical therapy is usually very effective. The duration required for radiation therapy to normalize serum prolactin levels is lengthy and may produce hypopituitarism as a last sequela. Radiation therapy is indicated in those with prolactinomas refractory to conventional therapy.43

Surgical treatment, mainly transsphenoidal adenectomy, has been effective in restoring ovulation in patients with small tumors.32 The cure rate (i.e. sustained normalization of serum prolactin concentrations) is about approximately 70% at both 5 and 10 years of follow up; the associated proportion of successful pregnancy was similar.44 The best results are obtained in patients with microadenomas with low initial serum prolactin levels and lack of abnormal postoperative residual tissue.45

A recommended treatment approach in patients who wish to conceive is summarized in Table 2. It is suggested that treatment with bromocriptine be continued for at least 12 months before conception because it seems to reduce the risk of tumor enlargement during pregnancy.46

Table 2. Management of women with pre-conception hyperprolactinemia

Visual field monthly

*Therapy for 1 year before conception

Acromegaly is a chronic disease caused by hypersecretion of growth hormone by the adenohypophysis of the pituitary gland. It is almost always associated with a benign pituitary tumor and is characterized by slow and progressive enlargement of the acral parts. Facial changes are typical, but they usually develop so gradually that neither the family nor the patient recognizes the changes. As in other endocrine disorders, comparison of the patient's photographs taken over many years may be the only clue to the progression of the disease. Symptoms may be due to local expansion of the tumor (i.e. headaches and visual field disturbances), or they may be due to the somatic effects of chronic excess growth hormone, such as hyperhidrosis, weight gain, arthralgias, and acroparesthesia (carpal tunnel syndrome). Most women with acromegaly have been reported to suffer from oligohypomenorrhea or amenorrhea. In addition to the bony deformities, organomegaly (particularly enlargement of the heart, thyroid, and liver) is not uncommon on physical examination. The skin appears coarse and leathery. Galactorrhea with hyperprolactinemia is a common finding.

Diagnosis

The diagnosis is confirmed by an elevation in plasma insulin-like growth factor 1 (IGF-1) levels and a lack of suppression of growth hormone following the administration of a glucose load.47 However, IGF-1 levels may not be reliable during pregnancy, as they can be physiologically increased48 or decreased during pregnancy.49

Thus, suspected cases of acromegaly among pregnant women should be confirmed with a growth hormone suppression test, which requires determination of plasma growth hormone levels before and 1 and 2 hours after the administration of a solution of 100 g glucose orally. A normal response is characterized by growth hormone levels lower than 1 g/L after glucose administration. Patients with acromegaly typically have elevated baseline IGF-1 levels and respond to the glucose load with no growth hormone suppression of growth hormone concentration or even occasionally with a paradoxical increase.

In patients with acromegaly, there are increased risks of several associated cormorbidities, including hypertension, diabetes mellitus, cardiovascular disease, osteoarthritis, and sleep apnea, which should be evaluated for upon the confirmed diagnosis of acromegaly.47

Treatment

Treatment is mandatory in patients with the disease because the long-term prognosis is poor; untreated individuals have an almost 3-fold increased mortality rate.48 Conventional pituitary irradiation, transsphenoidal hypophysectomy,50 and drug therapy with octreotide (or other somatostatin receptor analogues) or the growth receptor antagonist, pegvisomant51 are used most often and can improve disease survival.52

Acromegaly during pregnancy

There are limited data of successful pregnancies in women with acromegaly. In 1954, Abelove and colleagues reported two normal pregnancies in an acromegalic woman and reviewed 33 reported cases from the world literature.53 Since that time, several other cases have been published, including a recent report of ten pregnancies among eight acromegalic women in Brazil, in which plasma IGF-1 levels were not significantly changed during gestation.54 In most instances, the infants have been reported as being normal. However, in a case described by Fisch et al.,55 the infant was born with acromegalic features. In this infant, growth was above average during the neonatal period, but a normal growth pattern subsequently returned, although no serum laboratory measurements were obtained. The lack of acromegalic features in most cases is in accordance with the report by King and colleagues demonstrating no placental transfer of growth hormone from mother to fetus.56

Historically, bromocriptine has been used as a successful treatment to induce pregnancy in patients with acromegaly.57, 58 In each of these cases, pregnancy occurred in spite of persistent elevated serum growth hormone levels.

The current guidelines for management of acromegalic women during pregnancy have been summarized in the 2014 Endocrine Society guidelines for acromegaly.47 In general, discontinuation of long-acting medical therapy (somatostatin receptor analogues or pegvisomant) is recommended approximately 2 months prior to attempting to conceive; therapy can be replaced with short-acting octreotide instead during the pre-conception period. During gestation, medical therapy should only be administered only for tumor and headache control, and plasma growth hormone and IGF-1 levels should not be monitored.

Diabetes insipidus is an uncommon disease characterized by polyuria and polydipsia due to a deficiency of antidiuretic hormone (central or neurogenic diabetes insipidus) or the peripheral resistance to the antidiuretic hormone at the renal tubules (nephrogenic diabetes insipidus). Central diabetes insipidus may be a result of a lesion at the level of the hypothalamus or pituitary gland. It may arise following hypophysectomy, invasion of the neurohypophysis by tumors, malignant metastasis (i.e. breast cancer), trauma, granulomas, or infection. In 50% of cases, however, it is considered idiopathic, with some causes probably on an autoimmune basis. Nephrogenic diabetes insipidus is a hereditary disorder affecting males; therefore, symptomatic women carriers are extremely rare. Several cases of transient nephrogenic diabetes insipidus during pregnancy and/or postpartum have been reported. A third type of diabetes insipidus, called psychogenic, which is rarely reported in pregnancy,59 is differentiated from the other two in most cases by the results of the water deprivation test.

Diagnosis

Link:
Endocrine Diseases in Pregnancy | GLOWM

Recommendation and review posted by Bethany Smith

Please don't bother my friend!

I reckon that you are quiet young, so the thought of going bald scares you.

I had that too when I was in my early 20s, because baldness is a common thing too in my family.

I'm almost 40 now and YES I'm almost bald too LOL! But in reality going bald is a very slow process. Nobody (some rare cases excepted) is completely bald in their early 20s.

You see this is what I'm trying to say: -When you are 20 you don't wanna look like a bald old man (and that's not gonna happen I promise)

BUT: -When you are 40+ you don't wanna look like a 20 year old! (Although the media wants to make us believe that "young" is the way to be)

So when you reach the age of 40 you won't bother about a little or more baldness because all of of your male generation members have the same "problem" (which isn't a problem)

Since in prehistory man was hairy like an ape and now we are allmost hairless I think the ability of loosing hair is a step ahead in evolution! And I feel that being a little or more bald is very masculine!

View post:
male pattern baldness and genetics? | Yahoo Answers

Recommendation and review posted by Bethany Smith

Photo:via Imgur

Diabetes mellitus, commonly referred to as diabetes, is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period. Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger. If left untreated, diabetes can cause many complications. Acute complications include diabetic ketoacidosis and nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular disease, stroke, chronic kidney failure, foot ulcers, and damage to the eyes. Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced. There are three main types of ...more on Wikipedia

Symptoms: Polyphagia, Acanthosis nigricans, Hyperglycemia, Weight gain, Fatigue, + more

Treatments: Smoking cessation, Insulin lispro, Anti-diabetic medication, Physical examination, Chromium(III) picolinate, + more

Risk Factors: Tobacco smoking, Personal History of Gestational Diabetes, Indigenous peoples of the Americas, Asian American, Hispanic, + more

Parent Disease: Endocrine diseases, Nutrition disorder

Read more here:
List of Endocrine Disorders | Thyroid & Endocrine System ...

Recommendation and review posted by Bethany Smith

Are there enough stem cells in your knees to heal the damage of osteoarthritis? If yes, why arent those stem cells fixing your knees now? Is it a lack of numbers?

Marc Darrow MD, JD. Thank you for reading my article. You can ask me your questions about bone marrow derived stem cells using the contact form below.

In 2011, doctors at the University of Aberdeen published research in the journal Arthritis and rheumatism that provided the first evidence that resident stem cells in the knee joint synovium underwent proliferation (multiplied) and chondrogenic differentiation (made themselves into cartilage cells) following injury.(1)This paper, presenting the idea that stem cells in an injured knee increased in numbers in preparation of healing has been cited by more than 40 medical studies.

If the stem cells in your knee synovial lining are abundant and have the ability to rebuild cartilage after injury, why isnt your knee fixing itself?

One of those 40 studies was performed by researchers at theUniversity of Calgary in 2012. Among their questions, if the stem cells in the knee synovial lining are abundant and have the ability to rebuild cartilage after injury, why isnt the knee fixing itself? Here is what they published:

Since osteoarthritis leads to a progressive loss of cartilage and synovial progenitors (rebuilding) cells have the potential to contribute to articular cartilage repair, the inability of osteoarthritis synovial fluid Mesenchymal progenitor cells (stem cell growth factors) to spontaneously differentiate into chondrocytes suggests that cell-to-cell aggregation and/or communication may be impaired in osteoarthritis and somehow dampen the normal mechanism of chondrocyte replenishment from the synovium or synovial fluid. Should the cells of the synovium or synovial fluid be a reservoir of stem cells for normal articular cartilage maintenance and repair, these endogenous sources of chondro-biased cells would be a fundamental and new strategy for treating osteoarthritis and cartilage injury if this loss of aggregation & differentiation phenotype can be overcome.(2)

This research was supported in a study from December 2017 In Nature reviews. The paper suggested that recognizing that joint-resident stem cells are comparatively abundant in the joint and occupy multiple niches (from the center of the joint to the out edges) will enable the optimization of single-stage therapeutic interventions for osteoarthritis.(3) The idea is to get these native stem cells to repair.

Now we know that there are many stem cells in the knee, when there is an injury there are more stem cells. If we can figure out how to get these stem cells turned on to the healing mode, the knee could heal itself of early stage osteoarthritis. So the problem is not the number of stem cells, BUT, communication.

This failure to communicate was also seen in other research. In 2016, another heavily cited paper, this time fromTehran University for Medical Sciences, noted that despite their larger numbers,the native stem cells act chaotically and are unable to regroup themselves into a healing mechanism and repair the bone, cartilage and other tissue. Introducing bone marrow stem cells into this environmentgets the native stem cells in line and redirects them to perform healing functions. The joint environmentis changed from chaotic to healing because of communication.(4) It should be pointed out that 62 medical studies cited the research in this papers findings).

A recentpaper from a research team inAustralia confirms how this change of joint environment works. It starts with cell signalling a new communication network is built.

University of Iowa research published in theJournal of orthopaedic research

Serious meniscus injuries seldom heal and increase the risk for knee osteoarthritis; thus, there is a need to develop new reparative therapies. In that regard, stimulating tissue regeneration by autologous (from you, not donated) stem/progenitor cells has emerged as a promising new strategy.

(The research team) showed previously that migratory chondrogenic progenitor cells (mobile cartilage growth factors) were recruited to injured cartilage, where they showed a capability in situ (on the spot) tissue repair. Here, we tested the hypothesis that the meniscus contains a similar population of regenerative cells.

Explant studies revealed that migrating cells were mainly confined to the red zone (where the blood is and its growth factors) in normal menisci: However, these cells were capable of repopulating defects made in the white zone (the desert area where no blood flows. Migrating cell numbers increased dramatically in damaged meniscus. Relative to non-migrating meniscus cells, migrating cells were more clonogenic, overexpressed progenitor cell markers, and included a larger side population. (They were ready to heal) Gene expression profiling showed that the migrating population was more similar tochondrogenic progenitor cells (mobile cartilage growth factors) than other meniscus cells. Finally, migrating cells equaledchondrogenic progenitor cells in chondrogenic potential, indicating a capacity for repair of the cartilaginous white zone of the meniscus. These findings demonstrate that, much as in articular cartilage, injuries to the meniscus mobilize an intrinsic progenitor cell population with strong reparative potential.(6)

The intrinsic progenitor cell population with strong repair potential are in your knee waiting to be mobilized.

So what are we to make of this research?There are a lot of stem cells in a knee waiting to repair. The problem is they are confused and not getting the correct instructions. Stem cell therapy can fix the communication problem and begin the repair process anew.

A leading provider of bone marrow derived stem cell therapy, Platelet Rich Plasma and Prolotherapy11645 WILSHIRE BOULEVARD SUITE 120, LOS ANGELES, CA 90025

PHONE: (800) 300-9300

1 Kurth TB, Dellaccio F, Crouch V, Augello A, Sharpe PT, De Bari C. Functional mesenchymal stem cell niches in adult mouse knee joint synovium in vivo. Arthritis Rheum. 2011 May;63(5):1289-300. doi: 10.1002/art.30234.

2 Krawetz RJ, Wu YE, Martin L, Rattner JB, Matyas JR, Hart DA. Synovial Fluid Progenitors Expressing CD90+ from Normal but Not Osteoarthritic Joints Undergo Chondrogenic Differentiation without Micro-Mass Culture. Kerkis I, ed.PLoS ONE. 2012;7(8):e43616. doi:10.1371/journal.pone.0043616.

3 McGonagle D, Baboolal TG, Jones E. Native joint-resident mesenchymal stem cells for cartilage repair in osteoarthritis. Nature Reviews Rheumatology. 2017 Dec;13(12):719.

4Davatchi F, et al. Mesenchymal stem cell therapy for knee osteoarthritis: 5 years follow-up of three patients. Int J Rheum Dis. 2016 Mar;19(3):219-25.

5. Freitag J, Bates D, Boyd R, Shah K, Barnard A, Huguenin L, Tenen A.Mesenchymal stem cell therapy in the treatment of osteoarthritis: reparative pathways, safety and efficacy a review.BMC Musculoskelet Disord. 2016 May 26;17(1):230. doi: 10.1186/s12891-016-1085-9. Review.

6 Seol D, Zhou C, et al. Characteristics of meniscus progenitor cells migrated from injured meniscus. J Orthop Res. 2016 Nov 3. doi: 10.1002/jor.23472.

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Stem cell numbers in a damaged knee - Dr. Marc Darrow is a ...

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Step 1: Get ready to donate

Once you join the Be The Match Registry, you will be included in patient searches every day. If you match a patient, you will be contacted to confirm that you are willing to donate. If you agree to move forward, you will be asked to update your health information and participate in additional testing to see if you are the best match for the patient. If you are the best match, you will:

There are two methods of donation: PBSC and bone marrow. The patients doctor will choose which one is best for the patient.

The time it takes for a donor to recover varies. It depends on the person and type of donation. Most donors are able to return to work, school and other activities within 1 to 7 days after donation. Be The Match considers donor safety a top priority and will follow up with you regularly until you are able to resume normal activity.

Continued here:
Steps of PBSC or bone marrow donation - Be The Match

Recommendation and review posted by Bethany Smith

PUBMED NLM ID: 101586297 | Index Copernicus Value: 84.95 The Journal of Stem Cell Research & Therapy is an open access journal that showcases seminal research in the field of stem cell therapy. As stem-cells are flag-bearers of translational research, the field has an interdisciplinary feel by including oncology, clinical research, medicine and healthcare under the aegis of stem-cell therapy. It also includes scientific research related to the auxiliary areas of Biology by prioritizing scholarly communication milieu and transfers expert knowledge synthesized from the ever burgeoning stem-cell literature. In order to create such impactful content, the Journal of Stem Cell Research & Therapy brings together an expert Editorial Board, which comprises of noted scholars in the field of Cell Biology. Every single article is subjected to rigorous peer review by illustrious scientists. In addition to Research Articles, the Journal also publishes high quality Commentaries, Reviews, and Perspectives aimed at synthesizing the latest developments in the field, and putting forward new theories in order to provoke debates amongst the scholars in the field. The journal thus maintains the highest standards in terms of quality and comprehensive in its approach.The journal aims to provide the authors with an efficient and courteous editorial platform. The authors can be assured of an expeditious publishing process. In this regard, the journal also provides advance online posting of the accepted articles. The Journal of Stem Cell Research & Therapy ensures barrier-free, open access distribution of its content online and thus, helps in improving the citations for authors and attaining a good impact factor.

Scholarly Journal of Stem Cell Research & Therapy is using online manuscript submission, review and tracking systems of Editorial Manager for quality and quick review processing. Review processing is performed by the editorial board members of Journal of Stem Cell Research and Therapy or outside experts; at least two independent reviewers approval followed by editor approval is required for acceptance of any citable manuscript.

It is an undifferentiated cell which is capable of transforming into more cells of same type or multiple other types. They are found in multicellular organisms. They can differentiate into cells of blood, skin, heart, muscles, brain etc. In adult human being, they replenish the dead cells of various organs. Stem cells are being used for treatment of various diseases like diabetes, arthritis, few cancers, bone marrow failure etc.

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They can develop into any cell type or organ in the body. A single totipotent stem cell can give rise to an entire organism. Fertilized egg or a zygote is the best example. Zygote divides and produces more totipotent cells. After 4 days the cells lose totipotency and become pluripotent.

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They can differentiate into any cell type in the human body. Embryonic stem cells are mostly pluripotent stem cells. They have the ability to differentiate into any of three germ layers: endoderm, mesoderm, or ectoderm.

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These are multipotent stem cells normally found in the bone marrow and are derived from mesenchyme. They differentiate into adipocytes, chondrocytes, osteoblasts, myocytes and tendon. MSCs can also be extracted from blood, fallopian tube, fetal liver and lungs.

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They are the multipotent stem cells derived from mesoderm and located in red bone marrow. They are responsible for production of red blood cells, white blood cells and platelets. HSCs give rise to myeloid lineage (which forms erythrocytes, eosinophils, basophils, neutrophils, macrophages, mast cells and platelets) and lymphoid lineage (which forms T-lymphocytes, plasma cells and NK cells).

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They can differentiate into more than one cell type, but only into a limited number of cell types. Hematopoietic stem cells are considered multipotent as they can differentite into red blood cells, platelets, white blood cells but they cannot differentiate into hepatocytes or brain cells.

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Cells with stem cell like abilities have been observed breast cancer, colon cancer, leukemia, melanoma, prostate cancer which can form new cells and lead to tumorigenesis. They cause relapse and metastasis by giving rise to new tumors. Scientists are developing methods to destroy CSCs in place of traditional methods which focus on bulk of cancer cells.

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They are derived from Hematopoietic stem cells. They differentiate into Erythrocyte progenitor cell (forms erythrocytes), Thrombocyte progenitor cell (forms platelets) and Granulocyte-Monocyte progenitor cell (forms monocytes, macrophages, neutrophils, basophils, eosinophils, dendritic cells).

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They are the self-renewing, multipotent stem cells in the nervous system that differentiate into neurons, astrocytes and oligodendrocytes. They repair the nervous system after damage or an injury. They have potential clinical use the management of Parkinsons disease, Huntingtons disease and multiple sclerosis.

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They are derived from embryo in the blastocyst stage. They are pluripotent stem cells. They give rise to all derivatives of the three primary germ layers: endoderm (stomach, colon, liver, pancreas, intestines etc.), mesoderm (muscle, bone, cartilage, connective tissue, lymphatic system, circulatory system, genitourinary system etc.) and ectoderm (brain, spinal cord, epidermis etc.).

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Embryonic stem cells are derived from the fetus are used in treatment of various diseases. As ESCs are pluripotent, they can differentiate into any cell type. Researchers are able to grow ESCs into complex cells types like pancreatic -cells and cardiocytes. Fetal cell therapy is generating lot of controversy from religious groups and ethics committees.

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Research is being done to use stem cells for the treatment of diabetes mellitus. Human embryonic stem cells may be grown in vivo and stimulated to produce pancreatic -cells and later transplanted to the patient. Its success depends on response of the patients immune system and ability of the transplanted cells to proliferate, differentiate and integrate with the target tissue.

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The procedure to replace damaged cells (in cancers, aplastic anemia etc.) with healthy stem cells of the same person or in another compatible person to restore the normal production of cells. It can either be autologous or allogeneic. Bone marrow HSCs are generally used for the transplantation.

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They are the totipotent, undifferentiated cells present in the meristems (shoot and root apices) of a plant. They never undergo aging process and can grow into any cell in the plant throughout its lifetime. They have numerous applications in production of cosmetics, perfumes, pigments, insecticides and antimicrobials.

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Several types of dental stem cells have been isolated from mature and immature teeth, exfoliated deciduous teeth and apical papilla, MSCS from tooth germs and from human periodontal ligament. They are found to be multipotent and can give rise to osteogenic, adipogenic, myogenic and neurogenic cell lineages.

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Adipose tissue is a huge source of mesenchymal stem cells which differentiate into various cell types. They can be easily extracted in large numbers by a simple lipo-aspiration. They have good application potential in regenerative medicine. ASCs are found to have the ability to differentiate into bone cells, cartilage cells, nerve cells, adipocytes etc.

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Preservation of stem cells is critical for both research and clinical application of stem-cell based therapies. Properly preserved stem cells can be later used in the field of regenerative medicine for treating congenital disorders, heart defects etc. Currently there is no universal method for preserving stem cells and the existing methods are expensive.

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Oncology & Cancer Case Reports, Prostate Cancer, Fertilization: In Vitro - IVF-Worldwide, Reproductive Medicine, Genetics & Stem Cell Biology, Journal of Stem Cells and Regenerative Medicine, Stem Cells and Cloning: Advances and Applications, International Journal of Hematology-Oncology and Stem Cell Research, Open Stem Cell Journal, Stem Cell, Stem Cell Research Journal

MSCs can be applied in osteoarthritis treatment through implantation and microfracture as well as intra-articular injections. Single injection studies have showed improvement from pain which decreased overtime. Multiple, regular MSC injections into joints may be necessary.

Related Journals ofStem Cell Therapy for Osteoarthritis

Osteoporosis and Physical Activity, Osteoarthritis, Fertilization: In Vitro - IVF-Worldwide, Reproductive Medicine, Genetics & Stem Cell Biology, Osteoarthritis and Cartilage, Arthritis and Rheumatism, Arthritis Care and Research, Arthritis Research and Therapy, Seminars in Arthritis and Rheumatism

OMICS International through its Open Access Initiative is committed to make genuine and reliable contributions to the scientific community. OMICS International hosts over 700 leading-edge peer reviewed Open Access Journals and organizes over 1000 International Conferences annually all over the world. OMICS International journals have over 10 million readers and the fame and success of the same can be attributed to the strong editorial board which contains over 50000 eminent personalities that ensure a rapid, quality and quick review process. OMICS International signed an agreement with more than 1000 International Societies to make healthcare information Open Access. OMICS International Conferences make the perfect platform for global networking as it brings together renowned speakers and scientists across the globe to a most exciting and memorable scientific event filled with much enlightening interactive sessions, world class exhibitions and poster presentations.

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Read: Hidden Figures and the appeal of math in an age of inequality

One name sprang readily to mind: Jennifer Smith. Huerta-Snchez remembered reading a classic, decades-old paper in which Smith was thanked in the acknowledgments for ably programming and executing all the computations. That seemed odd. Today, programming is recognized as crucial work, and if a scientist did all the programming for a study, she would expect to be listed as an author. It was weird to me that Smith was not an author on that paper, Huerta-Snchez says. [Rori and I] wanted to see if there were more women like her.

The duo recruited five undergraduate students, who looked at every issue of a single journalTheoretical Population Biologypublished between 1970 and 1990. They pored through hard copies of almost 900 papers, pulled out every name in the acknowledgments, worked out whether they did any programming, and deduced their genders where possible. Rochelle Reyes, one of the students, says that she was extremely motivated to do this work, having grown up on stories of under-recognized pioneers like Rosalind Franklin, who was pivotal in deciphering the structure of DNA, and Henrietta Lacks, whose cells revolutionized medical research. I was fortunate to grow up in a diverse environment with a passion for science as well as social justice, Reyes says.

She and her colleagues found that in the 1970s, women accounted for 59 percent of acknowledged programmers, but just 7 percent of actual authors. That decade was a pivotal time for the field of population genetics, when the foundations of much modern research were laid. Based on authorship at the time, it seems that this research was conducted by a relatively small number of independent individual scientists, nearly all of whom were men, the team writes. But that wasnt the case.

Its hard to know what sort of contributions people in the past have made behind the scenes, says Jessica Abbott, a geneticist at Lund University. But this study shows that its possible to get the right kind of data if you think creatively.

Margaret Wu, for example, was thanked in a 1975 paper for help with the numerical work, and in particular for computing table I. She helped to create a statistical tool that scientists like Huerta-Snchez still regularly use to estimate how much genetic diversity there should be in a population of a given size. That tool is called the Watterson estimator, after the 1975 papers one and only authorG. A. Watterson. The paper has since been cited 3,400 times.

Skeptics might argue that the programmers listed in these old papers were just doing menial work that wasnt actually worthy of authorship. Rohlfs says thats unlikely, especially in the cases of Wu, Jennifer Smith, and Barbara McCann, who were repeatedly name-checked in many papers. They were doing work that was good enough that they were being called back again and again, she says. The team even talked with William Hill, Smiths former supervisor at the University of Edinburgh, who described her work as both technical and creative. (He didnt, unfortunately, know where Smith ended up, and the team never managed to track her down.)

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Where do stem cells come from? Learn the basics of master cells to better understand their therapeutic potential.

In this article:

Where do stem cells come from? You have probably heard of thewonders of stem cell therapy. Not only do stem cells make research for future scientific breakthroughs possible, but they also provide the basis for many medical treatments today. So, where exactly are they from, and how are they different from regular cells? The answer depends on the types of stem cells in question.

There are two main types of stem cells adult and embryonic:

Beyond the two broader categories, there are sub-categories. Each has its own characteristics. For researchers, the different types of stem cells serve specific purposes.

Many tissues throughout the adult human body contain stem cells. Scientists previously believed adult stem cells to be inferior to human embryonic stem cells for therapeutic purposes. Theydid not believe adult stem cells to be as versatile as embryonic stem cells (ESCs), because they are not capable of becoming all 200 cell types within the human body.

While this theoryhas notbeen entirely disproved, encouraging evidence suggests that adult stem cells can develop into a variety of new types of cells. They can also affect repair through other mechanisms.

In August 2017, the number of stem cell publications registered in PubMed, a government database, surpassed 300,000. Stem cells are also being explored in over 4,600 cell therapy clinical trials worldwide. Some of the earliest forms of adult stem cell use include bone marrow and umbilical cord blood transplantation.

It should be noted that while the term adult stem cell is used for this type of cell, it is not descriptive of age, because adult stem cells can come from children. The term simply helps to differentiate stem cells derived from living humans as opposed to embryonic stem cells.

Embryonic stem cells are controversial because they are made from embryos that are created but not used by fertility clinics.

Because adult stem cells are somewhat limited in the cell types they can become, scientists developed a way to genetically reprogram cells into what is called an inducedpluripotent stem cell or iPS cell. In creating inducedpluripotent stem cells, researchers hope to blend the usefulness of adult stem cells with the promise of embryonic stem cells.

Both embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are known as pluripotent stem cells.

Pluripotent stem cells are a type of cell that has the capacity to divide indefinitely and create any cell found within the three germ layers of an organism: ectoderm (cells forming the skin and nervous system), endoderm (cells forming pancreas, liver, endocrine gland, and gastrointestinal and respiratory tracts), and mesoderm (cells forming connective tissues, and other related tissues, muscles, bones, most of the circulatory system, and cartilage).

Embryonic stem cells can grow into a much wider range of cell types, but they also carry the risk of immune system rejection in patients. In contrast, adult stem cells are more plentiful, easier to harvest, and less controversial.

Embryonic stem cells come from embryos harvested shortly after fertilization (within 4-5 days). These cells are made when the blastocysts inner cell mass is transferred into a culture medium, allowing them to develop.

At 5-6 days post-fertilization, the cells within the embryo start to specialize. At this time, they no longer are able to become all of the cell types within the human body. They are no longer pluripotent.

Because they are pluripotent, embryonic stem cells can be used to generate healthy cells for disease patients. For example, they can be grown into heart cells known as cardiomyocytes. These cells may have the potential to be injected into an ailing patients heart.

Harvesting stem cells from embryos is controversial, so there are guidelines created by the National Institutes of Health (NIH) that allow the public to understand what practices are not allowed.

Scientists can harvest perinatal stem cells from a variety of tissues, but the most common sources include:

The umbilical cord attaches a mother to her fetus. It is removed after birth and is a valuable source of stem cells. The blood it contains is rich in hematopoietic stem cells (HSC). It also contains smaller quantities of another cell type known as mesenchymal stem cells (MSCs).

The placenta is a large organ that acts as a connector between the mother and the fetus. Both placental blood and tissue are also rich in stem cells.

Finally, there is amniotic fluid surrounding a baby while it is in utero. It can be harvested if a pregnant woman needs a specialized kind of test known as amniocentesis. Both amniotic fluid and tissue contain stem cells, too.

Adult stem cells are usually harvested in one of three ways:

The blood draw, known as peripheral blood stem cell donation, extracts the stem cells directly from a donors bloodstream. The bone marrow stem cells come from deep within a bone often a flat bone such as the hip. Tissue fat is extracted from a fatty area, such as the waist.

Embryonic donations are harvested from fertilized human eggs that are less than five days old. The embryos are not grown within a mothers or surrogates womb, but instead, are multiplied in a laboratory. The embryos selected for harvesting stem cell are created within invitro fertilization clinics but are not selected for implantation.

Amniotic stem cells can be harvested at the same time that doctors use a needle to withdraw amniotic fluid during a pregnant womans amniocentesis. The same fluid, after being tested to ensure the babys health, can also be used to extract stem cells.

As mentioned, there is another source for stem cells the umbilical cord. Blood cells from the umbilical cord can be harvested after a babys birth. Cells can also be extracted from the postpartumhuman placenta, which is typically discarded as medical waste following childbirth.

The umbilical cord and the placenta are non-invasive sources of perinatal stem cells.

People who donate stem cells through the peripheral blood stem cell donor procedure report it to be a relativelypainless procedure. Similar to giving blood, the procedure takes about four hours. At a clinic or hospital, an able medical practitioner draws the blood from the donors vein in one of his arms using a needle injection. The technician sends the drawn blood into a machine, which extracts the stem cells. The blood is then returned to the donors body via a needle injected into the other arm. Some patients experience cramping or dizziness, but overall, its considered a painless procedure.

If a blood stem cell donor has a problem with his or her veins, a catheter may be injected in the neck or chest. The donor receives local anesthesia when a catheter-involved donation occurs.

During a bone marrow stem cell donor procedure, the donor is put under heavy sedation in an operating room. The hip is often the site chosen to harvest the bone marrow. More of the desired red marrow is found in flat bones, such as those in the pelvic region. The procedure takes up to two hours, with several extractions made while the patient is sedated. Although the procedure is painless due to sedation, recovery can take a couple of weeks.

Bone marrow stem cell donation takes a toll on the donorbecause it involves the extraction of up to 10 percent of the donors marrow. During the recovery period, the donors body gradually replenishes the marrow. Until that happens, the donor may feel fatigued and sore.

Some clinics offer regenerative and cosmetic therapies using the patients own stem cells derived from the fat tissue located on the sides of the waistline. Considered a simple procedure, clinics do this for therapeutic reasons or as a donation for research.

Stem cells differ from the trillions of other cells in your body. In fact, stem cells make up only a small fraction of the total cells in your body. Some people have a higher percentage of stem cells than others. But, stem cells are special because they are the mothers from which specialized cells grew and developed within us. When these cells divide, they become daughters. Some daughter cells simply self-replicate, while others form new kinds of cells altogether. This is the main way stem cells differ from other body cells they are the only ones capable of generating new cells.

The ways in which stem cells can directly treat patients grow each year. Regenerative medicine now relies heavily on stem cell applications. This type of treatment replaces diseased cells with new, healthy ones generated through donor stem cells. The donor can be another person or the patient themselves.

Sometimes, stem cells also exert therapeutic effects by traveling through the bloodstream to sites that need repair or by impacting their micro-environment through signaling mechanisms.

Some types of adult stem cells, like mesenchymal stem cells (MSCs), are well-known for exerting anti-inflammatory and anti-scarring effects. MSCs can also positively impact the immune system.

Conditions and diseases which stem cell regeneration therapy may help include Alzheimers disease, Parkinsons disease, and multiple sclerosis (MS). Heart disease, certain types of cancer, and stroke victims may also benefit in the future. Stem cell transplant promises advances in treatment for diabetes, spinal cord injury, severe burns, and osteoarthritis.

Researchers also utilize stem cells to test new drugs. In this case, an unhealthy tissue replicates into a larger sample. This method enables researchers to test various therapies on a diseased sample, rather than on an ailing patient.

Stem cell research also allows scientists to study how both healthy and diseased tissue grows and mutates under various conditions. They do this by harvesting stem cells from the heart, bones, and other body areas and studying them under intensive laboratory conditions. In this way, they get a better understanding of the human body, whether healthy or sick.

With the following stem cell transplant benefits, its not surprising people would like to try the therapy as another treatment option.

Physicians harvest stem cell from either the patient or a donor. For an autologous transplant, there is no risk of transferring any disease from another person. For an allogeneic transplant, the donor is meticulously screened before the therapy to make sure they are compatible with the patient and have healthy sources of stem cells.

One common and serious problem of transplants is the risk of rejecting the transplanted organs, tissues, stem cells, and others. With autologous stem cell therapy, the risk is avoided primarily because it comes from the same person.

Because stem cell transplants are typically done through infusion or injection, the complex and complicated surgical procedure is avoided. Theres no risk of accidental cuts and scarring post-surgery.

Recovery time from surgeries and other types of treatments is usually time-consuming. With stem cell therapy, it could only take about 3 months or less to get the patient back to their normal state.

As the number of stem cell treatments dramatically grew over the years, its survival rate also increased. A study published in the Journal of Clinical Oncology showed there was a significant increase in survival rate over 12 years among participants of the study. The study analyzed results from over 38,000 stem cell transplants on patients with blood cancers and other health conditions.

One hundred days following transplant, the researchers observed an improvement in the survival rate of patients with myeloid leukemia. The significant improvements we saw across all patient and disease populations should offer patients hope and, among physicians, reinforce the role of blood stem cell transplants as a curative option for life-threatening blood cancers and other diseases.

With the information above, people now have a better understanding of the answer to the question Where do stem cells come from? Stem cells are a broad topic to comprehend, and its better to go back to its basics to learn its mechanisms. This way, a person can have a piece of detailed knowledge about these master cells from a scientific perspective.

If you found this blog valuable, subscribe to BioInformants stem cell industry updates.

As the first and only market research firm to specialize in the stem cell industry, BioInformant research is cited by The Wall Street Journal, Xconomy, AABB, and Vogue Magazine. Bringing you breaking news on an ongoing basis, we encourage you to join more than half a million loyal readers, including physicians, scientists, executives, and investors.

What do you understand aboutthe basics of stem cells? Share your thoughts in the comments section below.

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Where Do Stem Cells Come From? | Basics Of Stem Cell Therapy

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Genetic Testing Q&AQ: What are genes?

A: Genes are individual units of inheritance made of DNA. We all have two copies of each gene; we inherit one copy from each of our parents and pass one copy on to each child. The exact DNA sequence of a gene is a code with instructions to make a functioning protein (like a recipe). Changes to the DNA code can cause the gene not to work and stop its protein from being made.

A: Genetic testing is a process that looks for alterations in a person's genes. Alterations in certain genes may lead to an increased risk of cancer. Therefore, genetic testing results may be helpful in tailoring cancer screening recommendations.

Genetic testing involves sending a blood sample to a specialized lab for analysis. Results are returned to the ordering physician and genetic counselor, who then discloses them to the patient and arranges appropriate follow-up care.

A: Genetic counselors are trained licensed professionals who have earned a Master's degree in genetic counseling from an accredited program. Cancer genetic counselors specifically counsel patients about inherited cancer syndromes, the chance they might carry a gene in a form that confers increased risk of specific inherited cancer syndromes, the mechanics of genetic testing, the patient's chance of having an inherited susceptibility to cancer, and the implications of being found to carry or not carry a genetic risk for cancer.

The role of a genetic counselor is to assist individuals and families in understanding genetic disorders. Genetic counselors:

Genetic counselors often help to interpret confusing or uncertain test results, and also educate patients and providers on new testing options. For this reason, genetic counselors may maintain contact with patients over time.

A: During the visit, your genetic counselor will take a detailed family history in order to evaluate the likelihood that you could have an inherited predisposition to cancer. Features of a family history that suggest a hereditary susceptibility include:

The genetic counselor may then discuss the option of testing and will explain the relevant gene(s) and associated syndrome in terms of cancer risks and medical management issues. Common concerns of genetic testing, including issues of insurance discrimination and confidentiality, will be discussed. Possible results of genetic testing, as well as the cost and logistics of testing, insurance coverage, or options if insurance does not cover, will also be reviewed. Your genetic counselor will help to guide you in making the best decisions regarding genetic testing for yourself, as a decision to undergo genetic testing or not is truly a personal decision.

A: Information regarding personal and family cancer history including the specific cancer(s), age(s) at diagnosis or information about pre-cancerous conditions such as colon polyps and copies of personal or family genetic test results are requested for your visit. Other medical records such as pathology reports, surgical reports, or summary notes) are often useful. Also helpful are prior pathology reports.

A: We recommend general guidelines for a healthy lifestyle as endorsed by the American Cancer Society and the National Cancer Institute, as these may also help reduce your risk for developing cancer.

In the videos below, Dana-Farber cancer genetics specialists provide answers to a variety of questions about specific genetic tests, interpreting test results, and genetic risk for cancer.

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