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Stem Cell Treatment Cardiovascular Disease, Heart Disease …

Cardiovascular disease, also called heart disease, is a broad medical term used to describe a group of conditions that affect the blood vessels or the heart. It is the most common cause of death worldwide.1

Conditions of cardiovascular disease include:

The Stem Cells Transplant Institutein Costa Rica, uses adult autologous stem cells for the treatment of cardiovascular disease (heart disease). The symptoms of cardiovascular disease will depend on the specific type of heart disease.

Treatment at the Stem Cells Transplant Institute could help improve the symptoms of cardiovascular disease such as:

Heart disease and cardiovascular disease are often used interchangeably. These terms refer to a group of conditions that affect the blood vessels and heart. Valvular heart disease affects how the valves pump blood flow in and out of the heart. Cardiomyopathy affects the contractions of the heart muscle. Heart arrhythmias are disturbances in the electrical conduction making the heart beat irregular. Coronary artery disease is the most common cause of cardiovascular disease and stem cell therapy may be an effective treatment.

Coronary artery disease is caused by atherosclerosis, the buildup of plaque, causing a narrowing or blocking the blood vessels in the coronary arteries. Coronary artery disease is the leading cause of cardiovascular disease. Atherosclerosis can lead to chest pain, heart attack or stroke.

Coronary arteries carry oxygen rich blood to the heart. Plaque is caused by the presence of cholesterol, calcium, fat, and other substances in the blood. When plaque builds up in the blood vessels it narrows the arteries causing them to harden and weaken, reducing the amount of oxygen rich blood to the heart. As a result, the heart cannot pump blood effectively to the rest of the body potentially leading to heart failure and ultimately death.

If the plaque building up in the coronary arteries breaks, a blood clot forms around the plaque. If the clot cuts off the blood flow to the heart muscle completely, the heart muscle is unable to get the necessary oxygen and nutrients causing a part of the heart muscle to die. The result is a heart attack or myocardial infarction,

Coronary artery disease, high blood pressure or a previous heart attack can lead to the onset of heart failure. Heart failure is a chronic, progressive disease typically caused by another heart condition resulting in the heart muscle losing its ability to supply the rest of body with enough blood and oxygen.

Atherosclerosis can also cause peripheral artery disease. Peripheral arterial disease occurs when the narrowed peripheral arteries cannot send enough blood flow to the extremities, usually the legs. The most common symptoms of peripheral artery disease are; cramping, pain, and/or tiredness in the leg or hip muscles during exertion. The most severe symptom of peripheral artery disease is critical limb ischemia, pain at rest due to reduced blood flow to the limb.

Approximately 85% of strokes are ischemic strokes. Atherosclerosis is the most common cause of ischemic stroke. If the arteries become too narrow due to plaque buildup, the blood cells may collect and form a clot. A larger clot can block the artery where it is formed (thrombotic stroke) while a smaller clot may travel until it reaches an artery closer to the brain (embolic stroke). When the arteries to your brain become narrow or blocked, the required blood flow is reduced resulting in stroke. Other causes of ischemic stroke are clots due to an irregular heartbeat or heart attack.

Stem cell therapy at the Stem Cells Transplant Institute may be a good alternative for patients seeking a safe, non-surgical treatment for cardiovascular disease.

Notably, adult stem and progenitor cells including.mesenchymal stem cells have progressed into clinical trials and have shown positive benefits.5

Stem cell transplantation uses healthy cells to promote the repair of damaged cells and regeneration of healthy and functional cells to repair injured tissue.1 The therapeutic effect of stem cell transplantation in patients with cardiovascular disease may be due to the paracrine effect. The theory is transplanted stem cells repair damaged tissue by releasing factors that promote regeneration of healthy stem cells, reduce inflammation, promote the growth of new blood vessels, inhibit cell death, and reduce hypertrophy.1

The results of initial research using mesenchymal stem cell transplantation:

Heart Failure

Adipose derived stem cells improve left ventricular function, promote angiogenesis, lower fibrosis, and decrease inflammation. Several months following treatment, stem cells continue to migrate to the heart muscle regenerating and renewing healthy heart function. Stem cell therapy cannot help all patients with cardiovascular disease but for many patients stem cell therapy combined with lifestyle modification may be a safe, effective, non-surgical alternative treatment.

Lifestyle changes that can help improve cardiovascular disease include:

The Stem Cells Transplant Institute uses autologous mesenchymal stem cells for the treatment of cardiovascular disease. Autologous means the stem cells are collected from the recipient so the risk of rejection is virtually eliminated. Mesenchymal stem cells are one type of adult stem cells that are found in a variety of tissues including; adipose tissue, lung, bone marrow, and blood. Mesenchymal stem cells have several advantages over other types of stem cells; ability to migrate to sites of tissue injury, strong immunosuppressive effect, and better safety after infusion.2,3 Mesenchymal stem cells are a promising treatment for cardiovascular disease. Treatment at the Stem Cells Transplant Institute may improve the symptoms and long-term complications of cardiovascular disease.

A team of stem cell experts developed an FDA approved method and protocol for harvesting and isolating adipose derived stem cells for autologous reimplantation. The collection and use of adult stem cells does not require the destruction of embryos and for this reason, more U.S. federal funding is being spent on stem cell research.

The stem cells are administered intravenously.

Costa Rica has one of the best healthcare systems in world and is ranked among the highest for medical tourism. Using the most advanced technologies, the team of experts at The Stem Cells Transplant Institute believes in the potential of stem cell therapy for the treatment of cardiovascular disease. We are committed to providing personalized service and the highest quality of care to every patient. Contact us to see if stem cell therapy may be a treatment option for you.

1.Sun R.Advances in stem cell therapy for cardiovascular disease (Review). National Journal of Mol. Med. 38: 23-29, 2016. 2 Hare JM, Fishman JE, Gerstenblith G, DiFede Velazquez DL, Zambrano JP, Suncion VY, Tracy M, Ghersin E, Johnston PV, Brinker JA, et al: Comparison of allogeneic vs autologous bone marrow-derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. JAMA 308: 2369-2379, 2012.3 Miyahara Y, Nagaya N, Kataoka M, Yanagawa B, Tanaka K, Hao H, Ishino K, Ishida H, Shimizu T, Kangawa K, et al: Monolayered mesenchymal stem cells repair scarred myocardium after myocardial infarction. Nat Med 12: 459-465, 2006. 4 Mazo M, Planat-Bnard V, Abizanda G, Pelacho B, Lobon B, Gavira JJ, Peuelas I, Cemborain A, Pnicaud L, Laharrague P, et al: Transplantation of adipose derived stromal cells is associated with functional improvement in a rat model of chronic myocardial infarction. Eur J Heart Fail 10: 454-462, 2008. 5 Stem cell-based therapies to promote angiogenesis in ischemic cardiovascular disease Luqia Hou,1,2 Am J Physiol Heart Circ Physiol 310: H455H465, 2016. 6 Kinnaird T, Stabile E, Burnett MS, Lee CW, Barr S, Fuchs S, Epstein SE. Marrow-derived stromal cells express genes encoding a broad spectrum of arteriogenic cytokines and promote in vitro and in vivo arteriogenesis through paracrine mechanisms. Circ Res 94: 678685, 2004. 7 Kinnaird T, Stabile E, Burnett MS, Shou M, Lee CW, Barr S, Fuchs S, Epstein SE. Local delivery of marrow-derived stromal cells augments collateral perfusion through paracrine mechanisms. Circulation 109: 15431549, 2004.

8 Hare JM, Fishman JE, Gerstenblith G, DiFede Velazquez DL, Zambrano JP, Suncion VY, Tracy M, Ghersin E, Johnston PV, Brinker JA, Breton E, Davis-Sproul J, Schulman IH, Byrnes J, Mendizabal AM, Lowery MH, Rouy D, Altman P, Wong Po Foo C, Ruiz P, Amador A, Da Silva J, McNiece IK, Heldman AW, George R, Lardo A. Comparison of allogeneic vs autologous bone marrowderived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. JAMA 308: 23692379, 2012.

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Stem Cell Treatment Cardiovascular Disease, Heart Disease ...

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Autologous iPS cell therapy for Macular Degeneration: From bench-to-bedside

Presented At:Gibco - 24 Hours of Stem Cells Virtual Event

Presented By:Kapil Bharti - Stadtman Investigator, NIH, Unit on Ocular Stem Cell & Translational Research

Speaker Biography:Dr. Kapil Bharti holds a bachelor's degree in Biophysics from the Panjab University, Chandigarh, India, a master's degree in biotechnology from the M.S. Rao University, Baroda, India, and a diploma in molecular cell biology from Johann Wolfgang Goethe University, Frankfurt, Germany. He obtained his Ph.D. from the same institution, graduating summa cum laude. His Ph.D. work involved research in the areas of heat stress, chaperones, and epigenetics.

Webinar:Autologous iPS cell therapy for Macular Degeneration: From bench-to-bedside

Webinar Abstract:Induced pluripotent stem (iPS) cells are a promising source of personalized therapy. These cells can provide immune-compatible autologous replacement tissue for the treatment of potentially all degenerative diseases. We are preparing a phase I clinical trial using iPS cell derived ocular tissue to treat age-related macular degeneration (AMD), one of the leading blinding diseases in the US. AMD is caused by the progressive degeneration of retinal pigment epithelium (RPE), a monolayer tissue that maintains vision by maintaining photoreceptor function and survival. Combining developmental biology with tissue engineering we have developed clinical-grade iPS cell derived RPE-patch on a biodegradable scaffold. This patch performs key RPE functions like phagocytosis of photoreceptor outer segments, ability to transport water from apical to basal side, and the ability to secrete cytokines in a polarized fashion. We confirmed the safety and efficacy of this replacement patch in animal models as part of a Phase I Investigational New Drug (IND)-application. Approval of this IND application will lead to transplantation of autologous iPS cell derived RPE-patch in patients with the advanced stage of AMD. Success of NEI autologous cell therapy project will help leverage other iPS cell-based trials making personalized cell therapy a common medical practice.

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Is Male Infertility Genetic? | Hereditary Fertility Issues …

Why does it matter if infertility has a genetic cause?

Developed in the early 1990s, assisted reproduction in the form of IVF and ICSI (intracytoplasmic sperm injection) is a revolutionary laboratory technique in which a single sperm is placed directly inside an egg for fertilization. This technique has opened the door to fertility for men who formerly had few available treatment options, as it allows men who were previously considered severely infertile or sterile the possibility of fatherhood. However, with ICSI sperm are chosen by laboratory technicians and not by nature and because of this, it is not clear what barriers to natural selection are altered. Thus, along with this technology comes the possibility of passing on to a child certain genetic issues that may have caused the fathers infertility, or even more severe conditions. Another reason to know whether male infertility is genetic or not is because classic treatments such asvaricocelerepair or medications given to improve male infertility. In fact, Dr Turek was one of the first to publishonthis issue, showing thatvaricocelerepair was not effective in improving fertility in men with genetic infertility. Because he recognized these issues early on, Dr. Turek, while at UCSF in 1997, founded the first formal genetic counseling and testing program for infertility in the U.S. Called the Program in the Genetics of Infertility (PROGENI), Dr.Tureksprogram has helped over 2000 patients at risk for genetic infertility to navigate the decision-making waters that surround this condition.

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

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

Among the various infertility diagnoses that men have, some are more commonly associated with genetic causes. Diagnoses that can have genetic causes include men nonobstructive azoospermia (no sperm count), oligospermia (low sperm count), and congenital absence of the vas deferens. A list of some of the best- described causes of genetic male infertility and their frequencies and associated conditions are listed in Table 1.

Nonobstructiveazoospermiais defined aszero sperm countin the ejaculate due to an underlying sperm production problem within the testicles. This is quite different from obstructive azoospermia in which sperm production within the testes is normal, but there is a blockage in the reproductive tract ducts that prevents the sperm from leaving the body. There can be changes in the levels of reproductive hormones, such as follicle stimulating hormone (FSH), observed withnonobstructiveazoospermia. Most commonly, the FSH is elevated in this condition, which is an appropriate and safe hormone responseofthe pituitary gland to states of low or no sperm production. This diagnosis is associated with a 15%chance forhaving chromosome abnormalities(Figure 2) and a 13% chance for having gene regions missing on the Y chromosome (termed Y chromosome microdeletions, Figure3). To detect these changes, blood tests are typically offered to men with nonobstructive azoospermia.

Oligospermiathat places men at risk for genetic infertility occurs when the ejaculate contains a sperm concentration of <5 million sperm/mLsemen. Similar to nonobstructive azoospermia, this is most commonly due to an underlying sperm production problem. With this diagnosis, there is a 2% risk for chromosome abnormalities and 6-8% risk of Y chromosomemicrodeletions.Ingeneral, the lower the sperm count, the higher the chance that a genetic cause is present. Again the appropriate testing includes akaryotypeand Y chromosome microdeletion analysis. Thus far, there are noestablished guidelines for applying these genetic tests in cases of low spermmotility(movement) or poor sperm morphology (shape).

Congenital absence of the vas deferens is characterized by the malformation or absence of the ducts that allow sperm to pass from the testicles into the ejaculate and out of the body during ejaculation. The duct that is affectedinthis condition is thevasdeferens. This is the sameductthat is treated during a vasectomy, a procedure for men who want birth control. Men with this condition are essentially born with a natural vasectomy. This congenital condition is associated with mutations and/or variations in the genes for cystic fibrosis (the CFTR gene) in 70-80% men if thevasdeferensis absent on both sides, but less than this if the duct is missing on only one side. For most men with this condition with a mutation in the cystic fibrosis gene, the missingvasdeferensis the only problem that results from this genetic change and they do not have the full spectrum of symptoms associated with cystic fibrosis, the most common genetic disease in the U.S.andgenerally lethal in early adulthood.

A less common reason for mento havea zero sperm count (azoospermia) than nonobstructive azoospermia is obstructive azoospermia. In essence, this is an unexplained zero sperm count due to a blockage of the reproductive tract ducts leading from the testicle to the ejaculate. Blockages are most commonly found in theepididymisbut can also be located in thevasdeferensor ejaculatory ducts. Most cases of obstructive azoospermia are amendable to surgical repair and naturally fertility is common. However, a high proportion of these men (47%) have mutations in the cystic fibrosis gene (CFTR) or harbor variations in the CFTR gene, termed 5T alleles. As such, genetic counseling and testing is also important in these patients.

These conditions represent only the most common genetic conditions encountered when evaluating men for genetic infertility. For this reason, consider readingDr.Turekspublished paperthat discusses most of the currently understood syndromes and conditions that are associated with infertility. It is also important to remember that if all genetic test results are normal, there is still a possibility that the infertility has a genetic cause. However, in many cases, medical science is currently unable to offer testing to detect it.

If a man has a chromosome abnormality identified as the cause of infertility, then depending on the chromosome abnormality detected, there may be a higher risk for children to be born with birth defects or mental impairment. This occurs as a result of a child inheriting from the father an imbalance in chromosome material. A genetic counselor can provide more detailed information about such potential risks, and offer other resources for individuals who have been diagnosed with a chromosome abnormality. There may be support organizations available to help men with genetic diagnoses and their partners cope with the impact of this information. Some couples find it helpful to talk to others in similar circumstances.

If a man is diagnosed with a Y chromosome deletion, then he will pass on that Y chromosome deletion to anysonhe conceives. To his daughters, he will pass on his X chromosome, instead of the Y chromosome. It is assumed that any son inheriting a Y chromosome deletion from his father will also have infertility. It is unclear whether the type and severity of the infertility will be different from the fathers. So far, there have only been a few reports of sons born to fathers with Y chromosome deletions after conception by assisted reproduction. As expected, there has not been an increase in the rate of birth defects or other problems for these boys, although this group is still small in number, and too young to have fertility evaluations.

Transmission of CFTR mutations in cases of infertility due to congenital absence of the vasdeferensis somewhat more complex than either Ymicrodeletionsor a chromosome abnormality. This is because there are over 1400 described mutations in the CFTR gene and the impact of mutations differs depending on which one is present. In general, the partner of an affected man should be tested as well, so that the residual risk of a child having either congenital absence of the vas deferens or full-blown cystic fibrosis can be estimated.

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About Hormone Clinics – Hormone Clinics

Welcome to the Hormone Clinic !

At the hormone clinics we have been helping men and women to live well and achieve peak performance at any age through hormone therapy.

Our medical director, Dr. Richard Gaines was one of the pioneers in hormone therapy for men and women. He, and all of the staff with the hormone clinic possess a unique insight and decades of experience in the safe and effective use of hormone replacement therapies such as HGH Therapy,Testosterone Therapy and Bio-Identical Hormone Therapy.

We use hormone therapy to give you back what time and nature can take away.

The hormone clinic takes a very different approach to hormone therapy than you will find at Cenegenics, or any other provider of hormone therapy. At the hormone clinic you will always be treated as an individual.

We tailor your hormone therapy to your unique needs and lifestyle. Beyond that, we incorporate your hormone therapy into a program of Holistic Health and Wellness.

It is an approach to hormone therapy that is designed to help you get the most out of your treatments, in mind, body and spirit.

During your hormone therapy, you will be assigned one of our Holistic Wellness coaches. He or she will work with you to design a program of fitness, diet, stress reduction and exercise that will help you to maximize, and maintain the benefits of your hormone therapy.

You will also find the cost of hormone therapy more reasonable at the hormone clinic than you would at most other providers of hormone therapy. This is not only because of our precise and individualized dosing. We have developed long-standing relationships with certified local compounding pharmacies, which helps us to keep the costs of our bioidentical hormones low.

Also, unlike some other hormone centers, The Hormone Clinic will never lock you into a long term hormone therapy program. In addition, The Hormone Clinic will never try to sell you products or supplements along with your hormone therapy that you do not need.

All of the doctors, physicians assistants, and nurse practitioners at the Hormone Clinic are highly trained and experienced in hormone therapy. Many of them are over 45 and on the program themselves, and are running marathons, racing motorcycles, climbing mountains, and doing other great things!

The Hormone Clinic is led by well-known expert in hormone therapy Dr. Richard Gaines. For decades, Dr. Gaines has been helping men and women of any age stay young, healthy, and accomplish great things in life, by offering customized hormone therapy.

In our Miami Beach location, our hormone clinic can provide you with not only the very best in Miami hormone therapy, but is also within the building of South Floridas first integrated wellness center.

As soon as you step into any hormone clinic location, you will know immediately that you are in a unique ultra-modern facility.

At the Hormone Clinic you will be treated with the ultimate in individualized medicine. At every point of contact with our hormone therapy staff you will receive executive treatment, all delivered in a setting that is as unique as you are.

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Low Rates of Genetic Testing in Ovarian, Breast Cancer …

April 9, 2019, by NCI Staff

Many women diagnosed with ovarian and breast cancers are not receiving tests for inherited genetic mutations, according to a new study.

Credit: iStock

Tests for inherited genetic mutations can provide women diagnosed with ovarian or breast cancer with important information that can have implications for family members and potentially guide treatment decisions and longer-term screening for second cancers. However, many women with ovarian and breast cancers are not receiving these genetic tests, a new study suggests.

An NCI-funded analysis of data on more than 83,000 women from large cancer registries in California and Georgia found that, in 2013 and 2014, only about one-quarter of women with breast cancer and one-third of women with ovarian cancer underwent testing for known harmful variants in breast and ovarian cancer susceptibility genes.

The study also found that among patients who did receive genetic testing, 8% of breast cancer patients and 15% of ovarian cancer patients had actionable gene variants, meaning variants that might warrant changes in treatment, screening, and risk-reduction strategies.

The findings, published April 9, 2019, in the Journal of Clinical Oncology, were surprising, especially the low rate of testing among women with ovarian cancer, said lead author Allison Kurian, M.D., M.Sc., of Stanford University School of Medicine.

Genetic testing has become quite cheap and accessible, and this study includes a time period when it was becoming much cheaper, so its striking that we still see low rates of testing, Dr. Kurian said. I think that suggests that there are most likely other barriers outside of cost.

The study also revealed racial and socioeconomic disparities in testing rates among women diagnosed with ovarian cancer. Genetic testing rates were far lower for black women than for white women, and they were also lower for uninsured patients than for insured patients.

These findings have uncovered a [disparities] gap that is much more substantial than I would have thought, Dr. Kurian said.

About 15% of ovarian cancers are caused by inherited mutations, and several medical organizations recommend that all women diagnosed with ovarian cancer receive genetic testing.

For women with breast cancer, the recommendations for genetic counseling and testing are generally more limited, typically relying on factors such as age at cancer diagnosis and family history. However, some organizations, including the American Society of Breast Surgeons, recommend that genetic testing be made available to all women diagnosed with breast cancer.

There are many reasons why women with ovarian and breast cancer would get tested, Dr. Kurian explained.

We know that if patients have a specific inherited gene mutation, they will likely have more benefit from a new class of drugs called PARP inhibitors, she said.

The Food and Drug Administration has approved three PARP inhibitors for BRCA1-and BRCA2-associated ovarian cancer and two for BRCA1/2-associated metastatic breast cancer. Harmful variants of both BRCA1 and BRCA2 are known to increase the risk of breast and ovarian cancer, as well as of several other types of cancer.

Another reason to get tested is that patients with a genetic mutation that is associated with breast or ovarian cancer may be at higher risk of a second cancer, so you dont want to miss a second cancer that could be a problem, Dr. Kurian said.

The findings could also be life-saving information for a patients relatives. If you find that she carries a mutation, every first-degree relative, male or female, has a 50% chance of having the same mutation, she said.

Testing, then, could allow for enhanced screening and prevention for family members who are carriers, she explained.

The study included all women older than age 20 who were diagnosed with breast or ovarian cancer in California and Georgia from 20132014 and whose data were reported to NCIs Surveillance, Epidemiology and End Results (SEER) registries. There were 77,085 patients with breast cancer and 6,001 with ovarian cancer. The registry data were linked to results from four laboratories that performed nearly all the genetic testing for inherited, or germline, mutations in these states during the study period.

According to the authors, this is the first population study of hereditary cancer genetic testing in the United States with laboratory-confirmed testing results.

Weve never had this kind of linkage available before, giving us a baseline to let us know if the standard of care [for testing] was being followed, said study coauthor Lynne Penberthy, M.D., M.P.H., associate director for NCIs Surveillance Research Program. Thats why this is really important. These data can be used to see where we are and where were going. We can continue to provide this information, so people can see, hopefully, an increase in the appropriate use of genetic testing over time.

Linking the SEER registry data to the testing data in this study provides really objective data about the massive undertesting of ovarian cancer patients, said Susan Domchek, M.D., executive director of the Basser Center for BRCA at the University of Pennsylvania Abramson Cancer Center, who was not involved in the study.

Testing is recommended for all patients with ovarian cancer, she added, so the fact that only one-third of these patients had it done in this time period is a clear-cut example that were not testing ovarian cancer patients the way that we should be.

While large racial and socioeconomic disparities in testing rates were not observed among women with breast cancer, among women with ovarian cancer, testing rates were far lower in black women than white women (21.6% versus 33.8%) and in uninsured women than insured women (20.8% versus 35.3%).

Understanding why genetic testing rates are so low in women with ovarian cancer and why racial and socioeconomic disparities in testing exist among women with the disease is tricky, Dr. Kurian said.

Testing in ovarian cancer has not been widely studied beforedefinitely not at the population leveland not in such a diverse population, she added, so theres a lot we dont know about barriers.

For example, she said, its unclear whether genetic testing is on the radar screen of doctors treating patients with ovarian cancer as much as it is for patients with breast cancer. Dr. Domchek said there could also be misconceptions among patients about the costs of genetic testing.

But if access to genetic counseling or information on testing is difficult, clearing up these misconceptions can be a challenge, she said. So, trying to figure out how to better streamline [counseling and education] into practice to make sure all of these individuals with ovarian cancer get tested is a subject of ongoing research.

Dr. Domchek noted that NCI is looking to fund studies that offer genetic testing to women with a personal or family history of ovarian cancer to see if it can help to identify members of their families who may be at increased cancer risk.

Although variants in the BRCA1 and BRCA2 genes were the most frequently found in the study, the laboratories also looked for other inherited cancer-related genetic mutations using tests known as multigene panels.

The results provide an understanding, on a broader scale, of how common these mutations are, Dr. Kurian said.

The multigene panel testing led to other noteworthy findings, Dr. Penberthy said.

What was really interesting was that while BRCA1 and BRCA2 were the most common germline mutations that we found in the study, there were other mutations that were not uncommon and that were actionable in terms of treatment as well, she explained.

For example, 60 women with breast cancer in the study had a mutation in the CDH1, PALB2, or PTEN genes. These mutations are associated with a substantially increased breast cancer risk, Dr. Kurian said, so women who have these mutations may consider having both breasts removed (a risk-reducing bilateral mastectomy), rather than just the breast in which the tumor was found.

And widely used clinical guidelines recommend that women with breast cancer who have certain inherited genetic mutations,including in genes such as ATM and CHEK2,undergo more intensive screening for second cancers. In the study, mutations in ATM and CHEK2 were found in 0.7% and 1.6% of women with breast cancer, respectively.

Mutations in CHEK2 and PALB2and several other genes were found both in women with breast cancer and women with ovarian cancer. Studies havent yet linked these genes with increased ovarian cancer risk, so further study is warranted, the authors wrote.

However, the key message from this study is the undertesting of ovarian cancer patients, who clearly need it, Dr. Domchek said.

Its not to say we shouldnt debate population screening [for inherited mutations], or which genes to test for, and how were going to do it, she said. But first, for heavens sake, lets test the people who absolutely need testing, not only because it impacts family members, but also because now we have first-line therapy with PARP inhibitors. Every woman with ovarian cancer should know her BRCA1 or BRCA2 status.

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Genetic testing – Drugs.com

The originating document has been archived. We cannot confirm the completeness, accuracy and currency of the content.

Medically reviewed on Jul 19, 2018

Genetic testing involves examining your DNA, the chemical database that carries instructions for your body's functions. Genetic testing can reveal changes or alterations in your genes that may cause illness or disease.

Although genetic testing can provide important information for diagnosing, treating and preventing illness, there are limitations. For example, if you're a healthy person, a positive result from genetic testing doesn't always mean you will develop a disease. On the other hand, in some situations, a negative result doesn't guarantee that you won't have a certain disorder.

Talking to your doctor or a genetic counselor about what you will do with the results is an important step in the process of genetic testing.

Several types of genetic testing are done for different reasons:

Before you undergo genetic testing, gather as much information as you can about your family's medical history. Then, talk with your doctor or a genetic counselor about your personal and family medical history. This can help you better understand your risk. Discuss questions or concerns you have about genetic testing at that meeting. Also, talk about your options, depending on the results of the test.

If you are being tested for a genetic disorder that runs in families, you may want to consider discussing your decision to undergo genetic testing with your family. Having these conversations before testing can give you a sense of how your family might respond to your test results and how it will affect them.

Not all health insurance pays for genetic testing. So, before you have a genetic test, check with your insurance provider to see what will be covered. In the United States, the federal Genetic Information Nondiscrimination Act (GINA) helps prevent health insurers or employers from discriminating against you based on test results. Most states offer additional protection.

Your doctor, medical geneticist or nurse practitioner may administer a genetic test. Depending on the type of test, a sample of your blood, skin, amniotic fluid or other tissue will be collected and sent to a lab for analysis.

The amount of time it takes for you to receive your genetic testing results will depend on the type of test and your health care facility. Talk to your doctor before the test about when you can expect the results. The lab will likely provide the test results to your doctor in writing. Your doctor can then discuss them with you.

If the genetic test result is positive, that means the genetic alteration that was being tested for was detected. The steps you take after you receive a positive result will depend on the reason you underwent genetic testing. If the purpose was to diagnose a specific disease or condition, a positive result will help you and your doctor determine the right treatment and management plan.

If you were tested to find out if you are carrying an altered gene that could cause disease in your child, and the test is positive, your doctor or a genetic counselor can help you determine your child's risk of actually developing the disease. The test results can also provide information to consider as you and your partner make family planning decisions.

If you were having gene testing to determine if you might develop a certain disease, a positive test doesn't necessarily mean you will get that disorder. For example, having a breast cancer gene (BRCA1 or BRCA2) means you are at high risk of developing breast cancer at some point in your life, but it doesn't indicate with certainty that you will get breast cancer. However, there are some conditions, such as Huntington's disease, for which having the altered gene does indicate that the disease will eventually develop.

Talk to your doctor about what a positive result means for you. In some cases, you can make lifestyle changes that may decrease your risk of developing a disease, even if you have an altered gene that makes you more susceptible to a disorder. Results may also help you make choices related to family planning, careers and insurance coverage.

In addition, you may choose to participate in research or registries related to your genetic disorder or condition. These options may help you stay updated with new developments in prevention or treatment.

A negative result means a genetic alteration was not detected by the test. But a negative result doesn't guarantee that you don't have an alteration. The accuracy of genetic tests to detect alterations varies, depending on the condition being tested for and whether or not an alteration has been previously identified in a family member.

Even if you don't have the genetic alteration, that doesn't necessarily mean you will never get the disease. For example, people who don't have a breast cancer gene (BRCA1 or BRCA2) can still develop breast cancer. Also, genetic testing may not be able to detect all genetic defects.

In some cases, a genetic test may not be able to provide helpful information about the gene in question. Everyone has variations in the way genes appear (polymorphisms), and often, these variations don't affect your health. But sometimes it can be difficult to distinguish between a disease-causing gene alteration and a harmless gene variation. In these situations, follow-up testing may be necessary.

No matter what the results of your genetic testing, talk with your doctor or genetic counselor about questions or concerns you may have. This will help you understand what the results mean for you and your family.

Last updated: July 19th, 2013

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What are the types of genetic tests? – Genetics Home …

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

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

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

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

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

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

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

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

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Amazon.com: AncestryDNA: Genetic Testing Ethnicity: Health …

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Hypogonadism | California Center for Pituitary Disorders

Hypogonadism is separated into two types: primary hypogonadism (resulting from dysfunction of the testis or ovary) or central hypogonadism (resulting from pituitary or hypothalamic dysfunction that leads to loss of lutenizing horomne [LH] and follicle-stimulating hormone [FSH]).

Causes of hypogondaism include genetic, menopausual, autoimmune, viral, radiation, and chemotherapeutic agents. Central hypogonadism is often due to pituitary adenomas. Through compression of the gland, these tumors can cause destruction of pituitary tissue or interference with gonadotropin-releasing hormone (GnRH) input from the hypothalamus. Gonadotropin dysfunction is the second most common hormonal disorder from compression of the pituitary gland from a pituitary adenoma after GH suppression. Hypothalamic disorders such as tumors and hypothalamic amenorrhea, as well as exposure to radiation, can lead to hypogonadism. Fasting, weight loss, anorexia nervosa, bulimia, exercise, or stressful conditions result in defects in pulsatile GnRH secretion ("hypothalamic amenorrhea"). Elevated prolactin levels can also suppress GnRH pulses and lead to hypothalamic hypogonadism. Diagonisis requires measurement of LH, FSH, and testosterone or estrogen, with reference to age-adjusted normal values.

Hypogonadism in prepubertal children causes no symptoms, whereas in adolescents, it leads to delayed or absent sexual development.

In adult women, hypogonadism causes:

Prolonged periods of hypogonadism can cause osteoporosis.

In men, hypogonadism leads to:

Most cases of hypogonadism can be successfully treated. Treatment of hypogonadism in men and premenopausal women is effectively accomplished by replacement hormonal therapy. Fertility can be restored by administration of human chorionic gonadotropin, which acts like LH, often in combination with FSH, or by the pulsatile administration of GnRH. Treatment for hypogonadism resulting from a pituitary tumor includes surgery to remove the tumor.

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Banking Menstrual Stem Cells | What are Menstrual Stem …

Stem cells in menstrual blood have similar regenerative capabilities as thestem cells in umbilical cord blood and bone marrow. Cryo-Cell's patent-pendingmenstrual stem cell service offers women in their reproductive years the ability to store and preserve these cells for potential use by herself or a family memberfree from ethical or political controversy.

Cryo-Cell is the only stem cell bank in the world that can offer womenthe reassurance and peace of mind that comes with this opportunity.

What are menstrual stem cells?Stem cells in menstrual blood are highly proliferativeandpossess the unique ability to develop into various other types of healthy cells. During a womans menstrual cycle, these valuable stem cells are discarded.

Cryo-Cell'smenstrual stem cell bankingservice captures those self-renewing stem cells, processes and cryopreserves them for emerging cellular therapies that hold the promise of potentially treatinglife-threatening diseases.

How are menstrual stem cells collected, processed and stored?The menstrual blood is collected in a physicians officeusing a medical-grade silicone cup in place of a tampon orsanitary napkin. The sample is shipped to Cryo-Cell via a medical courier and processed in our state-of-the-art ISO Class 7 clean room.

The menstrual stem cells are stored in two cryovials that are overwrapped to safeguard them during storage. The overwrapped vials are cryogenically preserved in a facility that isclosely monitored at all times to ensure that your menstrual stem cells are safe and ready for future use.

What are the benefits of banking menstrual stem cells?Cryo-Cell's innovative menstrual stem cell banking service provides women with the exclusive opportunity to build their own personal healthcare portfolio with stem cells that will be a 100% match for the donor. Menstrual stem cells have demonstrated the capability of differentiating into many other types of stem cells such as cardiac, neural, bone, fat and cartilage.

Bankingmenstrual stem cells now is an investment in your future medical needs. Currently, they are being studied to treat stroke, heart disease, diabetes, neurodegenerative disease, and ischemic wounds in pre-clinical and clinical models.

Cryo-Cells activities for New York State residents are limited to collection, processing, and long-term storage ofmenstrual stem cells. Cryo-Cells possession of a New York State license for such collection, processing, and long-term storage does not indicate approval or endorsement of possible future uses or future suitability of these cells.

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Cryonics: does it offer humanity a chance to return from the …

The decision of a teenage girl to have her body cryogenically frozen in the hope of being reanimated by medical advances in the future is one with which many could sympathise. But does current evidence suggest the gamble will pay off, or does cryonics simply give desperate people false hope dressed up in the language of science?

There are two advances that make cryonics a little less far-fetched that it once was. The first is vitrification. As Arctic explorers and mountaineers have learned, humans are not designed to be frozen and defrosted. When our cells freeze, they fill with ice crystals, which break down cell walls as they expand, reducing our body to mush once it is warmed up again.

Vitrification prevents this by replacing the blood with a mixture of antifreeze-like chemicals and an organ preservation solution. When cooled to below -90C, the fluid becomes a glass-like solid.

The technique has substantially improved the reliability of freezing and thawing embryos, and particularly eggs, in fertility treatment and it works for small pieces of tissue and blood vessels. Earlier this year, scientists managed to cryogenically freeze the brain of a rabbit and recover it in an excellent state although it is not clear if the brains functions would have been preserved as well as its superficial appearance. However, even vitrifying larger structures, such as human kidneys for transplantation, has never been done clinically and remains some way off.

Barry Fuller, a professor in surgical science and low temperature medicine, at University College London, said: There is ongoing research into these scientific challenges, and a potential future demonstration of the ability to cryopreserve human organs for transplantation would be a major first step into proving the concept, but at the moment we cannot achieve that.

This is the growing appreciation that our personality, skills and memories are to some extent defined by the connections between neurons. This has led some to speculate that rather than bringing the actual body back to life, the brains contents could be downloaded on to a computer, allowing the person to live as a robot in the future.

This might have the whiff of nonsense, but Nick Bostrom, a professor of philosophy at the University of Oxfords Future of Humanity Institute, and his colleague, Anders Sandberg, are both banking on this possibility. As a head, my life would be limited, but by then we will be able to make real connections to computers, Anders said in a 2013 interview. So my hope is that, once revived, my memories and personality could be downloaded into a computer.

However, many neuroscientists have pointed out that even if you could code the astronomical number of connections between the brains 100bn neurons, even this would not capture the full complexity of the human mind.

From a purely scientific perspective, your money is probably better spent while you are still alive.

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Stem Cells For Heart Health: What The Current Research …

Stem cells are incredible. Science is only starting to scratch the surface of how these amazing cells can help people suffering from heart failure and other cardiovascular issues. Heres some information on what stem cells are, and how they may help heart attack patients and others who have problems involving their heart tissue.

There are more than 200 kinds of cells in the body, and each type is specifically structured for the job its supposed to do. There are skin cells, nerve cells, and cells that form heart tissue and other tissues in the body.1

Theyre found in bone marrow, blood vessels, the liver, the brain, and other parts of the body. Stem cells are even found in the umbilical cord. These sophisticated cells change over time as the body matures. Some of them disappear shortly after youre born, while others stay with you for a lifetime.2

There are three main types of stem cells tissue-specific (adult stem cells), embryonic stem cells, and induced pluripotent (iPS) stem cells. Heres a quick look at each type:

These typically reside in a specific organ, generating other cells to support the health of that organ. They replace those that are lost through injury, or through everyday living.3

Embryonic stem cells form about three to five days after a sperm fertilizes an egg. These are also known as pluripotent cells. This simply means they can develop into any sort of cell the body needs to develop.4

Embryonic cells have been the source of a massive controversy. The main reason is that harvesting these cells destroys the embryo.5 Scientists are working to develop iPS cells that come from adult stems cells rather than embryonic cells. Early research indicates that these cells may share many of the same characteristics of embryonic cells. But there are differences between the two, and there is more work to be done before scientists know exactly what those differences are.6

Research is ongoing into the potential use of stem cells for heart health. For example, work is being done to see if stem cells can help improve heart attack survival rates. Scientists are also looking into the potential for giving a patient their own cardiac stem cells after a heart attack, or even giving patients non-cardiac stem cells from a donor after an attack takes place.7

The goal of this research is to eventually provide cardiac patients with stem cells that can regenerate heart tissue that has been damaged. Some researchers feel that these advances are imminent, while others believe there is a great deal of work yet to be done.8

Early results from ongoing clinical trials involving stem cells for heart health are extremely promising. In one study, a group of 109 patients suffering from heart failure received either stem cell therapy or a placebo. According to the results, the patients who received stem cells were at significantly lower risk of hospitalization or death due to a sudden worsening of their condition.9

Heart failure affects more than 5 million people in the U.S.10 It occurs when the heart gradually weakens to the point to where it cant pump enough blood to meet the needs of the rest of the body. For those with severe heart failure, the only options are either to have a heart transplant or have a device planted to help the heart continue pumping. And even this is only a temporary measure theyll still need a transplant.11

Another study involved the use of stem cells from the umbilical cord. This trial involved 30 heart failure patients. Like the previous study, one group received stem cells while the other received a placebo. The umbilical cords were donated by healthy mothers whose babies were delivered through cesarean section.12

According to the results, the hearts of patients who received the umbilical cord stem cells pumped better than those of the placebo group. The stem cell patients also showed improved quality of life and day-to-day functioning. In addition, the stem cell group did not report any adverse effects, such as immune system reactions.13

As you can see, the use of stem cells to treat heart patients shows great promise. But this is still an extremely young scientific field, and a great deal more research must be performed. Many questions have to be answered, such as what approaches to stem cell harvesting will work the best and what types of side effects are possible from stem cell treatment.

However, this research does bring hope. And hope is something that is incredibly important to many of those suffering from severe cardiac illnesses.

Learn More:How Cardio Can Change Your Brain (And Why Thats Good News!)NEWS: A Vaccine For Arthritis Is Closer Than You ThinkAre Organ Donors At Risk of Becoming Obsolete?

Sources1.https://askabiologist.asu.edu/questions/human-cell-types2.https://www.medicalnewstoday.com/info/stem_cell3.http://www.closerlookatstemcells.org/learn-about-stem-cells/types-of-stem-cells4.https://stemcells.nih.gov/info/basics/3.htm5.http://www.cnn.com/2013/07/05/health/stem-cells-fast-facts/index.html6.http://www.closerlookatstemcells.org/learn-about-stem-cells/types-of-stem-cells#induced-pluripotent7.https://my.clevelandclinic.org/health/diseases/17508-stem-cell-therapy-for-heart-disease8.https://www.health.harvard.edu/heart-health/repairing-the-heart-with-stem-cells9.https://www.ncbi.nlm.nih.gov/pubmed/2705988710.https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_failure.htm11.http://www.heart.org/HEARTORG/Conditions/HeartFailure/TreatmentOptionsForHeartFailure/Devices-and-Surgical-Procedures-to-Treat-Heart-Failure_UCM_306354_Article.jsp#.WleO-yMrJ3k12.https://www.medicalnewstoday.com/articles/319552.php13.http://circres.ahajournals.org/content/early/2017/09/15/CIRCRESAHA.117.310712

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CRISPR gene editing explained: What is it and how does it …

We are in the midst of a gene-editing revolution.

For four decades, scientists have tinkered with our genes. Since the 1970s, they've experimentally switched them on and off, uncovering their functions; mapped their location within our genome; and even inserted or deleted them in animals, plants and human beings.

And in November 2018, aChinese scientist claimedto have created the world's first genetically modified human beings.

Though scientists have made great inroads into understanding human genetics, editing our genes has remained a complex process requiring imprecise, expensive technology, years of expertise and just a little luck, too.

In 2012, a pair of scientists developed a new tool to modify genes, reshaping the entire field of gene-editing forever: CRISPR. Often described as "a pair of molecular scissors," CRISPR is widely considered the most precise, most cost-effective and quickest way to edit genes. Its potential applications are far-reaching, affecting conservation, agriculture, drug development and how we might fight genetic diseases. It could even alter the entire gene pool of a species.

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3:36

The field of CRISPR research is still remarkably young, yet we've already seen how it might be used to fight HIV infection, combat invasive species and destroy antibiotic-resistant bacteria. Many unknowns remain, however, including how CRISPR might damage DNA, leading to pathologies such as cancer.

Such a monumental leap in genetic engineering is full of complexities that ask big, often philosophical questions about science, ethics, how we conduct research and the future of humanity itself. With the confirmation that two human embryos were modified using CRISPR and carried to term, those questions have come sharply into focus. The future of gene-editing seemingly arrived overnight.

But what exactly is CRISPR and what are the outstanding concerns about such a powerful tool?

Let's break it all down.

CRISPR has the potential to be used in editing human embryos to create "designer babies."

Few predicted how important CRISPR would become for gene editing upon its discovery 30 years ago.

As early as 1987, researchers at Osaka University studying the function of Escherichia coli genes first noticed a set of short, repeated DNA sequences, but they didn't understand the significance.

Six years later, another microbiologist, Francisco Mojica, noted the sequences in a different single-celled organism, Haloferax mediterranei. The sequences kept appearing in other microbes and in 2002, the unusual DNA structures were given a name: Clustered regularly interspaced short palindromic repeats.

CRISPR.

Studying the sequences more intensely revealed that CRISPR forms an integral part of the "immune system" in bacteria, allowing them to fight off invading viruses. When a virus enters the bacteria, it fights back by cutting up the virus' DNA. This kills the virus and the bacteria stores some of the leftover DNA.

The leftover DNA is like a fingerprint, stored in the CRISPR database. If invaded again, the bacteria produce an enzyme called Cas9 that acts like a fingerprint scanner. Cas9 uses the CRISPR database to match the stored fingerprints with those of the new invader. If it can find a match, Cas9 is able to chop up the invading DNA.

Nature often provides great templates for technological advances. For instance, the nose of a Japanese bullet train is modeled on the kingfisher's beak because the latter is expertly "designed" by evolution to minimize noise as the bird dives into a stream to catch fish.

In a similar way, CRISPR/Cas9's ability to efficiently locate specific genetic sequences, and cut them, inspired a team of scientists to ask whether that ability could be mimicked for other purposes.

The answer would change gene editing forever.

In 2012, pioneering scientists Jennifer Doudna, from UC Berkeley, and Emmanuelle Charpentier, at Umea University Sweden, showed CRISPR could be hijacked and modified. Essentially, they'd turned CRISPR from a bacterial defense mechanism into a DNA-seeking missile strapped to a pair of molecular scissors. Their modified CRISPR system worked marvelously well, finding and cutting any gene they chose.

An illustration of the CRISPR-Cas9 gene editing complex. The Cas9 nuclease protein (white and green) uses a guide RNA (red) sequence to cut DNA (blue) at a complementary site.

Several research groups followed up on the original work, showing that the process was possible in yeast and cultured mouse and human cells.

The floodgates opened, and CRISPR research, which had long been the domain of molecular microbiologists, skyrocketed. The number of articles referencing CRISPR in preeminent research journal Nature has increased by over 6,000 percent between 2012 and 2018.

While other gene-editing tools are still in use, CRISPR provides a gigantic leap because of its precision and reliability. It's really good at finding genes and making accurate cuts. That allows genes to be cut out with ease, but it also provides an opportunity to paste new genes into the gap. Previous gene-editing tools could do this, too, but not with the ease that CRISPR can.

Another huge advantage CRISPR has over alternative gene-editing techniques is its expense. While previous techniques might cost a laboratory upward of $500 to edit a single gene, a CRISPR kit can do the same thing for under $100.

The CRISPR/Cas9 system has been adapted to enable gene editing in organisms including yeast, fungi, rice, tobacco, zebrafish, mice, dogs, rabbits, frogs, monkeys, mosquitoes and, of course, humans -- so its potential applications are enormous.

For research scientists, CRISPR is a tool that provides better, faster tinkering with genes, allowing them to create models of disease in human cell lines and mouse models with much higher proficiency. With better models of say, cancer, researchers are able to fully understand the pathology and how it develops, and that could lead to improved treatment options.

One particular leap in cancer therapy options is the genetic modification of T cells, a type of white blood cell that's critical for the human immune system. A Chinese clinical trial extracted T cells from patients, used CRISPR to delete a gene that usually acts as an immune system brake, and then reintroduced them into the patients in an effort to combat lung cancer. And that's just one of the many trials underway using CRISPR edited cells to fight particular types of cancer.

Beyond cancer, CRISPR has the potential to treat diseases caused by a mutation in a single gene, such as sickle cell anemia or Duchenne muscular dystrophy. Correcting a defective gene is known as gene therapy, and CRISPR is potentially the most powerful way to perform it. Using mouse models, researchers have demonstrated the efficacy of such treatments but human gene therapies using CRISPR remain untested.

Mosquitoes will be targeted using CRISPR gene drives, which could potentially drive malaria-carrying species to extinction.

Then there are CRISPR gene drives, which use CRISPR to guarantee a genetic trait will be passed from parent to offspring -- essentially rewriting the rules of inheritance. Guaranteeing certain genes will spread through a population provides an unprecedented opportunity to tackle mosquito-borne diseases such as malaria, enabling scientists to create infertile mosquitoes in the lab and release them in the wild to crash the population -- or even render a species extinct. CNET published an extensive report of their proposed use and the ethical concerns that surround them in February 2019.

And CRISPR's potential benefits don't end there. The tool opens up new ways of creating antimicrobials to combat rising levels of antibiotic resistance, targeted manipulation of agricultural crops such as wheat to make them hardier or more nutritious, and, potentially, the ability to design human beings, gene by gene.

CRISPR may be the most precise way to cut DNA we've yet discovered, but it's not always perfect.

One of the chief barriers to getting CRISPR effectively working in humans is the risk of "off-target effects." When CRISPR is tasked with hunting down a gene, it sometimes finds genes that look very similar to its target and cuts them, too.

An unintended cut may cause mutations in other genes, leading to pathologies such as cancer, or it may have no effect at all -- but with safety a major concern, scientists will need to ensure CRISPR acts only on the gene it's intended to impact. This work has already begun, and several teams of researchers have tinkered with CRISPR/Cas9 to increase its specificity.

Now playing: Watch this: DNA data storage could solve a big problem

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To date, CRISPR work in humans has been confined to cells that don't pass on their genome to the next generation. But gene editing can also be used to edit embryos and thus, change the human gene pool. In 2015, an expert panel of CRISPR scientists suggested that such editing -- known as germline editing -- would be irresponsible until consensus can be reached on safety, efficacy, regulation and social concerns.

Still, research into germline editing has been occurring for several years. In 2017, scientists in the UK edited human embryos for the first time, and researchers in the US used CRISPR to correct a defective gene that causes heart disease. The ability to edit embryos begins to raise ethical concerns about so-called designer babies, wherein scientists may select beneficial genes to increase physical fitness, intelligence or muscle strength, creeping into the controversial waters of eugenics.

That particular future is likely a long way off -- but the era of editing the human genome has already begun.

On Nov. 25, 2018, Chinese scientist Jiankui He said he had created the world's first CRISPR babies. By using CRISPR, He was able to delete a gene known as CCR5. The modified embryos resulted in the birth of twin girls, known by the pseudonyms Lulu and Nana.

The scientific community widely condemned the research, criticizing He's lack of transparency and asking whether there was an unmet medical need for the two girls to receive such a modification. In the wake of the research, several high-profile researchers involved with CRISPR's creation even suggested a global moratorium on using the tool for germline editing.

Few would argue that He's work highlights a need for stricter regulatory controls and effective oversight of clinical trials in which embryos are edited. While He maintains his own experiment was concerned with improving the health of the twin girls by making them HIV-resistant, the experiment was deemed reckless and ethically wrong and the potential consequences overlooked. Recent research suggests that the deletion He created in the CCR5 gene may affect brain activity, after a study in mice showed that blocking CC5 improves cognition and recovery from stroke.

In January 2019, the Chinese government said that He acted both unlawfully and unethicallyand would face charges. He was later dismissed by his university.

Jiankui He claimed to have created the world's first gene-edited babies.

The most recent International Summit for Human Genome Editing, in November 2018, concluded, as it did in 2015, "the scientific understanding and technical requirements for clinical practice remain too uncertain and the risks too great to permit clinical trials of germline editing at the time."

He's work, which remains unpublished, heralds the first clinical trial and birth of genetically modified human beings -- which means, whether it was the intention or not, a new era for CRISPR has begun.

As the revolution surges forward, the greatest challenges will continue to be effective oversight and regulation of the technology, the technical hurdles that science must overcome to ensure it is precise and safe, and managing the larger societal concerns of tinkering with the stuff that makes usus.

CRISPR continues to make headlines as scientists refine its specificity and turn it toward myriad genetic diseases. On Feb. 4, researchers at UC Berkeley, including CRISPR pioneer Jennifer Douda, revealed that another enzyme, CasX, could be used to edit genes in place of Cas9.

The scientists identified CasX in a ground-dwelling bacteria not normally present in humans, which means our immune systems are less likely to rebel against it. Because it's smaller and potentially more specific than Cas9, it can clip genes with greater success and less chance of any negative effects.

Then, on Feb. 18, scientists at UC San Francisco revealedthey had used CRISPR to make stem cells "invisible" to the immune system. Stem cells are able to mature into adult cells of any tissue, so they have been proposed as a way to repair damaged organs. However, the immune system typically tries to annihilate any foreign invader and stem cells are seen as such. CRISPR has enabled the stem cells to evade the immune system so they can get to work at healing.

Only a day later, researchers at the Salk Institute for Biological Sciencespublished in Nature Medicine their findings on a CRISPR therapy for Hutchinson-Gilford progeria, a disease associated with rapid aging. The disease is caused by a genetic mutation that results in a buildup of abnormal proteins, ultimately leading to premature cell death. A single dose of CRISPR/Cas9 was shown to suppress the disease in a mouse model, paving the way for further exploration of CRISPR's therapeutic potential.

And still more CRISPR success stories continue to roll in. On Feb. 25, CRISPR Therapeutics, a company co-founded by CRISPR visionary Emmanuelle Charpentier, announced thatthe first human patients had been infused with a CRISPR/Cas9 drug to treat the disease beta-thalassemia. The illness is caused by a genetic mutation that results in red blood cells being unable to create the oxygen-transport molecule haemoglobin. To combat this, the CRISPR Therapeutics team takes stem cells from a patient, edits them with CRISPR/Cas9 outside the body to increase haemoglobin production and then transfuses them back into the bloodstream. The company plans to use a similar approach to treating the blood disease known as sickle cell anemia.

CRISPR research is advancing at a rapid pace, and it can be hard to keep up. In only seven years, CRISPR went from an evolutionary adaptation in bacteria to a gene-editing tool that created the very first genetically modified human beings. We've already seen CRISPR transform the entire field of molecular biology and that effect has rippled across the biological and medical fields.

First published, Jan. 23, 2019.Update, on Feb. 28 5 a.m. PT: Adds recent advances section

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Start genome editing with CRISPR-Cas9 | idtdna.com

Alt-R CRISPR-Cas9 System

Simple delivery of ribonucleoprotein complexes (crRNA:tracrRNA:Cas9 or sgRNA:Cas9).

CRISPR-Cas9 genome editing methods use a Cas9 endonuclease to generate double-stranded breaks in DNA. Cas9 endonuclease requires a CRISPR RNA (crRNA) to specify the DNA target sequence, and the crRNA must be combined with the transactivating crRNA (tracrRNA) to activate the endonuclease and create a functional editing ribonucleoprotein complex (Figure 1A). In an alternative approach, the crRNA and tracrRNA can be delivered as a single RNA oligonucleotide (Figure 1B). After cleavage, DNA is then repaired by non-homologous end-joining (NHEJ) or homology-directed recombination (HDR), resulting in a modified sequence. Alt-R CRISPR-Cas9 reagents and kits provide essential, optimized tools needed to use this pathway for genome editing research.

Option 1: Alt-R CRISPR-Cas9 crRNA:tracrRNA

Alt-R CRISPR-Cas9 crRNA

Alt-R CRISPR-Cas9 tracrRNA

The Alt-R CRISPR-Cas9 System offers two options for generating synthetic guide RNAs. The two-part system pairs an optimized, shortened universal tracrRNA oligonucleotide (67 nt) with an optimized, shortened, target-specific crRNA oligonucleotide (36 nt) for improved targeting of Cas9 to dsDNA targets (Figure 2). The single guide RNA (sgRNA) option combines the crRNA and tracrRNA segments into one long RNA molecule, reducing the number of components and simplifying the CRISPR workflow.

While delivering Cas9 nuclease as part of an RNP is the preferred method, the Alt-R CRISPR-Cas9 System is also compatible with S. pyogenes Cas9 from any source, including cells that stably express S. pyogenes Cas9 endonuclease, or when Cas9 is introduced as a DNA or mRNA construct.

All Alt-R CRISPR-Cas9 crRNAs are 3536 nt RNA oligos containing the 19 or 20 nt target-specific protospacer region, along with the 16 nt tracrRNA fusion domain. We recommend 20 nt protospacers for most applications. crRNAs must be duplexed with Alt-R CRISPR-Cas9 tracrRNA before RNP complex formation.

Alt-R CRISPR-Cas9 crRNAs are synthesized with proprietary chemical modifications, which protect the crRNA from degradation by cellular RNases and further improve on-target editing performance. When using 2-part gRNAs under highly challenging conditions (e.g., high nuclease environments or with Cas9 mRNA), use Alt-R CRISPR-Cas9 crRNA XT, which have additional chemical modifications for the highest level of stability and performance.

We guarantee* our predesigned guide RNAs targeting human, mouse, rat, zebrafish, or nematode genes. For other species, you may use our proprietary algorithms to design custom guide RNAs. If you have protospacer designs of your own or from publications, use our design checker tool to assess their on- and off-targeting potential before ordering guide RNAs that are synthesized using our Alt-R guide RNA modifications.

The 67 nt Alt-R tracrRNA is much shorter than the classical 89 bases of the natural S. pyogenes tracrRNA. We find that shortening the tracrRNA increases on-target performance. Alt-R CRISPR tracrRNA also contains proprietary chemical modifications that confer increased nuclease resistance.

Alt-R CRISPR-Cas9 tracrRNA labeled with ATTO 550 (ATTO-TEC) provide the same function as their unlabeled counterparts. However, the fluorescent dye allows you to monitor transfection or electroporation efficiency during preliminary experiments to optimize transfection conditions in your cell types (Figure 3).

Labeled tracrRNAs can also help concentrate transfected cells via FACS (fluorescence-activated cell sorting) analysis, which can simplify your screening process for cells with CRISPR events. (For more information and tips on using Alt-R CRISPR-Cas9 tracrRNA ATTO 550, see the application note.)

Alt-R CRISPR tracrRNA orders include Nuclease-Free Duplex Buffer for forming the complex between crRNA and tracrRNA oligos. Alt-R tracrRNA can be ordered in larger scale and paired with all of your target specific crRNAs, allowing for an easy and a cost-effective means of studying many CRISPR sites.

Alt-R CRISPR-Cas sgRNA

Alt-R CRISPR-Cas9 sgRNAs are long RNA oligonucleotides (99100 bases) containing the target-specific crRNA region and the Cas9-interacting tracrRNA region within a single molecule (i.e., 1920 base protospacer region and 80-base universal sgRNA region). Like other Alt-R RNAs, it contains chemical modifications to stabilize the RNA, increasing resistance to nuclease activity. For challenging conditions (e.g., high nuclease environments or with Cas9 mRNA), sgRNAs may provide increased potency.

The Alt-R S.p. Cas9 Nuclease V3 enzyme is a high purity, recombinant S. pyogenes Cas9. The enzymes include nuclear localization sequences (NLSs) and C-terminal 6-His tags. The S. pyogenes Cas9 enzyme must be combined with a gRNA to produce a functional, target-specific editing complex. For the best editing, combine the Alt-R S.p. Cas9 Nuclease V3 enzyme with the optimized Alt-R CRISPR gRNA in equimolar amounts.

The Alt-R S.p. HiFi Cas9 Nuclease V3 offers improved specificity over wild-type Cas9, greatly reducing the risk of off-target cutting events. This Cas9 variant also preserves the high level of editing efficiency expected from a Cas9 nuclease, maintaining 90100% on-target editing activity at most sites. For applications that are sensitive to off-target events, combining the Alt-R S.p. HiFi Cas9 Nuclease V3 with optimized Alt-R CRISPR-Cas9 gRNA (crRNA:tracrRNA) is highly recommended.

Cas9 nickases allow specific cutting of only one strand at the DNA target site. Cuts to both strands of DNA are accomplished by using either Alt-R S.p. Cas9 D10A Nickase V3 or Alt-R S.p. Cas9 H840A Nickase V3, with 2 gRNAs that target two neighboring Cas9 sites, one on either strand of the target region. This functionally increases the length of the recognition sequence from 20 to 40 bases. For more information about using Cas9 nickases, see the application note.

Alt-R S.p. dCas9 Protein V3 has mutations that result in the loss of nuclease activity. This protein can form RNP complexes with Alt-R gRNAs and bind to the target region specified by the gRNA without cutting the DNA.

In some cases, transfection of RNP or the creation of stably transfected cells is not possible. In those applications, AltR S.p. Cas9 Expression Plasmid is designed to provide expression of Cas9 endonuclease under CMV promoter control. Note that the plasmid contains no eukaryotic selectable marker, making expression of S.p. Cas9 transient. The Alt-R CRISPR-Cas9 System Plasmid User Guide provides instructions for using this plasmid.

Optional controls for human, mouse, and rat are available for the 2-part Alt-R CRISPR-Cas9 System.

We recommend using the appropriate Alt-R CRISPR-Cas9 Control Kit for studies in human, mouse, or rat cells. The control kits include an Alt-R CRISPR HPRT Positive Control crRNA targeting the HPRT (hypoxanthine phosphoribosyltransferase) gene and a computationally validated Alt-R CRISPR-Cas9 Negative Control crRNA. The kit also includes the Alt-R CRISPR-Cas9 tracrRNA for complexing with the crRNA controls, Nuclease-Free Duplex Buffer, and validated PCR primers for amplifying the targeted HPRT region in the selected organism. The inclusion of the PCR assay makes the kits ideal for verification of HPRT modification using the Alt-R Genome Editing Detection Kit.

Alt-R control kit components can also be ordered individually.

For information about sgRNA controls, contact applicationsupport@idtdna.com.

If you are studying primary or hard-to-transfect cells, electroporation is often a viable alternative to lipid-based transfection in CRISPR experiments. The Alt-R Cas9 Electroporation Enhancer is a Cas9-specific carrier DNA that is optimized to work with the Amaxa Nucleofector device (Lonza) and Neon System (Thermo Fisher) to increase transfection efficiency and thereby increase genome editing efficiency (Figure 4).

Alt-R HDR Enhancer is a small molecule compound that increases homology-directed repair. Alt-R HDR Enhancer exhibits its activity in multiple cell lines, including both adherent and suspension cell lines. Its activity is independent of the enzyme employed; for example, it can be used either with Alt-R S.p. Cas9 Nuclease V3 or Alt-R A.s. Cas12a (Cpf1) Nuclease V3.This versatile reagent is also compatible with electroporation and lipofection methods.

Use this kit to detect on-target genome editing and estimate genome editing efficiency in CRISPR experiments. Learn more >>

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Hypopituitarism | Johns Hopkins Medicine

What is hypopituitarism?Hypopituitarism happens when your pituitary gland is not active enough. The front lobe of the gland may only partly work. Or it may not work at all. As a result the gland does not make enough hormones.What causes hypopituitarism?

Causes of hypopituitarism can directly affect the pituitary gland. Or they can indirectly affect the glandthrough changes inthe hypothalamus. Direct causes are:

Indirect causes are:

Symptoms are different for each person. They happen over time or right away. They depend on which hormones the pituitary gland is not making enough of. The following are common symptoms linked to certain hormones:

These symptoms may look like other health problems. Always see your health care provider for a diagnosis.

Your health care provider will ask about your past health. You will also need an exam. Other tests you may need:

Your health care provider will figure out the best treatment for you based on:

Treatment of hypopituitarism depends on what is causing it. The goal of treatment is have the pituitary gland work as it should. Treatment may include:

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Female genetic hair loss? | Yahoo Answers

In women, hair loss usually begins at menopause. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, there has been rare cases reported, in which hair loss affects women as young as 15 or 16. However, unlike with men, hair loss in women typically begins later and is generally not to the full-head state that is generally seen in men.

Balding is genetic and hereditary, and it's thereby logical to think that by looking at family members can be helpful in determining the fate of one's hairline. Sometime it is the case that grandson and maternal grandfather will end up with the similar hairlines, but it's not that foolproof, not the ultimate reference point it's treated as, so better not to consider it at all when wondering if the baldness gene is one you have inherited. Genetic hair loss affects both men and women equally.

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hypogonadism | Definition, Causes, Symptoms, & Treatment …

Hypogonadism, in men, decreased testicular function that results in testosterone deficiency and infertility.

Hypogonadism is caused by hypothalamic, pituitary, and testicular diseases. Hypothalamic and pituitary diseases that may cause decreased testicular function include tumours and cysts of the hypothalamus, nonsecreting and prolactin-secreting pituitary tumours, trauma, hemochromatosis (excess iron storage), infections, and nonendocrine disorders, such as chronic illness and malnutrition. The primary testicular disorders that result in hypogonadism in postpubertal men include Klinefelter syndrome and related chromosomal disorders, although these disorders usually manifest at the time of puberty.

Other causes of hypogonadism in men include testicular inflammation (orchitis) caused by mumps; exposure to gonadal toxins, including alcohol, marijuana, and several anticancer drugs (e.g., cyclophosphamide, procarbazine, and platinum); and radiation with X-rays. Many of the disorders that cause delayed puberty are sufficiently mild that affected men do not seek care until well into adult life. This particularly applies to those disorders that decrease spermatogenesis and therefore fertility but spare Leydig cell function.

The clinical manifestations of hypogonadism in adult men include decreased libido, erectile dysfunction (inability to have or maintain an erection or to ejaculate), slowing of facial and pubic hair growth and thinning of hair in those regions, drying and thinning of the skin, weakness and loss of muscle mass, hot flashes, breast enlargement, infertility, small testes, and osteoporosis (bone thinning). The evaluation of men suspected to have hypogonadism should include measurements of serum testosterone, luteinizing hormone, follicle-stimulating hormone, and prolactin, in addition to the analysis of semen. Men with hypogonadism who have decreased or normal serum gonadotropin concentrations are said to have hypogonadotropic hypogonadism and may need to be evaluated for hypothalamic or pituitary disease with computerized axial tomography or magnetic resonance imaging (MRI) of the head. Men with hypogonadism who have increased serum gonadotropin concentrations are said to have hypergonadotropic hypogonadism, and their evaluation should be focused on the causes of testicular disease, including chromosomal disorders.

Men with hypogonadism caused by a hypothalamic disorder, pituitary disorder, or testicular disorder, such as Klinefelter syndrome, are treated with testosterone, which may be injected, applied transdermally (i.e., as a skin patch), or taken orally. Testosterone treatment reverses many of the symptoms and signs of hypogonadism but will not increase sperm count. Sperm count cannot be increased in men with testicular disease, although it is sometimes possible to increase sperm count in men with hypothalamic or pituitary disease by prolonged administration of gonadotropin-releasing hormone or gonadotropins. In men with testicular disease, viable sperm can sometimes be obtained by aspiration from the testes for in vitro fertilization.

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Human iPS cell-derived dopaminergic neurons function in a …

Kriks, S. et al. Dopamine neurons derived from human ES cells efficiently engraft in animal models of Parkinsons disease. Nature 480, 547551 (2011)

Doi, D. et al. Isolation of human induced pluripotent stem cell-derived dopaminergic progenitors by cell sorting for successful transplantation. Stem Cell Reports 2, 337350 (2014)

Perrier, A. L. et al. Derivation of midbrain dopamine neurons from human embryonic stem cells. Proc. Natl Acad. Sci. USA 101, 1254312548 (2004)

Chambers, S. M. et al. Highly efficient neural conversion of human ES and iPS cells by dual inhibition of SMAD signaling. Nat. Biotechnol. 27, 275280 (2009)

Kirkeby, A. et al. Generation of regionally specified neural progenitors and functional neurons from human embryonic stem cells under defined conditions. Cell Reports 1, 703714 (2012)

Doi, D. et al. Prolonged maturation culture favors a reduction in the tumorigenicity and the dopaminergic function of human ESC-derived neural cells in a primate model of Parkinsons disease. Stem Cells 30, 935945 (2012)

Hargus, G. et al. Differentiated Parkinson patient-derived induced pluripotent stem cells grow in the adult rodent brain and reduce motor asymmetry in Parkinsonian rats. Proc. Natl Acad. Sci. USA 107, 1592115926 (2010)

Nguyen, H. N. et al. LRRK2 mutant iPSC-derived DA neurons demonstrate increased susceptibility to oxidative stress. Cell Stem Cell 8, 267280 (2011)

Snchez-Dans, A. et al. Disease-specific phenotypes in dopamine neurons from human iPS-based models of genetic and sporadic Parkinsons disease. EMBO Mol. Med. 4, 380395 (2012)

Kikuchi, T. et al. Idiopathic Parkinsons disease patient-derived induced pluripotent stem cells function as midbrain dopaminergic neurons in rodent brains. J. Neurosci. Res. 95, 18291837 (2017)

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Imbert, C., Bezard, E., Guitraud, S., Boraud, T. & Gross, C. E. Comparison of eight clinical rating scales used for the assessment of MPTP-induced parkinsonism in the Macaque monkey. J. Neurosci. Methods 96, 7176 (2000)

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Hallett, P. J. et al. Successful function of autologous iPSC-derived dopamine neurons following transplantation in a non-human primate model of Parkinsons disease. Cell Stem Cell 16, 269274 (2015)

Freed, C. R. et al. Transplantation of embryonic dopamine neurons for severe Parkinsons disease. N. Engl. J. Med. 344, 710719 (2001)

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Li, W. et al. Extensive graft-derived dopaminergic innervation is maintained 24 years after transplantation in the degenerating parkinsonian brain. Proc. Natl Acad. Sci. USA 113, 65446549 (2016)

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Smith, S. M. Fast robust automated brain extraction. Hum. Brain Mapp. 17, 143155 (2002)

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Jucaite, A., Fernell, E., Halldin, C., Forssberg, H. & Farde, L. Reduced midbrain dopamine transporter binding in male adolescents with attention-deficit/hyperactivity disorder: association between striatal dopamine markers and motor hyperactivity. Biol. Psychiatry 57, 229238 (2005)

Leroy, C. et al. Assessment of 11C-PE2I binding to the neuronal dopamine transporter in humans with the high-spatial-resolution PET scanner HRRT. J. Nucl. Med. 48, 538546 (2007)

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Sossi, V., Holden, J. E., de la Fuente-Fernandez, R., Ruth, T. J. & Stoessl, A. J. Effect of dopamine loss and the metabolite 3-O-methyl-[18F]fluoro-dopa on the relation between the 18F-fluorodopa tissue input uptake rate constant Kocc and the [18F]fluorodopa plasma input uptake rate constantKi. J. Cereb. Blood Flow Metab. 23, 301309 (2003)

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Stem Cells from Fat vs. Bone Marrow Best Sources for …

Stromal vascular fraction was dramatically better than bone marrow concentrate in its ability to differentiate into cartilage.Two other important features were also well documented in this study. SVF created significantly more colony forming units than BMC, another significant predictor of healing response. Perhaps most importantly, SVF was dramatically better than BMC in its ability to differentiate into cartilage.

Second, a study by Han Chao et al has also demonstrated that fat derived stem cells also have a higher proliferation potential for neural tissue and are a better source for not only cartilage regeneration but also for nervous system regeneration.

The studies gave a very comprehensive look at comparing BMC and SVF in the ability to repair cartilage damage in a same procedure protocol. Every significant measurement comparing bone marrow to adipose tissue for stem cell harvesting demonstrated that adipose derived stem cells provided better cell content and superior ability to differentiate into cartilage than bone marrow. Our extensive clinical experience with the procedure for Colorado patients suffering from pain in the knees, other joints, soft tissue, and a wide range of back problems clearly demonstrates the same.

Using the most effective combination of autologous stem cell sources is one of several criteria to identify a legitimate stem cell clinic. Other important characteristics we recommend paying attention to when choosing a stem cell clinic, include the presence of a physician who owns and operates the clinic, X-ray guided injections administered by a trained injection specialist, and a clinic that takes time to discuss your questions. A review of your imaging and clinical data is needed in order to determine if stem cell therapy is right for you.

*Individual patient results may vary. Contact us today to find out if stem cell therapy may be able to help you.

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Stem Cells from Fat vs. Bone Marrow Best Sources for ...

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Supplements Archives – Dr. Jolene Brighten

This web site offers health, wellness, fitness and nutritional information and is provided for informational purposes only. This information is not intended as a substitute for the advice provided by your physician or other healthcare professional. You should not rely on this information as a substitute for, nor does it replace, professional medical advice, diagnosis, or treatment, Always speak with your physician or other healthcare professional before taking any medication or nutritional, herbal or homeopathic supplement, or using any treatment for a health problem. If you have or suspect that you have a medical problem, contact your health care provider promptly. Do not disregard professional medical advice or delay in seeking professional advice because of something you have read on this web site. The use of any information provided on this web site is solely at your own risk. Nothing stated or posted on this web site or available through any services offered by Dr. Jolene Brighten, ND and Brighten Wellness, LLC, are intended to be, and must not be taken to be, the practice of medicine. Information provided on this web site DOES NOT create a doctor-patient relationship between you and any doctor affiliated with our web site. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease.

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2009 Dr. Jolene Brighten.

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Supplements Archives - Dr. Jolene Brighten

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NSGC > Genetic Testing > About Genetic Testing

There are thousands of genetic tests, meaning we can test for many of these genetic mutations. But there are also many mutations that we dont have tests for.

Whether or not to have genetic testing is complicated. What will it tell you? What will you do about it once you get the results? Will having that information help you or not? Thats why the insight and guidance provided by a genetic counselor is invaluable. A genetic counselor can explain the different types of tests available and what they may and may not tell you as well as how they may or may not help you.

Genetic tests are generally performed as part of your clinical care. However, there are times when you may be offered one or more genetic tests as part of a research study. If this is the case, the genetic counselor or study staff will review the study in detail so that you can decide whether or not to participate

View thisresourcethat includes helpful information and critical points to consider throughout the genetic testing process.

Find a Genetic Counselor

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Male and female ability differences down to socialisation …

It is the mainstay of countless magazine and newspaper features. Differences between male and female abilities from map reading to multi-tasking and from parking to expressing emotion can be traced to variations in the hard-wiring of their brains at birth, it is claimed.

Men instinctively like the colour blue and are bad at coping with pain, we are told, while women cannot tell jokes but are innately superior at empathising with other people. Key evolutionary differences separate the intellects of men and women and it is all down to our ancient hunter-gatherer genes that program our brains.

The belief has become widespread, particularly in the wake of the publication of international bestsellers such as John Gray's Men Are from Mars, Women Are from Venus that stress the innate differences between the minds of men and women. But now a growing number of scientists are challenging the pseudo-science of "neurosexism", as they call it, and are raising concerns about its implications. These researchers argue that by telling parents that boys have poor chances of acquiring good verbal skills and girls have little prospect of developing mathematical prowess, serious and unjustified obstacles are being placed in the paths of children's education.

In fact, there are no major neurological differences between the sexes, says Cordelia Fine in her book Delusions of Gender, which will be published by Icon next month. There may be slight variations in the brains of women and men, added Fine, a researcher at Melbourne University, but the wiring is soft, not hard. "It is flexible, malleable and changeable," she said.

In short, our intellects are not prisoners of our genders or our genes and those who claim otherwise are merely coating old-fashioned stereotypes with a veneer of scientific credibility. It is a case backed by Lise Eliot, an associate professor based at the Chicago Medical School. "All the mounting evidence indicates these ideas about hard-wired differences between male and female brains are wrong," she told the Observer.

"Yes, there are basic behavioural differences between the sexes, but we should note that these differences increase with age because our children's intellectual biases are being exaggerated and intensified by our gendered culture. Children don't inherit intellectual differences. They learn them. They are a result of what we expect a boy or a girl to be."

Thus boys develop improved spatial skills not because of an innate superiority but because they are expected and are encouraged to be strong at sport, which requires expertise at catching and throwing. Similarly, it is anticipated that girls will be more emotional and talkative, and so their verbal skills are emphasised by teachers and parents.

The latter example, on the issue of verbal skills, is particularly revealing, neuroscientists argue. Girls do begin to speak earlier than boys, by about a month on average, a fact that is seized upon by supporters of the Men Are from Mars, Women Are from Venus school of intellectual differences.

However, this gap is really a tiny difference compared to the vast range of linguistic abilities that differentiate people, Robert Plomin, a professor at the Institute of Psychiatry in London, pointed out. His studies have found that a mere 3% of the variation in young children's verbal development is due to their gender.

"If you map the distribution of scores for verbal skills of boys and of girls you get two graphs that overlap so much you would need a very fine pencil indeed to show the difference between them. Yet people ignore this huge similarity between boys and girls and instead exaggerate wildly the tiny difference between them. It drives me wild," Plomin told the Observer.

This point is backed by Eliot. "Yes, boys and girls, men and women, are different," she states in a recent paper in New Scientist. "But most of those differences are far smaller than the Men Are from Mars, Women Are from Venus stereotypes suggest.

"Nor are the reasoning, speaking, computing, emphasising, navigating and other cognitive differences fixed in the genetic architecture of our brains.

"All such skills are learned and neuro-plasticity the modifications of neurons and their connections in response experience trumps hard-wiring every time."

The current popular stress on innate intellectual differences between the sexes is, in part, a response to psychologists' emphasis of the environment's importance in the development of skills and personality in the 1970s and early 1980s, said Eliot. This led to a reaction against nurture as the principal factor in the development of human characteristics and to an exaggeration of the influence of genes and inherited abilities. This view is also popular because it propagates the status quo, she added. "We are being told there is nothing we can do to improve our potential because it is innate. That is wrong. Boys can develop powerful linguistic skills and girls can acquire deep spatial skills."

In short, women can read maps despite claims that they lack the spatial skills for such efforts, while men can learn to empathise and need not be isolated like Mel Gibson's Nick Marshall, the emotionally retarded male lead of the film What Women Want and a classic stereotype of the unfeeling male that is perpetuated by the supporters of the hard-wired school of intellectual differences.

This point was also stressed by Fine. "Many of the studies that claim to highlight differences between the brains of males and females are spurious. They are based on tests carried out on only a small number of individuals and their results are often not repeated by other scientists. However, their results are published and are accepted by teachers and others as proof of basic differences between boys and girls.

"All sorts of ridiculous conclusions about very important issues are then made. Already sexism disguised in neuroscientific finery is changing the way children are taught."

So should we abandon our search for the "real" differences between the sexes and give up this "pernicious pinkification of little girls", as one scientist has put it?

Yes, we should, Eliot insisted. "There is almost nothing we do with our brains that is hard-wired. Every skill, attribute and personality trait is moulded by experience."

Cambridge University psychologist and autism expert Simon Baron-Cohen:

"The female brain is predominantly hard-wired for empathy. The male brain is predominantly hard-wired for understanding and building systems"

Writer and feminist Joan Smith:

"Very few women growing up in England in the late 18th century would have understood the principles of jurisprudence or navigation because they were denied access to them"

John Gray, author of Men are from Mars, Women are from Venus:

"A man's sense of self is defined through his ability to achieve results. A woman's sense of self is defined through her feelings and the quality of her relationships"

Sociologist Beth Hess:

"For two millennia, 'impartial experts' have given us such trenchant insights as the fact that women lack sufficient heat to boil the blood and purify the soul, that their heads are too small, their wombs too big, their hormones too debilitating, that they think with their hearts or the wrong side of the brain. The list is never-ending"

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Male and female ability differences down to socialisation ...

Recommendation and review posted by Bethany Smith

Advanced maturation of human cardiac tissue grown from …

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Advanced maturation of human cardiac tissue grown from ...

Recommendation and review posted by Bethany Smith

Addgene: CRISPR Pooled gRNA Libraries

Bassik Human CRISPR Knockout Library 101926 101934 Knockout Human Bassik 3rd 10 Varies Bassik Mouse CRISPR Knockout Library 1000000121 1000000130 Knockout Mouse Bassik 3rd 10 Varies Activity-optimized genome-wide library Discontinued Knockout Human Sabatini and Lander 3rd 10 178,896 Activity-optimized genome-wide library 1000000100 Knockout Human Sabatini and Lander 3rd 10 187,535 Broad GPP genome-wide Brunello 73179 (1 plasmid)73178 (2 plasmid) Knockout Human Doench and Root 3rd 4 76,441 Broad GPP genome-wide Brie 73632 (1 plasmid)73633 (2 plasmid) Knockout Mouse Doench and Root 3rd 4 78,637 Broad GPP kinome Brunello 75314, 75315 (1 plasmid)75312, 75313(2 plasmid) Knockout Human Doench and Root 3rd 4 3,052 Broad GPP kinome Brie 75317 (1 plasmid)75316 (2 plasmid) Knockout Mouse Doench and Root 3rd 4 2,852 Broad GPP activation Calabrese p65-HSF 92379 (Set A)92380 (Set B) Activation Human Doench and Root 3rd 36 56,762 (Set A)56,476 (Set B) Broad GPP activation Caprano p65-HSF 92383 (Set A)92384 (Set B) Activation Mouse Doench and Root 3rd 36 67,187 (Set A)66,889 (Set B) Broad GPP inhibition Dolcetto 92385 (Set A)92386 (Set B) Inhibition Human Doench and Root 3rd 36 57,050 (Set A)57,011 (Set B) Broad GPP inhibition Dolomiti 104090 (Set A)104091 (Set B) Inhibition Mouse Doench and Root 3rd 36 67,366 (Set A)67,194 (Set B) Cas13a/C2c2 Protospacer flanking site (PFS) Library 79153 Knockout E. coli Zhang N/A N/A - The protospacers contained in the library represent all 4096 (46) combinations of 6 nucleotides. N/A CRiNCL - Human CRISPRi Non-coding Libraries 86538 86550 Inhibition Human Weissman 3rd 10 Varies CRISPR/Cas9-assisted Removal of Mitochondrial DNA (CARM) Library 82480 Knockout Mouse Xie N/A N/A 395 CRISPRa Discontinued Activation Human Weissman 3rd 10 198,810 CRISPRa-v2 839781000000091 Activation Human Weissman 3rd 510 104,540209,080 CRISPRa-v2 839961000000093 Activation Mouse Weissman 3rd 510 107,105214,210 CRISPRi Discontinued Inhibition Human Weissman 3rd 10 206,421 CRISPRi-v2 839691000000090 Inhibition Human Weissman 3rd 510 104,535209,070 CRISPRi-v2 839871000000092 Inhibition Mouse Weissman 3rd 510 107,415214,830 Enriched subpools (kinase, nuclear, ribosomal, cell cycle) 51043 51048 Knockout Human Sabatini and Lander 3rd 10 Varies Focused Ras Synthetic Lethal Human CRISPR Knockout Library 92352 Knockout Human Sabatini and Lander 3rd 50 6,661 hCRISPRa-v2 subpooled libraries 83980 83986 Activation Human Weissman 3rd 5 Varies hCRISPRi-v2 subpooled libraries 83971 83977 Inhibition Human Weissman 3rd 5 Varies mCRISPRa-v2 subpooled libraries 83998 84004 Activation Mouse Weissman 3rd 5 Varies mCRISPRi-v2 subpooled libraries 83989 83995 Inhibition Mouse Weissman 3rd 5 Varies Human CRISPR Knockout Library 1000000132 Knockout Human X.S. Liu 3rd 10 185,634 Human GeCKO v2 1000000048 (1 plasmid)1000000049 (2 plasmid) Knockout Human Zhang 3rd 6 123,411 Human genome-wide library v1 69763 Knockout Human Wu 3rd 4 77,406 Human improved genome-wide library v1 67989 Knockout Human Yusa 3rd 5 90,709 Human CRISPR lncRNA Activation Pooled Library 1000000106 Activation Human Zhang 3rd 10 96,458 Human CRISPR Metabolic Gene Knockout Library 110066 Knockout Human Sabatini 3rd 10 30,290 Human miRNA CRISPR Knockout Library 112200 Knockout Human Lin 3rd 4-5 8,382 Human Paired-guide RNA (pgRNA) Library for Long Non-coding RNAs (lncRNAs) 89640 Knockout Human Wei 3rd Varies 12,472 pairs Mouse GeCKO v2 1000000052 (1 plasmid)1000000053(2 plasmid) Knockout Mouse Zhang 3rd 6 130,209 Mouse genome-wide library v1 Discontinued Knockout Mouse Yusa 3rd 5 87,897 Mouse improved genome-wide library v2 67988 Knockout Mouse Yusa 3rd 5 90,230 Oxford Fly 64750 Knockout D. melanogaster Liu N/A 3 40,279 Perturb-seq Guide Barcodes (GBC) 85968 Barcode Human Weissman 3rd N/A N/A SAM v1 - 3 plasmid system 1000000057 (Zeocin)1000000074 (Puromycin) Activation Human Zhang 3rd 3 70,290 SAM v1 - 3 plasmid system 1000000075 (Puromycin) Activation Mouse Zhang 3rd 3 69,716 SAM v2 - 2 plasmid system 1000000078 (Blasticidin) Activation Human Zhang 3rd 3 70,290 Toronto KnockOut - Version 1 1000000069 Knockout Human Moffat 3rd 12 176,500 Toronto KnockOut - Version 3 90294 Knockout Human Moffat 3rd 4 70,948 Toxoplasma Knockout 80636 Knockout T. gondii Lourido N/A 10 8,158 Two plasmid human activity-optimized genome-wide library 1000000095 Knockout Human Sabatini and Lander 3rd 10 187,536 Two plasmid mouse activity-optimized genome-wide library 1000000096 Knockout Mouse Sabatini and Lander 3rd 10 188,509

Original post:
Addgene: CRISPR Pooled gRNA Libraries

Recommendation and review posted by Bethany Smith

BONE MARROW – Stem Cell International

Inside of our bones is where we find this soft, sponge-like material called bone marrow. This bone marrow is filled with blood-forming stem cells that can either divide and form more blood-forming stem cells, or they can transform into three types of blood cells: white blood cells, red blood cells, or platelets.

This method of stem cell therapy is most commonly used for patients suffering from some types of cancer.

How it Works

There are two types of bone marrow transplants; autologous and allogeneic. An autologous bone marrow transplant is when the stem cells are taken from your own body, while an allogeneic process will use the stem cells from a healthy donor.

The procedure starts with an anesthesia being administered to the patient before a doctor begins harvesting the bone marrow from the hip bone, or sometimes, the sternum. The bone marrow is then moved through a process that removes blood and bone from the marrow. The stem cells are then isolate and will be released into your bloodstream, like a blood transfusion.

Who Can Benefit

The conditions most commonly treated with a bone marrow transplant include:

If you are suffering from any of the above diseases, it doesnt mean you are automatically a candidate for a bone marrow transplant. You need to meet with a physician first to be sure this is the most appropriate treatment for your needs. Here at Stem Cell International, our expert physicians would love to talk with you.

What You Can Expect

If you decide this therapy may be right for you, each one of our patients will meet with a physician to discuss your medical history and desired outcomes of the entire process. This is also important for you and the physician to become more comfortable with each other and be absolutely sure this is the best route for your needs.

Did You Know

If you decide a bone marrow transplant is the best route for your needs, you can expect to see and feel improvements anywhere from 2 to 8 weeks. Although, complete recovery of immune function could take several months.

If youre interested in being treated with a bone marrow transplant at Stem Cell International, one of our stem cell experts would be happy to help you decide. Get in touch today!

Read more here:
BONE MARROW - Stem Cell International

Recommendation and review posted by Bethany Smith


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