Federico Mingozzi: "Translational research in the in vivo gene therapy of monogenic diseases"
Educational Day* at ESGCT Conference in Madrid. Federico Mingozzi - Head of Immunology and Liver Gene Transfer at Gnthon in Paris - talks on "Translationa...

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Federico Mingozzi: "Translational research in the in vivo gene therapy of monogenic diseases" - Video

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Newswise LA JOLLA, CA November 20, 2014 Scientists at The Scripps Research Institute (TSRI) have discovered how one gene is essential to hearing, uncovering a cause of deafness and suggesting new avenues for therapies.

The new study, published November 20 in the journal Neuron, shows how mutations in a gene called Tmie can cause deafness from birth. Underlining the critical nature of their findings, researchers were able to reintroduce the gene in mice and restore the process underpinning hearing.

This raises hopes that we could, in principle, use gene-therapy approaches to restore function in hair cells and thus develop new treatment options for hearing loss, said Professor Ulrich Mller, senior author of the new study, chair of the Department of Molecular and Cellular Neuroscience and director of the Dorris Neuroscience Center at TSRI.

The Gene Responsible

The ear is a complex machine that converts mechanical sound waves into electric signals for the brain to process. When a sound wave enters the ear, the uneven ends (stereocilia) of the inner ears hair cells are pushed back, like blades of grass bent by a heavy wind. The movement causes tension in the strings of proteins (tip links) connecting the stereocilia, which sends a signal to the brain through ion channels that run through the tips of the hair cell bundles.

This process of converting mechanical force into electrical activity, called mechanotransduction, still poses many mysteries. In this case, researchers were in the dark about how signals were passed along the tip links to the ion channels, which shape electrical signals.

To track down this unknown component, researchers in the new study built a library of thousands of genes with the potential to affect mechanotransduction.

The team spent six months screening the genes to see if the proteins the genes produced interacted with tip link proteins. Eventually, the team found a gene, Tmie, whose protein, TMIE, interacts with tip link proteins and connects the tip links to a piece of machinery near the ion channel.

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TSRI Researchers Find How Mutant Gene Can Cause Deafness

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Kilian Before After Stemlogix Stem Cell Therapy
dog with arthritis treated with autologous stem cells.

By: mark Greenberg

Excerpt from:
Kilian Before & After Stemlogix Stem Cell Therapy - Video

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By: Adam Feuerstein | 11/18/14 - 10:16 AM EST

Inject a cocktail of undifferentiated stem cellsinto a patient who has suffered a heart attack, and days or even weekslater, the stem cells transform into cardiac cells and rebuild the damaged heart muscle. Months later, the patient has a "new" healthy heart.It's a great story. But so far, the proof remains elusive though not for a lack of trying.

The latest company to fulfill this ambitious scenario is NeoStem (NBS) which presented disappointing (but not surprising) results from a small study of its proprietary cardiac stem-cell therapy NBS10 at the American Heart Association annual meeting Monday. NeoStem tried to put some positive spin on the bad news but shares are down 25% to $5.10.

NBS10, formerly known as AMR-001, is an autologous stem-cell therapy derived from a patient's own bone marrow. When injected back into patients following a heart attack, the stem cells are supposed torestore blood flow, rebuild damaged cardiac muscle and improve function.

Except in NeoStem's study, NBS10 fell short on two primary endpoints designed to assess the therapy's efficacy. The study used non-invasive imaging to assess blood flow through the heart, six months after a single infusion of NBS10 or a placebo. There was no difference between NBS and placebo, NeoStem said.

The study's other co-primary efficacy endpoint was a measurement of adverse cardiac "MACE" events --defined as cardiovascular death, a repeatheart attack, heart failure hospitalization and coronary revascularization. To date, 17% of patientstreated with NBS10 have suffered a MACE event compared to 19% of patients in the placebo arm -- a difference which was not statistically significant.

NeoStem said NBS10 therapy was safe relative to placebo and that no patients treated with the stem cells have died compared to three deaths in the placebo patients. But with only one year of follow up on a small number of patients, any claims about a mortality benefit are clinically meaningless.

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NeoStem's Stem Cell Therapy Fails Mid-Stage Heart Attack Study

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Episode 6.1 Mesoblaste Inc THE STEM CELL REVIEW
Michael SCHUSTER, founding Executive gives a brilliant presentation of Angioblast and Mesoblast, 2 sister biotech companies in Stem Cell. Both companies are using Mesochemal adult precursor...

By: Jean-Loup Romet-Lemonne

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Episode 6.1 Mesoblaste Inc THE STEM CELL REVIEW - Video

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Congestive Heart Failure Treatment Using Stem Cells

Congestive Heart Failureor CHF is a state wherein the heart does not have the capability to properly function as a pump. As a result of the cardiac-malfunction the oxygen pumped into the body is insufficient. Congestive heart failure is generally caused bysimultaneousillnesses. Illnesses that weaken the heart muscle,or diseases that trigger the heart muscles to become stiff, or illnesses that create an increase in oxygen demands for the body which consequently increases the supply for fresh oxygen by the body when the heart is incapable of producing oxygen-rich blood at the level needed.

Congestive heart failure and ishchemic heart disease can have an impact on numerous organs in the body. For instance, the injured areas of the heart directly affected by the sickness does not have the capability to produce enough blood for the kidneys, which then affect their capability to excrete water and salt (sodium). The distressed kidney function may cause the body to retain more fluids than needed by the body. The lungs also may develop pulmonary edema (PE).

PE occurs when the fluid in the lungs diminishes a persons ability to exercise normally. Fluid might likewise accumulate inside the liver, which directly affects it function by impairing the livers capability to create important proteins and also in helping clear the body of harmful elements and/ortoxins. The intestines might also turn out to be much less effective in being able to absorb the vitamins, nutrients and medicines a human needs. The fluids in the body can also accumulate quickly which could result to edema (severe swelling) of the ankles and feet.

An Ejection fraction of 20% would be considered a dangerous level and therefore indicates a highly advanced stage of heart failure. Healthy people usually have ejection fractions in between 52% and 68%.

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Stem Cell Treatment Congestive Heart Failure | CHF Stem ...

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19-Nov-2014

Contact: Lauren Woods lauren.woods@mountsinai.org 646-634-0869 The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc

Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.

"Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack," says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.

In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.

"It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level," says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. "Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure."

cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.

According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the heart's decreased pumping efficiency.

"Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure," says Dr. Fish.

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Delivering stem cells into heart muscle may enhance cardiac repair and reverse injury

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New York, NY (PRWEB) November 19, 2014

Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.

Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack, says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.

In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.

It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level, says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure.

cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.

According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the hearts decreased pumping efficiency.

Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure, says Dr. Fish.

This study adds to the emerging evidence that a small population of adult stem cells can be recruited to the damaged areas of the heart and improve clinical outcomes, says Dr. Hajjar.

Other study co-authors included Kiyotake Ishikawa, MD, Jaume Aguero, MD, Lisa Tilemann, MD, Dongtak Jeong, PhD, Lifan Liang, PhD, Lauren Fish, Elisa Yaniz-Galende, PhD, and Krisztina Zsebo, PhD.

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Delivery of Stem Cells into Heart Muscle After Heart Attack May Enhance Cardiac Repair and Reverse Injury

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Woodland Hills, CA (PRWEB) November 19, 2014

Longtime skincare industry professional Nancy Ryan announces the launch of NR Skin, featuring a line of efficacious products that deliver various skin rejuvenation and age repair benefits for all skin types.

According to Dr. Lisa Benest, Board-certified dermatologist, Burbank, CA, the NR Skin line offers a range of daily skincare and skin rejuvenation products distinguished by high concentrations of powerhouse ingredients that are known for their anti-aging properties, such as antioxidant vitamins and minerals, plant stem cells, lipids, as well as peptides. Dr. Benest notes that NR Skin products offer pure, clean ingredients that feel great on the skin and deliver visible results.

Backed by more than 20 years of skincare industry experience and expertise, NR Skin Founder and CEO Nancy Ryan comments, the creation of NR Skin is a culmination of my lifes work and lifelong passion for excellence in skincare. Im thrilled to help people improve their quality of life by achieving healthy, beautiful skin through such pure and effective products.

Before establishing NR Skin in 2014, Ms. Ryan led Pro-Med Consulting, Inc. for 21 years, which was built upon the core mission of giving dermatologists, plastic surgeons and medical spas a viable way to build their own brand equity and expand their businesses with private label, medical-grade skin care products. Over the years, she developed numerous relationships with leading physicians, whose businesses grew significantly by offering patients her high-performance products that bore each doctors name.

Prior to this successful venture, she worked for two pioneering skin care companies, Ortho Dermatologics, (makers of Retin-A Micro/Renova) and NeoStrata, where she had the opportunity to learn about skin care chemistry and the most effective ways to treat various skin conditions with specific product ingredients.

The NR Skin product line consists of: the following clinically tested products: Age-defying Peptide Cream; Citrus Stem Cell Fusion Cream, Neuro-Peptide Serum. Retinol Complex Treatment Super Antioxidant Cream, Super C Serum Treatment, Comfort Cleanser, Lash Teez Eyelash Growth Serum and Sunscreen Lotion SPF30.

To view products and recommended regimens, visit: http://www.nrskin.com Follow us on Facebook: http://www.facebook.com/nrskin and on Twitter: @nrskincompany

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NR Skin Launches Anti-Aging Product Line

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TIME Health medicine Bubble Boy Disease Cured With Stem Cells Alysia Padilla-Vacarro and daughter Evangelina on the day of her gene therapy treatment. Evangelina, now two years old, has had her immune system restored and lives a healthy and normal life. Courtesy of UCLA Researchers have treated more than two dozen patients with a treatment made from their own bone marrow cells

Alysia Padilla-Vaccaro and Christian Vaccaro owe their daughters life to stem cells. Evangelina, now two, is alive today because she saved herself with her own bone marrow cells.

Evangelina, a twin, was born with a severe immune disorder caused by a genetic aberration that makes her vulnerable to any and all bacteria and viruses; even a simple cold could be fatal. But doctors at University of California Los Angeles (UCLA) Broad Stem Cell Research Center gave her a new treatment, using her own stem cells, that has essentially cured her disease. Shes one of 18 children who have been treated with the cutting-edge therapy, and the studys leader, Dr. Donald Kohn, says that the strategy could also be used to treat other gene-based disorders such as sickle cell anemia.

Known to doctors as adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID), its better known as bubble boy disease, since children born with the genetic disorder have immune systems so weak that they need to stay in relatively clean and germ-free environments. Until Evangelina and her sister Annabella were 11 months old, We were gowned and masked and did not go outside, says their mother Alysia Padilla-Vaccaro. Our children did not physically see our mouths until then because we were masked all the time. We couldnt take them outside to take a breath of fresh air, because there is fungus in the air, and that could kill her.

Both parents wore masks at work to lower the chances they would be exposed to germs that they might bring back home. And they took showers and changed clothes as soon as they entered the house.

MORE: Gene-Therapy Trial Shows Promise Fighting Bubble Boy Syndrome

SCID is caused by a genetic mutation in the ADA gene, which normally produces the white blood cells that are the front lines of the bodys defense against bacteria and viruses. The Vaccaros decided to treat Annabella in the same way that they cared for Evangelina; They were crawling and playing with each other, and every toy they sucked on, they stuck in each others hands and each others mouth, so we couldnt take one outside to have a grand old time and potentially bring something back that could harm her sister, says Padilla-Vaccaro.

The only treatments for SCID are bone marrow transplants from healthy people, ideally a matched sibling; the unaffected cells can then repopulate the immune system of the baby with SCID. But despite being her twin, Annabella wasnt a blood match for her sister, nor were her parents. Padilla-Vaccaro and her husband, Christian, were considering unrelated donors but were concerned about the risk of rejection. We would be trying to fix one problem and getting another, she says.

MORE: Stem Cells Allow Nearly Blind Patients to See

Thats when the doctors at the Childrens Hospital at Orange County, where Evangelina was diagnosed, told her parents about a stem cell trial for SCID babies at UCLA, led by Dr. Donald Kohn. As soon as they said trial, I thought, my kid is dead, says Padilla-Vaccaro of the last resort option. But a dozen children born with other forms of SCIDin which different mutations caused the same weak immune systemswho were successfully treated by Kohn convinced the couple that the therapy was worth trying. Kohn had one spot left in the trial and was willing to hold it for Evangelina until she matured more. Born premature, she was diagnosed at six weeks old and needed more time for what was left of her immune system to catch up to weather the procedure.

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Bubble Boy Disease Cured With Stem Cells

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Kilian Before After Stemlogix Stem Cell Therapy
dog with arthritis treated with autologous stem cells.

By: mark Greenberg

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Kilian Before & After Stemlogix Stem Cell Therapy - Video

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Damian Garcia Olmo: "Clinical trials with mesenchymal stromal cells in wound healing"
Educational Day* at ESGCT Conference in Madrid. Prof. Damin Garca Olmo: "Clinical trials with mesenchymal stromal cells in wound healing" http://iccam.es/prof-damian-garcia-olmo/

By: European Society for Gene and Cell Therapy

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Low back, neck, hip, shoulder, and knee arthritis 7 months after stem cell therapy by Adelson
Spence describes his outcome from his "full-body make-over" by Harry Adelson, N.D.. Seven months ago, Spence had his own bone marrow stem cells injected into his low back, neck, hips, shoulders,...

By: Harry Adelson, N.D.

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Low back, neck, hip, shoulder, and knee arthritis 7 months after stem cell therapy by Adelson - Video

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PUBLIC RELEASE DATE:

19-Nov-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

For years, scientists have considered the laboratory mouse one of the best models for researching disease in humans because of the genetic similarity between the two mammals. Now, researchers at the Stanford University School of Medicine have found that the basic principles of how genes are controlled are similar in the two species, validating the mouse's utility in clinical research.

However, there are important differences in the details of gene regulation that distinguish us as a species.

"At the end of the day, a lot of the genes are identical between a mouse and a human, but we would argue how they're regulated is quite different," said Michael Snyder, PhD, professor and chair of genetics at Stanford. "We are interested in what makes a mouse a mouse and a human a human."

The research effort, Mouse ENCODE, is meant to complement a project called the Encyclopedia of DNA Elements, or ENCODE, that began in 2003. ENCODE studied specific components in the human genome that guide genes to code for proteins that carry out a cell's function, a process known as gene expression. Surrounding the protein-coding genes are noncoding regulatory elements, molecules that regulate gene expression by attaching proteins, called transcription factors, to specific regions of DNA.

Why mice matter

Mouse ENCODE analyzed more than 100 mouse cell types and tissues to annotate the regulatory elements of the mouse genome and compare them to the regulatory elements in the human genome. Both ENCODE and Mouse ENCODE are funded and coordinated by the National Human Genome Research Institute. Because mice are used as model organisms for many human clinical studies and drug discovery, understanding the similarities and differences can help researchers understand how the results found in mouse studies can translate to humans.

"The mindset is when you compare things, it helps understand genome annotation," said Mark Gerstein, PhD, the Albert L. Williams Professor of Biomedical Informatics at Yale University. "It's making the mouse a more meaningful model organism." Gerstein collaborated on previous ENCODE research but is not part of the Mouse ENCODE consortium, which is composed of researchers from more than 30 institutions.

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Stanford researchers compare mammals' genomes to aid human clinical research

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Group 8 PSA Genetic Engineering

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A DNA-editing technique based on bacterial memories could revolutionize medicine. But some worry it could get out of control

The age of genetic engineering began in the 1970s, when Paul Berg spliced DNA from a bacterial virus into a monkey virus and Herbert W. Boyer and Stanley N. Cohen created organisms in which introduced genes remained active for generations. By the late 1970s Boyer's company, Genentech, was churning out insulin for diabetics using Escherichia coli modified to contain a synthetic human gene. And in laboratories around the country, researchers were using transgenic mice to study disease.

These triumphs changed the course of medicine. But the early methods had two big limitations: they were imprecise and hard to scale. Researchers overcame the first limit in the 1990s by designing proteins that could snip specific locations of DNA, a big improvement over inserting DNA into cells at random and hoping for a useful mutation. Yet they still had to devise a new protein tailored to every sequence of DNA that they wanted to targetand that was slow, painstaking work.

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Is the Gene-Editing Revolution Finally Here?

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18-Nov-2014

Contact: Nancy Solomon solomonn@slu.edu 314-977-8017 Saint Louis University

A new treatment for Marfan syndrome, a rare genetic disease that can lead to heart problems, works as well as the currently recommended medical therapy, beta blockers, according to an article in the New England Journal of Medicine.

Angela Sharkey, M.D., professor of pediatrics at Saint Louis University, and a study author, said researchers found losartan, which had been more effective in an animal model of Marfan syndrome, was equally effective to a high dose of the beta blocker atenolol.

"While there may be certain patients who respond better to one drug or another, we found no evidence that losartan is superior to atenolol, a beta blocker currently prescribed for Marfan syndrome," said Sharkey, who was honored earlier this year as the Marfan Foundation's Hero with a Heart. "Losartan appears to be a reasonable alternative treatment for patients who can't take beta blockers, which could give physicians another option to treat a rare and debilitating genetic disease."

Both medications are designed to relax the blood vessels so the heart doesn't have to work as hard to pump blood through the body. Atenolol slows the heart rate, which decreases blood pressure and losartan prevents certain natural substances in the body from tightening the blood vessel walls.

The multi-site, NIH-funded trial followed 608 patients between ages 6 months and 25 years who had enlarged aortas (the main artery carrying blood to the body) for three years. All received either losartan, the investigational medication, or a higher dose of atenolol than is typically prescribed.

Patients in both treatment groups showed no difference in the rate of growth of their aortas.

Additionally, the incidence of aortic-root surgery, aortic dissection, or death did not differ between treatment groups.

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Investigational drug may offer another option to treat Marfan syndrome

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Are people born gay or is it a choice? A new study of gay brothers, the largest to date, adds more scientific evidence that theres a genetic basis for homosexuality.

A genetic analysis of over 409 pairs of gay brothers found that two areas of the human genome, a portion of the X chromosome and a portion of chromosome 8, were associated with the mens sexual orientation. The findings gel with a smaller study conducted in 1993 that implicated the same area of the X chromosome.

Before proceeding, its important to be clear that this study did not discover a gay gene. The regions they identified contain many different genes, so scientists still have a lot of searching to do before finding the specific genes that underlie sexual orientation. With that said, heres how scientists established a broad genetic link.

Over several years, the studys lead author Alan Sanders, of the NorthShore Research Institute in Illinois, collected blood and saliva samples from 409 pairs of gay brothers, including sets of non-identical twins. Then, researchers went through each mans samples looking for unique genetic markers shared by all men in the study.

The 818 men varied in hair color, height, intelligence and other physical attributes. So each man had unique genetic markers matching their unique traits. The one thing they did have in common was that they were all gay. Therefore, if the same genetic variants are found in the same spots in each man, theres reason to believe these places have something to do with sexual orientation.

The two most frequently shared genetic markers were from the Xq28 region on the X chromosome and the 8q12 region on the 8 chromosome. This commonality suggests theres a genetic link for male homosexuality. They published their findings Monday in the journal Psychological Medicine.

One of the primary weaknesses of the study, as pointed out by Sciences Kelly Servick, is that researchers used a type of analysis, genetic linkage, thats been phased out by more precise techniques.

Genetic linkage studies only identify relationships between broad regions that could contain hundreds of different genes. Today, the linkage technique has been replaced by genome-wide association studies, which identify specific genes associated with traits being studied.

According to the Associated Press, other researchers have questioned the data as well:

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Study of Gay Brothers Suggests Genetic Basis of Male Homosexuality

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PUBLIC RELEASE DATE:

18-Nov-2014

Contact: Karen Astle karen.astle@heart.org 214-706-1392 American Heart Association @HeartNews

Adults counseled on their genetic risk of coronary heart disease believe they have more control over their fate, according to research presented at the American Heart Association's Scientific Sessions 2014.

Researchers examined the impact of disclosing risk of 10-year heart disease with or without genetic risk information to 207 patients (48 percent male, average age 58) participating in Myocardial Infarction GENES (MI-GENES), a randomized controlled study.

The study's key elements included a risk score based on established risk factors and a genetic risk score based on 28 single nucleotide polymorphisms; risk disclosure by a genetic counselor in a 30-minute session; and two questionnaires about patient satisfaction - perceived personal control and genetic counseling satisfaction.

Researchers found that patients who received the genetic risk information had a higher perceived personal control value compared to those who didn't (8.85 vs. 8.54). Patients who received genetic risk information also reported a higher genetic counseling satisfaction (9.08 vs. 8.3).

"We have shown that disclosure of genetic risk led to increased perceived personal control and counseling satisfaction, which are associated with the increased likelihood of adopting healthier behaviors that may reduce coronary heart disease risk," said Christopher L. Robinson, lead author of the study. MI-GENES Study information (PDF)

###

Christopher L. Robinson, M.D. candidate at Saint Louis University School of Medicine, St. Louis, Missouri

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Patients counseled on genetic heart disease risk feel they have more control over fate

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Newswise November 19, 2014, New York, NY A team led by Ludwig and Memorial Sloan Kettering (MSK) researchers has published a landmark study on the genetic basis of response to a powerful cancer therapy known as immune checkpoint blockade. Their paper, in the current issue of the New England Journal of Medicine, describes the precise genetic signatures in melanoma tumors that determine whether a patient will respond to one such therapy. It also explains in exquisite detail how those genetic profiles translate into subtle molecular changes that enable the immune system attack of cancer cells in response to immune checkpoint blockade.

The genetic signature we have found will be invaluable to understanding the biological mechanisms that drive therapeutic responses to immunotherapy for metastatic melanoma, says Jedd Wolchok, MD, PhD, director of the Ludwig Collaborative Laboratory and associate director of the Ludwig Center for Cancer Immunotherapy at MSK, who co-led the study with Timothy Chan, MD, PhD, of MSKs Human Oncology and Pathogenesis Program. Further, our strategy can now be applied to determine the genetic signatures associated with the efficacy of a number of other immunotherapies and cancers.

Few approaches to treating cancer have generated as much excitement as immunotherapy, in which the immune system is engaged to destroy malignancies. One class of such treatments targets CTLA-4, a molecule expressed on the surface of killer T cells that ordinarily blocks their proliferation. Antibody drugs that block CTLA-4 thus stimulate killer T cell responseswhich can target cancer cellsand significantly extend survival for many melanoma patients. Yet not all patients respond equally to this treatment: some, remarkably, survive many years; others fail to respond at all.

There is a subset of melanoma patients who are living far longer than anyone would have expected in the past, largely because of this treatment and other recently developed targeted and immunologic treatments, says Wolchok. But we did not know how to identify them, and thats what really drove this investigation.

Cancer cells are swift but sloppy proliferators, generating countless mutations across their genome as they multiply. Those mutations are often expressed as changes in the chains of amino acids that make protein molecules. Like all cells, cancer cells chop up and hold out short fragments of such proteinseach about 9 amino acids in lengthfor the immune system to assess. These peptides are held up and presented to immune cells by a protein complex known as MHC Class I, which varies significantly between people.

Previous studies by Jedd and others had shown that the particular MHC type of a patient doesnt appear to influence the efficacy of CTLA-4 blockade, says Chan. So we decided to see if the tumor genome has anything to say about whether or not people respond to this therapy. The result was entirely unexpected, and the answer is exceedingly important.

Chan, Wolchok and their colleagues initially hypothesized that tumors that harbored highly mutated cells would be most responsive to CTLA-4 blockade. To test that hypothesis, they sequenced and compared all of the genes expressed as proteins (collectively known as the exome) in tumors taken from 25 patients treated with anti-CTLA-4 antibodies and found that this was, to some degree, true. But looking at the data a little more deeply, says Wolchok, we saw that there were outlierspatients who had over one thousand mutations who didnt respond, and some with just a few dozen who did. This was a strong indication that the quality of the mutations matters.

A sophisticated computational analysis of the cancer genomes revealed that a set of core peptide sequenceseach four amino acids long (tetrapeptides)within MHC Class I-presented peptides were unequivocally associated with response to treatment. To test the prognostic power of this genetic signature, the researchers sequenced the exomes of tumors from another 39 melanoma patients treated with CTLA-4 blockade. They found that all those in this set who had responded to the therapy had at least one and typically several more of the tetrapeptides they had identified. Those who failed to respond did not. Their results show that the mutant DNA sequences, can occur anywhere in the genomenot just within mutant driver genes that are already known to contribute to cancer.

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A Signature for Success

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Let #39;s Play: The Sims 3 Perfect Genetics Challenge (Part 3)- Skill Day
In this part we do some house renovating and have skill day. Please Like, Share and Subscribe!

By: InstaSimmer

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Let's Play: The Sims 3 Perfect Genetics Challenge (Part 3)- Skill Day - Video

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I got me a new workout partner | Genetics
At the commercial gym doing bent over rows.

By: Herbie Sherman

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I got me a new workout partner | Genetics - Video

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Fertility Center Applied Genetics Sarasota Perfect Five Star Review
http://GeneticsAndFertility.com 941-342-1568 Fertility Center Applied Genetics Sarasota reviews 5 Star Rating Dr. Pabon is a wonderful clinician and has an amazing bedside...

By: Julio E. Pabon, MD, PA / Fertility Center and Applied Genetics of Florida

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Could There Be A Predisposition Weakness To The Ebola Virus Based On Genetics?
Could There Be A Predisposition Weakness To The Ebola Virus Based On Genetics? Ebola Doctor Surgeon Martin Salia Died Today In Nebraska 100 Percent of Black Males With Ebola In U.S. Have ...

By: Charles Walton

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Could There Be A Predisposition Weakness To The Ebola Virus Based On Genetics? - Video

Recommendation and review posted by Bethany Smith

How can GENETICS revolutionize medicine?
In 2003, researchers first sequenced the human genome. Since then our understanding of human genetics has exploded. How will this biological revolution actually improve medical care for you...

By: CuriousMinds

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How can GENETICS revolutionize medicine? - Video

Recommendation and review posted by Bethany Smith