PUBLIC RELEASE DATE:

24-Jul-2014

Contact: Jennifer Davis jdavis@hsl.harvard.edu 617-363-8282 Hebrew SeniorLife Institute for Aging Research

BOSTONA novel study shows that the age girls reach puberty is influenced by 'imprinted genes'a subset of genes whose activity differs depending on which parent contributes the gene. This is the first evidence that imprinted genes can control the rate of development after birth and details of this study were published today in the journal Nature.

Age of the first period, known as menarche, is a marker for the timing of puberty in females. Medical evidence shows that the onset of menses varies between girls, is an inherited trait, and is linked to breast cancer, diabetes and heart disease risks. "This research is the first step in understanding the genetics involved with the onset of puberty in girls," says Douglas P. Kiel, M.D., M.P.H., Director of the Musculoskeletal Research Center at Harvard Medical Schoolaffiliated Hebrew SeniorLife Institute for Aging Research (IFAR) in Boston, Mass. "By uncovering which genes influence menarche, we can then focus on its link to increased disease risks, such as osteoporosis or diabetes, in later life."

The findings come from an international study of more than 180,000 women involving scientists from 166 institutions around the globe. The researchers identified 123 genetic variations that were associated with the timing of when girls experienced their first menstrual cycle by analyzing the DNA of 182,416 women of European descent from 57 studies. Six of these variants were found to be clustered within imprinted regions of the genome.

The activity of imprinted genes differs depending on which parent the gene is inherited from some genes are only active when inherited from the mother, others are only active when inherited from the father. Both types of imprinted genes were identified as determining puberty timing in girls, indicating a possible biological conflict between the parents over their child's rate of development. Further evidence for the parental imbalance in inheritance patterns was obtained by analyzing the association between these imprinted genes and timing of puberty in a study of over 35,000 women in Iceland, for whom detailed information on their family trees were available.

David Karasik, Ph.D., an associate scientist with Hebrew SeniorLife IFAR who also was involved with the study adds, "The genetics involved in female reproductive maturation is complex. Our findings extend knowledge of genetic influences that could contribute to the development of age-related conditions including menopause and osteoporosis.

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About the Institute for Aging Research

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Could age of first period influence development of diseases in older women?

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Our species caused 322 animal extinctions over the past 500 years, with two-thirds of those occurring in the last two centuries, according to a paper published in a special issue of the journal Science this week.

Many animals are threatened with human-caused extinction now, with researchers expressing particular concern over amphibian and invertebrate (creatures without a backbone) losses. Numbers of the latter group have nearly halved as our population doubled in size over the past 35 years.

Ecologists, zoologists and other scientists believe that, without urgent steps to stem the losses, we are facing global scale tipping points from which we may never look back or recover.

"Indeed, if current rates (of human population growth) were to continue unchecked, population size would be, by 2100, about 27 billion persons -- clearly an unthinkable and unsustainable option," co-author Rodolfo Dirzo, professor of environmental sciences at Stanford University, told Discovery News.

Dirzo and his colleagues call for "decreasing the per capita human footprint," by developing and implementing carbon-neutral technologies, producing food and goods more efficiently, consuming less and wasting less.

They also say it is essential that we ensure lower human population growth projections are the "ones that prevail."

Haldre Rogers and Josh Tewksbury, authors of another paper in the same issue, believe that, "animals do matter to people, but on balance, they matter less than food, jobs, energy, money, and development."

They continued, "As long as we continue to view animals in ecosystems as irrelevant to these basic demands, animals will lose."

Keeping animals alive and ecosystems healthy translate to big bucks on a global scale. Tewksbury, director of the Luc Hoffmann Institute of the World Wide Fund for Nature, pointed out that Southeast Asia's Mekong River Basin, through its fisheries, supports 60 million people. Rogers, a researcher in Rice University's Department of Ecology & Evolutionary Biology, added that 73 percent of visitors to Namibia are nature-based tourists, with their money accounting for 14.2 percent of that nation's economic growth.

"Whale watching in Latin America alone generates over 275 million dollars a year," Tewksbury said. "Multiple studies have demonstrated how turtles are worth more alive than dead."

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Humans Caused 322 Animal Extinctions in Past 500 Years

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge: Cowgirl and Horse Edition Episode 25
Come join me on my latest journey into the complex world of sims 3 genetics, as I try to get perfect foals and perfect children. Will I succeed in getting pe...

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Linda Avey and Anne Wojcicki on genetics - The New Yorker Conference
Linda Avey and Anne Wojcicki talk with Michael Specter about genetics. Subscribe to the all-new The New Yorker channel here: http://www.youtube.com/channel/U...

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Let #39;s Play: Sims 3 Perfect Genetics Challenge - Episode 17
Thank you so much for watching! I greatly appreciate it! Please comment, like and subscribe for more great videos from my channel. Also, check out some more of my social media links below!...

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Latest NBR Member Subscriber winner John Monaghan from Eketahuna is NBR's latest winner of New Zealand's richest subscription prize, the all-new BMW 320i xDrive Touring valued at $83,800 Read More

Past Winner Stephen Tubbs is NBR's latest winner of New Zealand's richest subscription prize, a fabulous trip for two flying Business Class with Singapore Airlines and SilkAir to Cambodias newest ultimate "all-inclusive" luxury eco-resort Song Saa Private Island, valued at $59,000 Read More

Past Winner Matthew Horton (right) catching the keys to his new Peugeot 508 from NBR publisher Todd Scott (centre), with Sime Darby Automobiles divisional manager Simon Rose (left) Horton Media Chief Executive Matthew Horton is the lucky winner of NBRs latest subscription prize. Mr Horton won a Peugeot 508 worth $54,990, which brings the publications prize pool total to almost $500,000 since 1999.

Past Winner FMA chairman Simon Allen was the winner of NBR' s latest subscriber prize of a Luxury European Escape courtesy of Air NZ, flying Business Premier to London, with stopovers each way in either Hong Kong or Los Angeles, plus four weeks' accommodation staying at the Small Luxury Hotels of the World properties of his choice. So what did he do with this wonderful prize?

Past Winner Long-time NBR subscriber Peter Merton won a Mini Countryman Cooper S valued at $63,000 in NBR's latest subscriber competition, drawn on February 24, 2012.

Past Winner Congratulations to Justin and Janine Smith (owner-operators of the Oamaru New World) They won seven nights for two on board Seabourn Odyssey valued at $30,000 - Athens to Istanbul.

Past Winner Max and Christine Tarr of Max Tarr Electrical in Palmerston North, winners of the Ultimate NZ Experience valued at $40,000 Three nights for four people staying at each of these luxury NZ Lodges, Kauri Cliffs, The Farm at Cape Kidnappers and Matakauri Lodge in Queenstown. Max has been an NBR subscriber since Sept 1991

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Genetics company trades off profit for R&D investment

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DeGette and Upton Host Roundtable Discussion with Experts on Personalized Medicine

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Jack Jablonski Walks In Spinal Cord Injury Fundraiser
Former high school hockey player Jack Jablonski, who took a paralyzing hit three years ago, took part in a treadmill walkathon to raise money for the Christo...

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15 India #39;s Most Promising Anti Aging and Regenerative Medicine Specialist 2014

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Stem cell agency President C. Randal Mills (left) and Chairman of the Board Jonathan Thomas.

Responding to his predecessor's ethically controversial departure, the president and chief executive of California's stem cell agency said Thursday he is taking legal steps to minimize conflicts of interests with those who have business before the agency.

C. Randal Mills said he will not take a job with any company funded by the California Institute for Regenerative Medicine for one year after he departs the agency. In addition, he also will not accept gifts or travel payments from any company, institution or person who gets agency funding.

Mills' action, announced at the agency's meeting in Millbrae, will be enforced with a legal agreement he will sign. His action comes less than a month after he replaced Alan Trounson as the agency chief. One week after his departure, CIRM-funded StemCells Inc. announced it had appointed Trounson to its board. StemCells Inc. had received an award of nearly $20 million from the agency to develop a therapy for Alzheimers disease.

While Trounson's appointment wasn't illegal, critics said it was unseemly for him to join a company that had received agency funding so soon after he left CIRM. An ethical controversy could harm the agency's chances of getting more funding from California voters, who gave the agency $3 billion with the passage of Proposition 71 in 2004.

Mills said the new rules apply only to himself, because of his central role at CIRM.

"This specifically addresses an issue where an individual in an organization has a disproportionate amount of power, and I want to make sure it's known that power will not be abused," Mills said.

Mills made the right decision, said Jeanne Loring, a CIRM-funded stem cell researcher at The Scripps Research Institute.

"There's a difference between what is legal and what is ethical," said Loring, who attended the meeting. "And he's going to be pushing the needle a lot more toward the ethical side without worrying whether he can get away with stuff."

John Simpson of Santa Monica-based Consumer Watchdog, who has often criticized CIRM for conflicts of interest, also praised the decision.

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A US Leader in Stem Cell Therapy - StemGenex
http://www.stemgenex.com/ - StemGenex offer patients access to cutting-edge adipose stem cell therapies for degenerative diseases, cosmetic enhancements and ...

By: EMSearch C

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PUBLIC RELEASE DATE:

24-Jul-2014

Contact: Vera Siegler vera.siegler@tum.de 49-892-892-2731 Technische Universitaet Muenchen

This news release is available in German.

The immune system has evolved to recognize and respond to threats to health, and to provide life-long memory that prevents recurrent disease. A detailed understanding of the mechanism underlying immunologic memory, however, has remained elusive. Since 2001, various lines of research have converged to support the hypothesis that the persistence of immune memory arises from a reservoir of immune cells with stem-cell-like potential. Until now, there was no conclusive evidence, largely because experiments could only be carried out on populations of cells. This first strict test of the stem cell hypothesis of immune memory was based on mapping the fates of individual T cells and their descendants over several generations.

That experimental capability was developed through a long-term collaboration, focused on clinical cell processing and purification, between researchers based in Munich and Seattle. Since 2009, the groups of Prof. Dirk Busch at the Technische Universitt Mnchen (TUM) and Prof. Stanley Riddell at the Fred Hutchinson Cancer Research Center have combined their technological and clinical expertise under the auspices of the TUM Institute for Advanced Study. The University of Heidelberg, the University of Dsseldorf, the Helmholtz Center Munich, the German Cancer Research Center (DKFZ), and the National Center for Infection Research (DZIF) also contributed to the present study.

Homing In On The "Stemness" of T Cells

After generating an immune response in laboratory animals, TUM researchers Patricia Graef and Veit Buchholz separated complex "killer" T cell populations enlisted to fight the immediate or recurring infection. Within these cell populations, they then identified subgroups and proceeded with a series of single-cell adoptive transfer experiments, in which the aftermath of immune responses could be analyzed in detail. Here the ability to identify and characterize the descendants of individual T cells through several generations was crucial.

The researchers first established that a high potential for expansion and differentiation in a defined subpopulation, called "central memory T cells," does not depend exclusively on any special source such as bone marrow, lymph nodes, or spleen. This supported but did not yet prove the idea that certain central memory T cells are, effectively, adult stem cells. Further experiments, using and comparing both memory T cells and so-called naive T cells that is, mature immune cells that have not yet encountered their antigen enabled the scientists to home in on stem-cell-like characteristics and eliminate other possible explanations.

Step by step, the results strengthened the case that the persistence of immune memory depends on the "stemness" of the subpopulation of T cells termed central memory T cells: Individual central memory T cells proved to be "multipotent," meaning that they can generate diverse types of offspring to fight an infection and to remember the antagonist. Further, these individual T cells self-renew into secondary memory T cells that are, again, multipotent at the single-cell level. And finally, individual descendants of secondary memory T cells are capable of fully restoring the capacity for a normal immune response.

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Scientists at The New York Stem Cell Foundation (NYSCF) Research Institute are one step closer to creating a viable cell replacement therapy for multiple sclerosis from a patient's own cells.

For the first time, NYSCF scientists generated induced pluripotent stem (iPS) cells lines from skin samples of patients with primary progressive multiple sclerosis and further, they developed an accelerated protocol to induce these stem cells into becoming oligodendrocytes, the myelin-forming cells of the central nervous system implicated in multiple sclerosis and many other diseases.

Existing protocols for producing oligodendrocytes had taken almost half a year to produce, limiting the ability of researchers to conduct their research. This study has cut that time approximately in half, making the ability to utilize these cells in research much more feasible.

Stem cell lines and oligodendrocytes allow researchers to "turn back the clock" and observe how multiple sclerosis develops and progresses, potentially revealing the onset of the disease at a cellular level long before any symptoms are displayed. The improved protocol for deriving oligodendrocyte cells will also provide a platform for disease modeling, drug screening, and for replacing the damaged cells in the brain with healthy cells generated using this method.

"We are so close to finding new treatments and even cures for MS. The enhanced ability to derive the cells implicated in the disease will undoubtedly accelerate research for MS and many other diseases," said Susan L. Solomon, NYSCF Chief Executive Officer.

"We hope that this protocol will be helpful to the MS field and the larger scientific community to better understand human oligodendrocyte biology and the process of myelination. This is the first step towards very exciting studies: the ability to generate human oligodendrocytes in large amounts will serve as an unprecedented tool for developing remyelinating strategies and the study of patient-specific cells may shed light on intrinsic pathogenic mechanisms that lead to progressive MS". said Dr. Valentina Fossati, NYSCF Helmsley Investigator and senior author on the paper.

In multiple sclerosis, the protective covering of axons, called myelin, becomes damaged and lost. In this study, the scientists not only improved the protocol for making the myelin-forming cells but they showed that the oligodendrocytes derived from the skin of primary progressive patients are functional, and therefore able to form their own myelin when put into a mouse model. This is an initial step towards developing future autologous cell transplantation therapies in multiple sclerosis patients

This important advance opens up critical new avenues of research to study multiple sclerosis and other diseases. Oligodendrocytes are implicated in many different disorders, therefore this research not only moves multiple sclerosis research forward, it allows NYSCF and other scientists the ability to study all demyelinating and central nervous system disorders.

Multiple sclerosis is a chronic, inflammatory, demyelinating disease of the central nervous system, distinguished by recurrent episodes of demyelination and the consequent neurological symptoms. Primary progressive multiple sclerosis is the most severe form of multiple sclerosis, characterized by a steady neurological decline from the onset of the disease. Currently, there are no effective treatments or cures for primary progressive multiple sclerosis and treatments relies merely on symptom management.

Explore further: 'Master switch' for myelination in human brain stem cells is identified

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Scientists 1 step closer to cell therapy for multiple ...

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WATCH:An 11-year-old girl with a rare blood disease is in need of a stem cell transplant ideally from a match within the South Asian Community. Angie Seth reports.

Stem cell and bone marrow donations are critical for hundreds of people in Canada suffering from certain types of cancers or blood diseases.

Right now there are approximately 800 people on the transplant list. Among them is 11-year-old Cierra Singh.

Cierra has a rare blood disease calledMyelodysplastic Syndrome.

Mybone marrow and my bones are not producing enough healthy cells. So there are platelets and the white blood cells and the red blood cells. My mom tells me they are not working as well as they should work, Cierra tells Global News.

We had the opportunity to meet this incredible little girl who strives to give back to others in every which way.

Everyone says its a big deal, but I dont see it as a big deal. I just try to stay positive all the time, she says.

Cierra was diagnosed with the rare blood disease in April. A trip to Sick Kids hospital because of a swollen leg led doctors to discover Cierras immune system was not functioning properly.

Her Mothers fears paint a bleak picture.

If she were to get a fever of 38.5 and up we need to rush her into emergency within the hour . The risk of infectious diseases is very high so they need to pump her body with antibiotics because she wont be able to fight it. The only cure for Myelodysplastic Syndrome is a stem cell transplant, there is no other option, KiranBenet, Cierras Mom says.

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11-year-olds critical need for a stem cell transplant

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The immune system has evolved to recognize and respond to threats to health, and to provide life-long memory that prevents recurrent disease. A detailed understanding of the mechanism underlying immunologic memory, however, has remained elusive. Since 2001, various lines of research have converged to support the hypothesis that the persistence of immune memory arises from a reservoir of immune cells with stem-cell-like potential. Until now, there was no conclusive evidence, largely because experiments could only be carried out on populations of cells. This first strict test of the stem cell hypothesis of immune memory was based on mapping the fates of individual T cells and their descendants over several generations.

That experimental capability was developed through a long-term collaboration, focused on clinical cell processing and purification, between researchers based in Munich and Seattle. Since 2009, the groups of Prof. Dirk Busch at the Technische Universitt Mnchen (TUM) and Prof. Stanley Riddell at the Fred Hutchinson Cancer Research Center have combined their technological and clinical expertise under the auspices of the TUM Institute for Advanced Study. The University of Heidelberg, the University of Dsseldorf, the Helmholtz Center Munich, the German Cancer Research Center (DKFZ), and the National Center for Infection Research (DZIF) also contributed to the present study.

Homing in on the "stemness" of T cells

After generating an immune response in laboratory animals, TUM researchers Patricia Graef and Veit Buchholz separated complex "killer" T cell populations enlisted to fight the immediate or recurring infection. Within these cell populations, they then identified subgroups and proceeded with a series of single-cell adoptive transfer experiments, in which the aftermath of immune responses could be analyzed in detail. Here the ability to identify and characterize the descendants of individual T cells through several generations was crucial.

The researchers first established that a high potential for expansion and differentiation in a defined subpopulation, called "central memory T cells," does not depend exclusively on any special source such as bone marrow, lymph nodes, or spleen. This supported but did not yet prove the idea that certain central memory T cells are, effectively, adult stem cells. Further experiments, using and comparing both memory T cells and so-called naive T cells -- that is, mature immune cells that have not yet encountered their antigen -- enabled the scientists to home in on stem-cell-like characteristics and eliminate other possible explanations.

Step by step, the results strengthened the case that the persistence of immune memory depends on the "stemness" of the subpopulation of T cells termed central memory T cells: Individual central memory T cells proved to be "multipotent," meaning that they can generate diverse types of offspring to fight an infection and to remember the antagonist. Further, these individual T cells self-renew into secondary memory T cells that are, again, multipotent at the single-cell level. And finally, individual descendants of secondary memory T cells are capable of fully restoring the capacity for a normal immune response.

Insights with clinical potential

One implication is that future immune-based therapies for cancers and other diseases might get effective results from adoptive transfer of small numbers of individual T cells. "In principle, one individual T cell can be enough to transfer effective and long-lasting protective immunity for a defined pathogen or tumor antigen to a patient," says Prof. Dirk Busch, director of the Institute for Medicial Microbiology, Immunology and Hygiene at TUM. "Isn't that astonishing?"

"These results are extremely exciting and come at a time when immunotherapy is moving into the mainstream as a treatment for cancer and other diseases," says Prof. Stanley Riddell of the Fred Hutchinson Cancer Research Center and the University of Washington. "The results provide strong experimental support for the concept that the efficacy and durability of T cell immunotherapy for infections and cancer may be improved by utilizing specific T cell subsets."

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Denver, CO (PRWEB) July 23, 2014

Daily Face & Body is excited to announce that they have released a cheaper and safer alternative to Botox called Stem Cell Technology Facial Serum.

Stem Cell Technology Facial Serum is an anti-aging product used to help people smooth, tone, and rejuvenate dead skin cells..

Stem Cell Technology Facial Serum can be used as a safe alternative to Botox, a popular cosmetic injection, because the Stem Cell does not have any toxins or health risks as opposed to Botox. In addition, it is Alcohol, Ammonia, Paraben, Perfume, and Sulfate free, and it has not been tested on Animals.

According to the Daily Face & Body website, their Stem Cell Technology Facial Serum uses 100% active plant stem cell ingredient (All Even Sweet Iris) which has been clinically tested to reduce wrinkles with overall anti-aging effects.

Jason Palmer, a representative of Daily Face & Body, says that the clinical test results showed that after 28 days of treatment, 84% of women noted their wrinkles seem to have decreased. It also decreased the total surface by 35%, decreased the number of wrinkles by 26%, and decreased the length of wrinkles by 33%.

Ingredients The ingredients in Stem Cell Technology Facial serum are as follows:

Active ingredient: All Even Sweet Irs (Iris pallida). The other ingredients are: Water, Cyclomethicone, Avena sativa (Oat) Kernel Extract, Cichorium Intybus (Chicory) Root, Oligosaccharides (and) Glycerin (and) Caesalpinia Spinosa Gum, Dimethicone, Iris Pallida Leaf Cell Extract, Lauramidoyl Inulin, Oleth-10, Carbomer, Phenoxyethanol (and) Ethylhexylglycerin, Potassium Sorbate, Tromethamine.

About Daily Face & Body is a locally owned Denver company that has been operating since 2012. They sell Skin Care products and accessories as well as home Spa therapy products and weight loss supplements. To receive more information about Daily Face & Body please visit their website http://www.dailyfaceandbody.com.

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Local Denver Skin Care Company Releases Safer Alternative to Botox

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New York, NY (PRWEB) July 23, 2014

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

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

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

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

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

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

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

NYSCF is a world leader in stem cell research and production with a mission to find cures for the devastating diseases of our time, including juvenile Batten disease. NYSCF has developed the NYSCF Global Stem Cell ArrayTM, an automated robotic technology that standardizes and scales stem cell production and differentiation, enabling the manufacture and analysis of large numbers of identical cells from skin samples of patients. The Array technology allows for the production of large-scale iPS cells that have the potential to become any cell type in the body.

This collaboration brings together the expertise of these two leading non-profit organizations, the support of BDSRA, and the participation of affected families, to create and make available to researchers, juvenile Batten disease iPS cell lines. Building on the NYSCF Research Institutes leading stem cell expertise and unique automated technology and analytics, while taking advantage of the tremendous resources and expertise of BBDF, BDSRA and affected families, this collaboration will move research

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The New York Stem Cell Foundation Partners With Beyond Batten Disease Foundation to Fight Juvenile Batten Disease

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PUBLIC RELEASE DATE:

23-Jul-2014

Contact: Tom Vasich tmvasich@uci.edu 949-824-6455 University of California - Irvine

Irvine, Calif., July 23, 2014 A therapy combining salmon fibrin injections into the spinal cord and injections of a gene inhibitor into the brain restored voluntary motor function impaired by spinal cord injury, scientists at UC Irvine's Reeve-Irvine Research Center have found.

In a study on rodents, Gail Lewandowski and Oswald Steward achieved this breakthrough by turning back the developmental clock in a molecular pathway critical to the formation of corticospinal tract nerve connections and providing a scaffold so that neuronal axons at the injury site could grow and link up again.

Results appear in the July 23 issue of The Journal of Neuroscience.

The work expands on previous research at UCI. In 2010, Steward helped discover that axons flourish after the deletion of an enzyme called PTEN, which controls a molecular pathway regulating cell growth. PTEN activity is low during early development, allowing cell proliferation. PTEN subsequently turns on, inhibiting this pathway and precluding any ability to regenerate.

Two years later, a UCI team found that salmon fibrin injected into rats with spinal cord injury filled cavities at the injury site, giving axons a framework in which to reconnect and facilitate recovery. Fibrin is a stringy, insoluble protein produced by the blood clotting process and is used as a surgical glue.

"This is a major next step in our effort to identify treatments that restore functional losses suffered by those with spinal cord injury," said Steward, professor of anatomy & neurobiology and director of the Reeve-Irvine Research Center, of the current findings. "Paralysis and loss of function from spinal cord injury has been considered irreversible, but our discovery points the way toward a potential therapy to induce regeneration of nerve connections."

In their study, he and Lewandowski treated rodents with impaired hand movement due to spinal cord injury with a combination of salmon fibrin and a PTEN inhibitor called AAVshPTEN. A separate group of rodents got only AAVshPTEN.

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Gene inhibitor, salmon fibrin restore function lost in spinal cord injury

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Latest Mental Health News

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

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

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

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

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

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

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

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

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

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Gene Discoveries Could Shed New Light on Schizophrenia

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By Amy Norton HealthDay Reporter

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

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

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

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

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

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

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

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

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

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Gene study gives new insight into puberty in girls

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PUBLIC RELEASE DATE:

24-Jul-2014

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

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

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

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

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

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

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

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Mutated gene linked to both autism and intellectual disability

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PUBLIC RELEASE DATE:

24-Jul-2014

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

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

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

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

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

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

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

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

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

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

Unknown Mutations

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

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

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

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Genetics of cancer: Non-coding DNA can finally be decoded

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

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Let's Play The Sims 3 - Perfect Genetics Challenge: Cowgirl and Horse Edition Episode 24 - Video

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

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Christian Enemark. Panel 3: Manipulated Microbes: Genetics, Genomics and Global Health Security - Video

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