27-05-2012 09:27 Special upload for webkinzgirle12 and turebeliever24 I DO NOT OWN THIS SHOW S05E14 Selective Breeding Lu treats a young patient with Bi-Polar disease which causes her to act hazardously violent. Her mother must decide whether to keep her or give her up to a mental institution. Meanwhile, Andy helps a woman have an invitro fertilization. She uses new technology to help the couple have a boy because of a genetic female-only disease in the family but later a web of lies and deceivements is revealed. Peter gets jealous when Kayla dates a man he volunteers for at a zoo.

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Strong Medicine ''Selective Breeding'' 1/2 - Video

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EURANGIE Park Murray Greys principal Malcolm Carson is pushing the boundaries of the breed through the outcross of genetics.

His cattle, be it Murray Grey, Angus, or a composite, are all Breedplan recorded and society registered in a quest to breed great cattle, no matter what the breed.

While Mr Carson believes the grey and silver cattle he breeds are more suited to the Australian climate than other breeds, he aims to uses good genetics in his herd, regardless of the colour.

"When it comes to breeding cattle, I am not locked into any one colour, and I have been using the best proven genetics for 11 years, be it Angus or Murray Grey," he said.

"A majority of my herd are recorded on the multi-breed register with the Angus and Murray Grey societies, as well as performance recorded with Breedplan.

"I would say they are Grey Angus cattle."

Mr Carson said people get "stuck in the tram tracks" and should look past the colour of an animal.

He is now running pure-bred Angus cows and pure-bred Murray Grey cows and uses artificial insemination to produce composites that are either 25 per cent, 50pc or 75pc Murray Grey.

Popular genetics are used in the herd to expand the gene pool, with Te Mania, Ardrossan and Lawson Angus bloodlines now present in the cattle.

Mr Carson is targeting high intramuscular fat, eye muscle area, 600-day growth rate and milking ability, as well as focusing strongly on temperament.

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Eurangie Park's commitment to genetics

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For Jonathan Provost, choosing his Eagle Scout project was an easy choice. Jonathan's cousin, Matthew Zieman, passed away from Acute Lymphatic Leukemia in February at the age of 24. Because of this, Jonathan's Eagle Scout project is a bone marrow donor registry drive.

"Matt was at his apartment last year and noticed a few bumps on the back of his neck," Jonathan said. "He just ignored them for a few weeks and then he told one of his friends, and she said to get it checked out. So he went by the hospital, they did a few tests, and they found out it was leukemia."

Jonathan hopes the drive will find a number of donors who can help current cancer patients, due to the difficulty of finding donor matches. Immediate family members are generally the first place doctors look for bone marrow donors; Matthew's only sibling wasn't a match, however, which made finding a donor more difficult.

The drive will be held from noon to 4 p.m. on Saturday, June 9, at Brad Duren Dentistry, located at 4030 Justin Road, Suite 102, in Flower Mound. The office is past the Chinn Chapel Soccer Complex and across from the Crossroads Bible Church. Jonathan chose the office partly because of its location and partly because of a familiarity.

"It's also off a popular road, and [Brad] told me he'd let me host the donor drive for free," he said. "He's my dentist and my mom works here, too."

The process of becoming a donor is easy. After having a cheek swab done, potential donors merely have to fill out a donor consent form, which will place them in the national bone marrow donor registry. Testing is then done to determine a genetic match between cancer patients and their potential donor. Patients see better results the closer a donor's genetics match his or her own.

If an individual is chosen as a blood donor, he or she will be called to Carter BloodCare to donate blood.

"A lot of people don't know it's really easy to do this -- it's not a complicated process at all," Jonathan said. "They generally don't put a needle in your hip anymore; they normally just take blood and that's it. The process is a lot simpler than it used to be."

Following a successful blood donation, known as peripheral blood stem cell donation, doctors will obtain stem cells from the blood of the donor. Those stem cells will then be given to a cancer patient that's a genetic and blood match in order to stimulate healthy red blood cell production.

If a donor is selected to give a bone marrow donation, he or she will have liquid marrow extracted from the back of the pelvic bone. This type of donation is far less likely, however.

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Flower Mound boy hopes to add bone marrow donors: Jonathan Provost's Eagle Scout project could help save lives

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Burr, the drummer with Maiden from 1979 until 1982, has been in a wheelchair as a result of multiple sclerosis, which has been attacking his nervous system since before he was diagnosed in 2002.

MS reduces the ability of the brain and spinal cord to communicate with each other, resulting in a wide range of potentially severe symptoms. The cause is unknown and there is no cure; but in 2009 researchers made the first breakthrough in reversing symptoms through stem cell therapy.

Di'Anno tells Talking Metal Pirate Radio Burr's condition is "not very good at all." - He had a lot to say, read it here.

Classic Rock Magazine is an official news provider for antiMusic.com. Copyright Classic Rock Magazine- Excerpted here with permission.

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Di'Anno Wants Former Iron Maiden Bandmate To Undergo Stem Cell Therapy Recap

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For Jonathan Provost, choosing his Eagle Scout project was an easy choice. Jonathan's cousin, Matthew Zieman, passed away from Acute Lymphatic Leukemia in February at the age of 24. Because of this, Jonathan's Eagle Scout project is a bone marrow donor registry drive.

"Matt was at his apartment last year and noticed a few bumps on the back of his neck," Jonathan said. "He just ignored them for a few weeks and then he told one of his friends, and she said to get it checked out. So he went by the hospital, they did a few tests, and they found out it was leukemia."

Jonathan hopes the drive will find a number of donors who can help current cancer patients, due to the difficulty of finding donor matches. Immediate family members are generally the first place doctors look for bone marrow donors; Matthew's only sibling wasn't a match, however, which made finding a donor more difficult.

The drive will be held from noon to 4 p.m. on Saturday, June 9, at Brad Duren Dentistry, located at 4030 Justin Road, Suite 102, in Flower Mound. The office is past the Chinn Chapel Soccer Complex and across from the Crossroads Bible Church. Jonathan chose the office partly because of its location and partly because of a familiarity.

"It's also off a popular road, and [Brad] told me he'd let me host the donor drive for free," he said. "He's my dentist and my mom works here, too."

The process of becoming a donor is easy. After having a cheek swab done, potential donors merely have to fill out a donor consent form, which will place them in the national bone marrow donor registry. Testing is then done to determine a genetic match between cancer patients and their potential donor. Patients see better results the closer a donor's genetics match his or her own.

If an individual is chosen as a blood donor, he or she will be called to Carter BloodCare to donate blood.

"A lot of people don't know it's really easy to do this -- it's not a complicated process at all," Jonathan said. "They generally don't put a needle in your hip anymore; they normally just take blood and that's it. The process is a lot simpler than it used to be."

Following a successful blood donation, known as peripheral blood stem cell donation, doctors will obtain stem cells from the blood of the donor. Those stem cells will then be given to a cancer patient that's a genetic and blood match in order to stimulate healthy red blood cell production.

If a donor is selected to give a bone marrow donation, he or she will have liquid marrow extracted from the back of the pelvic bone. This type of donation is far less likely, however.

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Flower Mound boy hopes to add bone marrow donors: Jonathan Provost's Eagle Scout project could help save lives

Recommendation and review posted by Bethany Smith

I was browsing the Harappa results, and two new things jumped out at me. Zack now has enough St. Thomas Christian samples from Kerala that I think we need to accept as the likely model that this community does not derive from the Brahmins of Kerala, as some of them claim. Their genetic profile is rather like many non-Brahmin South Indians, except the Nair, who have a peculiar attested history with the Brahmins of their region.

But thats not the really interesting finding. Below is a table I constructed from Zacks data.

I was curious about the distribution of the Northeast European component in South Asia. This element is almost entirely lacking in non-Brahmin South Indians (except for the Nair), but, it is present in non-Brahmin Indo-European speaking Indians, including Biharis and Bengalis. And interestingly, it is present in the same rough fraction in North Indian and South Indian Brahmins regardless of locale, ~5 percent in the former case, and ~10-15 percent in the latter. I initially divided them into two language classes, but noticed that the Maharashtra samples were more like the South Indians.

Then I remembered something random: there is a tradition dividing Indians Brahmin communities in two, on a north-south split. The above partition does not perfectly reflect the oral history and custom, but it is very close. The Brahmins of South India are a particularly homogeneous lot. Id bet that their diversity is a function of cultural evolution and adaptation to local circumstances, not disparate origins. Rather, they derive from some initial migration from a specific North Indian Brahmin community, and then admixed somewhat with another South Indian population (explaining their profiles being closer to the Southern average than that of Northern Brahmins).

Finally, most readers will be aware that I broadly accept the outline in Reconstructing Indian History. But, I do think there were multiple waves of northwest population intrusions into South Asia. In particular, I think the demographically preponderant wave was probably West Asian, while a later group brought some Eastern European ancestry into the mix as well. I think this explains nicely the fact that North Indian Brahmins have a South Indian cline but not a Northeast European cline(compare Bengali Brahmins to Punjabi Brahmins, and youll see what I mean). One possible model is that a very rapid sweep of an Indo-European speaking population may have occurred across the North Indian plain, overlain upon a local set of populations which had an ANI-ASI cline. The Genographic Project reportedly is going to present results which suggest that the Indian caste system pre-dates the arrival of the Aryans. That would comport well with this model, where earlier groups of northwesterners established a caste-like system, which the Aryans, who later formed the core of the twice-born castes, simply suited to their own needs upon arrival. If you look at Zacks results using public data sets a very low proportion of Northeastern European, equivalent to what you see in South India, is found in a few groups:

- The Dravidian Brahui and Baloch

- Tribes and Dalits

- Austro-Asiatic populations

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Genetics’ random truths | Gene Expression

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SACRAMENTO California's stem cell agency today approved two grants to UC Davis Health System researchers for their innovative work in regenerative medicine.

Kyriacos A. Athanasiou, distinguished professor of orthopaedic surgery and professor and chair of biomedical engineering, and the Child Family Professor of Engineering at UC Davis, is investigating the use of skin-derived stem cells to heal cartilage injuries and debilitating conditions of the knee such as osteoarthritis.

W. Douglas Boyd, professor of surgery, plans to further refine a novel approach to treating cardiovascular injuries suffered during a heart attack by using stem cells and a tissue-like scaffold to repair cardiac damage.

The pair received individual grants totaling approximately $6.6 million from the California Institute for Regenerative Medicine's (CIRM) governing board.

Athanasiou's and Boyd's multi-year grants were among the proposals submitted to CIRM for its third round of Early Translational Awards, which are intended to enable clinical therapies to be developed more rapidly.

"Both of these scientists are conducting exciting research that could have far-reaching implications in health care," said Jan Nolta, director of the UC Davis Institute for Regenerative Cures and the university's stem cell program director. "Dr. Athanasiou is bioengineering new cartilage that could have the same physiological integrity as the cartilage a person is born with. Dr. Boyd is developing a treatment that uses a paper-thin patch embedded with stem cells to harness their regenerative powers to repair damaged heart muscle."

Boyd, who's a pioneering cardiothoracic surgeon, pointed out in his CIRM proposal that heart disease is the nation's number-one cause of death and disability. An estimated 16.3 million Americans over the age of 20 suffer from coronary heart disease, which in 2007 accounted for an estimated 1 in 6 deaths in the U.S. Boyd plans to use bone-marrow derived stem cells -- known as mesenchymal stem cells -- in combination with a bioengineered framework known as an extracellular matrix, to regenerate damaged heart tissue, block heart disease and restore cardiac function, something currently not possible except in cases of a complete and very invasive heart transplant.

An expert in biomedical engineering, Athanasiou is focusing on developing a cellular therapy using stem cells created from an individual's own skin -- known as autologous skin-derived stem cells -- which have shown great promise in animal models. He plans to use the new funding to conduct extensive toxicology and durability tests to determine the technique's long-term safety and efficacy. Such tests are among the many steps needed to advance toward human clinical trials.

Cartilage is the slippery tissue that covers the ends of bones in joints, allowing bones to glide over each other and absorbing the shock of movement. Cartilage defects from injuries and lifelong wear and tear can eventually degenerate into osteoarthritis. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, osteoarthritis is the most common form of arthritis and affects an estimated 27 million Americans over the age of 25.

"For anyone suffering from osteoarthritis or other debilitating cartilage conditions, Dr. Athanasiou's goal of using stem cells to regenerate new tissue could have enormous quality-of-life and economic benefits," said Nolta, who is the recipient of a prior translational grant from CIRM to develop potential therapies for Huntington's disease . "Dr. Boyd's work is equally promising because he's using a bioengineered structure to encourage cardiac tissue repair, which could have important benefits in the treatment of heart disease."

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State awards stem cell grants to medical researchers

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DUARTE, Calif.--(BUSINESS WIRE)--

City of Hope was granted a $5,217,004 early translational research award by the California Institute for Regenerative Medicine (CIRM) to support the development of a T cell-based immunotherapy that re-directs a patients own immune response against glioma stem cells. City of Hope has been awarded more than $49.7 million in grant support from CIRM since awards were first announced in 2006.

City of Hope is a pioneer in T cell immunotherapy research, helping to develop genetically modified T cells as a treatment for cancer. This strategy, termed adoptive T cell therapy, focuses on redirecting a patients immune system to specifically target tumor cells, and has the potential to become a promising new approach for treatment of cancer.

In this research, we are genetically engineering a central memory T cell that targets proteins expressed by glioma stem cells, said Stephen J. Forman, M.D., Francis and Kathleen McNamara Distinguished Chair in Hematology and Hematopoietic Cell Transplantation and director of the T Cell Immunotherapy Research Laboratory. Central memory T cells have the potential to establish a persistent, lifelong immunity to help prevent brain tumors from recurring.

The American Cancer Society estimates that more than 22,000 people in the U.S. will be diagnosed with a brain tumor this year, and 13,700 will die from the disease. Glioma is a type of brain tumor that is often difficult to treat and is prone to recurrence. Currently, less than 20 percent of patients with malignant gliomas are living five years after their diagnosis. This poor prognosis is largely due to the persistence of tumor-initiating cancer stem cells, a population of malignant cells similar to normal stem cells in that they are able to reproduce themselves indefinitely. These glioma stem cells are highly resistant to chemotherapy and radiation treatments, making them capable of re-establishing new tumors.

Researchers at City of Hope previously have identified several proteins as potential prime targets for the development of cancer immunotherapies, such as interleukin 13 receptor alpha 2, a receptor found on the surface of glioma cells, and CD19, a protein that is active in lymphoma and leukemia cells. Both investigational therapies are currently in phase I clinical trials. Forman is the principal investigator for the newly granted study which will develop a T cell that targets different proteins expressed by glioma stem cells. Christine Brown, Ph.D., associate research professor, serves as co-principal investigator, and Michael Barish, Ph.D., chair of the Department of Neurosciences, and Behnam Badie, M.D., director of the Brain Tumor Program, serve as co-investigators on the project.

Because cancer stem cells are heterogeneous, our proposed therapy will target multiple antigens to cast as wide a net as possible over this malignant stem cell population, said Brown.

While in this effort, we are targeting a neurological cancer, our approach will lead to future studies targeting other cancers, including those that metastasize to the brain, added Barish.

The CIRM grant will help us to build a targeted T cell therapy against glioma that can offer lasting protection, determine the best way to deliver the treatment, establish an efficient process to manufacture these T cells for treatment, and get approval for a human clinical trial, said Badie.

City of Hope is also a collaborative partner providing process development, stem cell-derived cell products and regulatory affairs support in two other CIRM-funded projects that received early translational research grants. Larry Couture, Ph.D., senior vice president of City of Hopes Sylvia R. & Isador A. Deutch Center for Applied Technology Development and director of the Center for Biomedicine & Genetics, is working with Stanford University and Childrens Hospital of Orange County Research Institute on their respective projects.

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City of Hope Receives $5 Million Grant to Develop T Cell Treatment Targeting Brain Tumor Stem Cells

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Photo by Rachel Denny Clow, Corpus Christi Caller-Times // Buy this photo

Rachel Denny Clow/Caller-Times Cristina Rodriguez sits with her dogs Coby (left) and Flower at her home Thursday. Rodriguez, who has non-Hodgkin lymphoma, is having a Zumba benefit on Sunday and inviting people to register to donate bone marrow. Rodriguez is a former Zumba instructor.

CORPUS CHRISTI Had Cristina Rodriguez's cancer been more aggressive, had it penetrated her bones, things might have been different.

And while she has had chemotherapy, she has lost her hair and needs a stem cell treatment, but she doesn't need a bone-marrow transplant.

And for that, she's lucky.

Hispanics needing bone marrow have a harder time finding matching donors than do other ethnicities because few Hispanics have registered to donate.

"That could've easily been me," Rodriguez said.

That's why Rodriguez, 31, is trying to raise awareness about the importance for Hispanics to give bone marrow. The former Zumba instructor is hosting a Zumba event Sunday afternoon that partly is a fundraiser for her ongoing cancer treatments and partly a campaign to encourage more people to become donors.

Among the 8 million people signed up as bone marrow donors, 800,000 or 10 percent, identify themselves as Hispanic or Latino. Though Hispanics comprise more than one-third of Texas' population, only 17 percent of registered bone marrow donors in the state are Hispanic.

Overall, Hispanics have a 72 percent chance of finding a bone marrow donor, compared with whites, who have a 93 percent chance, according to the donor program. Only blacks fare worse, with a 63 percent likelihood of finding a donor.

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Former Zumba instructor with cancer encourages Hispanics to donate bone marrow

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Scientists turn skin cells into healthy heart tissue

Kate Kelland (Reuters) / 26 May 2012

The researchers said there were still many years of testing and refining ahead. But the results meant they might eventually be able to reprogramme patients cells to repair their own damaged hearts.

We have shown that its possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young - the equivalent to the stage of his heart cells when he was just born, said Lior Gepstein, who led the work.

The researchers, whose study was published in the European Heart Journal on Wednesday, said clinical trials of the technique could begin within 10 years.

Heart failure is a debilitating condition in which the heart is unable to pump enough blood around the body. It has become more prevalent in recent decades as advances in medical science mean many more people survive heart attacks. At the moment, people with severe heart failure have to rely on mechanical devices or hope for a transplant.

Researchers have been studying stem cells from various sources for more than a decade, hoping to capitalise on their ability to transform into a wide variety of other kinds of cell to treat a range of health conditions.

There are two main forms of stem cells - embryonic stem cells, which are harvested from embryos, and reprogrammed human induced pluripotent stem cells (hiPSCs), often originally from skin or blood.

Gepsteins team took skin cells from two men with heart failure aged 51 and 61 and transformed them by adding three genes and then a small molecule called valproic acid to the cell nucleus.

They found that the resulting hiPSCs were able to differentiate to become heart muscle cells, or cardiomyocytes, just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for the study.

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Scientists turn skin cells into healthy heart tissue

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Washington, May 25 : A new study has described how a cell therapy might one day be used not only to quell some common types of persistent and difficult-to-treat pain, but also to cure the conditions that give rise to them.

UCSF scientists, working with mice, focused on treating chronic pain that arises from nerve injury -- so-called neuropathic pain.

In their study, the scientists transplanted immature embryonic nerve cells that arise in the brain during development and used them to make up for a loss of function of specific neurons in the spinal cord that normally dampen pain signals.

A small fraction of the transplanted cells survived and matured into functioning neurons. The cells integrated into the nerve circuitry of the spinal cord, forming synapses and signaling pathways with neighbouring neurons.

As a result, pain hypersensitivity associated with nerve injury was almost completely eliminated, the researchers found, without evidence of movement disturbances that are common side effects of the currently favoured drug treatment.

'Now we are working toward the possibility of potential treatments that might eliminate the source of neuropathic pain, and that may be much more effective than drugs that aim only to treat symptomatically the pain that results from chronic, painful conditions,' said the senior author of the study, Allan Basbaum, PhD, chair of the Department of Anatomy at UCSF.

Those who suffer from chronic pain often get little relief, even from powerful narcotic painkillers, according to Basbaum. Gabapentin, an anticonvulsant first used to treat epilepsy, now is regarded as the most effective treatment for neuropathic pain. However, it is effective for only roughly 30 percent of patients, and even in those people it only provides about 30 percent relief of the pain, he said.

The explanation for neuropathic pain, research showed, is that following injury neurons may be lost, or central nervous system circuitry may change, in ways that are maladaptive, compromising signals that normally help dampen pain. These changes contribute to a state of hyper-excitability, enhancing the transmission of pain messages to the brain and causing normally innocuous stimuli to become painful.

The inhibitory neurons that are damaged in the spinal cord to cause pain hypersensitivity release a molecule that normally transmits inhibitory signals ' the neurotransmitter GABA. A loss of GABA inhibition also is implicated in epilepsy and may play a role in Parkinson's disease. Gabapentin does not mimic GABA, but it helps to compensate for the loss of inhibition that GABA normally would provide.

Basbaum's UCSF colleagues, including study co-authors Arturo Alvarez-Buylla, PhD, and Arnold Kriegstein, MD, PhD, along with Scott Baraban, PhD, had already been experimenting with transplanting immature neurons that make GABA, using the transplanted neurons to bolster inhibitory signals in mouse models to prevent epileptic seizures and to combat a Parkinson's-like disease.

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Cell therapy may ease chronic pain

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Washington, May 25 : Researchers have identified a single gene that simultaneously controls inflammation, accelerated aging and cancer.

The principal investigator of the study is Robert J. Schneider, PhD, the Albert Sabin Professor of Molecular Pathogenesis, associate director for translational research and co-director of the Breast Cancer Program at NYU Langone Medical Center.

"This was certainly an unexpected finding," said Schneider.

"It is rather uncommon for one gene to have two very different and very significant functions that tie together control of aging and inflammation. The two, if not regulated properly, can eventually lead to cancer development. It's an exciting scientific find," he stated.

For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connection between them has remained largely a mystery, Dr. Schneider said.

What was known, due in part to past studies by Schneider and his team, was that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer.

When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. Now, more than a decade in the making, the mystery surrounding the connection between inflammation, advanced aging and cancer is finally being unravelled.

The current study revealed that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer, Dr. Schneider explained.

"AUF1 is a medical and scientific trinity. Nature has designed a way to simultaneously turn off harmful inflammation and repair our chromosomes, thereby suppressing aging at the cellular level and in the whole animal."Dr. Schneider said.

With this new information, Dr. Schneider and colleagues are examining human populations for specific types of genetic alterations in the AUF1 gene that are associated with the co-development of certain immune diseases, increased rates of aging and higher cancer incidence in individuals to determine exactly how the alterations manifest and present themselves clinically.

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Gene behind chronic inflammation, accelerated aging and cancer identified

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ScienceDaily (May 24, 2012) A new type of male contraceptive could be created thanks to the discovery of a key gene essential for sperm development.

The finding could lead to alternatives to the conventional male contraceptives that rely on disrupting the production of hormones, such as testosterone. These treatments can cause side-effects such as irritability, mood swings and acne.

Research, led by the University of Edinburgh, has shown how a gene -- Katnal1 -- is critical to enable sperm to mature in the testes.

If scientists can regulate the Katnal1 gene in the testes, they could prevent sperm from maturing completely, making them ineffective without changing hormone levels.

The research, which is published in the journal PLoS Genetics, could also help in finding treatments for cases of male infertility when malfunction of the Katnal1 gene hampers sperm development.

Dr Lee Smith, Reader in Genetic Endocrinology at the University of Edinburgh's Centre for Reproductive Health, said: "If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive.

"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm.

"Although other research is being carried out into non-hormonal male contraceptives, identification of a gene that controls sperm production in the way Katnal1 does is a unique and significant step forward in our understanding of testis biology."

Scientists found that male mice that were modified so they did not have the Katnal1 gene were infertile.

Further investigation showed that this was because the gene was needed to allow the sperm to develop and mature.

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New type of male contraceptive? Key gene essential for sperm development discovered

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(CBS News) A male birth control pill might not be so far-fetched, now that Scottish scientists have uncovered a key gene essential for sperm development.

The gene - called Katnal1 - is critical for sperm production because it enables sperm to mature in the testes. Thus, if scientists can somehow regulate this gene with a pill, sperm production will be stalled.

"If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive," study author Dr. Lee Smith, a reader in genetic endocrinology at the Medical Research Council Center for Reproductive Health at the University of Edinburgh in Scotland, said in a news release.

16 worst birth control mistakes Scientists zap sperm counts with ultrasound: Next male birth control? Fertility killers: 11 things that sock it to sperm

Non-hormonal is important, the researchers say, because some conventional male contraceptives that rely on disrupting production of the male hormone testosterone can cause side effects such as mood swings, acne and irritability. The new treatment would also provide an alternative to popular male birth control methods like condoms and vasectomy.

Katnal1 is needed to regulate scaffold-like structures called tubules, the study showed, which forms part of the cells that provide nutrients to developing sperm. When scientists genetically modified mice to not carry this gene, the mice were infertile. The findings are published in the May 24 issue of PLoS Genetics.

Smith said the effects from a drug targeting this gene would be reversible since it stops the sperm at the maturation stage.

"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm," he said.

Dr. Allan Pacey, a senior lecturer in andrology at the University of Sheffield in the U.K., told BBC News that a non-hormonal contraceptive for men has been the "Holy Grail" of research for years.

"The gene described by the research group in Edinburgh sounds like an exciting new possible target for a new male contraceptive, but it may also shed light on why some men are sub-fertile and why their sperm does not work properly," Pacey said.

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Sperm gene discovery may lead to male birth control

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University of Edinburgh researchers say they've identified a gene crucial to sperm development that could be a target for a new form of male birth control.

Oliver Cleve / Getty Images

Condoms or a vasectomy are basically the only contraceptive options currently available for men. But a new gene discovery by infertility researchers at theCentre for Reproductive Healthat the University of Edinburghsuggests that the development of a male contraceptive pill could someday be possible.

While studying infertility in mice, the researchers identified a gene called Katnal1 that appears to be critical during the late stages of sperm production. In the testes,Katnal1 regulates a protein needed by cells that support sperm maturation; without it, sperm do not develop properly and the body disposes of them.

In lab studies, the research team found that mice with genetic mutations that interrupted Katnal1 became infertile.

(MORE:Male Contraception May Be a Reality Sooner than We Think)

Although the research is still in the preliminary stages, the authors say that if a drug could be developed to hinder Katnal1, it could potentially serve as a reversible contraceptive.

If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive, researcherDr. Lee Smith of the University of Edinburgh said in a news release.The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm.

As Dr. Allan Pacey, a senior lecturer in andrology at the University of Sheffield,told BBC News:

The key in developing a non-hormonal contraceptive for men is that the molecular target needs to be very specific for either sperm or other cells in the testicle which are involved in sperm production.

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The New Era of Contraception, Thanks to Gene Discovery?

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Your DNA may hold valuable information about your health, but current genetic tests can't improve doctors' ability to predict your risk of major disease.

Don Bishop / Getty Images

Our genome the blueprint for what makes us who we are can provide valuable clues about our health and potentially help us predict our risk for various diseases. But a new study shows that knowledge of our DNA isnt actually as revealing as doctors hoped.

In a report published in the American Journal of Human Genetics, scientists at the Harvard School of Public Health found that incorporating genetic information did not improve doctors ability to predict disease risk above and beyond standard risk factors, including things like family history, lifestyle and behavior. So, having detailed genetic information didnt change doctors prevention or treatment plans.

For most people, your doctors advice before seeing your genetic test for a particular disease will be exactly the same as after seeing your tests, Peter Kraft, a co-author of the paper and an epidemiologist at the Harvard School of Public Health, said in a statement.

The researchers looked at risk factors both genetic and environmental for three common, chronic diseases, breast cancer, Type 2 diabetes and rheumatoid arthritis. All conditions are known to be influenced by some genetic and some lifestyle factors. The researchers wanted to determine whether adding information about the interplay of these factors would improve the sensitivity of disease risk prediction.

(MORE: Genetic Testing for Kids: Is It a Good Idea?)

For breast cancer, the scientists created a simulation that included 15 common genetic variants associated with increased risk of the disease, along with environmental factors, such as a womans age at first period, age when she gave birth to her first child and the number of close relatives affected by breast cancer. For Type 2 diabetes, researchers included 31 genetic variants, as well as lifestyle factors like obesity, physical activity, smoking status and family history of diabetes. Finally, for rheumatoid arthritis, they considered 31 genetic variants and two major lifestyle risk factors smoking and breast-feeding.

The researchers analyzed whether interactions among the genes, or interactions between genes and environmental factors, significantly changed the risk profile for any of these diseases. The disease models generated a variety of statistical combinations of genetic and environmental factors, but none produced any marked improvement in predicting disease risk over the lifestyle factors alone.

So, while genome sequencing has become a popular buzzword in medicine, the researchers conclude that given our current limited ability to interpret the genome or understand the complex interplay between genes and environment, getting genetic tests or whole-genome sequencing may not be as helpful as it could be when it comes to informing our health decisions. Even with the current list of 15 genetic variants associated with breast cancer, for example, scientists cant tell which variants are driving disease or are necessary to cause it, and which are merely along for the ride.

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Why Genetic Tests Don’t Help Doctors Predict Your Risk of Disease

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ScienceDaily (May 25, 2012) Chromosomal deletions in DNA often involve just one of two gene copies inherited from either parent. But scientists haven't known how a deletion in one gene from one parent, called a "hemizygous" deletion, can contribute to cancer.

A research team led by Stephen Elledge, a professor in the Department of Genetics at Harvard Medical School, and his post-doctoral fellow Nicole Solimini, has now provided an answer. The most common hemizygous deletions in cancer, their research shows, involve a variety of tumor suppressing genes called STOP genes (suppressors of tumorigenesis and proliferation) that scatter randomly throughout the genome, but that sometimes cluster in the same place on a chromosome. And these clusters, said Elledge, who is also a professor of medicine at Brigham and Women's Hospital, tend to be deleted as a group. "Eliminating the cluster gives a bigger bang for the deletion buck," he said.

This finding is especially interesting in light of the two-hit model of cancer formation, which holds that both copies of a recessive gene need to be inactivated to trigger a biological effect. Thus the loss of a single tumor suppressor copy should have little or no influence on tumor cell proliferation because the remaining copy located on the other chromosome is there to pick up the slack.

Elledge's research points to a different hypothesis, namely that STOP genes in a hemizygous deletion aren't recessive but are instead haploinsufficient, meaning that they depend on two copies to function normally. "If a tumor suppressor is haploinsufficient, then a single gene copy lacks the potency needed to fully restrain tumorigenesis," Elledge explained, who is also a Howard Hughes Medical Institute Investigator. "So by removing clusters of haploinsufficient genes all at once, the cancer cell immediately propels its growth forward without having to wait for the other copies to also be lost."

Angelika Amon, a professor of biology at the Massachusetts of Technology, said she's surprised by the findings. "We've known from a lot of human syndromes that haploinsufficiency is widespread in the development of complex multicellular organisms," she said. "But these data show it's also critical for individual cells and cell proliferation."

The results also offer a different take on the two-hit model in carcinogenesis, Amon said. Being remarkably unstable, cancer cells can delete gene copies at every turn of the corner. If the loss of a single tumor suppressor copy provides no survival advantage for the tumor, then the tumor has no incentive to retain the cell with that deletion. But if the loss of that copy boosts proliferation, then the probability of a second hit later is greatly increased. "So haploinsufficiency is a way for the cancer cell to dramatically accelerate the acquisition of growth beneficial mutations," Amon said.

In other words, all it takes is a 50 percent reduction in gene activity for a cancer cell to grow. "That tells us it's a lot easier to get cancer than we might have hoped," Amon said.

According to Elledge, the number of hemizygotic deletions averages roughly six per tumor, with some tumors -- breast and pancreatic, for instance -- averaging up to ten. Each deletion involves 25 to 40 genes, many of them STOP genes, but also a few GO genes (growth enhancers and oncogenes) that enhance proliferation. That the STOP genes substantially outnumber their GO counterparts is important, Elledge explained, because it means cancer cells can tilt scales toward proliferation without also compromising it at the same time.

"The data reveal a lot of haploinsufficient players that have small effects individually, but large effects in combination," Elledge said. "Unfortunately, it's not easy to see how to take advantage of that chemotherapeutically."

What's important about the results, he emphasized, is that they open up new views on how tumors evolve. Moreso, they underscore the importance of proliferation as a fundamental feature of tumor growth, he added.

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Cancer may require simpler genetic mutations than previously thought

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Washington, May 25 : Detailed knowledge about your genetic makeup'the interplay between genetic variants and other genetic variants, or between genetic variants and environmental risk factors'may only change your estimated disease prediction risk for three common diseases by a few percentage points, which is typically not enough to make a difference in prevention or treatment plans, say researchers.

The study by Harvard School of Public Health (HSPH) researchers is the first to revisit claims in previous research that including such information in risk models would eventually help doctors either prevent or treat diseases.

'While identifying a synergistic effect between even a single genetic variant and another risk factor is known to be extremely challenging and requires studies with a very large number of individuals, the benefit of such discovery for risk prediction purpose might be very limited,' said lead author Hugues Aschard, research fellow in the Department of Epidemiology.

Scientists have long hoped that using genetic information gleaned from the Human Genome Project and other genetic research could improve disease risk prediction enough to help aid in prevention and treatment. Others have been skeptical that such 'personalized medicine' will be of clinical benefit.

Still others have argued that there will be benefits in the future, but that current risk prediction algorithms underperform because they don't allow for potential synergistic effects'the interplay of multiple genetic risk markers and environmental factors'instead focusing only on individual genetic markers.

Aschard and his co-authors, including senior author Peter Kraft, HSPH associate professor of epidemiology, examined whether disease risk prediction would improve for breast cancer, type 2 diabetes, and rheumatoid arthritis if they included the effect of synergy in their statistical models. But they found no significant effect by doing so.

'Statistical models of synergy among genetic markers are not 'game changers' in terms of risk prediction in the general population,' said Aschard.

The researchers conducted a simulation study by generating a broad range of possible statistical interactions among common environmental exposures and common genetic risk markers related to each of the three diseases. Then they estimated whether such interactions would significantly boost disease prediction risk when compared with models that didn't include these interactions since, to date, using individual genetic markers in such predictions has provided only modest improvements.

For breast cancer, the researchers considered 15 common genetic variations associated with disease risk and environmental factors such as age of first menstruation, age at first birth, and number of close relatives who developed breast cancer.

For type 2 diabetes, they looked at 31 genetic variations along with factors such as obesity, smoking status, physical activity, and family history of the disease. For rheumatoid arthritis, they also included 31 genetic variations, as well as two environmental factors: smoking and breastfeeding.

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Genetic information may not significantly improve disease risk prediction

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ScienceDaily (May 24, 2012) Understanding the genetic diversity within and between populations has important implications for studies of human disease and evolution. This includes identifying associations between genetic variants and disease, detecting genomic regions that have undergone positive selection and highlighting interesting aspects of human population history.

Now, a team of researchers from the UCLA Henry Samueli School of Engineering and Applied Science, UCLA's Department of Ecology and Evolutionary Biology and Israel's Tel Aviv University has developed an innovative approach to the study of genetic diversity called spatial ancestry analysis (SPA), which allows for the modeling of genetic variation in two- or three-dimensional space.

Their study is published online this week in the journal Nature Genetics.

With SPA, researchers can model the spatial distribution of each genetic variant by assigning a genetic variant's frequency as a continuous function in geographic space. By doing this, they show that the explicit modeling of the genetic variant frequency -- the proportion of individuals who carry a specific variant -- allows individuals to be localized on a world map on the basis of their genetic information alone.

"If we know from where each individual in our study originated, what we observe is that some variation is more common in one part of the world and less common in another part of the world," said Eleazar Eskin, an associate professor of computer science at UCLA Engineering. "How common these variants are in a specific location changes gradually as the location changes.

"In this study, we think of the frequency of variation as being defined by a specific location. This gives us a different way to think about populations, which are usually thought of as being discrete. Instead, we think about the variant frequencies changing in different locations. If you think about a person's ancestry, it is no longer about being from a specific population -- but instead, each person's ancestry is defined by the location they're from. Now ancestry is a continuum."

The team reports the development of a simple probabilistic model for the spatial structure of genetic variation, with which they model how the frequency of each genetic variant changes as a function of the location of the individual in geographic space (where the gene frequency is actually a function of the x and y coordinates of an individual on a map).

"If the location of an individual is unknown, our model can actually infer geographic origins for each individual using only their genetic data with surprising accuracy," said Wen-Yun Yang, a UCLA computer science graduate student.

"The model makes it possible to infer the geographic ancestry of an individual's parents, even if those parents differ in ancestry. Existing approaches falter when it comes to this task," said UCLA's John Novembre, an assistant professor in the department of ecology and evolution.

SPA is also able to model genetic variation on a globe.

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Nnew genetic method developed to pinpoint individuals' geographic origin

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Option activity on Seattle Genetics, Inc. (SGEN - 20.51) has taken a bullish turn lately, with speculators showing an increased preference for calls over puts. During the past five sessions, traders on the International Securities Exchange (ISE) and Chicago Board Options Exchange (CBOE) have bought to open 2,334 calls on the biotech stock, along with just 96 puts. The resulting five-day call/put volume ratio of 24.31 points to a strong bias for bullish bets over bearish on SGEN.

Broadening our scope to include data from the NASDAQ OMX PHLX (PHLX), SGEN sports a 10-day ISE/CBOE/PHLX put/call volume ratio of 13.45. This ratio ranks higher than 78% of other such readings taken during the previous year, revealing that options traders are purchasing calls over puts at a faster-than-usual pace.

During this same 10-day time frame, open interest at SGEN's June 22.50 call has surged by over 3,000 contracts. This overhead strike is now home to peak front-month call open interest of 5,379 contracts, followed closely by the 5,312 contracts in residence at the June 25 call.

On the charts, SGEN has racked up a healthy gain of 23.5% so far in 2012, easily besting the broader equities market. The shares are currently trading above support at their 10-day and 80-day moving averages, and they're also in the process of establishing a foothold above the round-number $20 level.

However, the stock is trading just below its all-time highs in the $22-22.50 area. This region marked peaks for SGEN throughout the fourth quarter of 2011, and the equity peaked squarely at $21.99 on May 18 before pulling back to trendline support.

With resistance in this area showing no signs of weakening, SGEN is facing an uphill battle as it attempts to chart new record highs. Unfortunately, the glut of out-of-the-money calls at the June 22.50 strike could cause additional trouble for the stock during the short term. As the hedges related to these overhead calls are unwound, the resulting selling pressure could keep SGEN pinned below familiar resistance.

However, that could be exactly what call players are counting on. Short interest accounts for a formidable 27.2% of the stock's float, so it's entirely possible that bears have been buying calls to hedge their shorted shares. This theory is supported by the preference for June 22.50 and 25 calls, since out-of-the-money options provide a cheaper hedge than their in-the-money counterparts.

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Can Seattle Genetics Break Through Looming Resistance?

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ScienceDaily (May 24, 2012) Severe combined immunodeficiency is defect in the immune system that results in a loss of the adaptive immune cells known as B cells and T cells. Mutations in several different genes can lead to the development of severe combined immunodeficiency, including mutation of the adenosine deaminase (ADA) gene. Traditional treatment options, such as enzyme replacement therapy, are of limited efficacy, but bone marrow transplant from a compatible donor leads to a better response.

A recent clinical trial indicated that gene therapy to insert the correct ADA gene in the patient's own bone marrow cells can also lead to a good response.

However, patients were noted to have defects in B cell tolerance, meaning that some B cells that react to antigens from the body fail to be eliminated, leading to an autoimmune response. Dr. Eric Meffre and colleages at Yale University in New Haven, Connecticut and Alessandro Aiuti in Milan, Italy joined together to better understand why patients developed B cell tolerance problems. They found that loss of the ADA gene directly contributes to B cell tolerance problems and that these defects are mostly corrected after gene therapy.

Their results point to a previously unknown role for ADA in B cell response and support the use of gene therapy as an effective treatment option for ADA-deficient severe combined immunodeficiency patients.

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Gene therapy can correct forms of severe combined immunodeficiency, study suggests

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CONTRIBUTED PHOTO Former Zumba instructor Cristina Rodriguez leads a flash mob at La Palmera mall in December 2010, a month before she stopped teaching because she developed a pain in her hip. She later was diagnosed with non-Hodgkin lymphoma. Rodriguez is trying to raise awareness about the importance, especially among Hispanics, of donating bone marrow.

Photo by Rachel Denny Clow, Corpus Christi Caller-Times

Rachel Denny Clow/Caller-Times Cristina Rodriguez sits with her dogs Coby (left) and Flower at her home Thursday. Rodriguez, who has non-Hodgkin lymphoma, is having a Zumba benefit on Sunday and inviting people to register to donate bone marrow. Rodriguez is a former Zumba instructor.

Photo by Rachel Denny Clow, Corpus Christi Caller-Times

Rachel Denny Clow/Caller-Times Cristina Rodriguez sits with her dogs Coby (left) and Flower at her home Thursday.

CORPUS CHRISTI Had Cristina Rodriguez's cancer been more aggressive, had it penetrated her bones, things might have been different.

And while she has had chemotherapy, she has lost her hair and needs a stem cell treatment, but she doesn't need a bone-marrow transplant.

And for that, she's lucky.

Hispanics needing bone marrow have a harder time finding matching donors than do other ethnicities because few Hispanics have registered to donate.

"That could've easily been me," Rodriguez said.

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Former Zumba instructor with cancer encourages Hispanics to donate bone marrow

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Scientists turn skin cells into healthy heart tissue

Kate Kelland (Reuters) / 26 May 2012

The researchers said there were still many years of testing and refining ahead. But the results meant they might eventually be able to reprogramme patients cells to repair their own damaged hearts.

We have shown that its possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young - the equivalent to the stage of his heart cells when he was just born, said Lior Gepstein, who led the work.

The researchers, whose study was published in the European Heart Journal on Wednesday, said clinical trials of the technique could begin within 10 years.

Heart failure is a debilitating condition in which the heart is unable to pump enough blood around the body. It has become more prevalent in recent decades as advances in medical science mean many more people survive heart attacks. At the moment, people with severe heart failure have to rely on mechanical devices or hope for a transplant.

Researchers have been studying stem cells from various sources for more than a decade, hoping to capitalise on their ability to transform into a wide variety of other kinds of cell to treat a range of health conditions.

There are two main forms of stem cells - embryonic stem cells, which are harvested from embryos, and reprogrammed human induced pluripotent stem cells (hiPSCs), often originally from skin or blood.

Gepsteins team took skin cells from two men with heart failure aged 51 and 61 and transformed them by adding three genes and then a small molecule called valproic acid to the cell nucleus.

They found that the resulting hiPSCs were able to differentiate to become heart muscle cells, or cardiomyocytes, just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for the study.

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Scientists turn skin cells into healthy heart tissue

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Miami, FL (PRWEB) May 26, 2012

Muscle atrophy a major problem with arthritis, could be treated with regenerative medicine, according to A.J. Farshchian MD from the Center for Regenerative Medicine.

Muscle atrophy also known as Muscle wasting Is common in arthritis and is usually due to loss of muscle tissue which could be caused by disease or lack of use. Mostly it is caused from disuse. Some of the other causes of atrophy are: diabetes (diabetic neuropathy) burns poliomyelitis amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) Guillain-Barre syndrome muscular dystrophy myotonia congenita myotonic dystrophy some atrophy that occurs normally with aging cerebrovascular accident (stroke) spinal cord injury peripheral nerve injury (peripheral neuropathy) prolonged immobilization rheumatoid arthritis prolonged corticosteroid therapy

The Center for Regenerative Medicine in Miami, Florida concentrates on helping arthritic and injured people to get back to a functional level of life and their activities using non-surgical techniques and Orthopedic medicine. The center's expertise is in treatment of conditions of spine, knees, shoulders and other cartilage damages. We have developed non-surgical and rehabilitation techniques focused on treatment and management of joint pain. Our team includes health professionals organized around a central theme:

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Muscle Atrophy, a Major Problem with Arthritis, is Now being Treated at The Center for Regenerative Medicine

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Public release date: 25-May-2012 [ | E-mail | Share ]

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

Five scientists from the University of California, San Diego and its School of Medicine have been awarded almost $12 million in new grants from the California Institute for Regenerative Medicine (CIRM) to conduct stem cell-based research into regenerating spinal cord injuries, repairing gene mutations that cause amyotrophic lateral sclerosis and finding new drugs to treat heart failure and Alzheimer's disease.

The awards mark the third round of funding in CIRM's Early Translational Awards program, which supports projects that are in the initial stages of identifying drugs or cell types that could become disease therapies. More than $69 million in awards were announced yesterday, including funding for first-ever collaboratively funded research projects with China and the federal government of Australia.

"With these new awards, the agency now has 52 projects in 33 diseases at varying stages of working toward clinical trials," said Jonathan Thomas, JD, PhD and CIRM governing board chair. "Californians should take pride in being at the center of this worldwide research leading toward new cures. These projects represent the best of California stem cell science and the best international experts who, together, will bring new therapies for patients."

The five new UC San Diego awards are:

With a $1.8 million award, Lawrence Goldstein, PhD, professor in the Department of Cellular and Molecular Medicine, Howard Hughes Medical Institute Investigator and director of the UC San Diego Stem Cell Program, and colleagues will continue their work developing new methods to find and test drug candidates for Alzheimer's disease (AD). Currently, there is no effective treatment for AD. The researchers screen novel candidates using purified human brain cells made from human reprogrammed stem cells. Already, they have discovered that these human brain cells exhibit a unique biochemical behavior that indicates early development of AD in a dish.

Mark H. Tuszynski, MD, PhD, professor of neurosciences and director of the Center for Neural Repair at UC San Diego, and colleagues seek to develop more potent stem cell-based treatments for spinal cord injuries. By combining grafts of neural stem cells with scaffolds placed at injury sites, the researchers have reported substantial progress in restoring functional improvement in impaired animal models. The new $4.6 million grant will fund work to identify the optimal human neural stem cells for preclinical development and, in an unprecedented step, test this treatment in appropriate preclinical models of spinal cord injury, providing the strongest validation for human translation.

Amyotrophic lateral sclerosis or ALS (Lou Gehrig's disease) is a progressive neurological condition that is currently incurable. Gene Yeo, PhD, assistant professor in the Department of Cellular and Molecular Medicine, and colleagues will use a $1.6 million grant to exploit recent discoveries that specific mutations in RNA-binding proteins cause neuronal dysfunction and death. They will use neurons generated from patient cells containing the mutations to identify the unique RNA "signature" of these doomed neurons and screen for drug-like compounds that bypass the mutations to correct the RNA signature to obtain healthy neurons.

Eric David Adler, MD, an associate clinical professor of medicine and cardiologist, studies heart failure, including the use of stem cells to treat it. His $1.7 million award will fund research into Danon disease, a type of inherited heart failure that frequently kills patients by their 20s. Adler and colleagues will turn stem cells created from skin cells of patients with Danon disease into heart cells, then screen hundreds of thousands of drug candidates for beneficial effects. The most promising drugs will subsequently be tested on mice with a genetic defect similar to Danon disease, with the ultimate goal of identifying a suitable candidate for human clinical trials. The research may have broader applications for other conditions with similar pathogenesis, such as cancer and Parkinson's disease.

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UC San Diego researchers receive new CIRM funding

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