Learning and memory are regulated by a region of the brain known as the hippocampus. New research from City of Hope has found that stimulating a specific gene could prompt growth in adults of new neurons in this critical region, leading to faster learning and better memories.

Understanding the link between this gene and the growth of new neurons or neurogenesis is an important step in developing therapies to address impaired learning and memory associated with neurodegenerative diseases and aging. The new research was published June 9 in the Proceedings of the National Academy of Sciences.

The study, which used an animal model, found that over-expressing the gene a nuclear receptor called TLX resulted in smart, faster learners that retained information better and longer.

Memory loss is a major health problem, both in diseases like Alzheimers, but also just associated with aging, said Yanhong Shi, Ph.D., lead author of the study and a neurosciences professor at City of Hope. In our study, we manipulated the expression of this receptor by introducing an additional copy of the gene which obviously we cannot do outside the laboratory setting. The next step is to find the drug that can target this same gene.

The discovery creates a new potential strategy for improving cognitive performance in elderly patients and those who have a neurological disease or brain injury.

The bulk of the brains development happens before birth, and there are periods largely in childhood and young adulthood when the brain experiences bursts of new growth. In the past couple of decades, however, scientists have found evidence of neurogenesis in later adulthood occurring mostly in the hippocampus, the region of the brain associated with learning and memory.

The new study is the first to firmly link the TLX gene to a potential for enhancing learning and memory.

Researchers found that over-expression of the gene was actually associated with a physically larger brain, as well as the ability to learn a task quickly. Furthermore, over-expression of the gene was linked with the ability to remember, over a longer period of time, what had been learned.

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The above story is based on materials provided by City of Hope. Note: Materials may be edited for content and length.

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Specific gene linked to adult growth of brain cells, learning, memory

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The genetics of SLE, an update and what it means for de patient and (...) // Robert Kimberly (USA)
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A team of haematologists has engineered a particular white blood cell to be HIV resistant after hacking the genome of induced pluripotent stem cells (iPSCs).

The technique has been published in the Proceedings of the National Academy of Sciences and was devised by Yuet Wai Kan of the University of California, former President of the American Society of Haematology, and his peers.

The white blood cell the team had ideally wanted to engineer was CD+4 T, a cell that is responsible for sending signals to other cells in the immune system, and one that is heavily targeted by the HIV virus. When testing for the progress of HIV in a patient, doctors will take a CD4 cell count in a cubic millimetre of blood, with between 500 and 1,500 cells/mm3 being within the normal range. If it drops below around 250, it means HIV has taken hold -- the virus ravages these cells and uses them as an entry point.

HIV gains entry by attaching itself to a receptor protein on the CD+4 Tcell surface known as CCR5.If this protein could be altered, it could potentially stop HIV entering the immune system, however. A very small number of the population have this alteration naturally and are partially resistant to HIV as a result -- they have two copies of a mutation that prevents HIV from hooking on to CCR5 and thus the T cell.

In the past, researchers attempted to replicate the resistance by simply transplanting stem cells from those with the mutation to an individual suffering from HIV. The rarity of this working has been demonstrated by the fact that just one individual,Timothy Ray Brown(AKA the Berlin patient), has been publicly linked to the treatment and known to be HIV free today. The Californian team hoped to go right to the core of the problem instead, and artificially replicate the protective CCR5mutation.

Kan has been working for years on a precise process for cutting and sewing back together genetic information. His focus throughout much of his career has been sickle cell anaemia, and in recent years this has translated to researching mutations and how these can be removed at the iPSC stage, as they are differentiated into hematopoietic cells. He writes on his university web page: "The future goal to treatment is to take skin cells from patients, differentiate them into iPS cells, correct the mutations by homologous recombination, and differentiate into the hematopoietic cells and re-infuse them into the patients. Since the cells originate from the patients, there would not be immuno-rejection." No biggie.

This concept has now effectively been translated to the study of HIV and the CD+4 T cell.

Kan and his team used a system known as CRISPR-Cas9 to edit the genes of the iPSCs. It uses Cas9, a protein derived from bacteria, to introduce a double strand break somewhere at the genome, where part of the virus is then incorporated into the genome to act as a warning signal to other cells. An MIT team has already used the technique to correct a human disease-related mutation in mice.

When Kan and his team used the technique they ended up creating HIV resistant white blood cells, but they were not CD+4 T-cells. They are now speculating that rather than aiming to generate this particular white blood cell with inbuilt resistance, future research instead look at creating HIV resistant stem cells that will become all types of white blood cells in the body.

Of course, with this kind of therapy the risk is different and unexpected mutations could occur. In an ideal world, doctors will not want to be giving constant cell transplants, but generating an entirely new type of HIV resistant cells throughout the body carries its own risks and will need stringent evaluation if it comes at all close to being proven.

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Stem cells edited to produce an HIV-resistant immune system

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Cell Therapy for Parkinson #39;s 2
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New genomic research led by UC San Francisco (UCSF) scientists reveals that two common gene variants that lead to longer telomeres, the caps on chromosome ends thought by many scientists to confer health by protecting cells from aging, also significantly increase the risk of developing the deadly brain cancers known as gliomas.

The genetic variants, in two telomere-related genes known as TERT and TERC, are respectively carried by 51 percent and 72 percent of the general population. Because it is somewhat unusual for such risk-conferring variants to be carried by a majority of people, the researchers propose that in these carriers the overall cellular robustness afforded by longer telomeres trumps the increased risk of high-grade gliomas, which are invariably fatal but relatively rare cancers.

The research was published online in Nature Genetics on June 8, 2014.

"There are clearly high barriers to developing gliomas, perhaps because the brain has special protection," said Margaret Wrensch, MPH, PhD, the Stanley D. Lewis and Virginia S. Lewis Endowed Chair in Brain Tumor Research at UCSF and senior author of the new study. "It's not uncommon for people diagnosed with glioma to comment, 'I've never been sick in my life.'"

In a possible example of this genetic balancing act between risks and benefits of telomere length, in one dataset employed in the current study -- a massive genomic analysis of telomere length in nearly 40,000 individuals conducted at the University of Leicester in the United Kingdom -- shorter telomeres were associated with a significantly increased risk of cardiovascular disease.

"Though longer telomeres might be good for you as a whole person, reducing many health risks and slowing aging, they might also cause some cells to live longer than they're supposed to, which is one of the hallmarks of cancer," said lead author Kyle M. Walsh, PhD, assistant professor of neurological surgery and a member of the Program in Cancer Genetics at UCSF's Helen Diller Family Comprehensive Cancer Center.

In the first phase of the new study, researchers at UCSF and The Mayo Clinic College of Medicine analyzed genome-wide data from 1,644 glioma patients and 7,736 healthy control individuals, including some who took part in The Cancer Genome Atlas project sponsored by the National Cancer Institute and National Human Genome Research Institute. This work confirmed a link between TERT and gliomas that had been made in previous UCSF research, and also identified TERC as a glioma risk factor for the first time.

Since both genes have known roles in regulating the action of telomerase, the enzyme that maintains telomere length, the research team combed the University of Leicester data, and they found that the same TERT and TERC variants associated with glioma risk were also associated with greater telomere length.

UCSF's Elizabeth Blackburn, PhD, shared the 2009 Nobel Prize in Physiology or Medicine for her pioneering work on telomeres and telomerase, an area of research she began in the mid-1970s. In the ensuing decades, untangling the relationships between telomere length and disease has proved to be complex.

In much research, longer telomeres have been considered a sign of health -- for example, Blackburn and others have shown that individuals exposed to chronic stressful experiences have shortened telomeres. But because cancer cells promote their own longevity by maintaining telomere length, drug companies have searched for drugs to specifically target and block telomerase in tumors in the hopes that cancer cells will accumulate genetic damage and die.

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Longer telomeres linked to risk of brain cancer: Double-edged sword, gene variants may promote overall health while ...

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Newswise DUARTE, Calif. Learning and memory are regulated by a region of the brain known as the hippocampus. New research from City of Hope has found that stimulating a specific gene could prompt growth in adults of new neurons in this critical region, leading to faster learning and better memories.

Understanding the link between this gene and the growth of new neurons or neurogenesis is an important step in developing therapies to address impaired learning and memory associated with neurodegenerative diseases and aging. The new research was published June 9 in the Proceedings of the National Academy of Sciences.

The study, which used an animal model, found that over-expressing the gene a nuclear receptor called TLX resulted in smart, faster learners that retained information better and longer.

Memory loss is a major health problem, both in diseases like Alzheimers, but also just associated with aging, said Yanhong Shi, Ph.D., lead author of the study and a neurosciences professor at City of Hope. In our study, we manipulated the expression of this receptor by introducing an additional copy of the gene which obviously we cannot do outside the laboratory setting. The next step is to find the drug that can target this same gene.

The discovery creates a new potential strategy for improving cognitive performance in elderly patients and those who have a neurological disease or brain injury.

The bulk of the brains development happens before birth, and there are periods largely in childhood and young adulthood when the brain experiences bursts of new growth. In the past couple of decades, however, scientists have found evidence of neurogenesis in later adulthood occurring mostly in the hippocampus, the region of the brain associated with learning and memory.

The new study is the first to firmly link the TLX gene to a potential for enhancing learning and memory.

Researchers found that over-expression of the gene was actually associated with a physically larger brain, as well as the ability to learn a task quickly. Furthermore, over-expression of the gene was linked with the ability to remember, over a longer period of time, what had been learned.

View post:
City of Hope Links Specific Gene to Adult Growth of Brain Cells, Learning and Memory

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/ 06.06.2014 02:55PM

Quantel to Color Finish 4K 60p FIFA World Cup

Pablo Rio and Genetic Engineering 2 tapped

The Quantel GE2 system, which includes two Pablo Rio 4KO color correction and finishing systems sharing storage and workflow via a GenePool, will be used for the production of fast-turnaround 4K highlights packages. These will be distributed to broadcasters and Sony Stores worldwide as well as being displayed on 4K super-screens in fan parks around Brazil. The Quantel system will also be used for the post production of the Official FIFA World Cup film in 4K Ultra HD.

Pablo Rio runs on high-performance PC hardware and exploits Nvidia Maximus multi-GPU technology to deliver interactivity and productivity. Pablo Rio is available as software-only and as a range of Quantel-backed turnkey systems. Genetic Engineering 2 provides shared storage and workflow for up to four Pablo Rio systems.

The Quantel system will work with 4K 60p XAVC media recorded on either the Sony PMW-F55 cameras being used by FIFA Film crews throughout the competition or the Sony Servers used for the 4K live production of three matches played at the Maracana Stadium in Rio de Janeiro (one in the round of 16, one quarter final and the final itself). All XAVC media will be instantly available for viewing and editing on the Pablo Rio color and finishing systems thanks to their ability to begin work immediately with soft-mounted media without transcoding or importing. The Quantel system will also record live 4K 60p via Quad 3G SDI, which can be edited while recording. The Pablo Rios will be equipped with Fraunhofer IISs integrated easyDCP toolset for production of cinema deliverables.

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Quantel to Color Finish 4K 60p FIFA World Cup

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Beverly HIlls, California (PRWEB) June 09, 2014

The top stem cell doctor in Beverly Hills and Los Angeles at Beverly Hills Orthopedic Institute are now offering stem cell procedures for hip arthritis. The stem cell therapy typically provides pain relief along with being able to delay or avoid the need for joint replacement. Call (310) 438-5343 for more information and scheduling.

Dr. Raj, Medical Director at Beverly Hills Orthopedic Institute, is a Double Board Certified orthopedic doctor who has been a pioneer in stem cell therapy for musculoskeletal conditions. Several types of stem cell procedures are offered including bone marrow derived along with amniotic derived procedures.

For the bone marrow stem cell procedures, a short outpatient procedure involves harvesting bone marrow from the patient's iliac crest. The stem cells are immediately processed to concentrate the growth factors and cells, and then they are injected into the hip for pain relief and tissue regeneration.

For the amniotic derived procedures, the fluid is obtained from consenting donors after a scheduled c-section procedure. There is no fetal tissue utilized, and the fluid is processed at an FDA regulated laboratory. An immense amount of stem cells, growth factors and hyaluronic acid are present in the amniotic material.

Dr. Raj has performed a significant amount of stem cell procedures utilizing both methods for hip arthritis, with the results being stellar to date. Being Double Board Certified and a sports medicine expert, Dr. Raj also offers stem cell procedures for sports injuries such as tendonitis and ligament injuries. This includes rotator cuff tendonitis, knee injuries, elbow tendonitis and more.

Beverly Hills Orthopedic Institute is the premier stem cell clinic in Los Angeles and Beverly Hills. Dr. Raj is an ABC News Medical Correspondent and a WebMD Medical Expert. For information on how stem cell therapy can help, call Beverly Hills Orthopedic Institute at (310) 438-5343.

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Beverly Hills Orthopedic Institute Now Offering Revolutionary Stem Cell Procedures for Hip Arthritis to Avoid Joint ...

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