The Hope for Personalized Medicine in Myeloma
Dr. Mario Boccadoro, noted myeloma expert from Turin, Italy, shares his perspective on the improving prospects for patients with the disease. He also comments on efforts to tailor treatment for each patient in the quest for true "personalized medicine."

By: patientpower

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The Hope for Personalized Medicine in Myeloma - Video

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Medicinal Rice P5 based Formuls for Spinal cord injury: Pankaj Oudhia #39;s Medicinal Plant Database
Septenary Ingredients of Important Traditional Herbal Formulations from Pankaj Oudhia #39;s Medicinal Plant Database Medicinal Plants of India with reference to Healing Flora of Andhra Pradesh, Assam, Karnataka, Kerala, Chhattisgarh, Gujarat, Jharkhand, Madhya Pradesh, Maharashtra, Meghalaya, Sikkim, Arunachal Pradesh, Orissa, Rajasthan, Tamilnadu, Punjab, Haryana, West Bengal, Uttarakhand and Uttar Pradesh. - This video is a part of Compilation of Pankaj Oudhia #39;s Research Works at Indira Gandhi Agricultural University, Raipur, India (1990-2001), - This video is a part of Pankaj Oudhia #39;s report on Endangered Species of India. - This video is a part of Pankaj Oudhia #39;s report on Forgotten Herbal Formulations of the World with special reference to Asia. - This video is a part of Pankaj Oudhia #39;s report on North American and European Medicinal Species in Traditional Healing of Asia. - This video is a part of Pankaj Oudhia #39;s Traditional Knowledge Database on Medicinal Rice based Herbal Formulations. - This video is a part of Pankaj Oudhia #39;s Dream Project to Establish International Medicinal Rice Research Institute (IMRRI) in India. For details please visit http://www.pankajoudhia.com

By: Pankaj Oudhia

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Medicinal Rice P5 based Formuls for Spinal cord injury: Pankaj Oudhia's Medicinal Plant Database - Video

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Jan. 31, 2013 New research has shown the presence of a disease affecting small blood vessels, known as microangiopathy, in the bone marrow of diabetic patients. While it is well known that microangiopathy is the cause of renal damage, blindness and heart attacks in patients with diabetes, this is the first time that a reduction of the smallest blood vessels has been shown in bone marrow, the tissue contained inside the bones and the main source of stem cells.

These precious cells not only replace old blood cells but also exert an important reparative function after acute injuries and heart attacks. The starvation of bone marrow as a consequence of microangiopathy can lead to a less efficient healing in diabetic patients. Also, stem cells from a patient's bone marrow are the most used in regenerative medicine trials to mend hearts damaged by heart attacks. Results from this study highlight an important deficit in stem cells and supporting microenvironment that can reduce stem cells' therapeutic potential in diabetic patients.

The research team, led by Professor Paolo Madeddu, Chair of Experimental Cardiovascular Medicine in the School of Clinical Sciences and Bristol Heart Institute at the University of Bristol, investigated the effect of diabetes on bone marrow stem cells and the nurturing of small blood vessels in humans.

The new study, published in the American Heart Association journal Circulation Research, was funded by the British Heart Foundation (BHF).

The researchers have shown a profound remodelling of the marrow, which shows shortage of stem cells and surrounding vessels mainly replaced by fat, especially in patients with a critical lack of blood supply to a tissue (ischaemia). This means that, as peripheral vascular complications progress, more damage occurs in the marrow. In a vicious cycle, depletion of bone marrow stem cells worsens the consequences of peripheral ischaemia.

Investigation of underpinning mechanisms revealed that exposure of bone marrow stem cells to the high glucose level typical of diabetes mellitus impacts on "microRNAs," which are tiny RNA molecules controlling gene expression and hence biological functions. In particular, microRNA-155, that normally controls the production of stem cells, becomes dramatically reduced in bone marrow cells exposed to high glucose. Diabetes-induced deficits are corrected by reintroducing microRNA-155 in human stem cells. The authors foresee that microRNAs could be used to regain proper stem cells number in diabetes and fix stem cells before reintroduction into a patient's body.

Professor Paolo Madeddu said: "Our study draws attention to the bone marrow as a primary target of diabetes-induced damage. The research suggests that the severity of systemic vascular disease has an impact on bone marrow causing a precocious senescence of stem cells. More severe bone marrow pathologies can cause, or contribute to, cardiovascular disease and lead to worse outcomes after a heart attack, through the shortage of vascular regenerative cells. Clinical evidence indicates that achieving a good control of glucose levels is fundamental to prevent vascular complications, but is less effective in correcting microangiopathy. We need to work hard to find new therapies for mending damaged microvessels."

Professor Costanza Emanueli, Chair of Vascular Pathology and Regeneration at the University of Bristol and co-author of the paper, added: "MicroRNAs represent an attractive means to repair the marrow damage and generate "better" stem cells for regenerative medicine applications. We are working at protocols using microRNA targeting for enhancing the therapeutic potential of stem cells before their transplantation to cure heart and limb ischaemia, which are often associated with diabetes mellitus. More work is, however, necessary before using this strategy in patients."

The findings advance the current understanding of pathological mechanisms leading to collapse of the vascular niche and reduced availability of regenerative cells. The data provides a key for interpretation of diabetes-associated defect in stem cell mobilisation following a heart attack. In addition, the research reveals a new molecular mechanism that could in the future become the target of specific treatments to alleviate vascular complications in patients with diabetes.

Professor Jeremy Pearson, Associate Medical Director at the BHF said: "Professor Madeddu and his team have shown for the first time that the bone marrow in patients with diabetes can't release stem cells which are important for the repair of blood vessel damage commonly found in people with the disease.

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Diabetes distresses bone marrow stem cells by damaging their microenvironment

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Admit it or not, as you age your skin starts showing signs that you would rather hide. Spots, wrinkles, and even crow's feet are just some of those signs that you would camouflage with makeup and skin creams to make them disappear-temporarily. But fear not, for beauty experts have discovered that stem cell treatment can also help in maintaining youthful skin.

According to Ma Fe Doria, a skin care expert, stem cell therapy is an intervention strategy that introduces new adult stem cells into damaged tissue in order to treat disease or injury. As many may be aware, the most popular stem cell treatment is in Germany, where lots of celebrities and personalities (i.e. politicians) have flown to have stem cell injections for their ailments, using cells mostly harvested from the sheep. According to those who have undergone the procedure, the treatments have improved their body and the pains they've experienced have disappeared.

Today, many medical researchers continue to do experiments to determine if stem cell can help in curing various types of ailments from cancer to diabetes, which doctors have said may not be far behind. Aside from its healing benefits, stem cell is now being used by the beauty industry. Many cosmetic and beauty centers have started offering stem cell injections for the face, which is said to regenerate the skin where the cells are injected. While some continue to use sheep cells, plant and fat stem cells are now becoming the popular alternatives, with the fat stem cells being used to heal wounds, improve scars, and rejuvenate the skin.

But stem cell treatment is not cheap. Those who can afford it need to fly out of the country to avail of the treatment. Realizing the need in the market, Flawless Facial Center partnered with a local industry leader to produce Flawless' Stem Cell line, which uses the potent power of plant stem cells. Dubbed as the "superfood for the skin," Flawless' Stem Cell line is the epitome of skin nutrition.

"This new range of products allowed us to mark several milestones not just for Flawless but for the local beauty industry. Once again, we have taken something that, for the longest time, has remained exclusive to celebrities and other influential people, and made it affordable for the regular Juan and Juana," says Flawless ceo Ruby Sy.

For P2,500, the line includes a cleanser, day cream, and night serum. Flawless' Stem Cell line utilizes the plant stem cell technology to achieve the skin's youthful appearance by protecting it against oxidative stress and boosting the skin's repair and rejuvenation systems. "Times have really changed. No thanks to free radicals that are present in almost everything around us-from the food we eat to the air we breathe-people today age so much faster. This is especially true for people who like to spend late nights partying or spend too much time in front of the [TV/computer] monitor. Various studies have proven time and again the harmful effects such activities have on our skin," Sy said.

But with Flawless' latest baby, you can say goodbye to those ugly marks on your face. The Stem Cell line promises to solve all these, and more, by providing your skin with the right amount of nutrition and protection. Indeed, youthful glow is not only safe and available in a bottle, it's also now within reach of your pocket.

Go to http://www.flawless.com.ph for

store locations

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Beauty Innovation: Young-looking skin with stem cell therapy

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SAN DIEGO, Jan. 31, 2013 /PRNewswire/ -- ViaCyte, Inc., a leading regenerative medicine company focused on developing new approaches to treat major diseases through the application of a stem cell-derived cell therapy, announced today that the Company was granted 20 patents worldwide in 2012, eight U.S. and twelve foreign. These patents bolster the Company's already strong proprietary position for its ground-breaking diabetes product, VC-01, as well as other applications of its broad technology platform.

(Logo: http://photos.prnewswire.com/prnh/20121026/LA00871LOGO-a)

VC-01 is a very promising, development-stage product that consists of pancreatic precursor cells (called PEC-01) derived from a proprietary human embryonic stem cell line and encapsulated in a proprietary, immune isolating medical device (the ENCAPTRA device). When implanted under the skin in suitable animal models, the cells further differentiate into insulin producing and other endocrine cells that regulate blood glucose in a manner similar or identical to a normal pancreas. If VC-01 performs in humans as it has in animal studies, it could effectively cure type 1 diabetics and be an important new therapy for insulin dependent type 2 diabetics.

ViaCyte's significant intellectual property portfolio now includes over 300 issued patents and pending applications related to the growth, directed differentiation and use of human pluripotent stem cells such as human embryonic stem cells and induced pluripotent stem cells. This portfolio includes 51 issued U.S. and foreign patents specifically directed to the Company's VC-01 product. In addition to the protection afforded by patents, the Company also relies on significant proprietary know-how to develop its product offerings.

Dr. Paul Laikind, ViaCyte's president and chief executive officer said, "Our comprehensive and growing intellectual property portfolio helps to establish us as a leading company in the cell therapy and regenerative medicine field. Although the Company's resources are currently fully committed to the rapid development of VC-01 as a potentially transformative treatment for patients with insulin-dependent diabetes, our platform technology has many other important applications."

In July and August of 2012, the Board of Patent Appeals and Interferences of the U.S. Patent and Trademark Office (the "Board") also issued two decisions favoring ViaCyte on motions filed in the patent interference proceedings between ViaCyte and Geron Corporation (Menlo Park, California). The interferences involved ViaCyte's U.S. Patent No. 7,510,876 ("876 Patent"), which is directed to human definitive endoderm cell cultures in vitro. The Board upheld the claims of ViaCyte's '876 Patent in its entirety over Geron's applications. In September 2012, Geron appealed this decision in the United States District Court for the Northern District of California.

About ViaCyteViaCyte, a private company that has emerged as a leader in the field of regenerative medicine, is currently focused on developing a novel cell therapy for the treatment of diabetes. The Company's lead product is based on the production of pancreatic progenitors derived from human pluripotent stem cells. These cells are implanted in a durable and retrievable encapsulation device. Once implanted and matured, these cells secrete insulin and other regulatory factors in response to blood glucose levels. ViaCyte's goal for this potentially transformative diabetes product is long term insulin independence without immune suppression, and without risk of hypoglycemia and other diabetes-related complications.

ViaCyte is headquartered in San Diego, California with additional operations in Athens, Georgia. The Company is funded in part by the California Institute for Regenerative Medicine (CIRM) and JDRF.

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ViaCyte's Role as a Leading Cell Therapy Company Bolstered with the Issuance of 20 Patents in 2012

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PROVO A new discovery by BYU researchers may help doctors identify and better help patients with genetic potential for chemo and treatment resistance.

BYU and University of Iowa researchers discovered NEK2, a gene that seems to be a predictor of how cancer patients may react to therapy. When NEK2 is highly expressed, patients cancers often do not respond to chemotherapy, according to the study published in January in the journal Cancer Cell.

Just the expression of that gene could predict whether a patient would do well on therapy or not, said David Bearss, a BYU biology professor and co-author of the study. So that gene seemed to correlate with drug resistance.

NEK2 is found in normal dividing cells as well as cancer cells, but it becomes a problem as the levels increase.

Normal cells will have the NEK2 protein, but at much lower levels than the cancer cells, Bearss said. And really, thats how we distinguish patients that are predicted to do poorly versus ones that are predicted to do better on therapy is by the level of expression.

Michael Deininger, a physician and the chief of hematology at the University of Utah School of Medicine, said the research helps explain some of the main features of resistant cancer cells their instability and their ability to pump specific drugs out of the cells.

If it was, indeed, the case that NEK2 could be targeted and we would be able to shut down two major drug resistant mechanisms at the same time, that would be a very exciting development, Deininger said.

This breakthrough has positive ramifications for the cancer front: Doctors can give patients personalized treatment by examining NEK2 levels and, depending on how highly the gene is expressed, lead patients through a specialized, more aggressive process if needed.

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BYU professor co-authors breakthrough cancer research

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Newswise Brian Kaspar, PhD, principal investigator in the Center for Gene Therapy at The Research Institute at Nationwide Childrens Hospital, along with a team of Spinal Muscular Atrophy (SMA) researchers and clinicians, received $650,000 in grants in 2012 from Sophias Cure Foundation for SMA research and Phase 1 clinical trial development which is set to launch in 2013. Working together with Nationwide Childrens, Sophias Cure Foundation has raised more than $2.3 million dollars for Dr. Kaspars program during the last three years alone.

Grant dollars from Sophias Cure Foundation are being used to support the pivotal studies required to submit an Investigational New Drug application to initiate human clinical trials in SMA patients which we hope to do in 2013, said Dr. Kaspar, also a faculty member at The Ohio State University College of Medicine. SMA research and therapeutic development stands to gain from this generous investment as we all look forward to translating our research to advance human clinical trials. Sophias Cure Foundation has been the lead funder of this program and their incredible investment in this lab has accelerated our program by many years. We are honored and extremely appreciative for this significant support.

Spinal Muscular Atrophy (SMA) is a group of inherited debilitating neurological diseases that cause progressive muscle degeneration and weakness throughout the body. There is no treatment for the progressive weakness which is caused by the disease. It is estimated that SMA occurs between one-in-6,000 and one-in-20,000 births. One-in-40 to one-in-80 normal men and women carry the gene for SMA, and if both a man and woman carry the gene, there is a 25 percent chance that any of their children will manifest SMA.

Sophias Cure Foundation is a non-profit public charity which was formed by the Gaynor family in New York City shortly after their daughter, Sophia, was diagnosed with Spinal Muscular Atrophy in 2009. The foundation was created to assist in funding for clinical research towards finding a cure for SMA and to offer support to families affected by this disease by providing advocacy, awareness, education and support. The foundation was formed three years ago by Vincent Gaynor, a One World Trade Center construction worker, and Catherine Gaynor, who left her job to care for Sophia when they learned she was sick. With their leadership and 100 percent volunteer involvement the foundation has raised more than $3 million for SMA research to date.

We run our foundation from the heart, because when you lead with your heart good things will always happen, said Vincent Gaynor, co-founder of Sophias Cure Foundation. People gravitate toward that. They believe in us and Sophia and know we will get the funds into the right hands to find a cure. Our partnership with Dr. Kaspar and Nationwide Childrens Hospital will yield great results for Spinal Muscular Atrophy research.

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Sophia's Cure Foundation Donates $650,000 in 2012 to Nationwide Children's Hospital for Dr. Brian Kaspar's Work in SMA ...

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Public release date: 31-Jan-2013 [ | E-mail | Share ]

Contact: Marianne Slegers marianne.slegers@kcl.ac.uk 44-077-034-69550 King's College London

An international study led by King's College London has identified a new genetic variant associated with stroke. By exploring the genetic variants linked with blood clotting a process that can lead to a stroke scientists have discovered a gene which is associated with large vessel and cardioembolic stroke but has no connection to small vessel stroke.

Published in the journal Annals of Neurology, the study provides a potential new target for treatment and highlights genetic differences between different types of stroke, demonstrating the need for tailored treatments.

About 15 million people worldwide suffer a stroke each year. Of these, five million die and another five million are left permanently disabled, according to numbers from the World Health Organization (WHO). Risk factors for a stroke are high blood pressure, a heart rhythm disorder, high blood cholesterol, tobacco use, unhealthy diet, physical inactivity, diabetes and advancing age.

A stroke occurs when the blood supply to the brain is cut off, often due to a blood clot blocking an artery that carries blood to the brain, which then leads to brain cell damage. Coagulation (blood clotting) abnormalities, particularly easy clotting of the blood, are therefore common contributing factors in the development of stroke.

Dr Frances Williams, Senior Lecturer from the Department of Twin Research and Genetic Epidemiology at King's and lead author of the paper, said: 'Previous studies have demonstrated the influence of genetic factors on the components of coagulation. The goal of this study was to extend these observations to determine if they were further associated with different types of stroke.'

The research was carried out in three stages. The first consisted of a genome-wide association study (GWAS) in 2100 healthy volunteers which identified 23 independent genetic variants that were involved in coagulation. The second stage examined the 23 variants in 4200 stroke and non-stroke cases from centres across Europe (Wellcome Trust Case Control Consortium 2 and MORGAM collections) and found that a particular mutation on the ABO gene was significantly associated with stroke.

Stage three of the study used the MetaStroke cohort, a project of the International Stroke Genetics Consortium which comprises 8900 stroke cases recruited from centres in the Europe, USA and Australia, whose DNA has been collected and undergone GWA scan. It was confirmed that a variant in the ABO blood type gene was associated with stroke, a finding specific to large vessel and cardioembolic stroke.

Dr Williams said: 'The discovery of the association between this genetic variant and stroke identifies a new target for potential treatments, which could help to reduce the risk of stroke in the future. It is also significant that no association was found with small vessel disease, as this suggests that stroke subtypes involve different genetic mechanisms which emphasises the need for individualised treatment.'

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New stroke gene discovery could lead to tailored treatments

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Scientists have decoded the genetic blueprint of the rock pigeon, unlocking secrets about pigeons' Middle East origins, feral pigeons' kinship with escaped racing birds and how mutations give pigeons traits like feather head crests.

In the new study, "we've shown a way forward to find the genetic basis of traits--the molecular mechanisms controlling animal diversity in pigeons," he says. "Using this approach, we expect to be able to do this for other traits in pigeons, and it can be applied to other birds and many other animals as well."

Shapiro conducted the research with Jun Wang of China's BGI-Shenzhen (formerly Beijing Genomics Institute) and other scientists from BGI, the University of Utah, Denmark's University of Copenhagen and the University of Texas M.D. Anderson Cancer Center in Houston.

There are some 350 breeds of rock pigeons--all with different sizes, shapes, colors, color patterns, beaks, bone structure, vocalizations and arrangements of feathers on the feet and head--including head crests in shapes known as hoods, manes, shells and peaks.

The pigeon's genetic blueprint is among the few bird genomes sequenced so far, along with those of the chicken, turkey, zebra finch and a common parakeet known as a budgerigar or budgie. "This will give us new insights into bird evolution," Shapiro says.

Using software developed by paper co-author Mark Yandell, a geneticist at the University of Utah, the scientists revealed that a single mutation in a gene named EphB2 causes head and neck feathers to grow upward instead of downward, creating head crests.

"This same gene in humans has been implicated as a contributor to Alzheimer's disease, as well as prostate cancer and possibly other cancers," Shapiro says, noting that more than 80 of the 350 pigeon breeds have head crests, which play a role in attracting mates in many bird species.

The researchers compared the pigeon genome to those of chickens, turkeys and zebra finches. "Despite 100 million years of evolution since these bird species diverged, their genomes are very similar," Shapiro says.

A genome for the birds, a gene for head crests

The biologists assembled 1.1 billion base pairs of DNA in the rock pigeon genome; the researchers believe there are about 1.3 billion total, compared with 3 billion base pairs in the human genome. The rock pigeon's 17,300 genes compare in number with the approximately 21,000 genes in humans.

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Mutant Gene Responsible for Pigeons' Head Crests

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A stroke gene has been identified that could help scientists save lives and prevent disability.

People with a mutant form of the ABO gene that determines blood group are more likely to have certain types of stroke, researchers found. The research highlights differences between various of types of stroke, paving the way to personalised therapies.

Scientists unscrambled the DNA of 2,100 healthy volunteers and identified 23 genetic variants linked to blood clotting, one of the chief causes of strokes. Next, they focused on the 23 variants in 4,200 stroke patients and stroke-free individuals from centres across Europe.

The research - published in the Annals of Neurology journal - showed that a particular variant of the ABO gene was significantly associated with stroke.

In the final stage of the study, the scientists scanned the DNA of almost 900 stroke victims from Europe, the US and Australia. This linked the mutant ABO gene to two specific kinds of stroke known as "large vessel" and "cardioembolic". However, no association was found with "small vessel" strokes.

Lead researcher Dr Frances Williams, from King's College London, said: "The discovery of the association between this genetic variant and stroke identifies a new target for potential treatments which could help reduce the risk of stroke in the future.

"It is also significant that no association was found with small vessel disease, as this suggests that stroke sub-types involve different genetic mechanisms which emphasises the need for individualised treatments."

Each year, around 152,000 people in the UK have a stroke, costing the country more than 8.2 billion. More than half of the estimated 1.2 million stroke survivors in the UK suffer from disabilities that affect their daily lives.

All strokes result in damage to the brain, either due to blocked arteries or bleeding from ruptured blood vessels.

Cardioembolic strokes involve a blood vessel blockage, usually a clot, that originates in the heart and travels to the brain. They are especially severe and account for up to 30% of strokes. Large vessel strokes are the result of blood clots forming in the brain's larger arteries. Small vessel strokes are similar but affect small arterial vessels

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Scientists identify stroke gene

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Jan. 31, 2013 In the last decade, a new strain of MRSA has emerged that can spread beyond hospital walls, putting everyone at risk of contracting the dangerous bacterial infection. This particular strain of MRSA -- known as USA300 -- contains a chunk of genes not shared by any other strains, though it is unclear how this unique genetic material enables the bacteria to survive and persist in the community.

Now, research from the University of North Carolina School of Medicine has pinpointed a gene that causes the infection to linger on the skin longer than other strains, allowing it to be passed more readily from one person to the next.

The gene makes this strain of MRSA resistant to specific compounds on the skin called polyamines that are toxic to other forms of the bacteria. In uncovering this property, researchers have identified a novel target for developing new treatments against methicillin-resistant Staphylococcus aureus, particularly the USA300 strain that accounts for the vast majority of MRSA skin and soft tissue infections seen in emergency rooms.

"The problem is by the time you figure out how one strain comes into dominance, it often fades away and a new strain comes in. But because these compounds occur naturally and are so toxic, we still think they can lead to treatments that are effective against all MRSA. We will just have to put in a little extra work to block the gene and make this particular strain of MRSA susceptible to polyamines," said senior study author Anthony Richardson, PhD, assistant professor of microbiology and immunology at the UNC School of Medicine.

The UNC study, published Jan. 16, 2013, in the journal Cell Host & Microbe, follows an attribute of MRSA previously unexplored by other scientists -- its sensitivity to the naturally occurring compounds called polyamines.

Polyamines are critical to wound repair because they are anti-inflammatory and promote tissue regeneration. Scientists first observed that MRSA infections were killed by polyamines in the 1950s, but no one followed up until recently, when Richardson decided to twist this scientific observation into a treatment option.

He and his colleagues tested hundreds of MRSA strains and found that all of them except one -- USA300 -- were sensitive to polyamines. When they looked to see what was different about this particular strain, they found that it contained a chunk of 34 genes, called the arginine catabolic mobile element (ACME), that none of the other strains possessed.

Then the researchers mutated each of these genes, one by one, until they created a strain that could be killed off by the polyamines. To confirm that they had the right gene, the researchers added a normal, non-mutated version of the gene -- named SpeG -- to other strains of MRSA and showed that it could make them resistant to these compounds.

Finally, Richardson wanted to know if the gene exerts the same effects in the context of a real infection. Using mouse models of MRSA infection, he and his colleagues showed that the presence of the SpeG gene helped the potent USA300 strain to stay on the skin for anywhere from a day to a week, giving the infection time to spread to the next host.

"Previously, the field tried to understand MRSA by focusing on attributes that we already knew were important, such as the amount of toxins or virulence factors a given strain makes. Those elements may explain why the disease is so bad when you get it, but they don't explain how a particular strain takes over. Our work uncovers the molecular explanation for one strain's rapid and efficient spread to people outside of a crowded hospital setting," said Richardson.

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Gene finding may lead to treatments effective against all MRSA strains

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Jan. 31, 2013 Future research into the underlying causes of neurological disorders such as autism, epilepsy and schizophrenia, should greatly benefit from a first-of-its-kind atlas of gene-enhancers in the cerebrum (telencephalon). This new atlas, developed by a team led by researchers with the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) is a publicly accessible Web-based collection of data that identifies and locates thousands of gene-regulating elements in a region of the brain that is of critical importance for cognition, motor functions and emotion.

"Understanding how the brain develops and functions, and how it malfunctions in neurological disorders, remains one of the most daunting challenges in contemporary science," says Axel Visel, a geneticist with Berkeley Lab's Genomics Division. "We've created a genome-wide digital atlas of gene enhancers in the human brain -- the switches that tell genes when and where they need to be switched on or off. This enhancer atlas will enable other scientists to study in more detail how individual genes are regulated during development of the brain, and how genetic mutations may impact human neurological disorders."

Visel is the corresponding author of a paper in the journal Cell that describes this work. The paper is titled "A High-Resolution Enhancer Atlas of the Developing Telencephalon." (See below for a list of co-authors.)

The cerebrum is the most highly developed region of the human brain. It houses the cerebral cortex, the so-called "gray matter" where complex information processing events take place, and the basal ganglia, a brain region that helps control movement throughout the body and is involved in certain types of learning. Many of the genes responsible for development of the cerebrum have been identified but most of the DNA elements responsible for expressing these genes -- turning them on/off -- have not. This is especially true for gene enhancers, sequences of DNA that act to amplify the expression of a specific gene. Characterizing gene enhancers tends to be difficult because an enhancer does not have to be located directly adjacent to the gene it is enhancing, but can in fact be located hundreds of thousands of DNA basepairs away.

"In addition to acting over long distances and being located upstream, downstream or in introns of protein-coding genes, the sequence features of gene enhancers are poorly understood," Visel says. "However, gene-centric studies have provided strong evidence that gene enhancers are critical for normal embryonic development of the brain and have also linked human diseases to perturbed enhancer sequences."

Visel and an international team of researchers met the challenges of systematic identification and functional characterization of gene enhancers in the cerebrum through a combination of ChIP-seq studies and large-scale histological analyses in transgenic mice, in which the activity patterns of human telencephalon enhancers can be studied. ChIP-seq, which stands for "chromatin immunoprecipitation followed by sequencing," is a technique for genome-wide profiling of proteins that interact with DNA.

This combination of approaches enabled Visel and his colleagues to identify over 4,600 candidate embryonic forebrain enhancers. Furthermore, studying mouse embryos they mapped the activity of 145 of these enhancers at high resolution to define where exactly in the developing brain they drive the expression of their respective target genes. The result is a comprehensive, electronically accessible database for investigating the gene regulatory mechanisms of cerebrum development, and for studying the roles of distant-acting enhancers in neurodevelopmental disorders.

"By mapping hundreds of gene enhancer sequences and defining where exactly in the developing brain they are active, our enhancer atlas provides important information to connect non-coding mutations to actual biological functions," Visel says.

As an example of how the enhancer atlas could be used in this manner, Visel says that if through genetic studies a certain region of the human genome has been linked to a specific neurological disorder but that region does not contain any protein-coding genes, checking the atlas could reveal whether the region is home to any distant-acting gene enhancers.

"If there is a gene enhancer in the region," Visel says, "researchers could determine exactly how the enhancer or a mutated form is related to the disorder. This encompasses a lot of territory in the human genome. More than half of all the disease-related DNA sequence changes discovered in genome-wide screens to date fall within the 98-percent of human genome sequences that do not code for proteins. These 'non-coding' sequences were once dismissed by many as 'junk DNA' but are now known to harbor critical gene regulatory functions."

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Genome-wide atlas of gene enhancers in the brain online

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Experts in private hearing healthcare, Hidden Hearing, have responded to research that has identified a gene linked to progressive hearing loss.

(PRWEB UK) 31 January 2013

The findings published in Proceedings of the National Academy of Sciences identify a gene, called P2X2, which appears to be crucial to the preservation of life-long normal hearing and protection against noise.

A mutation in P2X2 increases the susceptibility to both age and noise related hearing loss that begins in early life, usually adolescence, and progresses with age. This is generally accompanied by high frequency tinnitus which can range from severe to profound over decades.

A spokesperson for Hidden Hearing Said:

These findings are very interesting in identify a genetic link in hearing loss. We look forward to seeing what this research will mean for hearing impairment.

With more than 40 years experience in treating hearing loss, Hidden Hearing is entrusted with the care of more than 100,000 people each year. The firm has 84 hearing centres across the UK, all catering for a range of needs and budgets. Specialising in hearing tests and hearing aids, the company also offer a variety of hearing aid accessories and in 2005, became the first dedicated hearing retailer to be recognised as an Investor in People.

Vicky Moore Hidden Hearing 01622 697590 Email Information

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Hidden Hearing Respond to Research that Identifies Gene Linked to Hearing Loss

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Less radiotherapy side-effects using oncolytic viruses? How to kill cancer cells. Future health
More: http://www.virttu.com. How oncolytic viruses can target radiotherapy - micro-dose radiation to kill cancer cells. Replication of oncolytic viruses inside tumours. Pre-clinical trials. Phase I, Phase II and Phase III clinical trials on oncolytics. Use of oncolytic viruses to treat advanced malignant melanoma and mestatases -- Amgen research using an oncolytic virus developed from HSV (Herpes Simplex Virus). Oncolytic virus conference 2013. Problems with traditional chemotherapy -- side effects. Why Amgen bought an oncolytic viruse for $500m in cash and $500m to be paid if oncolytic trials are fully successful. Investor interest in oncolytic viruses. Oncolytic virus fund. Lessons from the history of research and development in monoclonal antibodies in cancer treatment. Why targeted cancer therapy -- a so-called "magic bullet" is so needed. How oncolytic viruses have been modified so that they cannot replicate in normal cells, but are still able to divide in a wide variety of human cancer cells. History of oncolytic viruses. Arming oncolytic viruses. Using viruses like Seprehvir (HSV-1716), adapted to carry an additional payload extra genes which teach infected cancer cells to take up a compound containing radioactive iodine from the blood, delivering a micro-dose of radiation inside individual cancer calls. Or adding a gene which teaches cancer cells how to split a harmless pro-drug into two, inside the cell, releasing a very effective chemotherapy (alkylating agent ...

By: pjvdixon

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Less radiotherapy side-effects using oncolytic viruses? How to kill cancer cells. Future health - Video

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Micro-dose chemo for cancer using oncolytic viruses. Cancer therapy - future healthcare
More: http://www.virttu.com. How oncolytic viruses can target radiotherapy - micro-dose radiation to kill cancer cells. Replication of oncolytic viruses inside tumours. Pre-clinical trials. Phase I, Phase II and Phase III clinical trials on oncolytics. Use of oncolytic viruses to treat advanced malignant melanoma and mestatases -- Amgen research using an oncolytic virus developed from HSV (Herpes Simplex Virus). Oncolytic virus conference 2013. Problems with traditional chemotherapy -- side effects. Why Amgen bought an oncolytic viruse for $500m in cash and $500m to be paid if oncolytic trials are fully successful. Investor interest in oncolytic viruses. Oncolytic virus fund. Lessons from the history of research and development in monoclonal antibodies in cancer treatment. Why targeted cancer therapy -- a so-called "magic bullet" is so needed. How oncolytic viruses have been modified so that they cannot replicate in normal cells, but are still able to divide in a wide variety of human cancer cells. History of oncolytic viruses. Arming oncolytic viruses. Using viruses like Seprehvir (HSV-1716), adapted to carry an additional payload extra genes which teach infected cancer cells to take up a compound containing radioactive iodine from the blood, delivering a micro-dose of radiation inside individual cancer calls. Or adding a gene which teaches cancer cells how to split a harmless pro-drug into two, inside the cell, releasing a very effective chemotherapy (alkylating agent ...

By: pjvdixon

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Micro-dose chemo for cancer using oncolytic viruses. Cancer therapy - future healthcare - Video

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By Pranali Dalvi

Using microbes to manufacture chemicals is starting to be cheaper and greener than traditional chemistry. And their feedstock is sugar, not oil.

Source: 2010 Agricultural Biotechnology International Conference

On Friday,Dr. Michael Lynchspoke to an engaged audience about how microbes have ushered in a new era in metabolic and genetic engineering. Lynch is the co-founder and CSO ofOPX Biotechnologies, a Colorado-based company that makes bio-based chemicals and fuels from microbes. OPXBIO microbes produce fatty acids from hydrogen and carbon dioxide. In turn, the fatty acids are used to make cleaners, detergents, jet fuel, and diesel.

Lynch said its easier to understand the genetic circuits and enzymatic pathways of microbes, thanks to much cheaper DNA sequencing. What we still lack though, is an understanding of how to rationally design complex biological systems likely because we fail to recognize the interplay among an organisms genotype, phenotype, and environment.

Its a complex set of factors that go into making phenotypic traits such as color, size, or shape.

In an industrial setting [phenotypes] are equivalent to metabolism or higher production of the product of interest, Lynch said. In a clinical setting, [phenotypes] could be virulence or pathogenesis.

One approach to understanding how phenotypes are controlled has been through functional genomics.

Lets say we take a population of wildtype microorganisms and introduce genetic modifications in a controlled way. Next, we selectively screen for the phenotype of interest and compare the sequence of this phenotype to the wildtype to pinpoint the genetic mutations that made the difference.

Comparing phenotypes one at a time is inefficient, though. Lynch wanted to find a way to speed up this process.

Link:
Designing Microbial 'Factories' Rationally

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February 1, 2013

Connie K. Ho for redOrbit.com Your Universe Online

A new study by researchers from the University of North Carolina (UNC) may be able to help develop treatments that work against all MRSA strains, according to an article recently published in the journal Cell Host & Microbe.

According to the Mayo Clinic, methicillin-resistant Staphyloccoccus aureus (MRSA) infections can be found in people who stay in hospitals, nursing homes, dialysis centers or other healthcare settings. MRSA is a type of bacteria that is difficult to treat due to its resistance to antibiotics such as penicillins or cephalosporins. Another form of MRSA known as community-associated MRSA (CA-MRSA) occur among healthy individuals who have not recently been hospitalized and often begins as a painful skin boil. It is spread by skin-to-skin contact and those who are at risk for this form of MRSA often include child care workers, young people who play contact sports such as wrestling, and people who live in crowded areas.

The recent study focuses on a new strain of MRSA called USA300 that has appeared in the last 10 years. The strain has the ability to spread past hospital walls and individuals have a higher of risk of contracting the harmful bacterial infection. USA300 is unique in that it has a group of genes that are not shared by other strains of MRSA. During their study, scientists from the UNC School of Medicine found the gene that allows the infection to remain on the skin longer than other strains, making it easier to pass the infection on to other individuals.

The problem is by the time you figure out how one strain comes into dominance, it often fades away and a new strain comes in. But because these compounds occur naturally and are so toxic, we still think they can lead to treatments that are effective against all MRSA. We will just have to put in a little extra work to block the gene and make this particular strain of MRSA susceptible to polyamines, explained the studys senior author Anthony Richardson, Assistant Professor of Microbiology and Immunology, in a statement.

The researchers believe that the gene also causes this strain of MRSA to be resistant to polyamines, compounds that occur naturally on human skin and are typically toxic to other strains. The findings of this particular gene provided the researchers with additional information to develop new treatments against MRSA, including the USA 300 strain that is found in the majority of hospital visits related to MRSA skin and soft tissue infections.

For their research, the team of investigators was able to track an attribute of MRSA that had not previously been studied and were able to better understand why MRSA is so sensitive to polyamines. Polyamines play an important role in wound care as they are anti-inflammatory and aid in tissue regeneration.

The scientists tested hundreds of MRSA strains and found that all except for the USA300 strain were sensitive to polyamines. They also discovered that this specific MRSA strains had a group of 34 genes, known as the arginine catabolic mobile element (ACME), which were not found in other strains.

Following the discovery of the ACME, the scientists mutated each of the genes so that they could change the gene sequence and create a new strain that could be eliminated by the polyamines. The researchers then added a normal, non-mutated version of the gene called SpeG to the other strains of MRSA to verify that those strains had become resistant to polyamines. The goal of the researcher was to determine exactly which gene was preventing the bacteria from being killed by the toxic polyamines so that they could focus on that particular gene when possibly developing a treatment in the future.

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Study Seeks Treatment For All MRSA Strains In Genetic Vulnerabilities

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Two cancer genetics researchers at the Icahn School of Medicine at Mount Sinai have received a grant from the Liddy Shriver Sarcoma Initiative to support promising research on a genetic mutation in hereditary bone cancer called osteosarcoma.

New York, NY (PRWEB) February 01, 2013

John Martignetti, MD, PhD and Olga Camacho-Vanegas, PhD discovered that mutations in newly described and previously unknown forms of the methylthioadenosine phosphorylase (MTAP) gene result in hereditary osteosarcoma and Malignant Fibrous Histiocytoma (MFH)two rare bone cancers that usually affect children, adolescents and young adults.

Osteosarcoma and MFH are treated with a combination of aggressive therapies, but a significant number of patients deal with disease relapse and progression. With support from the Liddy Shriver Sarcoma Initiative Grant, the scientists hope to find out why MTAP mutations result in cancer and how common they are, then evaluate MTAP as a therapeutic target.

Our goal is to evaluate how common MTAP mutations are in bone cancer and determine their therapeutic relevance, said Dr. Martignetti, who is Associate Professor of Genetics and Genomics Sciences; Oncological Sciences; and Pediatrics at the Graduate School of Biomedical Sciences at Mount Sinai. We are honored to be recognized by the Liddy Shriver Sarcoma Initiative, and hope our efforts will lead to improved therapies for individuals with osteosarcoma.

The work that led to this study began with Dr. Martignetti's encounter with a family when he was a Pediatric Resident at Mount Sinai in which several members had a rare bone disease and bone cancer. This led Dr. Martignetti and his research team to identify six other families throughout the world, unrelated to the first family, with the same condition. Genetic studies revealed a common link among all the families and patientsmutations in a region of the MTAP gene which arose from ancient retroviruses in the human genome - a completely novel finding in cancer genetics.

We knew that the MTAP gene was relevant in other types of cancer, but the mutations in this gene are markedly higher in bone cancer than we expected, said Dr. Camacho- Vanegas, Assistant Professor of Genetics and Genomic Sciences. This indicates that currently available chemotherapies and novel drugs that target MTAP may benefit patients with this type of cancer.

Bruce D. Shriver, PhD, Director of the Research Grants Program at the Liddy Shriver Sarcoma Initiative, said, We are pleased to support the research of Drs. Martignetti and Camacho-Vanegas and hope that it will lead to important and useful contributions to the treatment of Osteosarcoma and Malignant Fibrous Histiocytoma (MFH) of the bone.

According to the Liddy Shriver Sarcoma Initiative, sarcoma is a cancer of the connective tissues, such as nerves, muscles, and bones. Sarcomas can arise anywhere in the body and are frequently hidden deep in the limbs. They are often misdiagnosed and assumed to be sports injuries or benign bumps. Sarcomas are rare tumors, comprising less than one percent of adults' cancers and nearly 21 percent of children's cancers.

The Liddy Shriver Sarcoma Initiative was founded in 2003. Its mission is to improve the quality of life for people dealing with sarcomas around the world. The Initiative increases public awareness of sarcoma, raises funds to award research grants, and provides support and timely information to sarcoma patients, their families, and medical professionals. These efforts are achieved through collaboration with numerous individuals and organizations that share a similar vision.

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John Martignetti, MD, PhD, and Olga Camacho-Vanegas, PhD, Awarded Grant from Liddy Shriver Sarcoma Initiative

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ForgeCraft Ep 8 - Solving lava issues plus bonus genetics tutorial!
Solving our issues with lava once and for all! Xycraft Tanks + Geothermal Generators go! ============================== Join the IRC channel! #iChun on espernet Follow me on Twitter! twitter.com

By: oHaiiChun

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ForgeCraft Ep 8 - Solving lava issues plus bonus genetics tutorial! - Video

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Genetics Puzzle Problem (#12)

By: WillBegoable

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Genetics Puzzle Problem (#12) - Video

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Hair Loss Genetics Video
do-you-inherit-hair-loss-from-your-mothers-side-of-the-family-with-sanusi-umar-md

By: AHJEarNoseAndThroat

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Hair Loss Genetics Video - Video

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UTEP Headlines Newscast 02.01.13
IT #39;S FRIDAY, FEBRUARY 1, 2013. HELLO, I #39;M VERONIQUE MASTERSON IN THE UTEP LIBRARY. HERE #39;S WHAT YOU NEED TO KNOW ABOUT WHAT #39;S HAPPENING AT THE UNIVERSITY OF TEXAS AT EL PASO. ### IT #39;S ORANGE FRIDAY! AS YOU CAN SEE BEHIND ME, THESE STUDENTS ARE RIGHT ON POINT! WE #39;D LIKE THE MINER NATION TO WEAR ORANGE ON FRIDAYS TO BUILD SCHOOL SPIRIT AS PART OF THE UNIVERSITY #39;S CENTENNIAL CELEBRATION. FOR MORE INFORMATION ABOUT ALL THINGS CENTENNIAL, VISIT UTEP100YEARS.COM. ### A UNITED NATIONS SENIOR ADVISER ON MIGRATION WILL SPEAK ABOUT HUMAN SECURITY ON THE BORDER AT 10 AM WEDNESDAY, FEBRUARY 6 AT THE UTEP UNION CINEMA IN UNION BUILDING EAST. THE LECTURE, TITLED "HUMAN SECURITY AT THE BORDERLANDS: WHY SHOULD IT MATTER?" WILL BE FREE AND OPEN TO THE PUBLIC. SENIOR ADVISER TO THE UNITED NATIONS SECRETARY-GENERAL ON MIGRATION AND DEVELOPMENT FRANCOIS FOUINAT, IS EXPECTED TO ADDRESS THE IMPORTANCE OF ENGAGING IN ALTERNATIVE CONVERSATIONS ABOUT SECURITY POLICY THAT CENTER ON CITIZENS #39; WELL-BEING, AND ON HUMANIZING BORDERS BEYOND MILITARIZATION AND SURVEILLANCE. FOUINAT HAS SERVED IN HIS CURRENT POSITION SINCE 2006. HE HAS PLAYED A CENTRAL ROLE IN THE CONCEPTION AND ESTABLISHMENT OF THE GLOBAL FORUM ON MIGRATION AND DEVELOPMENT, A GLOBAL GOVERNMENTAL PROCESS THAT CONSIDERS THE LINKS BETWEEN MIGRATION AND DEVELOPMENT THROUGH DIALOGUE AND COOPERATION. ### KYUNG-AN HAN, PH.D., ASSOCIATE PROFESSOR OF BIOLOGICAL SCIENCES AND DIRECTOR OF THE NEUROSCIENCE AND METABOLIC DISORDERS PROJECT AT UTEP, HAS ...

By: UTEP

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UTEP Headlines Newscast 02.01.13 - Video

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Vlad #39;s Grow Titan Genetics: Dawg #39;s Breath Ep. 1
Test grow for Titan Genetics: (Stardawg x Alien Kush f2) X Tennesee Hawg #39;s Breath For more information visit: http://www.nwgt.org

By: Vladamyr

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Vlad's Grow Titan Genetics: Dawg's Breath Ep. 1 - Video

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Virology Lecture 2013 #3 - Genomes and genetics
A discussion of the seven different types of viral genome, and the pathway to mRNA, followed by an overview of modern viral genetic analysis.

By: Vincent Racaniello

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Virology Lecture 2013 #3 - Genomes and genetics - Video

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TGA Dairy Queen Apollo 13 BX OG Kush Chem Dawg -TLO Style
TGA Dairy Queen Apollo 13 BX OG Kush Chem Dawg Giving a long needed update on the Garden. Finally have some real genetics in which are OG Kush, TGA Genetics Dairy Queen, TGA Genetics Apollo 13 BX Chem Dawg... Using the TLO Style of Growing or True Living Organics Style of Growing developed by The Rev of Skunk Magazine. You can use the link below to Purchase his book if you haven #39;t gotten it already. http://www.amazon.com

By: HowtoGrowCannabis

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TGA Dairy Queen Apollo 13 BX OG Kush

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