Denny Ross - 16 January 2015 - 2
Denny is a charismatic and resilient individual who loves to challenge himself with the latest and fastest adventures in life. His most recent adventure has ...

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Denny Ross - 16 January 2015 - 2 - Video

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Wheelchair Van Transfer Video: Jennifer Hastings | MedBridge
Watch a demonstration of a wheelchair van transfer. Read FREE related article: https://www.medbridgeeducation.com/h/october-newsletter-independent-transfers-exercise-filters-back-pain-stroke-rehab ...

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Wheelchair Van Transfer Video: Jennifer Hastings | MedBridge - Video

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Non-Surgical Regenerative Medicine For Joint Pain- Flexogenix
For millions of patients experiencing joint pain, facing the prospect of joint replacement surgery along with all of the associated risks and potential unwan...

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Genetically modified crops have long drawn fire from opponents worried about potential contamination of conventional crops and other plants. Now a plant gene discovered by University of Guelph scientists might help farmers reduce the risk of GM contamination and quell arguments against the use of transgenic food crops, says Sherif Sherif, lead author of a new research paper describing the findings.

This is believed to be the first-ever study to identify a gene involved in altering fruit trees that normally cross-pollinate -- needing one plant to fertilize another -- into self-pollinators, said Sherif.

The paper was published recently in the journal BMC Biology.

Sherif said researchers might one day insert this gene into GM crops to prevent their pollen from reaching other plants.

Plant agriculture professor Jay Subramanian, Sherif's PhD supervisor and a co-author on the paper, said: "There are a lot of transgenic crops worldwide. There is concern about pollen from them being able to fertilize something in the wild population, thus creating 'super weeds.'"

The researchers found a gene making a protein that naturally allows a small handful of plants to self-pollinate and make fruit before the flower opens. Peaches, for example, have closed flowers, unlike their showy-flowered plum and cherry cousins that need pollen from another tree to fertilize and set fruit.

Subramanian studies tree fruits at the Vineland Research and Innovation Centre in Vineland, Ont. Sherif worked with him on studies of plant responses to stresses such as drought or disease.

Other co-authors on the paper are Guelph professors Jaideep Mathur, Department of Molecular and Cellular Biology and Gopi Paliyath, Department of Plant Agiruclture, along with Islam El-Sharkawy, a former research associate with Subramanian; and colleagues at the National University of Singapore.

Besides aiding crop farmers and food producers, their discovery might be a boon to perfume-makers, said Subramanian.

Used in fragrant perennials such as jasmine, the gene might keep flowers closed and allow growers to collect more of the aromatic compounds prized by perfume-makers. "That's when volatile compounds are peaking," said Subramanian. "When the flower opens, you lose almost 80 per cent of those volatiles."

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Gene may help reduce GM contamination

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Single-letter genetic variations within parts of the genome once dismissed as 'junk DNA' can increase cancer risk through wormhole-like effects on far-off genes, new research shows.

Researchers found that DNA sequences within 'gene deserts' -- so called because they are completely devoid of genes -- can regulate gene activity elsewhere by forming DNA loops across relatively large distances.

The study, led by scientists at The Institute of Cancer Research, London, helps solve a mystery about how genetic variations in parts of the genome that don't appear to be doing very much can increase cancer risk.

Researchers developed a new technique to study the looping interactions and discovered that single-letter DNA variations linked to the development of bowel cancer were found in regions of the genome involved in DNA looping.

Their study, published today in Nature Communications, is the first to look comprehensively at these DNA interactions specifically in bowel cancer cells, and has implications for the study of other complex genetic diseases.

It was funded by the EU, Cancer Research UK, Leukaemia & Lymphoma Research, and The Institute of Cancer Research (ICR).

The researchers developed a technique called Capture Hi-C to investigate long-range physical interactions between stretches of DNA -- allowing them to look at how specific areas of chromosomes interact physically in more detail than ever before. Previous techniques used to investigate long-range DNA interactions were not sensitive enough to produce definitive results.

The researchers assessed 14 regions of DNA that contain single-letter variations previously linked to bowel cancer risk. They detected significant long-range interactions for all 14 regions, confirming their role in gene regulation.

These interactions are important because they can control how genes behave, and alterations in gene behaviour can lead to cancer -- in fact most genetic variations that have been linked to cancer risk are not in genes themselves, but in the areas of the genome that regulate them.

Study leader Professor Richard Houlston, Professor of Molecular and Population Genetics at The Institute of Cancer Research, London, said: "Our new technique shows that genetic variations are able to increase cancer risk through long-range looping interactions with cancer-causing genes elsewhere in the genome. It is sometimes described as analogous to a wormhole, where distortions in space and time could in theory bring together distant parts of the universe.

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Cancer risk linked to DNA 'wormholes'

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Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement and is fatal in the majority of cases. The next-generation genetic sequencing of the exomes (protein-coding portions) of 2,874 ALS patients and 6,405 controls represents the largest number of ALS patients to have been sequenced in a single study to date.

Though much is known about the genetic underpinnings of familial ALS, only a handful of genes have been definitively linked to sporadic ALS, which accounts for about 90 percent of all ALS cases. The newly associated gene, called TBK1, plays a key role at the intersection of two essential cellular pathways: inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components). The study, conducted by an international ALS consortium that includes scientists and clinicians from Columbia University Medical Center (CUMC), Biogen Idec, and HudsonAlpha Institute for Biotechnology, was published today in the online edition of Science.

"The identification of TBK1 is exciting for understanding ALS pathogenesis, especially since the inflammatory and autophagy pathways have been previously implicated in the disease," said Lucie Bruijn, PhD, Chief Scientist for The ALS Association. "The fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease. This study, which combines the efforts of over two dozen laboratories in six countries, also highlights the global and collaborative nature of ALS research today.

"This study shows us that large-scale genetic studies not only can work very well in ALS, but that they can help pinpoint key biological pathways relevant to ALS that then become the focus of targeted drug development efforts," said study co-leader David B. Goldstein, PhD, professor of genetics and development and director of the new Institute for Genomic Medicine at CUMC. "ALS is an incredibly diverse disease, caused by dozens of different genetic mutations, which we're only beginning to discover. The more of these mutations we identify, the better we can decipher--and influence--the pathways that lead to disease." The other co-leaders of the study are Richard M. Myers, PhD, president and scientific director of HudsonAlpha, and Tim Harris, PhD, DSc, Senior Vice President, Technology and Translational Sciences, Biogen Idec.

"These findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential points of intervention. We are following up by looking at the function of this pathway so that one day this research may benefit the patients living with ALS," said Dr. Harris. "The speed with which we were able to identify this pathway and begin our next phase of research shows the potential of novel, focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease. This synergy is vital for both industry and the academic community, especially in the context of precision medicine and whole-genome sequencing."

"Industry and academia often do things together, but this is a perfect example of a large, complex project that required many parts, with equal contributions from Biogen Idec. Dr. Tim Harris, our collaborator there, and his team, as well as David Goldstein and his team, now at Columbia University, as well as our teams here at HudsonAlpha, said Dr. Myers. "I love this research model because it doesn't happen very frequently, and it really shows how industry, nonprofits, and academic laboratories can all work together for the betterment of humankind. The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information, recruiting patients, as well as collecting DNA samples for us to do this study, were all critical to get this done."

Searching through the enormous database generated in the ALS study, Dr. Goldstein and his colleagues found several genes that appear to contribute to ALS, most notably TBK1 (TANK-Binding Kinase 1), which had not been detected in previous, smaller-scale studies. TBK1 mutations appeared in about 1 percent of the ALS patients--a large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein. The study also found that a gene called OPTN, previously thought to play a minor role in ALS, may actually be a major player in the disease.

"Remarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene, interact physically and functionally. Both proteins are required for the normal function of inflammatory and autophagy pathways, and now we have shown that mutations in either gene are associated with ALS," said Dr. Goldstein. "Thus there seems to be no question that aberrations in the pathways that require TBK1 and OPTN are important in some ALS patients."

The researchers are currently using patient-derived induced pluripotent embryonic stem cells (iPS cells) and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates. Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor-cell survival.

"This is a great example of the potential of precision medicine," said Tom Maniatis, PhD, the Isidore S. Edelman Professor, chair of biochemistry and molecular biophysics, and coauthor on the paper. Dr. Maniatis is also a member of the Zuckerman Mind Brain Behavior Institute and director of Columbia's university-wide precision medicine initiative. "It now seems clear that future ALS treatments will not be equally effective for all patients because of the disease's genetic diversity. Ultimately, as candidate therapies become available, we hope to be able to use the genetic data from each ALS patient to direct that person to the most appropriate clinical trials and, ultimately, use the data to prescribe treatment."

Link:
New ALS gene, signaling pathways identified

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Newswise NEW YORK, NY (February 19, 2015)Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS), or Lou Gehrigs disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement and is fatal in the majority of cases. The next-generation genetic sequencing of the exomes (protein-coding portions) of 2,874 ALS patients and 6,405 controls represents the largest number of ALS patients to have been sequenced in a single study to date.

Though much is known about the genetic underpinnings of familial ALS, only a handful of genes have been definitively linked to sporadic ALS, which accounts for about 90 percent of all ALS cases. The newly associated gene, called TBK1, plays a key role at the intersection of two essential cellular pathways: inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components). The study, conducted by an international ALS consortium that includes scientists and clinicians from Columbia University Medical Center (CUMC), Biogen Idec, and HudsonAlpha Institute for Biotechnology, was published today in the online edition of Science.

"The identification of TBK1 is exciting for understanding ALS pathogenesis, especially since the inflammatory and autophagy pathways have been previously implicated in the disease," said Lucie Bruijn, PhD, Chief Scientist for The ALS Association. "The fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease. This study, which combines the efforts of over two dozen laboratories in six countries, also highlights the global and collaborative nature of ALS research today.

This study shows us that large-scale genetic studies not only can work very well in ALS, but that they can help pinpoint key biological pathways relevant to ALS that then become the focus of targeted drug development efforts, said study co-leader David B. Goldstein, PhD, professor of genetics and development and director of the new Institute for Genomic Medicine at CUMC. ALS is an incredibly diverse disease, caused by dozens of different genetic mutations, which were only beginning to discover. The more of these mutations we identify, the better we can decipherand influencethe pathways that lead to disease. The other co-leaders of the study are Richard M. Myers, PhD, president and scientific director of HudsonAlpha, and Tim Harris, PhD, DSc, Senior Vice President, Technology and Translational Sciences, Biogen Idec.

These findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential points of intervention. We are following up by looking at the function of this pathway so that one day this research may benefit the patients living with ALS, said Dr. Harris. The speed with which we were able to identify this pathway and begin our next phase of research shows the potential of novel, focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease. This synergy is vital for both industry and the academic community, especially in the context of precision medicine and whole-genome sequencing.

Industry and academia often do things together, but this is a perfect example of a large, complex project that required many parts, with equal contributions from Biogen Idec. Dr. Tim Harris, our collaborator there, and his team, as well as David Goldstein and his team, now at Columbia University, as well as our teams here at HudsonAlpha, said Dr. Myers. I love this research model because it doesnt happen very frequently, and it really shows how industry, nonprofits, and academic laboratories can all work together for the betterment of humankind. The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information, recruiting patients, as well as collecting DNA samples for us to do this study, were all critical to get this done."

Searching through the enormous database generated in the ALS study, Dr. Goldstein and his colleagues found several genes that appear to contribute to ALS, most notably TBK1 (TANK-Binding Kinase 1), which had not been detected in previous, smaller-scale studies. TBK1 mutations appeared in about 1 percent of the ALS patientsa large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein. The study also found that a gene called OPTN, previously thought to play a minor role in ALS, may actually be a major player in the disease.

Remarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene, interact physically and functionally. Both proteins are required for the normal function of inflammatory and autophagy pathways, and now we have shown that mutations in either gene are associated with ALS, said Dr. Goldstein. Thus there seems to be no question that aberrations in the pathways that require TBK1 and OPTN are important in some ALS patients.

See the article here:
New ALS Gene and Signaling Pathways Identified

Recommendation and review posted by Bethany Smith

Chuck Bednar for redOrbit.com @BednarChuck

As a general rule, humans like to know exactly what it is that theyre eating. In the past, this was an easy task you could pick up a tomato, a can of corn and a pack of ground beef and be fairly confident that you knew where they came from. In recent years, however, scientists have become increasingly involved in food production, causing some confusion amongst consumers.

[Related story: GMO potato approved by USDA]

If youre one of the people who sometimes feel overwhelmed when you start hearing terms such as genetic modification and selective breeding, dont worry we here at RedOrbit feel your pain, so weve created this handy little guide to help clear up some of the confusion.

Genetic modification (GMO)

Genetically modified organisms (GMOs) have been at the center of much of the discussion over scientifically-manipulated food. While a 2010 EU-funded study found that eating GMO foods is no more risky that eating conventionally-grown products, there are laws requiring these goods to carry special labels in over 60 countries, and some remain concerned about their safety.

According to the nonprofit George Mateljan Foundation, a GMO is defined as any organism that has had its core genetic material altered using genetic engineering techniques. In other words, the crops or creatures have had their DNA or RNA fundamentally changed in a laboratory in order to add or enhance specific traits, allowing them to grow larger, stay fresh longer, and so on.

A good example of this is the Arctic apple, a genetically-modified apple produced by a Canadian company, Okanagan Specialty Fruits, that received USDA approval earlier this week. The Arctic apple underwent a process called RNA interference (RNAi), which blocked a normally-occurring enzyme and kept the apple from turning brown after it had been sliced. [Related story: GMO apple approved for sale in US]

Selective breeding

Like genetic modification, selective breeding is performed in order to promote specific traits in a plant or animal. However, the selective breeding process does not involve making any changes to the core biological makeup of a plants genetic makeup at least not directly. Rather, organisms which strongly exhibit specific characteristics are bred together to emphasize those traits.

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WTF is GMO?

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How can we keep more people from joining the ranks of the 29 million Americans already diagnosed with diabetes? What if we could tell with precision who has the highest risk of developing the disease, and figure out which preventive steps are most likely to help each of them individually?

Researchers have just released a "precision medicine" approach to diabetes prevention that could do just that -- using existing information like blood sugar levels and waist-to-hip ratios, and without needing new genetic tests.

Their newly published model examined 17 different health factors, in an effort to predict who stands to gain the most from a diabetes-preventing drug, or from lifestyle changes like weight loss and regular exercise. Seven of those factors turned out to matter most.

The model is published in the British Medical Journal by a team from the University of Michigan, VA Ann Arbor Healthcare System and Tufts Medical Center in Boston.

They hope to turn it into a tool for doctors to use with patients who have "pre-diabetes," currently defined by abnormal results on a test of blood sugar after fasting. They also hope their approach could be used to develop similar precise prediction models for other diseases and treatments.

"Simply having pre-diabetes is not everything," says lead author Jeremy Sussman, M.D., M.S. "This really shows that within the realm of pre-diabetes there's a lot of variation, and that we need to go beyond single risk factors and look holistically at who are the people in whom a particular approach works best." Sussman is an assistant professor of general medicine at the U-M Medical School and a research scientist at the VA Center for Clinical Management Research.

The team developed the model using data from a gold-standard clinical trial of diabetes prevention: the Diabetes Prevention Program, which randomly assigned people with an elevated risk of diabetes to placebo, the drug metformin, or a lifestyle-modification program.

The team developed and tested their model by carefully analyzing data from more than 3,000 people in the study, all of whom had a high body mass index and abnormal results on two fasting blood sugar tests. Most also had a family history of diabetes, and more than a third were African American or Latino -- all known to be associated with higher risks of diabetes. In all, they looked at 17 factors that together predicted a person's risk of diabetes -- and his or her chance of benefiting from diabetes-preventing steps. They found seven factors were most useful.

The seven were: fasting blood sugar, long-term blood sugar (A1C level), total triglycerides, family history of high blood sugar, waist measurement, height, and waist-to-hip ratio. They developed a scoring scale using the clinical trial data, assigning points to each measure to calculate total score.

Fewer than one in 10 of trial participants who scored in the lowest quarter would develop diabetes in the next three years, while almost half of those in the top quarter would develop diabetes in that time. Then, the team looked at what impact the two diabetes-preventing approaches had.

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Precision medicine to prevent diabetes? Researchers develop personalized way to steer prevention efforts

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Tucson, AZ. (PRWEB) February 19, 2015

Could genetic codedetermine someones coffee habit? Apparently so, according to a new study by researchers at the Harvard T.H. Chan School of Public Health (HSPH).

Produced with the support of the Coffee and Caffeine Genetics Consortium and published in the journal Molecular Psychiatry this past fall, the studyone of several recent HSPH investigations of the popular beverageinvolved a meta-analysis of genomic data from more than 120,000 regular coffee drinkers of European and African ancestry. The researchers analyzed their subjects genetic makeup through DNA sequencing, and compared those results to self-reported coffee-drinking figures, in an effort to understand why some people need more of the stimulant than others to feel the same effect. Their data suggest that people instinctively regulate their coffee intake in order to experience the optimal effects of caffeine.

Lead author Marilyn Cornelis, a former research associate in the HSPH nutrition department who is now assistant professor in preventive medicine at Northwestern, says their findings provide insight not only on why caffeine affects people differently, but also on how these effects influence coffee-drinking behavior. One individual, for example, may need three cups of coffee to feel invigorated, while another may need only one. If that one-cup-a-day person consumes four cups instead, Cornelis explains, any jitters or other ill effects that result may discourage that level of consumption in the future.

Given coffees widespread consumption, its effects on health have been the subject of continuing interest and debate. The newest edition of The Diagnostic and Statistical Manual of Mental Disorders, for example, lists both caffeine intoxication and withdrawal as disorders. On the other hand, a study released in January by other investigators at HSPH found that drinking up to six cups of coffee a day showed no association with any increased risk of death (including from cancer or cardiovascular disease). Going back several yearscoffee often had a bad rap, Cornelis says. I hope to finally account for those genetic variants and possibly other risk factors that might modify our response to coffee or caffeine.

Her team identified six new genetic variants associated with habitual coffee drinking, including twoPOR and ABCG2related to caffeine metabolism, and another two that may influence the psychological boost and possible physical health benefits of caffeine. The most surprising aspect of the study, Cornelis reports, was the discovery that two genes involved in glucose and lipid metabolismGCKR and MLXIPLare also linked for the first time to the metabolic and neurological effects of caffeine.

Coffee is possibly protective, Cornelis says. Eventually, she hopes to account for those genetic variants and possibly other risk factors that might modify our response to coffee or caffeine. We know coffee is one of the primary sources of antioxidants of the American diet. If some individuals can metabolize caffeine quickly, then theyre potentially getting rid of the adverse effects of caffeine yet still experiencing the beneficial effects of other coffee constituents.

When it comes experiencing the healthiest choice for coffee look no further than Tylers Acid Free Coffee. Their chemical free roasting process maintains double the natural caffeine. As well as being acid-free, the lack of bloomed tannins and lipids acids makes the coffee less bitter, pH neutral, safer on tooth enamel, safer on your GI tract and an overall healthy choice for all coffee drinkers around the world. Make the choice to start a healthy lifestyle, take care of your body and your body will take care of you.

Link:
Enhancing the Caffeine Experience and How Coffee Habits Relate to Our Genetic Code

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Innovation and research in Personalized Medicine. Rafael Lopez
Instituto Roche Forum on Personalized Medicine: Challenges for the next decade 25th september 2014, Palacio de Congresos y Exposiciones de Galicia. Session 2: Innovation, research and Public...

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Innovation and research in Personalized Medicine. Rafael Lopez - Video

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Jill Hagenkord | A Decade of Direct Access Genetics: What have we learned?
23andMe Chief Medical Officer, Jill Hagenkord, describes how their company is disrupting the healthcare industry by allowing people to access their own DNA. Genetic information is the basis...

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Jill Hagenkord | A Decade of Direct Access Genetics: What have we learned? - Video

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MCR Overview Edited
Overview of a few of Michael Riddle Jr. #39;s Projects.

By: Riddle Institute for Regenerative Medicine

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MCR Overview Edited - Video

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Platelet Rich Plasma - Howard Beach, Queens - Dr. Benjamin Bieber, MD - Regenerative Medicine
Platelet Rich Plasma (PRP) - Howard Beach, Ozone Park, Queens NY - Dr. Benjamin Bieber, MD - Regenerative Medicine http://www.crossbaypmr.com (718) 835-0100 Dr. Benjamin Bieber of Cross...

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A New Way to Reduce Chronic Pain - Denver Regenerative Medicine
For many people suffering from chronic pain, medication and surgery have been their only options to find relief. But Dr. Joel Cherdack of Denver Regenerative Medicine spoke with us about new...

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Posted by Richard Dietman (@rdietman) 3 day(s) ago

Mayo Clinic Radio: Cardiac Regeneration/Stop-Smoking Drug/Juicing

On this weeks Mayo Clinic Radio,fixing a broken heart. Cardiac regeneration uses the bodys own stem cells to repair damage done by heart disease. Mayo Clinic cardiologist Dr. Atta Behfar explains. Also on the program, nicotine dependency expert Dr. Richard Hurt discusses results of a new study about the stop-smoking drug varenicline (Chantix). And Mayo Clinic registered dietitian Katherine Zeratsky explains the risks of juice-only diets.

Myth or Matter-of-Fact: Cardiac regeneration may someday replace the need for surgery to repair heart damage.

To listen to the program at 9 a.m. Saturday, February 21, clickhere.

Follow#MayoClinicRadioand tweet your questions.

Mayo Clinic Radio is available oniHeartRadio.

Mayo Clinic Radiois a weeklyone-hour radio program highlighting health and medical informationfrom Mayo Clinic.

To find and listen toarchived shows,click here.

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Mayo Clinic Radio: Cardiac Regeneration/Stop-Smoking Drug/Juicing

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DALLAS, February 19, 2015 /PRNewswire/ --

The Global Cell Culture Protein Surface Coating Market 2015-2019 research report available with LifeScienceIndustryResearch.com provides information on the usage of different types of proteins derived from various sources for cell culture protein surface coating: Animal-derived protein, Human-derived protein, Synthetic protein and Plant-derived protein.

The Global Cell Culture Protein Surface Coating Market is expected to post 12.91% CAGR from 2014-2019, thanks to the wide range of applications for protein surface coatings include improved adhesion of cells, better proliferation and growth of cells, receptor-ligand binding studies, cell matrix studies, signal transduction studies, morphogenesis studies, differentiation of individual cell types, genetic engineering, metabolic pathway studies and drug screening. The high potential of stem cells in the treatment of severe diseases, including neurodegenerative diseases, cardiac diseases, and even diabetes, has resulted in demand for advanced cell culture products for stem cell production and study. Cell culture protein surface coating products help researchers improve the adhesion, proliferation, and growth of cultured cells. Complete report is available at http://www.lifescienceindustryresearch.com/global-cell-culture-protein-surface-coating-market-2015-2019.html .

Biopharmaceuticals are protein-based products such as vaccines, somatic cells, allergenics, and recombinant therapeutic proteins that are derived through cell culture. There has been increased demand for biopharmaceuticals, since they can be used to treat diseases and injuries more effectively than conventional drugs. Several big biopharmaceutical companies such as Roche, Novo Nordisk, and EMD Millipore are involved in biopharmaceutical production, and they require high accuracy and efficiency in their cell culture applications. Since cell culture protein surface coating has been shown to facilitate cell adhesion, and delivers high productivity in cell culture activities, these products are now in high demand in the biopharmaceuticals sector.

Cell culture protein surface coating is a procedure in which the cell culture surfaces are coated with proteins or extracellular matrix components to enhance the adhesion and proliferation of the cells in vitro. The following are the different types of available proteins: human-derived proteins, animal-derived proteins, plant-derived proteins, and synthetic proteins. Proteins such as fibronectin, laminin, collagen, vitronectin, and osteopontin are used for cell culture protein surface coating. Protein surface coating helps in the growth of various types of cells such as endothelial, epithelial, fibroblasts, leukocytes, myoblasts and muscle cells, neurons, and CHO cell lines. Cell culture protein surface coating provides improved adhesion, proliferation, and rapid growth of cells during isolation and cultivation.

This report covers the present scenario and the growth prospects of Global Cell Culture Protein Surface Coating market for the period 2015-2019. To calculate the market size, the report considers revenue generated from the sales of cell culture protein surface coating products including consumables and instruments.

Companies like Becton, Dickinson and Company, Corning, EMD Millipore, Sigma-Aldrich, Thermo Fisher Scientific, Abcam, BioMedTech Laboratories, Bio-Techne, Cedarlane Laboratories, Cell Guidance Systems, Cytoskeleton, Full Moon BioSystems, Greiner Bio-One, neuVitro, Orla Protein Technologies, Pall, PerkinElmer, PROGEN Biotechnik, PromoCell, RayBiotech, Sartorius Stedim Biotech, SouthernBiotech, Trevigen and Viogene BioTek are mentioned in this research available for purchase at http://www.lifescienceindustryresearch.com/purchase?rname=34847 .

The presence of developed healthcare infrastructure and government funding for companies is encouraging extensive R&D in the Global Cell Culture Surface Coating Market. Big pharmaceutical and biotechnology companies are investing extensively in R&D to develop innovative products to meet customer demand. High-end cell culture protein surface coating products can be used in many applications such as drug development, cell biology, tissue engineering, and biopharmaceutical production to increase efficiency and productivity.

The Global Cell Culture Protein Surface Coating Market 2015-2019 research report has been prepared based on an in-depth market analysis with inputs from industry experts. The report covers the Americas, and the EMEA and APAC regions; it also covers the Global Cell Culture Protein Surface Coating market landscape and its growth prospects in the coming years. The report includes a discussion of the key vendors operating in this market.

Other newly published research reports on the biotechnology market available with LifeScienceIndustryResearch.com can be accessed at http://www.lifescienceindustryresearch.com/category/biotechnology .

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Biopharma Demand Driving Cell Culture Protein Surface Coating Market Growth Globally, Along with Synthetic Proteins ...

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Under normal conditions, many of the different types of tissue-specific adult stem cells, including hematopoietic stem cells, exist in a state or dormancy where they rarely divide and have very low energy demands. "Our theory was that this state of dormancy protected hematopoietic stem cells from DNA damage and therefore protects them from premature aging," says Dr. Michael Milsom, leader of the study.

However, under conditions of stress, such as during chronic blood loss or infection, hematopoietic stem cells are driven into a state of rapid cell division in order to produce new blood cells and repair the damaged tissue. "It's like forcing you out of your bed in the middle of the night and then putting you into a sports car and asking you to drive as fast as you can around a race circuit while you are still half asleep," explains Milsom. "The stem cells go from a state of rest to very high activity within a short space of time, requiring them to rapidly increase their metabolic rate, synthesize new DNA and coordinate cell division. Suddenly having to simultaneously execute these complicated functions dramatically increases the likelihood that something will go wrong."

Indeed, experiments described in the study show that the increased energy demands of the stem cells during stress result in elevated production of reactive metabolites that can directly damage DNA. If this happens at the same time that the cell is trying to replicate its DNA, then this can cause either the death of the stem cell, or potentially the acquisition of mutations that may cause cancer.

Normal stem cells can repair the majority of this stress-induced DNA damage, but the more times you are exposed to stress, the more likely it is that a given stem cell will inefficiently repair the damage and then die or become mutated and act as a seed in the development of leukemia. "We believe that this model perfectly explains the gradual accumulation of DNA damage in stem cells with age and the associated reduction in the ability of a tissue to maintain and repair itself as you get older," Milsom adds.

In addition, the study goes on to examine how this stress response impacts on a mouse model of a rare inherited premature aging disorder that is caused by a defect in DNA repair. Patients with Fanconi anemia suffer a collapse of their blood system and have an extremely high risk of developing cancer. Mouse models of Fanconi anemia have exactly the same DNA repair defect as found in human patients but the mice never spontaneously develop the bone marrow failure observed in nearly all patients.

"We felt that stress induced DNA damage was the missing ingredient that was required to cause hematopoietic stem cell depletion in these mice," says Milsom. When Fanconi anemia mice were exposed to stimulation mimicking a prolonged viral infection, they were unable to efficiently repair the resulting DNA damage and their stem cells failed. In the same space of time that normal mice showed a gradual decline in hematopoietic stem cell numbers, the stem cells in Fanconi anemia mice were almost completely depleted, resulting in bone marrow failure and an inadequate production of blood cells to sustain life.

"This perfectly recapitulates what happens to Fanconi anemia patients and now gives us an opportunity to understand how this disease works and how we might better treat it," commented Milsom.

Prof. Dr. Andreas Trumpp, director of HI-STEM and head of the Division of Stem Cells and Cancer at the DKFZ believes that this work is a big step towards understanding a range of age-related diseases. "The novel link between physiologic stress, mutations in stem cells and aging is very exciting," says Trumpp, a co-author of the study. "By understanding the mechanism via which stem cells age, we can start to think about strategies to prevent or at least reduce the risk of damaged stem cells which are the cause of aging and the seed of cancer."

Story Source:

The above story is based on materials provided by German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ). Note: Materials may be edited for content and length.

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A good night's sleep keeps your stem cells young

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A devoted mum whose sick twins desperately need a double bone marrow transplant has begged the nation: Please save my boys.

Luis and Kian King, seven, have Juvenile Krabbe Disease, which quickly ravages the nervous system and the youngsters are getting worse by the week.

Parents Laura, 36, and Dean, 38, know the odds are stacked against the boys, as doctors battle to find donors for the UKs first twin transplant, before they become too weak to survive treatment.

The average life expectancy of a child with the rare disease is just 12.

Laura pleaded: If you are not on the donor register you could be the match who can give my boys back their lives and their futures and you dont even realise it.

All of us are giant medicine bottles walking around with the ability to help others in their hour of need. It only takes 10 minutes to join the register and you can change a familys life forever.

Juvenile Krabbe Disease which affects fewer than one in a million children has left the boys, who also have cerebral palsy, unable to walk unaided.

Experts have warned that without a stem cell transplant they only have three years left with any real quality of life.

The disease will rob them of their sight and ability to feed themselves, causing them to suffer more and more pain until they can no longer breathe unaided.

With the boys just five years off the average life expectancy of 12, Laura admits their illness haunts her.

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Luis and Kian King: Juvenile Krabbe Disease victims' mum in plea to help save her twin boys

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Fayetteville, Arkansas (PRWEB) February 19, 2015

CardioWise, Inc. has completed development of the first fully integrated version of its Multiparametric Strain Analysis Software (MPSA) and has installed it at the National Institutes of Health (NIH), National Heart, Lung, and Blood Institute (NHLBI). MPSA software is being used in clinical research protocol number 12-H-0078, sponsored by the NHLBI entitled, Preliminary Assessment of Direct Intra-Myocardial Injection of Autologous Bone Marrow-derived Stromal Cells on Patients Undergoing Revascularization for Coronary Artery Disease (CAD) with Depressed Left Ventricular Function. The Principle Investigator is Dr. Keith A. Horvath, the Director of Cardiothoracic Surgery at the NHLBI and Chief of Cardiothoracic Surgery at Suburban Hospital, where he leads the NIH Heart Center. Details of the study are available here: http://clinicalstudies.info.nih.gov/cgi/wais/bold032001.pl?A_12-H-0078.html@mesenchymal@@@@.

The recently completed integrated version of CardioWise analysis software has been installed at the NIH; and, Dr. Justin Miller, and Dr. Ming Li, both research fellows in the Cardiothoracic Surgery Research Program of the NHLBI, have been trained on its operation and use. They were assigned to the project by Dr. Horvath and Dr. Andrew Arai, Chief of the Advanced Cardiovascular Imaging Research Group in the NHLBIs Division of Intramural Research. CardioWise has completed validation testing of its software and the analyses of the first two patient cardiac MRI (CMR) data sets are in process. The patients who enrolled in the protocol received one baseline CMR scan and three additional follow-up CMR scans. Those CMR scans are being analyzed by CardioWise analysis software and the analyses will be compared to determine whether stem cell injections can improve the contractile function of the heart muscle by repairing damaged tissue.

The installation at the NIH under a Beta site agreement signed in 2014 marks the first clinical test of CardioWise MPSA software outside of Washington University School of Medicine in St. Louis, where it was developed. CardioWise has obtained the exclusive worldwide license for the patent-pending software and accompanying normal hearts database from Washington University in St. Louis. The companys MPSA software is uniquely capable of analyzing the three-dimensional motion of the heart that is acquired from cardiac MRI images and then comparing the analysis at 15,300 points to the motion of a normal heart model. The analysis detects portions of the heart that are moving abnormally and demonstrates to what degree the heart muscle has been affected. Since MRI uses no ionizing radiation or contrast, it is completely non-invasive and poses minimal risk to the patient. This allows the patient to be followed through the course of treatment and to measure outcomes of interventions such as the stem cell therapy currently being evaluated. In the near future, CardioWise MPSA may aid doctors to determine what intervention, such as surgery, stent insertion, or drug is most appropriate for the patient who presents with cardiovascular disease symptoms.

CardioWise is commercializing patent-pending, non-invasive Cardiac Magnetic Resonance Imaging (CMR) analysis software that produces a quantified 4D image model of the human heart, called Multiparametric Strain Analysis (MPSA). CardioWise heart analysis software combined with cardiac MRI is a single diagnostic test that is able to provide quantitative analysis of the myocardium, arteries and valves with an unprecedented level of detail. It has the opportunity to become the new gold standard of care for heart health analysis. CardioWise is a VIC Technology Venture Development portfolio company.

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CardioWise Completes Installation of the First Totally Integrated CardioWise Analysis Software at National Institutes ...

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Stemologica Review - Try Stemologica To Prevent Appearance Of Wrinkles
Click the link below to get a risk free trial; http://skincarebeautyshop.com/go/have-your-stemologica-free-trial/ Read the Terms and Condition before you ord...

By: Yvan B.

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Stemologica Review - Try Stemologica To Prevent Appearance Of Wrinkles - Video

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Negotiating the Mine Field in the Quest for a Parkinsons Disease Cell Therapy - Jeanne Loring
Rejuvenation Biotechnology 2014 Parkinson #39;s Disease Session (August 22, 2014, 1:00pm) "Negotiating the Mine Field in the Quest for a Parkinson #39;s Disease Cell...

By: SENS Foundation

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Negotiating the Mine Field in the Quest for a Parkinsons Disease Cell Therapy - Jeanne Loring - Video

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Stem Cell Therapy Using Bone Marrow - Howard Beach, Ozone Park, Queens NY - Dr. Benjamin Bieber, MD
http://www.crossbaypmr.com Stem Cell Therapy Using Bone Marrow - Howard Beach, Ozone Park, Queens NY - Dr. Benjamin Bieber, MD - Regenerative Medicine Phone:...

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Stem Cell Therapy Using Bone Marrow - Howard Beach, Ozone Park, Queens NY - Dr. Benjamin Bieber, MD - Video

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Like a car's front and back bumpers, your cell's chromosomes are capped by "telomeres" that protect this genetic material against deterioration. Still, after enough replications, a chromosome's telomeres break down and once they reach a certain point of degradation, the cell dies. This is one reason that cells are mortal: telomeres only last so long. That is, unless the enzyme telomerase builds new material onto the worn telomeres to reinforce these chromosomal "bumpers." Telomere repair can be a good thing, but in some cases it's not: overactive telomerase can lengthen telomeres until a cell becomes immortal...leading to cancer.

Previous studies blame the gene TERT for reactivating the enzyme telomerase long after its work in healthy cells should be done. And, as you might expect, mutations that turn on the TERT gene are found in many cancer types. Again: more TERT makes more telomerase, which reinforces telomeres, which makes a cell immortal, which causes cancer. The lesson seems simple: turn off TERT and you can stop cancer.

But, like many findings in cancer, it's not nearly so simple. Despite this seemingly linear storyline, previous studies have been unable to show that a cell's level of TERT mutations predicts anything about the course of a patient's cancer -- patients with tumors harboring many TERT mutations seem to do just as well as patients with tumors harboring few TERT mutations.

A study published in the journal Science by University of Colorado Cancer Center members at the University of Colorado at Boulder and Denver looks inside human bladder cancer cell lines and patient genetics to discover why. The answer may help doctors and researchers mark especially aggressive bladder cancers, allowing them to recommend appropriate treatments and improve patient outcomes.

"We show a lot of correlations in the cell lines: TERT mutations are associated with things like more TERT mRNA, more TERT protein, more telomerase activity, and longer telomere lengths. But which of these things that go together is most meaningful to patients' lives?" says Thomas R. Cech, CU Cancer Center investigator, distinguished professor in the Department of Chemistry and Biochemistry at CU Boulder, winner of the 1989 Nobel Prize in Chemistry, and senior author of the study.

Cech's research team worked with colleagues including Dan Theodorescu, MD, PhD, professor of Urology and Pharmacology, director of the CU Cancer Center to show that, while there may be little correlation between the presence of TERT mutation and bladder cancer patient outcomes, levels of TERT messenger RNA (mRNA) are highly predictive of cancers that will act aggressively to claim patients' lives.

"We don't mean to disregard the influence of TERT mutations. Only, it seems that after these mutations, there are additional mechanics that intercede to create higher telomerase activity, longer telomere length, and poorer patient outcomes," Theodorescu says.

In other words, it is not simply the presence of TERT gene mutations that lead to cell immortality, but other factors that determine how often the blueprints of the mutated gene are manufactured into the protein it encodes. Sure enough, even among cells that had the same TERT mutations, some cells acted more aggressively than others, and these aggressive cells had fivefold higher levels of TERT protein and fourfold higher levels of telomerase activity. It was not the gene but its expression that made aggressive cancer.

"TERT expression levels directly determine telomerase activity levels," the authors write. And it is this activity that reinforces degraded telomeres, allowing a cell's chromosomes to continue replicating into immortality.

The finding has two important implications for patients with bladder cancer. First, by assessing levels of TERT mRNA (which more directly determines TERT protein levels), doctors could in the future pinpoint which patients should be treated with the most aggressive therapies. Second, the finding reinforces the opinion that telomerase reactivation is important for the progression of bladder cancers (and many other types as well), and that perhaps by learning to interrupt the process of telomerase reactivation, we could someday interrupt the progression of the disease itself.

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Chromosome 'bumper repair' gene predicts cancer patient outcomes

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Cancer Center News

Duke Medicine researchers have shown how gene mutations may cause common forms of cartilage tumors. In a study published in the Feb. 16, 2015, issue of the Proceedings of the National Academy of Sciences, Duke researchers and their colleagues revealed that mutations in the isocitrate dehydrogenase (IDH) gene contribute to the formation of benign tumors in cartilage that can be a precursor to malignancies.

Click here to read the full press release.

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Among the research institutions NCI funds across the United States, it currently designates 68 as Cancer Centers. Largely based in research universities, these facilities are home to many of the NCI-supported scientists who conduct a wide range of intense, laboratory research into cancers origins and development. The Cancer Centers Program also focuses on trans-disciplinary research, including population science and clinical research. The centers research results are often at the forefront of studies in the cancer field.

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Duke scientists find that gene mutation drives cartilage tumor formation

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