Personalized Medicine – the Future of Healthcare – Video
Personalized Medicine - the Future of Healthcare
Where are we with healthcare delivery five years from now, ten years from now?
By: OracleHealthSciences
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Personalized Medicine - the Future of Healthcare - Video
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What Are the Symptoms of a Spinal Cord Injury? – Video
What Are the Symptoms of a Spinal Cord Injury?
Some of the most serious injuries dealt with by personal injury lawyers are spinal injuries. John Cooper of Norfolk-based Cooper Hurley Injury Lawyers talks ...
By: Cooper Hurley Injury Lawyers
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Another new beginning to my spinal cord injury – Video
Another new beginning to my spinal cord injury
I broke my neck in #39;98, but a bedsore while immobilized and in traction stopped me from getting long term inpatient therapy, many wounds (of flesh and heart)...
By: Ralph Raymond
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Replacing insulin through stem cell-derived pancreatic cells under the skin
PUBLIC RELEASE DATE:
24-Mar-2014
Contact: Susan Gammon Ph.D. sgammon@sanfordburnham.org 858-795-5012 Sanford-Burnham Medical Research Institute
LA JOLLA, Calif., March 25, 2014 Sanford-Burnham Medical Research Institute (Sanford-Burnham) and UC San Diego School of Medicine scientists have shown that by encapsulating immature pancreatic cells derived from human embryonic stem cells (hESC), and implanting them under the skin in animal models of diabetes, sufficient insulin is produced to maintain glucose levels without unwanted potential trade-offs of the technology. The research suggests that encapsulated hESC-derived insulin-producing cells hold great promise as an effective and safe cell-replacement therapy for insulin-dependent diabetes.
"Our study critically evaluates some of the potential pitfalls of using stem cells to treat insulin-dependent diabetes," said Pamela Itkin-Ansari, Ph.D., adjunct assistant professor in the Development, Aging, and Regenerative Program at Sanford-Burnham, with a joint appointment at UC San Diego.
"We have shown that encapsulated hESC-derived pancreatic cells are able to produce insulin in response to elevated glucose without an increase in the mass or their escape from the capsule. These results are important because it means that the encapsulated cells are both fully functional and retrievable," said Itkin-Ansari.
In the study, published online in Stem Cell Research, Itkin-Ansari and her team used bioluminescent imaging to see if encapsulated cells stay in the capsule after implantation.
Previous attempts to replace insulin-producing cells, called beta cells, have met with significant challenges. For example, researchers have tried treating diabetics with mature beta cells, but because mature cells are fragile and scarce, the method is fraught with problems. Moreover, since the cells come from organ donors, they may be recognized as foreign by the recipient's immune systemrequiring patients to take immunosuppressive drugs to prevent their immune system from attacking the donor's cells, ultimately leaving patients vulnerable to infections, tumors, and other adverse events.
Encapsulation technology was developed to protect donor cells from exposure to the immune systemand has proven extremely successful in preclinical studies.
Itkin-Ansari and her research team previously made an important contribution to the encapsulation approach by showing that pancreatic islet progenitor cells are an optimal cell type for encapsulation. They found that progenitor cells were more robust than mature beta cells to encapsulate, and while encapsulated, they matured into insulin-producing cells, which secreted insulin only when needed.
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A/Professor Dr Chin on Stem Cell Therapy – Video
A/Professor Dr Chin on Stem Cell Therapy
Interview on Bernama TV - Dr Chin Sze Piaw, Consultant Physician Cardiologist SUBSCRIBE: http://www.youtube.com/BeverlyWilshir... FACEBOOK: http://face...
By: Beverly Wilshire
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Need for Advanced Cancer Diagnostics Drives Demand for Circulating Tumor Cells & Cancer Stem Cells Technologies …
San Jose, California (PRWEB) March 25, 2014
Follow us on LinkedIn High prevalence of cancer worldwide and growing number of related casualties is creating an immediate need for effective diagnosis and therapy. Despite continuous research and the development of novel drugs, cancer remains unbeatable in most cases. The discovery of Circulating Tumor Cells (CTCs) and Cancer Stem Cells (CSCs) and their molecular mechanism is forecast to play an indispensable role in the future of cancer diagnostics and treatment. CTCs are cells dispersed from the primary tumor and found in peripheral blood circulation. The detection of CTCs and their numbers present important clues on the presence of cancer and the extent of its spread within the body. Clinical applications of CTC diagnostics are currently limited with high cost being the primary limiting factor. Unmet medical needs in the field of effective screening is however expected result in continuous flow of R&D investments in CTCs and CSCs. CTC based diagnostics involve a simple blood test and is increasingly being preferred over painful bone marrow aspirations and surgical biopsies to diagnose and analyze cancer metastasis.
CTC quantification and analyses based on molecular research also provides the potential to develop personalized cancer treatment regimens, which is garnering interest among scientific communities. Better, faster, and more user-friendly methods to detect and characterize CTCs will witness increased demand in the coming years. PCR-based (nucleic acid-based) identification methods are the most effective and sensitive for CTC genetic profiling, scoring over immunocytometric (protein-based) methods for molecular characterization of CTCs. RT-PCR and qPCR are highly specific techniques that are widely used to identify and amplify CTCs. CellSearch is the only FDA-approved automated system that offer combined enrichment, staining, and scanning of CTCs.
Cancer Stem Cells (CSCs) are the bulk cells within a tumor carrying its proliferative capability. CSCs remain unaffected by cancer treatment strategies, including chemotherapy and cause tumor relapse or re-occurrence thereby creating the need for new therapeutic drugs that destroy CSCs. The technology is still under extensive research. Biotechnology and pharmaceutical companies are increasingly shifting focus to anti-cancer therapeutics that target cancer stem cells and their regenerative mechanisms.
As stated by the new market research report on Circulating Tumor Cells and Cancer Stem Cells Technologies, the United States and Europe are the largest markets worldwide. The United States remains the undisputed leader in CTC diagnostics. Asia-Pacific is forecast to emerge as the fastest growing market driven by developing healthcare infrastructure, growing patient awareness, increasing per capita healthcare spends, focus on quality healthcare services, and the urgent need for advanced cancer diagnostics.
Key players covered in the report for CTC diagnostics include Adnagen GmbH, ApoCell Inc., Biocep LTD, Biocept Inc., Biofluidica Microtechnologies LLC, Celltrafix Inc., Clearbridge Biomedics, Creatv Microtech Inc., Cynvenio Biosystems Inc., Ikonisys Inc., IVDiagnostics Inc., Janssen Diagnostics LLC, Epic Biosciences Inc., Rarecells SAS, Screencell, Stemcell Technologies Inc. Market participants in CSC research include Alchemia Limited, Amgen Inc., Exelixis Inc., Formula Pharmaceuticals, GlaxoSmithKline Plc, Geron Corp, Infinity Pharmaceuticals, Kalobios Pharmaceuticals Inc., Novartis AG, OncoMed Pharmaceuticals Inc., Roche Diagnostics, and Verastem Inc., among others.
The research report titled Circulating Tumor Cells and Cancer Stem Cells Technologies: A Global Strategic Business Report announced by Global Industry Analysts Inc., provides a comprehensive review of market trends, drivers, key issues and challenges. The study also provides insights into CTC biology and CTC detection technologies, including CellSearch, ISET, CTC Chip, FAST, FISH, etc. The report provides market estimates and projections for CTC Diagnostics for all major geographic markets including the United States, Canada, Japan, Europe (France, Germany, Italy, UK, Spain, Russia, and Rest of Europe), Asia-Pacific, and Rest of World. Exclusive coverage is presented on Cancer Stem Cells biology, Surface Markers, Signaling Pathways, and Pipeline drugs.
For more details about this comprehensive market research report, please visit http://www.strategyr.com/Circulating_Tumor_Cells_CTCs_and_Cancer_Stem_Cells_CSCs_Technologies_Market_Report.asp
About Global Industry Analysts, Inc. Global Industry Analysts, Inc., (GIA) is a leading publisher of off-the-shelf market research. Founded in 1987, the company currently employs over 800 people worldwide. Annually, GIA publishes more than 1300 full-scale research reports and analyzes 40,000+ market and technology trends while monitoring more than 126,000 Companies worldwide. Serving over 9500 clients in 27 countries, GIA is recognized today, as one of the world's largest and reputed market research firms.
Global Industry Analysts, Inc. Telephone: 408-528-9966 Fax: 408-528-9977 Email: press(at)StrategyR(dot)com Web Site: http://www.StrategyR.com/
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Osteoarthritis breakthrough at NUI Galway
Tuesday 25 March 2014 16.58
Scientists at NUI Galway have achieved positive early stage results from a study looking at a possible treatment for osteoarthritis using stem cells.
Researchers at the Regenerative Medicine Institute said the results indicate that the treatment could be ready for use in patients within five years.
Osteoarthritis affects more than 400,000 people in Ireland, and 70 million across the EU. The disease causes the painful degeneration of cartilage in joints and is the most common form of arthritis.
The NUI Galway team are part of an EU funded projectinvolving partners in seven countries, which is examining whether stem cell therapy can help treat osteoarthritis by regenerating joints.
The group is testing stem cells derived from fat, which is injected into joints.
Fat stem cells are considered a good alternative to bone-marrow derived stem cells, as they are available in large quantities and can be harvested using minimally invasive techniques.
The scientists, who are involved in the 10m EU funded ADIPOA project, have just completed first phase clinical trials which sought to determine how adipose or fat-derived stem cells injected into diseased joints can activate the regeneration of cartilage.
According to Scientific Director of the Regenerative Medicine Institute, Professor Frank Barry, if the treatment continues to show promiseit could eventually lead to a cure for osteoarthritis.
Currently the only options for sufferers are joint replacement or life-long pain management.
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Stem Cell-Derived Beta Cells Under Skin Replace Insulin
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Newswise Scientists at University of California, San Diego School of Medicine and Sanford-Burnham Medical Research Institute have shown that by encapsulating immature pancreatic cells derived from human embryonic stem cells (hESC), and implanting them under the skin of diabetic mouse models, sufficient insulin is produced to maintain glucose levels without unwanted potential trade-offs of the technology.
The research, published online in Stem Cell Research, suggests that encapsulated hESC-derived insulin-producing cells may be an effective and safe cell replacement therapy for insulin dependent-diabetes.
Our study critically evaluates some of the potential pitfalls of using stem cells to treat insulin dependent-diabetes, said Pamela Itkin-Ansari, PhD, assistant project scientist in the UC San Diego Department of Pediatrics and adjunct assistant professor in Development, Aging and Regenerative program at Sanford-Burnham.
We have shown that encapsulated hESC-derived insulin-producing cells are able to produce insulin in response to elevated glucose without an increase in the mass or their escape from the capsule, said Itkin-Ansari. These results are important because it means that the encapsulated cells are both fully functional and retrievable.
Previous attempts to replace insulin producing cells, called beta cells, have met with significant challenges. For example, researchers have tried treating diabetics with mature beta cells, but because these cells are fragile and scarce, the method is fraught with problems. Moreover, since the cells come from organ donors, they may be recognized as foreign by the recipients immune system requiring patients to take immunosuppressive drugs to prevent their immune system from attacking the donors cells, ultimately leaving patients vulnerable to infections, tumors and other adverse events.
Encapsulation technology was developed to protect donor cells from exposure to the immune system and has proven extremely successful in preclinical studies.
Itkin-Ansari and her research team previously made an important contribution to the encapsulation approach by showing that pancreatic islet progenitor cells are an optimal cell type for encapsulation. They found that progenitor cells were more robust than mature beta cells to encapsulate, and while encapsulated, they matured into insulin-producing cells that secreted insulin only when needed.
In the study, Itkin-Ansari and her team used bioluminescent imaging to determine if encapsulated cells stay in the capsule after implantation.
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Stem Cell-Derived Beta Cells Under Skin Replace Insulin
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Stem Cells Shed Light on Bipolar Disorder
Researchers have grown embryonic-like stem cells from patients with bipolar disorder and transformed them into brain cells that are already answering questions about the condition.
The cells, which carry the precisely tailored genetic instructions from the patients own cells, behave differently than cells taken from people without the disorder, the researchers report.
Already, we see that cells from people with bipolar disorder are different in how often they express certain genes, how they differentiate into neurons, how they communicate, and how they respond to lithium," Sue O'Shea, a stem cell specialist at the University of Michigan who led the study, said in a statement.
The work, described in the journal Translational Psychiatry, helps fulfill one of the big promises of stem cells research using a patients own cells to study his or her disease.
Mental illness is especially hard to study. Getting into a living persons brain is almost impossible, and scientists cant deliberately cause it in people in order to study it.
Creating animals such as mice with what looks like human mental illness is imprecise at best.
The University of Michigan team turned instead to what are called induced pluripotent stem cells, or iPS cells. These are ordinary skin cells taken from a patient and tricked into turning back into the state of a just-conceived embryo.
These cells, grown from skin cells taken from people with bipolar disorder, arose from stem cells and were coaxed to become neural progenitor cells -- the kind that can become any sort of nervous system cell. The research showed differences in cell behavior compared with cells grown from people without bipolar disorder.
They are pluripotent, meaning they can become any type of cell there is. In this case, the Michigan team redirected the cells to become neurons the cells that make up much of the brain. "This gives us a model that we can use to examine how cells behave as they develop into neurons, OShea said.
Bipolar disorder, once called manic-depression, is very common, affecting an estimated 3 percent of the population globally. It runs in families, suggesting a strong genetic cause, and is marked by mood swings from depression to feelings of euphoria and creativity thats considered the manic phase.
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Stem Cells Shed Light on Bipolar Disorder
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Stem Cells Shed Light On Bipolar Disease
Researchers have grown embryonic-like stem cells from patients with bipolar disorder and transformed them into brain cells that are already answering questions about the condition.
The cells, which carry the precisely tailored genetic instructions from the patients own cells, behave differently than cells taken from people without the disorder, the researchers report.
Already, we see that cells from people with bipolar disorder are different in how often they express certain genes, how they differentiate into neurons, how they communicate, and how they respond to lithium," Sue O'Shea, a stem cell specialist at the University of Michigan who led the study, said in a statement.
The work, described in the journal Translational Psychiatry, helps fulfill one of the big promises of stem cells research using a patients own cells to study his or her disease.
Mental illness is especially hard to study. Getting into a living persons brain is almost impossible, and scientists cant deliberately cause it in people in order to study it.
Creating animals such as mice with what looks like human mental illness is imprecise at best.
The University of Michigan team turned instead to what are called induced pluripotent stem cells, or iPS cells. These are ordinary skin cells taken from a patient and tricked into turning back into the state of a just-conceived embryo.
These cells, grown from skin cells taken from people with bipolar disorder, arose from stem cells and were coaxed to become neural progenitor cells -- the kind that can become any sort of nervous system cell. The research showed differences in cell behavior compared with cells grown from people without bipolar disorder.
They are pluripotent, meaning they can become any type of cell there is. In this case, the Michigan team redirected the cells to become neurons the cells that make up much of the brain. "This gives us a model that we can use to examine how cells behave as they develop into neurons, OShea said.
Bipolar disorder, once called manic-depression, is very common, affecting an estimated 3 percent of the population globally. It runs in families, suggesting a strong genetic cause, and is marked by mood swings from depression to feelings of euphoria and creativity thats considered the manic phase.
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Finger-prick technique opens door for DIY stem cell donors
Harvesting samples for producing stem cells can be rather painful. Techniques can involve collecting large amounts of blood, bone marrow or skin scrapes. The reality is intrusive measures such as these can be very off-putting. But what if it was as simple as a finger-prick? Such a DIY approach, which is so easy it can be done at home or in the field without medical staff, has been developed by researchers at Singapore's A*STAR Institute of Molecular and Cell Biology (IMCB).
Unlike previous techniques that require comparatively large cell samples, the ICMB team has managed to successfully reprogram mature human cells into hiPSCs with high efficiency using less than a single drop of blood. Pluripotent stem cells are important in many forms of medical research and treatment as they have the potential to become any other cell type in the body.
"It all began when we wondered if we could reduce the volume of blood used for reprogramming," says Dr Loh Yuin Han Jonathan, Principal Investigator at IMCB. "We then tested if donors could collect their own blood sample in a normal room environment and store it. Our finger-prick technique, in fact, utilized less than a drop of finger-pricked blood."
It is hoped that this much less invasive method of sample collection will help attract more donors to increase the samples available to researchers. Blood samples have been found to remain viable for 48 hours after collection and in culture this can be extended to 12 days, opening up remote areas for potential cell harvesting. This could benefit research and treatment with the recruitment of donors with varied ethnicities, genotypes and diseases now possible. It is hoped the technique will also lead to the establishment of large-scale hiPSC banks.
"We were able to differentiate the hiPSCs reprogrammed from Jonathans finger-prick technique, into functional heart cells," says Dr Stuart Alexander Cook, Senior Consultant at the National Heart Centre Singapore and co-author of the paper. "This is a well-designed, applicable technique that can unlock unrealized potential of biobanks around the world for hiPSC studies at a scale that was previously not possible."
The team has filed a patent for their innovation and their paper has been published online at Stem Cell Translational Medicine.
Source: A*STAR
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Bipolar disorder breakthrough
When it comes to understanding bipolar disorder, many questions remain unanswered such as what truly causes the condition and why finding proper treatments is so difficult.
But now, researchers have taken a huge step towards solving some of the disorders complex mysteries.
Through groundbreaking stem cell research, scientists from the University of Michigan Medical School and the Heinz C. Prechter Bipolar Researcher Fund transformed skin cells from people with bipolar disorder into neurons that mimicked those found in their brains. They were then able to compare these nerve stem cells with cells derived from people without bipolar disorder and study how the neurons responded to medications for the condition.
Detailed in the journal Translational Psychiatry, this study marks the first time researchers have derived a stem cell line specific to bipolar disorder.
Once we have derived nerve cells, were able to study those cells and determine how they behave compared to other cells and how they behave in response to medications, principal investigator Dr. Melvin McInnis, of the Prechter Bipolar Research Fund, told FoxNews.com. So if we can understand the basic biological problems with these cells, we can potentially identify interventions that further how we understand the illness and how we treat it.
Also known as manic-depressive illness, bipolar disorder is a brain condition characterized by intense shifts in mood alternating between periods of high energy and mania to periods of severe anxiety and depression. While the condition is known to run in families, scientists still arent fully certain what causes its development, believing it to be a combination of genetics and other factors.
Additionally, the most common form of treatment for the disorder, lithium, is also somewhat of a mystery.
We really do not know and understand what drives these fluctuations in moods; we dont understand how the medications truly work that help individuals with variability in their moods, McInnis said. We dont know why an individual will become ill at a particular time. All we know is really at an observational level.
In order to better understand what is happening in the bipolar mind, McInnis and his team took small samples of skin from individuals who had been diagnosed with bipolar disorder. These samples were then exposed to specific growth factors, which coaxed the cells into becoming induced pluripotent stem cells (iPSCs) meaning they had the ability to turn into any type of cell. Subsequently, the cells were exposed to an additional set of growth factors, which coaxed them into becoming neurons.
This process has also been used to better understand other complex brain disorders, such as schizophrenia and conditions that cause seizures. According to McInnis, the technique allows researchers to examine how cells behave as they develop into a whole new type of cell, as well as how they function when they finally become neurons.
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Gene implicated in progression, relapse of deadly breast cancer finding points to potential Achilles' heel in triple …
Scientists from Weill Cornell Medical College and Houston Methodist have found that a gene previously unassociated with breast cancer plays a pivotal role in the growth and progression of the triple negative form of the disease, a particularly deadly strain that often has few treatment options. Their research, published in this week's Nature, suggests that targeting the gene may be a new approach to treating the disease.
About 42,000 new cases of triple negative breast cancer (TNBC) are diagnosed in the United States each year, about 20 percent of all breast cancer diagnoses. Patients typically relapse within one to three years of being treated.
Senior author Dr. Laurie H. Glimcher, the Stephen and Suzanne Weiss Dean of Weill Cornell Medical College, wanted to know whether the gene -- already understood from her prior work to be a critical regulator of immune and metabolic functions -- was important to cancer's ability to adapt and thrive in the oxygen- and nutrient-deprived environments inside of tumors. Using cells taken from patients' tumors and transplanted into mice, Dr. Glimcher's team found that the gene, XBP1, is especially active in triple negative breast cancer, particularly in the progression of malignant cells and their resurgence after treatment.
"Patients with the triple negative form of breast cancer are those who most desperately need new approaches to treat their disease," said Dr. Glimcher, who is also a professor of medicine at Weill Cornell. "This pathway was activated in about two-thirds of patients with this type of breast cancer. Now that we better understand how this gene helps tumors proliferate and then return after a patient's initial treatment, we believe we can develop more effective therapies to shrink their growth and delay relapse."
The group, which included investigators from nine institutions, examined several types of breast cancer cell lines. They found that XBP1 was particularly active in basal- like breast cancer cells cultivated in the lab and in triple negative breast cancer cells from patients. When they suppressed the activity of the gene in laboratory cell cultures and animal models, however, the researchers were able to dramatically reduce the size of tumors and the likelihood of relapse, especially when these approaches were used in conjunction with the chemotherapy drugs doxorubicin or paclitexel. The finding suggests that XBP1 controls behaviors associated with tumor-initiating cells that have been implicated as the originators of tumors in a number of cancers, including that of the breast, supporting the hypothesis that combination therapy could be an effective treatment for triple negative breast cancer.
The scientists also found that interactions between XBP1 and another transcriptional regulator, HIF1-alpha, spurs the cancer-driving proteins. Silencing XBP1 in the TNBC cell lines reduced the tumor cells' growth and other behaviors typical of metastasis.
"This starts to demonstrate how cancer cells co-opt the endoplasmic reticulum stress response pathway to allow tumors to grow and survive when they are deprived of nutrients and oxygen," said lead author Dr. Xi Chen, a postdoctoral associate at Weill Cornell, referring to the process by which healthy cells maintain their function. "It shows the interaction between two critical pathways to make the cells better able to deal with a hostile microenvironment, and in that way offers new strategies to target triple negative breast cancer."
Scientists still need to study how those strategies would help women with the disease.
"Obviously we need to know now whether what our group saw in models is what we'll see in patients," said coauthor Dr. Jenny Chang, professor of medicine at Weill Cornell and director of the Houston Methodist Cancer Center. "We are very excited about the prospect of moving this research forward as soon as possible for the benefit of patients."
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Deletion of FAT10 gene reduces body fat, slows down aging in mice
PUBLIC RELEASE DATE:
24-Mar-2014
Contact: Andrea Grossman 617-636-3728 Tufts University, Health Sciences Campus
Boston, MA [March 24, 2014, 3:00 p.m. EDT] A single gene appears to play a crucial role in coordinating the immune system and metabolism, and deleting the gene in mice reduces body fat and extends lifespan, according to new research by scientists at the Jean Mayer USDA Human Nutrition Research Center (USDA HNRCA) on Aging at Tufts University and Yale University School of Medicine. Their results are reported online today in the Proceedings of the National Academy of Sciences.
Based on gene expression studies of fat tissue conducted at the USDA HNRCA, the Tufts University researchers initiated studies of the role of FAT10 in adipose tissue and metabolism. "No one really knew what the FAT10 gene did, other than it was 'turned on' by inflammation and that it seemed to be increased in gynecological and gastrointestinal cancers." said co-author Martin S. Obin, Ph.D., an adjunct scientist in the Functional Genomics Core Unit at the USDA HNRCA at Tufts University. "Turning off the FAT10 gene produces a variety of beneficial effects in the mice, including reduced body fat, which slows down aging and extends lifespan by 20 percent."
Typically, mice gain fat as they age. The authors observed that activation of the FAT10 gene in normal mice increases in fat tissue with age. Mice lacking FAT10 consume more food, but burn fat at an accelerated rate. As a result, they have less than half of the fat tissue found in normal, aged mice. At the same time their skeletal muscle ramps up production of an immune molecule that increases their response to insulin, resulting in reduced circulating insulin levels, protection against type 2 diabetes and longer lifespan.
The authors note that eliminating FAT10 will not fully address the dilemma of aging and weight gain. "Laboratory mice live in a lab under ideal, germ-free conditions," said Obin, who is also an associate professor at the Friedman School of Nutrition Science and Policy at Tufts University. "Fighting infection requires energy, which can be provided by stored fat. Mice without the FAT10 gene might be too lean to fight infection effectively outside of the laboratory setting. More research is needed to know how to achieve that balance in mice and then hopefully, at some point, people."
The possibilities for future research of FAT10 are exciting. Recent high-profile studies reported that FAT10 interacts with hundreds of other proteins in cells. Now the Tufts and Yale researchers have demonstrated that it impacts immune response, lipid and glucose metabolism, and mitochondrial function.
"Now there is dramatic road map for researchers looking at all of the proteins that FAT10 gets involved with," said co-first and corresponding author Allon Canaan, Ph.D., an associate scientist in the Department of Genetics at Yale. "Blocking what FAT10 does to coordinate immunity and metabolism could lead to new therapies for metabolic disease, metabolic syndrome, cancer and healthy aging, because when we knock it out the net result is mice live longer."
Canaan and colleagues initially developed the FAT10-deficient mouse to study the role of FAT10 in sepsis. In an attempt to increase sensitivity for sepsis, Canaan aged the FAT10 knockout mice and made the discovery that mice lacking the gene were lean and aged more slowly. The mice appear younger and more robust than comparably-aged normal mice, have better muscle tone, and do not develop age-related tumors.
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Deletion of FAT10 gene reduces body fat, slows down aging in mice
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MRI reveals genetic activity: Deciphering genes' roles in learning and memory
Doctors commonly use magnetic resonance imaging (MRI) to diagnose tumors, damage from stroke, and many other medical conditions. Neuroscientists also rely on it as a research tool for identifying parts of the brain that carry out different cognitive functions.
Now, a team of biological engineers at MIT is trying to adapt MRI to a much smaller scale, allowing researchers to visualize gene activity inside the brains of living animals. Tracking these genes with MRI would enable scientists to learn more about how the genes control processes such as forming memories and learning new skills, says Alan Jasanoff, an MIT associate professor of biological engineering and leader of the research team.
"The dream of molecular imaging is to provide information about the biology of intact organisms, at the molecule level," says Jasanoff, who is also an associate member of MIT's McGovern Institute for Brain Research. "The goal is to not have to chop up the brain, but instead to actually see things that are happening inside."
To help reach that goal, Jasanoff and colleagues have developed a new way to image a "reporter gene" -- an artificial gene that turns on or off to signal events in the body, much like an indicator light on a car's dashboard. In the new study, the reporter gene encodes an enzyme that interacts with a magnetic contrast agent injected into the brain, making the agent visible with MRI. This approach, described in a recent issue of the journal Chemical Biology, allows researchers to determine when and where that reporter gene is turned on.
An on/off switch
MRI uses magnetic fields and radio waves that interact with protons in the body to produce detailed images of the body's interior. In brain studies, neuroscientists commonly use functional MRI to measure blood flow, which reveals which parts of the brain are active during a particular task. When scanning other organs, doctors sometimes use magnetic "contrast agents" to boost the visibility of certain tissues.
The new MIT approach includes a contrast agent called a manganese porphyrin and the new reporter gene, which codes for a genetically engineered enzyme that alters the electric charge on the contrast agent. Jasanoff and colleagues designed the contrast agent so that it is soluble in water and readily eliminated from the body, making it difficult to detect by MRI. However, when the engineered enzyme, known as SEAP, slices phosphate molecules from the manganese porphyrin, the contrast agent becomes insoluble and starts to accumulate in brain tissues, allowing it to be seen.
The natural version of SEAP is found in the placenta, but not in other tissues. By injecting a virus carrying the SEAP gene into the brain cells of mice, the researchers were able to incorporate the gene into the cells' own genome. Brain cells then started producing the SEAP protein, which is secreted from the cells and can be anchored to their outer surfaces. That's important, Jasanoff says, because it means that the contrast agent doesn't have to penetrate the cells to interact with the enzyme.
Researchers can then find out where SEAP is active by injecting the MRI contrast agent, which spreads throughout the brain but accumulates only near cells producing the SEAP protein.
Exploring brain function
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MRI reveals genetic activity: Deciphering genes' roles in learning and memory
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First stem cell study of bipolar disorder yields promising results
What makes a person bipolar, prone to manic highs and deep, depressed lows? Why does bipolar disorder run so strongly in families, even though no single gene is to blame? And why is it so hard to find new treatments for a condition that affects 200 million people worldwide?
New stem cell research published by scientists from the University of Michigan Medical School, and fueled by the Heinz C. Prechter Bipolar Research Fund, may help scientists find answers to these questions.
The team used skin from people with bipolar disorder to derive the first-ever stem cell lines specific to the condition. In a new paper in Translational Psychiatry, they report how they transformed the stem cells into neurons, similar to those found in the brain -- and compared them to cells derived from people without bipolar disorder.
The comparison revealed very specific differences in how these neurons behave and communicate with each other, and identified striking differences in how the neurons respond to lithium, the most common treatment for bipolar disorder.
It's the first time scientists have directly measured differences in brain cell formation and function between people with bipolar disorder and those without.
The researchers are from the Medical School's Department of Cell & Developmental Biology and Department of Psychiatry, and U-M's Depression Center.
Stem cells as a window on bipolar disorder
The team used a type of stem cell called induced pluripotent stem cells, or iPSCs. By taking small samples of skin cells and exposing them to carefully controlled conditions, the team coaxed them to turn into stem cells that held the potential to become any type of cell. With further coaxing, the cells became neurons.
"This gives us a model that we can use to examine how cells behave as they develop into neurons. Already, we see that cells from people with bipolar disorder are different in how often they express certain genes, how they differentiate into neurons, how they communicate, and how they respond to lithium," says Sue O'Shea, Ph.D., the experienced U-M stem cell specialist who co-led the work.
"We're very excited about these findings. But we're only just beginning to understand what we can do with these cells to help answer the many unanswered questions in bipolar disorder's origins and treatment," says Melvin McInnis, M.D., principal investigator of the Prechter Bipolar Research Fund and its programs.
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First stem cell study of bipolar disorder yields promising results
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Genetic cause of rare type of ovarian cancer discovered
The cause of a rare type of ovarian cancer that most often strikes girls and young women has been uncovered by an international research team led by the Translational Genomics Research Institute (TGen), according to a study published online today by the scientific journal, Nature Genetics.
By applying its groundbreaking work in genomics, TGen led a study that included Mayo Clinic, Johns Hopkins University, St. Joseph's Hospital and Medical Center; Evergreen Hematology and Oncology, Children's Hospital of Alabama, the Autonomous University of Barcelona, British Columbia Cancer Agency, University of British Columbia, and the University Health Network-Toronto.
The findings revealed a "genetic superhighway" mutation in a gene found in the overwhelming majority of patients with small cell carcinoma of the ovary, hypercalcemic type, also known as SCCOHT.
This type of cancer usually is not diagnosed until it is in its advanced stages. It does not respond to standard chemotherapy, and 65 percent of patients die within 2 years. It has affected girls as young as 14 months, and women as old as 58 years -- with a mean age of only 24 years old. In this study, the youngest patient was 9 years old.
"This is a thoroughly remarkable study. Many genetic anomalies can be like a one-lane road to cancer; difficult to negotiate. But these findings indicate a genetic superhighway that leads right to this highly aggressive disease," said Dr. Jeffrey Trent, President and Research Director of TGen, and the study's senior author. "The correlation between mutations in SMARCA4 and the development of SCCOHT is simply unmistakable."
Dr. Trent added that while the breakthrough is for a relatively rare cancer, discovering the origins of this type of ovarian cancer could have implications for more common diseases.
Much of the work in this study was inspired by the memory of Taryn Ritchey, a 22-year-old TGen patient who in 2007 lost her battle with ovarian cancer, the 5th leading cause of cancer death among American women.
"Taryn would be incredibly excited about this amazing new study, and she would be glad and thankful that other young women like her might now be helped because of TGen's ongoing research," said Taryn's mother Judy Jost of Cave Creek, Ariz. "My daughter never gave up, and neither has TGen."
The SMARCA4 gene -- previously associated with lung, brain and pancreatic cancer -- was the only recurrently mutated gene in the study's samples. The implications of this discovery, therefore, may be widespread.
"The findings in this study represent a landmark in the field. The work identifies SMARCA4 mutations as the culprit, and most future research on this disease will be based on this remarkable discovery," said Dr. Bert Vogelstein, Director of the Ludwig Center at Johns Hopkins University, Investigator at the Howard Hughes Medical Institute, and pioneer in the field of cancer genomics. He did not participate in the study but is familiar with its findings.
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Genetic cause of rare type of ovarian cancer discovered
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Two UMass Medical School students take home prestigious Weintraub Award
PUBLIC RELEASE DATE:
25-Mar-2014
Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School
WORCESTER, MA. Colin Conine and Emma Watson, PhD students in the Graduate School of Biomedical Sciences (GSBS) at the University of Massachusetts Medical School, received the 2014 Harold M. Weintraub Graduate Student Award for research into the mechanisms governing epigenetic inheritance and the complex interactions between diet, gene expression and physiology. Only 13 students from North America were chosen for the prestigious award sponsored by the Basic Sciences Division of the Fred Hutchinson Cancer Research Center. UMass Medical School was one of only two institutions to have multiple winners this year.
"I'm happy that both Colin and I won the award this year. I think it's a testament to the strong community of C. elegans biologists here at UMass Medical School, with whom we have both trained," said Watson, a doctoral candidate in the Program in Systems Biology. "We use the roundworm C. elegans to explore basic biological processes and find new angles of attack for human disease. C. elegans was the perfect model for me to study the genetic underpinnings that link diet and physiology. Its metabolic network and nutritional requirements are surprisingly a lot like ours, despite being a soil-dwelling nematode that eats bacteria all day long!"
Watson is working in the lab of Marian Walhout, PhD, co-director of the Program in Systems Biology and professor of molecular medicine.
"Emma is an outstanding graduate student who fully deserves this award," said Dr. Walhout. "It is a pleasure to work with her. She is hard working, smart, fun and has vision. If she sets the bar, it is very high!"
Conine is studying in the lab of 2006 Nobel Laureate Craig C. Mello, PhD.
"There is still so much we don't understand about inheritance. Genetics and DNA don't explain everything," said Conine, a doctoral candidate in molecular biology and genetics. "Epigenetic inheritance of RNA provides a new way of looking at how information is passed from generation to generation that could help us explain disease causes that have eluded DNA studies."
"The Weintraub Award is the Nobel of thesis awards," said Dr. Mello, Howard Hughes Medical Institute Investigator, the Blais University Chair in Molecular Medicine and distinguished professor of molecular medicine and cell biology. "It is a huge honor and a deserving award for Colin, who has a wonderful blend of curiosity and tenacity that has allowed him to tackle difficult problems. Colin has a rare attribute as a scientist to make connections that others miss. I expect great things from Colin and have no doubt that he will go on to become a leading independent researcher."
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Two UMass Medical School students take home prestigious Weintraub Award
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‘Stem Cell Tourism’ Takes Advantage of Patients, Says Law Professor
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Newswise MADISON, Wis. Desperate patients are easy prey for unscrupulous clinics offering untested and risky stem cell treatments, says law and bioethics Professor Alta Charo of the University of Wisconsin-Madison, who is studying stem cell tourism.
Stem cells are cells that can form many types of cells in the body, and that makes them inherently promising and dangerous. Stem cell tourism refers to people traveling, both within the U.S. and abroad, in pursuit of advertised stem cell therapies to purportedly treat a variety of medical conditions.
The evidence for therapeutic use of stem cells is very limited, except for bone marrow stem cells, but patients all over the world are convinced stem cells will cure their disease, says Charo. While there are some very promising results in the early clinical trials for stem cell therapies using embryonic and other kinds of stem cells, the treatments being advertised by these clinics are dubious, mostly ineffective, and sometimes positively harmful.
Patients are being hoodwinked, but there are dilemmas about tackling (the treatments) at regulatory or political levels.
The outrage over failures in stem cell tourism is limited, Charo says. Patients may pay tens of thousands of dollars for procedures that may carry no promise of success or carry grievous risks of failure. Most people have no reason to pay attention, and those who are paying attention are sick, so they are focused on trying anything, Charo says. If it does not work, they are already in a bad position with plenty to think about.
During a search for stem cell therapies on the web, Charo found products that supposedly enhance the natural formation of stem cells in the skin alongside approved and unapproved treatments in the United States, and stem cell clinics outside the United States, like a stem cell treatment for spinal conditions that might be innocuous, but is probably useless.
Some American operators are trying to slip through Food and Drug Administration regulation, says Charo, who served as senior policy advisor in the Office of the Commissioner of the FDA between 2009 and 2011. The FDA regulates medical devices, tissue transplants and drugs, but not organ transplants or the way medicine is practiced.
To sell a product that can heal without claiming it is a drug, some clinics remove stem cells from a patient, grow them with minimal manipulation, and then reinsert the resulting cells back to the same patient. There has been a long-running battle over whether that is a tissue transplant akin to organ transplantation and thus the practice of medicine, or a tissue transplant that is acting like drug, Charo says. If the latter, then what you do is subject to FDA [regulation], so you have to prove that your product is safe and effective, which almost always requires expensive clinical trials.
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'Stem Cell Tourism' Takes Advantage of Patients, Says Law Professor
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Should stem cell therapy be used in DLCBL? – Video
Should stem cell therapy be used in DLCBL?
Response based on the findings of the case study presented by Prof. Marek Trnn Transcript: The question to consider is whether a stem cell transplant is su...
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Heart Stem cell therapy – Video
Heart Stem cell therapy
Clara answers some questions regarding the stem-cell therapy she received for congenital heart disease. For more info visit: http://www.stemaid.com.
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Keys to Woman's Hormone Therapy | Personalized Medicine – Video
Keys to Woman #39;s Hormone Therapy | Personalized Medicine
Woman #39;s Hormone Therapy Treatment | Personalized Medicine The Institute of Nutritional Medicine Cardiovascular Research provides cutting-edge research, met...
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Employment Video – Spinal Cord Injury – Video
Employment Video - Spinal Cord Injury
This video is a part of a research project conducted by David B. Gray, PhD and associates at the Washington University School of Medicine Program in Occupati...
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Leading Surgeons Warn Against Media Hype About Tracheal Regeneration
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Newswise Beverly, MA, March 24, 2014 Reports of the two earliest tissue-engineered whole organ transplants using a windpipe, or trachea, created using the patient's own stem cells, were hailed as a breakthrough for regenerative medicine and widely publicized in the press. However, two leading transplant surgeons in Belgium warn of the dangers of media attention, and urge that tracheal bioengineering be demonstrated as both effective and safe before further transplants take place. Their views are published in an Editorial in The Journal of Thoracic and Cardiovascular Surgery, an official publication of the American Association for Thoracic Surgery.
In 2008, surgeons repopulated a donor trachea with cells from a 30-year-old woman, which they then transplanted into the patient. In 2011, a 36-year-old man who had been suffering from late-stage tracheal cancer was given a new trachea made from a synthetic scaffold seeded with his own stem cells. Both procedures were carried out by Professor Paolo Macchiarini and colleagues (Barcelona, 2008, and Sweden, 2011).
In 2012, an article in The New York Times, A First: Organs Tailor-Made With Bodys Own Cells, recognized tracheal regeneration as the first regenerative medicine procedure designed to implant bioartificial organs. The achievement was touted as the beginning of complex organ engineering for the heart, liver, and kidneys, and it was suggested that allotransplantation along with immunosuppression might become problems of the past.
Major medical breakthroughs deserve the necessary press attention to inform the medical community and public of the news, say Pierre R. Delaere, MD, PhD, and Dirk Van Raemdonck, MD, PhD, from the Department of Otolaryngology Head & Neck Surgery and the Department of Thoracic Surgery, University Hospital Leuven, Belgium. Unfortunately, misrepresentation of medical information can occur and is particularly problematic when members of the professional and public press are misled to believe unrealistic medical breakthroughs.
The authors raise doubts regarding whether a synthetic tube can transform into a viable airway tube, pointing out that the mechanism behind the transformation from nonviable construct to viable airway cannot be explained with our current knowledge of tissue healing, tissue transplantation, and tissue regeneration. Cells have never been observed to adhere, grow, and regenerate into complex tissues when applied to an avascular or synthetic scaffold and, moreover, this advanced form of tissue regeneration has never been observed in laboratory-based research, say the authors.
Delaere and Van Raemdonck reviewed the information gathered from published reports on three patients who received bioengineered tracheas and unpublished reports on an additional 11 patients. Although there were differences between the techniques used, production of the bioengineered trachea in all cases produced similar results, and the different approaches worked in comparable ways.
The results show that mortality and morbidity were very high. Several patients died within a three-month period, and the patients who survived longer functioned with an airway stent that preserved the airway lumen, they observe.
They also question whether the trachea can really be considered to be the first bioengineered organ. From the 14 reports reviewed, they concluded that the bioengineered tracheal replacements were in fact airway replacements that functioned only as scaffolds, behaving in a similar way to synthetic tracheal prostheses.
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GDNF transfection promotes neuronal differentiation of bone marrow mesenchymal stem cells
PUBLIC RELEASE DATE:
21-Mar-2014
Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research
Studies have shown that the differentiation rate of grafted bone marrow mesenchymal stem cells into mature neuron-like cells is very low. Therefore, it is very important to establish an effcient and stable induction protocol to promote the differentiation of bone marrow mesenchymal stem cells into neuron-like cells in vitro and elucidate the mechanisms underlying differentiation for the treatment of central nervous system diseases. Jie Du and colleagues from Sichuan University in China found that glial cell line-derived neurotrophic factor/bone marrow mesenchymal stem cells have a higher rate of induction into neuron-like cells, and this enhanced differentiation into neuron-like cells may be associated with up-regulated expression of glial cell line-derived neurotrophic factor, nerve growth factor and growth-associated protein-43. The researchers provide experimental support for the therapeutic use of glial cell line-derived neurotrophic factor gene-modified bone marrow mesenchymal stem cells in transplantation strategies for central nervous system diseases. The relevant paper has been published in the Neural Regeneration Research (Vol. 9, No. 1, 2014).
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Article: " Transfection of the glial cell line-derived neurotrophic factor gene promotes neuronal differentiation," by Jie Du1, 2, Xiaoqing Gao3, Li Deng3, Nengbin Chang2, Huailin Xiong2, Yu Zheng1 (1 Department of Physiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan Province, China; 2 Department of Anatomy, Luzhou Medical College, Luzhou 646000, Sichuan Province, China; 3 Research Center for Preclinical Medicine, Luzhou Medical College, Luzhou 646000, Sichuan Province, China)
Du J, Gao XQ, Deng L, Chang NB, Xiong HL, Zheng Y. Transfection of the glial cell line-derived neurotrophic factor gene promotes neuronal differentiation. Neural Regen Res. 2014;9(1):33-40.
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Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/
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GDNF transfection promotes neuronal differentiation of bone marrow mesenchymal stem cells
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