Mobile Health Care Innovation: TechNOW interview, David Farnes, CATA, Health Care Champion
CATA CEO, John Reid, interviews, CATA #39;s Mobile Health Care Lead, David Farnes on a new submission to the Advisory Panel on Healthcare Innovation, entitled, " Mobile Health in Canada: Turn Up...
By: John Reid CATAAlliance
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Mobile Health Care Innovation: TechNOW interview, David Farnes, CATA, Health Care Champion - Video
The Post Office Can Nickel and Dime Like Health Care
Can hidden fees can the answer to the revenue problems of the postal service?
By: Harry Dent
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The Post Office Can Nickel and Dime Like Health Care - Video
Tommy Chong Rips FOX #39;s stupidity Opposing universal health care based on rumors and lies
By: Omar Rivero
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Tommy Chong Rips FOX's stupidity Opposing universal health care based on rumors and lies - Video
Lung Cancer: It #39;s not just a "smoker #39;s disease"
Do you know which cancer is the leading cause of death in the U.S.? It kills more Americans than breast, colon, and prostate cancerscombined. Yet we are still very far behind in advancing...
By: Baylor Health Care System
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Lessons from the VA
Dr. Holm is joined by Carrie Carlson, DO, in studio and Mike Davies, MD, via Skype to discuss the health care of veterans in our time. Dr. Carlson is a primary care doctor and occupational...
By: Prairie Doc
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This is the last installment in a four-part series.
LOS ANGELES (MarketWatch) -- Health analysts agree that its time for the patient to start being more of a consumer.
Obamacare, controls on Medicare spending, cutting back on malpractice litigation, more preventive care and even healthier lifestyles have all been touted as ways to cut costs in the health-care system. But together theyve made little more than a dent in the ever-rising cost of health care, which has been outpacing inflation for decades.
Mark Smith, 61, a self-employed documentary and commercial producer in Jersey City, N.J., has been paying for an individual policy for his family for several years. He says hes been seeing 16% increases in his premiums every year, sometimes more. His last increase would have put his monthly premium at $1,850 a month, even though its just him and his wife on the policy now.
It will always outpace whatever the economic conditions are, by a lot, he said. I dont have an infinite budget for health insurance. So Smith is opting out of the individual market and latching on to a health plan through his wifes new job, which should cut his monthly premiums down to $500.
Health reforms will have little meaningful effect on prices that continue to outpace inflation unless consumers get in the game and start to push back, experts say.
They agree that if the U.S. is to maintain a free-market style of health care, those who buy health plans need to be active players in the system. Just as they would when buying a car or purchasing groceries, health-care consumers need to have enough information to know what a fair price is and to have enough leverage to demand that price.
(Read: 10 ways patients can lower their health-care costs.)
You cant be a citizen any longer and not realize there are no more magical solutions to these problems, said Dr. Reed Tuckson, a former executive for UnitedHealth Group Inc. and the American Medical Association, now an industry consultant. The increase in Medicare expenditures is so huge. And theres no way that youre going to have any kind of taxation that could possibly solve that dilemma.
Accomplishing the task of becoming price-conscious wont be easy, however, for a group of consumers that for decades had insurers screen their costs for them.
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Health Exchange: Health-care costs: Its time for patients to take control
PUBLIC RELEASE DATE:
20-Nov-2014
Contact: Scott LaFee slafee@ucsd.edu 619-543-5232 University of California - San Diego @UCSanDiego
While investigating a rare genetic disorder, researchers at the University of California, San Diego School of Medicine have discovered that a ubiquitous signaling molecule is crucial to cellular reprogramming, a finding with significant implications for stem cell-based regenerative medicine, wound repair therapies and potential cancer treatments.
The findings are published in the Nov. 20 online issue of Cell Reports.
Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, and colleagues were attempting to use induced pluripotent stem cells (iPSC) to create a "disease-in-a-dish" model for focal dermal hypoplasia (FDH), a rare inherited disorder caused by mutations in a gene called PORCN. Study co-authors V. Reid Sutton and Ignatia Van den Veyver at Baylor College of Medicine had published the observation that PORCN mutations underlie FDH in humans in 2007.
FDH is characterized by skin abnormalities such as streaks of very thin skin or different shades, clusters of visible veins and wartlike growths. Many individuals with FDH also suffer from hand and foot abnormalities and distinct facial features. The condition is also known as Goltz syndrome after Robert Goltz, who first described it in the 1960s. Goltz spent the last portion of his career as a professor at UC San Diego School of Medicine. He retired in 2004 and passed away earlier this year.
To their surprise, Willert and colleagues discovered that attempts to reprogram FDH fibroblasts or skin cells with the requisite PORCN mutation into iPSCs failed using standard methods, but succeeded when they added WNT proteins - a family of highly conserved signaling molecules that regulate cell-to-cell interactions during embryogenesis.
"WNT signaling is ubiquitous," said Willert. "Every cell expresses one or more WNT genes and every cell is able to receive WNT signals. Individual cells in a dish can grow and divide without WNT, but in an organism, WNT is critical for cell-cell communication so that cells distinguish themselves from neighbors and thus generate distinct tissues, organs and body parts."
WNT signaling is also critical in limb regeneration (in some organisms) and tissue repair.
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Newswise BOSTON (Nov. 20, 2014) Investigators at Massachusetts Eye and Ear and Harvard Medical School Department of Ophthalmology and colleagues reported the development and characterization of a comprehensive genetic test for inherited eye disorders in the online version of the Nature journal Genetics In Medicine today. The Genetic Eye Disease (GEDi) test includes all of the genes known to harbor mutations that cause inherited retinal degenerations, optic atrophy and early onset glaucoma. These disorders are important causes of vision loss, and genetic treatments such as gene therapy hold promise for preserving vision in affected individuals. The GEDi test is offered on a CLIA-certified basis through the Ocular Genomics Institute (OGI) at Mass. Eye and Ear.
The retina is the neural tissue in the back of the eye that initiates vision. It is responsible for receiving light signals and converting them into neurologic signals, which are then transmitted via the optic nerve to the brain so that we can see. Mutations that disrupt vision by damaging the retina and optic nerve have been identified in more than 200 genes. This genetic diversity made genetic diagnostic testing difficult until the recent development of high throughput genomic techniques. The GEDi test uses targeted capture and next generation sequencing techniques to sequence 226 genes known to cause inherited eye disorders. Future versions of the test will also include genes responsible for eye movement disorders (strabismus) and other inherited eye conditions.
Gene panel-based tests for inherited eye disorders have been previously reported, but none of these have been as thoroughly characterized with regard to their performance in a diagnostic setting as the GEDi test. Stringent tests of accuracy and reproducibility showed that the GEDi test is both highly accurate and reproducible. This type of validation testing is recommended by the American College of Medical Genetics and Genomics, but few other genetic tests have been characterized in as much detail as the GEDi test. The results reported show that the GEDi test is 98 percent accurate at detecting spelling variations or mutations in the genetic code of inherited eye disease genes, and is highly reproducible between test runs. In contrast, the technique whole exome sequencing in which the coding regions of all genes are sequenced, and which is being employed commonly in clinical settingswas 88 percent accurate at detecting genetic variants in the same genes.
The results we obtained for the GEDi test have broad implications and show that panel-based testing focused on the specific genes associated with genetic conditions offers important advantages over whole exome sequencing, said Janey Wiggs, M.D., Ph.D., director of the Genetic Diagnostic Testing Service of the OGI, and the Paul Austin Chandler Associate Professor of Ophthalmology, Harvard Medical School.
Investigators in the OGI and other centers around the United States and the world are optimistic that treatments targeting the underlying genetic cause of inherited eye disorders can be applied broadly to preserve vision. One especially promising approach is gene therapy, in which a correct copy of the misspelled or mutant gene responsible for disease is added to the affected cells in the retina. Reports of early results from clinical trials of gene therapies for two inherited retinal degenerative disorders have shown that this treatment can be performed safely, and that subjects treated in these trials experienced significant improvements in or preservation of vision. Clinical trials of gene therapies for three additional genetic forms of inherited retinal degeneration are currently in progress, and more are on the way. Given the potential of gene and genetic therapies, improved genetic diagnostic testing for patients with genetic eye disorders such as that offered with the GEDi test is especially important.
About Massachusetts Eye and Ear Mass. Eye and Ear clinicians and scientists are driven by a mission to find cures for blindness, deafness and diseases of the head and neck. After uniting with Schepens Eye Research Institute in 2011, Mass. Eye and Ear in Boston became the world's largest vision and hearing research center, offering hope and healing to patients everywhere through discovery and innovation. Mass. Eye and Ear is a Harvard Medical School teaching hospital and trains future medical leaders in ophthalmology and otolaryngology, through residency as well as clinical and research fellowships. Internationally acclaimed since its founding in 1824, Mass. Eye and Ear employs full-time, board-certified physicians who offer high-quality and affordable specialty care that ranges from the routine to the very complex. U.S. News & World Reports Best Hospitals Survey has consistently ranked the Mass. Eye and Ear Departments of Otolaryngology and Ophthalmology as among the top hospitals in the nation. Mass. Eye and Ear is home to the Ocular Genomics Institute which aims to translate the promise of precision medicine into clinical care for ophthalmic disorders. For more information about life-changing care and research, or to learn how you can help, please visit MassEyeAndEar.org.
Reference: Consugar MB*, Navarro-Gomez D*, Place EM*, Bujakowska KM, Sousa ME, Fonseca-Kelly ZD, Taub DG, Janessian M, Wang DY, Au ED, Sims KB, Sweetser DA, Fulton AB, Liu Q, Wiggs JL,Gai X, Pierce EA. Panel-based Genetic Diagnostic Testing for Inherited Eye Diseases is Highly Accurate and Reproducible and More Sensitive for Variant Detection Than Exome Sequencing. Genetics In Medicine, In Press. (*Co-first authors).
Grant support: This work was supported by grants from the National Institutes of Health (EY012910, and P30EY014104), the March of Dimes and the Foundation Fighting Blindness.
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Newswise Denver, Colorado -- The American College of Veterinary Internal Medicine Foundation (ACVIMF), in partnership with the Veterinary Pharmacology Research Foundation (VPRF), announced today that they have funded a new study for animal health with a pharmacologic focus. The study will be conducted by Dr. Lauren Trepanier of the University of Wisconsin-Madison for the Genetic risk for cyclophosphamide toxicity in dogs.
The strategic partnership between VPRF and ACVIMF began in 2009 in an effort to solicit, review and administer research grants with a pharmacologic focus. The Veterinary Pharmacology Research Foundation (VPRF) was formed by the governing bodies of American Academy of Veterinary Pharmacology and Therapeutics (AAVPT) and the American College of Veterinary Clinical Pharmacology (ACVCP) in June of 2006. These organizations recognized that the lack of funding for basic pharmacology research was limiting both growth and innovation in the development of new veterinary therapeutics and the number of trained researchers in the field. As such, they sought to invest their collective resources in the growth of veterinary pharmacology through research grants and training programs. Jane Owens, President, VPRF.
The first call for proposals went out in November 2009. Since then, the partnership has awarded over $88,250 to six ACVIM Board-certified researchers along with their research team members. The first VPRF grant was awarded in June 2010 to Drs. Kenneth Simpson, Melanie Craven and Belgin Dogan from Cornell University for the development of a novel amikacin delivery method for treatment of E. coli associated with Granulomatous Colitis of Boxer dogs.
In 2011, the second grant was awarded to Drs. Butch KuKanich and Kate KuKanich from Kansas State University for a study to determine the effect of CYP inhibition on tramadol disposition and pharmacological effects in dogs. In 2012, Drs. Chen Gilor and Christopher Adin of the Veterinary Clinical Sciences Department at the Ohio State University received funding for evaluating Exenatide extended release in cats. Grant monies were also awarded to Drs. Jennifer Myers, Janice Bright, Christopher Orton, Daniel Gustafson and Christine Swardson Olver from the College of Veterinary Medicine & Biomedical Sciences, Colorado State University for evaluation of the pharmacokinetics and pharmacodynamics of Apibaxin in cats. The 2013 VPRF funds were awarded to Dr. Dawn Boothe and resident Jacqueline Gimmler of Auburn University for establishing terbinafine doses for treatment of canine Malassezia infection.
The grants encourage investigators to submit proposals that focus on research to evaluate the safety, effectiveness and duration of effect of therapies for veterinary species, explore new drug therapies for animals, develop and validate methods of evaluating effects of drugs in animal diseases or conditions, or ensure that a safe food supply is not compromised by drug therapy. As this grant is a partnership between veterinary internists and VPRF, collaborations between pharmacologists and Diplomates of ACVIM were strongly encouraged.
About Veterinary Pharmacology Research Foundation The Veterinary Pharmacology Research Foundation provides grant funding to support research into new and currently approved medications for combating diseases of companion and food animals, projects that ensure the safety of food products from treated livestock, and training programs for veterinary pharmacologists. These areas have been unmet needs in veterinary medicine for over 30 years. To donate to the Foundation, please access the following: http://aavpt.affiniscape.com/associations/12658/files/VPRFDonationForm3.pdf
About the ACVIM Foundation The American College of Veterinary Internal Medicine (ACVIM) Foundation is a non-profit 501(c)(3) organization dedicated to pioneering the healthcare of animals through the work of specialists in the American College of Veterinary Internal Medicine (ACVIM): small and large animal internists, cardiologists, neurologists, and oncologists. By supporting the work of these groundbreaking scientists, by raising awareness of specialty medicine, and by mobilizing the animal-loving public, we aim to revolutionize current treatments and spark the discovery of future cures. The ACVIM Foundation recognizes the need for advanced care, research dollars, awareness, and the need to support the Resident-in-training and the future scientist. Learn more at http://www.ACVIMFoundation.org.
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Genetic Engineering Recast
English 1001 recast project.
By: Brent Ufkes
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BIOLOGY: Genetic Engineering - Robin Hesketh
Good News for cancer therapy. Trials show genetic engineering of T-cells in the treatment of B-Cell Acute Lymphocitic Leukemia works.
By: Hay Levels
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PUBLIC RELEASE DATE:
20-Nov-2014
Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline
New Rochelle, NY, November 20, 2014-Women are more sensitive to the effects of cocaine and more susceptible to cocaine abuse than men. Cocaine's ability to disrupt a woman's estrus cycle may explain the sex differences in cocaine addiction, and new evidence that caffeine may be neuroprotective and able to block cocaine's direct effects on the estrus cycle reveals novel treatment possibilities, according to an article published in Journal of Caffeine Research: The International Multidisciplinary Journal of Caffeine Science, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Caffeine Research website at http://online.liebertpub.com/doi/full/10.1089/jcr.2014.0015 until December 20, 2014.
In the article "Cocaine Shifts the Estrus Cycle Out of Phase and Caffeine Restores It", Patricia Broderick, PhD and Lauren Malave, City College of New York, City University of New York Graduate Center, City University of New York, and NYU Langone Medical Center, New York, NY, show that cocaine shifts the estrus cycle, thereby changing a woman's estrogen levels. Caffeine can block these changes, suggesting that antagonists of the adenosine system may have a role in treating cocaine addiction.
"This is cutting-edge work that has never been shown before. It is critical knowledge relevant to women's reproductive health," says Patricia A. Broderick, PhD, Editor-in-Chief of Journal of Caffeine Research and Medical Professor in Physiology, Pharmacology & Neuroscience, The Sophie Davis School of Biomedical Education, The City College of New York, The City University of New York, and Adjunct Professor in Neurology, New York University Langone Medical Center and Comprehensive Epilepsy Center.
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About the Journal
Journal of Caffeine Research: The International Multidisciplinary Journal of Caffeine Science is a quarterly journal published in print and online. The Journal covers the effects of caffeine on a wide range of diseases and conditions, including mood disorders, neurological disorders, cognitive performance, cardiovascular disease, and sports performance. Journal of Caffeine Research explores all aspects of caffeine science including the biochemistry of caffeine; its actions on the human body; benefits, dangers, and contraindications; and caffeine addiction and withdrawal, across all stages of the human life span from prenatal exposure to end-of-life. Tables of content and a sample issue may be viewed on the Journal of Caffeine Research website at http://www.liebertpub.com/jcr.
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Caffeine counters cocaine's effects on women's estrus cycles
Chiara Bonini: "Bases of Gene Therapy in leukemias"
Chiara Bonini, dept. of Experimental Hematology at Fondazione San Raffaele del Monte Tabor - Milano, talks about "Bases of Gene Therapy in leukemias". http:/...
By: European Society for Gene and Cell Therapy
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Federico Mingozzi: "Translational research in the in vivo gene therapy of monogenic diseases"
Educational Day* at ESGCT Conference in Madrid. Federico Mingozzi - Head of Immunology and Liver Gene Transfer at Gnthon in Paris - talks on "Translational research in the in vivo gene...
By: European Society for Gene and Cell Therapy
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Gene Therapy: Progeria
Biol 298A Project 2 BioloG-Unit.
By: Ben Rein
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Delivering stem cell factor directly into damaged heart muscle after a heart attack may help repair and regenerate injured tissue, according to a study led by researchers from Icahn School of Medicine at Mount Sinai presented November 18 at the American Heart Association Scientific Sessions 2014 in Chicago, IL.
"Our discoveries offer insight into the power of stem cells to regenerate damaged muscle after a heart attack," says lead study author Kenneth Fish, PhD, Director of the Cardiology Laboratory for Translational Research, Cardiovascular Research Center, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai.
In the study, Mount Sinai researchers administered stem cell factor (SCF) by gene transfer shortly after inducing heart attacks in pre-clinical models directly into damaged heart tissue to test its regenerative repair response. A novel SCF gene transfer delivery system induced the recruitment and expansion of adult c-Kit positive (cKit+) cardiac stem cells to injury sites that reversed heart attack damage. In addition, the gene therapy improved cardiac function, decreased heart muscle cell death, increased regeneration of heart tissue blood vessels, and reduced the formation of heart tissue scarring.
"It is clear that the expression of the stem cell factor gene results in the generation of specific signals to neighboring cells in the damaged heart resulting in improved outcomes at the molecular, cellular, and organ level," says Roger J. Hajjar, MD, senior study author and Director of the Cardiovascular Research Center at Mount Sinai. "Thus, while still in the early stages of investigation, there is evidence that recruiting this small group of stem cells to the heart could be the basis of novel therapies for halting the clinical deterioration in patients with advanced heart failure."
cKit+ cells are a critical cardiac cytokine, or protein receptor, that bond to stem cell factors. They naturally increase after myocardial infarction and through cell proliferation are involved in cardiac repair.
According to researchers there has been a need for the development of interventional strategies for cardiomyopathy and preventing its progression to heart failure. Heart disease is the number one cause of death in the United States, with cardiomyopathy or an enlarged heart from heart attack or poor blood supply due to clogged arteries being the most common causes of the condition. In addition, cardiomyopathy causes a loss of cardiomyocyte cells that control heartbeat, and changes in heart shape, which lead to the heart's decreased pumping efficiency.
"Our study shows our SCF gene transfer strategy can mobilize a promising adult stem cell type to the damaged region of the heart to improve cardiac pumping function and reduce myocardial infarction sizes resulting in improved cardiac performance and potentially increase long-term survival and improve quality of life in patients at risk of progressing to heart failure," says Dr. Fish.
"This study adds to the emerging evidence that a small population of adult stem cells can be recruited to the damaged areas of the heart and improve clinical outcomes," says Dr. Hajjar.
Other study co-authors included Kiyotake Ishikawa, MD, Jaume Aguero, MD, Lisa Tilemann, MD, Dongtak Jeong, PhD, Lifan Liang, PhD, Lauren Fish, Elisa Yaniz-Galende, PhD, and Krisztina Zsebo, PhD.
This research study was performed in collaboration with the Celladon Corporation in San Diego, CA. Dr. Hajjar is the scientific cofounder of the company Celladon, which is developing his AAV1/SERCA2a gene therapy for the treatment of heart failure. He holds equity in Celladon and receives financial compensation as a member of its advisory board.
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Newswise LA JOLLA, CA November 20, 2014 Scientists at The Scripps Research Institute (TSRI) have discovered how one gene is essential to hearing, uncovering a cause of deafness and suggesting new avenues for therapies.
The new study, published November 20 in the journal Neuron, shows how mutations in a gene called Tmie can cause deafness from birth. Underlining the critical nature of their findings, researchers were able to reintroduce the gene in mice and restore the process underpinning hearing.
This raises hopes that we could, in principle, use gene-therapy approaches to restore function in hair cells and thus develop new treatment options for hearing loss, said Professor Ulrich Mller, senior author of the new study, chair of the Department of Molecular and Cellular Neuroscience and director of the Dorris Neuroscience Center at TSRI.
The Gene Responsible
The ear is a complex machine that converts mechanical sound waves into electric signals for the brain to process. When a sound wave enters the ear, the uneven ends (stereocilia) of the inner ears hair cells are pushed back, like blades of grass bent by a heavy wind. The movement causes tension in the strings of proteins (tip links) connecting the stereocilia, which sends a signal to the brain through ion channels that run through the tips of the hair cell bundles.
This process of converting mechanical force into electrical activity, called mechanotransduction, still poses many mysteries. In this case, researchers were in the dark about how signals were passed along the tip links to the ion channels, which shape electrical signals.
To track down this unknown component, researchers in the new study built a library of thousands of genes with the potential to affect mechanotransduction.
The team spent six months screening the genes to see if the proteins the genes produced interacted with tip link proteins. Eventually, the team found a gene, Tmie, whose protein, TMIE, interacts with tip link proteins and connects the tip links to a piece of machinery near the ion channel.
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InnerSpace: Futurist
Explorations of the future have always been the domain of Sci Fi writers, but now there #39;s a relatively new occupation that #39;s increasingly in demand: The Futu...
By: Space
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The Future of Fashion on Futurist
From LED wardrobe to solar powered outfits, the future of what #39;s hanging in your closet is looking bright. The List #39;s Bradley Hasemeyer is taking a look at f...
By: The List TV Show
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