Hospice UK annual conference 2014 - second plenary (day one)
The second plenary of the first day of the Hospice UK 2014 annual conference #39;The value and importance of research in measuring, demonstrating and improving the quality of end of life care #39;,...
By: Hospice UK (previously Help the Hospices)
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Hospice UK annual conference 2014 - second plenary (day one) - Video
5 Benefits Of Physical Exercise To Elders
CrestHire is the best resource used by home health care agencies to find quality home health care and senior care services in NJ, USA.
By: Sree Alangad
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AP Photo/Damian Dovarganes, File FILE - In this Oct. 1, 2013, file photo, Rosa Guerra, 52, right, gets a free eye exam during the Binational Health Week event held at the Mexican Consulate in Los Angeles. Health care advocates say President Obamas immigration action should enable hundreds of thousands of low-income immigrants in Calif., to qualify for Medi-Cal even as state officials say its premature to comment.
SACRAMENTO, Calif. President Barack Obama's executive order to spare some immigrants from deportation has galvanized Democrats, immigration groups and health care advocates in California to push for expanding health coverage to a segment of the population that remains uninsured.
The president's action excludes immigrants who came to the country illegally from qualifying for federal health benefits. But California has its own policy of providing health coverage with state money to low-income immigrants with so-called "deferred action" that allow them to avoid deportation. Immigrant and health care advocates say that means Obama's executive order will enable hundreds of thousands of low-income immigrants in California to apply for Medi-Cal, California's version of Medicaid.
Anthony Wright, executive director of Health Access California, said allowing this expanded group of immigrants to participate in the Medicaid program will enable people to get primary and preventive care, "rather than just at the emergency room."
The California Department of Health Care Services, however, has yet to receive formal guidance. A state official said it's too early to tell how the immigration program will impact the overall Medi-Cal program, which is consuming an increasing share of state funds.
Medi-Cal is a health program for the poor paid for by the federal government and the state. It has grown by about 3 million people in California under federal health care reform and now covers more than 11 million Californians, about 30 percent of the state's population. The federal government is paying for the expansion, but the state will eventually pay 10 percent of additional costs to cover low-income adults, many of whom are childless.
The state is expected to spend more than $17 billion of its own money on the program this year, up 3.5 percent a year ago, according to the Legislative Analyst's Office.
AP Photo/Damian Dovarganes, File FILE - In this Oct. 1, 2013, file photo, Alberto Pizon, right, a representative of Anthem BlueCross BlueShield Latino Health Access group provides free information to Paulino Zarate, 65, left, on the new health options available during a health fair promoted at the Binational Health Week event held at the Mexican Consulate in Los Angeles. Health care advocates say President Obamas immigration action should enable hundreds of thousands of low-income immigrants in Calif. to qualify for Medi-Cal even as state officials say its premature to comment.
"We are assessing what some of the potential impacts could be, but it would be premature for us to comment until we have more specific information available," said Norman Williams, a spokesman for the Department of Health Care Services.
The president's action has also emboldened a Democratic lawmaker to revive a bill that would provide health coverage to all Californians, regardless of their immigration status.
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When private prices for health care services decrease, Medicare spending increases, according to a new study. The finding raises the possibility that physicians and hospitals may be shifting some services to Medicare when they stand to make more money by doing so -- though further research will be needed to clearly identify the cause, according to the study's authors.
The study, conducted by the Leonard D. Schaeffer Center for Health Policy and Economics, is the first in a series of attempts to mine reams of health care spending data gathered by the Institute of Medicine in 2013.
"It turns out that what happens in private health care may not stay in private health care," said John Romley, research assistant professor at the USC Price School of Public Policy and lead researcher on the study. "If a private health plan manages to negotiate lower prices with health care providers, they may make up the difference by providing additional health care to Medicare beneficiaries."
Romley collaborated with Sarah Axeen, Darius Lakdawalla and Dana Goldman of the USC Schaeffer Center as well as Michael Chernew of Harvard University and Jay Bhattacharya of Stanford University. The findings were published online by Health Services Research on Nov. 27.
The team examined data from more than 300 geographic regions covering the United States, exploring Medicare spending on inpatient and outpatient care and prescription drugs for fee-for-service beneficiaries.
The researchers found that a 10 percent lower private price for health care is associated with a 3 percent increase in Medicare spending per member per year, and 4.3 percent more specialist visits.
Next, Romley plans to explore how mergers among insurers affect private health care prices, and ultimately Medicare utilization and spending.
"We've known for a long time that some parts of the U.S. have much higher Medicare spending than others, but not necessarily a higher quality of care. But Medicare is only 20 percent of U.S. health care spending, and we're only now beginning to understand how private health care differs throughout the U.S.," Romley said.
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The above story is based on materials provided by University of Southern California. The original article was written by Robert Perkins. Note: Materials may be edited for content and length.
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Cheaper private health care prices mean more Medicare spending
At least 5,000 Russians marched on a frosty Sunday afternoon in Moscow to protest plans to lay off thousands of doctors and close hospitals against the backdrop of a flagging economy. Alexander Zemlianichenko/AP hide caption
At least 5,000 Russians marched on a frosty Sunday afternoon in Moscow to protest plans to lay off thousands of doctors and close hospitals against the backdrop of a flagging economy.
In the numbing cold, several thousand demonstrators marched in Moscow on Sunday, protesting plans to make drastic cuts in the city's health care system. It was the second protest in the past month over a pocketbook issue that affects most Russian consumers especially as people feel the effects of a weakening economy.
Protesters waved flags and carried banners with slogans like "Save money on war, not on doctors." It was a relatively small demonstration, but it drew broad support. And it signaled that while Russian President Vladimir Putin has been facing growing international isolation for his foreign policy, he's also under pressure at home.
The demonstrators ranged from doctors and patients groups saying the medical system desperately needs reform to Communists who want to return to a Soviet-style system of free medical care.
They all say the government's reform plan is a heavy-handed scheme concocted by government bureaucrats who never consulted the medical community.
"They haven't explained anything to anybody," says Tatiana Korshunova, a blood technician on a heart-surgery team. "They haven't explained why they're cutting the number of hospitals or how they're going to do that. They haven't explained why they're cutting the number of doctors."
The government's plan would eliminate jobs for up to 10,000 doctors and close 28 of Moscow's hospitals and clinics by early next year. Korshunova says it is humiliating that medical workers weren't consulted on something that impacts so many of them.
The city administration says the closed hospitals will eventually be replaced by neighborhood outpatient clinics. Pavel, a 30-year-old cardiologist, says that's just doing things backwards.
"We do need reforms, but not the way they're doing it," he says. "They need to build up the clinics before they close hospitals and lay people off."
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Protesters In Moscow Demand Explanation For Health Care Cuts
An Australian health company will be investigated for a second time over evidence it potentially put profits ahead of patients through over-servicing.
The Federal Government has launched a second investigation after the ABC obtained evidence that Primary Health Care offered its doctors bonuses to see extra patients each day.
The bonus scheme was offered to doctors working in Primary Health Care clinics across Australia between September and February next year.
GPs were offered a bonus for seeing three extra patients each day and incentives to write extra diabetes and asthma management plans.
When doctors write up a plan they can bill an extra charge to Medicare on top of the scheduled appointment.
Health groups have been outraged by the offer and said patients were being treated like numbers to help the health company's bottom line.
Primary Health Care is the country's number one provider of large medical centres and made a profit of $162 million last year.
Legal experts said the bonus scheme was not a direct breach of health laws unless the result of the offer was for doctors to charge for extra unnecessary visits, called over-servicing.
The majority of Primary Health Care clinics bulk-bill, and extra billings mean extra costs to the taxpayer.
Primary Health Care said there was a problem with under-servicing in the health care system and the Government was trying to encourage more management plans for asthma and diabetes.
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Primary Health Care investigated again over claims of incentives for GPs to over-service
PUBLIC RELEASE DATE:
1-Dec-2014
Contact: Emmanouil Dermitzakis emmanouil.dermitzakis@unige.ch 41-223-795-483 Universit de Genve @UNIGEnews
Personalized medicine uses methods of molecular analysis, especially genetic sequencing and transcription, in order to simultaneously identify genetic mutations to evaluate each individual's risk of contracting a given disease. It seems that there is more than a single mechanism at hand, as proven by the work of a team of geneticists at the University of Geneva's (UNIGE) Faculty of Medicine, and the Swiss Institute for Bioinformatics (SIB). They have sequenced the RNA of 400 pairs of twins; with this information, they can quantify the roles of both genetic and environmental context on the expression of genes. They concluded that establishing the list of mutations present in a person's genome is not sufficient to predict that person's future health. The study can be found in the latest online edition of Nature Genetics.
What influence does the environment have on genes activity? How do certain types of mutations interact with one another in a single individual? These are the complex interactions that Emmanouil Dermitzakis, Louis-Jeantet Professor in the Department of Genetic Medicine and Development at the UNIGE's Faculty of Medicine, and his team have sought to understand, working together with scientists from Kings College London and the Wellcome Trust Sanger Institute.
Although we know that carriers of the same mutation do not necessarily both develop the same disease, how much of this discrepancy is due to genetics and how much is environmental remains unclear. Understanding how a mutation behaves when confronted with another mutation, on the one hand, and assessing the person's environmental context, on the other, forms the basis of the complex challenge of true personalized medicine.
Twins that are similar, but not identical
In Geneva, the scientists sequenced the RNA of 400 pairs of monozygotic and dizygotic twins and combined this information with genetic variations that had already been identified in these subjects. In this large sample, they identified a significant series of mutations that controlled gene expression. The researchers discovered that the influence that purely genetic (between genes) and environmental interactions (between a gene and the environment) had on gene expression were both substantial. They conclude that genetic or environmental context contributes significantly to the way in which a person's genetic composition is expressed, as well as to their risk of developing certain diseases.
The researchers used the differences between monozygotic twins, whose genomes are identical, to identify mutations that interact with the environment. Dizygotic twins, who only share half of their genome, but who were raised in the same environment, allowed researchers to separate purely genetic effects from effects caused by the similar environmental context in which the twins were raised.
We have discovered that the genetic and environmental contexts of a mutation have a much greater influence on its expression in a given individual than we previously thought, emphasized Dr Alfonso Buil, lead author of this study. Understanding the architecture of genetic expression constitutes an essential step in understanding the genetic bases of complex diseases, he adds.
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Genes and environment: Complex interactions at the heart of personalized medicine
PUBLIC RELEASE DATE:
1-Dec-2014
Contact: David Slotnick newsmedia@mssm.edu The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc
(NEW YORK - December 1, 2014) Kidneys donated by people born with a small variation in the code of a key gene may be more likely, once in the transplant recipient, to accumulate scar tissue that contributes to kidney failure, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai and published today in the Journal of Clinical Investigation.
If further studies prove the variation to cause fibrosis (scarring) in the kidneys of transplant recipients, researchers may be able to use it to better screen potential donors and improve transplant outcomes. Furthermore, uncovering the protein pathways that trigger kidney fibrosis may help researchers design drugs that prevent this disease process in kidney transplant recipients, and perhaps in all patients with chronic kidney disease.
"It is critically important that we identify new therapeutic targets to prevent scarring within transplanted kidneys, and our study has linked a genetic marker, and related protein pathways, to poor outcomes in kidney transplantation," said Barbara Murphy, MD, Chair, Department of Medicine, Murray M. Rosenberg Professor of Medicine (Nephrology) and Dean for Clinical Integration and Population Health at the Icahn School of Medicine at Mount Sinai. "Drug designers may soon be able to target these mechanisms."
A commonly used study type in years, the genome-wide association study (GWAS) looks at differences at many points in the genetic code to see if, across a population, any given variation in the genetic code is found more often in those with a given trait; in the case of the current study, with increased fibrosis in recipients of donated kidneys.
Even the smallest genetic variations, called single nucleotide polymorphisms (SNPs), can have a major impact on a trait by swapping just one of 3.2 billion "letters" making up the human DNA code. The current study found a statistically significant association between SNP identified as rs17319721 in the gene SHROOM3 and progressive kidney scarring (fibrosis) and function loss in a group of kidney donors, mostly of European descent. In many cases, certain SNPs will be more common in families or ethnic groups.
The kidneys filter the blood to remove extra blood sugar and waste products that trickle down the kidney tubes to become urine, while re-absorbing key nutrients. The build-up of scar tissue in these delicate structures over time interferes with proper renal function.
Chronic kidney disease already affects 10 percent of US adults and its prevalence is increasing. Along with leading to kidney failure in many cases, chronic kidney disease increases the risk of cardiovascular disease. Fibrosis in kidney tubules is a common pathogenic process for many types of chronic kidney disease, and a central part of chronic disease in donated kidneys (chronic allograft nephropathy, or CAN).
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Genetic marker may help predict success of kidney transplants
Released: 1-Dec-2014 5:00 PM EST Source Newsroom: Mayo Clinic Contact Information
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Newswise ROCHESTER, Minn. Most patients with triple-negative breast cancer should undergo genetic testing for mutations in known breast cancer predisposition genes, including BRCA1 and BRCA2, a Mayo Clinic-led study has found. The findings come from the largest analysis to date of genetic mutations in this aggressive form of breast cancer. The results of the research appear in the Journal of Clinical Oncology.
Clinicians need to think hard about screening all their triple-negative patients for mutations because there is a lot of value in learning that information, both in terms of the risk of recurrence to the individual and the risk to family members. In addition, there may be very specific therapeutic benefits of knowing if you have a mutation in a particular gene, says Fergus Couch, Ph.D., professor of laboratory medicine and pathology at Mayo Clinic and lead author of the study.
The study found that almost 15 percent of triple-negative breast cancer patients had deleterious (harmful) mutations in predisposition genes. The vast majority of these mutations appeared in genes involved in the repair of DNA damage, suggesting that the origins of triple-negative breast cancer may be different from other forms of the disease. The study also provides evidence in support of the National Comprehensive Cancer Network (NCCN) guidelines for genetic testing of triple-negative breast cancer patients.
Triple-negative breast cancer is a specific subset of breast cancer that makes up about 12 to 15 percent of all cases. The disease is difficult to treat because the tumors are missing the estrogen, progesterone and HER-2 receptors that are the target of the most common and most effective forms of therapy. However, recent studies have suggested that triple-negative breast cancer patients might harbor genetic mutations that make them more likely to respond to alternative treatments like cisplatin, a chemotherapy agent, or PARP inhibitors, anti-cancer agents that inhibit the poly (ADP-ribose) polymerase (PARP) family of enzymes.
Dr. Couch and his colleagues decided to assess the frequency of mutations in predisposition genes in patients with triple-negative breast cancer to further delineate the role of genetic screening for individuals with the disease. The researchers sequenced DNA from 1,824 triple-negative breast cancer cases seen at 12 oncology clinics in the U.S. and Europe, as part of the Triple-Negative Breast Cancer Consortium.
They found deleterious mutations in almost 15 percent of triple-negative breast cancer patients. Of these, 11 percent had mutations in the BRCA1 and BRCA2 genes and the rest had mutations in 15 other predisposition genes, including the DNA repair genes PALB2, BARD1, and RAD51C. No mutations were found in predisposition genes involved in other processes like the cell cycle.
Triple-negative breast cancers are different from all the other breast cancers, says Dr. Couch. Other studies have suggested that this form of the disease might be associated with some defect in DNA repair, and our study verifies that. Our findings generate a whole new set of hypotheses about how triple-negative breast cancer might be arising, which could give us better ideas for prevention or new therapies for this disease.
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Triple-Negative Breast Cancer Patients Should Undergo Genetic Screening: Mayo Clinic
PUBLIC RELEASE DATE:
1-Dec-2014
Contact: Renatt Brodsky renatt.brodsky@mountsinai.org The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc
The most commonly used medications for osteoporosis worldwide, bisphosphonates, may also prevent certain kinds of lung, breast and colon cancers, according to two studies led by researchers at the Icahn School of Medicine at Mount Sinai and published today in the Proceedings of the National Academy of Sciences (PNAS).
Bisphosphonates had been associated by past studies with slowed tumor growth in some patients but not others, and the mechanism behind these patterns was unknown. In the studies published today, an international research team showed that bisphosphonates block the abnormal growth signals passed through the human EGF receptors (HER), including the forms of this protein family that make some tumors resistant to leading treatments. The connection between bisphosphonates and HER receptors was detected first in a genetic database analysis and confirmed in studies of human cancer cells and in mice.
"Our study reveals a newfound mechanism that may enable the use of bisphosphonates in the future treatment and prevention of the many lung, breast and colon cancers driven by the HER family of receptors," said lead study author Mone Zaidi, MD, Professor of Medicine and of Structural and Chemical Biology within the Icahn School of Medicine at Mount Sinai, Director of the Mount Sinai Bone Program and a member of the Tisch Cancer Institute at Mount Sinai. "Having already been approved by the FDA as effective at preventing bone loss, and having a long track record of safety, these drugs could be quickly applied to cancer if we can confirm in clinical trials that this drug class also reduces cancer growth in people. It would be much more efficient than starting drug design from scratch."
Of the two newly published PNAS papers, one describes the evidence that bisphosphonates block abnormal growth signals through HER family receptors, while the second examines the potential applications for this new mechanism: cancer prevention, combination with existing treatments, and use against treatment-resistant tumors.
Stop Abnormal Growth
The study results revolved around the human epidermal growth factor receptor (HER/EGFR) family, which consists of four types of transmembrane tyrosine kinase receptors: HER1, HER2, HER3, and HER4. HER family members occur on the surfaces of many cell types and regulate cell division and proliferation, processes closely linked to both normal tissue growth and the abnormal growth seen in cancer.
A variety of human cancers, including nonsmall cell lung (NSCLC), breast, and colon cancers, are driven by random genetic changes (somatic mutations) that make HER family receptor tyrosine kinases more active drivers of abnormal growth. About of 30 percent of nonsmall cell cancers (NSCLCs) and 90 percent of colon cancers are driven by small genetic changes in HER1, while 25 percent of breast cancers proceed from genetic changes that result in excessive amounts of HER2.
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Widely used osteoporosis drugs may prevent breast, lung and colon cancers
8 hours ago Streptococcus pyogenes is one of the bacteria in which the HZI scientists have studied the CRISPR-Cas system. Credit: HZI / M. Rohde
Genome engineering with the RNA-guided CRISPR-Cas9 system in animals and plants is changing biology. It is easier to use and more efficient than other genetic engineering tools, thus it is already being applied in laboratories all over the world just a few years after its discovery. This rapid adoption and the history of the system are the core topics of a review published in the renowned journal Science. The review was written by the discoverers of the system Prof. Emmanuelle Charpentier, who works at the Helmholtz Centre for Infection Research (HZI) and is also affiliated to the Hannover Medical School and Ume University, and Prof. Jennifer Doudna from the University of California, Berkeley, USA.
Many diseases result from a change of an individual's DNA - the letter code that genes consist of. The defined order of the letters within a gene usually codes for a protein. Proteins are the workforce of our body and responsible for almost all processes needed to keep us running. When a gene is altered, its protein product may lose its normal function and disorders can result. "Making site-specific changes to the genome therefore is an interesting approach to preventing or treating those diseases", says Prof Emmanuelle Charpentier, head of the HZI research department "Regulation in Infection Biology". Due to this, ever since the discovery of the DNA structure, researchers have been looking for a way to alternate the genetic code.
First techniques like zinc finger nucleases and synthetic nucleases called TALENs were a starting point but turned out to be expensive and difficult to handle for a beginner. "The existing technologies are dependent on proteins as address labels and customizing new proteins for any new change to introduce in the DNA is a cumbersome process", says Charpentier. In 2012, while working at Ume University, she described what is now revolutionising genetic engineering: the CRISPR-Cas9 system.
It is based on the immune system of bacteria and archaea but is also of value in the laboratory. CRISPR is short for Clustered Regularly Interspaced Palindromic Repeats, whereas Cas simply stands for the CRISPR-associated protein. "Initially we identified a novel RNA, namely tracrRNA, associated to the CRISPR-Cas9 system, which we published in 2011 in Nature. We were excited when Krzysztof Chylinski from my laboratory subsequently confirmed a long term thinking: Cas9 is an enzyme that functions with two RNAs", says Charpentier.
Together the system has the ability to detect specific sequences of letters within the genetic code and to cut DNA at a specific point. In this process the Cas9 protein functions as the scissors and an RNA snippet as the address label ensuring that the cut happens in the right place. In collaboration with Martin Jinek and Jennifer Doudna, the system could be simplified to use it as a universal technology. Now the user would just have to replace the sequence of this RNA to target virtually any sequence in the genome.
After describing the general abilities of CRISPR-Cas9 in 2012 it was shown in early 2013 that it works as efficiently in human cells as it does in bacteria. Ever since, there has been a real hype around the topic and researchers from all over the world have suggested new areas in which the new tool can be used. The possible applications extend from developing new therapies for genetic disorders caused by gene mutations to changing the pace and course of agricultural research in the future all the way to a possible new method for fighting the AIDS virus HIV.
"The CRISPR-Cas9 system has already breached boundaries and made genetic engineering much more versatile, efficient and easy", Charpentier says. "There really does not seem to be a limit in the applications."
Explore further: RCas9: A programmable RNA editing tool
Viruses cannot only cause illnesses in humans, they also infect bacteria. Those protect themselves with a kind of 'immune system' which simply put consists of specific sequences in the genetic material ...
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Revolutionizing genome engineering: Review on history and future of the CRISPR-Cas9 system published
Genome engineering with the RNA-guided CRISPR-Cas9 system in animals and plants is changing biology. It is easier to use and more efficient than other genetic engineering tools, thus it is already being applied in laboratories all over the world just a few years after its discovery. This rapid adoption and the history of the system are the core topics of a review published in the journal Science. The review was written by the discoverers of the system Prof. Emmanuelle Charpentier, who works at the Helmholtz Centre for Infection Research (HZI) and is also affiliated to the Hannover Medical School and Ume University, and Prof. Jennifer Doudna from the University of California, Berkeley, USA.
Many diseases result from a change of an individual's DNA -- the letter code that genes consist of. The defined order of the letters within a gene usually codes for a protein. Proteins are the workforce of our body and responsible for almost all processes needed to keep us running. When a gene is altered, its protein product may lose its normal function and disorders can result. "Making site-specific changes to the genome therefore is an interesting approach to preventing or treating those diseases," says Prof Emmanuelle Charpentier, head of the HZI research department "Regulation in Infection Biology." Due to this, ever since the discovery of the DNA structure, researchers have been looking for a way to alternate the genetic code.
First techniques like zinc finger nucleases and synthetic nucleases called TALENs were a starting point but turned out to be expensive and difficult to handle for a beginner. "The existing technologies are dependent on proteins as address labels and customizing new proteins for any new change to introduce in the DNA is a cumbersome process," says Charpentier. In 2012, while working at Ume University, she described what is now revolutionising genetic engineering: the CRISPR-Cas9 system.
It is based on the immune system of bacteria and archaea but is also of value in the laboratory. CRISPR is short for Clustered Regularly Interspaced Palindromic Repeats, whereas Cas simply stands for the CRISPR-associated protein. "Initially we identified a novel RNA, namely tracrRNA, associated to the CRISPR-Cas9 system, which we published in 2011 in Nature. We were excited when Krzysztof Chylinski from my laboratory subsequently confirmed a long term thinking: Cas9 is an enzyme that functions with two RNAs," says Charpentier.
Together the system has the ability to detect specific sequences of letters within the genetic code and to cut DNA at a specific point. In this process the Cas9 protein functions as the scissors and an RNA snippet as the address label ensuring that the cut happens in the right place. In collaboration with Martin Jinek and Jennifer Doudna, the system could be simplified to use it as a universal technology. Now the user would just have to replace the sequence of this RNA to target virtually any sequence in the genome.
After describing the general abilities of CRISPR-Cas9 in 2012 it was shown in early 2013 that it works as efficiently in human cells as it does in bacteria. Ever since, there has been a real hype around the topic and researchers from all over the world have suggested new areas in which the new tool can be used. The possible applications extend from developing new therapies for genetic disorders caused by gene mutations to changing the pace and course of agricultural research in the future all the way to a possible new method for fighting the AIDS virus HIV.
"The CRISPR-Cas9 system has already breached boundaries and made genetic engineering much more versatile, efficient and easy," Charpentier says. "There really does not seem to be a limit in the applications."
Story Source:
The above story is based on materials provided by Helmholtz Centre for Infection Research. Note: Materials may be edited for content and length.
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Futurist Herb OHeron on the value of a degree
Herb O #39;Heron is Canada #39;s own educational futurist. Working with the Association of Universities and Colleges of Canada (AUCC), as Director of Research and Po...
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SEEMF Skopje 2014 - Press Freedom Panel The Censorship disquised in free countries
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SEEMF Skopje 2014 - Press Freedom Panel The Censorship disquised in free countries - Video
2015 Jeep Wrangler Unlimited Oscar Mike Freedom Edition Billet Silver
My new jeep wrangler. Filmed with gopro hero 4 black @1080p/120fps.
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2015 Jeep Wrangler Unlimited Oscar Mike Freedom Edition Billet Silver - Video
sds antiwar monument holy cross Colorado aria Joe Hill Honda Freedom Trail
There is an influence from Bernard DeVoto, Robert Service and Elmer Bernstein in this poem/song To just get away from the sickening reality of Social Problems, Wars, from the ritual of college...
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sds antiwar monument holy cross Colorado aria Joe Hill Honda Freedom Trail - Video
Freedom! Forum Formal w/ SuperKan
Freedom Forum Formal http://freedom.community.tm/threads/the-freedom-forum-formal-december-19th-2014.81773/ Kan #39;s Channel http://www.youtube.com/WeKanGame Get your own Video CMS ...
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Zumba with Jan @ Freedom Fitness / Hideaway
No copyright infringement intended. For choreography purposes only. Choreography inspired by Medora Cesarano. Buy this song here: ...
By: Tracy Cox
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Zumba with Jan @ Freedom Fitness / Menea La Pera
No copyright infringement intended. For choreography purposes only. Buy this song here: http://www.amazon.com/gp/product/B00LI9P17Y/ref=dm_ws_sp_tlw_trk1?ie=UTF8 qid=1417399944 sr=1-1.
By: Tracy Cox
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Two Steps From Hell: "My Freedom" (feat.Merethe Soltvedt)
Two Steps From Hell: ~ My Freedom (feat.Merethe Soltvedt) ~ Beautiful Epic composition from Thomas Bergersen!
By: Miracles ~ http://www.twostepsfromhell.com/ Links for pics: http://wall.alphacode.
By: THESTORMWOLF9
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Two Steps From Hell: "My Freedom" (feat.Merethe Soltvedt) - Video