With Facebook deciding to hide monthly and daily active users, we have lost the one game platform that could give us reasonably objective data about game performance. We are back to the Dark Ages of vanity metrics as a result. This is something that needs to change.Source: http://feedproxy.google.com/~r/Techcrunch/~3/XaMGVBGVQKc/
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New research reveals a potential way for how parents' experiences could be passed to their offspring's genes. The research was published today, 25 January, in the journal Science.
Epigenetics is a system that turns our genes on and off. The process works by chemical tags, known as epigenetic marks, attaching to DNA and telling a cell to either use or ignore a particular gene.
The most common epigenetic mark is a methyl group. When these groups fasten to DNA through a process called methylation they block the attachment of proteins which normally turn the genes on. As a result, the gene is turned off.
Scientists have witnessed epigenetic inheritance, the observation that offspring may inherit altered traits due to their parents' past experiences. For example, historical incidences of famine have resulted in health effects on the children and grandchildren of individuals who had restricted diets, possibly because of inheritance of altered epigenetic marks caused by a restricted diet.
However, it is thought that between each generation the epigenetic marks are erased in cells called primordial gene cells (PGC), the precursors to sperm and eggs. This 'reprogramming' allows all genes to be read afresh for each new person - leaving scientists to question how epigenetic inheritance could occur.
The new Cambridge study initially discovered how the DNA methylation marks are erased in PGCs, a question that has been under intense investigation over the past 10 years. The methylation marks are converted to hydroxymethylation which is then progressively diluted out as the cells divide. This process turns out to be remarkably efficient and seems to reset the genes for each new generation. Understanding the mechanism of epigenetic resetting could be exploited to deal with adult diseases linked with an accumulation of aberrant epigenetic marks, such as cancers, or in 'rejuvenating' aged cells.
However, the researchers, who were funded by the Wellcome Trust, also found that some rare methylation can 'escape' the reprogramming process and can thus be passed on to offspring ? revealing how epigenetic inheritance could occur. This is important because aberrant methylation could accumulate at genes during a lifetime in response to environmental factors, such as chemical exposure or nutrition, and can cause abnormal use of genes, leading to disease. If these marks are then inherited by offspring, their genes could also be affected.
Dr Jamie Hackett from the University of Cambridge, who led the research, said: "Our research demonstrates how genes could retain some memory of their past experiences, revealing that one of the big barriers to the theory of epigenetic inheritance - that epigenetic information is erased between generations - should be reassessed."
"It seems that while the precursors to sperm and eggs are very effective in erasing most methylation marks, they are fallible and at a low frequency may allow some epigenetic information to be transmitted to subsequent generations. The inheritance of differential epigenetic information could potentially contribute to altered traits or disease susceptibility in offspring and future descendants."
"However, it is not yet clear what consequences, if any, epigenetic inheritance might have in humans. Further studies should give us a clearer understanding of the extent to which heritable traits can be derived from epigenetic inheritance, and not just from genes. That could have profound consequences for future generations."
Professor Azim Surani from the University of Cambridge, principal investigator of the research, said: "The new study has the potential to be exploited in two distinct ways. First, the work could provide information on how to erase aberrant epigenetic marks that may underlie some diseases in adults. Second, the study provides opportunities to address whether germ cells can acquire new epigenetic marks through environmental or dietary influences on parents that may evade erasure and be transmitted to subsequent generations, with potentially undesirable consequences."
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University of Cambridge: http://www.cam.ac.uk
Thanks to University of Cambridge for this article.
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Source: http://www.labspaces.net/126467/Scientists_discover_how_epigenetic_information_could_be_inherited
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If that's the situation, let me discuss some of my healthy epidermis care guidance and perhaps we can get some of those concerns eliminated.
First let's get one factor clear: there is no particular age or time frame you should definitely begin using anti aging items. It all relies on your genetics, way of life, choices and also on your kind of epidermis. Some individuals have excellent genetics and look like youngsters into their 40s, the relax of us must manage what we eat strategy, work out program and remain non-smokers to arrive at the same impact (and even then there's no guarantee). Those who greasy epidermis or a few excess weight usually look young for more time, but slimmer individuals and dry-skinned individuals need to begin actions against the ravages of time previously.
So when do you individually need to begin with using anti aging cream? My healthy epidermis care guidance is to begin with when the first experience lines begin to appear, usually around the sight or oral cavity. Based on the aspects detailed above, this could be when you are 21, or it could be when you are 31 or even mature. Keep an eye on your experience and take activity as soon as you see the first wrinkles-in-the-making.
Some individuals suggest getting safety actions before any ravages of time are noticeable, but in my perspective this is not necessary.
But what anti aging items should I use, you ask. Again, you need to look at yourself and your epidermis to choose. Most individuals can begin with an anti aging day cream and a experience clean with some anti aging advantages. But if you have dry epidermis, you might want to use an anti aging evening cream right away. Using covers every few several weeks is also a wise decision - at first you can use any (all-natural) covers and later on shift to ones with more juvenating substances.
Source: http://b1b2kombonganandes.blogspot.com/2013/01/when-to-begin-using-stop-ageing-lotion.html
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ST. CATHARINES ? At least 14 people have fallen victim to a ?paving scam? in St. Catharines, Niagara Regional Police say.
According to investigators, a male going door-to-door approaches victims offering to pave their driveway at a much reduced cost.
Once the suspect receives the cash up front, he claims he will return with his equipment.
In some cases, the suspect has even asked the victim to drive him to a location to pick up his equipment.
The male then disappears with the cash and never returns.
While legitimate businesses seek customers through door-to-door sales, there are others that use the opportunity to defraud unsuspecting victims who are quick to respond to a great offer.
The Niagara Regional Police Service cautions the public that before paying cash for a service, or agreeing to a contract, ensure you know who you are doing business with.
Information on crimes can be submitted anonymously using Crime Stoppers of Niagara.
To leave an anonymous tip, please contact Crime Stoppers via: Telephone: 1-800-222-8477 (TIPS) Online: www.niagaratips.com Text: 274637 (CRIMES), keyword ?Niagara,? then your tip.
Crime Stoppers guarantees that you will remain anonymous through any of the methods offered to provide tips.
You may also be eligible to receive a cash reward of up to $2,000 if the information leads to an arrest.
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Jan. 25, 2013 ? At least one in five people in countries for which data are available were infected with influenza during the first year of the 2009 H1N1 pandemic, according to a new study.
The highest rates of infection were in children, with 47 per cent of those aged five to 19 showing signs of having caught the virus. Older people were affected less, with only 11 per cent of people aged 65 or older becoming infected.
The findings come from an international collaboration led by the World Health Organization and Imperial College London, which analysed data from 19 countries, including the UK, US, China and India, to assess the global impact of the 2009 influenza pandemic.
The results, published in the journal Influenza and Other Respiratory Viruses, showed that 20-27 per cent of people studied were infected in the pandemic during the first year of circulation. The researchers believe the incidence of influenza is likely to have been similar in countries where data were not available, meaning that as many as a quarter of the world's population may have been infected.
The study collated results from more than two dozen research studies involving more than 90,000 blood samples collected before, during and after the pandemic. The samples were tested for antibodies produced by the body in response to the specific flu strain that caused the pandemic.
While this study did not set out to look at mortality, the authors also used previously published estimates of pandemic influenza mortality together with mortality estimates that are still in progress, to estimate the proportion of people infected who died from the pandemic virus. Based on an estimate of approximately 200,000 deaths, they suggest that the case fatality ratio was less than 0.02 per cent.
Multiple exposures to previously circulating influenza viruses may have given older people some protection against the strain that emerged in 2009. Blood samples from before the pandemic showed that 14 per cent of people aged 65 or over already had antibodies that reacted to the 2009 strain.
Dr Maria Van Kerkhove, from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial College London, one of the lead authors of the study, said: "This study is the result of a combined effort by more than 27 research groups worldwide, who all shared their data and experience with us to help improve our understanding of the impact the pandemic had globally."
Dr Anthony Mounts of the World Health Organization, the senior author, said: "Knowing the proportion of the population infected in different age groups and the proportion of those infected who died will help public health decision-makers plan for and respond to pandemics. This information will be used to quantify severity and develop mathematical models to predict how flu outbreaks spread and what effect different interventions may have."
The study was funded by the Medical Research Council.
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Source: http://feeds.sciencedaily.com/~r/sciencedaily/most_popular/~3/G_N230ahFTk/130125104058.htm
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Public release date: 24-Jan-2013
Share ] Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
BOSTONTwo new mutations that collectively occur in 71 percent of malignant melanoma tumors have been discovered in what scientists call the "dark matter" of the cancer genome, where cancer-related mutations haven't been previously found.
Reporting their findings in the Jan. 24 issue of Science Express, the researchers from Dana-Farber Cancer Institute and the Broad Institute said the highly "recurrent" mutations occurring in the tumors of many people may be the most common mutations in melanoma cells found to date.
The researchers said these cancer-associated mutations are the first to be discovered in the vast regions of DNA in cancer cells that do not contain genetic instructions for making proteins. The mutations are located in non-protein-coding DNA that regulates the activity of genes.
This non-coding DNA, much of which was previously dismissed as "junk," accounts for 99 percent of a cell's genome. A large number of oncogenic mutations in cancer have been identified in the past several decades, but all have been found within the actual genetic blueprints for proteins.
"This new finding represents an initial foray into the 'dark matter' of the cancer genome," said Levi Garraway, MD, PhD, of Dana-Farber and the Broad and the article's senior author.
"In addition, this represents the discovery of two of the most prevalent melanoma gene mutations. Considered as a whole, these two TERT promoter mutations are even more common than BRAF mutations in melanoma. Altogether, this discovery could cause us to think more creatively about the possible benefits of targeting TERT in cancer treatment or prevention."
The mutations affect a promoter region a stretch of DNA code that regulates the expression of a gene adjacent to the TERT gene. TERT contains the recipe for making telomerase reverse transcriptase, an enzyme that can make cells virtually immortal, and is often found overexpressed in cancer cells. A promoter region of DNA controls the rate of a gene's transcription the copying of its DNA recipe into a message used by the cell to manufacture a protein.
"We think these mutations in the promoter region are potentially one way the TERT gene can be activated," said Franklin Huang, MD, PhD, co-first author of the report along with Harvard MD-PhD student Eran Hodis, of Dana-Farber and the Broad Institute.
To investigate the mutation's effect, the researchers hooked the mutant TERT promoter to a gene that makes luciferase a light-emitting protein. They observed that the mutant promoter increased the production of luciferase in laboratory cell lines. In the same way, the scientists presume, the mutant promoter in human pigmented skin cells can send the TERT gene into overdrive, potentially contributing to the development of melanoma.
The mutations were discovered when the scientists sifted through data from whole-genome sequencing of malignant melanoma tumors. Unlike "whole-exome" searches that examine only the protein-coding DNA of a cell's genome, whole-genome searches scan all of the DNA, including the non-coding regions.
In analyzing whole-genome data, the investigators discovered the two somatic, or not-inherited, mutations in 17 of 19 (89 percent) of the tumors. Next, they sequenced a larger number of melanoma tumors and found that the two mutations were present in 71 percent of tumors in total.
The researchers said the same mutations are present in cell lines from some other malignancies, and that preliminary evidence showed they might be unusually common in bladder and liver cancers. They also noted that the discovery of these important mutations in DNA previously not linked to cancer-causing alterations highlights the value of whole-genome searches of tumor DNA.
###
Other authors include Mary Jue Xu, a student at Harvard Medical School; Gregory V. Kryukov, PhD, of the Broad; and Lynda Chin, MD, of M.D. Anderson Cancer Center.
The research was supported in part by the National Institutes of Health (T32 CA009172, T32GM07753, DP2OD002750, and R33CA126674), the Mittelman Family Fellowship, the American Cancer Society, the Novartis Institutes for Biomedical Research, the Melanoma Research Alliance, and the Starr Cancer Consortium.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook.
About the Broad Institute of MIT and Harvard
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to www.broadinstitute.org.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 24-Jan-2013 Share ] Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
BOSTONTwo new mutations that collectively occur in 71 percent of malignant melanoma tumors have been discovered in what scientists call the "dark matter" of the cancer genome, where cancer-related mutations haven't been previously found.
Reporting their findings in the Jan. 24 issue of Science Express, the researchers from Dana-Farber Cancer Institute and the Broad Institute said the highly "recurrent" mutations occurring in the tumors of many people may be the most common mutations in melanoma cells found to date.
The researchers said these cancer-associated mutations are the first to be discovered in the vast regions of DNA in cancer cells that do not contain genetic instructions for making proteins. The mutations are located in non-protein-coding DNA that regulates the activity of genes.
This non-coding DNA, much of which was previously dismissed as "junk," accounts for 99 percent of a cell's genome. A large number of oncogenic mutations in cancer have been identified in the past several decades, but all have been found within the actual genetic blueprints for proteins.
"This new finding represents an initial foray into the 'dark matter' of the cancer genome," said Levi Garraway, MD, PhD, of Dana-Farber and the Broad and the article's senior author.
"In addition, this represents the discovery of two of the most prevalent melanoma gene mutations. Considered as a whole, these two TERT promoter mutations are even more common than BRAF mutations in melanoma. Altogether, this discovery could cause us to think more creatively about the possible benefits of targeting TERT in cancer treatment or prevention."
The mutations affect a promoter region a stretch of DNA code that regulates the expression of a gene adjacent to the TERT gene. TERT contains the recipe for making telomerase reverse transcriptase, an enzyme that can make cells virtually immortal, and is often found overexpressed in cancer cells. A promoter region of DNA controls the rate of a gene's transcription the copying of its DNA recipe into a message used by the cell to manufacture a protein.
"We think these mutations in the promoter region are potentially one way the TERT gene can be activated," said Franklin Huang, MD, PhD, co-first author of the report along with Harvard MD-PhD student Eran Hodis, of Dana-Farber and the Broad Institute.
To investigate the mutation's effect, the researchers hooked the mutant TERT promoter to a gene that makes luciferase a light-emitting protein. They observed that the mutant promoter increased the production of luciferase in laboratory cell lines. In the same way, the scientists presume, the mutant promoter in human pigmented skin cells can send the TERT gene into overdrive, potentially contributing to the development of melanoma.
The mutations were discovered when the scientists sifted through data from whole-genome sequencing of malignant melanoma tumors. Unlike "whole-exome" searches that examine only the protein-coding DNA of a cell's genome, whole-genome searches scan all of the DNA, including the non-coding regions.
In analyzing whole-genome data, the investigators discovered the two somatic, or not-inherited, mutations in 17 of 19 (89 percent) of the tumors. Next, they sequenced a larger number of melanoma tumors and found that the two mutations were present in 71 percent of tumors in total.
The researchers said the same mutations are present in cell lines from some other malignancies, and that preliminary evidence showed they might be unusually common in bladder and liver cancers. They also noted that the discovery of these important mutations in DNA previously not linked to cancer-causing alterations highlights the value of whole-genome searches of tumor DNA.
###
Other authors include Mary Jue Xu, a student at Harvard Medical School; Gregory V. Kryukov, PhD, of the Broad; and Lynda Chin, MD, of M.D. Anderson Cancer Center.
The research was supported in part by the National Institutes of Health (T32 CA009172, T32GM07753, DP2OD002750, and R33CA126674), the Mittelman Family Fellowship, the American Cancer Society, the Novartis Institutes for Biomedical Research, the Melanoma Research Alliance, and the Starr Cancer Consortium.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook.
About the Broad Institute of MIT and Harvard
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to www.broadinstitute.org.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2013-01/dci-rdn012413.php
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