Powerful 6.1 Mag. EARTHQUAKE Jolts SOLOMON ISLANDS - N of Australia
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Powerful 6.1 Mag. EARTHQUAKE Jolts SOLOMON ISLANDS - N of Australia - Video
phi phi islands tailandia
phi phi islands tailandia Ms en nuestro blog: http://moisesyana.blogspot.com.es.
By: Moiss Iniesta
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Taste of the Islands - Day 1 of 100 Things to Do on Sanibel Captiva
Day 1 of 100 Things to do on Sanibel Captiva takes us to Taste of the Islands on November 16, 2014 at The Dunes Golf Tennis Club! Check out the blog post at http://www.sellsanibelcaptivarealest...
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Taste of the Islands - Day 1 of 100 Things to Do on Sanibel & Captiva - Video
Dance Tunes at Taste of the Islands
Food, live music, dancing, sunshine and a worthy cause - Taste of the Islands on Sanibel supports CROW, a non-profit clinic that treats thousands of Lee County area wildlife patients annually....
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TX5W Raivavae Island Austral Islands. From dxing.at-communication.com
KK6BT will be active from Raivavae Island (IOTA OC-114), Austral Islands 5-11 January 2015 as TX5W. http://dxing.at-communication.com/en/tx5w-raivavae-austral/
By: Alexander Teimurazov
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TX5W Raivavae Island Austral Islands. From dxing.at-communication.com - Video
Rollercoaster Tycoon scenario #23 Iceberg Islands
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Battle Islands attack revanche contre JAGC_ALUMBRES
mon attack contre JAGC_ALUMBRES.
By: Utitu V
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Venice Island up for grabs at a cool 9.6m ($15m) with easy access to Venice and its luxurious lifestyles John Lennon used to own Dorinish Island, now known as 'Beatle Island' available for 240,290 ($376,000) CEO of privateislands.com describes owning as a 'unique lifestyle that not everyone is cut out for'
By John Hutchinson for MailOnline
Published: 07:52 EST, 19 November 2014 | Updated: 21:05 EST, 19 November 2014
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If you're on the lookout for your next property venture then why not consult the 'islands for sale' list?
Private islands are available from as nearby to the Isle of Man as Ireland, to as far away as Australia.
The idea of owning your own private islands seems like a luxury most of us can only dream of, but some are actually more affordable than you might think, while some may well indeed remain a dream.
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Mary Heanue, Inis Turk; John Walsh, Bere Island; Simon Murray, Inis Boffin; Aisling Moran, Sherkin Island and Mairtin O Mealid, Cape Clear met to discuss a move by two government departments to temporarily avert funding cuts for development offices. Photograph: Nick Bradshaw/The Irish Times
English-speaking island communities say they are not one bit happy with a move by two government departments to temporarily avert funding cuts for development offices.
Representatives from nine offshore islands, who had to organise boat trips and bed nights in Dublin to make their case, said that a promise by two ministers today to extend funding for three months of next year was a sop and insufficient.
Some hours before the islanders press conference, Minister of State for the Gaeltacht Joe McHugh announced that funding for non-Gaeltacht islands would continue to the end of March 2015.
He promised that in the meantime, both his department and the Department of Environment would examine ways of supporting the continuation of these vital island structures and services.
The islands have called on Minister for Environment Alan Kelly to provide core investment under a dedicated islands development programme which would secure vital services, such as educational training and childcare, waste management, management community buildings, festivals and tourism projects.
Inishbofin off Co Galway, Inishturk and Clare Island off Co Mayo, and the Cork islands of Bere, Sherkin, Dursey, Whiddy, Long and Heir are the main communities affected by the funding cut this December.
The island development programme put in place by a Fine Gael-led coalition government from the mid-1990s was discontinued in 2009.
A 1996 interdepartmental report on islands chaired by former Fine Gael junior minister Donal Carey had identified the Leader programme as the mechanism for supporting the programme.
Since 2009, English and Irish-speaking islands have availed of separate funding streams.
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Islanders reject ministerial move to resolve funding cuts row
Islands of Fuerteventura and Tenerife have cheapest in-resort costs For a family of four, a week-long trip to the Canaries comes in at 525 Caribbean ranks among the priciest with trips costing up to 3,952
By Katie Amey for MailOnline
Published: 07:45 EST, 19 November 2014 | Updated: 09:21 EST, 19 November 2014
For a winter break on a budget, British holidaymakers should look no further than the Canaries.
The islands of Fuerteventura and Tenerife have the cheapest in-resort costs for Britons while Caribbean hotspots Turks and Caicos and Barbados rank among the priciest destinations, a study says.
For a family of four, the cost of a week-long trip could amount to just 525 in Fuerteventura and 574 in Tenerife.
For a budget-friendly holiday in the sun, look no further than the Canary Islands (pictured: Fuerteventura)
Tenerife is another popular winter destination for Britons (pictured: Beach Las Vistas in Los Cristianos)
The TripAdvisor survey analysed the cost of rented accommodation, car hire, dinner at a restaurant and basic groceries at 29 destinations.
While the Canaries proved wallet-friendly, Caribbean favourites such as Turks and Caicos and Barbados can cost up to as much as 3,952 and 2,095, respectively.
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Canary Islands named best value winter sun destination for Brits
'With the lack of support from the government, it is our responsibility as private citizens to contribute and support this ignored sector of our society'
MANILA, Philippines In the Philippines, persons born with and afflicted with rare disorders are a vulnerable and largely unsupported population.
A disease is considered rare if it affects 1 in 20,000 individuals or less, as defined by the Institute of Human Genetics of the National Institute of Health. Pompe disease, Maple Syrup Urine disease, Menkes syndrome, Lowe Syndrome are only a few of the registered 6,000-8,000 rare diseases globally. Because of the relatively low number afflicted by these disorders, support from the Philippine government is absent and access to basic health benefits such as insurance coverage is unavailable to patients with rare diseases.
Rare diseases in the Philippines
Statistics show that 1 in 20,000 Filipinos are afflicted with one of the 30 Rare diseases registered in the country, 75% of which affect children.
Without help from the government and private sector, treatment and medication is elusive for these patients due to their prohibitive cost and accessibility, most of which can only be sourced from the United States.
Formed with the help of the Institute of Human Genetics (IHG), the Philippine Society for Orphan Disorders, Inc. (PSOD), is a non-profit organization dedicated to be the central network for the advocacy and effective administration of sustainable support for the treatment and medication for rare disease sufferers.
Pairing up with Rare
In support of PSOD's advocacy and efforts, Il Ponticello Cucina Italiana will be holding RARE PAIRS, a Charity Dinner and Wine Pairing fundraising event on November 22, 2014 to help fund and contribute to the growing needs of the increasing number Filipino patients afflicted with rare disorders.
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PUBLIC RELEASE DATE:
19-Nov-2014
Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine
For years, scientists have considered the laboratory mouse one of the best models for researching disease in humans because of the genetic similarity between the two mammals. Now, researchers at the Stanford University School of Medicine have found that the basic principles of how genes are controlled are similar in the two species, validating the mouse's utility in clinical research.
However, there are important differences in the details of gene regulation that distinguish us as a species.
"At the end of the day, a lot of the genes are identical between a mouse and a human, but we would argue how they're regulated is quite different," said Michael Snyder, PhD, professor and chair of genetics at Stanford. "We are interested in what makes a mouse a mouse and a human a human."
The research effort, Mouse ENCODE, is meant to complement a project called the Encyclopedia of DNA Elements, or ENCODE, that began in 2003. ENCODE studied specific components in the human genome that guide genes to code for proteins that carry out a cell's function, a process known as gene expression. Surrounding the protein-coding genes are noncoding regulatory elements, molecules that regulate gene expression by attaching proteins, called transcription factors, to specific regions of DNA.
Why mice matter
Mouse ENCODE analyzed more than 100 mouse cell types and tissues to annotate the regulatory elements of the mouse genome and compare them to the regulatory elements in the human genome. Both ENCODE and Mouse ENCODE are funded and coordinated by the National Human Genome Research Institute. Because mice are used as model organisms for many human clinical studies and drug discovery, understanding the similarities and differences can help researchers understand how the results found in mouse studies can translate to humans.
"The mindset is when you compare things, it helps understand genome annotation," said Mark Gerstein, PhD, the Albert L. Williams Professor of Biomedical Informatics at Yale University. "It's making the mouse a more meaningful model organism." Gerstein collaborated on previous ENCODE research but is not part of the Mouse ENCODE consortium, which is composed of researchers from more than 30 institutions.
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Stanford researchers compare mammals' genomes to aid human clinical research
Released: 17-Nov-2014 1:00 PM EST Embargo expired: 19-Nov-2014 1:00 PM EST Source Newsroom: Johns Hopkins Medicine Contact Information
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Newswise When the mouse and human genomes were catalogued more than 10 years ago, an international team of researchers set out to understand and compare the mission control centers found throughout the large stretches of DNA flanking the genes. Their long-awaited report, published Nov. 19 in the journal Nature suggests why studies in mice cannot always be reproduced in humans. Importantly, the scientists say, their work also sheds light on the function of DNAs regulatory regions, which are often to blame for common chronic human diseases.
Most of the differences between mice and humans come from regulation of gene activity, not from genes themselves, says Michael Beer, Ph.D., assistant professor of biomedical engineering at the Johns Hopkins University School of Medicine, and a member of the international team of investigators. Because mice are an important model for human biology, we have to understand these differences to better interpret our results.
Particularly in the early days of genetics, Beer says, researchers tended to ignore regulatory DNA, searching instead for single or multiple gene mutations linked to disease. But genes are only as good as their mission control centers. Without them, they cannot produce protein at the right time, in the right place nor in the right amount. Thats why it is becoming clearer, he adds, that most human disorders, from diabetes to attention deficit hyperactivity disorder to Parkinsons disease, actually stem from off-kilter gene regulation.
Almost all human genes have a clearly related gene in mice, which makes mice a good model for studying questions in biology that cannot be studied in human beings. But protein coding genes make up only 1.5 percent of either genome, analysis shows, accounting for the fact, for instance, that the history of drug development is littered with compounds that cured rodents but failed in human trials.
The reasons for these failures and why people dont have tails or whiskers likely lies outside of our genes, Beer explains, in the regulatory regions, which compose a larger fraction of the genome, but are less conserved or similar in mice and men.
To delve into the details of those regions, the team analyzed 124 types of mouse cells and tissues, including brain, heart, blood, kidney, liver and skin. Together, the consortium generated more than 1,000 datasets representing regions of DNA where genes were active, where the DNA was open and accessible, where specific proteins were binding to DNA, and where DNA replication was happening.
To exploit the information in similar datasets previously created using human tissues, Beer developed a mathematical tool to compare all of the datasets and identify the most similar and most rapidly evolving regulatory regions in mice and humans.
The analysis showed that while mouse genes involved in core intracellular processes, like protein production, have activity patterns very similar to those in humans, the activity profiles of mouse genes involved in processes at the surfaces of cells are quite different a finding with broad implications for researchers using mice to study cell-to-cell communication, immunity, cardiovascular disease and a host of other disorders, Beer notes.
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Introduction:
A genetic condition is an sickness because of to abnormalities in genetics or chromosomes, specially a predicament that is current from ahead of beginning. Most genetic problems are really unusual and influence 1 person in each many 1000s or thousands and thousands.
.A genetic problem may or may possibly not be a heritable difficulty. Some genetic issues are accredited down from the mother or father genes, but other individuals are usually or almost thanks to new mutations or alterations to the DNA. In other situations, the very same condition this sort of as some kinds of most cancers, may be due to inherited genetic situation in some people, by new mutations in other people, and by nongenetic leads to in still other folks.
Fundamental Details:
Here we have different varieties of genetic ailments. They are:
One-gene Multifactorial Chromosomal Mitochondrial
Solitary-gene:
This is 1 of the kind of the genetic condition, it could brings about by the alterations of the mutations happen in the DNA sequence of one particular gene. Genetic code for essential proteins, the substances that have out most of the function. And also execute most daily life characteristics and even make up by the vast majority of cellular factors. When a gene is mutated so that its protein solution can be no longer to bring out its regular operate,a problem can result.
Multi factorial:
This is also a single of the variety of genetic condition thanks to mixture of ecological variables and strains in several genes.When interacting with the avoidance of multifactorial diseases, there are several pitfalls working at many diverse phases. Some are obtainable at the social stage, other people at the neighborhood or group phase, other people at the stage of specific actor, and other folks at the biological phase. Prevention packages for multifactorial ailments have to be developed to offer with as a lot of of these phases as achievable.
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PUBLIC RELEASE DATE:
18-Nov-2014
Contact: Nancy Solomon solomonn@slu.edu 314-977-8017 Saint Louis University
A new treatment for Marfan syndrome, a rare genetic disease that can lead to heart problems, works as well as the currently recommended medical therapy, beta blockers, according to an article in the New England Journal of Medicine.
Angela Sharkey, M.D., professor of pediatrics at Saint Louis University, and a study author, said researchers found losartan, which had been more effective in an animal model of Marfan syndrome, was equally effective to a high dose of the beta blocker atenolol.
"While there may be certain patients who respond better to one drug or another, we found no evidence that losartan is superior to atenolol, a beta blocker currently prescribed for Marfan syndrome," said Sharkey, who was honored earlier this year as the Marfan Foundation's Hero with a Heart. "Losartan appears to be a reasonable alternative treatment for patients who can't take beta blockers, which could give physicians another option to treat a rare and debilitating genetic disease."
Both medications are designed to relax the blood vessels so the heart doesn't have to work as hard to pump blood through the body. Atenolol slows the heart rate, which decreases blood pressure and losartan prevents certain natural substances in the body from tightening the blood vessel walls.
The multi-site, NIH-funded trial followed 608 patients between ages 6 months and 25 years who had enlarged aortas (the main artery carrying blood to the body) for three years. All received either losartan, the investigational medication, or a higher dose of atenolol than is typically prescribed.
Patients in both treatment groups showed no difference in the rate of growth of their aortas.
Additionally, the incidence of aortic-root surgery, aortic dissection, or death did not differ between treatment groups.
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Investigational drug may offer another option to treat Marfan syndrome
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Newswise November 19, 2014, New York, NY A team led by Ludwig and Memorial Sloan Kettering (MSK) researchers has published a landmark study on the genetic basis of response to a powerful cancer therapy known as immune checkpoint blockade. Their paper, in the current issue of the New England Journal of Medicine, describes the precise genetic signatures in melanoma tumors that determine whether a patient will respond to one such therapy. It also explains in exquisite detail how those genetic profiles translate into subtle molecular changes that enable the immune system attack of cancer cells in response to immune checkpoint blockade.
The genetic signature we have found will be invaluable to understanding the biological mechanisms that drive therapeutic responses to immunotherapy for metastatic melanoma, says Jedd Wolchok, MD, PhD, director of the Ludwig Collaborative Laboratory and associate director of the Ludwig Center for Cancer Immunotherapy at MSK, who co-led the study with Timothy Chan, MD, PhD, of MSKs Human Oncology and Pathogenesis Program. Further, our strategy can now be applied to determine the genetic signatures associated with the efficacy of a number of other immunotherapies and cancers.
Few approaches to treating cancer have generated as much excitement as immunotherapy, in which the immune system is engaged to destroy malignancies. One class of such treatments targets CTLA-4, a molecule expressed on the surface of killer T cells that ordinarily blocks their proliferation. Antibody drugs that block CTLA-4 thus stimulate killer T cell responseswhich can target cancer cellsand significantly extend survival for many melanoma patients. Yet not all patients respond equally to this treatment: some, remarkably, survive many years; others fail to respond at all.
There is a subset of melanoma patients who are living far longer than anyone would have expected in the past, largely because of this treatment and other recently developed targeted and immunologic treatments, says Wolchok. But we did not know how to identify them, and thats what really drove this investigation.
Cancer cells are swift but sloppy proliferators, generating countless mutations across their genome as they multiply. Those mutations are often expressed as changes in the chains of amino acids that make protein molecules. Like all cells, cancer cells chop up and hold out short fragments of such proteinseach about 9 amino acids in lengthfor the immune system to assess. These peptides are held up and presented to immune cells by a protein complex known as MHC Class I, which varies significantly between people.
Previous studies by Jedd and others had shown that the particular MHC type of a patient doesnt appear to influence the efficacy of CTLA-4 blockade, says Chan. So we decided to see if the tumor genome has anything to say about whether or not people respond to this therapy. The result was entirely unexpected, and the answer is exceedingly important.
Chan, Wolchok and their colleagues initially hypothesized that tumors that harbored highly mutated cells would be most responsive to CTLA-4 blockade. To test that hypothesis, they sequenced and compared all of the genes expressed as proteins (collectively known as the exome) in tumors taken from 25 patients treated with anti-CTLA-4 antibodies and found that this was, to some degree, true. But looking at the data a little more deeply, says Wolchok, we saw that there were outlierspatients who had over one thousand mutations who didnt respond, and some with just a few dozen who did. This was a strong indication that the quality of the mutations matters.
A sophisticated computational analysis of the cancer genomes revealed that a set of core peptide sequenceseach four amino acids long (tetrapeptides)within MHC Class I-presented peptides were unequivocally associated with response to treatment. To test the prognostic power of this genetic signature, the researchers sequenced the exomes of tumors from another 39 melanoma patients treated with CTLA-4 blockade. They found that all those in this set who had responded to the therapy had at least one and typically several more of the tetrapeptides they had identified. Those who failed to respond did not. Their results show that the mutant DNA sequences, can occur anywhere in the genomenot just within mutant driver genes that are already known to contribute to cancer.
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Group 8 PSA Genetic Engineering
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Genetic Engineering - Restriction Enzymes - Part 3 - Anytime Education
http://www.anytimeeducation.com for more awesome free biology lessons. http://www.twitter.com/James_Dundon http://www.facebook.com/anytimeeducation Restriction enzymes, also known as ...
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Genetic Engineering - Restriction Enzymes - Part 3 - Anytime Education - Video
PUBLIC RELEASE DATE:
17-Nov-2014
Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline
New Rochelle, NY, November 17, 2014--In the future, as space exploration takes astronauts on longer missions and more female astronauts participate, "The Impact of Sex and Gender on Adaptation to Space" will become increasingly critical to astronaut safety and mission success, as explored in a special collection of articles published in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The articles are available Open Access on the Journal of Women's Health website at http://online.liebertpub.com/toc/jwh/23/11.
In the Executive Summary, Drs. Saralyn Mark, Graham Scott, Dorit Donoviel, Lauren Leveton, John Charles, and Bette Siegel and Ms. Erin Mahoney from National Aeronautics and Space Administration (NASA), National Space Biomedical Research Institute (NSBRI), and Valador, Inc. provide an overview of six individual articles in the November issue of the Journal derived from the findings of workgroups formed to report on the current research related to sex- and gender-based differences in how humans adapt to spaceflight. Each workgroup and article focuses on a specific type of adaptation: cardiovascular, immunological, sensorimotor, musculoskeletal, reproductive, and behavioral.
In her Commentary, Dr. Mark remarks that in addition to ongoing missions for the purpose of space exploration and research, "NASA has promoted the development of the commercial space sector for the transport of payloads and eventually humans." The impact of sex and gender should influence "the development of equipment, machine-human interfaces, and countermeasures including the use of personalized medicine and genomics or -'astro-omics.'"
"Understanding sex and gender differences in physiological and psychological adaptation to space is increasingly important as the number of female astronauts increases," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.
###
About the Journal
Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the official journal of the Academy of Women's Health and the Society for Women's Health Research.
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New NASA and NSBRI report on sex and gender differences in adaptation to space flight
Wheat diseases caused by a host of viruses that might include wheat streak mosaic, triticum mosaic, soil-borne mosaic and barley yellow dwarf could cost producers 5 to 10 percent or more in yield reductions per crop, but a major advance in developing broad disease-resistant wheat is on the horizon.
John Fellers, molecular biologist for the U.S. Department of Agriculture's Agricultural Research Service, and Harold Trick, plant geneticist for Kansas State University, have led an effort to develop a patent-pending genetic engineering technology that builds resistance to certain viruses in the wheat plant itself. And although genetically engineered wheat is not an option in the market today, their research is building this resistance in non-genetically engineered wheat lines as well.
"(Wheat viruses) are a serious problem," Trick said. "Wheat streak mosaic virus is one of the most devastating viruses we have. It's prevalent this year. In addition to that, we have several other diseases, triticum mosaic virus and soil-borne mosaic virus, that are serious diseases."
Knowing how costly these diseases can be for producers, Fellers has worked on finding solutions for resistance throughout his career. As a doctoral student at the University of Kentucky, he used a technology in his research called pathogen-derived resistance, or RNA-mediated resistance -- a process that requires putting a piece of a virus into a plant to make it resistant to that particular virus. Most of the viruses that infect wheat are RNA viruses, he said.
"The plant has its own biological defense system," Fellers said. "We were just triggering that with this technology."
Now Fellers, with the help of Trick, his wheat transformation facility and K-State graduate students, have developed transgenic wheat lines that contain small pieces of wheat streak mosaic virus and triticum mosaic virus RNA.
"It's kind of like forming a hairpin of RNA," Fellers said. "What happens is the plant recognizes this RNA isn't right, so it clips a piece of it and chops it up, but then it keeps a copy for itself. Then we have a resistance element."
Fellers compared the process to the old days of viewing most wanted posters on the post office wall. The piece of foreign RNA from the virus, which is a parasite, is one of those most wanted posters. Because the virus is a parasite, it has to seize or hijack part of the plant system to make proteins that it needs to replicate.
When the virus comes into the plant, the plant holds up that poster from the post office wall, recognizes the virus, and doesn't allow the virus to replicate and go through its lifecycle.
A broad resistance goal
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