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Thursday, March 14, 2013
Imprevionism: Where Classic Art and Digital Media Collide
Monday, March 11, 2013
Publishers File Formal Complaints Over Amazon's Bid to Secure the .Book Domain
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Saturday, March 9, 2013
Glaciers will melt faster than ever and loss could be irreversible warn scientists
Mar. 7, 2013 ? Canada's Arctic Archipelago glaciers will melt faster than ever in the next few centuries. Research by European funded scientists has shown that 20 per cent of the Canadian Arctic glaciers may have disappeared by the end of this century which would amount to an additional sea level rise of 3.5 cm.
The results of the research, part of the EU funded ice2sea programme, will be published in Geophysical Research Letters this week, and the paper is now available online.
The researchers developed a climate model for the island group of the north of Canada in which they simulated the shrinking and growing of glaciers in this area.
The researchers show that the model correctly "predicted" the ice mass loss measured over the last ten years and then used the same model to project the effect of future climate change on Canada's Arctic Archipelago glaciers.
The most important result of the research is it shows the probable irreversibility of the melting process, according to lead author Dr Jan Lenaerts of Utrecht University who says, "Even if we assume that global warming is not happening quite so fast, it is still highly likely that the ice is going to melt at an alarming rate. The chances of it growing back are very slim."
One of the main reasons for the irreversibility lies in the fact that snow melting on tundra, and sea ice loss from around the glaciers, actually reinforce regional warming, with significant consequences on the glaciers of Northern Canada. Snow and sea ice reflect the sunlight, and when the snow and sea ice have disappeared, a large part of the sunlight will be absorbed by the land and the sea, which will significantly increase the local temperature.
In one scenario 20 per cent of volume of the glaciers disappears by the end of this century. In this scenario the average global temperature increases by 3 degrees Centigrade but the rise in temperature around Canadian ice caps is 8 degrees Centigrade. Dr Lenaerts emphasises this is not an extreme scenario.
Canada's Arctic Archipelago glaciers represent the third largest ice body in the world after Greenland and the Antarctic. Should the Canadian ice caps melt completely, the global average sea level will rise by 20 centimetres. Since the year 2000 the temperature in this area has risen by 1 to 2 degrees Centigrade and the ice volume has already significantly decreased. If a fifth of the Canadian ice caps have melted by the end of this century, this leads to an additional sea rise of 3.5cm.
Co-author Professor Michiel van den Broeke of Utrecht University says , "Most attention goes out to Greenland and Antarctica which is understandable because they are the two largest ice bodies in the world. However, with this research we want to show that the Canadian ice caps should be included in the calculations."
Professor David Vaughan programme leader of ice2sea, who is based at the British Antarctic Survey in Cambridge, says, "The Canadian archipelago is an area where climate is changing rapidly, and the glaciers here contain enough ice that we should not ignore their contribution to sea-level rise. Added to glaciers in Alaska, the Russian Arctic and Patagonia, these apparently small contributions add up to significant sea-level rise. A key success of this study was in showing that the model performed well in reproducing recently observed changes. That success gives us confidence in how the model predicts future changes."
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The above story is reprinted from materials provided by British Antarctic Survey, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Jan T. M. Lenaerts, Jan H. van Angelen, Michiel R. van den Broeke, Alex S. Gardner, Bert Wouters, Erik van Meijgaard. Irreversible mass loss of Canadian Arctic Archipelago Glaciers. Geophysical Research Letters, 2013; DOI: 10.1002/grl.50214
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
Thursday, March 7, 2013
Key to heart failure: New therapies on horizon
Mar. 5, 2013 ? Some 5.8 million Americans suffer from heart failure, a currently incurable disease. But scientists at Temple University School of Medicine's (TUSM) Center for Translational Medicine have discovered a key biochemical step underlying the condition that could aid the development of new drugs to treat and possibly prevent it.
"Drugs we currently use for heart failure are not very effective," explained lead investigator Walter J. Koch, PhD, Professor and Chairman of the Department of Pharmacology at TUSM, and Director of the Center for Translational Medicine at TUSM. But, he added, "The more we learn about the disease mechanism, the more drug targets we'll find."
That is what Koch and colleagues at Thomas Jefferson University and the University of California, Davis, achieved in their latest study, which appears in the March 5 issue of the online journal PLOS ONE. The report is the first to show that an enzyme called GRK5 (G-protein coupled receptor kinase 5) can gain access to a heart cell's nucleus -- its command center, where control of its genes is maintained -- by way of a transport mechanism involving calcium and a protein known as calmodulin. Once calcium and calmodulin deliver GRK5 to the nucleus, the enzyme usurps control over specific genes, ultimately causing hypertrophy, in which heart cells grow larger in size. Hypertrophy is a biological hallmark of heart failure.
GRK5 had previously been identified as a key player in maladaptive cardiac hypertrophy, which is the end stage of heart failure, when the heart muscle becomes enlarged and unable to pump enough blood to keep vital organs functioning. While GRK5's ability to get inside the nucleus was known, Koch and colleagues worked to fill in the missing links in its transport mechanism. Those links, they hope, will not only allow them to better understand GRK5's role in causing heart cells to increase in size but also find ways to block that process to more effectively treat heart failure.
The GRK5 enzyme is a unique member of the GRK family, owing to its presence in the nucleus. Its journey begins at the cell membrane, where signals received by a molecule at the cell surface known as a Gq-coupled receptor prompt "escorts" -- one of which is calmodulin, as the researchers discovered -- to attach to GRK5 and guide it to the nucleus.
The team found that GRK5's transport requires calmodulin after examining different places on the enzyme where various escort molecules attach. They then introduced mutations that altered the attachment sites. Only when calmodulin-binding residues on GRK5 were mutated was the enzyme prevented from reaching the nucleus. Those mutations led to dramatic decreases in nuclear GRK5 levels and corresponding declines in the activity of genes known to drive cardiac hypertrophy. Calmodulin's ability to bind to GRK5 is in turn dependent on calcium. The same results were obtained both in vitro, using human heart muscle cells cultivated under laboratory conditions, and in vivo, in mice.
The team's research also marks a breakthrough in scientists' understanding of the role of neurohormones in hypertrophy. Released by specialized neurons into the bloodstream, neurohormones have long been cited as a cause of heart cell enlargement.
"One of the novel findings to fall out of this paper is that not all hypertrophic signals from neurohormones are the same," Koch explained. "That's something to keep in mind as we move forward."
The next step, according to Koch, is to test the ability of different agents to keep GRK5 out of the nucleus. "We are now discussing a trial on inhibition of another cardiac GRK, GRK2," he said. He cautioned, however, that trials in patients with GRK5 inhibition are years away. First, agents capable of blocking GRK5 transport must be identified and tested in animals.
The work is an important advance for Temple's Center for Translational Medicine. GRK5 enters the pipeline of novel drug targets under investigation by the Center's scientists and clinicians, who share the common goal of coordinating clinical practice and basic research to speed the delivery of new therapies to patients.
"It's another entry into larger, pre-clinical animal studies," Koch said. "Something new to start down the path of translational medicine."
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Story Source:
The above story is reprinted from materials provided by Temple University Health System, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Jessica I. Gold, Jeffrey S. Martini, Jonathan Hullmann, Erhe Gao, J. Kurt Chuprun, Linda Lee, Douglas G. Tilley, Joseph E. Rabinowitz, Julie Bossuyt, Donald M. Bers, Walter J. Koch. Nuclear Translocation of Cardiac G Protein-Coupled Receptor Kinase 5 Downstream of Select Gq-Activating Hypertrophic Ligands Is a Calmodulin-Dependent Process. PLoS ONE, 2013; 8 (3): e57324 DOI: 10.1371/journal.pone.0057324
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/ro7vXNjnLys/130305174655.htm
Wednesday, March 6, 2013
What Makes Apple's iWatch Tick?
The long-held belief that Apple is working on an iWatch gained more steam Monday, thanks to new rumors focusing on a launch later this year, along with what the watch might actually do for users. Apple may have filed scores of patent applications that include the word "wrist," but the number and detailed nature of the leaks about its plans raise the question of whether the company has loosened its famously tight grip on security.
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