Sunday, January 8, 2012

SvetlanaFadeeva: Photo: fan-photo of Alex Meraz with fan at Vampire Baseball game in Portland, 2009 . photo by SandeeDandee http://t.co/QC0m7QZ8

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Photo: fan-photo of Alex Meraz with fan at Vampire Baseball game in Portland, 2009 . photo by SandeeDandee tmblr.co/ZSqoPxEMTbFO SvetlanaFadeeva

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Source: http://twitter.com/SvetlanaFadeeva/statuses/155376544397799424

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Saturday, January 7, 2012

Sony Ericsson LT26i 'Nozomi' gets leaked again ahead of inevitable CES unveiling

Android Central

Ready for yet another Sony Ericsson "Nozomi" leak? Following on from the slew of images that worked their way onto the web in November and December, some new photos of the upcoming SE device have appeared on ITProPortal today, seemingly confirming much of what we already knew from earlier leaks.

To recap, inside the LT26i (or Nozomi, if you prefer codenames), you've apparently got a 1.5GHz dual-core Qualcomm Snapdragon CPU, the same sort that powers the HTC Sensation XE, along with 1GB of RAM. Software-wise, there's Android 2.3.7 Gingerbread, skinned with a new version of SE's Xperia UI. On the outside, there's said to be a 720p Bravia Engine display, tucked inside a chassis of similar size to the Arc S, albeit a little chunkier around the back. The rear camera is said to be an impressive 12MP Sony Exmor R sensor, a step up from the 8MP camera of the Arc and Arc S. Interestingly, ITProPortal refers to the device as the Xperia HD, rather than the Xperia Arc HD, which we've heard from other sources.

For its part, Sony Ericsson has been dropping some pretty serious hints that it'll be showing off its new hotness at CES 2012 next week. So, only a few more days and we should be able to get our hands on this and other CES-bound devices on the show floor in Las Vegas. Maybe then we'll find out what's going on with that weird transparent cut-out section along the bottom of the phone.

Source: ITProPortal



Source: http://feedproxy.google.com/~r/androidcentral/~3/bYuCzUa-bMw/story01.htm

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Video: Obama shows off football skills in Hawaii

President Obama was spotted playing football on the beach in Hawaii. NBC?s Brian Williams reports.

>>> the photos that come out today may make it tougher for men of a certain age at the beach this summer. a lot of guys will be expected to dive for every football that comes remotely close to them. this is the 50-year-old president of the united states on new year's day in what appears to be a hard-core beach football game. somebody snapped these pictures even though the president was on the grounds of a protected u.s. marine base on oahu during the first family's ten-day vacation. recently you

Source: http://video.msnbc.msn.com/nightly-news/45877527/

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Friday, January 6, 2012

Crucial gene activator in slow-killing parasite identified

Crucial gene activator in slow-killing parasite identified [ Back to EurekAlert! ] Public release date: 5-Jan-2012
[ | E-mail | Share Share ]

Contact: Kevin Mayhood
kevin.mayhood@case.edu
216-368-4442
Case Western Reserve University

A potential target for schistosomiasis vaccine

In the complicated life cycle of ancient flatworms that cause schistosomiasis, Case Western Reserve University researchers have identified a gene activator crucial to development of the parasites within humans a potential target for a vaccine.

A description of the activator, which turns on rapid growth, is in the online journal PLoS Neglected Tropical Diseases.

Schistosomiasis, which causes organ damage and failure, afflicts more than 200 million people worldwide, killing 280,000 annually. Another 400 million people are at risk for the disease.

For decades, a single drug, praziquantel, has been used to kill the worms, and scientists are concerned the drug may become useless. The worms, called schistosomes, have shown they can develop resistance to praziquantel in the lab and there is currently no other drug to treat the disease.

Beyond that concern, the lack of a vaccine leaves human hosts in a cycle of their own: becoming infected, taking praziquantel, becoming reinfected - multiple times - due to the prevalence and ease of contracting the parasite in rivers and ponds in Asia, Africa and South America. Repeated exposure can add up to illness and death.

"This is really a disease of poor people," said Emmitt Jolly, professor of biology at Case Western Reserve and senior author of the paper. "The strategy to combat the disease cannot be expensive."

Jolly and John Milligan, a technician in Jolly's lab and lead author, spent two years studying, identifying and characterizing the protein, and gene activator, myocyte enhancer factor 2, commonly referred to at Mef2, in the flatworm's life cycle.

Depending on the phase of development, the schistosome lives in snails, in freshwater or in humans. From the snail, it becomes a tiny free swimmer that penetrates human skin. The parasite enters blood vessels and feeds on blood cells.

Sexually mature schistosomes congregate in blood vessels in a part of the abdomen called the mesentery. They mate and lay 300 to 1,000 eggs per day that migrate through the liver. About half the eggs are passed outside with urine and feces, depending on the species, and half get stuck in the body.

Upon reaching fresh water, the half excreted hatch into free swimmers that enter and grow in snails.

The half that remain in the body build up and cause an immune response. The eggs become encapsulated in granulomas, immune cells that wall off the foreign material. The result is significant organ damage, particularly in the liver, spleen, and intestine, but also other organs. Schistosomes can live and lay eggs for decades, the build-up of the granulomas slowly sickening and killing the host.

Mef2 is found in plants and yeast on up to humans. The activator is essential to muscle, nerve and bone development in humans, but how it works in flatworms was unknown.

Jolly and Milligan found, by homology, the protein appeared similar to Mef2 in yeast. Mef2 has two parts that act independently: one part binds to DNA, the second part activates gene expression.

When the researchers combined the schistosome gene activator with the DNA binder of yeast, the combination switched on the same yeast gene as the pure yeast gene activator.

They found that in the Schistosome, Mef2 expression is turned up right after the swimmer enters the human host. During this time, the parasites grow from 100 micrometers in length to 10 to 16-millimeter worms.

Praziquantel is most effective when schistosomes start producing eggs inside human hosts. A vaccine could prevent the parasite from reaching sexual maturity and laying eggs inside of hosts thereby preventing schistosomiasis, the researchers say.

Although Mef2 is present in humans, the portion of schistosome Mef2 that switches on gene activity is so different from human Mef2 that "We can target that part, and not affect the host," Jolly said.

Milligan and Jolly are working with other researchers to further understand schistosome Mef2 and are hopeful the work will lead to an alternative to praziquantel or a complimentary drug.

###

The research was funded the Case Western Reserve Department of Biology.



[ Back to EurekAlert! ] [ | E-mail | Share 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.


Crucial gene activator in slow-killing parasite identified [ Back to EurekAlert! ] Public release date: 5-Jan-2012
[ | E-mail | Share Share ]

Contact: Kevin Mayhood
kevin.mayhood@case.edu
216-368-4442
Case Western Reserve University

A potential target for schistosomiasis vaccine

In the complicated life cycle of ancient flatworms that cause schistosomiasis, Case Western Reserve University researchers have identified a gene activator crucial to development of the parasites within humans a potential target for a vaccine.

A description of the activator, which turns on rapid growth, is in the online journal PLoS Neglected Tropical Diseases.

Schistosomiasis, which causes organ damage and failure, afflicts more than 200 million people worldwide, killing 280,000 annually. Another 400 million people are at risk for the disease.

For decades, a single drug, praziquantel, has been used to kill the worms, and scientists are concerned the drug may become useless. The worms, called schistosomes, have shown they can develop resistance to praziquantel in the lab and there is currently no other drug to treat the disease.

Beyond that concern, the lack of a vaccine leaves human hosts in a cycle of their own: becoming infected, taking praziquantel, becoming reinfected - multiple times - due to the prevalence and ease of contracting the parasite in rivers and ponds in Asia, Africa and South America. Repeated exposure can add up to illness and death.

"This is really a disease of poor people," said Emmitt Jolly, professor of biology at Case Western Reserve and senior author of the paper. "The strategy to combat the disease cannot be expensive."

Jolly and John Milligan, a technician in Jolly's lab and lead author, spent two years studying, identifying and characterizing the protein, and gene activator, myocyte enhancer factor 2, commonly referred to at Mef2, in the flatworm's life cycle.

Depending on the phase of development, the schistosome lives in snails, in freshwater or in humans. From the snail, it becomes a tiny free swimmer that penetrates human skin. The parasite enters blood vessels and feeds on blood cells.

Sexually mature schistosomes congregate in blood vessels in a part of the abdomen called the mesentery. They mate and lay 300 to 1,000 eggs per day that migrate through the liver. About half the eggs are passed outside with urine and feces, depending on the species, and half get stuck in the body.

Upon reaching fresh water, the half excreted hatch into free swimmers that enter and grow in snails.

The half that remain in the body build up and cause an immune response. The eggs become encapsulated in granulomas, immune cells that wall off the foreign material. The result is significant organ damage, particularly in the liver, spleen, and intestine, but also other organs. Schistosomes can live and lay eggs for decades, the build-up of the granulomas slowly sickening and killing the host.

Mef2 is found in plants and yeast on up to humans. The activator is essential to muscle, nerve and bone development in humans, but how it works in flatworms was unknown.

Jolly and Milligan found, by homology, the protein appeared similar to Mef2 in yeast. Mef2 has two parts that act independently: one part binds to DNA, the second part activates gene expression.

When the researchers combined the schistosome gene activator with the DNA binder of yeast, the combination switched on the same yeast gene as the pure yeast gene activator.

They found that in the Schistosome, Mef2 expression is turned up right after the swimmer enters the human host. During this time, the parasites grow from 100 micrometers in length to 10 to 16-millimeter worms.

Praziquantel is most effective when schistosomes start producing eggs inside human hosts. A vaccine could prevent the parasite from reaching sexual maturity and laying eggs inside of hosts thereby preventing schistosomiasis, the researchers say.

Although Mef2 is present in humans, the portion of schistosome Mef2 that switches on gene activity is so different from human Mef2 that "We can target that part, and not affect the host," Jolly said.

Milligan and Jolly are working with other researchers to further understand schistosome Mef2 and are hopeful the work will lead to an alternative to praziquantel or a complimentary drug.

###

The research was funded the Case Western Reserve Department of Biology.



[ Back to EurekAlert! ] [ | E-mail | Share 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/2012-01/cwru-cga010512.php

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SIAP - Jeff Goodman of CBS - NBA Scout on Meyers Leonard (Last post on 01/04/2012 at 2:25 PM PST)

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Copyright ? 2012? InsideIllini.com and Scout.com. All rights reserved. This website is an unofficial independent source of news and information, and is not affiliated with any school, team, or league.

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Source: http://mbd.scout.com/mb.aspx?S=169&F=2616&T=8521734&P=1

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Thursday, January 5, 2012

Aging-related degeneration caused by defects of energy metabolism in tissue stem cells?

Aging-related degeneration caused by defects of energy metabolism in tissue stem cells?

Tuesday, January 3, 2012

Aging-related tissue degeneration can be caused by mitochondrial dysfunction in tissue stem cells. The research group of Professor Anu Suomalainen Wartiovaara in Helsinki University, with their collaborators in Max Planck Institute for Biology of Aging, Karolinska Institutet and University of Wisconsin reported on the 3rd January in Cell Metabolism their results on mechanisms of aging-associated degeneration.

Stem cells are called the spare parts for tissues, as they maintain and repair tissues during life. They are multipotent and can produce a variety of different cell types, from blood cells to neurons and skin cells. Mitochondria are the cellular engine: they transform the energy of nutrients to a form that cells can use, and in this process they burn most of the inhaled oxygen. If this nutrient 'burning' is inefficient, the engine will produce exhaust fumes, oxygen radicals, which damage cellular structures, including the genome. Antioxidants target to scavenge these radicals.

Already in 2004 and 2005 a research model was created in Sweden and USA, which accumulated a heavy load of mitochondrial genome defects. This led to symptoms of premature aging: thin skin, graying of hair, baldness, osteoporosis and anemia.

In the current publication, scientist Kati Ahlqvist in Professor Suomalainen Wartiovaara's group showed that these symptoms were partially explained by stem cell dysfunction. The number of stem cells did not reduce, but their function was modified: the progeny cells in blood and the nervous system were dysfunctional. The researchers also found out that these defects could be partially prevented by early antioxidant treatment.

"This suggests that oxygen radicals can regulate stem cell function and that these cells are very susceptible for mitochondrial dysfunction. These findings may also be important to understand mechanisms of mitochondrial disease", Professor Suomalainen Wartiovaara says.

The results are a breakthrough in revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance. These findings increase the understanding of mechanisms of aging-related degeneration.

###

University of Helsinki: http://www.helsinki.fi

Thanks to University of Helsinki for this article.

This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.

This press release has been viewed 10 time(s).

Source: http://www.labspaces.net/116382/Aging_related_degeneration_caused_by_defects_of_energy_metabolism_in_tissue_stem_cells__

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Trailer for Netflix?s first original series hits the web (Yahoo! News)

Despite a somewhat rough year, streaming media and DVD rental giant?Netflix is updating its viewing options with new original content, including its first original series. Called?Lilyhammer, it's the unlikely story of an American mobster who relocates to the small Norwegian town of Lilyhammer as part of the witness protection program.

The Sopranos actor Stephen Van Zandt plays the mobster, and the trailer offers some tantalizing glimpses of what should prove to be an interesting fish-out-of-water story as an East Coast gangster who may or may not be completely over his less-than-legal ways tries to adjust to life in a completely different environment.

Lilyhammer isn't the first original content purchased by Netflix. Back in March, the company announced that it had outbid giants including HBO and AMC for a series called?House of Cards. According to?Netflix's blog, that series will air in late 2012.

Interestingly, Netflix has decided to release the entire?Lilyhammer series ? eight episodes total?? at the same time, so viewers will be able to watch it all at once if they'd like. It's an interesting and potentially risky move, but we assume that they're banking on fans helping spread the word virally, linking and sharing episodes to build buzz. Only time will tell if Netflix's gamble pays off!

Business Insider via?Gizmodo

This article was written by Katherine Gray and originally appeared on Tecca

More from Tecca:

Source: http://us.rd.yahoo.com/dailynews/rss/tech/*http%3A//news.yahoo.com/s/yblog_technews/20120105/tc_yblog_technews/trailer-for-netflixs-first-original-series-hits-the-web

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