Source: http://news.feedzilla.com/en_us/stories/politics/top-stories/296710950?client_source=feed&format=rss
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বৃহস্পতিবার, ৪ এপ্রিল, ২০১৩
Celebs Without Makeup: See Demi Lovato & More!
The X Factor judge is the latest celeb to go makeup-free! Take a look at more stars who have shared their au naturel looks.
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Same-day water pollution test could keep beaches open more often
Apr. 3, 2013 ? With warm summer days at the beach on the minds of millions of winter-weary people, scientists are reporting that use of a new water quality test this year could prevent unnecessary beach closures while better protecting the health of swimmers. A study analyzing the accuracy of the test appears in ACS' journal Environmental Science & Technology.
Meredith B. Nevers and colleagues point out that decisions on whether water is safe for recreational use have been based on tests that actually show the condition of water in the past. Those tests involve sampling water for the E. coli bacteria used as red flags for fecal contamination, putting the samples in culture dishes and waiting to see if any bacteria grow. As a result, managers might close a beach based on fecal contamination that existed in the past, but posed no current threat. Likewise, they might keep a contaminated beach open because the water was clean in the past.
They describe analysis and validation of a new rapid water-quality test that could prevent beaches from being closed by providing accurate, same-day results of bacteria levels. Developed by the U.S. Environmental Protection Agency, the test's same-day results could help managers across the country determine whether beaches are safe for swimming.
The authors acknowledge funding from USGS Great Lakes Science Center
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The above story is reprinted from materials provided by American Chemical Society.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Meredith B. Nevers, Muruleedhara N. Byappanahalli, Richard L. Whitman. Choices in Recreational Water Quality Monitoring: New Opportunities and Health Risk Trade-Offs. Environmental Science & Technology, 2013; 130318093351008 DOI: 10.1021/es304408y
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.
Source: http://feeds.sciencedaily.com/~r/sciencedaily/living_well/~3/7p17p7d-lVY/130403104220.htm
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শুক্রবার, ২২ মার্চ, ২০১৩
Georges St-Pierre?s camp says he beat Nick Diaz with an injured Achilles tendon
The UFC gave a backstage look at Georges St-Pierre's win over Nick Diaz at UFC 158, complete with an adorable shot at the end of GSP high-fiving a young fan who was dressed like the champ from head to toe.
According the GSP's trainer, Firas Zahabi, it's a fight the UFC welterweight champion went through with despite an injury. Zahabi said GSP injured his Achilles tendon during training for the fight, and it may have worsened during the bout.
"I was worried it would tear during the fight," Zahabi told MMAFighting.com. "We had to cut his last sparring [session] short due to his injury. He had a week to rest it and then the fight."
Does finding out that GSP was injured changed your opinion of his performance? Speak up in the comments, on Facebook or on Twitter.
Other popular content on Yahoo! Sports:
? Friends Junior dos Santos and 'Big Foot' Silva ready to fight if UFC title is at stake
? Timothy Bradley managed to change public opinion with thrilling fight tactic
? Photo gallery: Best action from the NCAA tournament
? Flurry of offseason departures not new to Ravens
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বৃহস্পতিবার, ২১ মার্চ, ২০১৩
Study could aid development of new drugs to treat gout
Wednesday, March 20, 2013
Findings from a Loyola University Chicago Stritch School of Medicine study could lead to the development of new drugs to treat gout.
The study, led by Liang Qiao, MD, and his colleagues and collaborators, was published March 19 in the journal Nature Communications.
Gout is caused by a buildup of uric acid around joints, typically the big toe, knee or ankles. The immune system revs up to attack uric acid salt crystals, and this immune response causes painful inflammation.
The innate immune response is mainly activated by calcium that enters a macrophage immune cell through an opening called the calcium channel. There are several types of calcium channels. Researchers found that a particular type of calcium channel, called TRPM2, is responsible for initiating the immune response. (TRPM2 stands for transient receptor potential melastatin 2.)
In lab mice, study collaborators from Japan knocked out a gene that is responsible for this calcium channel. Qiao's team then exposed these "knockout" mice and a comparison group of normal mice to uric acid salt crystals and to a liposome, a compound that also causes inflammation. They found that inflammation was significantly lower in the knockout mice that lacked the TRPM2 calcium channel. They therefore concluded that disabling the TRPM2 calcium channel could be key to reducing painful inflammation from gout.
The next step will be to design a compound that would block the TRPM2 calcium channel, and then test how well this compound reduces inflammation in an animal model.
The study's findings might also apply to Alzheimer's disease and arteriosclerosis (hardening of the arteries). These two diseases, like gout, have been linked to inflammation. And it is possible that the TRPM2 calcium channel may be key to initiating the inflammatory response in these two diseases as well. But this has not been proven yet, Qiao said.
The study also could aid in the development of new vaccines. Researchers elsewhere are studying whether liposomes could serve as more effective adjuvants in new vaccines. (An adjuvant is the component in a vaccine that stimulates the immune system to attack a pathogen such as a virus or bacterium). The Loyola study found that only liposomes with either a positive or a negative electric charge are effective in stimulating the immune system.
Liposomes with a neutral charge did not stimulate the immune system.
Qiao, senior author of the study, is a professor in the Department of Microbiology and Immunology at Loyola University Chicago Stritch School of Medicine. Co-authors of the study are Zhenyu Zhong (first author, significant contributor), Yougang Zhai, Shuang Liang and Renzhi Han, all of Loyola University Chicago; Yasou Mori of Kyoto University in Japan; and Fayyaz S. Sutterwala of the University of Iowa.
###
Loyola University Health System: http://www.luhs.org
Thanks to Loyola University Health System 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.
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Source: http://www.labspaces.net/127370/Study_could_aid_development_of_new_drugs_to_treat_gout
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Eric Schmidt says Google Now for iOS hinges upon Apple
Sometimes, it's what you don't say that matters. When asked at Google's Big Tent Summit about when Google Now might show on the iPhone, the company's Eric Schmidt told a questioner that he'll "need to discuss that with Apple," and that there was no certainty Apple would approve what Google sent. Conspicuously non-committal? You bet -- but the statement also suggests that a Google Now release is just a question of whether or not Apple gives the thumbs up, not whether the iOS port exists at all. We'd add that the remarks sound eerily familiar. Schmidt was saying similar things about Apple's responsibility when he downplayed the odds of a stand-alone Google Maps release for iOS, and we all know how that turned out. Skip forward to about 17:50 in the video at the source link for Schmidt's own words.
Filed under: Cellphones, Internet, Mobile, Apple, Google
Via: TechCrunch
Source: NDTV
Source: http://www.engadget.com/2013/03/21/eric-schmidt-says-google-now-for-ios-hinges-upon-apple/
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It?s All in the Nerves: How to Really Treat Depression
Exercise, Prozac and electroconvulsive therapy (ECT) may ultimately relieve depression in the same way.
That?s what the latest research, conducted on mice, suggests, and the scientists are encouraged that similar processes are at work in the human brain as well. According to the findings, published in the journals Cell Stem Cell and Molecular Psychiatry, all of these therapies can spur the growth of brain cells. And it seems that such neurogenesis, which perhaps results from changes in levels of brain chemicals like serotonin, can lift the symptoms of depression.
Since the mid-1990s, researchers have been piecing together a theory of depression that accounts for the seemingly disparate triggers of the mental illness, as well as the variety of treatments that seem to counteract the negative mood.
And so far, this is what they believe: extreme or uncontrollable stress, particularly early in life, can lead to excessive release of the neurotransmitter glutamate in the brain.? At these high levels, glutamate can damage or even kill certain cells in the hippocampus, a region known for its role in memory.? This can lead to a thinning of the neural network in this area, which contributes to depression for reasons that are not yet clear. But antidepressant treatments all seem to promote the birth of new brain cells in that part of the brain.
Moreover, ?It?s not just growth of new nerve cells [in this region],? says Bruce McEwen, professor of neuroscience at Rockefeller University,??There?s also plasticity of nerve cells all over the brain? that is ongoing and can be facilitated or blocked.? ?These changes may start in the hippocampus, where new cells can be born, but older cells can be revitalized elsewhere as well, perhaps even changing the circuit of nerve activity that keeps people stuck in depressive thoughts and feelings.
MORE:?Antidepressants: Are They Effective or Just a Placebo?
Now, Hongjun Song, professor of neurology and neuroscience at Johns Hopkins University, documents how disparate treatments, from exercise to antidepressants that manipulate serotonin levels, and even electrical stimulation of certain brain regions, can ultimately trigger this nerve growth that fights depression.
The brain must maintain a delicate balance, with complex chains of signals keeping various opposing processes in check.? One protein that stymies the growth of brain cells, sFRP3, is useful in controlling cell growth from getting out of hand, but could be harmful if it hampers necessary growth. Working with mice, Song and his colleagues showed that antidepressant medications, ECT and exercise all affect levels of sFRP3.
?If you treat with different classes of antidepressants or ECT, they all lead to changes in expression of sFRP3,? says Song, who studied Prozac (fluoxetine), a selective serotonin reuptake inhibitor (SSRI) and imipramine, an antidepressant in another class of drugs called tricyclics, which regulate multiple neurotransmitters.? The research showed that these drugs reduced levels of sFRP3 levels in the hippocampus, which allowed new cells and connections to grow.
To further confirm the effect of sFRP3 on depression, Song and his colleagues also genetically engineered mice without the sFRP3 protein; these animals were less likely to show depressive responses when they were forced to swim until exhaustion, an indication that they were less prone to experiencing the negative mood state.
The research also found that in human patients, genes associated with the protein affected how long it took depressed people to respond to medication. Taken together, the latest data suggests that presence of elevated levels of sFRP3 protein may increase vulnerability to depression by preventing new nerve cells from growing in the hippocampal region.?Similarly, mice given ECT, and those that exercised regularly, also showed lower levels of sFRP3.
MORE:?Ketamine: Leading the Way Toward Fast-Acting Antidepressants
So how do things as different as ECT, drugs and exercise change the same protein? They all?affected a single type of cell in?the hippocampus, known as granule cells.? ?What matters is that you want to activate [these] granule cells,? says Song.??If the animals do running, that leads to firing of those neurons,? he says, explaining that all of the other treatments did so as well.
Further studies are needed to confirm whether consistently high levels of the protein increase the likelihood of depression in human patients, but if that?s the case, then activating granule cells, by way of suppressing the release of sFRP3, might be a promising new way of treating depression. So far, ?no drugs are known [to affect it directly],? says Song, ?The next step is trying to find an approach where we can modulate the function of sFRP3 as an antidepressant.?
Source: http://news.yahoo.com/nerves-really-treat-depression-190012361.html
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