Source: http://news.feedzilla.com/en_us/stories/politics/top-stories/304215041?client_source=feed&format=rss
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Tuesday, May 7, 2013
Optimal workout partner encourages less to motivate more
May 7, 2013 ? The best workout partner may be one who understands that silence is golden, according to one Kansas State University researcher in the College of Human Ecology.
Brandon Irwin, assistant professor of kinesiology, recently found that individuals tend to work out longer when their partner was perceived to be more skilled and was one who kept verbal encouragement to a minimum.
Irwin worked with researchers at Michigan State University on the study "You Can Do It: the Efficacy of Encouragement in Motivating the Weak Link to Exercise Longer During an Online Exercise Video Game," which will be published in the Journal of Medical Internet Research. He said the team's goal was to determine how to increase motivation during physical activity.
"People like to exercise with other people," Irwin said. "In exercise groups, people tend to encourage each other, saying things like, 'Come on, you can do it.' We wanted to find out what effect this had on motivation."
In a separate study, Irwin discovered the optimal exercise partner is 40 percent better than the other, motivating the less skilled partner to exercise for a longer period of time and at an increased rate. In this study, 115 participants were told to do planks, an abdominal exercise, for as long as they could.
Next, the researchers told a group of participants they would be exercising with a partner who was slightly better, although the partner was a looped video recording. A third group was told they would be exercising with a partner -- also a recording -- but this time, the partner verbally encouraged them.
"Initially, it made sense to us that encouragement would be motivating," Irwin said. "However, we found almost the opposite to be true. When exercising with someone who is slightly better and who is not verbally encouraging, participants exercised longer than if conditions were the same but that person was verbally encouraging them. We didn't expect that."
Irwin said the researchers' best guess for why this happened is that those who received encouragement from a partner whom they perceived as more skilled may have interpreted the comments as condescending.
"If two individuals are exercising together and one is constantly saying 'you can do this' to the other, it may be taken as patronizing," Irwin said. "Those who received encouragement may have felt condescended, or even that their virtual partner was encouraging themselves, since no names were used."
Participants in the study were not aware that their partner was a recording and would never stop the exercise. The researchers told all participants that as soon as they stopped, their partner had to stop.
"Being the 'weak link' is a big motivator in partner or group exercise," Irwin said. "You don't want to let your partner down. We're honing in on that aspect of group exercise."
Irwin said this research could be used in designing electronic media, including both video games and social media. In a video game, the research findings could help develop the best virtual character in an exercise-based video game, like the Nintendo Wii Fit.
"Our research suggests that the best virtual workout partner is someone who is a little better than you and doesn't encourage you under certain conditions," he said.
Irwin added that these principles could also be applied to real workout partners on a proposed social media fitness website. Partners could be matched through an algorithm that would be used to dictate how much communication they should have.
"When you're communicating through an electronic medium, the designer puts restrictions on what and how you communicate with each other," Irwin said. "If you're partnered with your ultimate workout buddy, your communication could be facilitated or inhibited, depending on your preferences."
Irwin was the principle investigator of this study, which was supported by a $149,000 grant from the Robert Wood Johnson Foundation to Michigan State University.
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/~3/7P8hAv6LLT8/130507103028.htm
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New insights into Ebola infection pave the way for much-needed therapies
May 7, 2013 ? The Ebola virus is among the deadliest viruses on the planet, killing up to 90% of those infected, and there are no approved vaccines or effective therapies. A study published by Cell Press on May 7th in the Biophysical Journal reveals how the most abundant protein making up the Ebola virus -- viral protein 40 (VP40) -- allows the virus to leave host cells and spread infection to other cells throughout the human body. The findings could lay the foundation for the development of new drugs and strategies for fighting Ebola infection.
"Little research is available on how the Ebola virus buds from the plasma membrane of human cells," says senior study author Robert Stahelin of Indiana University School of Medicine. "By shedding light on this process, our study will help us to identify potential drug candidates that could interfere with this step in the viral life cycle."
The Ebola virus is made up of seven proteins, including VP40, which plays a key role in enabling the virus to leave host cells and infect other cells in the human body. Past studies have shown that a part of VP40 called the C-terminal domain penetrates the plasma membrane surrounding host cells. But until now, it was not known exactly how VP40 binds to the plasma membrane to allow the virus to escape host cells.
To address this question, Stahelin and his team made vesicles designed to mimic the plasma membrane of host cells and exposed these vesicles to VP40. Observing their interactions under the microscope, they found that VP40's C-terminal domain penetrates more than halfway into one layer of the vesicles. VP40 also caused the vesicle membranes to bend into the shape of the Ebola virus, paving the way for its escape. When the researchers mutated the C-terminal domain of VP40, the protein was much less effective at binding to and bending membranes and forming virus-like particles that could escape from host cells.
Altogether, the findings reveal how VP40's C-terminal domain allows the Ebola virus to spread infection. "Currently, we are trying to find small molecules that can inhibit VP40 interactions with the plasma membrane," Stahelin says. "This effort could lead to the discovery of potential drug candidates that could form the basis of much-needed therapies for this deadly virus."
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The above story is reprinted from materials provided by Cell Press, 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:
- Soni et al. The Ebola Virus Matrix Protein Deeply Penetrates the Plasma Membrane: An Important Step in Viral Egress. Biophysical Journal, 2013
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.
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Monday, May 6, 2013
BMC Software agrees to be sold for $6.6 billion
NEW YORK (AP) ? BMC Software Inc. has agreed to be sold to a private investor group for about $6.6 billion in cash.
The Houston-based maker of system management software for businesses said Monday that the deal is for $46.25 per share. That's less than 2 percent above Friday's closing stock price of $45.42.
With roughly 143 million shares outstanding, according to FactSet, that values the deal at $6.6 billion. The companies said the deal is worth $6.9 billion.
The investor group is led Bain Capital and Golden Gate Capital and also includes Special Investments and Insight Venture Partners.
BMC said that Elliott Management, which owns 9.6 percent of the BMC's stock, has agreed to vote its shares in favor of the deal, which is expected to close later this year. The hedge fund had asked the company to consider selling itself last year. The stock then jumped in March after reports surfaced that the company was considering buyout offers from several private equity firms.
Under the terms of the deal, BMC can solicit alternative proposals for 30 days.
Shares of BMC slipped 8 cents to $45.34 in morning trading. The stock is up 14.6 percent year-to-date, slightly more than the Standard & Poor's 500, which is up 13.2 percent.
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New Jersey Gov. Chris Christie squashes spider; PETA not pleased
Come election time, Chris Christie will not get the spider lover vote.
The New Jersey governor demonstrated his bug killing skills to a group of fourth-graders when the unwelcome guest crawled across the desk in his office. Video captured the crowd of kids pointing out the arachnid, and the governor making an executive decision: He kills it with his hand, then wipes the remains on his pants.
?That's also one of the fun parts of being governor. Any bugs on your desk, you're allowed to kill them and not get in trouble," the governor is heard saying on video posted by his office.
Not everyone seems to agree. Ingrid Newkirk, president of People for the Ethical Treatment of Animals, said the governor missed a teachable moment.
"He probably did it without thinking,? Newkirk said in a statement. ?Some people put the spider outside, but spiders are often scary to people, and that can prevent them from pondering their worth."
PETA?s insect activism is bipartisan, it should be noted. The organization sent President Barack Obama a ?humane fly catcher? after he caught and killed a fly during an interview with CNBC back in 2009.
?We support compassion for the even the smallest animals," Bruce Friedrich, vice president for policy at PETA, said at the time. ?We support giving insects the benefit of the doubt."
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Thousands of leftists protest Hollande's 1st year
Leader of the French leftist party, Jean Luc Melenchon, delivers a speech before a rally to protest against the austerity measures announced by the French government, in Paris, Sunday, May 5, 2012. (AP Photo/Michel Spingler)
Leader of the French leftist party, Jean Luc Melenchon, delivers a speech before a rally to protest against the austerity measures announced by the French government, in Paris, Sunday, May 5, 2012. (AP Photo/Michel Spingler)
Leader of the French leftist party, Jean Luc Melenchon, smiles before a rally to protest against the austerity measures announced by the French government, in Paris, Sunday, May 5, 2012. (AP Photo/Michel Spingler)
Leader of the French leftist party, Jean Luc Melenchon, delivers a speech before a rally to protest against the austerity measures announced by the French government, in Paris, Sunday, May 5, 2012. (AP Photo/Michel Spingler)
Leader of the French leftist party, Jean Luc Melenchon, delivers a speech before a rally to protest against the austerity measures announced by the French government, in Paris, Sunday, May 5, 2012. (AP Photo/Michel Spingler)
PARIS (AP) ? Tens of thousands of supporters of leftist parties are marching through central Paris to express disappointment with President Francois Hollande's first year in power, criticizing the leader for reneging on his promises to rein in the world of finance and enact economic stimulus.
Hollande, a Socialist, won the presidency last May, promising to spare France the austerity measures enacted elsewhere in Europe. He has raised taxes, especially on the rich, and made limited cuts to spending.
France's economy has continued to deteriorate, with growth stagnating and unemployment rising well above 10 percent. Hollande now has the lowest popularity rating of any post-war president.
Supporters of French leftist parties, which together call themselves the Left Front, marched through Paris on Sunday to call on Hollande to change his policies.
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Sunday, May 5, 2013
Engadget Podcast 342 - 05.03.13
With something old, and something new (we'll let you figure out what), this podcast has the makings of a wedding. There's even a brief mention of something blue... hmmm.
Hosts: Tim Stevens, Brian Heater, Peter Rojas
Guest: Ryan Block
Producers: James Trew, Joe Pollicino
Hear the podcast:
Filed under: Podcasts
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Saturday, May 4, 2013
Possible lead in case of missing U.S. journalist in Syria
BOSTON (AP) ? The New Hampshire-based family of a journalist missing for five months now believe "with a very high degree of confidence" that he is being held in a Syrian prison.
James Foley was last seen on Nov. 22 in northwest Syria, where he was contributing videos to Agence France-Press for the media company GlobalPost. His family in Rochester, N.H., says he was kidnapped by unknown gunmen.
GlobalPost CEO Philip Balboni said Friday that an exhaustive investigation has determined that Foley was likely abducted by a pro-Syrian government military group. Investigators believe he is being held with one or more Western journalists in a detention facility near Damascus.
Foley's family and the company have appealed to the Syrian government to release him.
The family spoke at World Press Freedom Day in Boston.
Source: http://news.yahoo.com/nh-family-missing-us-journalist-syrian-prison-151219097.html
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Friday, May 3, 2013
Iowa jury awards $240 million to mentally disabled turkey plant workers
(Reuters) - A jury on Wednesday awarded $240 million to 32 mentally disabled workers at an Iowa turkey processing plant to compensate for what government attorneys described as abuse by the Texas company that employed and housed them.
A federal jury in Davenport found that Hill Country Farms, doing business as Henry's Turkey Service, of Goldthwaite, Texas, had created an unlawful hostile environment for the men and discriminated against them on the basis of their disability. Jurors awarded them $7.5 million each, following a week-long trial, according to court documents.
According to the lawsuit filed by the U.S. Equal Employment Opportunity Commission against Hill Country Farms, workers at the West Liberty, Iowa plant were hit and kicked by Hill Country employees, called names, denied bathroom breaks and restrained or confined to rooms. Injuries and complaints of pain or requests for doctor's visits were ignored, the complaint said.
Henry's Turkey Service shut down in February 2009, the EEOC said.
Neither EEOC attorney Robert A. Canino nor an attorney for Hill Country Farms, David L. Scieszinski of Wilton, Iowa, were immediately available for comment.
A federal judge last September found that Henry's Turkey Service had violated the Americans with Disabilities Act by paying the workers "severely substandard wages" -- $65 a month rather than the average of $11 to $12 per hour given to non-disabled workers who performed the same work, according to the EEOC. Senior U.S. District Judge Charles R. Wolle awarded the workers $1.3 million for the pay discrimination.
The EEOC offered evidence that the 100-year-old former schoolhouse being used as living quarters for the men was bug- and rodent-infested, inadequately heated and had a leaky roof. The state fire marshal closed it down as unsafe, the EEOC said.
(Reporting by Mary Wisniewski; Editing by Nick Zieminski)
Source: http://news.yahoo.com/iowa-jury-awards-240-million-mentally-disabled-turkey-192037167.html
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New molecule heralds hope for muscular dystrophy treatment
May 1, 2013 ? There's hope for patients with myotonic dystrophy. A new small molecule developed by researchers at the University of Illinois has been shown to break up the protein-RNA clusters that cause the disease in living human cells, an important first step toward developing a pharmaceutical treatment for the as-yet untreatable disease.
Steven C. Zimmerman, the Roger Adams Professor of Chemistry at the U. of I., led the group in developing and demonstrating the compound. The National Institutes of Health supported the work published in the journal ACS Chemical Biology.
Myotonic dystrophy type 1 is the most common form of muscular dystrophy in adults, affecting one in 8,000 people in North America. It causes progressive weakness as the muscles deteriorate over time. There is no treatment available for the disease; though a few measures can help ease some symptoms, nothing can halt their inevitable progression.
"This is a disease that currently doesn't have any treatment, so we have a huge interest in finding therapeutic agents," said graduate student Amin Haghighat Jahromi, the first author of the paper.
Myotonic dystrophy type 1, called DM1 for short, is caused by a mutation to one gene. In a healthy person, one small segment of the gene -- a DNA sequence of CTG -- is repeated a few times. In someone with DM1, the sequence is repeated more than 50 times, even up to thousands of repeats. The sequence is transcribed into RNA over and over, like a skipping record stuck in a loop. The repetitive RNA binds to the protein MBNL1, which is essential for regulating protein balance in cells. The RNA traps the MBNL1 protein in aggregates within the cell's nucleus.
"The RNA is functioning in an abnormal way, and unfortunately, it's toxic," Zimmerman said. "MNBL regulates a process called alternative splicing that controls how much of different proteins are made. Affected cells make the proteins, just not at the right levels, so all the levels are imbalanced. There are more than 100 proteins that are affected."
The Illinois group developed a small molecule that could infiltrate the nucleus and bind to the RNA, forcing it to let go of MBNL1 so the protein can do its job. The molecule is small and water-soluble so it can cross the membrane into the cell, which has been a challenge for researchers attempting to use methods with larger molecules. It specifically targets only the repeating RNA sequence so as not to interfere with other cellular functions.
The researchers administered the molecule to live cells that have the disease features of DM1. Using advanced microscopy methods, they were able to watch the cells over time to see how they responded to the molecule. In only a few hours, they saw the clusters within the nucleus break up and were able to measure that the MBNL1 protein had increased its regulatory activity.
"This is the first study that gives direct evidence for the function of the compound," Jahromi said. "We track how the cell is changing upon treatment with the compound and see the effect directly."
Next, the researchers plan to begin collaborating with other groups to test their molecule in fruit flies and mice. Although the molecule will need many rounds of testing for toxicity, efficacy, metabolism and possible side effects before human trials can begin, finding a molecule that works in living cells is an important first step toward making a drug that could treat myotonic dystrophy.
"We're close to developing drug candidates that can be tested in animals. And if it works in animals, then we move hopefully into clinical trials with humans," Zimmerman said. "It's heartbreaking, at one level, to say we're years away from something that's going to be in the clinic. On the other hand, we now have targets. We now know how to go after this disease. It gives patients and their families a bit of hope."
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The above story is reprinted from materials provided by University of Illinois at Urbana-Champaign.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Amin Haghighat Jahromi, Lien Nguyen, Yuan Fu, Kali A. Miller, Anne M. Baranger, Steven C. Zimmerman. A Novel CUGexp?MBNL1 Inhibitor with Therapeutic Potential for Myotonic Dystrophy Type 1. ACS Chemical Biology, 2013; : 130320091510009 DOI: 10.1021/cb400046u
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/PHaBqIkW16E/130501145107.htm
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