CAIRO (AP) ? Thousands of opponents and supporters of Egypt's Islamist president began massing in city squares in competing rallies Sunday, gearing up for a day of massive nationwide protests that many fear could turn deadly as the opposition seeks to push out Mohammed Morsi.
Waving Egyptian flags, crowds descended on Tahrir Square in the heart of Cairo, one of multiple sites in Cairo and around the country where they plan rallies.
On the other side of Cairo, thousands of the Islamist leader's backers gathered not far from the presidential palace in a show of support.
The demonstrations on Sunday, the anniversary of Morsi's inauguration as Egypt's first freely elected leader, are the culmination of growing polarization since he took office.
The president is joined in one camp by his Islamist allies, including the Muslim Brotherhood and more hard-line groups. The other is an array of secular and liberal Egyptians as well as moderate Muslims and Christians ? and what the opposition says is a broad sector of the general public that has turned against the Islamists.
There is a sense among opponents and supporters of Morsi that Sunday's rally is a make-or-break day, hiking worries of violence. Already at least seven people, including an American, have been killed in clashes between the two camps over the past week, mainly in Nile Delta cities and the coastal city of Alexandria.
The opposition believes that with sheer numbers in the street, it can pressure Morsi to step down ? perhaps with the added weight of the powerful military if it signals the president should go. But Islamists have vowed to defend Morsi.
In an interview published Sunday in The Guardian, Morsi said he had no plans to meet the protesters' demand for early presidential election.
"If we changed someone in office who (was elected) according to constitutional legitimacy ? well, there will (be) people or opponents opposing the new president too, and a week or a month later, they will ask him to step down," Morsi told the British daily.
"There is no room for any talk against this constitutional legitimacy," he said.
As the crowds swelled in Tahrir, birthplace of the 2011 uprising that toppled Mubarak, traffic in the normally capital's normally clogged streets was light at midday as many residents chose to stay home for fear of violence. Banks were closing early and most government departments were either closed for the day or were thinly staffed.
Thousands of Morsi's supporters have staged a sit-in since Friday in front of the Rabia al-Adawiya Mosque near the Ittihadiya presidential palace. In the evening, anti-Morsi crowds plan to march on the palace, and Morsi supporters have vowed to defend it if it is attacked.
The opposition protests emerge from a petition campaign by a youth activist group known as Tamarod, Arabic for "rebel." For several months, the group has been collecting signatures on a call for Morsi to step down. On Saturday the group announced it had more than 22 million signatures ? proof, it claims, that a broad sector of the public no longer wants Morsi in office.
It was not possible to verify the claim. Morsi's supporters have questioned the authenticity and validity of the signatures, but have produced no evidence of fraud.
Morsi, who has three years left in his presidential term, claims that Mubarak loyalists are behind the planned protests. His supporters say Tamarod is a cover for thugs loyal to Mubarak.
The 22 million signatures, while they have no legal weight, deal a symbolic blow to Morsi at a time when he is widely seen by Egyptians to have failed to tackle the country's most pressing problems, from surging crime rates and high unemployment to fuel shortages and power outages.
If verified, the number of people who signed the petition calling on Morsi to step down would be nearly twice the number who voted for him a year ago in a run-off that he won with around 52 percent of the vote.
Adding to his troubles, eight lawmakers from the country's interim legislature announced their resignation Saturday to protest Morsi's policies. The 270-seat chamber was elected early last year by less than 10 percent of Egypt's eligible voters, and is dominated by Islamists.
A legal adviser to Morsi also announced his resignation late Saturday in protest of what he said was Morsi's insult of judges in his latest speech on Wednesday.
With a sense of doom hanging over the country, Defense Minister Gen. Abdel-Fattah el-Sissi last week gave the president and his opponents a week to reach a compromise and warned that the military would intervene to prevent the nation from entering a "dark tunnel."
Morsi had called for national reconciliation talks in a Wednesday speech but offered no specifics. Opposition leaders dismissed the call as cosmetics.
Asked by The Guardian whether he was confident that the army would not intervene if the country becomes ungovernable, Morsi replied, "Very."
The Egyptian leader, however, said he did not know in advance of el-Sissi's last week's comments.
Mobile virtualization startup BlueStacks only recently revealed the GamePop, its mobile home gaming console that offers all-you-can play gaming for a flat monthly fee, but it's already expanding the line. Today, the company is announcing GamePop Mini, a version of the GamePop that offers completely free hardware with a standard $6.99 monthly GamePop service subscription, with smaller hardware that's yours to keep after 12 months even if you decide to cancel your GamePop account.
The Amzer Skin Case is made out of 100% premium silicone and is a great, lightweight option for protecting your iPhone 5. The durable silicone absorbs any shock your device may receive from accidental drops or bumps, keeping it just like new. The smooth silicone gives you a sure and lasting grip on your iPhone 5 and prevents slides on flat surfaces.
June 20, 2013 ? Men who are diagnosed as azoospermic -- infertile because of an absence of sperm in their ejaculate -- are more prone to developing cancer than the general population, a study led by a Stanford University School of Medicine urologist has found. And a diagnosis of azoospermia before age 30 carries an eight-fold cancer risk, the study says.
"An azoospermic man's risk for developing cancer is similar to that for a typical man 10 years older," said Michael Eisenberg, MD, PhD, assistant professor of urology at the medical school and director of male reproductive medicine and surgery at Stanford Hospital & Clinics. Eisenberg is lead author of the study, published online June 20 in Fertility and Sterility.
Diagnoses of male infertility and azoospermia are surprisingly common in the United States. About 4 million American men -- 15 percent of those ages 15-45 -- are infertile. Of these, some 600,000 -- about 1 percent of those of reproductive age -- are azoospermic. "There is evidence that infertility may be a barometer for men's overall health," Eisenberg said, "and a few studies have found an association of male infertility with testicular cancer." The new study, he said, not only assigns the bulk of infertile men's increased cancer risk to those with azoospermia, but also suggests that this risk extends beyond testicular cancer.
Eisenberg conducted most of the analysis for the study at Stanford, using data gathered from the Texas Cancer Registry and the Baylor College of Medicine in Houston, where he completed his medical training. The study's senior authors are Larry Lipshultz, MD, and Dolores Lamb, PhD, professors of urology at Baylor.
The study population consisted of 2,238 infertile men who were seen at a Baylor andrology clinic from 1989 to 2009. Their median age was 35.7 when they were first evaluated for the cause of their infertility. Of those men, 451 had azoospermia, and 1,787 did not. There were otherwise no apparent initial differences between the two groups.
Azoospermia can arise for two reasons. Obstructive azoospermia is caused by a blockage that prevents otherwise plentiful, fit sperm produced in the testes from reaching the ejaculate. But a screen of about one-fourth of the azoospermic men in the study population indicated that the vast majority suffered from the non-obstructive variety: Their testes didn't produce enough sperm for any to reach their ejaculate, most likely because of genetic deficiencies of one sort or another. Fully one-fourth of all the genes in the human genome play some role in reproduction, Eisenberg noted, so there are a lot of ways for the capacity to sire offspring to go astray.
After undergoing a semen analysis, the men were followed for an average of 6.7 years to see which of them turned up in the Texas Cancer Registry. (Fortunately for the analysis, most people tend to stay in the state where they've grown up, said Eisenberg.) Their rates of diagnosed cancer incidence were then compared with age-adjusted cancer-diagnosis statistics of Texas men in general.
In all, a total of 29 of the 2,238 infertile men developed cancer over a 5.8-year average period from their semen analysis to their cancer diagnosis. This contrasted with an expected 16.7 cases, on an age-adjusted basis, for the male Texas population in general (which, Eisenberg said, closely reflects cancer incidence rates for the entire U.S. population). This meant that infertile men were 1.7 times as likely to develop cancer as men in the general population. This is considered a moderately increased risk.
But comparing the cancer risk of azoospermic and nonazoospermic infertile men revealed a major disparity: The azoospermic men were at a substantially elevated risk -- nearly three times as likely to receive a diagnosis of cancer as men in the overall population. Infertile men who weren't azoospermic, in contrast, exhibited a statistically insignificant increased cancer risk of only 1.4 times that of men in the overall population.
By excluding men whose cancer diagnosis came within two or three years of their infertility evaluation, the researchers were able to rule out the possibility that azoospermia caused by an undiagnosed cancer had affected the statistics.
While the study wasn't large enough to delineate which specific types of cancer pushed azoospermic men's incidence rates up, the diagnoses they received covered a wide range of cancers: brain, prostate and stomach tumors, as well as melanoma, lymphoma, testicular cancer and cancer of the small intestine. The findings suggest that genetic defects that result in azoospermia may also broadly increase a man's vulnerability to cancer, Eisenberg said, supporting the notion that azoospermia and cancer vulnerability may share common genetic causes.
The study, which was funded by the National Institute for Child Health and Human Development, is the first to examine the cancer risk of azoospermia in particular, or to link it to non-germ-cell cancers. Previous studies have failed to consistently identify any increased risk for nontesticular cancers in infertile men, whether azoospermic or otherwise. In those previous studies, however, azoospermic men couldn't be separately examined because sperm analyses weren't available.
Most striking of all, said Eisenberg, was the cancer risk among azoospermic men who first had their semen analyzed before age 30. They were more than eight times as likely to subsequently develop cancer than Texas males in the general population of the same age. In contrast, there was no relationship between age of semen analysis and risk of cancer for nonazoospermic men.
The good news, Eisenberg said, is that while the cancer risk among young azoospermic men was quite large compared to their same-age peers, their relative youth means that their absolute risk of contracting cancer during the follow-up period remained small. The bad news, he said, is that men in their 30s often don't have a primary health-care provider. He advised that young men who are diagnosed as azoospermic should be aware of their heightened risk and make sure to get periodic checkups with that in mind.
All Critics (95) | Top Critics (34) | Fresh (86) | Rotten (9)
This is an odd film (creepier than it knows), and even if you feel the atmospheric company of Dunham-ism, with a little of Whit Stillman, Henry Jaglom, and Woody Allen, the core influence on Noah Baumbach's film is fifty years older or more.
Baumbach usually builds his films around difficult protagonists, but Frances is entirely endearing, at once silly and deep, hopeless and promising.
The dialogue and editing are zippy and generally charming, combining with the tart observations of 20-something culture to create a nice frisson.
A black-and-white salute to the French New Wave (the score is borrowed from Georges Delerue, composer of many a Truffaut and Godard film) that manages to be very much of this moment ...
The movie's a love letter to an actress and her character, but by the end you may feel like an intervention is more in order.
The obvious love of New York City echoes Woody Allen at his best. But "Frances Ha" is very much its own film, a story of life and love and messy rooms.
A refreshing amount of buoyancy to dance and charm its way through Quarter-Life Crisis territory. One of the best performances of Greta Gerwig's career to date
Frances Ha is a sympathetic but not uncritical depiction of a girl's gradual evolution into a woman; one that never condescends by forcing her to abandon all her quirks and impish qualities in the final act... An absolute delight, this is.
Indie darling Gerwig has a great deal to do with the picture's success: she's disarmingly likable...
There's a level of audacity beneath the lightweight whimsy in this unassuming low-budget comedy.
"Frances Ha makes a star out of Gerwig, and she's the kind of star we need: a goofy one we can feel tender about but never underestimate."
'I can't account for my own bruises,' Frances says, as if she were a clumsy kid with an adult's vocabulary. Does the remark refer to more than the abrasions on her skin?
A celebration of cinema, New York City and the distinctive charms of actress Greta Gerwig, Frances Ha was co-written by Gerwig and its director, Noah Baumbach, and it's the best film either has made.
There's a thin line between comedy and tragedy, and Greta Gerwig walks it remarkably well.
There's depth and realism in the way Frances Ha shows aspiration versus reality.
Gerwig, beyond a doubt, is immeasurably appealing, and Frances Ha is tailor-made to showcase her gifts better than anything she's ever been in.
...if you hold your nose and simply wallow through the stench of self-aggrandizement, you'll be rewarded with an experience that will actually tug on your emotions.
Frances Ha provides a sharp, fleet, and very funny look at female friendship and the acceptance of adult responsibilities.
This is very minimalist storytelling much of which feels improvised in front of the camera. The film is more of a character situation than a character story.
Frances Ha is endearing, kind and, in many ways, Noah Baumbach's best movie to date.
It's a film that bears all of the zingy dialogue and sharp characterizations of Baumbach's other films ("The Squid and the Whale," "Greenberg") but with more of a generosity of spirit towards its characters.
Funny and touching, Frances Ha may very well be the most eloquent take yet on a generation in flux.
The light Frances Ha provides skittish moments of heartbreak and confusion on the humorous path to adulthood, but it sends a comforting message that our fate may use the same language as our dreams even if it doesn't tell the same story.
Easily Baumbach's warmest and most upbeat film to date.
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I figure this is simply a result of adulthood. Granted, it's a truth that I bemoan and groan and fight, kicking and screaming against, but a truth nonetheless.?
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People grow up, people get jobs, people move to Japan. It happens and in my brief adult-life-so-far I've found that generally one of two things happen when close friends move away: good intentions are set but touch is lost or you carry on -- and in some magic, cosmic way, your friendship gets forged in candy-colored steel. (My steel is candy-colored because my friendships are one of the few things I get all sappy and hearts/butterflies over, but your steel may be any style of your choosing. May I suggest skulls?)?
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I move around a lot. Since I was a kid, moving around to new neighborhoods, states, there was even a new country in the mix, was something I just got used to. Very early on, I developed a motto that still serves me really well: "Don't hold on to a friendship that doesn't want you, but cling like a pit bull to one that does." Awwwwww, I'll wait while all of y'all sew that into pillows. (Note: I've since learned that pit bulls do NOT have "locking jaws"; just don't want to perpetuate any mean doggie stereotypes.)
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But really, while there is always a mourning period of losing the intimacy of the everyday with a friend or partner (my husband moving to Japan for a year to study nerd things), I've found that with a little effort, dedication and forgiveness, long-distance friendships can be the antidote to when nobody knows your name, and you need the comfort of someone "just getting it."
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A few months into living in O'ahu, I went out with some of my husband's new classmates. I tried to be on my best behavior -- witty, weird, wise-ass -- I thought I was charming the crowd. Turns out "charming" was not the way most people thought of me that night. Try "loud" and "overly aggressive" and "Did Louise just steal that woman's lighter?" (For the record I DID NOT.)?
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If it hadn't been for the knowledge that I have a small army of people 3000+ miles away who love me not only in spite of my social disgraces but BECAUSE of them, I would have let that incident fester and boil and keep me away from social situations for my duration in O'ahu. The magic of a late night phone call with someone who wishes that they had been there with you during "the lighter incident," if only to laugh at the absurdity of it all, does wonders to restore one's confidence.?
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So in the spirit of National Long Distance Friendship Day (I made that up, but don't you have a friend you need to call?), here is a list of the tips, tricks and forgivable blunders that have allowed me to delight in a collection of real friends across the country and internationally.?
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1. Make regular phone dates.
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I am officially the worst at calling people. Everyone who knows me knows this, and it's not OK.?
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Making weekly phone dates make you prioritize your long distance friend for a certain amount of time, carve out a part of your schedule to just "hang out" with them. Just like old times.?
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More than that, sometimes spontaneously picking up your phone and reporting the big and little things to your friends restores a sense of normalcy to a far apart friendship. Yes, it's not the same as everyday contact, but by it does keep you in each other's lives.?
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Sometimes it does take some effort, like when my husband was living in Japan. Aside from Skype (more on that later), buying a calling card was one of the best things I did. When exciting things happened to me, I could call him, granted with a few more digits to dial, and yelp and holler over the phone almost like he was just across town.
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I have a phone date with my friend Bethany later today, and I programmed an alarm in my phone to remind myself to call. Bethany is the very best at forgiving me for not making our dates, and for this reason alone, I started using my phone alarm so that I wouldn't abuse that kindness.?
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Behold! My reminder on my piece of crap phone!?
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Which brings me to?
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2. Forgive.
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Birthdays will be wished late, people will feel left out, tons of texts or e-mails will be misinterpreted, "Why didn't you tell me?!" stuff will happen.
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Forgive, forgive, forgive. Apologize. Forgive.?
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Having long distance friendships is hard, and life happens, so sometimes things fall by the wayside, but holding grudges only creates more distance. In my experience, as hurt as you are by your friend forgetting your birthday, they feel twice as horrible and panicked when they REALIZE they missed your birthday.?
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I'm telling you, the cell phone calendar with reminders is the greatest invention of the modern age.?
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3. Don't hesitate to do the nice stuff.
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My friend Liz, one of my oldest and most skilled long distance friends, once said to me, "When I see something that might make my friend happy, if I can afford it, I will get it for them, because you shouldn't hesitate when you could do something nice for your friends." MY GOD, I have nice people in my life.?
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But it's true. Nothing makes me shed tears of joy quicker or laugh real laughs faster than getting a little gift in the mail, or a "This made me think of you" picture of a dog in a dress sent to my phone. And inversely, there is something really uplifting about sending a little surprise to someone you care about.?
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Sometimes I really have to force myself off my lazy ass to get to the post office to mail shit, but in the end I'm always glad I did. You will be too.?
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4. Skype.
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What did people do before Skype??
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My friend Joy, her boyfriend and her cat, Deryk, just moved to a new apartment, and while I'm SO BUMMED that I can't be there to break it in with her, an upcoming Skype session will allow me to get a tour and be not QUITE so out of the loop. Thanks, Skype!
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When my husband was living in Japan, Skype single-handedly preserved, if not strengthened our relationship. Unlike phones, you have to make a little more effort to actually be in a certain place, at a certain time, and look at a person.?
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Not to mention, you can Skype someone into a show, party, bat mitzvah -- anything! And for a moment, it's like they're not so far away.?
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5. Save up for a visit.
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Money sucks. I say that almost everyday. But really, coming from one of the cheapest people ever born, save up for that rendezvous with your BFF, it's worth it.?
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And you know what's even more fun than planning a trip to see a friend? Surprising them on a special occasion.?
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I screamed, cried, and peed a little when, on my first birthday in Hawai'i, my friend Joy surprised me by flying all the way from LA just to see me (and hang in Hawai'i, let's be honest).?
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There's something so renewing about spending even a few days with a dear friend. You'll fly or drive away from each other with your roots a little deeper intertwined and feeling, I promise, a little less lonely in the world.?
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If you can make the big trip to see your friend, it's like the phone date, Skype session, and "I miss you!" gift all rolled up into one.?
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Not flying across the Pacific, but one of the happiest days of my life. My friends, Joy and Marty, surprised me at LAX when I had a three hour layover at 1am. I'm the luckiest.?
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So that's what I do.?
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It may seem simplistic, but in my experience, just seeing, spelled out, how easy it can be to evolve a friendship from near distance to long distance can assuage the FREAK OUT that can occur when faced with leaving your friend-family.?
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So I want to know: What do you do?
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How do you stay in touch with your long distance friends? How far away is your farthest friend? Do you also collect friends across the world?
In this June 9, 2011 file photo, U.S actor and auto racing driver Patrick Dempsey poses for photographs in Le Mans, France. The only all-American lineup at the 24 Hours of Le Mans might very well be the one that draws the most interest from non-racing fans. The No. 77 Dempsey Del Piero-Proton Porsche will be headlined by Patrick Dempsey. (AP Photo/Vincent Michel, File)
The only all-American lineup at the 24 Hours of Le Mans might very well be the one that draws the most interest from non-racing fans.
The No. 77 Dempsey Del Piero-Proton Porsche will be headlined by Patrick Dempsey ? you know, ?McDreamy? of ?Grey?s Anatomy? fame. He is joining co-drivers Joe Foster and Patrick Long in the GTE Am division and driving a Porsche 911 GT3 RSR.
?I think anybody who?s a road racer wants to race here,? Dempsey said. ?Having done it in the past and coming back and doing it with an all-American driver lineup with Patrick Long and Joe Foster with a great team at Proton-Dempsey-Del Piero, it?s a tremendous honor. It means everything to us, and it?s humbling, it?s exciting, it?s inspirational, and it?s so moving to be a part of this event. It?s a dream come true to come back here.?
It will be the actor?s second time competing in the endurance race in Le Mans, France, but this time he appears to have a legitimate shot at a class victory.
The 47-year-old Dempsey shared a Ferrari at Le Mans in 2009 with Foster, his motorsports business partner. New to the entry this year is Long, a two-time Le Mans winner making his 10th start in the race. Long turned the third-fastest lap in class during the one-day Le Mans pre-test earlier this month.
The team was also buoyed by its second-place result at Laguna Seca last month in Dempsey?s last outing. The team appeared poised to win until co-driver Andy Lally was passed for the class lead following a restart on the final lap of the four-hour race.
To be considered a contender has Dempsey on the cusp of what once seemed to be an unreachable goal.
?We would sit around the kitchen or in the trailer dreaming about when we?d go to Le Mans and getting on the podium,? he said. ?This has always been a dream and a goal. So to come back here ? it was a dream come true and a turning point in my life to have done it in 2009, and I haven?t had a win yet, and I would love to if I could get my first win to be at Le Mans. It would just be so, so special. It would be deeply moving certainly. I know the drivers on the team can do it.?
It will be Long?s first race teaming with Dempsey and Foster. He was a late addition to the team in place of Dempsey Del Piero team principal Michael Avenatti, whose business commitments outside of racing prevented him from competing at Le Mans. But it didn?t take him long to feel comfortable with the team assembled.
?Once Patrick and Joe got in the car and picked it up really quickly, I started to feel really positive about our chances,? Long said. ?That was sort of capped off by the test that we had just two weeks ago.?
Dempsey has been an active participant in sports car racing now for nearly a decade, and Long has been impressed by his progress.
?He definitely is underrated,? Long said. ?I?ve watched him and Joe partner up and go very seriously at racing a little bit from a distance. Working alongside him has certainly been a different experience. He?s a very intense competitor, very focused. What I underestimated was his fitness. We went testing in (in Italy) and the team was worn out. They were looking at me. I?ve run with them previously over here in Europe and they were like, ?We?re out of tires; we?re out of fuel.? I?m like, ?This guy still wants to drive and he?s here to put the numbers up and not just show up and look the part.??
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DOUBLE DUTY: Brian Vickers has a lot of road in front of him this weekend as the only driver attempting double duty in the Sprint Cup and Nationwide Series races.
Vickers is scheduled to run the Nationwide race on Saturday at Road America for Joe Gibbs Racing before heading West to Sonoma, Calif., for the Cup race in a Michael Waltrip Racing entry on Sunday.
?I?m looking forward to both of them,? said Vickers. ?It?s going to take a little different mentality and technique going from Road America which is a little bit faster place to Sonoma which is a slower, more technical road race, but I?m up for the challenge and excited.?
In the past, most Cup drivers have spent the majority of their time in Sonoma and flew to the Nationwide race just in time for the start. Vickers, though, will spend most of the weekend in Wisconsin with JGR as he focuses on his Nationwide effort. He?s currently 10th in the championship race, 100 points behind leader Regan Smith.
Jason Bowles will drive MWR?s No. 55 for him at Sonoma in practice and qualifying, and Vickers will have to start at the back of the field when he arrives Sunday. Vickers was able to find a silver lining in knowing he?ll start at the back.
?I think there?s opportunities at Sonoma to get to do a little bit different pit strategy,? he said. ?Knowing that you don?t really have track position to protect kind of can create opportunities. We?ve been there in the past where we?ve had either bad qualifying or something happened during the race and we had to come in and pit or penalties on pit road, like last year we had the penalty on pit road and had to go to the back and we worked our way back up to fourth, but as much as it hurt us, it also created opportunities.?
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It?s been a rough few weeks for Gustavo Yacaman, the Grand-AM Series driver who was placed on two-race probation by series officials for ?his involvement in various incidents? during the June 1 race in Detroit.
His first stint back on the track since the hand-slapping couldn?t have gone any worse.
The Colombian started eighth at Mid-Ohio on Saturday and was trying to make a pass on Memo Rojas ? the same driver he wrecked at Detroit ? when the two made contact. It led to a flat tire for Yacaman, who drove off the track and through a gravel trap, which ruptured the oil line.
The Michael Shank Racing entry then burst into flames, causing significant damage to the No. 6 Ford-Riley. It also led to harsh criticism of Yacaman from racers from various series, many who instantly took to social media to lambast the 22-year-old.
Among those showing zero sympathy was Scott Pruett, Rojas? co-driver who never got a chance to drive at Detroit because of the accident with Yacaman.
?I feel really bad for Mike Shank, but not the driver,? Pruett said. ?It will be interesting to see what Grand-Am does, since he?s on probation.?
Shank on Sunday supported his driver through a series of tweets, saying Yacaman drives for the team this season and ?that is not changing? while acknowledging he ?has made bad decisions and I promise u that we will correct this path.?
Shank said the team has obligations to the sponsor and the 10 employees that work on the car, and tweeted, ?Our focus is now on the massive rebuild effort to try and get the 6 car to Watkins.?
All wasn?t lost at Mid-Ohio for the Shank organization. Ozz Negri marked his return to the No. 60 with a fourth-place finish with co-driver John Pew. The car had to come back from significant damage of its own suffered in Detroit, and Negri had missed three races while he continued to recover from an offseason training injury to his leg.
?It?s great having Ozz back, it?s like a missing family member that?s finally back,? Pew said. ?The whole team is excited that he?s back. The guys did a tremendous job getting the car back from Detroit. Right down to the last nut and bolt it rolled off the trailer just about perfect. It was an awesome car. It?s too bad we couldn?t get a podium, but I?m pretty happy with a fourth place.?
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Restoring appropriate movement to immune cells may save seriously burned patientsPublic release date: 19-Jun-2013 [ | E-mail | Share ]
Contact: Sue McGreevey smcgreevey@partners.org 617-724-2764 Massachusetts General Hospital
Treatment with recently identified molecule helps neutrophils travel to site of injury, may reduce sepsis, other complications
Advances in emergency medicine and trauma surgery have had a significant impact on survival of patients in the days immediately after major injuries, including burns. Patients who survive the immediate aftermath of their injuries now are at greatest risk from infections particularly the overwhelming, life-threatening immune reaction known as sepsis or from inflammation-induced multiorgan failure. Now, a device developed by Massachusetts General Hospital (MGH) investigators that measures the movement of key immune cells may help determine which patients are at greatest risk for complications, and a novel treatment that directly addresses the cause of such complications could prevent many associated deaths.
"One in every three patients with burn injuries that dies in an intensive care unit does so because of septic complications," says Daniel Irimia, MD, PhD, of the MGH Department of Surgery, corresponding author of a report in the June FASEB Journal. "In the days immediately after injury, white blood cells called neutrophils can lose their ability to move to the site of an injury. In an animal model of burn injury, we found that death due to septic complications can be prevented by a treatment that restores the proper movement of neutrophils."
The most abundant type of white blood cell, neutrophils are part of the innate immune system and the body's first line of defense against infections. Normally, neutrophils are drawn towards the site of a infection by chemical signals from bacteria or injured cells. However, it has recently been discovered that in patients with serious burn injuries neutrophils' ability to follow these signals becomes impaired soon after the injury. Not only does that impairment reduce the availability of the cells to fight infection at the site of injury, but misguided neutrophils also can attack healthy tissue, contributing to organ failure. The current study was designed to analyze changes in the speed and direction of neutrophil movement after burn injury and to investigate whether recently identified molecules called resolvins, which normally act to terminate the inflammatory process after an infection has cleared, could also restore normal neutrophil motion after burns.
Using a microfluidic device that measures neutrophil movement developed at the MGH BioMEMS Resource Center, the investigators first confirmed that the ability of neutrophils from burn-injured rats to move towards a chemical signal of injury progressively deteriorates in both speed and accuracy as time passes. While cells from uninjured animals moved quickly and directly through a series of microchannels towards the injury signal, cells from blood samples taken 9 days after the injury became trapped in the device or reversed direction. The researchers then showed that application of resolvin D2 significantly improved the in vitro migratory ability of neutrophils from burned animals.
Experiments in living rats revealed that treatment with resolvin D2 restored appropriate neutrophil motion, an effect that lasted at least two days after treatment ended. In addition, when burn-injured animals were subjected to a second sepsis-inducing injury, treatment with resolvin D2 significantly increased survival. For example, in a group of rats injected with a bacterial toxin nine days after a burn injury, all of those pre-treated with resolvin survived, while all untreated animals died.
"Our ability to measure neutrophil movement in great detail gave us the information we needed to develop the optimal dosage and duration of resolvin treatment for the burned rats. Our results also indicate that neutrophil motility could be a useful biomarker for the actual risk of septic complications in patients," says Irimia, an assistant professor of Surgery at Harvard Medical School who is also affiliated with Shriner's Hospital for Children. "Our experiments in the animal model suggest that a resolvin-based treatment could prevent those complications by restoring the body's own resources, allowing it to respond to secondary infections, which could save hundreds of patients with burns every year. "
###
Lead author of the paper is Tomohiro Kurihara, MD, previously of the MGH Department of Surgery and now at Keio University in Tokyo . Additional co-authors are Caroline Jones, PhD, Yong-Ming Yu, MD, PhD, Susumu Watada, MD, Ronald Tompkins, MD, ScD, and Shawn Fagan, MD, MGH Surgery; and Alan Fischman, MD, MGH Radiology. The study was supported by grants from Shriners Burns Hospital and by National Institutes of Health grants GM-092804, GM-007035, and DE-019938.
Massachusetts General Hospital (http://www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine. In July 2012, MGH moved into the number one spot on the 2012-13 U.S. News & World Report list of "America's Best Hospitals."
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Restoring appropriate movement to immune cells may save seriously burned patientsPublic release date: 19-Jun-2013 [ | E-mail | Share ]
Contact: Sue McGreevey smcgreevey@partners.org 617-724-2764 Massachusetts General Hospital
Treatment with recently identified molecule helps neutrophils travel to site of injury, may reduce sepsis, other complications
Advances in emergency medicine and trauma surgery have had a significant impact on survival of patients in the days immediately after major injuries, including burns. Patients who survive the immediate aftermath of their injuries now are at greatest risk from infections particularly the overwhelming, life-threatening immune reaction known as sepsis or from inflammation-induced multiorgan failure. Now, a device developed by Massachusetts General Hospital (MGH) investigators that measures the movement of key immune cells may help determine which patients are at greatest risk for complications, and a novel treatment that directly addresses the cause of such complications could prevent many associated deaths.
"One in every three patients with burn injuries that dies in an intensive care unit does so because of septic complications," says Daniel Irimia, MD, PhD, of the MGH Department of Surgery, corresponding author of a report in the June FASEB Journal. "In the days immediately after injury, white blood cells called neutrophils can lose their ability to move to the site of an injury. In an animal model of burn injury, we found that death due to septic complications can be prevented by a treatment that restores the proper movement of neutrophils."
The most abundant type of white blood cell, neutrophils are part of the innate immune system and the body's first line of defense against infections. Normally, neutrophils are drawn towards the site of a infection by chemical signals from bacteria or injured cells. However, it has recently been discovered that in patients with serious burn injuries neutrophils' ability to follow these signals becomes impaired soon after the injury. Not only does that impairment reduce the availability of the cells to fight infection at the site of injury, but misguided neutrophils also can attack healthy tissue, contributing to organ failure. The current study was designed to analyze changes in the speed and direction of neutrophil movement after burn injury and to investigate whether recently identified molecules called resolvins, which normally act to terminate the inflammatory process after an infection has cleared, could also restore normal neutrophil motion after burns.
Using a microfluidic device that measures neutrophil movement developed at the MGH BioMEMS Resource Center, the investigators first confirmed that the ability of neutrophils from burn-injured rats to move towards a chemical signal of injury progressively deteriorates in both speed and accuracy as time passes. While cells from uninjured animals moved quickly and directly through a series of microchannels towards the injury signal, cells from blood samples taken 9 days after the injury became trapped in the device or reversed direction. The researchers then showed that application of resolvin D2 significantly improved the in vitro migratory ability of neutrophils from burned animals.
Experiments in living rats revealed that treatment with resolvin D2 restored appropriate neutrophil motion, an effect that lasted at least two days after treatment ended. In addition, when burn-injured animals were subjected to a second sepsis-inducing injury, treatment with resolvin D2 significantly increased survival. For example, in a group of rats injected with a bacterial toxin nine days after a burn injury, all of those pre-treated with resolvin survived, while all untreated animals died.
"Our ability to measure neutrophil movement in great detail gave us the information we needed to develop the optimal dosage and duration of resolvin treatment for the burned rats. Our results also indicate that neutrophil motility could be a useful biomarker for the actual risk of septic complications in patients," says Irimia, an assistant professor of Surgery at Harvard Medical School who is also affiliated with Shriner's Hospital for Children. "Our experiments in the animal model suggest that a resolvin-based treatment could prevent those complications by restoring the body's own resources, allowing it to respond to secondary infections, which could save hundreds of patients with burns every year. "
###
Lead author of the paper is Tomohiro Kurihara, MD, previously of the MGH Department of Surgery and now at Keio University in Tokyo . Additional co-authors are Caroline Jones, PhD, Yong-Ming Yu, MD, PhD, Susumu Watada, MD, Ronald Tompkins, MD, ScD, and Shawn Fagan, MD, MGH Surgery; and Alan Fischman, MD, MGH Radiology. The study was supported by grants from Shriners Burns Hospital and by National Institutes of Health grants GM-092804, GM-007035, and DE-019938.
Massachusetts General Hospital (http://www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine. In July 2012, MGH moved into the number one spot on the 2012-13 U.S. News & World Report list of "America's Best Hospitals."
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June 17, 2013 ? Discovery of a mutant gene responsible for a disease is a milestone, but for most conditions, it may be only a first step towards a treatment or cure. Understanding Rett Syndrome, an autism spectrum disorder, is further complicated by the fact that the implicated gene controls a suite of other genes. Two papers, published in today's Nature Neuroscience and Nature, reveal key steps in how mutations in the gene for methyl CpG-binding protein (MECP2) cause the condition. The Rett Syndrome Research Trust (RSRT) funded this work with generous support from partners Rett Syndrome Research Trust UK and Rett Syndrome Research & Treatment Foundation.
Rett Syndrome is a single-gene neurological disorder that affects girls. Development slows during the first year of life, then regresses, as toddlers lose speech, mobility, and hand use. Many girls have seizures, orthopedic and severe digestive problems, as well as breathing and other autonomic impairments. Most live into adulthood and require total, round-the-clock care. Rett Syndrome affects about 1 in 10,000 girls born each year.
The papers result from a collaboration between the labs of Adrian Bird, Ph.D., Buchanan Professor of Genetics at the Wellcome Trust Centre for Cell Biology at the University of Edinburgh, and Michael Greenberg, Ph.D., Department Chair and Nathan Marsh Pusey Professor of Neurobiology at Harvard Medical School.
The Bird and Greenberg labs have been working together since 2011 as members of the MECP2 Consortium along with Gail Mandel, a Howard Hughes Investigator at Oregon Health and Sciences University. The Consortium, launched by RSRT with a $1 million lead gift by RSRT Trustee Tony Schoener and his wife Kathy, fosters novel alliances among leading scientists to interrogate the molecules at the root of the syndrome.
Professor Bird discovered the MeCP2 protein in 1992. In 2007, he showed that affected brain cells in a mouse model of Rett Syndrome can regain function, even in late stages of the disease, suggesting that the disorder is curable. Despite this unexpected breakthrough the function of the Rett protein remains elusive.
In search of the function, the Bird lab set out to identify the key domains of the protein. Mutations found in individuals suffering from Rett led them to their answer. By focusing only on "missense" mutations, which alter a single amino acid, the researchers were able to hone in on two key domains where the mutations aggregated. The first was the well-known methyl binding domain (MBD) which is the site where MeCP2 binds to methylated DNA, thereby modulating the expression of downstream genes. The second key domain is where MeCP2 binds to a molecule called NCoR/SMRT, a large multi-protein machine that shuts down genes. The Bird lab coined this domain the NCoR/SMRT Interaction Domain (NID).
"Further proof of the importance of the MBD and the NID came from mining the genomes of 6503 healthy people. The result was the exact mirror image of the situation seen in Rett. All along the MECP2 gene normal people have non-disease causing alterations, known as polymorphisms. However, no alterations of any kind could be found in the MBD and the NID, indicating that these domains are prized real estate that cannot be tampered with," said Matthew Lyst, postdoctoral researcher and lead author on the NatureNeuroscience paper.
The most frequent Rett mutation in the NID is at amino acid # 306. When the researchers recapitulated the mutation in mice, the animals suffered symptoms similar to girls with Rett. At fault: loss of the interaction between the MeCP2 and NCoR/SMRT proteins and further evidence of the importance of the NID.
"We knew that MeCP2 binds to the genome at methylated sites, but nothing more than that. We now know that its function depends on the ability to bring NCoR/SMRT co-repressors to the DNA," Prof. Bird summed up.
The Nature paper continues the story through another amino acid location, 308, which is very near the 306 mutation in the human version of the gene. Sensory input leads to the addition of a phosphate group at the 308 site and this alters the ability of the MeCP2 protein to interact with the NCoR/SMRT co-repressor, thereby affecting the expression of downstream proteins. The Greenberg lab created mice with a mutation at 308 that are unable to attach a phosphate group. As a result, genes that MeCP2 normally controls are mis-regulated.
"The MeCP2 308 mice have reduced brain weight, motor system abnormalities, and lower seizure thresholds that correspond to the deceleration of head growth, motor system impairments and seizure disorders found in Rett. This suggests that the modification of 308 is critical for the normal function of MeCP2 and its disruption might contribute to Rett," said Daniel Ebert, postdoctoral researcher and lead author on the Nature paper.
Whether the phosphates are added to MeCP2 depends on activity of the neuron. The Greenberg lab has found that in early life, sensory input leads to modification of MeCP2 at multiple sites, including 308. These changes appear to be critical for proper brain development, and their absence in Rett Syndrome may begin to explain what goes wrong in the brains of girls with this devastating disorder.
Each step deciphered in the genetic choreography behind Rett Syndrome is a step towards treatment. "To design an effective small molecule therapy, one needs to understand the underlying mechanisms of how MeCP2 functions and how mutations in MeCP2 lead to disease. Both papers published today make significant progress by providing compelling evidence for dysregulation of the MeCP2-NCoR interaction underlying key aspects of Rett Syndrome," said Prof. Greenberg.
What still isn't known is which genes the co-repressors target. And that will be the next leap in traveling the road from a mutant gene to a little girl who wrings her hands, has seizures and can't talk or walk. Discovering the other molecular events might reveal intersecting or redundant genetic pathways that drug developers can tweak in the search for treatments.
A team of archaeologists from Australia has found an ancient city buried for more than 1,000 years beneath Cambodia's soupy jungles.
By Elizabeth Barber,?Contributor / June 17, 2013
Hidden in the depths of the Cambodian jungle lays an ancient city, undiscovered until now (News2242).
If at seems at times that our globe is already thoroughly mapped and explored, all its corridors charted and its mysteries explained, then the latest news out of Southeast Asia is solacing ? there are, it seems, still lost worlds to be discovered, combed out from beneath a millennium of accumulated jungle in remote Cambodia.
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A team of archaeologists from Australia has found an ancient city that has for more than 1,000 years escaped detection ? not even looters had found the mysterious place, buried in Cambodia?s otherwise heavily trafficked Siem Reap province, which sees about a million tourists each year, Australia's The Age reported.
Known as Mahendraparvata, the lost world is some 1,200-years old, about 350 years older than the Angkor Wat temple complex, also in Siem Reap. Like Angkor, it was part of the Hindu-Buddhist Khmer Empire that from about 800 A.D. to 1400 A.D. ruled?Southeast Asia, using slave labor to construct opulent, arrestingly beautiful stone temples.
Damian Evans, director of the University of Sydney's archaeological research center in Cambodia, and a small group of colleagues working in Cambodia?s northwestern corridor first mapped the area, Cambodia?s Phnom Kulen mountain, using airborne Lidar, a remote-sensing technology that uses lasers. The Lidar data revealed structures hidden beneath Technicolor green of rural Cambodia?s thick jungles, giving scientists the basic outline of the almost mythical place ??as well as the wish to know more.
Weeks later, guided by an ex-Khmer Rogue soldier familiar with the terrain, the team hacked their way to the remnants of this once-booming cosmopolis:?abandoned, overgrown temples, as well as evidence of roads and canals.
Scientists are unsure why Mahendraparyata was abandoned ??possibly, the area had suffered too much?environmental degradation to support the empire?s burgeoning population. Turned over to time, the royal city was worked to rubble as a millennium of industrious vegetation and monsoon rains did their worst. The mountain itself, once home to the peak of Cambodian culture, would go on to witness one of its worst moments, becoming a Khmer Rouge stronghold in the 1970s.
Throughout all that, the mountain has remained a spiritual place, host to tens of thousands of pilgrims each year.
Mayo Clinic: Rotavirus vaccine given to newborns in Africa is effectivePublic release date: 17-Jun-2013 [ | E-mail | Share ]
Contact: Bob Nellis newsbureau@mayo.edu 507-284-5005 Mayo Clinic
Vaccine may save thousands of lives annually
ROCHESTER, Minn. -- Mayo Clinic and other researchers have shown that a vaccine given to newborns is at least 60 percent effective against rotavirus in Ghana. Rotavirus causes fever, vomiting and diarrhea, which in infants can cause severe dehydration. In developed nations, the condition often results in an emergency room visit or an occasional hospitalization, but is rarely fatal. In developing countries, however, rotavirus-related illness causes approximately 500,000 deaths per year. The findings appear this week in the Journal of Infectious Diseases.
Currently, there is no neonatal rotavirus vaccine available and infants do not receive their first dose of a rotavirus vaccine until they are approximately 2 months old, leaving younger infants at serious risk of rotavirus infection. In the study, the first of two doses was administered within the first 29 days of life (neonatal dosing), and the second dose before 60 days of age.
"For the first time in a large-scale study, we have demonstrated that protection against rotavirus gastroenteritis can be achieved earlier in life," says co-author and pediatrician Robert M. Jacobson, M.D., of the Mayo Clinic Children's Center. "The next step should be additional studies in neonates to provide earlier protection against life-threatening rotavirus diarrhea. The rotavirus vaccines used in America and Europe are administered later -- when babies are 2 to 4 months old -- but younger infants also contract the virus in the first two months of life."
Two vaccines serve as standard protection in developed countries, but are not especially effective in African or Asian countries, says Dr. Jacobson. Besides, he says, protection is also needed from birth due to the widespread risk of the virus.
"There is a huge protection gap right now in the first months of life," says Dr. Jacobson. "This study points to a clear and practical solution."
In Ghana, 998 newborns were selected for the randomized, double-blind, placebo trial from two of the poorest parts of the country. Half received the oral reassortant rotavirus tetravalent vaccine (RRV-TV) in the first two months of life, half received a placebo. Results showed a significant response in parameters of efficacy, safety and immune impact of the vaccine.
###
The study was funded by the International Medical Foundation. Co-authors include George Armah, Ph.D., University of Ghana; Albert Kapikian, M.D., National Institutes of Health; Timo Vesikari, M.D., Ph.D., University of Tampere, Finland; Nigel Cunliffe, M.D., Ph.D., University of Liverpool, U.K.; D. Bruce Burlington, M.D., Gaithersburg, Md.; and Leonard Ruiz Jr., Ph.D., International Medica Foundation, Rochester.
About Mayo Clinic
Mayo Clinic is a nonprofit worldwide leader in medical care, research and education for people from all walks of life. For more information, visit http://www.mayoclinic.org/about and http://www.mayoclinic.org/news.
Journalists can become a member of the Mayo Clinic News Network for the latest health, science and research news and access to video, audio, text and graphic elements that can be downloaded or embedded.
MULTIMEDIA ALERT: Video of Dr. Jacobson
is available on the Mayo Clinic News Network.
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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.
Mayo Clinic: Rotavirus vaccine given to newborns in Africa is effectivePublic release date: 17-Jun-2013 [ | E-mail | Share ]
Contact: Bob Nellis newsbureau@mayo.edu 507-284-5005 Mayo Clinic
Vaccine may save thousands of lives annually
ROCHESTER, Minn. -- Mayo Clinic and other researchers have shown that a vaccine given to newborns is at least 60 percent effective against rotavirus in Ghana. Rotavirus causes fever, vomiting and diarrhea, which in infants can cause severe dehydration. In developed nations, the condition often results in an emergency room visit or an occasional hospitalization, but is rarely fatal. In developing countries, however, rotavirus-related illness causes approximately 500,000 deaths per year. The findings appear this week in the Journal of Infectious Diseases.
Currently, there is no neonatal rotavirus vaccine available and infants do not receive their first dose of a rotavirus vaccine until they are approximately 2 months old, leaving younger infants at serious risk of rotavirus infection. In the study, the first of two doses was administered within the first 29 days of life (neonatal dosing), and the second dose before 60 days of age.
"For the first time in a large-scale study, we have demonstrated that protection against rotavirus gastroenteritis can be achieved earlier in life," says co-author and pediatrician Robert M. Jacobson, M.D., of the Mayo Clinic Children's Center. "The next step should be additional studies in neonates to provide earlier protection against life-threatening rotavirus diarrhea. The rotavirus vaccines used in America and Europe are administered later -- when babies are 2 to 4 months old -- but younger infants also contract the virus in the first two months of life."
Two vaccines serve as standard protection in developed countries, but are not especially effective in African or Asian countries, says Dr. Jacobson. Besides, he says, protection is also needed from birth due to the widespread risk of the virus.
"There is a huge protection gap right now in the first months of life," says Dr. Jacobson. "This study points to a clear and practical solution."
In Ghana, 998 newborns were selected for the randomized, double-blind, placebo trial from two of the poorest parts of the country. Half received the oral reassortant rotavirus tetravalent vaccine (RRV-TV) in the first two months of life, half received a placebo. Results showed a significant response in parameters of efficacy, safety and immune impact of the vaccine.
###
The study was funded by the International Medical Foundation. Co-authors include George Armah, Ph.D., University of Ghana; Albert Kapikian, M.D., National Institutes of Health; Timo Vesikari, M.D., Ph.D., University of Tampere, Finland; Nigel Cunliffe, M.D., Ph.D., University of Liverpool, U.K.; D. Bruce Burlington, M.D., Gaithersburg, Md.; and Leonard Ruiz Jr., Ph.D., International Medica Foundation, Rochester.
About Mayo Clinic
Mayo Clinic is a nonprofit worldwide leader in medical care, research and education for people from all walks of life. For more information, visit http://www.mayoclinic.org/about and http://www.mayoclinic.org/news.
Journalists can become a member of the Mayo Clinic News Network for the latest health, science and research news and access to video, audio, text and graphic elements that can be downloaded or embedded.
MULTIMEDIA ALERT: Video of Dr. Jacobson
is available on the Mayo Clinic News Network.
[ | E-mail | 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.
Quality of waking hours determines ease of falling sleepPublic release date: 17-Jun-2013 [ | E-mail | Share ]
Contact: Deborah Wormser deborah.wormser@utsouthwestern.edu 214-648-3404 UT Southwestern Medical Center
DALLAS June 17, 2013 The quality of wakefulness affects how quickly a mammal falls asleep, UT Southwestern Medical Center researchers report in a study that identifies two proteins never before linked to alertness and sleep-wake balance.
"This study supports the idea that subjective sleepiness is influenced by the quality of experiences right before bedtime. Are you reluctantly awake or excited to be awake?" said Dr. Masashi Yanagisawa, professor of molecular genetics and a Howard Hughes Medical Institute investigator at UT Southwestern. He is principal author of the study published online in May in the Proceedings of the National Academy of Sciences.
Co-author Dr. Robert Greene, UT Southwestern professor of psychiatry and a physician at the Dallas VA Medical Center, said the study is unique in showing that the need for sleep (called sleep homeostasis) can be separated from wakefulness both behaviorally and biochemically, meaning the two processes can now be studied individually.
"Two of the great mysteries in neuroscience are why do we sleep and what is sleep's function? Separating sleep need from wakefulness and identifying two different proteins involved in these steps represents a fundamental advance," he said.
If borne out by further research, this study could lead to new ways of assessing and possibly treating sleep disorders, perhaps by focusing more attention on the hours before bedtime because the quality of wakefulness has a profound effect on sleep, Dr. Yanagisawa said.
The experiment featured three groups of mice with virtually identical genes. The control group slept and woke at will and followed the usual mouse pattern of sleeping during the day and being awake at night. The two test groups were treated the same and had the same amount of sleep delay six hours but they were kept awake in different ways, said lead author Dr. Ayako Suzuki, a postdoctoral researcher who works in the laboratories of both Dr. Yanagisawa and Dr. Greene.
The first test group's sleep was delayed by a series of cage changes. Mice are intensely curious, so each cage change was followed by an hour spent vigorously exploring the new surroundings. This behavior would roughly correspond to teenagers voluntarily delaying bedtime with a new and stimulating event like a rock concert or video game.
Researchers kept the second group awake as gently as possible, usually by waving a hand in front of the cage or tapping it lightly whenever the mice appeared to be settling down to sleep. That test group would more resemble parents reluctantly staying awake awaiting a child's return from a concert.
Both test groups experienced the same amount of sleep deprivation, but their reactions to the different forms of alertness were striking, Dr. Yanagisawa said. In one test, the cage-changing group took longer to fall asleep than the gentle-handling group even though an analysis of their brain waves indicated equal amounts of sleep need in both test groups.
"The need to sleep is as high in the cage-changing group as in the gentle-handling group, but the cage-changers didn't feel sleepy at all. Their time to fall asleep was nearly the same as the free-sleeping, well-rested control group," he said.
The researchers identified two proteins that affected these responses, each linked to different aspects of sleep: phosphorylated dynamin 1 levels were linked to how long it took to fall asleep, while phosphorylated N-myc downstream regulated gene 2 protein levels tracked the amount of sleep deprivation and corresponded to the well-known brain-wave measure of sleep need, they report.
"The two situations are different biochemically, which is a novel finding," Dr. Yanagisawa said, adding, "These proteins are completely new to sleep research and have never before been linked to sleep need and wakefulness."
From an evolutionary perspective, an arousal mechanism that adapts to environmental stimuli is crucial because sleeping on a rigid schedule could be dangerous. "Animals, including humans, must be able to keep themselves at least temporarily alert, say during a natural disaster," he said.
###
Drs. Yanagisawa and Greene are both corresponding authors on the study, and both have dual appointments at the International Institute for Integrative Sleep Medicine, University of Tsukuba, Tsukuba, Japan. Former Associate Professor of Internal Medicine Dr. Christopher M. Sinton, now at the University of Arizona, was also involved in the study.
The study was funded by the Japan Society for the Promotion of Science through the Funding Program for World-Leading Innovative R&D on Science and Technology; the Perot Family Foundation; and the Department of Veterans Affairs.
About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including five who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 90,000 hospitalized patients and oversee more than 1.9 million outpatient visits a year.
This news release is available on our home page at http://www.utsouthwestern.edu/home/news/index.html
To automatically receive news releases from UT Southwestern via email, subscribe at http://www.utsouthwestern.edu/receivenews
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Quality of waking hours determines ease of falling sleepPublic release date: 17-Jun-2013 [ | E-mail | Share ]
Contact: Deborah Wormser deborah.wormser@utsouthwestern.edu 214-648-3404 UT Southwestern Medical Center
DALLAS June 17, 2013 The quality of wakefulness affects how quickly a mammal falls asleep, UT Southwestern Medical Center researchers report in a study that identifies two proteins never before linked to alertness and sleep-wake balance.
"This study supports the idea that subjective sleepiness is influenced by the quality of experiences right before bedtime. Are you reluctantly awake or excited to be awake?" said Dr. Masashi Yanagisawa, professor of molecular genetics and a Howard Hughes Medical Institute investigator at UT Southwestern. He is principal author of the study published online in May in the Proceedings of the National Academy of Sciences.
Co-author Dr. Robert Greene, UT Southwestern professor of psychiatry and a physician at the Dallas VA Medical Center, said the study is unique in showing that the need for sleep (called sleep homeostasis) can be separated from wakefulness both behaviorally and biochemically, meaning the two processes can now be studied individually.
"Two of the great mysteries in neuroscience are why do we sleep and what is sleep's function? Separating sleep need from wakefulness and identifying two different proteins involved in these steps represents a fundamental advance," he said.
If borne out by further research, this study could lead to new ways of assessing and possibly treating sleep disorders, perhaps by focusing more attention on the hours before bedtime because the quality of wakefulness has a profound effect on sleep, Dr. Yanagisawa said.
The experiment featured three groups of mice with virtually identical genes. The control group slept and woke at will and followed the usual mouse pattern of sleeping during the day and being awake at night. The two test groups were treated the same and had the same amount of sleep delay six hours but they were kept awake in different ways, said lead author Dr. Ayako Suzuki, a postdoctoral researcher who works in the laboratories of both Dr. Yanagisawa and Dr. Greene.
The first test group's sleep was delayed by a series of cage changes. Mice are intensely curious, so each cage change was followed by an hour spent vigorously exploring the new surroundings. This behavior would roughly correspond to teenagers voluntarily delaying bedtime with a new and stimulating event like a rock concert or video game.
Researchers kept the second group awake as gently as possible, usually by waving a hand in front of the cage or tapping it lightly whenever the mice appeared to be settling down to sleep. That test group would more resemble parents reluctantly staying awake awaiting a child's return from a concert.
Both test groups experienced the same amount of sleep deprivation, but their reactions to the different forms of alertness were striking, Dr. Yanagisawa said. In one test, the cage-changing group took longer to fall asleep than the gentle-handling group even though an analysis of their brain waves indicated equal amounts of sleep need in both test groups.
"The need to sleep is as high in the cage-changing group as in the gentle-handling group, but the cage-changers didn't feel sleepy at all. Their time to fall asleep was nearly the same as the free-sleeping, well-rested control group," he said.
The researchers identified two proteins that affected these responses, each linked to different aspects of sleep: phosphorylated dynamin 1 levels were linked to how long it took to fall asleep, while phosphorylated N-myc downstream regulated gene 2 protein levels tracked the amount of sleep deprivation and corresponded to the well-known brain-wave measure of sleep need, they report.
"The two situations are different biochemically, which is a novel finding," Dr. Yanagisawa said, adding, "These proteins are completely new to sleep research and have never before been linked to sleep need and wakefulness."
From an evolutionary perspective, an arousal mechanism that adapts to environmental stimuli is crucial because sleeping on a rigid schedule could be dangerous. "Animals, including humans, must be able to keep themselves at least temporarily alert, say during a natural disaster," he said.
###
Drs. Yanagisawa and Greene are both corresponding authors on the study, and both have dual appointments at the International Institute for Integrative Sleep Medicine, University of Tsukuba, Tsukuba, Japan. Former Associate Professor of Internal Medicine Dr. Christopher M. Sinton, now at the University of Arizona, was also involved in the study.
The study was funded by the Japan Society for the Promotion of Science through the Funding Program for World-Leading Innovative R&D on Science and Technology; the Perot Family Foundation; and the Department of Veterans Affairs.
About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including five who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 90,000 hospitalized patients and oversee more than 1.9 million outpatient visits a year.
This news release is available on our home page at http://www.utsouthwestern.edu/home/news/index.html
To automatically receive news releases from UT Southwestern via email, subscribe at http://www.utsouthwestern.edu/receivenews
[ | E-mail | Share ]
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Mobile virtualization startup BlueStacks only recently revealed the GamePop, its mobile home gaming console that offers all-you-can play gaming for a flat monthly fee, but it's already expanding the line. Today, the company is announcing GamePop Mini, a version of the GamePop that offers completely free hardware with a standard $6.99 monthly GamePop service subscription, with smaller hardware that's yours to keep after 12 months even if you decide to cancel your GamePop account.
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Public release date: 19-Jun-2013
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