McDreamy part of all-American team at Le Mans ? Artesia News

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.??

___

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.?

___

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.?

This entry was posted on June 19, 2013, 11:36 am and is filed under Entertainment. You can follow any responses to this entry through RSS 2.0. Both comments and pings are currently closed.

Source: http://www.artesianews.com/2013/06/19/ap-news/entertainment-ap-news/mcdreamy-part-of-all-american-team-at-le-mans/

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Restoring appropriate movement to immune cells may save seriously burned patients

Public release date: 19-Jun-2013
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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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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.

Public 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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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-06/mgh-ram061913.php

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White House says they have nearly completed executive actions on gun control (Washington Bureau)

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Rett Syndrome protein surrenders some of its secrets

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 Nature Neuroscience 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.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/health_medicine/genes/~3/ohn4IuWHhU8/130617122506.htm

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In Cambodia's jungles, a lost world is found (+ video)

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.

Source: http://rss.csmonitor.com/~r/feeds/science/~3/B3ccJe-9oA4/In-Cambodia-s-jungles-a-lost-world-is-found-video

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Mayo Clinic: Rotavirus vaccine given to newborns in Africa is effective

Public release date: 17-Jun-2013
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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.

Public 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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Source: http://www.eurekalert.org/pub_releases/2013-06/mc-mcr061713.php

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Quality of waking hours determines ease of falling sleep

Public release date: 17-Jun-2013
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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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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.

Public 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 ]

?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-06/usmc-qow061713.php

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