LONDON (AP) — A forgetful British bridegroom who made a hoax bomb threat rather than admit he'd neglected to book the venue for his wedding was sentenced Tuesday to a year in jail.
Neil McArdle called Liverpool's St. George's Hall from a phone booth on his scheduled wedding day in April, claiming a bomb was due to go off in 45 minutes.
His fiancee, Amy Williams, was left standing in the street in her wedding gown while the building was evacuated.
McArdle, 36, was arrested the same day and admitted that he made the call because he had forgotten to fill out the paperwork for the wedding.
"He did say several times how embarrassed and ashamed he was and how sorry he was," said prosecutor Derek Jones.
A judge at Liverpool Crown Court in northwest England sentenced McArdle to 12 months in jail.
Judge Norman Wright said that McArdle had frightened staff at the venue with his hoax —which came days after the Boston marathon bombings — and let down his fiancee.
"She was getting ready, expecting you were going to be man and wife and a very solemn public event in her life and you knew that was not going to take place," the judge said.
"You did not say 'We need to talk.' You tried to weasel your way out by creating a bomb hoax so the wedding would not take place."
Defense lawyer Charles Lander said McArdle and Williams are still together.
"The fact that she stands with him speaks volumes for her, and I hope volumes for him," Lander said.
Contact: Marie Rippen lytal@med.usc.edu University of Southern California - Health Sciences
Without sweat, we would overheat and die. In a recent paper in the journal PLOS ONE, USC faculty member Krzysztof Kobielak and a team of researchers explored the ultimate origin of this sticky, stinky but vital substance sweat gland stem cells.
Kobielak and his team used a system to make all of the sweat gland cells in a mouse easy to spot: labeling them with green fluorescent protein (GFP), which is visible under ultraviolet light.
Over time, the GFP became dimmer as it was diluted among dividing sweat gland cells. After four weeks, the only cells that remained fluorescent were the ones that did not divide or divided very slowly a known property among stem cells of certain tissues, including the hair follicle and cornea. Therefore, these slow-dividing, fluorescent cells in the sweat gland's coiled lower region were likely also stem cells.
Then, the first author of this paper, graduate student Yvonne Leung, tested whether these fluorescent cells could do what stem cells do best differentiate into multiple cell types. To the researchers' surprise, these glowing cells generated not only sweat glands, but also hair follicles when placed in the skin of a mouse without GFP.
The researchers also determined that under certain conditions, the sweat gland stem cells could heal skin wounds and regenerate all layers of the epidermis.
"That was a big surprise for us that those very quiescent sweat gland stem cells maintain multilineage plasticity participating not only in their own regeneration, but also in the regeneration of hair follicles and skin after injury," said Kobielak, assistant professor of pathology at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC.
This offers exciting possibilities for developing future stem cell-based treatments for skin and sweat gland-related conditions, such as hyperhidrosis or hypohidrosis (excessive or insufficient sweating). It could also lay the foundation for creating fully functional skin containing both sweat glands and hair follicles for burn victims.
###
Additional co-authors on the study were Eve Kandyba, Yi-Bu Chen and Seth Ruffins from the Broad Center.
The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health (grant numbers R03-AR061028 and R01-AR061552).
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USC researcher learns how to break a sweat
PUBLIC RELEASE DATE:
23-Oct-2013
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Contact: Marie Rippen lytal@med.usc.edu University of Southern California - Health Sciences
Without sweat, we would overheat and die. In a recent paper in the journal PLOS ONE, USC faculty member Krzysztof Kobielak and a team of researchers explored the ultimate origin of this sticky, stinky but vital substance sweat gland stem cells.
Kobielak and his team used a system to make all of the sweat gland cells in a mouse easy to spot: labeling them with green fluorescent protein (GFP), which is visible under ultraviolet light.
Over time, the GFP became dimmer as it was diluted among dividing sweat gland cells. After four weeks, the only cells that remained fluorescent were the ones that did not divide or divided very slowly a known property among stem cells of certain tissues, including the hair follicle and cornea. Therefore, these slow-dividing, fluorescent cells in the sweat gland's coiled lower region were likely also stem cells.
Then, the first author of this paper, graduate student Yvonne Leung, tested whether these fluorescent cells could do what stem cells do best differentiate into multiple cell types. To the researchers' surprise, these glowing cells generated not only sweat glands, but also hair follicles when placed in the skin of a mouse without GFP.
The researchers also determined that under certain conditions, the sweat gland stem cells could heal skin wounds and regenerate all layers of the epidermis.
"That was a big surprise for us that those very quiescent sweat gland stem cells maintain multilineage plasticity participating not only in their own regeneration, but also in the regeneration of hair follicles and skin after injury," said Kobielak, assistant professor of pathology at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC.
This offers exciting possibilities for developing future stem cell-based treatments for skin and sweat gland-related conditions, such as hyperhidrosis or hypohidrosis (excessive or insufficient sweating). It could also lay the foundation for creating fully functional skin containing both sweat glands and hair follicles for burn victims.
###
Additional co-authors on the study were Eve Kandyba, Yi-Bu Chen and Seth Ruffins from the Broad Center.
The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health (grant numbers R03-AR061028 and R01-AR061552).
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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.
Months after Apple apologized to consumers in China, Korean rival Samsung is doing the same after the country's state media criticized the vendor for failing to fix glitches in several of its phone models.
"We welcome the scrutiny from the media," Samsung posted to its China website on Wednesday. "Due to problems with management that brought inconvenience to our customers, the company expresses its sincerest of apologies."
Earlier this week, the country's state-controlled China Central Television aired a 30-minute segment that put a spotlight on flaws found in Samsung phones. The affected models include handsets that are part of Samsung's Galaxy S3 and Note 2 product line.
According to CCTV's report, a software glitch in the phones can permanently damage a memory chip within the device's motherboard. This can cause the phone to frequently crash, from 20 to 30 times a day, according to one Galaxy S3 owner interviewed in the segment.
Samsung, however, refused to properly acknowledge the problem, CCTV claimed in its report. Instead, the company said the glitch could be fixed with a software update, rather than replacing the phone's hardware.
In response, Samsung issued an apology on Wednesday and said it would offer free repairs or replace phones with persistent problems. In addition, all affected phone models will receive another year of warranty protection, regardless of whether they showed any glitches.
The flaws in the phones could be unique to the Chinese market. Samsung said the problems stem from certain local third-party apps installed on the handsets. These unspecified apps cause the phone's application processor and memory to overrun when "waking up," and they will continue to contact servers even when in "sleep" mode.
"This issue can be prevented through a simple firmware over-the-air (FOTA) software update," the company said in an email.
Samsung is just the latest tech company to be scrutinized by China's state press. In March, Apple faced similar criticism over its warranty policies, which CCTV alleged treated U.S. customers more favorably than those in China.
Other foreign companies have also been targets. This past week, Starbucks has been defending itself after CCTV criticized the company for pricing its coffee products higher in China than in the United States.
China's state press will regularly scrutinize companies, both foreign and domestic, as a way to regulate them, according to analysts. Apple and Samsung are two of the largest smartphone vendors in the country.
Sometimes companies do stupid things to market their products. A silly commercial here. A ridiculous junket there. That's all fine and good, but sometimes companies overdo it, companies like Samsung who just got slapped with a $340,000 fine in Taiwan for illegally paying people to trash talk HTC in forums.
She knows what she likes! Kate Middleton accessorized her stunning cream-colored ensemble with her favorite pair of pumps at son Prince George's christening at St. James' Palace on Wednesday, Oct. 23. The 31-year-old Duchess of Cambridge carefully carried the heir to the British throne out of the Chapel Royal wearing a pair of off-white "Sledge" pumps by L.K. Bennett.
The British brand's stylish heels paired perfect with Middleton's Sarah Burton for Alexander McQueen dress and matching fascinator. Prince William's wife has been spotted wearing the same shoes many times before including cousin Zara Philips' wedding in 2011 and during the couple's North American tour that same year.
In March 2012, Middleton's go-to footwear choice became available at Nordstrom and norstrom.com for stateside shoppers. The 4-inch heels with a 1/2-inch platform retailed for $325.
Not only did the nude pumps match the rest of Middleton's ensemble perfectly on Wednesday, but they also coordinated with Prince George's christening gown. The adorable 3-month-old little boy wore a white satin and Honiton lace robe, which was a replica of the one created for Victoria, Princess Royal, back in 1841. The replica was commissioned by Queen Elizabeth II in 2008 in order to "preserve the original," which is now on display at the Museum of London.
AT&T won't be matching T-Mobile's offer of free wireless data for the iPad Air when the device debuts at the company's stores across the U.S. next month.
AT&T, the country's second-largest cellular carrier, said it will offer a $100 discount to customers who sign a two-year contract for tablet data service.
For customers who don't want to sign a contract, AT&T will offer recently announced plans costing between $5 for 250MB of data for one day and $50 for 5GB for one month. Those customers won't get the $100 discount.
Subscribers will also be able to add the iPad Air to an existing data plan for an additional $10 per month.
On Wednesday, T-Mobile said it will give tablet owners 200MB of data per month for no cost. Once that's used up, customers will have the option of paying $5 for 500MB of data for one day or $10 for 1GB of data for a week.
T-Mobile, which is the fourth-largest of the country's four major carriers, is aggressively courting customers with cheaper pricing plans. It recently said customers heading overseas would get unlimited 2G data at no additional cost.
A spokesman for AT&T declined to comment on T-Mobile's announcement.
Martyn Williams covers mobile telecoms, Silicon Valley and general technology breaking news for The IDG News Service. Follow Martyn on Twitter at @martyn_williams. Martyn's e-mail address is martyn_williams@idg.com
This undated image released Sunday Oct. 13, 2013, by the London Metropolitan Police, shows missing British girl Madeleine McCann before she went missing from a Portuguese holiday complex on Thursday, May 3, 2007. British police are making a fresh appeal Monday Oct. 14, 2013, with new information about their investigation, with e-fit computer images of men allegedly seen in the Portuguese town of Praia da Luz around the time of Madeleine McCann's disappearance. (AP Photo/London Metropolitan Police)
This undated image released Sunday Oct. 13, 2013, by the London Metropolitan Police, shows missing British girl Madeleine McCann before she went missing from a Portuguese holiday complex on Thursday, May 3, 2007. British police are making a fresh appeal Monday Oct. 14, 2013, with new information about their investigation, with e-fit computer images of men allegedly seen in the Portuguese town of Praia da Luz around the time of Madeleine McCann's disappearance. (AP Photo/London Metropolitan Police)
LISBON, Portugal (AP) — More than six years after British girl Madeleine McCann vanished from her bedroom during a family vacation in Portugal and five years after Portuguese police gave up trying to find her, authorities reopened the case Thursday, citing new evidence.
Madeleine's parents, Kate and Gerry McCann, had long campaigned from their home in central England for the Portuguese investigation to resume. In a statement Thursday, they said they were "very pleased" at the development.
"We hope that this will finally lead to (Madeleine) being found and to the discovery of whoever is responsible for this crime," Kate and Gerry McCann said. The couple, both doctors, continue to care for Madeleine's younger siblings, twins Sean and Amelie.
Madeleine went missing shortly before her fourth birthday. Her disappearance sparked global interest as pictures of her and her grieving parents beamed around the world. Her parents briefly met with Pope Benedict XVI in St. Peter's Square in June 2007, a month after Madeleine disappeared, and the pontiff held a picture of their daughter.
Then, in a stunning twist, Portuguese police briefly considered the parents suspects before they were cleared and returned home.
Portuguese police closed the case in 2008 because authorities had detected no crime. However, a team of detectives from Porto, in northern Portugal, began reviewing the evidence in March 2011. They had not been involved in the original investigation.
The public prosecutor's office in Lisbon said it decided to reopen the investigation after new leads emerged during the case review. It did not elaborate. The case is subject to Portugal's judicial secrecy law, which forbids the release of information about investigations.
British police, meanwhile, launched Operation Grange in 2011 to try to find out what happened to Madeleine. British detectives have been sifting through the case files in Portugal and say they also have identified new avenues of investigation. They say both the timeline and the version of events surrounding the girl's disappearance have changed significantly as new information has emerged.
Madeleine disappeared from her family's resort apartment in Praia da Luz, a coastal town 200 kilometers (120 miles) south of Lisbon, while her parents and their friends were eating dinner nearby.
British detectives say it's possible that Madeleine is still alive.
Ten days ago, British police released a computer-generated image of a person they were interested in questioning about the girl's disappearance. Police asked the public for help and worked with the BBC on a "Crimewatch" TV show, which drew more than 2,000 calls offering possible new leads.
Police said the images were based on information from witnesses who spotted a man in the Portuguese resort the day Madeleine was last seen.
In London, Scotland Yard said the reopened Portuguese investigation will run parallel to the British police's efforts, and British police will be traveling regularly to Portugal.
"Both sides of the investigation are at relatively early stages, with much work remaining to be done," Scotland Yard said in a statement. "This new momentum is encouraging, but we still have a way to go."
Experts say all those efforts are worthwhile.
Even after so many years, officials should "do whatever it takes" to ensure that grieving parents get closure, said Delphine Moralis of Missing Children Europe, an umbrella group of 28 non-governmental organizations in 19 European Union countries and Switzerland.
"It's essential to keep the ball rolling" on efforts to find missing children, Moralis said by telephone from Brussels.
She cited as examples the cathartic resolution provided in the cases involving Natascha Kampusch, who was found eight years after being kidnapped in 1998 in Austria, and three women rescued in May after being held captive in a Cleveland house for about a decade.
____
Gregory Katz in London contributed to this report.
The first trailer for next year’s sequel film X-Men: Days of Future Past won’t be released until October 29 but today director Bryan Singer gives us a quick taste of what’s to come. Singer posted a short 6 second teaser preview of the full trailer due out next week. Click the embed above to watch the teaser for the trailer to get your first taste of X-Men: Days of Future Past.
In recent years, we've watched with wonder as boring old yellow halogen car headlights have been replaced with futuristic, Tron-like LEDs. Now, that transition is about to take place on the city scale, as New York City prepares to replace its street lamps—all 250,000 of them—with LEDs.
You may not have been bitten by a radioactive spider, but thanks to Marvel's new Creativity Studio and its accompanying stylus, you can at least draw the person who did. The app and pen combo, which is the fruit of a collaboration between Marvel and eKids, is a tool for those young imaginations out ...
In it, astronaut Karen Nyberg, one of the six people now aboard the International Space Station, demonstrates how little effort it takes to move around in microgravity.
She takes a single strand of hair from her head, stretches it across a handrail and pushes off. You can watch as Nyberg then floats across the station. (And, yes, there's a connection to Sandra Bullock and the movie Gravity, as you'll see.)
The 44-year-old Nyberg, who has a doctorate in mechanical engineering from the University of Texas, flew on a Space Shuttle Discovery mission to the space station in 2008. Her second trip to space began on May 28. She's scheduled to return to Earth on Nov. 10.
Contact: David Bricker dmbricker@houstonmethodist.org 832-667-5811 Houston Methodist
HOUSTON -- ( Oct. 24, 2013 ) -- Just 13 days in space may be enough to cause profound changes in eye structure and gene expression, report researchers from Houston Methodist, NASA Johnson Space Center, and two other institutions in the October 2013 issue of Gravitational and Space Research.
The study, which looked at how low gravity and radiation and oxidative damage impacts mice, is the first to examine eye-related gene expression and cell behavior after spaceflight.
"We found many changes in the expression of genes that help cells cope with oxidative stress in the retina, possibly caused by radiation exposure," said Houston Methodist pathologist Patricia Chvez-Barrios, M.D., the study's principal investigator. "These changes were partially reversible upon return to Earth. We also saw optic nerve changes consistent with mechanical injury, but these changes did not resolve. And we saw changes in the expression of DNA damage repair genes and in apoptotic pathways, which help the body destroy cells that are irreparably damaged."
Since 2001, studies have shown astronauts are at increased risk of developing eye problems, like premature age-related macular degeneration. Experts suspect the cause is low gravity, heightened exposure to solar radiation, or a combination of the two.
In Nov. 2011, a NASA-sponsored Ophthalmology study of seven astronauts showed that all seven had experienced eye problems after spending at least six months in space. Doctors saw a flattening of the back of the eyeball, folding of the choroid (vascular tissue behind the retina), excess fluid around and presumed swelling of the optic nerve, or some combination of these.
High-energy radiation from the Sun can cause nasty, extremely damaging chemical reactions in cells, collectively called oxidative stress. Earth's atmosphere reflects or absorbs much of this radiation and is, ironically, a much better shield than the thick metal hulls of space shuttles and the International Space Station.
Damage to eyes isn't merely a long-term health issue for some astronauts back on Earth -- it could interfere with future missions in which any loss of focus or vision makes it difficult for humans to complete long missions, such as round-trip travel to Mars (12 to 16 months) or to the moons of Jupiter (about two years). If both radiation exposure and gravity loss are to blame, one solution to save astronauts' eyes might be a spacecraft with a more protective hull and inside, a spinning hamster wheel that simulates gravity similar to those envisioned by futurist author Arthur C. Clarke and realized in Stanley Kubrick's film, 2001: A Space Odyssey.
To determine the impact of radiation exposure on eyes, Chvez-Barrios and lead author Susana Zanello, Ph.D., a space life scientist at NASA Johnson Space Center, examined mouse retinal gene expression on the 1st, 5th, and 7th days following a 13-day trip aboard space shuttle Discovery (STS-133), measuring indicators of oxidative and cellular stress. The researchers also examined the eyes and surrounding tissues for broad changes in structure and shape that could relate to low gravity. They maintained two controls on Earth -- one in which mice were kept in the same general conditions as those aboard the shuttle, and one in which mice were maintained in typical, Earth-based care facilities.
Mice returning to Earth showed immediate evidence of oxidative stress in their retinas. But the increased expression of six oxidative stress response genes appeared to return to normal by the seventh day on Earth. An indicator of oxidative stress in the cornea was also elevated one day after mice had returned from orbit, but returned to near-normal levels by the seventh day.
"This suggests oxidative stress in the retina and lens are at least partially reversible under the circumstances of the experiment," Chvez-Barrios said. "This was after a relatively short time in orbit. We don't know if damage caused by longer periods of oxidative stress will be more severe. Only more studies with longer exposure times may help answer this question."
In the mice that had been to orbit, the researchers also found an increase in beta-amyloid in their optic nerves, and this increase persisted after seven days on Earth. Beta-amyloid is associated with traumatic brain injury in humans, and was not detected in the mice that remained on Earth. The researchers also found an increased number of glial cells -- cells that respond to injury -- in the optic nerves of mice that had been to space. It is not known whether the deposit of beta-amyloid and increased glial cells were caused by sustained low gravity or during the trips to or from Earth orbit. The researchers also found orbiting mice were expressing elevated levels of caspase-3 in the retinal pigment epithelium. Caspaces are enzyme precursors that help the immune system destroy damaged cells in a process called apoptosis. Abnormalities of the epithelium are associated with development of age-related macular degeneration.
Chvez-Barrios and colleagues found changes in cell and tissue shape and fluid balance similar to what has been reported from previous studies, specifically studies of astronauts who had experienced optic nerve changes.
The study described in the Gravitational and Space Research paper was small -- 18 mice in nine different condition groups. Space is limited aboard orbital missions.
"We say in the paper these results should be thought of as preliminary, like a pilot study," Chvez-Barrios said. "We think our results are plausible based on what we know from previous studies of structural changes and damage caused by oxidative stress and changes in the eyes of astronauts returning to Earth, but additional experiments are needed to confirm what we are reporting about gene expression, cellular behavior and mechanisms of damage."
Chvez-Barrios also said the strain of mice used in the study are known to be unusually sensitive to light, and that the severity of oxidative, cellular, and tissue problems her group saw would probably be milder in healthy human eyes.
###
Chvez-Barrios is the director of Houston Methodist's Ocular Pathology Research Laboratory and is a Weill Cornell Medical College professor of ophthalmology and of pathology and laboratory medicine. Zanello is affiliated with the Universities Space Research Association, a consortium founded by NASA and the National Academy of Sciences. Also contributing to the Gravitational and Space Research paper were Corey Theriot, Ph.D. (University of Texas Medical Branch at Galveston) and Claudia Prospero Ponce, M.D. (University of Arizona Health Sciences Center). Work was funded by the NASA Human Research Program.
To speak with Dr. Chvez-Barrios, please contact David Bricker, Houston Methodist, at 832-667-5811 or dmbricker@houstonmethodist.org.
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Just 2 weeks in orbit causes changes in eyes
PUBLIC RELEASE DATE:
24-Oct-2013
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Contact: David Bricker dmbricker@houstonmethodist.org 832-667-5811 Houston Methodist
HOUSTON -- ( Oct. 24, 2013 ) -- Just 13 days in space may be enough to cause profound changes in eye structure and gene expression, report researchers from Houston Methodist, NASA Johnson Space Center, and two other institutions in the October 2013 issue of Gravitational and Space Research.
The study, which looked at how low gravity and radiation and oxidative damage impacts mice, is the first to examine eye-related gene expression and cell behavior after spaceflight.
"We found many changes in the expression of genes that help cells cope with oxidative stress in the retina, possibly caused by radiation exposure," said Houston Methodist pathologist Patricia Chvez-Barrios, M.D., the study's principal investigator. "These changes were partially reversible upon return to Earth. We also saw optic nerve changes consistent with mechanical injury, but these changes did not resolve. And we saw changes in the expression of DNA damage repair genes and in apoptotic pathways, which help the body destroy cells that are irreparably damaged."
Since 2001, studies have shown astronauts are at increased risk of developing eye problems, like premature age-related macular degeneration. Experts suspect the cause is low gravity, heightened exposure to solar radiation, or a combination of the two.
In Nov. 2011, a NASA-sponsored Ophthalmology study of seven astronauts showed that all seven had experienced eye problems after spending at least six months in space. Doctors saw a flattening of the back of the eyeball, folding of the choroid (vascular tissue behind the retina), excess fluid around and presumed swelling of the optic nerve, or some combination of these.
High-energy radiation from the Sun can cause nasty, extremely damaging chemical reactions in cells, collectively called oxidative stress. Earth's atmosphere reflects or absorbs much of this radiation and is, ironically, a much better shield than the thick metal hulls of space shuttles and the International Space Station.
Damage to eyes isn't merely a long-term health issue for some astronauts back on Earth -- it could interfere with future missions in which any loss of focus or vision makes it difficult for humans to complete long missions, such as round-trip travel to Mars (12 to 16 months) or to the moons of Jupiter (about two years). If both radiation exposure and gravity loss are to blame, one solution to save astronauts' eyes might be a spacecraft with a more protective hull and inside, a spinning hamster wheel that simulates gravity similar to those envisioned by futurist author Arthur C. Clarke and realized in Stanley Kubrick's film, 2001: A Space Odyssey.
To determine the impact of radiation exposure on eyes, Chvez-Barrios and lead author Susana Zanello, Ph.D., a space life scientist at NASA Johnson Space Center, examined mouse retinal gene expression on the 1st, 5th, and 7th days following a 13-day trip aboard space shuttle Discovery (STS-133), measuring indicators of oxidative and cellular stress. The researchers also examined the eyes and surrounding tissues for broad changes in structure and shape that could relate to low gravity. They maintained two controls on Earth -- one in which mice were kept in the same general conditions as those aboard the shuttle, and one in which mice were maintained in typical, Earth-based care facilities.
Mice returning to Earth showed immediate evidence of oxidative stress in their retinas. But the increased expression of six oxidative stress response genes appeared to return to normal by the seventh day on Earth. An indicator of oxidative stress in the cornea was also elevated one day after mice had returned from orbit, but returned to near-normal levels by the seventh day.
"This suggests oxidative stress in the retina and lens are at least partially reversible under the circumstances of the experiment," Chvez-Barrios said. "This was after a relatively short time in orbit. We don't know if damage caused by longer periods of oxidative stress will be more severe. Only more studies with longer exposure times may help answer this question."
In the mice that had been to orbit, the researchers also found an increase in beta-amyloid in their optic nerves, and this increase persisted after seven days on Earth. Beta-amyloid is associated with traumatic brain injury in humans, and was not detected in the mice that remained on Earth. The researchers also found an increased number of glial cells -- cells that respond to injury -- in the optic nerves of mice that had been to space. It is not known whether the deposit of beta-amyloid and increased glial cells were caused by sustained low gravity or during the trips to or from Earth orbit. The researchers also found orbiting mice were expressing elevated levels of caspase-3 in the retinal pigment epithelium. Caspaces are enzyme precursors that help the immune system destroy damaged cells in a process called apoptosis. Abnormalities of the epithelium are associated with development of age-related macular degeneration.
Chvez-Barrios and colleagues found changes in cell and tissue shape and fluid balance similar to what has been reported from previous studies, specifically studies of astronauts who had experienced optic nerve changes.
The study described in the Gravitational and Space Research paper was small -- 18 mice in nine different condition groups. Space is limited aboard orbital missions.
"We say in the paper these results should be thought of as preliminary, like a pilot study," Chvez-Barrios said. "We think our results are plausible based on what we know from previous studies of structural changes and damage caused by oxidative stress and changes in the eyes of astronauts returning to Earth, but additional experiments are needed to confirm what we are reporting about gene expression, cellular behavior and mechanisms of damage."
Chvez-Barrios also said the strain of mice used in the study are known to be unusually sensitive to light, and that the severity of oxidative, cellular, and tissue problems her group saw would probably be milder in healthy human eyes.
###
Chvez-Barrios is the director of Houston Methodist's Ocular Pathology Research Laboratory and is a Weill Cornell Medical College professor of ophthalmology and of pathology and laboratory medicine. Zanello is affiliated with the Universities Space Research Association, a consortium founded by NASA and the National Academy of Sciences. Also contributing to the Gravitational and Space Research paper were Corey Theriot, Ph.D. (University of Texas Medical Branch at Galveston) and Claudia Prospero Ponce, M.D. (University of Arizona Health Sciences Center). Work was funded by the NASA Human Research Program.
To speak with Dr. Chvez-Barrios, please contact David Bricker, Houston Methodist, at 832-667-5811 or dmbricker@houstonmethodist.org.
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The Wolverine 2 clawed its way to the top of the Chinese box office charts this week, taking $18.17 million (111.2 million yuan) in its first week despite bowing weeks after it originally premiered in Hong Kong and other overseas markets.
The China haul helped to push Twentieth Century Fox International's global ticket sales for 2013 past the $2 billion mark.
The movie opened in July in most other markets. Normally, a late release in China means viewers will have already accessed the film via pirate DVDs and illegal downloads, hurting ticket sales.
However, the movie's spectacular action scenes and strong performance by Hugh Jackman seem to have successfully lured the local fanboy audiences into China's cinemas. Jackman came to China for the premiere, and made a big splash in local press.
There were 2.96 million admissions for the film in the first week.
According to data from Beijing-based Entgroup, for the week of Oct. 14-20, Wolverine beat out Donnie Yen's Shenzhen-set cop movie Special ID, which took $10.9 million (66.52 million yuan), while LouisLeterrier's Now You See Me continued its respectable if unspectacular run, taking in another $7.95 million to bring its total to $17.91 million.
Love Will Tear Us Apart appeared to pick up pace during the week, taking in $6.36 million. The movie features martial arts specialist Feng Shaofeng and Ni Ni, best known internationally for her role in ZhangYimou's Flowers of War.
Meanwhile, Tsui Hark's Young Detective Dee: Rise of the Sea Dragon continued to edge closer to the $100 million box office mark. The fantasy prequel took $5.92 million during the week, bringing its cumulative total in the first 23 days on release to $94.7 million.
The latest episode of "Weird and Bitchin'" takes the Gnu and Lib Tech Snowboard teams to High Cascade for some camp-hammers and summer fun. The whole gang gathers, including Ted Borland, Max Warbington, Forest Bailey, Jason Robinson, Jesse and Pica Burtner, Brandon Reis, Cameron Gorby, and many more. Remember some of these tricks when you're knee-deep in powder and you'll be in the perfect mindset for some creative freeriding.
KUALA LUMPUR, Malaysia (AP) — A Malaysian university is facing public criticism for awarding an honorary doctorate in economics to North Korean leader Kim Jong Un.
The privately run HELP University said a "simple ceremony" to mark the conferment was held in early October at North Korea's embassy in Kuala Lumpur.
The event initially went unnoticed in this Southeast Asian nation but was reported briefly by North Korea's official news agency, KCNA. It attracted criticism on social networks in Malaysia this week after the U.S.-based Foreign Policy magazine posted a blog article that expressed surprise about the decision.
The university's president, Paul Chan, said in an undated statement released this week that the decision was about "building a bridge to reach the people."
Chan's office said he was not available for further comments Thursday.
Contact: Dr. Andreas Battenberg andreas.battenberg@tum.de 49-892-891-0510 Technische Universitaet Muenchen
Activation mechanism of a protective protein in the ocular lens resolved
This news release is available in German.
The lens of the human eye is made up of a highly concentrated protein solution that imparts the eye its high refractive power. Yet, despite this high protein content the ocular lens must remain clear and transparent. To this end ocular lens cells have developed a remarkable strategy: They have thrown overboard the complex machinery present in all other cells of the human body for building up and breaking down proteins. Instead, lens proteins are created only once in a lifetime during embryonic development. They are as old as the organism itself. To make them last a lifetime, the proteins are kept permanently in a dissolved state. If they clump together, the lens clouds over and the patient gets cataracts.
Alternative to surgery
To date, this condition could only be treated surgically by replacing the clouded lens with an artificial one. However, if the precise mechanism by which lens proteins are kept in a dissolved state were understood, it would open up new avenues for treatment. So, how does the cell manage to keep the proteins soluble for so long? The magic lies in two proteins, αA-crystallin and its relative, αB-crystallin. They are the best-known representatives of the class of so-called small heat shock proteins. They play an important role in all human cells, since they prevent other proteins from turning into useless clumps when subjected to strong heat or cell stress.
What exactly these protective proteins look like and how they act remained shrouded in mystery for a long time, in spite of intensive research. "The great challenge in the analysis of these two crystallin types lies in their inordinate variety," explains Johannes Buchner, professor for biotechnology at the Technische Universitaet Muenchen. "These proteins exist as a mixture of very different forms, each comprising a variable number of subunits. This makes it very difficult to distinguish the individual structures from one another."
Molecular switch
In 2009, in very close collaboration with Sevil Weinkauf, professor for electron microscopy at the Technische Universitaet Muenchen, the first part of the αB-crystallin puzzle fell into place. The team successfully deciphered the molecular structure of the most important form of this versatile protein a molecule comprising 24 subunits. Under normal conditions, i.e. when the cell is not exposed to stress, this complex is the most common variant. However, it is merely an idle form that contributes little to the prevention of clumping in other proteins. It was clear that there must be another molecular switch that triggers the protective protein.
It is this trigger mechanism that the team headed by Buchner and Weinkauf uncovered now. When a cell is exposed to stress, for instance when subjected to heat, phosphate groups are attached to a specific region of the protein. The negative charges of these phosphates break the links between the subunits and the large complexes consequently disintegrate into numerous smaller ones of only six or twelve subunits each. As a result of this breakup, the regions at the ends of the complexes become more flexible allowing the molecules to dock up with different partners, thereby preventing them from clumping the protective protein is now active.
Interdisciplinary cooperation
The success of the scientists can be traced back above all to the interdisciplinary combination of biochemical and electron-microscopic methodologies. Aligning the information from the two-dimensional protein disintegration images with the manifold three-dimensional structures of αB-crystallin proved particularly difficult. "Imagine you only have a few pictures of a coffee cup's shadow cast and want to infer the shape of the cup from that," Weinkauf explains to illustrate the problem. "Now, if you think that sounds difficult, try to imagine you have not just a single cup, but a cupboard full of china that you want to deduce from the shadow casts. It is precisely this daunting challenge that we met for αB-crystallin."
The newly acquired insights into the αB-crystallin mode of action form a solid footing for new therapeutic approaches. For instance, medication to treat cataracts could be developed: it would trigger the αB-crystallin activation mechanism to clear up clouded ocular lenses. But αB-crystallin also plays a role in other tissue cells. In cancer cells, for example, it is overly active and interferes with the so-called programmed cell death. In this case new medication would aim at inhibiting the protein.
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The work has been funded by German Research Foundation (Cluster of Excellence Center for Integrated Protein Science Munich (CIPSM) and SFB 1035).
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A protein safeguards against cataracts
PUBLIC RELEASE DATE:
23-Oct-2013
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Contact: Dr. Andreas Battenberg andreas.battenberg@tum.de 49-892-891-0510 Technische Universitaet Muenchen
Activation mechanism of a protective protein in the ocular lens resolved
This news release is available in German.
The lens of the human eye is made up of a highly concentrated protein solution that imparts the eye its high refractive power. Yet, despite this high protein content the ocular lens must remain clear and transparent. To this end ocular lens cells have developed a remarkable strategy: They have thrown overboard the complex machinery present in all other cells of the human body for building up and breaking down proteins. Instead, lens proteins are created only once in a lifetime during embryonic development. They are as old as the organism itself. To make them last a lifetime, the proteins are kept permanently in a dissolved state. If they clump together, the lens clouds over and the patient gets cataracts.
Alternative to surgery
To date, this condition could only be treated surgically by replacing the clouded lens with an artificial one. However, if the precise mechanism by which lens proteins are kept in a dissolved state were understood, it would open up new avenues for treatment. So, how does the cell manage to keep the proteins soluble for so long? The magic lies in two proteins, αA-crystallin and its relative, αB-crystallin. They are the best-known representatives of the class of so-called small heat shock proteins. They play an important role in all human cells, since they prevent other proteins from turning into useless clumps when subjected to strong heat or cell stress.
What exactly these protective proteins look like and how they act remained shrouded in mystery for a long time, in spite of intensive research. "The great challenge in the analysis of these two crystallin types lies in their inordinate variety," explains Johannes Buchner, professor for biotechnology at the Technische Universitaet Muenchen. "These proteins exist as a mixture of very different forms, each comprising a variable number of subunits. This makes it very difficult to distinguish the individual structures from one another."
Molecular switch
In 2009, in very close collaboration with Sevil Weinkauf, professor for electron microscopy at the Technische Universitaet Muenchen, the first part of the αB-crystallin puzzle fell into place. The team successfully deciphered the molecular structure of the most important form of this versatile protein a molecule comprising 24 subunits. Under normal conditions, i.e. when the cell is not exposed to stress, this complex is the most common variant. However, it is merely an idle form that contributes little to the prevention of clumping in other proteins. It was clear that there must be another molecular switch that triggers the protective protein.
It is this trigger mechanism that the team headed by Buchner and Weinkauf uncovered now. When a cell is exposed to stress, for instance when subjected to heat, phosphate groups are attached to a specific region of the protein. The negative charges of these phosphates break the links between the subunits and the large complexes consequently disintegrate into numerous smaller ones of only six or twelve subunits each. As a result of this breakup, the regions at the ends of the complexes become more flexible allowing the molecules to dock up with different partners, thereby preventing them from clumping the protective protein is now active.
Interdisciplinary cooperation
The success of the scientists can be traced back above all to the interdisciplinary combination of biochemical and electron-microscopic methodologies. Aligning the information from the two-dimensional protein disintegration images with the manifold three-dimensional structures of αB-crystallin proved particularly difficult. "Imagine you only have a few pictures of a coffee cup's shadow cast and want to infer the shape of the cup from that," Weinkauf explains to illustrate the problem. "Now, if you think that sounds difficult, try to imagine you have not just a single cup, but a cupboard full of china that you want to deduce from the shadow casts. It is precisely this daunting challenge that we met for αB-crystallin."
The newly acquired insights into the αB-crystallin mode of action form a solid footing for new therapeutic approaches. For instance, medication to treat cataracts could be developed: it would trigger the αB-crystallin activation mechanism to clear up clouded ocular lenses. But αB-crystallin also plays a role in other tissue cells. In cancer cells, for example, it is overly active and interferes with the so-called programmed cell death. In this case new medication would aim at inhibiting the protein.
###
The work has been funded by German Research Foundation (Cluster of Excellence Center for Integrated Protein Science Munich (CIPSM) and SFB 1035).
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