SAVAR, Bangladesh (AP) ? The heat in the rubble was sweltering. It closed in on his body like the darkness around him, making it hard to breathe. Working by the faint glow of a flashlight, he slithered through the broken concrete and spotted a beautiful young woman, her crushed arm pinned beneath a pillar. She was dying, and the only way to get her out was to amputate.
But Saiful Islam Nasar had no training, and almost no equipment. He's a mechanical engineer who just days earlier rushed hundreds kilometers from his hometown in southern Bangladesh when he heard the Rana Plaza factory building had collapsed and hundreds, perhaps thousands, of garment workers were trapped.
He also understood that maimed women can be cast from their homes.
"I asked her, 'Sister, are you married?' She said 'Yes.' I asked her, 'If I cut off your arm, will your husband take you again?' She said, 'My husband loves me very much.' And then I started to cut," he said.
He had brought a syringe loaded with pain-killer ? his father was a village medic, and had taught him how to give injections ? and he cut through her arm with a small surgical blade. It was easier than he expected because the arm had already been so badly damaged.
He pointed at fading specks of blood staining his vest and pants. He began to cry.
"There was no alternative," he said.
Bangladesh is well-versed in tragedy, a country where floods, ferry sinkings, fires and cyclones strike with cruel regularity. But with state services riven by dysfunction and corruption, often the only hope is the person beside you.
It is a country that makes heroes out of everyday citizens.
Many of the first responders at Rana Plaza were men like Nasar ? neighborhood residents, fellow garment workers, relatives of the missing and charity workers ? and they repeatedly took some of the most dangerous work. Using little more than hammers, hacksaws and their bare hands, they crawled into tiny holes in the wreckage, breaking through concrete and steel bars and working around the clock to drag out the victims.
They knew they were risking their lives.
Hemaet Ali, a 50-year-old construction worker who came to volunteer, told the people around him that his identity card, with his home address, was in his shirt pocket.
"If I die inside, please make sure that my body reaches my family," he told them.
Nasar came to Savar with 50 other men from the small volunteer organization he runs, Sunte Ki Pao. Normally, they assist people who have been in traffic accidents, offering basic first aid, securing valuables and contacting relatives. During seasonal floods, they help however they can when the waters rush into town. Nothing had prepared them to work the front line of their country's largest industrial accident.
"It was beyond imagination," he said Monday, six days after the collapse, when the search for survivors had given way to the search for bodies, and heavy equipment had replaced the rescuers.
Thin and lanky, the 24-year-old was well-suited for crawling through the tight tunnels he cut. At first, he had only his mobile phone to light the tiny spaces. He could see shattered chairs and tables. Sewing machines and fabric. And the battered bodies of the men and women who were crushed when the walls and ceilings came crashing down.
"I could just fit my shoulders in," he said. "I often felt like I would die and I would call out to my God."
The rescues, each of which could take many hours, were exhausting, both physically and emotionally.
"We would shout 'Is there anybody here? Please make a sound.' Sometimes you would hear an 'Oooh, oooh' and you knew someone was there," he said.
Over six days, he pulled six people out alive, and removed dozens of bodies. He would work until exhaustion set in and then attempt to sleep ? the first night on the roof of the collapsed building, the next two in a nearby field. Even now that he has moved into a tent, rest does not come easy.
"The images of the bodies flash in my mind," he said.
Eating also has been a problem.
"I have lost my taste," he explained. "I just keep smelling the smell of dead bodies."
The sickly sweet waft of rot from the building was ever present, and rescuers routinely sprayed cheap floral air freshener around the site in a futile attempt to control it.
Not all of the rescue workers at Rana Plaza were untrained. The government sent some 1,000 soldiers and firefighters to the site. But from all appearances, the majority of the rescuers who went into the rubble were volunteers. Altogether, some 2,500 people were brought out alive from the wreckage. The death toll stands at 386, but will surely climb as the largest pieces of rubble are moved.
The military, which oversaw much of the rescue efforts, dismisses the notion that they let volunteers take the lead.
"I have not heard of rescuing so many people in recent history anywhere in the world in case of such disaster," said Maj. Gen. Chowdhury Hasan Suhrawardy, a top military officer in the Savar area. "What we have done is excellent."
But it is clear that volunteers once again carried more than their share of the country's burden.
Sayed Shohel Harman, an unpaid community volunteer for the fire department, found a survivor whose arm was pinned under a concrete slab. The man begged Harman to give him a knife so he could cut off his own arm and free himself. Harman refused, saying he would go and get help.
"The doctors said it was too risky for them to go inside," Harman said. "They told me to go back and try to drag him out."
When he returned, the man was there, but his arm was gone. Another volunteer had given the man a knife and he had cut through his own flesh and crushed bones.
"I just sat down after seeing that," Harman said. "It was horrible."
Nasar said he will soon return to his hometown, where he will comfort his worried mother and look for a new job. He was forced to resign from his to join in the rescue. But most of all, he will think of the beautiful young woman whose name he never heard and whose fate he never learned.
"I pray to Allah that she has been saved, is alive and can return to her husband."
Metasploit software developer Joe Vennix has detailed a vulnerability in Safari?s webarchive file format along with how it can be exploited. The post on Rapid7 indicates that after being reported to Apple back in February, the bug was closed last month with a status of ?wontfix?, indicating that Apple has no plans to address the bug. So what is it and why is that?
In Safari, if you go to save a web page, one of the options for the format to use is Web Archive. In many browsers when you save a web page locally, it only consists of the HTML source code itself. This means that any images, embedded videos, linked stylesheets or JavaScript will be lost. When you open a copy of the locally saved page, it will be missing all of the additional content, often not showing much more than text from the page and broken images. Safari?s Web Archive format works by not only saving the HTML of the page, but any linked content. When you open a Web Archive file, you will see the page as it would have originally appeared on the Internet, with all images, styling, and linked content preserved.
The bug found in Safari?s security model is a lack of restriction on what data can be accessed by the files in the web archive. Normally a page like Apple.com would be restricted to reading cookies that belonged to only the apple.com domain. It could not read cookies from another domain, such as Gmail.com. This is critical because if all of your cookies were readable by any website, it would be trivial for a malicious site to send your cookies back to an attacker, who could then log in to your accounts on any number of websites. In the case of Safari?s web archives, it?s possible for a malicious web archive to not only access content storied by another site, but potentially any file on the victim?s computer.
With such a serious sounding vulnerability, you might be wondering why Apple wouldn?t want to fix it? The answer seems to be that an exploit like this cannot be accomplished without user action. You couldn?t actually be affected by this unless you were to download and open a malicious .webarchive file. Users can avoid being attacked by employing the age old advice of not opening strange files from the Internet (or anywhere for that matter). That said, some people still do and surely will continue to do so. Given the potential impact of a vulnerability like this on users, it certainly seems like something Apple would want to fix at some point.
If you?re interesting in understanding more about how this bug works or can be exploited, Joe?s blog post covers several real world examples of how it could be used.
Barack Obama is a controversial president, but we hope everyone can agree on one thing: The guy can land a punchline. At Saturday's annual White House Correspondents Dinner, the president gave a scathingly funny speech, lampooning himself, the press, Congress, and a few A-list celebrities. If he wasn't funnier than the evening's host Conan O'Brien, he definitely gave him a run for his money! Check out Obama's 7 best zingers, including shots at Jay-Z and Taylor Swift, below.
When Mary Thate and her now ex-husband divorced, she had no idea where her children would go to college. As a couple, they had put aside money for their three children's college education. Early on in the divorce process, they decided to stay in touch and save individually for the collegiate needs of their children.
Saving for college after a divorce is a process of communication. However, the communication is easier if a framework is set up during the divorce settlement, says Mike Fitzgerald, chairman of the College Savings Plans Network.
The framework could include freezing the current 529 plan account (a tax-advantaged investment account used for higher education), splitting 529 plan accounts when needed and deciding what proportion each parent will pay toward their children's education.
[Learn more ways to save for college.]
First, freezing a 529 plan account means no more deposits are made to the account. The money already in it can only be used toward education for the child designated, Fitzgerald says.
Under normal circumstances, an account owner could withdraw money at any time for any reason - a car, a vacation or another purpose - though they would have to pay a tax penalty for non-education spending. Freezing the account prevents former spouses from doing so during what is often a very tense process, he says. Freezing the account would also prevent a parent from using account funds to pay for the education of a child from a new marriage.
The other issue that should be discussed or decreed is what to do with money left over after the child completes his or her education, says Ernest Almonte, a certified public accountant. Possible options include one of the parents using funds to return to school or a sibling using leftover funds, he says.
Once the account is frozen, there are still investment decisions, Fitzgerald says, which are made by the account owner. The legal owner could decide to change the investment strategy to a riskier, more stock-based one or take a more conservative route with a greater percentage of short-term bonds and money market and savings accounts, he says.
[Examine your college savings strategy.]
There is a solution to the problem of one parent having full investment control. "The judge can order splitting an existing 529 plan, and the state has to abide by it," Fitzgerald says.
That means each half of the plan would be set up as a new account and owned by one spouse, who would make investment decisions on his or her half of the account. If a 529 plan had $5,000 in assets, each spouse would be responsible for a new account containing $2,500.
"That money could eventually be used by each parent to help pay for his or her share of the college costs as outlined in the divorce settlement," Fitzgerald says. The court can mandate the percentage each parent will pay toward the child's education, he says. However, each parent will make their own decisions as far as how and where the savings is held or invested.
Thate set a goal of saving $4,000 a year, which she deposits into Idaho's Ideal College Savings Program 529 plan. Her new husband also deposits $4,000, for a total of $8,000. Her ex-husband makes his own decisions about how he will save.
[Avoid the college savings mistakes parents make.]
Each child's education had a different price tag, and that cost wasn't known until college neared. It varied per child based on scholarships awarded, the tuition at time of graduation and high school grades, Thate says. Their oldest won a scholarship and the former couple adjusted what each needed to contribute toward their daughter's education accordingly.
They have an open discussion with each child and say they will pay the full cost of tuition if the child chooses which college to attend from among a set list of schools, she says. If the child chooses a more expensive school, she and her ex-husband will pay a certain amount.
Parents have to keep working together and be in agreement when it comes to education, Thate says. She and her ex-husband managed to get two children started in college by working together.
Trying to fund your education? Get tips and more in the U.S. News Paying for College center.
Apr. 28, 2013 ? From which ancestors have turtles evolved? How did they get their shell? New data provided by the Joint International Turtle Genome Consortium, led by researchers from RIKEN in Japan, BGI in China, and the Wellcome Trust Sanger Institute in the UK provides evidence that turtles are not primitive reptiles but belong to a sister group of birds and crocodiles. The work also sheds light on the evolution of the turtle's intriguing morphology and reveals that the turtle's shell evolved by recruiting genetic information encoding for the limbs.
Turtles are often described as evolutionary monsters, with a unique body plan and a shell that is considered to be one of the most intriguing structures in the animal kingdom.
"Turtles are interesting because they offer an exceptional case to understand the big evolutionary changes that occurred in vertebrate history," explains Dr. Naoki Irie, from the RIKEN Center for Developmental Biology, who led the study.
Using next-generation DNA sequencers, the researchers from 9 international institutions have decoded the genome of the green sea turtle and Chinese soft-shell turtle and studied the expression of genetic information in the developing turtle.
Their results published in Nature Genetics show that turtles are not primitive reptiles as previously thought, but are related to the group comprising birds and crocodilians, which also includes extinct dinosaurs. Based on genomic information, the researchers predict that turtles must have split from this group around 250 million years ago, during one of the largest extinction events ever to take place on this planet.
"We expect that this research will motivate further work to elucidate the possible causal connection between these events," says Dr. Irie.
The study also reveals that despite their unique anatomy, turtles follow the basic embryonic pattern during development. Rather than developing directly into a turtle-specific body shape with a shell, they first establish the vertebrates' basic body plan and then enter a turtle-specific development phase. During this late specialization phase, the group found traces of limb-related gene expression in the embryonic shell, which indicates that the turtle shell evolved by recruiting part of the genetic program used for the limbs.
"The work not only provides insight into how turtles evolved, but also gives hints as to how the vertebrate developmental programs can be changed to produce major evolutionary novelties." explains Dr. Irie.
Another unexpected finding of the study was that turtles possess a large number of olfactory receptors and must therefore have the ability to smell a wide variety of substances. The researchers identified more than 1000 olfactory receptors in the soft-shell turtle, which is one of the largest numbers ever to be found in a non-mammalian vertebrate.
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The above story is reprinted from materials provided by RIKEN, via AlphaGalileo.
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Journal Reference:
Zhuo Wang, Juan Pascual-Anaya, Amonida Zadissa, Wenqi Li, Yoshihito Niimura, Zhiyong Huang, Chunyi Li, Simon White, Zhiqiang Xiong, Dongming Fang, Bo Wang, Yao Ming, Yan Chen, Yuan Zheng, Shigehiro Kuraku, Miguel Pignatelli, Javier Herrero, Kathryn Beal, Masafumi Nozawa, Qiye Li, Juan Wang, Hongyan Zhang, Lili Yu, Shuji Shigenobu, Junyi Wang, Jiannan Liu, Paul Flicek, Steve Searle, Jun Wang, Shigeru Kuratani, Ye Yin, Bronwen Aken, Guojie Zhang, Naoki Irie. The draft genomes of soft-shell turtle and green sea turtle yield insights into the development and evolution of the turtle-specific body plan. Nature Genetics, 2013; DOI: 10.1038/ng.2615
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Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
Bill Gates triggered a media uproar with a 'disrespectful' one-handed shake upon meeting the new South Korean president. What should Bill Gates have done?
By David Clark Scott,?Staff writer / April 23, 2013
South Korean President Park Geun-hye, left, shakes hands with Microsoft founder Bill Gates before their meeting at the presidential Blue House in Seoul, South Korea, Monday, April 22, 2013. Gates has his left hand in his pocket.
(AP Photo/Lee Jin-man
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Global etiquette can be tricky. Just ask Bill Gates.
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The Microsoft chairman (who is also co-chair of one of the world's biggest charitable organizations)? is no stranger to international travel or meeting heads of state. But, on Monday, when he shook hands with South Korea's first female president, Park Geun-hye, Gates made a serious faux pas, which resulted in a cultural kerfuffle.
Gates shook her hand with just one hand. In South Korea, and much of Asia, that's only done in casual settings, with good friends. To top it off, Gates had his left hand in his pocket, signaling his superiority.
"How rude!" was the response in South Korea media. Almost every news organizations carried the photo on the front page.
The proper way to show respect would have been for Gates to clasp the South Korean leader's hand with both of his hands.
Was Gates sending a blunt signal of political disapproval to the new government leader? Was Gates ignorant of Asian etiquette??
There was enough media buzz that the South Korean president's office felt it needed to issue an official statement on the matter: "Bill Gates took a similar pose for a picture when he met former President Lee Myung-bak five years ago. Just think of it as an American style of greeting," according to Dong.com, the website of Dong-a Ilbo, a leading newspaper in Korea with daily circulation of more than 1.2 million.?
[Editor's note: Since publication, the president's office contacted The Christian Science Monitor to say that it had issued no official statement about the Bill Gates handshake.]
The first part of that statement is true. In fact, the Atlantic Wire compiled a series of Bill Gates One-Hand Shaking, One-Hand-in-Pocket photos from previous meetings with other world dignitaries, including UN Secretary General Ban Ki-moon, China's President Xi Jinping, and French President Nicolas Sarkozy.
Apparently Gates is consistently casual about his handshakes ? with whomever he meets.
While the one-handed Western handshake has become more common in Asia, business etiquette also suggests that one never looks directly in the eyes of the person you're meeting. An exception to that rule is the Philippines. And in many places, a bow is also part of the greeting.
In Cambodia, for example, if you meet a prominent businessman, the proper way to show respect is to place your palms together at chest height and bow at your waist.
There's also a culturally correct way to exchange business cards in Asia, too. Each card should be in English on one side, and the recipient's native language on the other. You present your card with both hands, native language side up and readable to the recipient. When you receive a card, it's also a two-handed affair. Look at it, thank the person, and put in gently in a coat pocket.
For more tips on global etiquette, check out The Christian Science Monitor's quiz on the globally savvy traveler.
JUNEAU, Alaska (AP) -- Build-out of a large-scale mine near the headwaters of a world-class salmon fishery in Alaska could wipe out as many as 90 miles of streams and alter flows in other waterways, the U.S. Environmental Protection Agency said in a revised assessment released Friday.
The report said mining activity would claim at least 24 miles of streams in the Bristol Bay region, based on the scenarios evaluated, with the loss of wetlands ranging from 1,200 to 4,800 acres.
The EPA focused on the Pebble deposit and took into account information related to the proposed Pebble Mine but also noted the potential for multiple mines in the region, given the resource base, which would lead to further elimination or blocking of streams and wetland losses.
EPA initiated the review process in response to concerns raised by tribes and others about the impact large-scale mining could have on Bristol Bay fisheries.
Pebble Limited Partnership, the group behind the proposed Pebble Mine, has called the mine deposit one of the largest of its kind in the world, with the potential of producing 80.6 billion pounds of copper, 107.4 million ounces of gold and 5.6 billion pounds of molybdenum over decades.
EPA regional administrator Dennis McLerran said the revised report generally affirms conclusions reached in the initial report last year while including more details on transportation corridors, possible culvert failures and other factors.
It noted, for example, that culvert blockages or other failures would inhibit fish passage. It said production of fish could be lost or diminished if blockages occurred during adult salmon immigration or juvenile salmon emigration and were not cleared for several days.
Extended blockages aren't likely during mine operations, but there could be a greater impact once mine operations end, the report states.
The report also noted that salmon could be affected by in-stream copper levels because leaching could occur during routine mine operations.
Tailing storage facilities and dams to hold mine waste are likely to be in place for hundreds to thousands of years because there is no plan for removal when mining operations end, according to the report. A tailings dam failure could wipe out or degrade rivers and streams for decades, though the risk of that is considered fairly low, the report states.
Conservationists said it was clear the mine would harm salmon and destroy streams, even if nothing ever goes wrong.
"Pebble is far bigger and more threatening to renewable resource jobs than any other mine proposal in Alaska and it's planned for the worst location possible," Tim Bristol, director of Trout Unlimited's Alaska program, said in a news release.
The new report updates an assessment EPA released last year and is meant to address concerns that were raised about things like missing data and incomplete information.
For example, rather than using a hypothetical mine scenario, EPA said it drew from plans developed for Northern Dynasty Minerals, which has a stake in the Pebble Mine; data collected by Pebble Limited Partnership; and its own experts to come up with three different mine scenarios.
EPA said the scenarios realistically represent the type of development expected to happen in the Bristol Bay region. McLerran said it also accounts for modern mining techniques. He said the focus has been on getting the science right so informed decisions can be made in the future.
Critics of the EPA review ? including the state of Alaska and the Pebble Partnership ? fear it could lead to the agency vetoing mining activity in the region.
U.S. Sen. Mark Begich, D-Alaska, said he opposes a pre-emptive veto of the Pebble Mine or other projects and added "an open, public process that answers Alaskans' questions and puts better science on the table is a good thing."
The revised assessment will undergo a new round of peer review and public comment before EPA releases a final report that could affect permitting decisions for the proposed mine.
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Follow Becky Bohrer on Twitter at http://twitter.com/beckybohrerap .
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Online:
EPA's Bristol Bay assessment: http://www2.epa.gov/bristolbay
The Disrupt NY 2013 Hackathon has kicked off and here's one of the new hack team pairings hoping to claim tomorrow's prize after a long night of coding. Michal Shaffer, left, from New York and Peter Ma, right from San Francisco -- met at the event and are now collaborating on a proximity art app that will be using Samsung's API and the Galaxy Note plus S Pen to power random collaborative doodling.
NEW YORK (Reuters) - Moody's Investors Service and Standard & Poor's on Friday said they have settled two long-running lawsuits seeking to hold them responsible for misleading investors about the safety of risky debt vehicles that they had rated.
The lawsuits had accused Moody's, a unit of Moody's Corp , and S&P, a unit of McGraw-Hill Cos, of negligent misrepresentation over their activities regarding the Cheyne and Rhinebridge structured investment vehicles (SIVs).
Morgan Stanley, which marketed both SIVs and helped structure the Rhinebridge SIV, also settled.
Settlement terms were not disclosed in the cases, which had been brought in 2008 and had sought more than $700 million (452 million pounds) of damages. Both lawsuits were dismissed with prejudice, meaning they cannot be brought again.
Moody's spokesman Michael Adler, McGraw-Hill spokesman Jason Feuchtwanger and Morgan Stanley spokesman Mark Lake confirmed their companies' respective settlements.
"This settlement allows us to put the significant legal defence and related costs, as well as the distraction, of these very protracted litigations behind us," Adler said.
Feuchtwanger said McGraw-Hill's settlement involved no admission of wrongdoing.
Lawyers for the plaintiff investors did not immediately respond to several requests for comment.
A trial in the Cheyne case had been scheduled for May 6 before U.S. District Judge Shira Scheindlin in Manhattan, who oversaw both lawsuits.
Credit rating agencies have been accused by investors, regulators and politicians of inflating the ratings of risky mortgage-backed and structured securities in a bid to win new business.
Critics said these activities also fuelled demand from investors who believed the ratings were objective, but prices collapsed once the risks materialized, helping to trigger the 2008 global financial crisis.
S&P still faces the U.S. Department of Justice's $5 billion civil fraud lawsuit filed in February over its ratings, the government's first major post-crisis action against a credit rating agency. The credit rating agency is trying to dismiss that case.
FIRST AMENDMENT
In the Cheyne and Rhinebridge cases, investors accused rating agencies of collaborating with banks to ensure that SIVs received ratings as high as "triple-A," though much of the underlying collateral was low-quality or subprime mortgage debt.
The Abu Dhabi Commercial Bank, King County in Washington state, and other investors sought $638 million of damages related to losses they claimed to have suffered when the Cheyne SIV went bankrupt in August 2007. The similarly-named firm that managed the SIV did not go bankrupt.
King County and the Iowa Student Loan Liquidity Corp, meanwhile, had been seeking $70 million of damages over Rhinebridge, which had been structured by Germany's IKB Deutsche Industriebank AG and was wound down in August 2008.
IKB settled the Rhinebridge case last year, and credit rating agency Fitch Ratings, a unit of France's Fimalac SA , settled last month.
Among the defences raised by the rating agencies were that their ratings were opinions that deserved free speech protection under the First Amendment to the U.S. Constitution.
Scheindlin limited that defence in a 2009 ruling, saying that ratings on notes sold to select investors were not "matters of public concern" deserving broad free speech protection.
The government has not hit Moody's and Fitch with lawsuits similar to the case it is pursuing against S&P.
The cases are Abu Dhabi Commercial Bank et al v. Morgan Stanley & Co et al, U.S. District Court, Southern District of New York, No. 08-07508; and King County, Washington et al v. IKB Deutsche Industriebank AG et al in the same court, No. 09-08387.
(Reporting by Nate Raymond and Jonathan Stempel in New York; Editing by Gary Hill and Lisa Shumaker)
Apr. 26, 2013 ? A potential new treatment strategy for patients with Charcot-Marie-Tooth disease is on the horizon, thanks to research by neuroscientists now at the University at Buffalo's Hunter James Kelly Research Institute and their colleagues in Italy and England.
The institute is the research arm of the Hunter's Hope Foundation, established in 1997 by Jim Kelly, Buffalo Bills Hall of Fame quarterback, and his wife, Jill, after their infant son Hunter was diagnosed with Krabbe Leukodystrophy, an inherited fatal disorder of the nervous system. Hunter died in 2005 at the age of eight. The institute conducts research on myelin and its related diseases with the goal of developing new ways of understanding and treating conditions such as Krabbe disease and other leukodystrophies.
Charcot-Marie-Tooth or CMT disease, which affects the peripheral nerves, is among the most common of hereditary neurological disorders; it is a disease of myelin and it results from misfolded proteins in cells that produce myelin.
The new findings sere published online earlier this month in The Journal of Experimental Medicine.
They may have relevance for other diseases that result from misfolded proteins, including Alzheimer's disease, Parkinson's, multiple sclerosis, Type 1 diabetes, cancer and mad cow disease.
The paper shows that missteps in translational homeostasis, the process of regulating new protein production so that cells maintain a precise balance between lipids and proteins, may be how some genetic mutations in CMT cause neuropathy.
CMT neuropathies are common, hereditary and progressive; in severe cases, patients end up in wheelchairs. These diseases significantly affect quality of life but not longevity, taking a major toll on patients, families and society, the researchers note.
"It's possible that our finding could lead to the development of an effective treatment not just for CMT neuropathies but also for other diseases related to misfolded proteins," says Lawrence Wrabetz, MD, director of the institute and professor of neurology and biochemistry in UB's School of Medicine and Biomedical Sciences and senior author on the paper. Maurizio D'Antonio, of the Division of Genetics and Cell Biology of the San Raffaele Scientific Institute in Milan is first author; Wrabetz did most of this research while he was at San Raffaele, prior to coming to UB.
The research finding centers around the synthesis of misfolded proteins in Schwann cells, which make myelin in nerves. Myelin is the crucial fatty material that wraps the axons of neurons and allows them to signal effectively. Many CMT neuropathies are associated with mutations in a gene known as P0, which glues the wraps of myelin together. Wrabetz has previously shown in experiments with transgenic mice that those mutations cause the myelin to break down, which in turn, causes degeneration of peripheral nerves and wasting of muscles.
When cells recognize that the misfolded proteins are being synthesized, cells respond by severely reducing protein production in an effort to correct the problem, Wrabetz explains. The cells commence protein synthesis again when a protein called Gadd34 gets involved.
"After cells have reacted to, and corrected, misfolding of proteins, the job of Gadd34 is to turn protein synthesis back on," says Wrabetz. "What we have shown is that once Gadd34 is turned back on, it activates synthesis of proteins at a level that's too high -- that's what causes more problems in myelination.
"We have provided proof of principle that Gadd34 causes a problem with translational homeostasis and that's what causes some neuropathies," says Wrabetz. "We've shown that if we just reduce Gadd34, we actually get better myelination. So, leaving protein synthesis turned partially off is better than turning it back on, completely."
In both cultures and a transgenic mouse model of CMT neuropathies, the researchers improved myelin by reducing Gadd34 with salubrinal, a small molecule research drug. While salubrinal is not appropriate for human use, Wrabetz and colleagues at UB and elsewhere are working to develop derivatives that are appropriate.
"If we can demonstrate that a new version of this molecule is safe and effective, then it could be part of a new therapeutic strategy for CMT and possibly other misfolded protein diseases as well," says Wrabetz.
And while CMT is the focus of this particular research, the work is helping scientists at the Hunter James Kelly Research Institute enrich their understanding of myelin disorders in general.
"What we learn in one disease, such as CMT, may inform how we think about toxins for others, such as Krabbe's," Wrabetz says. "We'd like to build a foundation and answer basic questions about where and when toxicity in diseases begin."
The misfolded protein diseases are an interesting and challenging group of diseases to study, he continues. "CMT, for example, is caused by mutations in more than 40 different genes," he says. "When there are so many different genes involved and so many different mechanisms, you have to find a unifying mechanism: this problem of Gadd34 turning protein synthesis on at too high a level could be one unifying mechanism. The hope is that this proof of principle applies to more than just CMT and may lead to improved treatments for Alzheimer's, Parkinson's, Type 1 diabetes and the other diseases caused by misfolded proteins."
Co-authors with D'Antonio and Wrabetz are M. Laura Feltri, MD, professor of neurology and biochemistry at UB and a researcher with UB's Hunter James Kelly Research Institute at the NYS Center of Excellence in Bioinformatics and Life Sciences; Nicolo Musner, Cristina Scapin Daniela Ungaro and Ubaldo Del Carro from the San Raffaele Scientific Institute and David Ron of Cambridge and the National Institute for Health Research Cambridge Biomedical Research Centre.
Funding was provided by the National Institutes of Health, the European Community and an award to D'Antonio from the Italian Ministry of Health.
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The above story is reprinted from materials provided by University at Buffalo. The original article was written by Ellen Goldbaum.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
M. D'Antonio, N. Musner, C. Scapin, D. Ungaro, U. Del Carro, D. Ron, M. L. Feltri, L. Wrabetz. Resetting translational homeostasis restores myelination in Charcot-Marie-Tooth disease type 1B mice. Journal of Experimental Medicine, 2013; 210 (4): 821 DOI: 10.1084/jem.20122005
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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NEW YORK/WASHINGTON (Reuters) - The two brothers suspected of carrying out last week's deadly Boston Marathon bombing decided, after the FBI released photos of them, to drive to Manhattan and detonate more explosives in Times Square, New York City officials said on Thursday.
Their plan unraveled when they realized a Mercedes sport utility vehicle they had hijacked on April 18, three days after the Boston bombing, did not have enough gasoline for the journey, said New York Police Commissioner Ray Kelly.
New York has been on heightened alert since the September 11, plane hijackings in 2001 destroyed the World Trade Center and officials said the plan by the Boston bombing suspects, ethnic Chechens Tamerlan and Dzhokhar Tsarnaev, showed America's most populous city remained a magnet for attackers.
Manhattan's Times Square was the target of an attempted car bombing by a Pakistan-born U.S. citizen in May 2010.
In the sharpest criticism of President Barack Obama's security policies since the blasts, a Republican senator said the Boston bombing, which killed three people and wounded 264, illustrated a "broken" national security system.
This week, lawmakers demanded answers about what the U.S. government knew about the suspects before the bombing, especially Tamerlan Tsarnaev, 26, who Russia had asked the FBI to question in 2011 over concerns he may have been a radical Islamist. He died on Friday in a shootout with police.
The surviving brother, 19-year-old Dzhokhar Tsarnaev, is recovering from wounds in a Boston hospital since he was captured on Friday night and told investigators of the alleged Times Square plan.
"Questioning of Dzhokhar revealed that he and his brother decided spontaneously on Times Square as a target," Kelly told a news conference with New York Mayor Michael Bloomberg. "They would drive to Times Square that same night.
"That plan, however, fell apart when they realized that the vehicle that they hijacked was low on gas and ordered the driver to stop at a nearby gas station," Kelly said.
At the time, the men still had six explosive devices, including a pressure-cooker bomb of the type used at the marathon and six pipe bombs, he said.
When they stopped to refuel, the driver of the vehicle escaped, Kelly said. The driver alerted authorities and set off a late-night chase and shootout in suburban Watertown, where police say the suspects threw improvised explosives at officers. Hours earlier, the brothers had shot and killed a Massachusetts Institute of Technology campus police officer in Cambridge, authorities said.
Earlier on April 18, the FBI released photos and video of the at the scene of the Boston bombing.
One Republican congressman said investigators have identified "persons of interest" in the United States to whom they would like to speak, some of them because of calls made from Tamerlan Tsarnaev's cell phone.
"There are also persons of interest here that we would like to more fully understand," said Mike Rogers, the chairman of the House of Representatives Intelligence Committee. "Their relationship and what role, if any, they may have played in that whole radicalization process. They are just still persons of interest, so they are not named."
Rogers also said investigators want to learn more about Tamerlan Tsarnaev's 2012 visit to Russia.
PARENTS SAY SONS INNOCENT
Dzhokhar Tsarnaev was formally charged on Monday in the hospital with crimes that could carry the death penalty.
His lawyer, Miriam Conrad, declined to comment on whether her client was still talking with investigators.
The U.S. Marshals Service, which is responsible for holding and transporting suspects outside of prison, declined to comment on whether or when Tsarnaev might be moved from the Beth Israel Deaconess Medical Center.
The brothers' father said he planned to travel to the United States from Russia to bury his older son, Tamerlan Tsarnaev.
"I am going to the United States. I want to say that I am going there to see my son, to bury the older one. I don't have any bad intentions. I don't plan to blow up anything," Anzor Tsarnaev told reporters in Makhachkala, the capital of Russia's Dagestan region.
Massachusetts Governor Deval Patrick said investigators might be interested in speaking to the parents.
"There are a lot of questions unanswered about the whys and the hows, and anybody who may be able to shed some light on that is of interest to law enforcement," Patrick said.
Anzor Tsarnaev's former wife, Zubeidat Tsarnaeva, angrily denied that her son had any role in the attack and criticized police for shooting him while apprehending him.
Tsarnaeva does not plan to accompany her former husband on his trip. One factor that may have influenced her decision is an outstanding arrest warrant for her in Massachusetts.
A warrant for Zubeidat Tsarnaeva's arrest was issued on October 25 after she failed to make a court appearance on shoplifting-related charges, according to Natick District Court Clerk Brian Kearney.
'WITCH HUNT'
In Washington, the focus remained on intelligence leading up to the Boston Marathon bombing. Tamerlan Tsarnaev had been on a federal database of potential terrorism suspects and the United States had twice been warned about him by Russian authorities. Congressional testimony this week focused on whether the FBI made mistakes in tracking him.
"We're in the post-event witch-hunt phase, which is predictable," said James Clapper, director of national intelligence, at a conference in Crystal City, Virginia. "I think it would be a real good idea to not hyperventilate for a while now until we actually get all the facts."
Nonetheless, Republican Senator Lindsey Graham blamed the administration for failing to stop the attack.
"I just know the system is broken. The ultimate blame I think is with the administration," the South Carolina senator told reporters, linking the bombings with last year's killing of a U.S. diplomat during an attack on a diplomatic compound in Benghazi, Libya.
"Between Benghazi and Boston, to me we're going backwards, not forward, in terms of national security," Graham said.
(Additional reporting by Tim McLaughlin, Svea Herbst-Bayliss, Aaron Pressman, Ross Kerber in Boston, Deborah Charles in Crystal City, Virginia, Alissa de Carbonnel in Makhachkala, Russia, and Atossa Araxia Abrahamian in New York; Writing by Scott Malone and Alex Dobuzinskis; Editing by Paul Thomasch, Mary Milliken and Christopher Wilson)
A Noblesville family that has gone through peaks and valleys over the past couple of years is now on a mountain top. There have been some pretty big scares during their little girl?s battle with cancer. The most recent shock for the family was the surprise of a lifetime: a trip to Disney World.
The third time was the charm.
?Mom!? screamed Izzy Mattocks.
?We are going to get on a plane right now,? said Molly Mattocks, Izzy?s mother.
?Mom, you never told me,? said Izzy.
Izzy Mattocks set off for Disney World Thursday.
?Thank you,? said Izzy. ?Let?s go, let?s go!?
The family is celebrating the 5-year-old?s fight against cancer. They tried to make the trip two other times, but each time Izzy?s health took a turn for the worse and she had to be rushed to the hospital.
?It did not happen because I got a fever and stuff,? said Izzy.
That was why this time, the trip was a secret.
?I am going to tell you this is a really awesome present and you do not want to lose it,? said Molly before the surprise was unveiled.
In 2011, Izzy started having sharp, severe pain in her stomach. At first, no one could figure out what was wrong with her. Then the discovery.
?Neuroblastoma is one of the most difficult pediatric cancers to cure,? said Molly. ?It is vicious.?
Neuroblastoma, like other forms of cancer, is a cold-blooded killer. Izzy was diagnosed with Stage 4. It had spread to her bones. The little girl?s fight for life began right away. She was put through intense rounds of chemotherapy and radiation.
?It is medicine that made my cancer go away,? said Izzy.
And that was not all.
?And I had surgeries,? she said. Reporter: ?How many?? What did they do?? Izzy: ?I don?t know.? Molly: ?Did they take the rock out? Izzy: ?They took the rock out.?
The ?rock? was the cancer. The neuroblastoma battle rocked the family.
?It was just a nightmare,? said Molly. ?Some days you would feel joy and you would feel peace and know that you conquered something. Then, at any moment, something would go wrong.?
It tested their faith.
?Some days I would say, ?Really God?? Are you kidding me??? But at the end of the day, just to fall back on seeing how far He has gotten us through this journey,? said Molly.
Then, after all that worry, all of those sleepless nights, and all of that pain- a reason to smile, a clear scan. No evidence of disease. Izzy, ?Warrior Princess? was allowed to leave the hospital.
Izzy is far from being 100 percent healthy, though. She is still on an IV, and she wears a breathing mask when she is in public. None of that mattered as the family boarded their plane, the family was focused on their next journey, to ?The Happiest Place on Earth.?
Sadly, Izzy?s battle is not over. She still must to go through six more months of treatment, and there is still a chance the disease could come back. If that happens the family said they are ready to answer that challenge.
Decisions being taken by a government advisory board on children in care, not to allow abusive parents to meet children during supervised access visits, are sometimes ignored, according to a social worker.
There were occasions when the Children and Young Persons Advisory Board recommended that a child who was living in foster care, for example, did not meet his or her abusive parent during family access time.
However, the abusive parents still turned up for the visit leaving the child traumatised.
This was recounted by social worker Daniella Zerafa during a conference entitled The Rights of the Child in Foster Care.
Ms Zerafa, who also lectures at the University of Malta, presented the case study of a fostered child, who she referred to as Katya.
The true story highlighted shortcomings in the system such as delays in deciding whether to issue a care order to remove a child from an abusive family.
Another problem highlighted was the fact that although Maltese law technically allowed the Government to strip parents of parental rights, in cases of abuse, this was not done in practice.
As a result, children were not being allowed to be adopted and live in a stable home.
During the conference Family Minister Marie-Louise Coleiro Preca said that her Government put the rights of children at the centre of its policies. She will work to ensure that children are given a stronger voice and that children in care are freed up for adoption. She said that there were about 600 children who lived in out of home care of which some 230 were being fostered.
Nationalist Party spokesman for the Family Chris Said also spoke about the need to strengthen legislation in the best interest of children. ?
MOGADISHU (Reuters) - In a sign of growing optimism that Somalia is winning a struggle against pirates and al Qaeda-linked insurgents, Britain opened an embassy on Thursday in a set of four metal cabins at Mogadishu airport.
It was the first such move by a Western power since Somalia began to emerge from more than two decades of conflict. Turkey and Iran are among others vying for influence in the Horn of Africa country, with growing commercial ties and diplomatic missions already up and running.
"It is a symbol of our confidence and belief in the future of Somalia," said British Foreign Secretary William Hague, who flew in on an unannounced visit to watch the Union Jack flag hoisted above the cabins, generator and satellite dish within the airport perimeter fence.
"This is a sign of where Somalia is now heading to," said Somali President Hassan Sheikh Mohamud.
"Somalia is going back to the international arena," he added, expressing hope that other Western states would follow suit.
The country is enjoying a delicate recovery but remains heavily dependent on others for its security. An African Union military offensive has driven weakened al Shabaab insurgents from bases in Mogadishu and other cities, and piracy in the strategic sea lanes off Somalia is at an all-time low, thanks largely to a heavy foreign naval presence.
REGIONAL BOOST
A stable Somalia would boost regional economies like Kenya and Ethiopia which have been rattled by their neighbor's insecurity, and would reassure Western capitals which have long worried Somalia provides a base for militant Islam to flourish.
The British government says now is "the best time in a generation for Somalia to get back onto the road to recovery." Britain will host an international conference in London on May 7 on ways to bolster security, impose the rule of law and rebuild the nation.
At the new embassy, due to be fully operational from late July, diplomats will live and work for a few weeks at a time in rotation behind two big blast walls, squeezed between the airport runway on one side and the Indian Ocean on the other.
Other countries with embassies in Mogadishu include Turkey, Libya, Ethiopia, Sudan, Yemen and Iran.
Britain's previous diplomatic mission lies in ruins: it closed in 1991 as a civil war broke out that led to first warlords and then Islamist militants stepping into the political vacuum.
Once written off as a failed state, Somalia now has its most legitimate government for decades since Mohamud's election in September. But the government still struggles to exert influence beyond the capital.
Foreign diplomats say they are spending more time in Somalia and will not be far behind the growing number of U.N. officials and aid workers slowly moving to Somalia from Kenya, where many organizations have been running their Somali operations.
Pictorious is a photo sharing startup that is faced with the unenviable task of crawling its way out of Instagram?s gigantic shadow. Today they?re releasing a bevy of updates to their iOS app, which will hopefully help it mount a better challenge against the photo sharing juggernaut.
CHICAGO (Reuters) - Five people were slain early on Wednesday in Manchester, Illinois, and a suspect died after a shootout with police, Illinois State Police said.
State Police spokeswoman Monique Bond confirmed the killings and also said that a 6-year-old girl had been injured and taken to hospital. Initial reports were that the victims had been shot, but Bond could not confirm this.
State Police did not discuss any motive nor did they say if the victims were related. The Chicago Tribune reported, citing relatives, that they were a grandmother, a young couple, and two children.
A suspect fled in a white Chevy Lumina, police said, citing witnesses. At about 7:13 a.m., the car was spotted and chased by state and local police who exchanged gunfire with the suspect, state police said.
About 15 minutes later, the suspect was arrested and taken to hospital, and later pronounced dead, Bond said. Police did not release the person's name.
Police said there was no reason to believe that the 300 or so residents of Manchester were in danger.
"Scott County is a small community. Fortunately, this type of thing doesn't happen very often, but this is proof they can happen," Scott County State's Attorney Michael Hill said at the news conference.
"It's been a very tragic scene," said Larry Balthis, pastor of the Manchester Baptist Church. Balthis said he knew the people involved, but he declined additional comment.
Jacksonville School District 117 was closed for the day, according to Debbie McKean, secretary to Superintendent Steve Ptacek. The school district covers 222 square miles and includes the area where the suspect was reportedly apprehended, McKean said.
(Reporting by Mary Wisniewski; Editing by Greg McCune; Editing by Lisa Von Ahn)
Apr. 24, 2013 ? Stanford University School of Medicine scientists have created a mouse model of muscular dystrophy in which degenerating muscle tissue gives off visible light.
The observed luminescence occurs only in damaged muscle tissue and in direct proportion to cumulative damage sustained in that tissue, permitting precise monitoring of the disease's progress in the mice, the researchers say.
While this technique cannot be used in humans, it paves the way to quicker, cheaper and more accurate assessment of the efficacy of therapeutic drugs. The new mouse strain is already being employed to test stem cell and gene therapy approaches for muscular dystrophies, as well as drug candidates now in clinical trials, said Thomas Rando, MD, PhD, professor of neurology and neurological sciences and director of Stanford's Glenn Laboratories for the Biology of Aging.
Rando is the senior author of a study, published online April 24 in the Journal of Clinical Investigation, describing his lab's creation of the experimental mouse strain in which an inserted gene coding for luciferase, the protein that causes fireflies' tails to glow, is activated only in an important class of rare stem cells that, collectively, serve as a reserve army of potential new muscle tissue. Under normal circumstances, these muscle stem cells, or "satellite cells," sit quietly adjacent to muscle fibers. But muscular injury or degeneration prompts satellite cells to start dividing and then to integrate themselves into damaged fibers, repairing the muscle tissue.
Muscular dystrophy is a genetically transmitted, progressive condition whose hallmark is the degeneration of muscle tissue. There are many different forms, whose severity, time of onset and preference for one set of muscles versus another depends on which gene is defective. But as a general rule, the disease begins to develop well before symptoms show up.
As the muscle fibers of someone with muscular dystrophy die off, nearby satellite cells -- which are normally dormant in the tissue -- begin replicating in an attempt to replace the lost muscle tissue. "But in the end, satellite cells' attempt to restore tissue is overwhelmed," said Rando, who is the founding director of Stanford's Muscular Dystrophy Association Clinic.
No truly effective treatments for muscular dystrophy exist. "Drug therapies now available for muscular dystrophy can reduce symptoms a bit, but do nothing to prevent or slow disease progression," said Rando. Testing a drug's ability to slow or arrest muscular dystrophy in one of the existing mouse models means sacrificing a few of them every couple of weeks and conducting labor-intensive, time-consuming microscopic and biochemical examinations of muscle-tissue samples taken from them, he said.
So Rando decided to design a better mouse. Dozens of mouse models of different varieties of muscular dystrophy, designed to best reflect different forms of the disease, already exist. Rando's team chose to start with a strain whose human analog is called limb-girdle muscular dystrophy. This steadily progressive form of the disease, whose clinical manifestations typically are most pronounced in limb muscles close to the torso (the thigh versus calf, or upper arm versus forearm), begins during the second or third decade of life, after the muscle-building burst of childhood is largely complete.
From that "starter" mouse strain, Rando's team developed another strain of mice that were prone to the same disease process but whose muscle cells contained the luciferase gene. When these mice are 2 months old, Rando and his associates use a sophisticated laboratory technique to activate the luciferase gene in the mice's satellite cells.
Once a luciferase gene is activated in a satellite cell, it stays "on" permanently in that cell and in all of its progeny, including mature muscle cells, causing them to glow whenever the mice are given a compound that gives off light in the presence of luciferase. So, as the muscular dystrophy progressed in the new mouse strain, the damage it inflicted on muscle fibers and the ensuing recruitment of neighboring satellite cells resulted in the affected muscle tissue's being increasingly luminescent. This luminescence, which could be observed through the mice's skin, was strong enough to be monitored and attributed to a precise anatomical location by a highly sensitive camera.
Invasive microscopic and biochemical methods are first able to detect disease symptoms in mice with the limb-girdle-analog strain when they are about 6 months old. In contrast, using this new method, the Stanford team could literally "see" the first signs of the disease's manifestation as early as 3 months.
Rando and his colleagues confirmed the validity of their luminescence assay with parallel examinations of the mice by standard microscopy and biochemical analysis. They also confirmed, in potentially luminescent but otherwise normal mice not suffering from progressive muscle deterioration, that healthy muscle tissue is ordinarily quiescent. In these mice, the Stanford scientists observed negligible luminescent output reflecting the less than 1 percent of all cells in muscle tissue that are satellite cells.
"In these luminescent mice, we could pick up the disease's pathological changes well before they could be seen otherwise," said Rando. "The readout was so sensitive we could observe those changes within a two-week period. Not only that, but we got our measurements instantaneously, without killing the mice."
The new assay's speed, accuracy and relative noninvasiveness will advance the pace of preclinical work, Rando said. "A lot of head-to-head comparisons of muscular-dystrophy therapies, including drugs already in clinical trials as well as stem cell therapies and gene therapies on the near horizon, can now be made that couldn't have been tried before, because they would have been too expensive and time-consuming to make them worth the effort."
The study was funded by the Jain Foundation and the National Institutes of Health (grant DP1OD000392). The first author was research associate Katie Maguire, PhD. Additional co-authors were Leland Lim, MD, PhD, clinical assistant professor of neurology and neurological sciences; and undergraduate student Sedona Speedy.
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The above story is reprinted from materials provided by Stanford University Medical Center. The original article was written by Bruce Goldman.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Katie K. Maguire, Leland Lim, Sedona Speedy, Thomas A. Rando. Assessment of disease activity in muscular dystrophies by noninvasive imaging. Journal of Clinical Investigation, 2013; DOI: 10.1172/JCI68458
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Apr. 24, 2013 ? The LHCb collaboration at CERN today submitted a paper to Physical Review Letters on the first observation of matter-antimatter asymmetry in the decays of the particle known as the B0s. It is only the fourth subatomic particle known to exhibit such behaviour.
Matter and antimatter are thought to have existed in equal amounts at the beginning of the universe, but today the universe appears to be composed essentially of matter. By studying subtle differences in the behaviour of particle and antiparticles, experiments at the LHC are seeking to cast light on this dominance of matter over antimatter.
Now the LHCb experiment has observed a preference for matter over antimatter known as CP-violation in the decay of neutral B0s particles. The results are based on the analysis of data collected by the experiment in 2011. "The discovery of the asymmetric behaviour in the B0S particle comes with a significance of more than 5 sigma -- a result that was only possible thanks to the large amount of data provided by the LHC and to the LHCb detector's particle identification capabilities," says Pierluigi Campana, spokesperson of the LHCb collaboration. "Experiments elsewhere have not been in a position to accumulate a large enough number of B0s decays."
Violation of the CP symmetry was first observed at Brookhaven Laboratory in the US in the 1960s in neutral particles called kaons. About 40 years later, experiments in Japan and the US found similar behaviour in another particle, the B0 meson. More recently, experiments at the so-called B factories and the LHCb experiment at CERN have found that the B+ meson also demonstrates CP violation.
All of these CP violation phenomena can be accounted for in the Standard Model, although some interesting discrepancies demand more detailed studies. "We also know that the total effects induced by Standard Model CP violation are too small to account for the matter-dominated Universe," says Campana. "However, by studying these CP violation effects we are looking for the missing pieces of the puzzle, which provide stringent tests of the theory and are a sensitive probe for revealing the presence of physics beyond the Standard Model."
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Journal Reference:
LHCb collaboration. First observation of CP violation in the decays of Bs mesons. Physical Review Letters, 2013 (submitted); [link]
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Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
T2 Bio publishes data supporting diagnostic test T2Candida in Science Translational MedicinePublic release date: 24-Apr-2013 [ | E-mail | Share ]
Contact: Karen Sharma ksharma@macbiocom.com 781-235-3060 MacDougall Biomedical Communications, Inc.
Breakthrough approach to rapid detection of Candida species directly from whole blood with T2 Magnetic resonance demonstrated in first patient samples
Lexington, MA, April 24, 2013 (Embargoed until 2:00 PM US Eastern Time) T2 Biosystems, a company developing direct detection products enabling superior diagnostics, today announced the publication of research supporting the Company's flagship diagnostic test, T2Candida, in Science Translational Medicine. The research highlights T2Candida as a breakthrough approach to rapid and sensitive identification of species-specific Candida, a sepsis-causing fungus, directly from whole blood in approximately three hours, or up to 25 times faster than the current gold standard of blood culture. This publication marks the first clinical study of patient samples with T2 Magnetic Resonance (T2MR) technology. Bloodstream infections of Candida, known as candidemia, are associated with a 40% mortality rate, largely due to the elapsed time from infection onset to pathogen diagnosis and treatment, which can take from two to five days with blood culture. With early identification of the specific species, this high mortality rate can be reduced to 11%.
"The rapid detection of Candida is of critical need within the healthcare community, where time is of the essence to enable life-saving treatment decisions," said Eleftherios Mylonakis, MD, Dean's Professor of Medicine, Chief, Infectious Disease Division, Warren Alpert Medical School of Brown University, and investigator in this study. "Studies have shown that each hour of delayed treatment increases the mortality of sepsis patients significantly, by up to 8% or more. This research outlines how T2 magnetic resonance can revolutionize the field, with great implications on mortality rates and healthcare costs."
"This research represents the first time that Candida has been identified directly from whole blood in patient samples with highly sensitive T2MR technology that affords limits of detection as low as 1 CFU/mL," added Tom Lowery, PhD, Vice President, Diagnostics Research & Development, T2 Biosystems, and principle investigator of the study. "Importantly, this T2MR approach to Candida identification is also amenable to virtually any molecular, immunoassay or hemostasis target, and we are currently developing a portfolio of products where high sensitivity and rapid detection will have the greatest impact on healthcare."
"T2MR represents a revolutionary, highly-sensitive nanotechnology solution, which can rapidly detect pathogens leading to early intervention that can save lives," said Robert S. Langer, D. Sc., David H. Koch Institute Professor, MIT, and co-founder and board member of T2 Biosystems. "T2Candida exemplifies the potential of nanotechnology to create great advances in healthcare in the near term."
In the paper entitled "T2 magnetic resonance enables nanoparticle-mediated rapid detection of candidemia in whole blood", the authors introduce a novel diagnostic method based on T2 magnetic resonance (T2MR). The T2Candida assay uses blood-compatible polymerase chain reaction (PCR) to amplify Candida DNA, which then binds to superparamagnetic nanoparticles coated with a complementary DNA strand. The binding event causes the nanoparticles to cluster, which changes the sample's T2MR signal. Using this approach, the researchers tested both Candida-spiked and patient samples and were able to rapidly, accurately and reproducibly detect five Candida species within human whole blood with a limit of detection as low as 1 CFU/mL and a time-to-result of approximately three hours. Spiked samples showed 98% positive agreement and 100% negative agreement between T2MR and blood culture. Clinical samples demonstrated similar concordance with blood culture with the important distinction that T2MR was able to identify Candida species in the presence of antifungals, whereas blood culture could not. This study suggests that rapid diagnosis of specific Candida species is achievable with T2MR technology, which is fully automated and applicable to a broad variety of targets.
###
Study authors included Lori A. Neely, Mark Audeh, Nu Ai Phung, Michael Min, Adam Suchocki, Daniella Plourde, Matthew Blanco, Vasiliki Demas, Lynell R. Skewis, Parris Wellman and Thomas J. Lowery of T2 Biosystems, Theodora Anagnostou of Brown University and Jeffrey J. Coleman and Eleftherios Mylonakis of Brown University and Massachusetts General Hospital.
T2Candida is for research use only. The test has not been cleared by FDA, and is not available for diagnostic use at this time.
About Sepsis & Candidemia
Sepsis is a potentially life-threatening illness caused by the body's severe reaction to infection by bacteria, fungi, viruses or parasites. It is one of the top 10 leading causes of death in the United States, and each hour of delayed treatment increases the mortality of these patients by 8%. Candida is a fungal pathogen known to cause sepsis, and it is associated with approximately 100,000 cases of candidemia in the U.S. annually, making it the fourth-leading cause of hospital-acquired infections. Currently, candidemia has a 40% mortality rate, which can be reduced to 11% with early identification of the specific species. Current detection methods rely on blood culture, a process that can take two to five days before identifying a Candida infection. The T2MR platform is able to detect species-specific Candida directly from whole blood without the limits experienced with optical detection technology, even at low copy numbers, and provide results in approximately three hours.
About T2 Biosystems
T2 Biosystems is disrupting the landscape of clinical diagnostics with T2MR, the Company's proprietary magnetic biosensor detector. The T2MR technology enables healthcare professionals to save lives and reduce costs by providing sensitive, accurate and rapid assay results. The Company's products detect molecular, hemostasis or immunoassay targets directly from unpurified clinical samples in hospitals, labs and physicians' offices. For more information, please visit http://www.t2biosystems.com.
Special Notes to Reporters
More information, including a copy of the paper, can be found online at the Science Translational Medicine press package at http://www.eurekalert.org/jrnls/scitransmed. You will need your user ID and password to access this information. For multimedia only associated with this release, please visit: http://www.t2biosystems.com/media.
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T2 Bio publishes data supporting diagnostic test T2Candida in Science Translational MedicinePublic release date: 24-Apr-2013 [ | E-mail | Share ]
Contact: Karen Sharma ksharma@macbiocom.com 781-235-3060 MacDougall Biomedical Communications, Inc.
Breakthrough approach to rapid detection of Candida species directly from whole blood with T2 Magnetic resonance demonstrated in first patient samples
Lexington, MA, April 24, 2013 (Embargoed until 2:00 PM US Eastern Time) T2 Biosystems, a company developing direct detection products enabling superior diagnostics, today announced the publication of research supporting the Company's flagship diagnostic test, T2Candida, in Science Translational Medicine. The research highlights T2Candida as a breakthrough approach to rapid and sensitive identification of species-specific Candida, a sepsis-causing fungus, directly from whole blood in approximately three hours, or up to 25 times faster than the current gold standard of blood culture. This publication marks the first clinical study of patient samples with T2 Magnetic Resonance (T2MR) technology. Bloodstream infections of Candida, known as candidemia, are associated with a 40% mortality rate, largely due to the elapsed time from infection onset to pathogen diagnosis and treatment, which can take from two to five days with blood culture. With early identification of the specific species, this high mortality rate can be reduced to 11%.
"The rapid detection of Candida is of critical need within the healthcare community, where time is of the essence to enable life-saving treatment decisions," said Eleftherios Mylonakis, MD, Dean's Professor of Medicine, Chief, Infectious Disease Division, Warren Alpert Medical School of Brown University, and investigator in this study. "Studies have shown that each hour of delayed treatment increases the mortality of sepsis patients significantly, by up to 8% or more. This research outlines how T2 magnetic resonance can revolutionize the field, with great implications on mortality rates and healthcare costs."
"This research represents the first time that Candida has been identified directly from whole blood in patient samples with highly sensitive T2MR technology that affords limits of detection as low as 1 CFU/mL," added Tom Lowery, PhD, Vice President, Diagnostics Research & Development, T2 Biosystems, and principle investigator of the study. "Importantly, this T2MR approach to Candida identification is also amenable to virtually any molecular, immunoassay or hemostasis target, and we are currently developing a portfolio of products where high sensitivity and rapid detection will have the greatest impact on healthcare."
"T2MR represents a revolutionary, highly-sensitive nanotechnology solution, which can rapidly detect pathogens leading to early intervention that can save lives," said Robert S. Langer, D. Sc., David H. Koch Institute Professor, MIT, and co-founder and board member of T2 Biosystems. "T2Candida exemplifies the potential of nanotechnology to create great advances in healthcare in the near term."
In the paper entitled "T2 magnetic resonance enables nanoparticle-mediated rapid detection of candidemia in whole blood", the authors introduce a novel diagnostic method based on T2 magnetic resonance (T2MR). The T2Candida assay uses blood-compatible polymerase chain reaction (PCR) to amplify Candida DNA, which then binds to superparamagnetic nanoparticles coated with a complementary DNA strand. The binding event causes the nanoparticles to cluster, which changes the sample's T2MR signal. Using this approach, the researchers tested both Candida-spiked and patient samples and were able to rapidly, accurately and reproducibly detect five Candida species within human whole blood with a limit of detection as low as 1 CFU/mL and a time-to-result of approximately three hours. Spiked samples showed 98% positive agreement and 100% negative agreement between T2MR and blood culture. Clinical samples demonstrated similar concordance with blood culture with the important distinction that T2MR was able to identify Candida species in the presence of antifungals, whereas blood culture could not. This study suggests that rapid diagnosis of specific Candida species is achievable with T2MR technology, which is fully automated and applicable to a broad variety of targets.
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Study authors included Lori A. Neely, Mark Audeh, Nu Ai Phung, Michael Min, Adam Suchocki, Daniella Plourde, Matthew Blanco, Vasiliki Demas, Lynell R. Skewis, Parris Wellman and Thomas J. Lowery of T2 Biosystems, Theodora Anagnostou of Brown University and Jeffrey J. Coleman and Eleftherios Mylonakis of Brown University and Massachusetts General Hospital.
T2Candida is for research use only. The test has not been cleared by FDA, and is not available for diagnostic use at this time.
About Sepsis & Candidemia
Sepsis is a potentially life-threatening illness caused by the body's severe reaction to infection by bacteria, fungi, viruses or parasites. It is one of the top 10 leading causes of death in the United States, and each hour of delayed treatment increases the mortality of these patients by 8%. Candida is a fungal pathogen known to cause sepsis, and it is associated with approximately 100,000 cases of candidemia in the U.S. annually, making it the fourth-leading cause of hospital-acquired infections. Currently, candidemia has a 40% mortality rate, which can be reduced to 11% with early identification of the specific species. Current detection methods rely on blood culture, a process that can take two to five days before identifying a Candida infection. The T2MR platform is able to detect species-specific Candida directly from whole blood without the limits experienced with optical detection technology, even at low copy numbers, and provide results in approximately three hours.
About T2 Biosystems
T2 Biosystems is disrupting the landscape of clinical diagnostics with T2MR, the Company's proprietary magnetic biosensor detector. The T2MR technology enables healthcare professionals to save lives and reduce costs by providing sensitive, accurate and rapid assay results. The Company's products detect molecular, hemostasis or immunoassay targets directly from unpurified clinical samples in hospitals, labs and physicians' offices. For more information, please visit http://www.t2biosystems.com.
Special Notes to Reporters
More information, including a copy of the paper, can be found online at the Science Translational Medicine press package at http://www.eurekalert.org/jrnls/scitransmed. You will need your user ID and password to access this information. For multimedia only associated with this release, please visit: http://www.t2biosystems.com/media.
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Public release date: 24-Apr-2013
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