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WASHINGTON (AP) ? Russian authorities secretly recorded a telephone conversation in 2011 in which one of the Boston bombing suspects vaguely discussed jihad with his mother, officials said Saturday, days after the U.S. government finally received details about the call.
In another conversation, the mother of now-dead bombing suspect Tamerlan Tsarnaev was recorded talking to someone in southern Russia who is under FBI investigation in an unrelated case, officials said.
The conversations are significant because, had they been revealed earlier, they might have been enough evidence for the FBI to initiate a more thorough investigation of the Tsarnaev family.
As it was, Russian authorities told the FBI only that they had concerns that Tamerlan and his mother were religious extremists. With no additional information, the FBI conducted a limited inquiry and closed the case in June 2011.
Two years later, authorities say Tamerlan and his brother, Dzhohkar, detonated two homemade bombs near the finish line of the Boston Marathon, killing three and injuring more than 260. Tamerlan was killed in a police shootout and Dzhohkar is under arrest.
In the past week, Russian authorities turned over to the United States information it had on Tamerlan and his mother, Zubeidat Tsarnaeva. The Tsarnaevs are ethnic Chechens who emigrated from southern Russia to the Boston area over the past 11 years.
Even had the FBI received the information from the Russian wiretaps earlier, it's not clear that the government could have prevented the attack.
In early 2011, the Russian FSB internal security service intercepted a conversation between Tamerlan and his mother vaguely discussing jihad, according to U.S. officials who spoke on condition of anonymity because they were not authorized to discuss the investigation with reporters.
The two discussed the possibility of Tamerlan going to Palestine, but he told his mother he didn't speak the language there, according to the officials, who reviewed the information Russia shared with the U.S.
In a second call, Zubeidat Tsarnaeva spoke with a man in the Caucasus region of Russia who was under FBI investigation. Jacqueline Maguire, a spokeswoman for the FBI's Washington Field Office, where that investigation was based, declined to comment.
There was no information in the conversation that suggested a plot inside the United States, officials said.
It was not immediately clear why Russian authorities didn't share more information at the time. It is not unusual for countries, including the U.S., to be cagey with foreign authorities about what intelligence is being collected.
The FSB said Sunday that it would not comment.
Jim Treacy, the FBI's legal attache in Moscow between 2007 and 2009, said the Russians long asked for U.S. assistance regarding Chechen activity in the United States that might be related to terrorism.
"On any given day, you can get some very good cooperation," Treacy said. "The next you might find yourself totally shut out."
Zubeidat Tsarnaeva has denied that she or her sons were involved in terrorism. She has said she believed her sons have been framed by U.S. authorities.
But Ruslan Tsarni, an uncle of the Tsarnaev brothers and Zubeidat's former brother-in-law, said Saturday he believes the mother had a "big-time influence" as her older son increasingly embraced his Muslim faith and decided to quit boxing and school.
After receiving the narrow tip from Russia in March 2011, the FBI opened a preliminary investigation into Tamerlan and his mother. But the scope was extremely limited under the FBI's internal procedures.
After a few months, they found no evidence Tamerlan or his mother were involved in terrorism.
The FBI asked Russia for more information. After hearing nothing, it closed the case in June 2011.
In the fall of 2011, the FSB contacted the CIA with the same information. Again the FBI asked Russia for more details and never heard back.
At that time, however, the CIA asked that Tamerlan's and his mother's name be entered into a massive U.S. terrorism database.
The CIA declined to comment Saturday.
Authorities have said they've seen no connection between the brothers and a foreign terrorist group. Dzhohkar told FBI interrogators that he and his brother were angry over wars in Afghanistan and Iraq and the deaths of Muslim civilians there.
Family members have said Tamerlan was religiously apathetic until 2008 or 2009, when he met a conservative Muslim convert known only to the family as Misha. Misha, they said, steered Tamerlan toward a stricter version of Islam.
Two U.S. officials say investigators believe they have identified Misha. While it was not clear whether the FBI had spoken to him, the officials said they have not found a connection between Misha and the Boston attack or terrorism in general.
___
Associated Press writer Adam Goldman in Washington and Michael Kunzelman in Boston contributed to this report.
Source: http://news.yahoo.com/russia-caught-bomb-suspect-wiretap-105240857.html
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In case you missed it, Samsung released a new phone over the weekend and now the company's put together a quick video describing the design notions behind its Galaxy S 4. Expect to hear the word "intuitive" a fair few times, mostly in regard to those new software features and a return of those nature-inspired design licks. Samsung adds that it's has also cranked up the attention to detail on the hardware design, in search of the "perfect line" for its new flagship, though we're not exactly sure if it can be both "unlike anything you've ever seen before" and "not a radical difference, but more an evolution," as mentioned in the clip. Take in some sun-kissed vistas and the chilled-out soundtrack right after the break.
Filed under: Cellphones, Mobile, Samsung
Source: Samsung Tomorrow (YouTube)
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Apr. 25, 2013 ? Researchers at Washington University School of Medicine in St. Louis have described a missing link in understanding how damage to the body's cellular power plants leads to Parkinson's disease and, perhaps surprisingly, to some forms of heart failure.
These cellular power plants are called mitochondria. They manufacture the energy the cell requires to perform its many duties. And while heart and brain tissue may seem entirely different in form and function, one vital characteristic they share is a massive need for fuel.
Working in mouse and fruit fly hearts, the researchers found that a protein known as mitofusin 2 (Mfn2) is the long-sought missing link in the chain of events that control mitochondrial quality.
The findings are reported April 26 in the journal Science.
The new discovery in heart cells provides some explanation for the long known epidemiologic link between Parkinson's disease and heart failure.
"If you have Parkinson's disease, you have a more than two-fold increased risk of developing heart failure and a 50 percent higher risk of dying from heart failure," says senior author Gerald W. Dorn II, MD, the Philip and Sima K. Needleman Professor of Medicine. "This suggested they are somehow related, and now we have identified a fundamental mechanism that links the two."
Heart muscle cells and neurons in the brain have huge numbers of mitochondria that must be tightly monitored. If bad mitochondria are allowed to build up, not only do they stop making fuel, they begin consuming it and produce molecules that damage the cell. This damage eventually can lead to Parkinson's or heart failure, depending on the organ affected. Most of the time, quality-control systems in a healthy cell make sure damaged or dysfunctional mitochondria are identified and removed.
Over the past 15 years, scientists have described much of this quality-control system. Both the beginning and end of the chain of events are well understood. And since 2006, scientists have been working to identify the mysterious middle section of the chain -- the part that allows the internal environment of sick mitochondria to communicate to the rest of the cell that it needs to be destroyed.
"This was a big question," Dorn says. "Scientists would draw the middle part of the chain as a black box. How do these self-destruct signals inside the mitochondria communicate with proteins far away in the surrounding cell that orchestrate the actual destruction?"
"To my knowledge, no one has connected an Mfn2 mutation to Parkinson's disease," Dorn says. "And until recently, I don't think anybody would have looked. This isn't what Mfn2 is supposed to do."
Mitofusin 2 is known for its role in fusing mitochondria together, so they might exchange mitochondrial DNA in a primitive form of sexual reproduction.
"Mitofusins look like little Velcro loops," Dorn says. "They help fuse together the outer membranes of mitochondria. Mitofusins 1 and 2 do pretty much the same thing in terms of mitochondrial fusion. What we have done is describe an entirely new function for Mfn2."
The mitochondrial quality-control system begins with what Dorn calls a "dead man's switch."
"If the mitochondria are alive, they have to do work to keep the switch depressed to prevent their own self-destruction," Dorn says.
Specifically, mitochondria work to import a molecule called PINK. Then they work to destroy it. When mitochondria get sick, they can't destroy PINK and its levels begin to rise. Then comes the missing link that Dorn and his colleague Yun Chen, PhD, senior scientist, identified. Once PINK levels get high enough, they make a chemical change to Mfn2, which sits on the surface of mitochondria. This chemical change is called phosphorylation. Phosphorylated Mfn2 on the surface of the mitochondria can then bind with a molecule called Parkin that floats around in the surrounding cell.
Once Parkin binds to Mfn2 on sick mitochondria, Parkin labels the mitochondria for destruction. The labels then attract special compartments in the cell that "eat" and destroy the sick mitochondria. As long as all links in the quality-control system work properly, the cells' damaged power plants are removed, clearing the way for healthy ones.
"But if you have a mutation in PINK, you get Parkinson's disease," Dorn says. "And if you have a mutation in Parkin, you get Parkinson's disease. About 10 percent of Parkinson's disease is attributed to these or other mutations that have been identified."
According to Dorn, the discovery of Mfn2's relationship to PINK and Parkin opens the doors to a new genetic form of Parkinson's disease. And it may help improve diagnosis for both Parkinson's disease and heart failure.
"I think researchers will look closely at inherited Parkinson's cases that are not explained by known mutations," Dorn says. "They will look for loss of function mutations in Mfn2, and I think they are likely to find some."
Similarly, as a cardiologist, Dorn and his colleagues already have detected mutations in Mfn2 that appear to explain certain familial forms of heart failure, the gradual deterioration of heart muscle that impairs blood flow to the body. He speculates that looking for mutations in PINK and Parkin might be worthwhile in heart failure as well.
"In this case, the heart has informed us about Parkinson's disease, but we may have also described a Parkinson's disease analogy in the heart," he says. "This entire process of mitochondrial quality control is a relatively small field for heart specialists, but interest is growing."
This work was supported by the National Institutes of Health (NIH) grants R01 HL059888 and R21 HL107276.
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The above story is reprinted from materials provided by Washington University School of Medicine. The original article was written by Julia Evangelou Strait.
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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/~3/QSYvGCfVQ78/130425142357.htm
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Apr. 25, 2013 ? Among the many planets detected orbiting other stars (exoplanets) over the last twenty years, a little less than three hundred periodically pass in front of their star. This is what astronomers call a planetary transit. Exoplanets that "transit" their stars are key objects for the study of other planetary systems, because they are the only planets beyond our solar system that can be studied in detail, both in terms of their physical parameters (mass, radius, orbital parameters) and their atmospheric properties (thermal structure, dynamics, composition).
The University of Liege (ULg) is deeply involved in this exciting research topic, notably through its TRAPPIST[1] robotic telescope installed in 2010 in one of the best astronomical sites of the world, the La Silla European Southern Observatory in the Chilean Atacama desert. One of the scientific objectives of this telescope is the detection and study of exoplanets via the accurate measurement of their transits. In just three years, it has fully demonstrated its great potential in this area. Indeed, TRAPPIST participated in the detection of thirty planets, representing ten percent of all transiting exoplanets known to date. This important contribution is the result of the excellent expertise of the Liege astronomers, and their active collaboration with other international teams of "planet hunters," including the Swiss team of Professor Didier Queloz, co-discoverer of the first exoplanet in 1995.
Among the thirty exoplanets co-detected by TRAPPIST, most are gas giants similar to Jupiter, but in much closer orbits. "With the intense radiation that they undergo from their star, these planets are real gold mines for the study of other worlds," says Micha?l Gillon, Principal Investigator of the TRAPPIST exoplanets program. "Indeed, it makes possible a number of measurements that give us access to valuable information on their atmospheric properties. " TRAPPIST also detected the transit of a planet twice smaller than Jupiter orbiting a nearby star much less massive than the Sun. "The name of this small planet is GJ3470b" continues Micha?l Gillon, "and it has a mass and a size comparable to those of Uranus and Neptune, suggesting a composition rich in water ice. The detection of this planet much smaller than Jupiter is very exciting, not only for its own study, but also because it demonstrates that by focusing on even less massive stars, TRAPPIST should be able to detect rocky planets similar in size and mass to Earth. Our current projects go in that direction. "
Probably dreaming of other Earths too, TRAPPIST continues to observe the gorgeous Chilean sky night after night, to the delight of Liege astronomers that analyze its valuable data thirteen thousand kilometers away ...
[1] TRAPPIST stands for TRAnsiting Planets and PlanetesImals Small Telescope.
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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/~3/4DOSGoWcq2k/130425103237.htm
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STOCKHOLM (Reuters) - Swedish police said on Thursday they found drugs on teen idol Justin Bieber's tour bus in Stockholm, but had no suspects and were unlikely to pursue the case further.
A police officer on crowd duty smelled marijuana on an empty tour bus outside the hotel where Bieber was staying just before his concert in the capital on Wednesday night, police spokesman Kjell Lindgren said.
Police searched the empty bus after it had taken 10 to 15 individuals to the concert venue.
"The police went onto the bus and searched it and found a small amount of narcotics," Lindgren said. "We don't know who had the drugs or who smoked them, so it will be hard to link them with any individual."
The drugs have been sent for analysis and Lindgren said the police did not plan further action unless they got more information.
Bieber is travelling Europe on his "Believe" tour and is due in Finland for a concert on Friday.
Bieber got into trouble earlier this month after a museum dedicated to Anne Frank said the 19-year-old had written that he hoped the young Holocaust victim would have been a "belieber", the word used by his fans to describe themselves.
Anne Frank, who died aged 15 at the Bergen-Belsen concentration camp in 1945, is one of the best-known Jewish victims of the Holocaust due to her diary.
(Reporting by Simon Johnson; Editing by Alistair Scrutton and Alistair Lyon)
Source: http://news.yahoo.com/swedish-police-drugs-justin-bieber-bus-no-suspects-132755019.html
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