Source: http://www.thehollywoodgossip.com/2013/03/nyc-subway-ads-put-shameful-face-on-teen-pregnancy/
taylor allderdice vincent jackson vicki gunvalson pierre garcon brown recluse spider wiz khalifa taylor allderdice eddie royal
Tuesday, March 26, 2013
Monday, March 25, 2013
Gladstone scientists discover that DNA damage occurs as part of normal brain activity
![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_uuvdApXBB6r58if3xKWmPloAQGezlQYhN1JrY0F_6Y9Bs4INTbDYrYJ0XvL-zOLDtbpgeBBDzMZDaPKQdHeQgx5IjrJCFMfFe4tP3sHTo=s0-d){kind=small}
Public release date: 24-Mar-2013[ | E-mail |
Share ] Contact: Anne Holden
anne.holden@gladstone.ucsf.edu
415-734-2534
Gladstone Institutes
Findings provide additional support for strategies to fight Alzheimer's disease
SAN FRANCISCO, CAMarch 24, 2013Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer's diseaseand identified two therapeutic strategies that reduce these disruptions.
Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer's. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learningas long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brainwidely thought to be a major cause of Alzheimer's diseaseincreases the number of neurons with DSBs and delays their repair.
"It is both novel and intriguing team's finding that the accumulation and repair of DSBs may be part of normal learning," said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. "Their discovery that the Alzheimer's-like mice exhibited higher baseline DSBs, which weren't repaired, increases these findings' relevance and provides new understanding of this deadly disease's underlying mechanisms."
In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer's, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.
The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environmentbut after being returned to their home environment, DSB levels dropped.
"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper's lead author. "But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."
The group of mice modified to simulate Alzheimer's had higher DSB levels at the startlevels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.
To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studiesone of which was led by Dr. Mucke and his teamthat showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer's and in humans in the disease's earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tauanother protein implicated in Alzheimer's. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.
The team's findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer'sperhaps by maintaining the delicate balance between DNA damage and repair.
"Currently, we have no effective treatments to slow, prevent or halt Alzheimer's, from which more than 5 million people suffer in the United States alone," said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. "The need to decipher the causes of Alzheimer's and to find better therapeutic solutions has never been more importantor urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memoryand in the disruption of these important brain functions by Alzheimer's disease."
###
Other scientists who participated in this research at Gladstone include Pascal Sanchez, PhD, Alexxai Kravitz, PhD, Xin Wang, Kaitlyn Ho, Kirsten Eilertson, PhD, Nino Devidze, PhD, and Anatol Kreitzer, PhD. This research was supported by grants from the National Institutes of Health and the S.D. Bechtel, Jr. Foundation.
About the Gladstone Institutes
Gladstone is an independent and nonprofit biomedical-research organization dedicated to accelerating the pace of scientific discovery and innovation to prevent, treat and cure cardiovascular, viral and neurological diseases. Gladstone is affiliated with the University of California, San Francisco.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 24-Mar-2013[ | E-mail |
Share ] Contact: Anne Holden
anne.holden@gladstone.ucsf.edu
415-734-2534
Gladstone Institutes
Findings provide additional support for strategies to fight Alzheimer's disease
SAN FRANCISCO, CAMarch 24, 2013Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer's diseaseand identified two therapeutic strategies that reduce these disruptions.
Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer's. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learningas long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brainwidely thought to be a major cause of Alzheimer's diseaseincreases the number of neurons with DSBs and delays their repair.
"It is both novel and intriguing team's finding that the accumulation and repair of DSBs may be part of normal learning," said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. "Their discovery that the Alzheimer's-like mice exhibited higher baseline DSBs, which weren't repaired, increases these findings' relevance and provides new understanding of this deadly disease's underlying mechanisms."
In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer's, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.
The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environmentbut after being returned to their home environment, DSB levels dropped.
"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper's lead author. "But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."
The group of mice modified to simulate Alzheimer's had higher DSB levels at the startlevels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.
To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studiesone of which was led by Dr. Mucke and his teamthat showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer's and in humans in the disease's earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tauanother protein implicated in Alzheimer's. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.
The team's findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer'sperhaps by maintaining the delicate balance between DNA damage and repair.
"Currently, we have no effective treatments to slow, prevent or halt Alzheimer's, from which more than 5 million people suffer in the United States alone," said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. "The need to decipher the causes of Alzheimer's and to find better therapeutic solutions has never been more importantor urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memoryand in the disruption of these important brain functions by Alzheimer's disease."
###
Other scientists who participated in this research at Gladstone include Pascal Sanchez, PhD, Alexxai Kravitz, PhD, Xin Wang, Kaitlyn Ho, Kirsten Eilertson, PhD, Nino Devidze, PhD, and Anatol Kreitzer, PhD. This research was supported by grants from the National Institutes of Health and the S.D. Bechtel, Jr. Foundation.
About the Gladstone Institutes
Gladstone is an independent and nonprofit biomedical-research organization dedicated to accelerating the pace of scientific discovery and innovation to prevent, treat and cure cardiovascular, viral and neurological diseases. Gladstone is affiliated with the University of California, San Francisco.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2013-03/gi-gsd031813.php
Macho Camacho Rise of the Guardians Pumpkin Pie Jack Taylor Apple Pie Recipe black friday How long to cook a turkey
Cyprus's Plan B: What will happen if Moscow won't foot the bill?
Cypriot officials have now lingered in Moscow for a second day of talks regarding a potential bailout deal. Meanwhile, the government is also looking into internal options to drum up funds.
Cyprus?s Central Bank chief, Panicos Demetriades, leaves after a meeting at the presidential palace in Nicosia Thursday. The European Central Bank says it will keep emergency aid for Cyprus's troubled banks in place at least until Monday, but will have to cut it off after that unless an international rescue program is drawn up.
Petros Karadjias/AP
EnlargeThe clock in Nicosia is ticking a lot louder: Tiny Cyprus has four days to come up with about ?6 billion ($7.5 billion) or lose its current lender of last resort, the European Central Bank (ECB).
Skip to next paragraph Robert MarquandStaff writer
Over the past three decades, Robert Marquand has reported on a wide variety of subjects for?The Christian Science Monitor, including American education reform,?the wars in the Balkans, the Supreme Court, South Asian politics, and the oft-cited "rise of China." In the past 15 years he has served as the Monitor's bureau chief in Paris, Beijing, and New Delhi.?
Recent posts
' +
google_ads[0].line2 + '
' +
google_ads[0].line3 + '
Subscribe Today to the Monitor
Tensions and emotions are high after ECB officials declared on Thursday that Cyprus must guarantee a ?10 billion ($13 billion) bailout by Monday or forfeit and presumably go into default, with unknown consequences for the eurozone economy and beyond.
Cypriot officials are scrambling to conjure new sources of revenue ? a so-called Plan B ? including a look at pension fund leveraging and sales of offshore gas exploration prospects. The finance minister and energy minister have now lingered in Moscow for a second day of talks regarding a potential bailout deal with Russia.?
Cypriot banks will remain closed this weekend even as bankers there worry about huge outflows of capital next week if some kind of deal, whether with the European Union or Moscow, is not in the offing. (Reportedly Russian officials yesterday told their EU counterparts they would not add to a current ?2.5 billion ($3 billion) loan to Cyprus.)?
Cypriot lawmakers vowed Thursday that they would not raise again the idea of a levy or tax on private accounts. However, EU and ECB authorities continue to state that available resources are so limited that the Cyprus parliament will need to revisit the issue, perhaps in a smaller percentage.
Meanwhile, Reuters notes, EU officials?continue to up the ante and put pressure on Cyprus. "I cannot rule out a Cyprus insolvency," Austrian Finance Minister Maria Fekter told the newspaper Oesterreich. "A euro exit would not achieve anything. Cyprus must act now."?
The ECB hard deadline comes a day after Cypriot lawmakers rejected the controversial EU terms of the bailout, engineered mysteriously last week, which require a ?tax? allowing Cypriot authorities to reach into the accounts of private bank deposits and withdraw some 10 percent of funds in accounts over ?100,000 ($130,000) and about 7 percent in accounts under that figure.
The idea of such a tax brings mingled perplexity and outrage in many parts of the world, but especially in Russia, which uses Cyprus as an offshore tax haven.
The Washington Post calculates?that:
Deposits in Cyprus?s banks were seven times the size of its economy at the end of 2012, an unusual situation fostered by low taxes and reputation for lax regulation. Many European policymakers suspect it is a hub for Russian money laundering. Cypriot banks hold $88 billion in deposits, of which $49 billion is in the form of deposits over $129,000, according to analysts? estimates.?
The Christian Science Monitor reports?that Moscow is playing ?hardball? with the Cypriot finance minister in order to protect its massive stake in Cyprus' banking system.
According to official Russian figures, more than $114 billion has flowed into Russia since 2007 from Cyprus, almost all of it in the form of dividends paid by Cyprus-registered holding companies. Big Russian firms, including most metals giants, the state-owned banks Sberbank and VTB, and the independent gas producer Novatek all have important holdings in Cyprus.
"The price of crisis in Cyprus is very high for Russia," says Igor Nikolayev, director of strategic planning for one of Russia's leading auditing firms.
bruno mars the Grammys 2013 State of the Union 2013 katy perry Rihanna Katy Perry Grammys 2013 taylor swift
Genomes of peregrine and saker falcons throw lights on evolution of a predatory lifestyle
Mar. 24, 2013 ? In a collaborative study published online in Nature Genetics, researchers from Cardiff University, BGI, International Wildlife Consultants, Ltd., and Abu Dhabi Falcon Hospital, have completed the genome sequencing and analysis of two iconic falcons, the peregrine (Falco peregrinus) and saker (Falco cherrug). The work provides an invaluable resource for the deep understanding of the adaptive evolution in raptors and the genetic basis of their wide distribution.
Peregrine and saker falcons are widespread, and their unique morphological, physiological and behavioral adaptations make them successful hunters. The peregrine is renowned as the world's fastest animal, and the falcon is the national emblem of United Arab Emirate. In recent decades, peregrine and saker falcons have been listed as endangered due to rapid population declines caused by a wide range of factors including environmental change, overharvesting for falconry, habitat loss and bioaccumulation of pesticides (e.g. DDT, PCBs).
In this study, researchers focused on the evolutionary basis of predatory adaptations underlying peregrine and saker. They conducted whole genome sequencing and assembled the high quality ~1.2 Gb reference genomes for each falcon species. Phylogenic analysis suggested that the two falcon species might diverged 2.1 million years ago.
Comparing with chicken and zebra finch, researchers found the transposable element composition of falcons was most similar to that of zebra finch. Large segmental duplications in falcons are less frequent than that in chicken and zebra finch, and comprise less than 1% of both falcon genomes. They also found that a gene expansion in the olfactory receptor ?-c clade in chicken and zebra finch is not present in falcons, possibly reflecting their reliance on vision for locating prey.
Observing genome-wide rapid evolution for both falcons, chicken, zebra finch and turkey, researchers found that the nervous system, olfaction and sodium ion trans-port have evolved rapidly in falcons, and also the evolutionary novelties in beak development related genes of falcons and saker-unique arid-adaptation related genes.
Shengkai Pan, bioinformatics expert from BGI, said, "The two falcon genomes are the first predatory bird genome published. The data presented in this study will advance our understanding of the adaptive evolution of raptors as well as aid the conservation of endangered falcon species."
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by BGI Shenzhen.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Xiangjiang Zhan, Shengkai Pan, Junyi Wang, Andrew Dixon, Jing He, Margit G Muller, Peixiang Ni, Li Hu, Yuan Liu, Haolong Hou, Yuanping Chen, Jinquan Xia, Qiong Luo, Pengwei Xu, Ying Chen, Shengguang Liao, Changchang Cao, Shukun Gao, Zhaobao Wang, Zhen Yue, Guoqing Li, Ye Yin, Nick C Fox, Jun Wang, Michael W Bruford. Peregrine and saker falcon genome sequences provide insights into evolution of a predatory lifestyle. Nature Genetics, 2013; DOI: 10.1038/ng.2588
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
Source: http://feeds.sciencedaily.com/~r/sciencedaily/most_popular/~3/nKjE34V6NSI/130325111216.htm
national enquirer whitney houston casket photo jk rowling qnexa kingdom of heaven national enquirer whitney houston arizona republican debate arizona debate
Family connections a big part of NCAA tournament
In this photo combo, Utah Jazz guard John Stockton, left, drives towards the basket during an NBA basketball game, Thursday, May 30, 1996, in Salt Lake City; while at right, Gonzaga's David Stockton, John's son, brings the ball up the court during an NCAA college basketball game, Thursday, March 21, 2013, in Salt Lake City. Family connections are a big part of the 2013 NCAA college basketball tournament. (AP Photo/Douglas C. Pizac, George Frey)
In this photo combo, Utah Jazz guard John Stockton, left, drives towards the basket during an NBA basketball game, Thursday, May 30, 1996, in Salt Lake City; while at right, Gonzaga's David Stockton, John's son, brings the ball up the court during an NCAA college basketball game, Thursday, March 21, 2013, in Salt Lake City. Family connections are a big part of the 2013 NCAA college basketball tournament. (AP Photo/Douglas C. Pizac, George Frey)
Michigan guard Tim Hardaway Jr. (10) drives against South Dakota State guard Brayden Carlson (12) in the second half of a second-round game of the NCAA men's college basketball tournament in Auburn Hills, Mich., Thursday, March 21, 2013. Michigan won 71-56. (AP Photo/Paul Sancya)
Gonzaga's David Stockton brings the ball upcourt against Southern University in the second half during a second-round game in the NCAA college basketball tournament in Salt Lake City Thursday, March 21, 2013. Gonzaga won 64-58. (AP Photo/George Frey)
AUBURN HILLS, Mich. (AP) ? Tim Hardaway Jr. can take the questions in stride at this point.
Any time Michigan is in the national spotlight, his familiar name stands out ? and the queries about his father seem inevitable.
"It was hard just to try to follow his footsteps, and you try not to worry about it," Hardaway said. "You try to leave a legacy of your own. It takes a long time to do that."
Hardaway is one of three Michigan players with fathers who were in the NBA, and the Wolverines aren't the only team with some famous names in this NCAA tournament. John Stockton's son plays for Gonzaga, and Danny Manning's is with Kansas. Several of college basketball's top performers are from athletic families, and some of these players have already conjured memories of generations past.
Hardaway scored 21 points to lead Michigan over South Dakota State on Thursday night, and he had plenty of help from Glenn Robinson III, who added 21 of his own for the Wolverines. Hardaway's father, of course, was a standout in the NBA, and Robinson's was a star at Purdue who scored 44 points in a win over Kansas during the 1994 NCAA tournament.
The Wolverines also have a backup forward named Jon Horford. His brother Al plays for the Atlanta Hawks, and his father Tito made it to the pros too. It's a coincidence that Hardaway, Robinson and Horford all ended up at Michigan, but coach John Beilein isn't shying away from the story line.
"We really feel good about it because their dads do know basketball," Beilein said. "We think that's always been a feather in our cap to have families. It's not just the dad involved with all these. There's a strong mother involved with every single one of these young men, and they've had a big part to do with their success as well."
David Stockton has played in all 34 games this season for Gonzaga, the same school his father attended. Kansas actually has three familiar names: Tyler Self, Evan Manning and Niko Roberts.
Self is the freshman son of Kansas coach Bill Self, and Manning is the freshman son of Danny Manning, who led the Jayhawks to the 1988 national title. Roberts, a junior guard, is the son of Norm Roberts, the former St. John's coach who is in his second year on Self's staff with the Jayhawks. All three play sparingly off the bench.
Don't think for a moment that they receive any sort of favoritism just because of the name on the back of their jerseys.
"Coaches want everybody to play, but obviously it's not equal opportunity," Bill Self said. "My wife even understands it, so it's not a big deal."
Then there's Montana coach Wayne Tinkle, whose Grizzlies lost to Syracuse on Thursday night in San Jose, Calif. At least the location was convenient. Tinkle's daughter Joslyn plays at Stanford and took a break from preparing for her own NCAA tournament to watch her dad coach.
Joslyn Tinkle watched the game with her brother, mother and two teammates. Her younger sister, Elle, was back at Gonzaga preparing for her NCAA tournament opener on Saturday against Iowa State.
"I was actually in the midst of finishing my take-home final and watching the selection show. I was hoping Montana would pop up in the San Jose bracket," Joslyn Tinkle said. "As soon as it happened the whole family got excited. It's really fun to be able to hang out with the family, except my sister. Maybe we'll get to see her next week. It's really awesome."
The Tinkle family was juggling two different NCAA tournaments, but the Larkin family extends across two sports. Miami guard Shane Larkin is the son of former Cincinnati Reds star Barry Larkin.
The Hall of Fame shortstop conceded he was "crushed" when his son gave up baseball, but Shane is making quite an impact on the basketball court, leaving a mark of his own.
That's what all these young athletes are trying to do. They may not be going about it the exact same way their parents did, but they're trying to enjoy their own competitive experiences ? with the support of family members who have already done it, like Hardaway's father.
"He just tells me to go out there, have fun, just play my hardest," Hardaway said. "And he's behind me 100 percent."
___
AP Sports Writers Josh Dubow and Dave Skretta contributed to this report.
Associated Pressmitt romney tax return flip saunders academy award nominations cynthia nixon cspan state of the union drinking game oscar noms
Sunday, March 24, 2013
Russian tycoon Berezovsky found dead in London
Exiled Russian oligarch Boris Berezovsky, a prominent Russian opposition figure, was found dead at his home near London on Saturday. NBC's Lester Holt reports.
By Becky Bratu, Staff Writer, NBC News
Exiled Russian oligarch Boris Berezovsky, a prominent Russian opposition figure, was found dead at his home near London on Saturday, British officials told NBC News. He was 67.
His death was also reported in a Facebook post by his son-in-law, Egor Schuppe. "Boris Berezovsky dead," the post read.
Ben Stansall / AFP - Getty Images, file
A picture dated Oct. 4, 2011 shows Russian tycoon Boris Berezovsky leaving the Court of Appeal in Central London. Berezovsky, the exiled Russian oligarch and long-time opponent of the Kremlin, has died in Britain at the age of 67, his spokesman said on March 23, 2013, without giving further details.
Police said in a statement that they were investigating "the unexplained death of a 67-year-old man, believed to be Russian national Boris Berezovsky." Officials were combing through a property in Ascot, Berkshire, which is about 25 miles west of London.?
Officers trained in dealing with chemical, biological, radiological and nuclear threats conducted a number of searches as a precaution but found "nothing of concern in the property," according to the police statement.?One road block in the area remained closed, police said.
Police said Berezovsky's body was still in the property Saturday night, police said.
"I would like to reassure residents that we are confident there is no risk to the wider community," Supt. Stuart Greenfield said in an earlier statement. "The property is part of a large estate so a number of roads are closed off at the moment and will remain so for the time being."
Berezovsky accumulated his wealth in the early 1990s, when Russia's privatization of state assets turned chaotic. He orchestrated the re-election of Boris Yeltsin in 1996 and played a role in Vladimir Putin's rise to prominence, but he fell out of favor with the latter after Putin became president of Russia in 2000.?
Berezovsky fled Russia for Britain in 2001 after criticizing Putin's government. He was granted political asylum in Britain in 2003.
Berezovsky was a close friend of Russian dissident Alexander Litvinenko, who was fatally poisoned with radioactive polonium in London in 2006.
Last year, a court ordered him to pay $53.3 million in legal costs to fellow Russian tycoon Roman Abramovich, the billionaire owner of Chelsea Football Club, after losing a legal battle against him. The legal and other costs of that lawsuit amounted to about $250 million.
?
This story was originally published on Sat Mar 23, 2013 3:55 PM EDT
hunger games Joey Kovar Expendables 2 Pussy Riot National Hurricane Center Zeek Rewards vanessa bryant
Congregation of burned Clearfield church hold Palm Sunday services
(Scott Sommerdorf | The Salt Lake Tribune) The burned Clearfield Community Church sits behind a fire line fence while Palm Sunday services were conducted at Wasatch Elementary School in Clearfield, Sunday, March 24, 2013.
Renewal ? Church members say they will rebuild after Tuesday fire.
Clearfield ? The sun didn?t filter through the stained glass windows. There was no organ music echoing off the solid timbers of the high ceiling, or a procession of children with palm fronds. Congregants held white printer paper instead of song books.
It didn?t matter.
"We may not be in our old building," Tina Ramirez told the Clearfield Community Church members Sunday morning, "but we are still here."
The church held Palm Sunday services at the Wasatch Elementary gym after a Tuesday fire gutted their church building a few blocks away. With a simple table-top cross, potted palms and a collection of daffodils decorating the space, the day?s message of renewal seemed particularly fitting.
Pastor John Parsley held a large blue parade banner salvaged from the flames as he preached, sending the smell of smoke wafting through the room.
"This may be a symbol of you, of us," he said, and paraphrased Winston Churchill. "?Never, never, never, never give up.?"
Parsley was working on a sermon in his office Tuesday when someone came to warn him about the fire, and left the book open to Matthew chapter 5 as he left. The blaze had started after a computer used as a card catalog at the church library overheated.
"It was an old, old computer," said Gerald Nichols, a small group coordinator at the church. "It got turned on once a month."
"It?s such a small, inconsequential thing, to have cause to much pain," said his wife, Cathy. Though there are often dozens of children at the church for home schooling, that day there were only about 13 junior high-age kids, and everyone got out safely.
The fire burned fast and hot, in part because the 35-year-old sanctuary didn?t have a sprinkler system ? it was grandfathered in under old rules, said North Davis Fire Chief Mark Becraft.
story continues below
"It was a very, very dangerous fire," he said, one that forced his firefighters out as the stairs started to fall. At one point, firefighters turned off their hoses to allow the blaze to consume the heavy timber on the building?s west side, removing the fuel. "If we hadn?t done that, it would still be smoldering today."
The blaze caused $750,000 to $1 million worth of damage. Though some of the brick walls still stand, the inside of the building is now a nest of twisted, blackened beams, the stained glass windows that were near the ceiling destroyed. Seven of those were handmade by member Edward Isler, who is retired from Hill Air Force Base.
"The pastor was just saying, ?Isn?t that something, when the sun is low, it casts [shadows of] the etchings on the floor??" said Isler on Sunday. One window, an image of a wafer and a wheat stalk, was created in memory of his wife.
"We would always say ?We?ve got to remember to take a picture of them,? but we never did," said his daughter, Tine Wolfe.
The congregation ? about 170 people on Sunday ?will hold services at Wasatch Elementary for the foreseeable future, but are insured and plan to rebuild. The less-damaged part of the building, including the fellowship hall, could be repaired in five months, said Bill Storing, chairman of the stewardship and finance committee, but it will likely be at about two years before the full church is rebuilt.
"The congregation is the church," said Clearfield Mayor Don Wood. "The goodness and the heart of the people."
April Ehrig of West Point has been attending the church of 20 years, and got her seminary degree and did a mission to the Czech Republic. She seemed to hold back tears as she talked about the fire.
Still, "situations like this tend to bring people together," she said. "It tells you what?s important."
lwhitehurst@sltrib.com
Twitter: @lwhitehurst
Copyright 2013 The Salt Lake Tribune. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
Source: http://www.sltrib.com/sltrib/news/56054072-78/church-fire-building-sunday.html.csp
reggie bush pope google reader carnival cruise nfl nfl lil wayne
Subscribe to:
Posts (Atom)