"Come See Our New Home on Android," the invitation sent to members of the press on Thursday declared. Does this mean the long-rumored Facebook phone is about to become official? What is the social network's next move? And does it stand a chance?
Facebook is intending to introduce a modified version of Google's Android operating system, according to sourcing from TechCrunch's Josh Constine, the New York Times' Nick Bilton and Brian X. Chen, and the Wall Street Journal's Evelyn M. Rusli and Amir Efrati. This version of Android will put Facebook front and center and "will debut on a handset made by HTC, according to a Facebook employee and another person who were briefed on the announcement," Chen and Bilton explain.
"Imagine Facebook?s integration with iOS 6, but on steroids, and built by Facebook itself," Constine adds. "It could have a heavy reliance on Facebook?s native apps like Messenger, easy social sharing from anywhere on the phone, and more."
?It?s putting Facebook first,? a person familiar with the matter emphasized to Wall Street Journal reporters. But unlike competitors such as Amazon and Google, it is not putting Facebook itself into the hardware game.
"With Amazon, it's pretty clear," mobile industry consultant Chetan Sharma told NBC News. "They want to sell their content and services. They're building their own devices, which is different from what Facebook is doing."
However, the idea of a modified version of Android may be viewed as an act of hostility directed at Facebook's frenemy, Google.
"The reaction from Google will be interesting to see," Sharma pointed out. "There's obviously overlap ... It seems to Google that it's underpinning their Google+ efforts. Longer term, I don't see them letting it go and letting other people do their work."
But even if Google lets Facebook's plans fly, there are other issues to consider, Sharma says. "If it's just a phone that's going to be pushed by HTC, its chances are going to be limited," he explains. "[HTC] doesn't have the marketing powers." To truly stand a shot, Facebook needs to join hands with carriers.
Of course, some might wonder whether any carriers would be game. After all, Facebook's VoIP efforts and its baked-in Messenger service might conflict with carriers' business agendas, right?
Not necessarily so, says Sharma. "In certain markets [VoIP and Messenger] would be challenging," he elaborates. "In markets where unlimited voice and messaging is already bundled in ? in those scenarios operators have less resistance to the idea. They already make money on voice and messaging and they'll also make money on the data used by Facebook."
Initial whispers don't suggest that "Facebook Home," as the social network's device/software combo is expected to be named, is going to be pitched by any carriers, so we'll have to see how things fare with merely HTC. (Of course, that's assuming all these rumors and reports pan out.)
Things will be official on Thursday, April 4, and we'll be in Menlo Park, Calif., to report live.
Want more tech news or interesting links? You'll get plenty of both if you keep up with Rosa Golijan, the writer of this post, by following her on Twitter, subscribing to her Facebook posts, or circling her on Google+.
HONOLULU (Reuters) - When Japanese warplanes strafed the USS Honolulu in the surprise attack on Pearl Harbor, Navy sailor Ray Emory fired back with a machine gun, so the World War Two veteran knows all about being on the front line of America's defenses.
But North Korea's latest threats of a pre-emptive nuclear strike and rocket attacks on Hawaii do not faze him.
"They're not gonna do anything," Emory, 91, said at his Honolulu home. "They can't even control their missiles. North Korea doesn't bother me. It really doesn't," he added.
Emory's attitude seems to be the norm in the lush, tropical islands, where this week residents and tourists appeared to be pretty much ignoring Pyongyang's rhetoric.
If anybody was seriously preparing for the worst, Jared Aiwohi would know. He is the owner of a store called Uncle Jesse's Place in Wailuku, Maui, that specializes in camouflage clothing, martial arts gear, hunting and bow supplies - the kind of gear favored by survivalists who fear a Doomsday scenario.
"The lifestyle here is laid back and people don't tend to be concerned about these things," Aiwohi said. "We always have the regulars prepping for things like this, but they haven't come in."
The U.S. military announced on March 15 it was bolstering missile defenses in response to the threats from North Korea, which has specifically mentioned Hawaii and the Pacific Island territory of Guam as potential targets.
"Yes, I'm concerned, but what can I do?" said Hawaiian homemaker Cheryl Yamamoto, 57. "Nothing."
Few believe North Korea will risk starting a full-out war - and Yamamoto said the ritual of going to work, getting dinner and taking care of her family weighed more on her mind than what the North Koreans might or might not do.
"I can't let them run my life," she said.
Joey Augustine and Doug Tojeiro, visiting from the continental United States, took time out from enjoying the local wild life (sea turtles) to discuss the threats as they walked up a rocky path from the beach. Both were skeptical.
"I think they're just trying to intimidate us, to see if they can get a rise out of us," Tojeiro said, as he wiped the salt water from his face. "We have the greatest military in the world to stay at peace."
On Guam, which lies about 2,500 miles closer to Pyongyang than Honolulu, the island's flow of tourists has been unaffected by rhetoric from North Korea, residents said.
While still on peoples' minds, concerns over the tension have receded somewhat as residents of the predominantly Catholic island have turned their attention to Easter celebrations.
Tammy Cruz, 38, a teacher from the village of Santa Rita, admitted she'd been a little worried: "Of course it's a scare to hear that our island is threatened." But she was focused on more immediate things: "Our tradition is to get together as a family and to come together to eat as well as have the kids play and to do an Easter Egg hunt."
While U.S. Stealth bombers and a B-52 bomber flew practice runs over South Korea this week, Honolulu's Department of Emergency Management said it had not received any particular alert about potential threats.
"In the event of a rocket attack, then the national defense system would render it useless," said Mel Kaku, director of the Department of Emergency Management. "The best recommendation to our people would be to shelter in place until the threat was eliminated," he added.
In the event of any attack, Kaku's advice to residents is "stay away from windows, or open areas, stay indoors."
"Kind of like during a hurricane, the blast would be similar, with high winds and projectiles," he said.
The Pentagon has declined to define the range of North Korea's rockets, saying it is classified. But Admiral James Winnefeld, vice chairman of the Joint Chiefs of Staff, acknowledged on March 15 that one type of North Korean missile likely had the range to reach the United States.
(Additional reporting by Maureen N. Maratita in Guam; Editing by Tim Gaynor and Claudia Parsons)
ATLANTA (AP) ? In another embarrassing blow to Atlanta public schools, nearly three dozen former educators, including the ex-superintendent, were indicted Friday in one of the nation's largest test cheating scandals.
Former Superintendent Beverly Hall faced charges including racketeering, false statements and theft because prosecutors said some of the bonuses she received were tied to falsified scores.
Hall retired just days before a state probe was released in 2011. She has long denied knowing about the cheating or ordering it.
During a news conference Friday, Fulton County District Attorney Paul Howard provided examples of two students who demonstrated "the plight of many children" in the Atlanta school system. He described a third-grader who failed a benchmark exam and received the worst score in her reading class in 2006. The girl was held back, yet when she took a separate assessment test not long after, she passed with flying colors.
Howard said the girl's mother, Justina Collins, knew something was awry, but was told by school officials that the child simply was a good test-taker. The girl is now in ninth grade, reading at a fifth-grade level.
"I have a 15-year-old now who is behind in achieving her goal of becoming what she wants to be when she graduates. It's been hard trying to help her catch up," Collins said.
The criminal investigation lasted 21 months and the allegations date back to 2005. In addition to Hall, 34 people were indicted: four high-level administrators, six principals; two assistant principals; six testing coordinators; 14 teachers; a school improvement specialist and a school secretary.
All of the people named in the indictment face conspiracy charges. Other charges in the 65-count indictment include false statements and writings, false swearing, theft and influencing witnesses.
The investigation involved at least 50 schools as well as hundreds of interviews with school administrators, staff, parents and students. The district has about 50,000 students.
Howard would not directly answer a question about whether Hall led the conspiracy.
"What we're saying is that without her, this conspiracy could not have taken place," he said. "It would not have taken place if her actions had not made that possible."
Hall faces up to 45 years in prison, Howard said.
Richard Deane, an attorney for Hall, did not immediately return a call seeking comment.
The tests were the key measure the state used to determine whether it met the federal No Child Left Behind law. Schools with good test scores get extra federal dollars to spend in the classroom or on teacher bonuses.
It wasn't immediately clear how much bonus money Hall received. Howard did not say and the amount wasn't mentioned in the indictment.
"Those results were caused by cheating. ... And the money that she received, we are alleging that money was ill-gotten," Howard said.
The previous state investigation in 2011 found cheating by nearly 180 educators in 44 Atlanta schools. Educators gave answers to students or changed answers on tests after they were turned in, investigators said. Teachers who tried to report it faced retaliation, creating a culture of "fear and intimidation" in the district.
State schools Superintendent John Barge said last year he believed the state's new accountability system would remove the pressure to cheat on standardized tests because it won't be the sole way the state determines student growth. The pressure was part of what some educators in Atlanta Public Schools blamed for their cheating.
Hall served as superintendent for more than a decade, which is rare for an urban schools chief. She was named Superintendent of the Year by the American Association of School Administrators in 2009 and credited with raising student test scores and graduation rates, particularly among the district's poor and minority students. But the award quickly lost its luster as her district became mired in the scandal.
In a video message to schools staff before she retired, Hall warned that the state investigation launched by former Gov. Sonny Perdue would likely reveal "alarming" behavior.
"It's become increasingly clear that a segment of our staff chose to violate the trust that was placed in them," Hall said. "There is simply no excuse for unethical behavior and no room in this district for unethical conduct. I am confident that aggressive, swift action will be taken against anyone who believed so little in our students and in our system of support that they turned to dishonesty as the only option."
The cheating came to light after The Atlanta Journal-Constitution reported that some scores were statistically improbable.
Most of the 178 educators named in the special investigators' report in 2011 resigned, retired, did not have their contracts renewed or appealed their dismissals and lost. Twenty-one educators have been reinstated and three await hearings to appeal their dismissals, said Atlanta Public Schools spokesman Stephen Alford.
Superintendent Erroll Davis said the district was focused on nurturing an ethical environment, providing quality education and supporting the employees who were not implicated.
"I know that our children will succeed when the adults around them work hard, work together, and do so with integrity," he said in a statement.
The Georgia Professional Standards Commission is responsible for licensing teachers and has been going through the complaints against teachers, said commission executive secretary Kelly Henson. Of the 159 cases the commission has reviewed, 44 resulted in license revocations, 100 got two-year suspensions and nine were suspended for less than two years, Henson said. No action was taken against six of the educators.
Mar. 27, 2013 ? Scientists at Harvard may have new hope for anyone who's tried to fight the battle of the bulge.
New research, conducted in collaboration with researchers at Massachusetts General Hospital, has found that the gut microbes of mice undergo drastic changes following gastric bypass surgery. Transfer of these microbes into sterile mice resulted in rapid weight loss. The study is described in a March 27 paper in Science Translational Medicine.
"Simply by colonizing mice with the altered microbial community, the mice were able to maintain a lower body fat, and lose weight -- about 20% as much as they would if they underwent surgery," said Peter Turnbaugh, a Bauer Fellow at Harvard's Faculty of Arts and Sciences (FAS) Center for Systems Biology, and one of two senior authors of the paper.
But as striking as those results were, they weren't as dramatic as they might have been.
"In some ways we were biasing the results against weight loss," Turnbaugh said, explaining that the mice used in the study hadn't been given a high-fat, high-sugar diet to increase their weight beforehand. "The question is whether we might have seen a stronger effect if they were on a different diet."
"Our study suggests that the specific effects of gastric bypass on the microbiota contribute to its ability to cause weight loss and that finding ways to manipulate microbial populations to mimic those effects could become a valuable new tool to address obesity," said Lee Kaplan, director of the Obesity, Metabolism and Nutrition Institute at MGH and the other senior author of the paper.
"We need to learn a good deal more about the mechanisms by which a microbial population changed by gastric bypass exert its effects, and then we need to learn if we can produce these effects -- either the microbial changes or the associated metabolic changes -- without surgery," Kaplan, an associate professor of Medicine at Harvard Medical School, added. "The ability to achieve even some of these effects without surgery would give us an entirely new way to treat the critical problem of obesity, one that could help patients unable or unwilling to have surgery."
While the results were exciting, Turnbaugh warned that it may be years before they could be replicated in humans, and that such microbial changes shouldn't be viewed as a way to lose those stubborn last 10 pounds without going to the gym. Rather, the technique may one day offer hope to dangerously obese people who want to lose weight without going through the trauma of surgery.
"It may not be that we will have a magic pill that will work for everyone who's slightly overweight," he said. "But if we can, at a minimum, provide some alternative to gastric bypass surgery that produces similar effects, it would be a major advance."
While there had been hints that the microbes in the gut might change after bypass surgery, the speed and extent of the change came as a surprise to the research team.
In earlier experiments, researchers had shown that the guts of both lean and obese mice are populated by varying amounts of two types of bacteria, Firmicutes and Bacteroidetes. When mice undergo gastric bypass surgery, however, it "resets the whole picture," Turnbaugh said.
"The post-bypass community was dominated by Proteobacteria and Proteobacteria, and had relatively low levels of Firmicutes," he said. What's more, Turnbaugh said, those changes occurred within a week of the surgery, and weren't short-lived -- the altered gut microbial community remained stable for months afterward.
While the results may hold out the hope for weight loss without surgery, both Turnbaugh and Kaplan warned that future studies are needed to understand exactly what is behind the weight loss seen in mice.
"A major gap in our knowledge is the underlying mechanism linking microbes to weight loss," Turnbaugh said. "There were certain microbes that we found at higher abundance after surgery, so we think those are good targets for beginning to understand what's taking place."
In fact, Turnbaugh said, the answer may not be the specific types of microbes, but a by-product they excrete.
In addition to changes in the microbes found in the gut, researchers found changes in the concentration of certain short-chain fatty acids. Other studies, Turnbaugh said, have suggested that those molecules may be critical in signaling to the host to speed up metabolism, or not to store excess calories as fat.
Going forward, Turnbaugh and Kaplan hope to continue to explore those questions.
"We think such studies will allow us to understand how host/microbial interactions in general can influence the outcome of a given diet," Kaplan said. "To some degree, what we're learning is a comfort for people who have an issue with their weight, because more and more we're learning that the story is more complicated than just how much you exercise and how much you eat."
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The above story is reprinted from materials provided by Harvard University, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
A. P. Liou, M. Paziuk, J.-M. Luevano, S. Machineni, P. J. Turnbaugh, L. M. Kaplan. Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity. Science Translational Medicine, 2013; 5 (178): 178ra41 DOI: 10.1126/scitranslmed.3005687
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.
Several Windows 8 apps, including Calendar, Mail and People, received updates just yesterday, and today Microsoft's Xbox Music is getting a refresh of its own. The music app's update brings both performance improvements to Windows RT devices and some new functionality. Among the new features is a volume control that sets the app's volume independent of the system's volume. The update also brings the ability to automatically sync your music collection to the cloud and add songs from your collection to other devices running Xbox music. Finally, as you can see in the screen grab above, there's a new playing UI that displays all tracks from an album in addition to the song currently playing. You can check out the update yourself by clicking through to the Windows Store via the source link.
Mar. 25, 2013 ? In an animal study, researchers at the University of Washington show that it was possible to use gene therapy to boost heart muscle function. The finding suggests that it might be possible to use this approach to treat patients whose hearts have been weakened by heart attacks and other heart conditions.
Led by University of Washington (UW) Professor and Vice Chair of Bioengineering Michael Regnier and Dr. Chuck Murry, director of the Center for Cardiovascular Biology and co-director of the Institute for Stem Cell and Regenerative Medicine at UW, the study appears online today in the journal Proceedings of the National Academy of Sciences (PNAS).
Normally, muscle contraction is powered by a molecule, the nucleotide called Adenosine-5'-triphosphate (ATP). Other naturally occurring nucleotides can also power muscle contraction, but, in most cases, they have proven to be less effective than ATP.
In an earlier study of isolated muscle, however, Regnier, Murry and colleagues had found that one naturally occurring molecule, called 2 deoxy-ATP (dATP), was actually more effective than ATP in powering muscle contraction, increasing both the speed and force of the contraction, at least over the short-term.
In the new PNAS study, the researchers wanted to see whether this effect could be sustained. To do this, they used genetic engineering to create a strain of mice whose cells produced higher-than-normal levels of an enzyme called Ribonucleotide Reductase, which converts the precursor of ATP, adenosine-5'-diphosphate or ADP, to dADP, which, in turn, is rapidly converted to dATP.
"This fundamental discovery, that dATP can act as a 'super-fuel' for the contractile machinery of the heart, or myofilaments, opens up the possibility to treat a variety of heart failure conditions," Regnier said. "An exciting aspect of this study and our ongoing work is that a relatively small increase in dATP in the heart cells has a big effect on heart performance."
The researchers found that increased production of the enzyme Ribonucleotide Reductase increased the concentration of dATP within heart cells approximately tenfold, and even though this level was still less than one to two percent of the cell's total pool of ATP, the increase led to a sustained improvement in heart muscle function, with the genetically engineered hearts contracting more quickly and with greater force.
"It looks as though we may have stumbled on an important pathway that nature uses to regulate heart contractility," Murry added. "The same pathway that heart cells use to make the building blocks for DNA during embryonic growth makes dATP to supercharge contraction when the adult heart is mechanically stressed."
Importantly, the elevated dATP effect was achieved without imposing additional metabolic demands on the cells, suggesting the modification would not harm the cell's functioning over the long-term.
The finding, the authors write, suggest that treatments that elevate dATP levels in heart cells may prove to be an effective treatment for heart failure.
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The above story is reprinted from materials provided by University of Washington - Health Sciences, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Sarah G. Nowakowski, Stephen C. Kolwicz, Frederick Steven Korte, Zhaoxiong Luo, Jacqueline N. Robinson-Hamm, Jennifer L. Page, Frank Brozovich, Robert S. Weiss, Rong Tian, Charles E. Murry, and Michael Regnier. Transgenic overexpression of ribonucleotide reductase improves cardiac performance. PNAS, March 25, 2013 DOI: 10.1073/pnas.1220693110
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.
Author: Mishel Roserberg | Total views: 79 Comments: 0 Word Count: 837 Date:
SEO is the process where a webmaster tweaks his or her site around to get the highest search engine ranking. It is a massive business and a powerful process. Some Internet marketers might say that SEO is too advanced for the regular site owner. Don't listen to that!
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2: Why You Need To Build Multiple Streams of Income For Yourself
Being an entrepreneur and earning multiple streams of income is a dream that many have, but in reality it does take some initial hard work to achieve this. Earning multiple streams of income is the wave of the future, and here are some tips and advice for you when you are looking for ways in which to do this for yourself.
3: What is Cyber Marketing And Why It Is So Important For The Success Of Your Website
Cyber marketing has now become an indispensable segment of e-commerce as well as the internet and World Wide Web related topics. Cyber marketing simply refers to a technique of attracting potential customers by advertising your products or services through such means as websites, emails, and banners.
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Businesses go to so much trouble when there is one sure-fire, simple, very inexpensive way to attract new clients to a business: Teach a free class. That is what article marketing is like. Your articles are just like free classes. You teach your target readers something helpful in your article. Your resource box then says, "If you enjoyed this article you can visit my website and apply what you have learned."
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If you want your SEO to work you now need to concentrate on appeasing Google Panda, and to do this you need to know what Google Panda's spiders/bots will be looking for. Find out here how to search engine optimise your website for the latest Google Panda algorithm, and achieve the success you deserve.
I'm up, up, and away later today for San Francisco, California and the Game Developer Conference (GDC 2013). I certainly don't have to tell anyone here how great the iPhone, iPod touch, and iPad are for gaming. Whether or not Apple "gets" gaming, they've enabled a lot of technology that a lot of developers have used to make great games. That's why, increasingly, iOS is a big deal in the gaming industry, and at events like GDC.
I'll be there along with our gaming editor Simon Sage, and Windows Phone Central's Paul Acevado. Our goal at the show is to get a better idea of where mobile gaming is going in 2013, get a look at some upcoming titles, and do our very best to bring you all with us. As always, the official stuff will go up right here on iMore, Android Central, CrackBerry, and Windows Phone Central, and if you want the behind-the-scenes shenanigans, you should follow us on Twitter @reneritchie, @simonsage, and @segacon.
Because I'm flying today, I recorded the iMore show on Friday, and with Dieter Bohn from the Verge to boot. (Dieter started the show way back in 2007, and the first podcast I ever did was with Dieter, so it was great to have him back on.) He's one of the mightiest minds in mobile, and the show was a blast, so if you haven't already, check it out.
We've also got what might be the biggest episodes of Debug in the history of Debug coming your way Monday, so make sure you check back here in the morning. You won't want to miss it.
We've gotten a ton of applications already, but since I'll be away, we won't even be able to start going through them until next week. That means there's still plenty of time. Also, We may also be looking for a few more part-time writers in the near future, so if you don't have the experience necessary to help run a site like iMore -- and frankly, that skill set isn't too common yet -- there'll be ways to get a start too. More on that soon!
Also, If you're a developer, designer, gamer, or iMore reader in SF, don't hesitate to say hello. I'd love to talk to you.
Gladstone scientists discover that DNA damage occurs as part of normal brain activityPublic 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."
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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.
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Gladstone scientists discover that DNA damage occurs as part of normal brain activityPublic 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."
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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.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
NEW YORK (Reuters) - Stocks rose on Friday, rebounding from their biggest decline in nearly a month, as a banking deal between Greece and Cyprus eased some concerns about the island nation as it tries to avoid a financial meltdown.
Cyprus agreed with Greece on a takeover of the Greek units of Cypriot banks, which ended uncertainty over the fate of those operations.
But Russia rebuffed Cypriot entreaties for aid, leaving the island's leaders scrambling to strike a bailout deal with the European Union by next week or face the collapse of its financial system and an exit from the euro that could roil the euro zone.
"While the market may be vulnerable because it's up so much, the U.S. economy is in a better shape and better position to withstand the whole euro zone and Cyprus situation," said Randy Frederick, managing director of active trading and derivatives at Charles Schwab.
The Dow Jones industrial average <.dji> was up 76.82 points, or 0.53 percent, at 14,498.31. The Standard & Poor's 500 Index <.spx> was up 8.81 points, or 0.57 percent, at 1,554.61. The Nasdaq Composite Index <.ixic> was up 14.50 points, or 0.45 percent, at 3,237.09.
On Thursday, the S&P 500 fell 0.8 percent while the Dow ended down 0.6 percent, as Oracle's revenue fell far short of expectations and worries intensified about the effect of Cyprus' troubles on the euro zone.
On Friday, retail stocks were the top gainers.
Tiffany & Co reported a slightly higher profit for the quarter that included the holiday season and said net worldwide sales would rise 6 percent to 8 percent this fiscal year, with growth in all regions. The stock was up 2 percent at $69.29.
Nike Inc shares jumped 11 percent to $59.50 as several brokerages upgraded the stock after the company's quarterly profit beat Wall Street expectations.
Blackstone Group LP and General Electric Co's lending arm have discussed jointly pursuing Dell Inc's financial-services business, the Wall Street Journal reported, citing people familiar with the matter.
Blackstone shares were down 0.3 percent at $19.84. GE shares were little changed at $23.30 and Dell shares were also flat at around $14.14.
The European Union has given Cyprus until Monday to raise 5.8 billion euros to secure a 10-billion euro international bailout. Parliament has already rejected one deal.
NICOSIA/MOSCOW (Reuters) - Russia rebuffed Cypriot entreaties for aid on Friday, leaving the island's increasingly isolated leaders scrambling to strike a bailout deal with the European Union by next week or face the collapse of its financial system.
In Nicosia, the country's biggest bank urged politicians to make haste and cut a deal with their EU partners as parliament considered proposals to nationalize pension funds, pool state assets and split the country's second-largest bank in a desperate effort to satisfy those exasperated European allies.
The governor of the Central Bank, Panicos Demetriades, warned political leaders the country would face a disorderly bankruptcy on Tuesday unless they approved the bills, an official present at the talks said.
"The next few hours will determine the future of the country," government spokesman Christos Stylianides said before the parliamentary debate. "We must all assume our share of the responsibility."
Even if the measures are approved, there was no confirmation they would raise the 5.8 billion euros demanded by the EU in return for a 10 billion euro ($12.9 billion) bailout to avoid a default.
The biggest local bank, the Bank of Cyprus, urged the government to go back and make a deal from the European Union, under which larger deposits over 100,000 euros, would be taxed. It was preferable, it said, to a collapse of the system and a return to the Cypriot pound which would wipe out assets.
"There must be no further delay," the bank said.
Cypriot insistence on taxing even small savers - in hopes of limiting damage to an offshore banking sector heavily dependent on larger Russian depositors - saw a bailout deal that had been agreed with the EU a week ago rejected by parliament on Tuesday.
Several hundred people rallied peacefully outside parliament on Friday, holding banners saying 'No to the victimization of banks'. "Our so-called friends and partners sold us out," said Marios Panayides, 65.
"They have completely abandoned us on the edge of an abyss."
Elsewhere, depositors, who have been besieging bank cash machines all week, queued again to withdraw what they could.
The clock was running down to a Monday deadline set by the European Central Bank for a deal to be in struck before it cuts funds to Cyprus's stricken banks, potentially pushing it out of Europe's single currency.
RUSSIAN REFUSAL
Nicosia angrily rejected a proposed levy on tax deposits in exchange for the EU bailout on Tuesday and turned to the Kremlin to renegotiate a loan deal, win more financing and lure Russian investors to Cypriot banks and gas reserves.
"The talks have ended as far as the Russian side is concerned," Russian Finance Minister Anton Siluanov told reporters after two days of crisis talks with his Cypriot counterpart, Michael Sarris.
Russians have billions of euros at stake in Cyprus's outsized and now crippled banking sector, a factor in the EU's unprecedented demand that bigger depositors take a hit in the interests of keeping Cyprus afloat.
But Siluanov said Russian investors were not interested in Cypriot gas and that the talks had ended without result. Sarris was due to fly home, where lawmakers were locked in yet more crisis talks.
New bills submitted to the Cypriot parliament included a "solidarity fund" to bundle state assets, including future gas revenues and nationalized semi-state pension funds, as the basis for an emergency bond issue.
JP Morgan likened it to "a national fire sale", and euro zone paymaster Germany indicated it opposed the nationalization of pension funds.
They were also considering a bank restructuring bill that officials said would see the country's second largest lender, Cyprus Popular Bank, split into good and bad assets, and a government call for the power to impose capital controls to stem a flood of funds leaving the island when banks reopen on Tuesday after a week-long shutdown.
"PLAYING WITH FIRE"
There was no silver bullet, however, and Cyprus's partners in the 17-nation currency bloc were increasingly unimpressed. It was unclear whether parliament would even vote on the bills on Friday.
"I still believe we will get a settlement, but Cyprus is playing with fire," Volker Kauder, a leading conservative ally of German Chancellor Angela Merkel, told public television ARD.
Merkel told lawmakers that nationalization of pension funds was unacceptable as a way to plug a hole in finances and clinch the bailout, parliamentary sources said.
Two lawmakers quoted the chancellor as saying debt sustainability and bank restructuring would have to be the core of any deal, which she called a matter of "credibility".
They also quoted Merkel as saying: "There is no way we can accept that", and "I hope it does not come to a crash".
Her finance minister, Wolfgang Schaeuble, said he did not know whether euro zone finance ministers would meet over the weekend. "I can't say in advance if and when Cyprus will deliver results," he said.
Cypriots have been stunned by the pace of the unfolding drama, having elected conservative President Nicos Anastasiades barely a month ago on a mandate to secure a bailout.
News that the deal would involve a levy on bank deposits, even for smaller savers, outraged Cypriots.
While EU lenders, notably Germany, had wanted larger, uninsured bank depositors to bear some of the cost of recapitalizing the banks, Cyprus feared for its reputation as an offshore banking haven and planned to spread the levy to deposits under 100,000 were covered by state insurance.
Senior euro zone officials acknowledged in a confidential conference call on Wednesday that they were "in a mess" and discussed imposing capital controls to insulate the currency area from a possible collapse of the small Cypriot economy.
Cyprus itself refused to take part in the call, minutes of which were seen by Reuters. Several participants described its absence as troubling and reflecting the wider confusion surrounding the island's predicament.
In Brussels, a senior European Union official told Reuters an ECB withdrawal would mean Cyprus's biggest banks being wound up, wiping out the large deposits it has sought to protect, and probably forcing the country to abandon the euro.
"If the financial sector collapses, then they simply have to face a very significant devaluation, and faced with that situation, they would have no other way but to start having their own currency," the EU official said.
Cypriot banks have been crippled by their exposure to Greece, the center of the euro zone debt crisis.
On Friday, Greece began transferring the Greek units of Cypriot banks to a Greek banking group, in coordination with the central bank in Cyprus, ending uncertainty for local savers.
(Additional reporting by Jan Strupczewski and Luke Baker in Brussels, Karolina Tagaris and Costas Pitas in Nicosia, Georgina Prodhan in Vienna, Lidia Kelly and Darya Korsunskaya in Moscow, Paul Carrel in Frankfurt and Gernot Heller in Berlin; Writing by Matt Robinson; Editing by Philippa Fletcher and Alastair Macdonald)
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From gas to new -- dating services different different things co leader -- 798. Darlene Joseph Louis bonded out for a federal charge of theft by taking. Head stolen over non thousand dollars from the girl scout. Tracy Williams -- co leader for the past three years told me by phone that dipping into the funds appears to become an easy habit for her. Had a PayPal account to that the debit card and we just making our own personal purchases off of the entry account. According to Williams it wasn't until she became a co leader with Lewis in 2010. That Lewis had anyone to answer to. Williams said she continually asked to -- bank statements and always got excuses. Lewis even commenting to Williams wants. I looked at the balance and I thought there was more than that the account typically held 151000 dollars in it. In this instance it was it 6000. She did pay some money back over -- But out of the ever 101000 dollars joint pay back a few hundred. We went to lewis' home to get a comment there was no answer at the door she was home however and did call that Carroll county sheriffs on us she had. Couple years and she was taken the money out she could have put it back -- and probably no 11 another's.
This transcript has been automatically generated and may not be 100% accurate.
Mar. 18, 2013 ? A study in the Journal of the American Medical Association Neurology suggests that controlling or preventing risk factors, such as hypertension, earlier in life may limit or delay the brain changes associated with Alzheimer's disease and other age-related neurological deterioration.
Dr. Karen Rodrigue, assistant professor in the UT Dallas Center for Vital Longevity (CVL), was lead author of a study that looked at whether people with both hypertension and a common gene had more buildup of a brain plaque called amyloid protein, which is associated with Alzheimer's disease. Scientists believe amyloid is the first symptom of Alzheimer's disease and shows up a decade or more before symptoms of memory impairment and other cognitive difficulties begin. The gene, known as APOE 4, is carried by 20 percent of the population.
Until recently, amyloid plaque could be seen only at autopsy, but new brain scanning techniques allow scientists to see plaque in living brains of healthy adults. Findings from both autopsy and amyloid brain scans show that at least 20 percent of typical older adults carry elevated levels of amyloid, a substance made up mostly of protein that is deposited in organs and tissues.
"I became interested in whether hypertension was related to increased risk of amyloid plaques in the brains of otherwise healthy people," Rodrigue said. "Identifying the most significant risk factors for amyloid deposition in seemingly healthy adults will be critical in advancing medical efforts aimed at prevention and early detection."
Based on evidence that hypertension was associated with Alzheimer's disease, Rodrigue suspected that the combination of hypertension and the presence of the APOE-e4 gene might lead to particularly high levels of amyloid plaque in healthy adults.
Rodrigue's research was part of the Dallas Lifespan Brain Study, a comprehensive study of the aging brain in a large group of adults of all ages funded by the National Institute on Aging. Rodrigue's group recruited 147 participants (ages 30-89) to undergo cognitive testing, magnetic resonance imaging (MRI) and PET imaging using Amyvid. Amyvid is a compound that when injected travels to the brain and binds with amyloid proteins, allowing the scientists to visualize the amount of amyloid plaque. Blood pressure also was measured at each visit.
Rodrigue classified participants in the study as hypertensive if they reported a current physician diagnosis of hypertension or if their blood pressure exceeded the established criteria for diagnosis. The participants were further divided into groups based on whether they were taking anti-hypertensive medications or if they were unmedicated and showed blood pressure elevations consistent with a diagnosis of hypertension. Finally, study subjects were classified in the genetic risk group if they were in the 20 percent of adults who had one or two copies of an APOE ?4 allele, a genetic variation linked to dementia.
The most striking result of the study was that nonmedicated hypertensive adults who also carried a genetic risk factor for Alzheimer's disease showed much higher amyloid levels than all other groups. Adults with medication-controlled hypertension, even those with genetic risk, had levels of amyloid plaque equivalent to participants without hypertension or genetic risk.
The study suggests that controlling hypertension may significantly decrease the risk of developing amyloid deposits, even in those with genetic risk. Rodrigue noted that long-term studies are needed to be certain that the use of hypertensive medications decreased amyloid deposits. Nevertheless, this early finding provides a window into the potential benefits of controlling hypertension that goes beyond lowering the risk of strokes and other cardiovascular complications.
Scientists cannot fully explain the neural mechanisms underlying the effect of hypertension and APOE ?4 on amyloid accumulation. But earlier research in animal models has shown that chronic hypertension may enable easier penetration of the blood-brain barrier, resulting in more amyloid deposition.
The recent study is significant because it focuses on a group of healthy and cognitively normal middle-aged and older adults, which enables the examination of risk factors and amyloid burden before the development of preclinical dementia. The team plans for long-term, longitudinal follow-up with participants to determine the proportion of the subjects who eventually develop the disease.
The study's co-authors included Dr. Denise Park, director of the Dallas Lifespan Brain Study and co-director of the Center for Vital Longevity, Dr. Kristen Kennedy and doctoral student Jennifer Rieck, all from The University of Texas at Dallas. The team also included Dr. Michael Devous and Dr. Ramon Diaz-Arrastia from UT Southwestern Medical Center and the Uniformed Services University of the Health Sciences. In addition to the National Institute on Aging support, the Alzheimer's Association provided funds for the study and Avid Radiopharmaceutical provided doses of Amyvid used in scanning.
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The above story is reprinted from materials provided by University of Texas at Dallas.
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Journal Reference:
Karen M. Rodrigue et al. Risk Factors for ?-Amyloid Deposition in Healthy AgingVascular and Genetic EffectsFactors for ?-Amyloid Deposition in Healthy Aging. JAMA Neurology, 2013; : 1 DOI: 10.1001/jamaneurol.2013.1342
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Public release date: 24-Mar-2013
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