LOS ANGELES (Reuters) - R&B singer Chris Brown, on probation for beating his former girlfriend, was charged on Tuesday with a hit-and-run and driving without a valid license in connection with a May 21 traffic accident in Los Angeles. Brown, 24, allegedly rear-ended another car and faces up to six months in jail on each misdemeanor charge, L.A. City Attorney spokesman Frank Mateljan said. He will be arraigned in Los Angeles Superior Court on July 15, Mateljan said. ...
Study identifies protein that contributes to cognitive decline in Alzheimer'sPublic release date: 25-Jun-2013 [ | E-mail | Share ]
Contact: Karin Eskenazi ket2116@columbia.edu 212-342-0508 Columbia University Medical Center
Findings highlight potential therapeutic targets
NEW YORK, NY (June 25, 2013) Researchers at Columbia University Medical Center (CUMC) have demonstrated that a protein called caspase-2 is a key regulator of a signaling pathway that leads to cognitive decline in Alzheimer's disease. The findings, made in a mouse model of Alzheimer's, suggest that inhibiting this protein could prevent the neuronal damage and subsequent cognitive decline associated with the disease. The study was published this month in the online journal Nature Communications.
One of the earliest events in Alzheimer's is disruption of the brain's synapses (the small gaps across which nerve impulses are passed), which can lead to neuronal death. Although what drives this process has not been clear, studies have indicated that caspace-2 might be involved, according to senior author Michael Shelanski, MD, PhD, the Delafield Professor of Pathology & Cell Biology, chair of the Department of Pathology & Cell Biology, and co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC.
Several years ago, in tissue culture studies of mouse neurons, Dr. Shelanski found that caspace-2 plays a critical role in the death of neurons in the presence of amyloid beta, the protein that accumulates in the neurons of people with Alzheimer's. Other researchers have shown that caspase-2 also contributes to the maintenance of normal synaptic functions.
Dr. Shelanski and his team hypothesized that aberrant activation of caspase-2 may cause synaptic changes in Alzheimer's disease. To test this hypothesis, the researchers crossed J20 transgenic mice (a common mouse model of Alzheimer's) with caspase-2 null mice (mice that lack caspase-2). They compared the animals' ability to negotiate a radial-arm water maze, a standard test of cognitive ability, with that of regular J20 mice and of normal mice at 4, 9, and 14 months of age.
The results for the three groups of mice were similar at the first two intervals. At 14 months, however, the J20/caspase-2 null mice did significantly better in the water maze test than the J20 mice and similarly to the normal mice. "We showed that removing caspase-2 from J20 mice prevented memory impairment without significant changes in the level of soluble amyloid beta," said co-lead author Roger Lefort, PhD, associate research scientist at CUMC.
Analysis of the neurons showed that the J20/caspase-2 null mice had a higher density of dendritic spines than the J20 mice. The more spines a neuron has, the more impulses it can transmit.
"The J20/caspase-2 null mice showed the same dendritic spine density and morphology as the normal miceas opposed to the deficits in the J20 mice," said co-lead author Julio Pozueta, PhD. "This strongly suggests that caspase-2 is a critical regulator in the memory decline associated with beta-amyloid in Alzheimer's disease."
The researchers further validated the results in studies of rat neurons in tissue culture.
Finally, the researchers found that caspase-2 interacts with RhoA, a critical regulator of the morphology (form and structure) of dendritic spines. "It appears that in normal neurons, caspase-2 and RhoA form an inactive complex outside the dendritic spines," said Dr. Lefort. "When the complex is exposed to amyloid beta, it breaks apart, activating the two components." Once activated, caspase-2 and RhoA enter the dendritic spines and contribute to their demise, possibly by interacting with a third molecule, the enzyme ROCK-II.
"This raises the possibility that if you can inhibit one or all of these molecules, especially early in the course of Alzheimer's, you might be able to protect neurons and slow down the cognitive effects of the disease," said Dr. Lefort.
###
The paper is titled, "Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice." The other contributors are Julio Pozueta, PhD (co-lead author), Elena M. Ribe, Carol M. Troy, and Ottavio Arancio, all based at CUMC at the time of the study.
Dr. Pozueta was an associate research scientist at CUMC at the time of this research and is currently a senior analyst at Prescient Life Sciences. The remaining authors declare no financial or other conflicts of interests.
The study was supported by grants from the National Institutes of Health (NIHAG08702 and NS15076), the Wallace Foundation for Research, and the Taub Foundation.
The Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center is a multidisciplinary group that has forged links between researchers and clinicians to uncover the causes of Alzheimer's, Parkinson's, and other age-related brain diseases and to discover ways to prevent and cure these diseases. It has partnered with the Gertrude H. Sergievsky Center at Columbia University Medical Center, which was established by an endowment in 1977 to focus on diseases of the nervous system, and with the Departments of Pathology & Cell Biology and of Neurology to allow the seamless integration of genetic analysis, molecular and cellular studies, and clinical investigation to explore all phases of diseases of the nervous system. For more information, visit The Taub Institute at http://www.cumc.columbia.edu/dept/taub/.
Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org.
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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.
Study identifies protein that contributes to cognitive decline in Alzheimer'sPublic release date: 25-Jun-2013 [ | E-mail | Share ]
Contact: Karin Eskenazi ket2116@columbia.edu 212-342-0508 Columbia University Medical Center
Findings highlight potential therapeutic targets
NEW YORK, NY (June 25, 2013) Researchers at Columbia University Medical Center (CUMC) have demonstrated that a protein called caspase-2 is a key regulator of a signaling pathway that leads to cognitive decline in Alzheimer's disease. The findings, made in a mouse model of Alzheimer's, suggest that inhibiting this protein could prevent the neuronal damage and subsequent cognitive decline associated with the disease. The study was published this month in the online journal Nature Communications.
One of the earliest events in Alzheimer's is disruption of the brain's synapses (the small gaps across which nerve impulses are passed), which can lead to neuronal death. Although what drives this process has not been clear, studies have indicated that caspace-2 might be involved, according to senior author Michael Shelanski, MD, PhD, the Delafield Professor of Pathology & Cell Biology, chair of the Department of Pathology & Cell Biology, and co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC.
Several years ago, in tissue culture studies of mouse neurons, Dr. Shelanski found that caspace-2 plays a critical role in the death of neurons in the presence of amyloid beta, the protein that accumulates in the neurons of people with Alzheimer's. Other researchers have shown that caspase-2 also contributes to the maintenance of normal synaptic functions.
Dr. Shelanski and his team hypothesized that aberrant activation of caspase-2 may cause synaptic changes in Alzheimer's disease. To test this hypothesis, the researchers crossed J20 transgenic mice (a common mouse model of Alzheimer's) with caspase-2 null mice (mice that lack caspase-2). They compared the animals' ability to negotiate a radial-arm water maze, a standard test of cognitive ability, with that of regular J20 mice and of normal mice at 4, 9, and 14 months of age.
The results for the three groups of mice were similar at the first two intervals. At 14 months, however, the J20/caspase-2 null mice did significantly better in the water maze test than the J20 mice and similarly to the normal mice. "We showed that removing caspase-2 from J20 mice prevented memory impairment without significant changes in the level of soluble amyloid beta," said co-lead author Roger Lefort, PhD, associate research scientist at CUMC.
Analysis of the neurons showed that the J20/caspase-2 null mice had a higher density of dendritic spines than the J20 mice. The more spines a neuron has, the more impulses it can transmit.
"The J20/caspase-2 null mice showed the same dendritic spine density and morphology as the normal miceas opposed to the deficits in the J20 mice," said co-lead author Julio Pozueta, PhD. "This strongly suggests that caspase-2 is a critical regulator in the memory decline associated with beta-amyloid in Alzheimer's disease."
The researchers further validated the results in studies of rat neurons in tissue culture.
Finally, the researchers found that caspase-2 interacts with RhoA, a critical regulator of the morphology (form and structure) of dendritic spines. "It appears that in normal neurons, caspase-2 and RhoA form an inactive complex outside the dendritic spines," said Dr. Lefort. "When the complex is exposed to amyloid beta, it breaks apart, activating the two components." Once activated, caspase-2 and RhoA enter the dendritic spines and contribute to their demise, possibly by interacting with a third molecule, the enzyme ROCK-II.
"This raises the possibility that if you can inhibit one or all of these molecules, especially early in the course of Alzheimer's, you might be able to protect neurons and slow down the cognitive effects of the disease," said Dr. Lefort.
###
The paper is titled, "Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice." The other contributors are Julio Pozueta, PhD (co-lead author), Elena M. Ribe, Carol M. Troy, and Ottavio Arancio, all based at CUMC at the time of the study.
Dr. Pozueta was an associate research scientist at CUMC at the time of this research and is currently a senior analyst at Prescient Life Sciences. The remaining authors declare no financial or other conflicts of interests.
The study was supported by grants from the National Institutes of Health (NIHAG08702 and NS15076), the Wallace Foundation for Research, and the Taub Foundation.
The Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center is a multidisciplinary group that has forged links between researchers and clinicians to uncover the causes of Alzheimer's, Parkinson's, and other age-related brain diseases and to discover ways to prevent and cure these diseases. It has partnered with the Gertrude H. Sergievsky Center at Columbia University Medical Center, which was established by an endowment in 1977 to focus on diseases of the nervous system, and with the Departments of Pathology & Cell Biology and of Neurology to allow the seamless integration of genetic analysis, molecular and cellular studies, and clinical investigation to explore all phases of diseases of the nervous system. For more information, visit The Taub Institute at http://www.cumc.columbia.edu/dept/taub/.
Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org.
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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.
25 June 2013Last updated at 09:18 ETBy Jonathan AmosScience correspondent, BBC News
Scientists have identified three new planets around a star they already suspected of hosting a trio of worlds.
It means this relatively nearby star, Gliese 667C, now has three so-called super-Earths orbiting in its "habitable zone".
This is the region where temperatures ought to allow for the possibility of liquid water, although no-one can say for sure what conditions are really like on these planets.
Gliese 667C is 22 light-years away.
Astronomers can see it on the sky in the constellation of Scorpius (The Scorpion).
Previous studies of Gliese 667C had established there were very likely three planets around it, with its habitable zone occupied by one super-Earth - an object slightly bigger than our home world, but probably still with a rocky surface.
Now, a team of astronomers led by Guillem Anglada-Escude of the University of G?ttingen, Germany, and Mikko Tuomi, of the University of Hertfordshire, UK, has re-examined the system and raised the star's complement of planets.
The researchers used a suite of telescopes including the 3.6m telescope at the Silla Observatory in Chile. This incorporates the high-precision Harps instrument. Harps employs an indirect method of detection that infers the existence of orbiting planets from the way their gravity makes a parent star appear to twitch in its motion across the sky.
Full to bursting
The planets' presence needs to be disentangled from this complex signal but the Harps instrument is recognised as having tremendous success in identifying smaller worlds.
Gliese 667C is a low-luminosity "M-dwarf" star just over one-third the mass of our Sun.
This means its habitable zone can be much closer in before temperatures make liquid water impossible. The team is now confident that three rocky worlds occupy this region at Gilese 667C.
"Their estimated masses range from 2.7 to 3.8 that of the Earth's," Mikko Tuomi told BBC News.
"However, we can only estimate the physical sizes by assuming certain compositions that is, well, only educated guessing.
"Their orbital periods are 28, 39, and 62 days, which means that they all orbit the star closer to its surface than Mercury in our own system. Yet, the estimated surface temperatures enable the existence of liquid water on them because of the low luminosity and low mass of the star."
These planets are said to completely fill the habitable zone. There are no more stable orbits in which to fit another planet.
That said, the team has found tantalising evidence for what may be another rocky world on the inner-edge of the zone. This would be a seventh planet in the system.
Fruitful targets
The planets would need an atmosphere to sustain liquid water on their surfaces, but at a distance of more than 200 trillion km, there are no means currently to determine what the precise conditions are like or whether life would have any chance of establishing itself.
Nonetheless, Dr Tuomi believes M-dwarf stars are good candidates to go hunting for potentially habitable worlds.
They are small enough that close-in rocky planets will show up well in the Harps Doppler spectroscopy data, but they are also dim enough that those close-orbiting worlds will not be roasted.
"This discovery single-handedly demonstrates that low-mass stars can be hosts of several potentially habitable planets," explained Dr Tuomi.
"In practice, it means that we might have to double or treble our estimates for the occurrence rate of habitable-zone planets around M-dwarf stars.
"There might, in fact, be more habitable-zone planets in the Universe than there are stars, which makes it much easier for the future space missions to obtain images of these planets.
"So, although only a rather simple discovery, its implications might force us to re-think how common habitable-zone planets are in the Universe."
The research has been written up for the journal Astronomy & Astrophysics.
Jonathan.Amos-INTERNET@bbc.co.uk and follow me on Twitter: @BBCAmos
Former Yahoo engineers Brian Acton and Jan Koum are making millions of dollars per year.
They could make hundreds of millions of dollars ? maybe a billion or two.
All it would take is a?relatively brief flurry of paperwork, signatures, and handshakes.
But so far, Acton and Koum?have chosen not to.
Mostly, this is because they hate advertising.
Acton and Koum are making millions because they are the creators of an app called WhatsApp.?It's a text messaging replacement.
Acton and Koum make money from WhatsApp in two ways. They charge iPhone users a one-time $.99 fee upon installation.?They charge Android users $.99 every year (after the first year).?Lots of people have paid Acton and Koum $.99.?The Wall Street Journal reports that?250 million people use WhatsApp every month.
It doesn't take a very complicated estimation to figure out that 250 million people paying $.99 once or annually adds up to a lot of money ? millions and millions of dollars.
Acton and Koum haven't said so (they are very press shy), but you have to assume?huge percentage of that money is going straight into their pockets. ?The company has taken little to zero outside investment. A year ago this time, Acton and Koum told a reporter they only employ 30 people.?Their company does all its development in Russia, where there is cheap talent.
The millions Acton and Koum are making is obviously nice.
But they could make much more ?if they chose to.
They are two ways they could do this:
Acton and Koum could potentially make a lot more money over time by taking venture capital investment and growing WhatsApp into a larger corporation.?Two industry sources tell us that late stage startup investors would love to fund Acton and Koum's project, giving it a valuation north of a billion dollars.
According to several reports, Acton and Koum could make a ton of money right away by selling their app to Google or Facebook.?
So far, Acton and Koum have declined to go down either path.
They haven't explained why.?
But it's pretty clear the reason Acton and Koum have turned all offers down (so far) is that Google, Facebook, and venture capitalists would each demand the same thing for their money: that WhatsApp sell advertising.
Acton and Koum hate advertising.
A couple of days ago, Koum posted a note to the WhatsApp company blog explaining "why we don?t sell ads."
It began with a ?quote from the character Tyler Durden in the book "Fight Club."
"Advertising has us chasing cars and clothes, working jobs we hate so we can buy shit we don?t need."
It went on:
Brian and I spent a combined 20 years at Yahoo!, working hard to keep the site working. And yes, working hard to sell ads, because that?s what Yahoo! did. It gathered data and it served pages and it sold ads.
We watched Yahoo! get eclipsed in size and reach by Google? a more efficient and more profitable ad seller. They knew what you were searching for, so they could gather your data more efficiently and sell better ads.
These days companies know literally everything about you, your friends, your interests, and they use it all to sell ads.
When we sat down to start our own thing together three years ago?we wanted to make something that wasn?t just another ad clearinghouse. We wanted to spend our time building a service people wanted to use because it worked and saved them money and made their lives better in a small way. We knew that we could charge people directly if we could do all those things. We knew we could do what most people aim to do every day: avoid ads.
No one wakes up excited to see more advertising, no one goes to?sleep thinking about the ads they?ll see tomorrow. We know people go to sleep excited about who they chatted with that day (and disappointed about who they didn?t). We want WhatsApp to be the product that keeps you awake? and that you reach for in the?morning. No one jumps up from a nap and runs to see an advertisement.
Advertising isn?t just the disruption of aesthetics, the insults to your intelligence and the interruption of your train of thought. At every company that sells ads, a significant portion of their engineering team spends their day tuning data mining, writing better code to collect all your personal data, upgrading the servers that hold all the data and making sure it?s all being logged and collated and sliced and packaged and shipped out? And at the end of the day the result of it all is a slightly different advertising banner in your browser or on your mobile screen.
Remember, when advertising is involved?you the user?are the product.
At WhatsApp, our engineers spend all their time fixing bugs, adding new features and ironing out all the little intricacies in our task of bringing rich, affordable, reliable messaging to every phone in the world. That?s our product and that?s our passion. Your data?isn?t even in the picture. We are simply not interested in any of it.
When people ask us why we charge for WhatsApp, we say ?Have you considered the alternative??
In Silicon Valley, industry sources are at once amazed by WhatsApp's success and skeptical that Acton and Koum can sustain it.
LinkedIn
Jan Koum's Linkedin Profile
One industry source told us?WhatsApp's?strong and distinct company culture is modeled after Craigslist.
This was not a compliment.
Despite being world famous, Craigslist is still operated as a small, profitable company by its founder, Craig Newmark.
It has made Newmark very wealthy individually, but many believe it could have been a company the size of eBay by now, if it had taken outside money and had been run by someone with greater ambitions.
This source said WhatsApp's company culture makes it?less likely Acton and Koum will be able to build?what?many in the Valley would consider to be a real business and company.
But the thing is ? from where we sit, it doesn't look like Acton and Koum much care if the rest of Silicon Valley views WhatsApp as "a real business and company."
They are already making millions off an app which is used by hundreds of millions of people.
Also, both were relatively early employees at Yahoo, and it's likely that made them financially secure.
The?best evidence that the WhatsApp founders don't care about how the rest of the Valley views them is Jan Koum's Twitter account.?
His avatar for it is not your typical founder's studio head shot. His bio doesn't brag about his title. It's a quote. He is followed by just 4,000 people ? a lot for most people, but not very much for a Silicon Valley star. He only follows one account. It's?@jesus94306, the account for Jesus Christ Silicon Valley, a witheringly satirical blog about the tech business. One of his most recent tweets is a quote from a Kanye West lyric.
"You think you free but you a slave to the funds, baby."
Forward-thinking financial institution Wells Fargo is offering its customers the choice of receiving a text message receipt -- in addition to its e-receipt and email options -- whenever you use one of the bank's ATMs. All that's required to take part in the environmentally friendly scheme is to attach your cellphone number to your account, either online, over the phone or at your local branch. The service is available starting today, and if you'd like to learn more, we've tucked the official release below the fold.
We have a perfect ending for "Mad Men's" season finale: Don Draper jumping out the window.
Obviously there's no chance of that happening. He's the star of the show, and besides, two season-ending suicides in a row (RIP, Lane Pryce) would be awfully repetitive. (Like juggling two juice accounts. RIP, Ocean Spray.)
But nothing is more redundant than Don Draper himself. Other than his brief interlude as a faithful newlywed, you just can't teach this dog new tricks.
Even a year ago, the thought of losing Don would have been inconceivable -- even though the businessman's freefall in the opening title sequence seems to imply that is his ultimate fate. Yeah, yeah, yeah, it's a metaphor, we get it. But the wretched ad exec has become so dull, predictable and dislikable that we really wouldn't miss him if he took a shortcut down to Madison Ave.
Everyone with sense agrees that Jon Hamm is a nearly perfect human creature, but we'd much rather see him in another role -- like his hilarious bubble boy Drew on "30 Rock." And you know what? "Mad Men's" ensemble cast would be just fine without him -- especially Roger Sterling and Sally Draper, who could easily front their own spin-off series.
Here are all the reasons we're over Don Draper:
Serial cheating: He's not unique among his colleagues at Sterling Cooper & Partners, but at least infidelity isn't a full-time hobby for Roger, Pete, Ted (maybe) and the gang. And yes, we know it's a manifestation of Dick Whitman's childhood in a whorehouse, but the backstory doesn't make his adultery any less boring.
Alcoholism: Another snoozer story line. But would Don be more interesting if he were sober? Doubtful. Another Roger acid trip, on the other hand ...
The sads: He wept on Peggy's shoulder and curled up in a fetal position on his disgusted daughter's bed, but we have lost all sympathy for depressed Don. In fact, our reaction is the same as his: Wah, wah, wah.
Tyranny: Don really is a monster, as Peggy called him after he humiliated her and Ted in the season's penultimate episode. He's spiteful, insensitive and downright cruel. So is Pete Campbell -- but at least we love to hate the snarky stair-tumbler. Don we just hate.
Impostor: Once upon a time, Don's identify theft was a thrilling narrative. Now nearly everyone knows the truth, and no one seems to care. Sterling Cooper's creative director works about five minutes a day, is trashed or asleep the rest of the time, insults his clients and colleagues and betrays his family. So why haven't they publicly outed him? Not that we'd really care. Bob Benson's fraud is so much more fascinating now.
Grim Reaper: Don isn't directly to blame for all the show's deaths, but they sure do seem to follow him like Pig Pen's cloud of dirt. And speculation is rampant that Megan might be the next to go, thanks to a number of clues connecting her to Charles Manson victim Sharon Tate. (Megan's obsession with "Rosemary's Baby" -- directed by Tate's husband, Roman Polanski -- only added fuel to the fire.) Her murder would paradoxically breathe new life into "Mad Men" -- but not if it means we'll be subjected to a final season devoted to her widower's grief.
Are you ready for Don to take a flying leap (literally or figuratively)? What do you hope to see in the season finale? Click on "Talk about it" below and share your thoughts!
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Public release date: 25-Jun-2013
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