Ahead of the Federal Reserve‘s policy-setting meeting this week, it’s worth taking a look at the latest figures from the Fed’s balance sheet.
Assets on the Fed’s balance sheet sit at around $2.8 trillion as of last Wednesday. The level has held pretty stable since June 2011, when the central bank ended its bond-buying program, commonly known as QE2.
The central bank has been engaged in a program known as Operation Twist since September of last year. The action shifts the Fed’s holdings into longer-dated government bonds without substantially increasing the size of the balance sheet.
The balance sheet is up from less than $1 trillion prior to the recession. During the downturn the Fed expanded its balance sheet through several programs aimed at keeping markets functioning. As markets stabilized the Fed shifted out of emergency programs and into purchases of U.S. Treasurys, mortgage-backed securities and agency debt securities to drive down interest rates and encourage more borrowing and growth in two separate rounds of what is known as quantitative easing.
The makeup of the balance sheet is moving back toward the long-term trend. The MBS and agency debt holdings, which were part of the first round of quantitative easing, have steadily declined as loans are paid off or mature. The Fed still holds more than $900 billion in MBS and agency debt, but now owns more Treasurys — over $1.65 trillion. The Treasurys holdings are likely to continue to rise, as the central bank purchases bonds with money reinvested from its shrinking MBS portfolio. Amid a continued high unemployment rate and uncertainties surrounding Europe, the Fed has already shifted its Treasurys holdings to focus on longer-term maturities. If conditions deteriorated, the central bank has options on the table including buying MBS or more Treasurys.
Meanwhile, other assets tied to emergency programs are disappearing. The Term Asset-Backed Securities Loan Facility, or TALF, ended in March 2010, and continues to fall due primarily to voluntary prepayments as the market improves and other financing options become more attractive. Direct-bank lending has fallen to the tens of millions of dollars. The Fed has sold off most of the assets related to the rescue of Bear Stearns and AIG and now just holds some $10 billion.
In an effort to track the Fed’s actions, Real Time Economics created an interactive graphic marking the expansion of the central bank’s balance sheet. The chart is updated as often as possible with the latest data released by the Fed.
In an effort to simplify the composition of the balance sheet, some elements have been consolidated. Portfolios holding assets from the Bear Stearns and AIG rescues have been put into one category, as have facilities aimed at supporting commercial paper and money markets. The direct bank lending group includes term auction credit, as well as loans extended through the discount window and similar programs.
Central bank liquidity swaps refer to Fed programs with foreign central banks that allow the institutions to lend out foreign currency to their local banks. Repurchase agreements are short-term temporary purchases of securities from banks, which are looking for liquidity and agree to repurchase them on a specified date at a specified price.
Tuesday, July 31, 2012
Monday, July 30, 2012
Who's the hottest star at Comic-Con so far?
Every year, it seems like Comic-Con becomes less about comics and more about movie stars. This year is no exception, and so far, the annual convention has been dominated by "Twilight."
SODAHEAD SLIDESHOW: See the hottest stars at Comic-Con.
Have you already marked your calendar for November's premiere of "Breaking Dawn - Part 2"? Today's your lucky day ... Kristen Stewart, Robert Pattinson and Taylor Lautner were all on hand at Comic-Con, looking sexy in their respective ways and causing the usual fan frenzy.
PHOTOS: See the latest celebrity pictures to hit the Internet.
Are you a "Twilight" hater? You might prefer to see what A-listers like Mila Kunis and Michelle Williams are doing at Comic-Con. From K-Stew to Mila to Ashley Greene, let us know: Who's the hottest star at Comic-Con ... so far?
SODAHEAD SLIDESHOW: See the hottest stars at Comic-Con.
Have you already marked your calendar for November's premiere of "Breaking Dawn - Part 2"? Today's your lucky day ... Kristen Stewart, Robert Pattinson and Taylor Lautner were all on hand at Comic-Con, looking sexy in their respective ways and causing the usual fan frenzy.
PHOTOS: See the latest celebrity pictures to hit the Internet.
Are you a "Twilight" hater? You might prefer to see what A-listers like Mila Kunis and Michelle Williams are doing at Comic-Con. From K-Stew to Mila to Ashley Greene, let us know: Who's the hottest star at Comic-Con ... so far?
Thursday, July 12, 2012
Washington Nationals: 5 Questions for the Second Half of the Season
The Washington Post News Service with Bloomberg News
(c) 2012, The Washington Post.
What happens when the Nationals shut down Stephen Strasburg?
At the All-Star Game, Stephen Strasburg said in a radio interview that the Nationals will have to "rip the ball out of my hands." But the decision has been made. Once Strasburg's season ends, likely after about 165 innings in early September, his starts will likely be transferred to John Lannan, a capable, veteran left-hander who has gone 6-8 with a 4.60 ERA at Class AAA Syracuse. In the National League, Gio Gonzalez, Jordan Zimmermann, Edwin Jackson and Ross Detwiler still stack up against any contender. But Strasburg sets them apart, and only time will tell the impact his absence has on clubhouse morale.
Who's the closer?
Drew Storen saved 43 games last year, and so the Nationals will have a very accomplished set-up man when he returns from elbow surgery as the second half starts. Tyler Clippard has become the closer, allowing one run in 18 1/3 innings since he took over the role. The decision for now is easy - Clippard has been great and Storen hasn't pitched all year. The Nationals will ease Storen back into the majors. From there the roles will shake out based on performance and keeping each reliever fresh. Either way, Storen-or-Clippard is a good problem to have.
How will Jayson Werth affect the lineup?
No matter what happens at the trade deadline, the Nationals will receive a boost around July 31, when Jayson Werth is expected to return. The Nationals will use an everyday outfield of Michael Morse, Bryce Harper and Werth, making Steve Lombardozzi a utility player off the bench. Manager Davey Johnson would prefer to make Danny Espinosa the everyday leadoff hitter, but Werth himself could hit leadoff against right-handed starters if Espinosa does not improve hitting from the left side of the plate.
What will the Nationals do at the trade deadline?
Despite their status as a contender, the Nationals are still approaching the trade deadline with an eye on the future. The Nationals could look to trade for a top starter to replace Strasburg, but they are staunchly against selling the farm for a rental player. The Nationals would like to add offensive depth, ideally a left-handed bat. When he worked for the Diamondbacks, General Manager Mike Rizzo drafted reportedly available outfielder Justin Upton, which may spark rumors or even real interest in a megadeal. The fit seems unlikely. Upton is still only 24 and finished fourth in MVP voting last year, so the price would be astronomical. The Nationals would have to revamp their roster if they added an everyday outfielder - Michael Morse or Adam LaRoche would have to go. The Nationals are looking to upgrade, not to overhaul.
Will Ryan Zimmerman's shoulder hold up?
Third baseman Ryan Zimmerman changed the Nationals' offense in mid-June and offered a reminder: When he's healthy, he rakes. Now he just has to stay healthy. Zimmerman's surge over the past 14 games - he's hitting .333/.394/.683 - began when he received a cortisone shot in his inflamed shoulder joint. Zimmerman hopes rest over the break means no more procedures. But if necessary he'll receive another shot, and relatively minor offseason surgery remains possible.
(c) 2012, The Washington Post.
What happens when the Nationals shut down Stephen Strasburg?
At the All-Star Game, Stephen Strasburg said in a radio interview that the Nationals will have to "rip the ball out of my hands." But the decision has been made. Once Strasburg's season ends, likely after about 165 innings in early September, his starts will likely be transferred to John Lannan, a capable, veteran left-hander who has gone 6-8 with a 4.60 ERA at Class AAA Syracuse. In the National League, Gio Gonzalez, Jordan Zimmermann, Edwin Jackson and Ross Detwiler still stack up against any contender. But Strasburg sets them apart, and only time will tell the impact his absence has on clubhouse morale.
Who's the closer?
Drew Storen saved 43 games last year, and so the Nationals will have a very accomplished set-up man when he returns from elbow surgery as the second half starts. Tyler Clippard has become the closer, allowing one run in 18 1/3 innings since he took over the role. The decision for now is easy - Clippard has been great and Storen hasn't pitched all year. The Nationals will ease Storen back into the majors. From there the roles will shake out based on performance and keeping each reliever fresh. Either way, Storen-or-Clippard is a good problem to have.
How will Jayson Werth affect the lineup?
No matter what happens at the trade deadline, the Nationals will receive a boost around July 31, when Jayson Werth is expected to return. The Nationals will use an everyday outfield of Michael Morse, Bryce Harper and Werth, making Steve Lombardozzi a utility player off the bench. Manager Davey Johnson would prefer to make Danny Espinosa the everyday leadoff hitter, but Werth himself could hit leadoff against right-handed starters if Espinosa does not improve hitting from the left side of the plate.
What will the Nationals do at the trade deadline?
Despite their status as a contender, the Nationals are still approaching the trade deadline with an eye on the future. The Nationals could look to trade for a top starter to replace Strasburg, but they are staunchly against selling the farm for a rental player. The Nationals would like to add offensive depth, ideally a left-handed bat. When he worked for the Diamondbacks, General Manager Mike Rizzo drafted reportedly available outfielder Justin Upton, which may spark rumors or even real interest in a megadeal. The fit seems unlikely. Upton is still only 24 and finished fourth in MVP voting last year, so the price would be astronomical. The Nationals would have to revamp their roster if they added an everyday outfielder - Michael Morse or Adam LaRoche would have to go. The Nationals are looking to upgrade, not to overhaul.
Will Ryan Zimmerman's shoulder hold up?
Third baseman Ryan Zimmerman changed the Nationals' offense in mid-June and offered a reminder: When he's healthy, he rakes. Now he just has to stay healthy. Zimmerman's surge over the past 14 games - he's hitting .333/.394/.683 - began when he received a cortisone shot in his inflamed shoulder joint. Zimmerman hopes rest over the break means no more procedures. But if necessary he'll receive another shot, and relatively minor offseason surgery remains possible.
In Preventing Alzheimer’s, Mutation May Aid Drug Quest
A study of a rare gene mutation that protects people against Alzheimer’s disease provides the strongest evidence yet that excessive levels of a normal brain substance, beta amyloid, are a driving force in the disease — bolstering hopes that anti-amyloid drugs already under development might alter the disease’s course or even prevent it.
So far, the drugs have not succeeded. But scientists not connected with the new study said it suggested that the drug companies’ big bets on anti-amyloid treatments could yet pay off.
The implication for drug development “is hugely important,” said Dr. David Altshuler, a genomics expert at Harvard Medical School and the Broad Institute of Harvard and M.I.T.
And Dr. Samuel Gandy, an Alzheimer’s researcher who directs the Mount Sinai Center for Cognitive Health, called the finding the most significant in the field in two decades, since researchers first reported a mutation that leads to the disease.
The protective mutation, whose discovery was reported online Wednesday in the journal Nature, is highly uncommon — it is not the reason most people do not develop Alzheimer’s. But what intrigues researchers is how it protects the brain.
Mutations that cause Alzheimer’s lead to excessive amounts of beta amyloid in the brain; by contrast, the protective mutation slows beta amyloid production, so people make much less.
“This paper provides strong evidence that it would work in the general population if you did it right,” Dr. Altshuler said.
Scientists at the drug companies agreed. “We are thrilled,” said Ryan Watts, one of the authors of the new paper and head of the neurodegeneration labs at Genentech, which is developing two drugs to reduce brain amyloid levels.
Dr. Richard Mohs, leader of neuroscience early clinical development at Eli Lilly, said the company was “very encouraged by these study results.” They show, he said, that despite an initial failure, the strategy of focusing on drugs to reduce beta amyloid levels is “a logical path for the development of effective therapies that may slow disease progression.”
Many questions remain, of course. Most people do not have the protective gene mutation, but as common as Alzheimer’s is, most people do not get it. It is not clear why. And most who develop Alzheimer’s do not have one of the rare gene mutations that cause it. The reasons for their disease are unclear.
The discovery of the protective gene mutation, a product of the revolution that has taken place in genetics, arose when researchers scanned the entire DNA of 1,795 Icelanders.
About 1 in 100 had a mutation in the gene for a large protein that is sliced to form beta amyloid. Then the investigators studied people who had been given an Alzheimer’s diagnosis, and a group of people 85 and older. Those with the mutation appeared to be protected from Alzheimer’s disease.
The investigators, led by Dr. Kari Stefansson, chief executive at DeCode Genetics, an Icelandic company, looked at genomes of North Americans and found the gene mutation in only about 1 in 10,000 people. That indicates, Dr. Stefansson said, that the mutation arose relatively recently in Scandinavia.
The protective gene even appears to override a very strong risk factor for Alzheimer’s disease in old age — two copies of a gene known as ApoE4. Ninety percent of people with two ApoE4 genes get Alzheimer’s by age 80. But Dr. Stefansson says there are 25 people in his study with two copies of ApoE4. None have Alzheimer’s disease.
The research “is obviously right,” said John Hardy, an Alzheimer’s researcher at University College London and a discoverer of the first gene mutation found to cause the disease. “The statistics and the finding are pretty secure.”
The discovery is part of a continuing story that implicates beta amyloid as a central and crucial player in this destructive brain disease. The idea began two decades ago with the discovery of very rare gene mutations that always cause Alzheimer’s in those who inherit them, usually by middle age. The mutations were different in different families, but all had the same effect: They increased the amount of beta amyloid in the brain. That meant that a buildup of amyloid was sufficient to cause the disease.
Elderly people with Alzheimer’s — who typically do not have these gene mutations — also had excess amyloid in the brain. So researchers reasoned that might mean that excess amyloid was causing the disease in them, too.
Additional evidence of the role of beta amyloid was reported on Wednesday in The New England Journal of Medicine. Using spinal taps and brain scans to track the protein, investigators found that people with one of the Alzheimer’s-causing mutations start making too much beta amyloid as long as 20 years before they have symptoms of the disease.
Researchers and drug companies focused on the amyloid hypothesis to the extent that almost every experimental drug being tested to slow or halt Alzheimer’s disease is designed to reduce the amount of amyloid in the brain. Most of those drugs are still being tested in clinical trials, but a Lilly drug that failed spectacularly in 2010, semagacestat, actually made people with Alzheimer’s worse and gave rise to soul-searching in the field.
It emphasized a crucial question that hung over the endeavor. Was amyloid really causing Alzheimer’s in elderly people? Might the protein instead be a bystander, accumulating, for example, as part of the brain’s response to damage?
The discovery of the protective gene mutation provides strong clues. People with the mutation make substantially less beta amyloid, but other than that they are no different from anyone else. And they do not get Alzheimer’s.
People could be tested to see if they have the protective mutation, Dr. Stefansson said, but he added, “The benefits of doing so are not obvious to me.” He explained that since the gene is so rare, chances that a person being tested would have it — especially if that person is not Scandinavian — are extremely low. Almost everyone would end up with the same uncertainty they have now. There is as yet no way to prevent Alzheimer’s and, outside of families with one of the rare disease-causing gene mutations, no way to know who is going to get it.
Still, Dr. Hardy noted, as provocative as the discovery of the protective gene mutation is, the strategy of reducing amyloid levels — the ultimate test of the amyloid hypothesis — still must be evaluated in typical Alzheimer’s disease. For example, perhaps people need to have lower levels of beta amyloid from birth to really be protected.
Researchers and companies explain away the failure of the first few experimental drugs to reduce beta amyloid levels or to block the protein by saying they were not powerful enough and were studied in people who already had the disease and clear symptoms of mental decline. By then it might be too late to make any difference. When brain cells have died, nothing can bring them back.
The strategy now is to use new brain scans and other methods to find and treat people before they have symptoms of mental decline.
“The idea is that treatment has to start early to make a difference,” Dr. Watts said.
Of course, people with the newly discovered mutation have lower levels of beta amyloid for their entire lives.
“You couldn’t start earlier than that,” Dr. Watts said.
So far, the drugs have not succeeded. But scientists not connected with the new study said it suggested that the drug companies’ big bets on anti-amyloid treatments could yet pay off.
The implication for drug development “is hugely important,” said Dr. David Altshuler, a genomics expert at Harvard Medical School and the Broad Institute of Harvard and M.I.T.
And Dr. Samuel Gandy, an Alzheimer’s researcher who directs the Mount Sinai Center for Cognitive Health, called the finding the most significant in the field in two decades, since researchers first reported a mutation that leads to the disease.
The protective mutation, whose discovery was reported online Wednesday in the journal Nature, is highly uncommon — it is not the reason most people do not develop Alzheimer’s. But what intrigues researchers is how it protects the brain.
Mutations that cause Alzheimer’s lead to excessive amounts of beta amyloid in the brain; by contrast, the protective mutation slows beta amyloid production, so people make much less.
“This paper provides strong evidence that it would work in the general population if you did it right,” Dr. Altshuler said.
Scientists at the drug companies agreed. “We are thrilled,” said Ryan Watts, one of the authors of the new paper and head of the neurodegeneration labs at Genentech, which is developing two drugs to reduce brain amyloid levels.
Dr. Richard Mohs, leader of neuroscience early clinical development at Eli Lilly, said the company was “very encouraged by these study results.” They show, he said, that despite an initial failure, the strategy of focusing on drugs to reduce beta amyloid levels is “a logical path for the development of effective therapies that may slow disease progression.”
Many questions remain, of course. Most people do not have the protective gene mutation, but as common as Alzheimer’s is, most people do not get it. It is not clear why. And most who develop Alzheimer’s do not have one of the rare gene mutations that cause it. The reasons for their disease are unclear.
The discovery of the protective gene mutation, a product of the revolution that has taken place in genetics, arose when researchers scanned the entire DNA of 1,795 Icelanders.
About 1 in 100 had a mutation in the gene for a large protein that is sliced to form beta amyloid. Then the investigators studied people who had been given an Alzheimer’s diagnosis, and a group of people 85 and older. Those with the mutation appeared to be protected from Alzheimer’s disease.
The investigators, led by Dr. Kari Stefansson, chief executive at DeCode Genetics, an Icelandic company, looked at genomes of North Americans and found the gene mutation in only about 1 in 10,000 people. That indicates, Dr. Stefansson said, that the mutation arose relatively recently in Scandinavia.
The protective gene even appears to override a very strong risk factor for Alzheimer’s disease in old age — two copies of a gene known as ApoE4. Ninety percent of people with two ApoE4 genes get Alzheimer’s by age 80. But Dr. Stefansson says there are 25 people in his study with two copies of ApoE4. None have Alzheimer’s disease.
The research “is obviously right,” said John Hardy, an Alzheimer’s researcher at University College London and a discoverer of the first gene mutation found to cause the disease. “The statistics and the finding are pretty secure.”
The discovery is part of a continuing story that implicates beta amyloid as a central and crucial player in this destructive brain disease. The idea began two decades ago with the discovery of very rare gene mutations that always cause Alzheimer’s in those who inherit them, usually by middle age. The mutations were different in different families, but all had the same effect: They increased the amount of beta amyloid in the brain. That meant that a buildup of amyloid was sufficient to cause the disease.
Elderly people with Alzheimer’s — who typically do not have these gene mutations — also had excess amyloid in the brain. So researchers reasoned that might mean that excess amyloid was causing the disease in them, too.
Additional evidence of the role of beta amyloid was reported on Wednesday in The New England Journal of Medicine. Using spinal taps and brain scans to track the protein, investigators found that people with one of the Alzheimer’s-causing mutations start making too much beta amyloid as long as 20 years before they have symptoms of the disease.
Researchers and drug companies focused on the amyloid hypothesis to the extent that almost every experimental drug being tested to slow or halt Alzheimer’s disease is designed to reduce the amount of amyloid in the brain. Most of those drugs are still being tested in clinical trials, but a Lilly drug that failed spectacularly in 2010, semagacestat, actually made people with Alzheimer’s worse and gave rise to soul-searching in the field.
It emphasized a crucial question that hung over the endeavor. Was amyloid really causing Alzheimer’s in elderly people? Might the protein instead be a bystander, accumulating, for example, as part of the brain’s response to damage?
The discovery of the protective gene mutation provides strong clues. People with the mutation make substantially less beta amyloid, but other than that they are no different from anyone else. And they do not get Alzheimer’s.
People could be tested to see if they have the protective mutation, Dr. Stefansson said, but he added, “The benefits of doing so are not obvious to me.” He explained that since the gene is so rare, chances that a person being tested would have it — especially if that person is not Scandinavian — are extremely low. Almost everyone would end up with the same uncertainty they have now. There is as yet no way to prevent Alzheimer’s and, outside of families with one of the rare disease-causing gene mutations, no way to know who is going to get it.
Still, Dr. Hardy noted, as provocative as the discovery of the protective gene mutation is, the strategy of reducing amyloid levels — the ultimate test of the amyloid hypothesis — still must be evaluated in typical Alzheimer’s disease. For example, perhaps people need to have lower levels of beta amyloid from birth to really be protected.
Researchers and companies explain away the failure of the first few experimental drugs to reduce beta amyloid levels or to block the protein by saying they were not powerful enough and were studied in people who already had the disease and clear symptoms of mental decline. By then it might be too late to make any difference. When brain cells have died, nothing can bring them back.
The strategy now is to use new brain scans and other methods to find and treat people before they have symptoms of mental decline.
“The idea is that treatment has to start early to make a difference,” Dr. Watts said.
Of course, people with the newly discovered mutation have lower levels of beta amyloid for their entire lives.
“You couldn’t start earlier than that,” Dr. Watts said.
Tuesday, July 10, 2012
Game console Ouya to bring gaming back to the TV
Startup hopes to attract both gamers and developers with a $99 console and an open gaming platform. Disrupting the system comes with a hefty price tag: a $950,000 fundraising campaign.
Hard-core gamers like a challenge. Just ask gaming business veteran Julie Uhrman.
Uhrman wants to disrupt the gaming industry with an affordable console called Ouya, a name she hopes will become the battle cry of game developers. Her company is soliciting developers to help build an open ecosystem of games on Android, essentially bringing the openness of mobile games back to the TV set.
"It's very ambitious -- it's hardware, it's software, it's building an ecosystem," Uhrman said.
But Uhrman said she believes her team has what it takes to challenge the status quo. The company starts its Kickstarter.com-based campaign today, with a goal of raising a very ambitious $950,000. The funding will allow Ouya to take its console prototype -- designed by Jawbone designer Yves Behar -- to production along with its controller counterpart. They hope to launch the product early next year.
The company's got some solid names on its angel investors list, including Jay Adelson, founder of Digg; Joe Greenstein, founder of Flixster; Hosain Rahman, founder of Jawbone; and Eric Hautemont, publisher of the Ticket to Ride board game.
With mobile games being less expensive to create, developers have moved away from making games for consoles, leaving an industry that, in Uhrman's eyes, has done very little innovation in terms of gaming content.
And despite the stalled creativity, Uhrman said TV remains the best platform for gamers when it comes to graphics and overall experience. (She said it's definitely her favorite.) She and the many developers backing Ouya want to see this new console bring developers back to that platform by offering an affordable way to create games for Ouya.
Built on Android and made to plug into your TV set, Ouya can play games in HD with a Tegra3 chipset.
"Our focus is on games -- we want to provide a phenomenal game experience," she said.
The only rule Ouya has is that the games must be free to try before purchase (so gamers don't ever feel like they wasted their money after downloading a game for the first time). Otherwise, Ouya is embracing the economic model of mobile games -- a 70/30 percent split for developers and Ouya. The company's Kickstarter.com campaign also touts special developer packages with consoles that comes rooted, a sign that it's built to be hacked.
"We are trying to leverage all that is great -- free to play, openness, touch screen, bringing what is familiar to TV -- and we want to wrap it up in this great bow -- affordability and game-ability for gamers and developers alike," Uhrman said.
While Uhrman said she believes consoles will eventually become a chip in a TV set, the market isn't dead yet, despite what some folks said during this year's E3 conference. And she thinks Ouya will prove that.
Developers certainly hope so. The company already has a slough of supporters, including Brian Fargo of inXile.
Fargo, who is also an investor in Ouya, said that the greatest innovation in the gaming industry is taking place in the open environments of PC, iOS, and tablet, and that Ouya can provide an exciting opportunity for TV gaming.
"It's probably the first time anybody has talked about releasing a console system that's clearly and purely dedicated to the development community," Fargo said, adding that other console have walled-off systems. "They would talk to developers but at the end of the day, they really weren't part of the plan. You get a lot of lip service."
And that's too bad, he said, because an open environment brings out the best ideas.
"Ultimately, no company or person can compete with what the crowd can do," Fargo said. "They're just going to have more ideas."
His own team raised almost $3 million on Kickstarter.com for its game Wasteland 2, which showcases the power of the developer community. He said it's critical to get developers on board because they inspire one another to make better apps and all it takes is "one killer app" to change the playing field.
He thinks Ouya can hit its $950,000 goal if the company effectively conveys its message.
"If there's that sense to try and support something to open it up, there's a chance to reach that number -- it's a bold number," Fargo said.
Hard-core gamers like a challenge. Just ask gaming business veteran Julie Uhrman.
Uhrman wants to disrupt the gaming industry with an affordable console called Ouya, a name she hopes will become the battle cry of game developers. Her company is soliciting developers to help build an open ecosystem of games on Android, essentially bringing the openness of mobile games back to the TV set.
"It's very ambitious -- it's hardware, it's software, it's building an ecosystem," Uhrman said.
But Uhrman said she believes her team has what it takes to challenge the status quo. The company starts its Kickstarter.com-based campaign today, with a goal of raising a very ambitious $950,000. The funding will allow Ouya to take its console prototype -- designed by Jawbone designer Yves Behar -- to production along with its controller counterpart. They hope to launch the product early next year.
The company's got some solid names on its angel investors list, including Jay Adelson, founder of Digg; Joe Greenstein, founder of Flixster; Hosain Rahman, founder of Jawbone; and Eric Hautemont, publisher of the Ticket to Ride board game.
With mobile games being less expensive to create, developers have moved away from making games for consoles, leaving an industry that, in Uhrman's eyes, has done very little innovation in terms of gaming content.
And despite the stalled creativity, Uhrman said TV remains the best platform for gamers when it comes to graphics and overall experience. (She said it's definitely her favorite.) She and the many developers backing Ouya want to see this new console bring developers back to that platform by offering an affordable way to create games for Ouya.
Built on Android and made to plug into your TV set, Ouya can play games in HD with a Tegra3 chipset.
"Our focus is on games -- we want to provide a phenomenal game experience," she said.
The only rule Ouya has is that the games must be free to try before purchase (so gamers don't ever feel like they wasted their money after downloading a game for the first time). Otherwise, Ouya is embracing the economic model of mobile games -- a 70/30 percent split for developers and Ouya. The company's Kickstarter.com campaign also touts special developer packages with consoles that comes rooted, a sign that it's built to be hacked.
"We are trying to leverage all that is great -- free to play, openness, touch screen, bringing what is familiar to TV -- and we want to wrap it up in this great bow -- affordability and game-ability for gamers and developers alike," Uhrman said.
While Uhrman said she believes consoles will eventually become a chip in a TV set, the market isn't dead yet, despite what some folks said during this year's E3 conference. And she thinks Ouya will prove that.
Developers certainly hope so. The company already has a slough of supporters, including Brian Fargo of inXile.
Fargo, who is also an investor in Ouya, said that the greatest innovation in the gaming industry is taking place in the open environments of PC, iOS, and tablet, and that Ouya can provide an exciting opportunity for TV gaming.
"It's probably the first time anybody has talked about releasing a console system that's clearly and purely dedicated to the development community," Fargo said, adding that other console have walled-off systems. "They would talk to developers but at the end of the day, they really weren't part of the plan. You get a lot of lip service."
And that's too bad, he said, because an open environment brings out the best ideas.
"Ultimately, no company or person can compete with what the crowd can do," Fargo said. "They're just going to have more ideas."
His own team raised almost $3 million on Kickstarter.com for its game Wasteland 2, which showcases the power of the developer community. He said it's critical to get developers on board because they inspire one another to make better apps and all it takes is "one killer app" to change the playing field.
He thinks Ouya can hit its $950,000 goal if the company effectively conveys its message.
"If there's that sense to try and support something to open it up, there's a chance to reach that number -- it's a bold number," Fargo said.
Glaxo Wins Approval for Child Meningitis Vaccine
Physicians have another weapon in the battle against childhood meningitis. On Thursday, the
U.S. Food & Drug Administration granted approval for a combination vaccine designed to
prevent bacterial meningitis in children.
The new vaccine, called MenHibrix, was developed GlaxoSmithKline (NYSE:GSK). It becomes the
first meningitis vaccine approved for use in children as young as six weeks old, Dow Jones
noted. The vaccine can be given to babies in four doses spaced between two and 15 months.
That puts it in line with the typical vaccination schedule for very young children.
Physicians have another weapon in the battle against childhood meningitis. On Thursday, the
U.S. Food & Drug Administration granted approval for a combination vaccine designed to
prevent bacterial meningitis in children.
The new vaccine, called MenHibrix, was developed GlaxoSmithKline (NYSE:GSK). It becomes the
first meningitis vaccine approved for use in children as young as six weeks old, Dow Jones
noted. The vaccine can be given to babies in four doses spaced between two and 15 months.
That puts it in line with the typical vaccination schedule for very young children.
U.S. Food & Drug Administration granted approval for a combination vaccine designed to
prevent bacterial meningitis in children.
The new vaccine, called MenHibrix, was developed GlaxoSmithKline (NYSE:GSK). It becomes the
first meningitis vaccine approved for use in children as young as six weeks old, Dow Jones
noted. The vaccine can be given to babies in four doses spaced between two and 15 months.
That puts it in line with the typical vaccination schedule for very young children.
Physicians have another weapon in the battle against childhood meningitis. On Thursday, the
U.S. Food & Drug Administration granted approval for a combination vaccine designed to
prevent bacterial meningitis in children.
The new vaccine, called MenHibrix, was developed GlaxoSmithKline (NYSE:GSK). It becomes the
first meningitis vaccine approved for use in children as young as six weeks old, Dow Jones
noted. The vaccine can be given to babies in four doses spaced between two and 15 months.
That puts it in line with the typical vaccination schedule for very young children.
Monday, July 2, 2012
Life & Style Told You First: Tom Cruise and Katie Holmes Divorcing After Five Years of Marriage!
After spending months apart, Tom Cruise and Katie Holmes have decided to divorce after five years marriage. "This is a personal and private matter for Katie and her family," Katie's attorney Jonathan Wolfe tells Life & Style. "Katie's primary concern remains, as it always has been, her daughter's best interest."
Life & Style first broke the news that their marriage was in crisis in mid-June, after Katie was a no-show as Tom was named an entertainment icon by the Friar's Club in NYC on June 12. "My wife couldn't be here tonight," explained Tom, who was with their daughter Suri, 6, and his son, Connor, 17. "She's in China, actually, working." (She was at an ice-skating event.)
Katie, 33, also missed all of the premieres for Tom's new movie, Rock of Ages, and the two haven't been photographed together since Feb. 26. She's been spending the bulk of her time alone with Suri in NYC, taking her daughter to the movies (the two caught the new Disney movie Brave at a local theater on June 23), hitting the gym, going to see Evita on Broadway, picking up groceries at the supermarket and dining out at trendy eateries like Serendipity and ABC Kitchen.
"Katie's been out and about doing normal things," an insider tells Life & Style. "She's looking very relaxed and has been all smiles."
The tension built as Tom filmed one film after another in Germany, Russia and Dubai. He's currently in Iceland shooting yet another movie, Oblivion. In fact, Tom has been so busy he missed Suri's birthday in April. The little girl was photographed crying hysterically while out with Katie in NYC on the evening of June 18. "With her parents apart, poor Suri has been spending more time by herself," a friend of Katie's tells Life & Style. "She must be so lonely."
The divorce announcement -- delivered by Katie's camp -- came just four days before Tom's 50th birthday on July 3. Katie is seeking sole custody.
Life & Style first broke the news that their marriage was in crisis in mid-June, after Katie was a no-show as Tom was named an entertainment icon by the Friar's Club in NYC on June 12. "My wife couldn't be here tonight," explained Tom, who was with their daughter Suri, 6, and his son, Connor, 17. "She's in China, actually, working." (She was at an ice-skating event.)
Katie, 33, also missed all of the premieres for Tom's new movie, Rock of Ages, and the two haven't been photographed together since Feb. 26. She's been spending the bulk of her time alone with Suri in NYC, taking her daughter to the movies (the two caught the new Disney movie Brave at a local theater on June 23), hitting the gym, going to see Evita on Broadway, picking up groceries at the supermarket and dining out at trendy eateries like Serendipity and ABC Kitchen.
"Katie's been out and about doing normal things," an insider tells Life & Style. "She's looking very relaxed and has been all smiles."
The tension built as Tom filmed one film after another in Germany, Russia and Dubai. He's currently in Iceland shooting yet another movie, Oblivion. In fact, Tom has been so busy he missed Suri's birthday in April. The little girl was photographed crying hysterically while out with Katie in NYC on the evening of June 18. "With her parents apart, poor Suri has been spending more time by herself," a friend of Katie's tells Life & Style. "She must be so lonely."
The divorce announcement -- delivered by Katie's camp -- came just four days before Tom's 50th birthday on July 3. Katie is seeking sole custody.
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