HONOLULU (Reuters) - The United States stands by its assertion that the North Korean government was behind the massive cyberattack on Sony Pictures, a spokesman for the White House National Security Council said on Saturday.
Asked about North Korea's statement on Saturday denying involvement in the strike against the Hollywood studio, NSC spokesman Mark Stroh said: "As the FBI made clear, we are confident the North Korean government is responsible for this destructive attack. We stand by this conclusion."
"The Government of North Korea has a long history of denying responsibility for destructive and provocative actions," he said.
"If the North Korean government wants to help, they can admit their culpability and compensate Sony for the damages this attack caused," Stroh added. North Korea called earlier for a joint U.S.-North Korean probe into the incident.
(Reporting by Julia Edwards in Honolulu; Writing by Susan Heavey in Washington; Editing by Frances Kerry)
The European Union wants Google to extend the range and impact of the "right to be forgotten" measures that passed earlier this year. The proposal would take the current limitation of EU-only domains like those ending in ".fr" and ".co.uk," and open ...
It's what you've all been waiting for! Engadget Expand is the place this week. We're taking over the Javits Center in Manhattan on November 7th and 8th. We're pretty damn excited for what's on tap this year, and we think you should be too. But, in...
When you land in a strange new city, your first instinct may be to see what there is to do near your hotel. However, searching Google for nearby attractions can be a hassle if you don't remember your hotel's name or address by heart. That...
If you regularly jailbreak your iPhone, you are no doubt familiar with Auxo. If you don't use it, you've at least heard of it. The original version of Auxo brought with it multitasking that was actually usable in an iOS 6 world. Auxo 2 is now available for iOS 7 and takes the multitasking game to an entirely new level.
When you launch Auxo 2 for the first time, you'll immediately notice that it has become a fusion between iOS 7 multitasking and Control Center. This new view is what Auxo 2 calls Multi-Center. It can be triggered by swiping up from the bottom of the screen or by double tapping the Home button. If you prefer to not have Control Center and multitasking merged into one view, you can disable it in Settings and keep them separate.
If you have the Multi-Center view enabled in Auxo 2, you'll notice some changes. Along the top and bottom of the screen you have access to common controls such as AirPlay, AirDrop, and system toggles such as WiFi, Camera, calculator, and more. If you don't like this view, which I don't know why you wouldn't, you can hide it in Auxo's settings.
The Quick Switcher, arguably Auxo 2's most prominent feature, lets you access recently used apps with one simple gesture. Just drag your finger up from the bottom left of the screen to launch the Quick Switcher. Now scrub left and right and let go on the app you'd like to launch. You can also drag your finger up from the bottom right corner of the screen in order to return to the Home screen instantly. As with any other settings for Auxo 2, these gestures can be disabled and customized in Auxo's settings section.
If you purchased the original version of Auxo, you'll get a discount on Auxo 2 which brings the price to $1.99. If you didn't purchase the original, the full price of Auxo 2 is $3.99, which in our opinion isn't bad for what's arguably one of the best jailbreak tweaks we've seen for iOS 7 thus far. Auxo 2 isn't currently available for iPad but will be eventually, as a free update to the existing Auxo 2 app.
If you try out Auxo 2, let me know what you think of it in the comments! What's your favorite feature of Auxo 2? Let me know that too!
Japanese artist Ei Wada, who was born in 1987, belongs to a generation that spent middle school feverishly poring over cassettes to make mix tapes—until, of course, they were quickly outmoded by CDs, and then MP3s. Now, Ei makes art using the outmoded technologies he grew up with.
Yahoo's been working hard to include support for Apple services in its Screen iOS app, now it's gone one better and launched its video-discovery app on Apple TV. With an emphasis on comedy, Yahoo Screen has been designed to collate the best of web video, including clips from Saturday Night Live, The Colbert Report, and The Daily Show, as well as live news, events and music. You'll also be able to browse trending videos and watch Yahoo Originals programming, which are delivered direct to your Apple TV without the need to AirPlay them across. AllThingsD reports that PBS has also quietly pushed a new app, letting users get their Nova, Frontline or Antiques Roadshow fix (older episodes of Downton Abbey will be available shortly after PBS begins re-airing seasons early next year). Today's update may only available to US users but Apple isn't being shy about broadening the number of Apple TV apps available across the globe.
Blocking signal-transmitting cellular pores may prevent damage to kidneys
PUBLIC RELEASE DATE:
15-Nov-2013
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Contact: Mike Morrison mdmorrison@partners.org 617-724-6425 Massachusetts General Hospital
One of the most devastating side effects of diabetes is kidney failure, and one of the earliest signs of kidney damage is a disruption of the organ's filtering capacity. Diabetes patients who develop kidney failure must go on dialysis, seriously limiting their quality of life and placing them at significantly increased risk of death. The incidence of kidney disease is increasing with rising rates of obesity-associated type 2 diabetes, but very little progress has been made towards protecting the kidney's filter barrier during the past 50 years.
Now a group of Massachusetts General Hospital (MGH) investigators has identified a molecule that plays a key role in the breakdown of the kidney filter, presenting a potential therapeutic target for stopping the damage before it becomes irreversible. Their report will appear in the December issue of the Journal of Clinical Investigation and is receiving early online release.
"Our study shows that blocking the ion channel TRPC5 may be a new treatment for diseases in which the kidney's filter barrier is damaged," says Anna Greka, MD, PhD, of the Division of Nephrology in the MGH Department of Medicine, who led the current study. "One in three Americans is at risk for developing chronic kidney disease from obesity, diabetes or high blood pressure; and kidney failure has been described as an emergent pandemic of our time."
TRPC5 is an ion channel, a pore in the cell membrane that transmits metabolic signals by allowing charged molecules in this case calcium to pass into or out of cells. Disrupted calcium signaling was suggested as a possible early event in damage to podocytes the cells that make up the kidney's filter barrier several decades ago, but the particular calcium channel that was involved had never been identified. Some families with a rare, inherited form of kidney disease were known to have activating mutations in a related calcium channel called TRPC6, which led Greka's team to investigate its role in kidney filtration. They were surprised to find that, in addition to TRPC6 channels, TRPC5 channels were also present in podocytes and that their activity was more damaging to the kidney filter, even in the absence of any mutations.
The current article describes a series of experiments by which Greka's team first confirmed the presence of TRPC5 channels in rodent podocytes; they then showed that animals in which TRPC5 expression was knocked out did not experience the type of kidney damage typically caused by a bacterial toxin or by a chemical known to damage podocytes. More detailed studies revealed that those damaging agents cause TRPC5 channels to open in podocytes, admitting excess calcium which causes the cytoskeleton the cells' internal structural support system to collapse, breaking down the filter formed by podocytes.
The researchers went on to show that a recently identified TRPC5 inhibitor, called ML204 discovered in the lab of study co-author Craig Lindsley, PhD, of Vanderbilt University Medical Center blocked the inrush of calcium into podocytes, preventing cytoskeletal breakdown and the damage to the kidney's filtering function. This protective effect was seen not only in cells and tissues but also in living mice.
"Future work needs to focus on optimizing ML204 and other potential TRPC5 blockers to be more potent. But generally our intention is to fervently pursue TRPC5 inhibition as a possible new treatment for the kidney diseases affecting hundreds of millions of people worldwide," says Greka, who is an assistant professor of Medicine at Harvard Medical School.
###
Thomas Schaldecker, Sookyung Kim, and Constantine Tarabanis of the Division of Nephrology in MGH Department of Medicine are co-lead authors of the Journal of Clinical Investigation article. Support for the study includes National Institutes of Health grants P30DK057521, DK083511 and DK093746 and an American Society of Nephrology Career Development grant.
Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.
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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.
Blocking signal-transmitting cellular pores may prevent damage to kidneys
PUBLIC RELEASE DATE:
15-Nov-2013
[
| E-mail
]
Share
Contact: Mike Morrison mdmorrison@partners.org 617-724-6425 Massachusetts General Hospital
One of the most devastating side effects of diabetes is kidney failure, and one of the earliest signs of kidney damage is a disruption of the organ's filtering capacity. Diabetes patients who develop kidney failure must go on dialysis, seriously limiting their quality of life and placing them at significantly increased risk of death. The incidence of kidney disease is increasing with rising rates of obesity-associated type 2 diabetes, but very little progress has been made towards protecting the kidney's filter barrier during the past 50 years.
Now a group of Massachusetts General Hospital (MGH) investigators has identified a molecule that plays a key role in the breakdown of the kidney filter, presenting a potential therapeutic target for stopping the damage before it becomes irreversible. Their report will appear in the December issue of the Journal of Clinical Investigation and is receiving early online release.
"Our study shows that blocking the ion channel TRPC5 may be a new treatment for diseases in which the kidney's filter barrier is damaged," says Anna Greka, MD, PhD, of the Division of Nephrology in the MGH Department of Medicine, who led the current study. "One in three Americans is at risk for developing chronic kidney disease from obesity, diabetes or high blood pressure; and kidney failure has been described as an emergent pandemic of our time."
TRPC5 is an ion channel, a pore in the cell membrane that transmits metabolic signals by allowing charged molecules in this case calcium to pass into or out of cells. Disrupted calcium signaling was suggested as a possible early event in damage to podocytes the cells that make up the kidney's filter barrier several decades ago, but the particular calcium channel that was involved had never been identified. Some families with a rare, inherited form of kidney disease were known to have activating mutations in a related calcium channel called TRPC6, which led Greka's team to investigate its role in kidney filtration. They were surprised to find that, in addition to TRPC6 channels, TRPC5 channels were also present in podocytes and that their activity was more damaging to the kidney filter, even in the absence of any mutations.
The current article describes a series of experiments by which Greka's team first confirmed the presence of TRPC5 channels in rodent podocytes; they then showed that animals in which TRPC5 expression was knocked out did not experience the type of kidney damage typically caused by a bacterial toxin or by a chemical known to damage podocytes. More detailed studies revealed that those damaging agents cause TRPC5 channels to open in podocytes, admitting excess calcium which causes the cytoskeleton the cells' internal structural support system to collapse, breaking down the filter formed by podocytes.
The researchers went on to show that a recently identified TRPC5 inhibitor, called ML204 discovered in the lab of study co-author Craig Lindsley, PhD, of Vanderbilt University Medical Center blocked the inrush of calcium into podocytes, preventing cytoskeletal breakdown and the damage to the kidney's filtering function. This protective effect was seen not only in cells and tissues but also in living mice.
"Future work needs to focus on optimizing ML204 and other potential TRPC5 blockers to be more potent. But generally our intention is to fervently pursue TRPC5 inhibition as a possible new treatment for the kidney diseases affecting hundreds of millions of people worldwide," says Greka, who is an assistant professor of Medicine at Harvard Medical School.
###
Thomas Schaldecker, Sookyung Kim, and Constantine Tarabanis of the Division of Nephrology in MGH Department of Medicine are co-lead authors of the Journal of Clinical Investigation article. Support for the study includes National Institutes of Health grants P30DK057521, DK083511 and DK093746 and an American Society of Nephrology Career Development grant.
Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.
[
| E-mail
Share
]
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Of all of the potential shortcomings of the cloud, trust is perhaps the largest. "Seeing is believing" is a truism that certainly applies to IT. Although you could have the worst-run internal IT shop ever, there's a comfort in being able to walk down to the data center and put your hands on what makes it tick. Moving critical pieces of your application infrastructure into the cloud removes that (sometimes false) sense of security and leaves many people feeling exposed.
Of course, that's completely natural -- any time you trust anyone to do anything for you, you are exposing yourself to risk. If a provider tells you it's taking nightly backups of your cloud-hosted ERP application and it turns out not to be true, you're the one who'll suffer in the event of a failure. The same is true with a traditional IT department, but at least you can wander down and ask to see tapes and backup logs if you're concerned that your people might not be on the ball. That's not so easy to do when systems might be hosted hundreds or even thousands of miles away in a nameless data center and you're customer No. 20,000 out of 100,000.
From the cloud provider's perspective, this lack of trust is a tough problem to solve. Assuming you're doing a thorough job, how exactly do you get a potential client to trust your operation well enough to give you its business? Aside from having a good track record with existing clients that might recommend you, publishing audit reports such as SAS-70, SOC-1 (aka SSAE 16), SOC-2, and SOC-3 has been a great way to go about instilling that trust by having an independent third party vouch that you're doing what you say you're doing.
Virginia’s governors race was close — closer than the pre-election polls suggested it would be. Dissatisfaction with President Obama’s health-care law appears to have fueled a last-minute surge for Republican Ken Cuccinelli II. Analysts are latching onto how he exceeded expectations, and what a political liability Obamacare might turn out to be in next year’s midterm elections.
But Republicans must take the right lesson from their loss. They should have won this election. Why didn’t Cuccinelli pull it out?
The European Union wants Google to extend the range and impact of the "right to be forgotten" measures that passed earlier this year. The proposal would take the current limitation of EU-only domains like those ending in ".fr" and ".co.uk," and open ...
It's what you've all been waiting for! Engadget Expand is the place this week. We're taking over the Javits Center in Manhattan on November 7th and 8th. We're pretty damn excited for what's on tap this year, and we think you should be too. But, in...
When you land in a strange new city, your first instinct may be to see what there is to do near your hotel. However, searching Google for nearby attractions can be a hassle if you don't remember your hotel's name or address by heart. That...
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