NSA collecting 5 billion cellphone location records per day

Galaxy Nexus and iPhone 4S in Korea

Hey everyone, the government’s tracking you. Quelle surprise. In what has to be one of the least shocking pieces of news to come from the Edward Snowden leaks, The Washington Post is reporting that the National Security Agency has been gathering surveillance data on foreign cellphone users’ whereabouts globally, with some Americans potentially caught in the net. The database, which collects about 5 billion records per day, is so vast that not even the NSA has the proper tools to sift through it all. That’s not to say the agency hasn’t been able to make “good” use of it with analytics programs, though.

One such program, ominously labeled Co-Traveler, allows the NSA to determine “behaviorally relevant relationships” based on data from signals intelligence activity designators (or sigads for short) located around the world, including one codenamed “Stormbrew.” That’s a lot of jargon for what are essentially data hubs that collect geolocation information down to the cell tower level. Co-Traveler can locate targets of interest based on cellphone users moving in tandem, even if they’re unknown threats — frequent meetups with an existing suspect could reveal a close associate, for instance.

As we’ve come to expect by now, both the NSA and the Office of the Director for National Intelligence argue that this location-based surveillance is legal. Agency representatives tell the Post that the collection system doesn’t purposefully track Americans. However, the NSA also says it can’t determine how many US residents get swept up in these location scans; there are concerns that it’s following targets protected by Fourth Amendment search rights.

Joseph Volpe contributed to this report.

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Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/6WkPM3j8hvI/
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HTC One developer and unlocked models start receiving Android 4.4 KitKat in the US

HTC's Peter Chou wants you to have KitKat

If you were bold enough to buy a Developer Edition HTC One or its unlocked sibling, today is your lucky day. HTC’s US division has announced that it’s rolling out an Android 4.4 KitKat upgrade to both One variants, weeks ahead of the expected update for carrier-locked models. Sense 5.5 should also be a part of the package. While the KitKat upgrade isn’t reaching these units as quickly as it did for the Google Play Edition, it’s safe to say that many One owners will have another reason to celebrate this Thanksgiving weekend.

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Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/t5bpH3pIXLo/
Category: cooking a turkey   Apple Pie Recipe   Katherine Webb   Lara Flynn Boyle   derek hough  

Obamacare Questions No One Asked Ahead of Time

‘If we had to do it all over again . . . there would have been a whole lot more questions that were asked,” President Obama told NBC last week.

In this now-famous TV interview, Mr. Obama was referring to his health-care rollout, but there are plenty of other questions somebody should have asked. Here are a few: During the 2008 primary race, Mr. Obama, you rejected Hillary Clinton’s proposed individual mandate. You said if health insurance were a good deal, nobody would have to be forced to buy it.

Source: http://www.realclearpolitics.com/2013/11/14/obamacare_questions_no_one_asked_ahead_of_time_319951.html
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UFC 167 Preliminary Recaps: High, Pettis, and Villante Win

UFC 167 kicked off with a three fight preliminary stream earlier this evening. In the third fight of the evening, Jason High would defeat Anthony Lapsley in a fun ground fight. In other action, Sergio Pettis and Gian Villante would kick off the night with wins.

High Tops Lapsley

Strikeforce import Jason High would improve to 2-1 in the UFC with a solid decision victory over Anthony Lapsley. High controlled the majority of the fight from top position and he constantly sought submission finishes. High has now won two straight in the Octagon after dropping his debut to Erick Silva on short notice.

Pettis Defeats Campuzano

Sergio Pettis got a victory but it did not come easy in his debut fight with Will Campuzano. Pettis showed flashes of potential brilliance tonight, but the move back up to bantamweight clearly took some of his finishing ability tonight. Pettis is now 10-0 in his MMA career, while Campuzano sees his five fight streak snapped.

Villante Rebounds to Floor Donovan 

Late replacement Gian Villante was not sharp to start off the UFC 167 card but he certainly finished strong against Cody Donovan. Villante would turn the fight around in an instant after finally getting his timing on Donovan’s headkick and delivering a perfectly timed counter punch. The Strikeforce import gets to 1-1 in the Octagon and he is now 4-1 in his last five.

UFC 167 Results:

  • Jason High def. Anthony Lapsley via unanimous decision (29-28, 29-28, 29-28)
  • Sergio Pettis def. Will Campuzano via unanimous decision (30-27,30-27,29-28)
  • Gian Villante def. Cody Donovan via TKO (strikes) 1:22 of Round 2

Source: http://mmafrenzy.com/96247/ufc-167-preliminary-recaps-high-pettis-and-villante-win/
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Bar Refaeli Makes Mole Removal Look Good

She’s practically perfect as far as millions of men are concerned, but Bar Refaeli had to have mole removal surgery earlier this week to get rid of a pesky mark on her side.

The 28-year-old Israeli supermodel posted a pre-surgery photo to her Instagram account on Tuesday (November 12), and despite the hospital trappings she looked positively gorgeous.

After the procedure was complete, Bar added another snap, though this time she was wearing a bikini on the beach, with just a small band aid covering her stitches.

Refaeli added the caption, “Heaven is a place on earth,” followed by the personal motto, “live #your #life.”

Source: http://celebrity-gossip.net/bar-refaeli/bar-refaeli-makes-mole-removal-look-good-1112002
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Former Apple Siri engineer now building connected device platform at Samsung

An engineer who oversaw some development of Apple’s Siri technology is now at Samsung building an online service for linking together the Internet of things. Luc Julia, a vice president at Samsung’s innovation lab in Menlo Park, Calif., demonstrated the project, called SAMI, or the Samsung Architecture for Multimodal Interactions, at a conference north of San Francisco on Friday.

Still in its early stages, SAMI aims to be a platform that can collect data from any connected device, including wearable computers like the Fitbit, and make that data available for consumption by other devices. It’s designed for use by companies that make wearable computers, home automation equipment and automobiles, as a common platform they can use to build additional services for their customers.

[ Get expert advice about planning and implementing your BYOD strategy with InfoWorld's 29-page "Mobile and BYOD Deep Dive" PDF special report. | Keep up on key mobile developments and insights with the Mobilize newsletter. ]

To demonstrate the service, Julia showed how SAMI might be used to build a personal health service. He donned a Fitbit and a wearable heart monitor, weighed himself on an Internet-connected scale, then ran around the stage a few times by way of putting himself through an exercise routine.

He showed how data from the devices, which is normally viewed in standalone apps, can be collected by SAMI, processed, and then presented to the user in the form of a single app.

In Siri-like fashion, he also asked the service, “SAMI, how am I doing?” The app told him he had reached his exercise goal for the day. The idea is that it could do more sophisticated analysis, such as telling him when he needs to train harder or take a break.

Julia showed the technology at the MEMS Executive Congress in Napa, California, an event for companies that make sensors for smartphones and other devices.

A big benefit of SAMI, according to Julia, is that it will be able to collect and store data from any device in its original format. Samsung will “normalize” the data and make it available as a feed — he called it a firehose, using the Twitter metaphor — that can be consumed by other applications.

“We’re doing this normalization and delivering the data through an API [application programming interface], because people don’t want to learn all the APIs for all the individual products,” he said.

Julia was a director of Apple’s Siri project for about 10 months until he left Apple last year. It’s easy to see similarities between the projects: Both collect data from a variety of services and deliver them through a single app. But while Siri is specific to Apple, Samsung wants its platform to be used by many companies. Julia didn’t give a lot of technical details but said Samsung wants it to be as “open” as possible, and it’s not interested in defining standards.

In a brief interview, Julia acknowledged some of the challenges SAMI faces. Chief among them, Samsung is a hardware company with little experience in developing online services, and its bitter rivalry with Apple would almost certainly preclude the iPhone maker from ever joining the same platform. “It’s something Samsung doesn’t know very well today, because Samsung is a hardware company. But we want to enter the space, and offer something different from iCloud,” he said.

Source: http://www.infoworld.com/d/mobile-technology/former-apple-siri-engineer-now-building-connected-device-platform-samsung-230559?source=rss_mobile_technology
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Today’s Horror Icons: Gareth Evans Of ‘The Raid’ And ‘V/H/S/2′

Gareth Evans is known for his inventive Indonesian martial arts actioner “The Raid,” but the filmmaker has contributed to fright cinema. Trading “The Raid’s” bleak tenement slum for a terrifying compound where a strange cult traps a news crew, his segment in horror anthology “V/H/S/2,” “Safe Haven,” blew fans away. The horror short contains the […]Source: http://moviesblog.mtv.com/2013/11/08/todays-horror-icons-gareth-evans-of-the-raid-and-vhs2/
Tags: Bill De Blasio   janelle monae   emmy awards   big brother spoilers   kim zolciak  

Effects of chronic stress can be traced to your genes

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5-Nov-2013

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Contact: John Sheridan
John.Sheridan@osumc.edu
614-293-3571
Ohio State University

Researchers find similar stress response characteristics in mice and humans

COLUMBUS, Ohio New research shows that chronic stress changes gene activity in immune cells before they reach the bloodstream. With these changes, the cells are primed to fight an infection or trauma that doesn’t actually exist, leading to an overabundance of the inflammation that is linked to many health problems.

This is not just any stress, but repeated stress that triggers the sympathetic nervous system, commonly known as the fight-or-flight response, and stimulates the production of new blood cells. While this response is important for survival, prolonged activation over an extended period of time can have negative effects on health.

A study in animals showed that this type of chronic stress changes the activation, or expression, of genes in immune cells before they are released from the bone marrow. Genes that lead to inflammation are expressed at higher-than-normal levels, while the activation of genes that might suppress inflammation is diminished.

Ohio State University scientists made this discovery in a study of mice. Their colleagues from other institutions, testing blood samples from humans living in poor socioeconomic conditions, found that similarly primed immune cells were present in these chronically stressed people as well.

“The cells share many of the same characteristics in terms of their response to stress,” said John Sheridan, professor of oral biology in the College of Dentistry and associate director of Ohio State’s Institute for Behavioral Medicine Research (IBMR), and co-lead author of the study. “There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that’s going to be pro-inflammatory.

“So what this suggests is that if you’re working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system.”

The findings suggest that drugs acting on the central nervous system to treat mood disorders might be supplemented with medications targeting other parts of the body to protect health in the context of chronic social stress.

Steven Cole, a professor of medicine and a member of the Cousins Center for Psychoneuroimmunology at UCLA, is a co-corresponding author of the study. The research is published in a recent issue of the journal Proceedings of the National Academy of Sciences.

The mind-body connection is well established, and research has confirmed that stress is associated with health problems. But the inner workings of that association exactly how stress can harm health are still under investigation.

Sheridan and colleagues have been studying the same mouse model for a decade to reveal how chronic stress and specifically stress associated with social defeat changes the brain and body in ways that affect behavior and health.

The mice are repeatedly subjected to stress that might resemble a person’s response to persistent life stressors. In this model, male mice living together are given time to establish a hierarchy, and then an aggressive male is added to the group for two hours at a time. This elicits a “fight or flight” response in the resident mice as they are repeatedly defeated by the intruder.

“These mice are chronically in that state, so our research question is, ‘What happens when you stimulate the sympathetic nervous system over and over and over, or continuously?’ We see deleterious consequences to that,” Sheridan said.

Under normal conditions, the bone marrow in animals and humans is making and releasing billions of red blood cells every day, as well as a variety of white blood cells that constitute the immune system. Sheridan and colleagues already knew from previous work that stress skews this process so that the white blood cells produced in the bone marrow are more inflammatory than normal upon their release as if they are ready to defend the body against an external threat.

A typical immune response to a pathogen or other foreign body requires some inflammation, which is generated with the help of immune cells. But when inflammation is excessive and has no protective or healing role, the condition can lead to an increased risk for cardiovascular diseases, diabetes and obesity, as well as other disorders.

In this work, the researchers compared cells circulating in the blood of mice that had experienced repeated social defeat to cells from control mice that were not stressed. The stressed mice had an average fourfold increase in the frequency of immune cells in their blood and spleen compared to the normal mice.

Genome-wide analysis of these cells that had traveled to the spleen in the stressed mice showed that almost 3,000 genes were expressed at different levels both higher and lower compared to the genes in the control mice. Many of the 1,142 up-regulated genes in the immune cells of stressed mice gave the cells the power to become inflammatory rapidly and efficiently.

“There is no traditional viral or bacterial challenge we’re generating the challenge via a psychological response,” said study first author Nicole Powell, a research scientist in oral biology at Ohio State. “This study provides a nice mechanism for how psychology impacts biology. Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it’s directly due to the sympathetic nervous system.”

The researchers confirmed that the sympathetic nervous system was activated by showing that a beta blocker reduced symptoms associated with chronic stress. The beta receptors that were turned off by this intervention are major participants in the sympathetic nervous system response.

Meanwhile, UCLA’s Cole performs specialized statistical analyses of genome function to determine how people’s perception of their surroundings affects their biology. He and colleagues analyzed blood samples both from Sheridan’s mice and from healthy young adult humans whose socioeconomic status had been previously characterized as either high or low.

The human analysis identified differing levels of expression of 387 genes between the low- and high-socioeconomic status adults and as in the mice, the up-regulated genes were pro-inflammatory in nature. The researchers also noted that almost a third of the genes with altered expression levels in immune cells from chronically stressed humans were the same genes differentially expressed in mice that had experienced repeated social defeat a much higher similarity than would occur by chance.

This same pro-inflammatory immune-cell profile has been seen in research on parents of children with cancer.

“What we see in this study is a convergence of animal and human data showing similar genomic responses to adversity,” Cole said. “The molecular information from animal research integrates nicely with the human findings in showing a significant up-regulation of pro-inflammatory genes as a consequence of stress and not just experimental stress, but authentic environmental stressors humans experience in everyday life.”

###

This work was supported by the National Institutes of Health; the Mind, Body, Brain and Health Initiative of the John D. and Catherine T. MacArthur Foundation; the British Columbia Ministry of Child and Family Development via the Human Early Learning Partnership; and the Allergy, Genes and Environment Research Network.

Additional co-authors are Erica Sloan of UCLA and the Monash Institute of Pharmaceutical Sciences in Australia; Michael Bailey (associate professor of oral biology) and Brenda Reader of Ohio State’s IBMR; Jesusa Arevalo of UCLA; Gregory Miller and Edith Chen of Northwestern University; and Michael Kobor of the University of British Columbia.


Contacts: John Sheridan, (614) 293-3571, John.Sheridan@osumc.edu; or Nicole Powell, (614) 366-3492, powell.424@osu.edu

Written by Emily Caldwell, (614) 292-8310; Caldwell.151@osu.edu



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[ Back to EurekAlert! ]

PUBLIC RELEASE DATE:

5-Nov-2013

[

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]


Share Share

Contact: John Sheridan
John.Sheridan@osumc.edu
614-293-3571
Ohio State University

Researchers find similar stress response characteristics in mice and humans

COLUMBUS, Ohio New research shows that chronic stress changes gene activity in immune cells before they reach the bloodstream. With these changes, the cells are primed to fight an infection or trauma that doesn’t actually exist, leading to an overabundance of the inflammation that is linked to many health problems.

This is not just any stress, but repeated stress that triggers the sympathetic nervous system, commonly known as the fight-or-flight response, and stimulates the production of new blood cells. While this response is important for survival, prolonged activation over an extended period of time can have negative effects on health.

A study in animals showed that this type of chronic stress changes the activation, or expression, of genes in immune cells before they are released from the bone marrow. Genes that lead to inflammation are expressed at higher-than-normal levels, while the activation of genes that might suppress inflammation is diminished.

Ohio State University scientists made this discovery in a study of mice. Their colleagues from other institutions, testing blood samples from humans living in poor socioeconomic conditions, found that similarly primed immune cells were present in these chronically stressed people as well.

“The cells share many of the same characteristics in terms of their response to stress,” said John Sheridan, professor of oral biology in the College of Dentistry and associate director of Ohio State’s Institute for Behavioral Medicine Research (IBMR), and co-lead author of the study. “There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that’s going to be pro-inflammatory.

“So what this suggests is that if you’re working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system.”

The findings suggest that drugs acting on the central nervous system to treat mood disorders might be supplemented with medications targeting other parts of the body to protect health in the context of chronic social stress.

Steven Cole, a professor of medicine and a member of the Cousins Center for Psychoneuroimmunology at UCLA, is a co-corresponding author of the study. The research is published in a recent issue of the journal Proceedings of the National Academy of Sciences.

The mind-body connection is well established, and research has confirmed that stress is associated with health problems. But the inner workings of that association exactly how stress can harm health are still under investigation.

Sheridan and colleagues have been studying the same mouse model for a decade to reveal how chronic stress and specifically stress associated with social defeat changes the brain and body in ways that affect behavior and health.

The mice are repeatedly subjected to stress that might resemble a person’s response to persistent life stressors. In this model, male mice living together are given time to establish a hierarchy, and then an aggressive male is added to the group for two hours at a time. This elicits a “fight or flight” response in the resident mice as they are repeatedly defeated by the intruder.

“These mice are chronically in that state, so our research question is, ‘What happens when you stimulate the sympathetic nervous system over and over and over, or continuously?’ We see deleterious consequences to that,” Sheridan said.

Under normal conditions, the bone marrow in animals and humans is making and releasing billions of red blood cells every day, as well as a variety of white blood cells that constitute the immune system. Sheridan and colleagues already knew from previous work that stress skews this process so that the white blood cells produced in the bone marrow are more inflammatory than normal upon their release as if they are ready to defend the body against an external threat.

A typical immune response to a pathogen or other foreign body requires some inflammation, which is generated with the help of immune cells. But when inflammation is excessive and has no protective or healing role, the condition can lead to an increased risk for cardiovascular diseases, diabetes and obesity, as well as other disorders.

In this work, the researchers compared cells circulating in the blood of mice that had experienced repeated social defeat to cells from control mice that were not stressed. The stressed mice had an average fourfold increase in the frequency of immune cells in their blood and spleen compared to the normal mice.

Genome-wide analysis of these cells that had traveled to the spleen in the stressed mice showed that almost 3,000 genes were expressed at different levels both higher and lower compared to the genes in the control mice. Many of the 1,142 up-regulated genes in the immune cells of stressed mice gave the cells the power to become inflammatory rapidly and efficiently.

“There is no traditional viral or bacterial challenge we’re generating the challenge via a psychological response,” said study first author Nicole Powell, a research scientist in oral biology at Ohio State. “This study provides a nice mechanism for how psychology impacts biology. Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it’s directly due to the sympathetic nervous system.”

The researchers confirmed that the sympathetic nervous system was activated by showing that a beta blocker reduced symptoms associated with chronic stress. The beta receptors that were turned off by this intervention are major participants in the sympathetic nervous system response.

Meanwhile, UCLA’s Cole performs specialized statistical analyses of genome function to determine how people’s perception of their surroundings affects their biology. He and colleagues analyzed blood samples both from Sheridan’s mice and from healthy young adult humans whose socioeconomic status had been previously characterized as either high or low.

The human analysis identified differing levels of expression of 387 genes between the low- and high-socioeconomic status adults and as in the mice, the up-regulated genes were pro-inflammatory in nature. The researchers also noted that almost a third of the genes with altered expression levels in immune cells from chronically stressed humans were the same genes differentially expressed in mice that had experienced repeated social defeat a much higher similarity than would occur by chance.

This same pro-inflammatory immune-cell profile has been seen in research on parents of children with cancer.

“What we see in this study is a convergence of animal and human data showing similar genomic responses to adversity,” Cole said. “The molecular information from animal research integrates nicely with the human findings in showing a significant up-regulation of pro-inflammatory genes as a consequence of stress and not just experimental stress, but authentic environmental stressors humans experience in everyday life.”

###

This work was supported by the National Institutes of Health; the Mind, Body, Brain and Health Initiative of the John D. and Catherine T. MacArthur Foundation; the British Columbia Ministry of Child and Family Development via the Human Early Learning Partnership; and the Allergy, Genes and Environment Research Network.

Additional co-authors are Erica Sloan of UCLA and the Monash Institute of Pharmaceutical Sciences in Australia; Michael Bailey (associate professor of oral biology) and Brenda Reader of Ohio State’s IBMR; Jesusa Arevalo of UCLA; Gregory Miller and Edith Chen of Northwestern University; and Michael Kobor of the University of British Columbia.


Contacts: John Sheridan, (614) 293-3571, John.Sheridan@osumc.edu; or Nicole Powell, (614) 366-3492, powell.424@osu.edu

Written by Emily Caldwell, (614) 292-8310; Caldwell.151@osu.edu



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| E-mail


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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.

Source: http://www.eurekalert.org/pub_releases/2013-11/osu-eoc110513.php
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Germany: Babies can be registered as neither sex

(AP) — A new law has gone into effect allowing German parents to register their newborn babies as neither male nor female if they were born with traits of both sexes.

The German Parliament in January approved the law that went into effect Friday. The German Ethics Council, an advisory group, had urged the change to take the pressure off parents to make a hasty decision and possibly commit to surgery immediately after birth, the dpa news agency reported.

The council had argued, among other things, that many people born with both sex characteristics who were operated on as children say they wouldn’t have consented to the surgery.

Parents had previously been required by law to register their children’s name and gender within one week with authorities.

Associated PressSource: http://hosted2.ap.org/APDEFAULT/bbd825583c8542898e6fa7d440b9febc/Article_2013-11-01-Germany-Gender%20Registration/id-f4d8ebe337be4cd8ba65924d94e6fb38
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