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Source: http://www.engadget.com/2013/11/07/star-wars-episode-vii-launch-date-december-2015/?ncid=rss_truncated"I am sorry that they are finding themselves in this situation based on assurances they got from me," President Obama said Thursday, speaking about Americans who will lose their current health insurance plans.
In speeches before parts of the Affordable Care Act took effect, the president promised that people who were content with the plans they already had would be able to keep them. But that hasn't always been the case, as The Two-Way reported in October.
Obama spoke about the troubled rollout of the new health care system with NBC's Chuck Todd Thursday. Todd asked the president about the pledge he often repeated when critics of the Affordable Care Act said it would mean thousands of cancelled policies.
"I meant what I said," Obama answered. "And we worked hard to try to make sure that we implemented it properly. But obviously, we didn't do a good enough job. And I regret that."
In addition to his apology, the president pledged to help those who have complained that the new law is forcing them to sign up for a more expensive plan.
"We've got to work hard to make sure that they know we hear them," Obama said, "and that we're going to do everything we can to deal with folks who find themselves in a tough position as a consequence of this."
The appearance on NBC marks "a more apologetic tone" for the president on this issue, NPR's Ari Shapiro reports.
"Until now, the White House had taken a defensive response to people being forced to change health plans. The president insisted that people losing their plans would get better and, in some cases, cheaper ones," Ari says in a report for our Newscast unit.
"The White House is also still struggling to get the HealthCare.gov website up and running," Ari adds. "It's functioning better than before, but it's still not up to speed."
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PUBLIC RELEASE DATE: 7-Nov-2013
ShareContact: Derik Hertel
derik.hertel@dartmouth.edu
603-650-1203
The Geisel School of Medicine at Dartmouth
Professor of Genetics Scott Williams, PhD, of the Institute for Quantitative Biomedical Sciences (iQBS) at Dartmouth's Geisel School of Medicine, has made two novel discoveries: first, a person can have several DNA mutations in parts of their body, with their original DNA in the restresulting in several different genotypes in one individualand second, some of the same genetic mutations occur in unrelated people. We think of each person's DNA as unique, so if an individual can have more than one genotype, this may alter our very concept of what it means to be a human, and impact how we think about using forensic or criminal DNA analysis, paternity testing, prenatal testing, or genetic screening for breast cancer risk, for example. Williams' surprising results indicate that genetic mutations do not always happen purely at random, as scientists have previously thought. His work, done in collaboration with Professor of Genetics Jason Moore, PhD, and colleagues at Vanderbilt University, was published in PLOS Genetics journal on November 7, 2013.1
Genetic mutations can occur in the cells that are passed on from parent to child and may cause birth defects. Other genetic mutations occur after an egg is fertilized, throughout childhood or adult life, after people are exposed to sunlight, radiation, carcinogenic chemicals, viruses, or other items that can damage DNA. These later or "somatic" mutations do not affect sperm or egg cells, so they are not inherited from parents or passed down to children. Somatic mutations can cause cancer or other diseases, but do not always do so. However, if the mutated cell continues to divide, the person can develop tissue, or a part thereof, with a different DNA sequence from the rest of his or her body.
"We are in reality diverse beings in that a single person is genetically not a single entityto be philosophical in ways I do not yet understandwhat does it mean to be a person if we are variable within?" says Williams, the study's senior author, and founding Director of the Center for Integrative Biomedical Sciences in iQBS. "What makes you a person? Is it your memory? Your genes?" He continues, "We have always thought, 'your genome is your genome.' The data suggest that it is not completely true."
In the past, it was always thought that each person contains only one DNA sequence (genetic constitution). Only recently, with the computational power of advanced genetic analysis tools that examine all the genes in one individual, have scientists been able to systematically look for this somatic variation. "This study is an example of the type of biomedical research project that is made possible by bringing together interdisciplinary teams of scientists with expertise in the biological, computational and statistical sciences." says Jason Moore, Director of the iQBS, who is also Associate Director for Bioinformatics at the Cancer Center, Third Century Professor, and Professor of Community and Family Medicine at Geisel.
Having multiple genotypes from mutations within one's own body is somewhat analogous to chimerism, a condition in which one person has cells inside his or her body that originated from another person (i.e., following an organ or blood donation; or sometimes a mother and childor twinsexchange DNA during pregnancy. Also, occasionally a person finds out that, prior to birth, he or she had a twin who did not survive, whose genetic material is still contained within their own body).2 Chimerism has resulted in some famous DNA cases: one in which a mother had genetic testing that "proved" that she was unrelated to two of her three biological sons.3
Williams says that, although this was a small study, "there is a lot more going on than we thought, and the results are, in some ways, astoundingly weird."
Because somatic changes are thought to happen at random, scientists do not expect unrelated people to exhibit the same mutations. Williams and colleagues analyzed the same 10 tissue samples in two unrelated people. They found several identical mutations, and detected these repeated mutations only in kidney, liver and skeletal body tissues. Their research examined "mitochondrial DNA" (mtDNA)a part of DNA that is only inherited from the mother.4 Technically all women would share mtDNA from one common female ancestor, but mutations have resulted in differences. The importance of Williams' finding is that these tissue-specific, recurrent, common mutations in mtDNA among unrelated study subjectsonly detected in three body tissuesare "not likely being developed and maintained through purely random processes," according to Williams. They indicate "a completely different model . a decidedly non-random process that results in particular mutations, but only in specific tissues."
If our human DNA changes, or mutates, in patterns, rather than randomly; if such mutations "match" among unrelated people; or if genetic changes happen only in part of the body of one individual, what does this mean for our understanding of what it means to be human? How may it impact our medical care, cancer screening, or treatment of disease? We don't yet know, but ongoing research may help reveal the answers.
Christopher Amos, PhD, Director of the Center for Genomic Medicine and Associate Director for Population Sciences at the Cancer Center, says, "This paper identifies mutations that develop in multiple tissues, and provides novel insights that are relevant to aging. Mutations are noticed in several tissues in common across individuals, and the aging process is the most likely contributor. The theory would be that selected mutations confer a selective advantage to mitochondria, and these accumulate as we age." Amos, who is also a Professor of Community and Family Medicine at Geisel, says, "To confirm whether aging is to blame, we would need to study tissues from multiple individuals at different ages." Williams concurs, saying, "Clearly these do accumulate with age, but how and why is unknownand needs to be determined."
As more and better data become available from high-throughput genetic analyses and high-powered computers, researchers are identifying an increasing number of medical conditions that result from somatic mutations, including neurological, hematological, and immune-related disorders. Williams and colleagues are conducting further research to examine how diseases, other than cancer or even benign conditions, may result from somatic changes.5 Williams, Moore and Amos will employ iQBS's Discovery supercomputer for next-generation sequencing to process subjects' DNA data.6 Future analyses will include large, whole-genome sequencing of the data for the two individuals studied in the current report.
Williams explains, "We know that cancer is caused by mutations that cause a tumor. But in this work, we chose to study mutations in people without any cancer. Knowing how we accumulate mutations may make it easier to separate genetic signals that may cause cancer from those that accumulate normally without affecting disease. It may also allow us to see that many changes that we thought caused cancer do not in many situations, if we find the same mutations in normal tissues."
Just as our bodies' immune systems have evolved to fight disease, interestingly, they can also stave off the effects of some genetic mutations. Williams states that, "Most genetic changes don't cause disease, and if they did, we'd be in big trouble. Fortunately, it appears our systems filter a lot of that out."
Mark Israel, MD, Director of Norris Cotton Cancer Center and Professor of Pediatrics and Genetics at Geisel, says, "The fact that somatic mutation occurs in mitochondrial DNA apparently non-randomly provides a new working hypothesis for the rest of the genome. If this non-randomness is general, it may affect cancer risks in ways we could not have previously predicted. This can have real impact in understanding and changing disease susceptibility."
###
1 Williams, Scott, et al., Recurrent tissue-specific mtDNA mutations are common in humans. http://www.plosgenetics.org/doi/pgen.1003929.
2 Strain L, Dean JC, Hamilton MP, Bonthron D. A true hermaphrodite chimera resulting from embryo amalgamation after in vitro fertilization. N Engl J Med 1998;(338):166-9/
3 Norton AT and Zehner O. Project MUSE: Today's Research, Tomorrow's Inspiration. http://www.academia.edu/202539/Which_Half_Is_Mommy_Tetragametic_Chimerism_and_Trans-Subjectivity.
4 The Bradshaw Foundation [online learning resource with main areas of focus on archaeology, anthropology and genetic research]: Mitochondrial DNA: The EVE Gene. http://www.bradshawfoundation.com/journey/eve.htm.
5 Li, Chun and Williams, Scott M. Human somatic variation: It's not just for cancer anymore. Current Genetic Medicine Reporter (In Press).
6 Discovery iQBS website. http://iqbs.org/resources/discovery-supercomputer/.
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.
PUBLIC RELEASE DATE: 7-Nov-2013
ShareContact: Derik Hertel
derik.hertel@dartmouth.edu
603-650-1203
The Geisel School of Medicine at Dartmouth
Professor of Genetics Scott Williams, PhD, of the Institute for Quantitative Biomedical Sciences (iQBS) at Dartmouth's Geisel School of Medicine, has made two novel discoveries: first, a person can have several DNA mutations in parts of their body, with their original DNA in the restresulting in several different genotypes in one individualand second, some of the same genetic mutations occur in unrelated people. We think of each person's DNA as unique, so if an individual can have more than one genotype, this may alter our very concept of what it means to be a human, and impact how we think about using forensic or criminal DNA analysis, paternity testing, prenatal testing, or genetic screening for breast cancer risk, for example. Williams' surprising results indicate that genetic mutations do not always happen purely at random, as scientists have previously thought. His work, done in collaboration with Professor of Genetics Jason Moore, PhD, and colleagues at Vanderbilt University, was published in PLOS Genetics journal on November 7, 2013.1
Genetic mutations can occur in the cells that are passed on from parent to child and may cause birth defects. Other genetic mutations occur after an egg is fertilized, throughout childhood or adult life, after people are exposed to sunlight, radiation, carcinogenic chemicals, viruses, or other items that can damage DNA. These later or "somatic" mutations do not affect sperm or egg cells, so they are not inherited from parents or passed down to children. Somatic mutations can cause cancer or other diseases, but do not always do so. However, if the mutated cell continues to divide, the person can develop tissue, or a part thereof, with a different DNA sequence from the rest of his or her body.
"We are in reality diverse beings in that a single person is genetically not a single entityto be philosophical in ways I do not yet understandwhat does it mean to be a person if we are variable within?" says Williams, the study's senior author, and founding Director of the Center for Integrative Biomedical Sciences in iQBS. "What makes you a person? Is it your memory? Your genes?" He continues, "We have always thought, 'your genome is your genome.' The data suggest that it is not completely true."
In the past, it was always thought that each person contains only one DNA sequence (genetic constitution). Only recently, with the computational power of advanced genetic analysis tools that examine all the genes in one individual, have scientists been able to systematically look for this somatic variation. "This study is an example of the type of biomedical research project that is made possible by bringing together interdisciplinary teams of scientists with expertise in the biological, computational and statistical sciences." says Jason Moore, Director of the iQBS, who is also Associate Director for Bioinformatics at the Cancer Center, Third Century Professor, and Professor of Community and Family Medicine at Geisel.
Having multiple genotypes from mutations within one's own body is somewhat analogous to chimerism, a condition in which one person has cells inside his or her body that originated from another person (i.e., following an organ or blood donation; or sometimes a mother and childor twinsexchange DNA during pregnancy. Also, occasionally a person finds out that, prior to birth, he or she had a twin who did not survive, whose genetic material is still contained within their own body).2 Chimerism has resulted in some famous DNA cases: one in which a mother had genetic testing that "proved" that she was unrelated to two of her three biological sons.3
Williams says that, although this was a small study, "there is a lot more going on than we thought, and the results are, in some ways, astoundingly weird."
Because somatic changes are thought to happen at random, scientists do not expect unrelated people to exhibit the same mutations. Williams and colleagues analyzed the same 10 tissue samples in two unrelated people. They found several identical mutations, and detected these repeated mutations only in kidney, liver and skeletal body tissues. Their research examined "mitochondrial DNA" (mtDNA)a part of DNA that is only inherited from the mother.4 Technically all women would share mtDNA from one common female ancestor, but mutations have resulted in differences. The importance of Williams' finding is that these tissue-specific, recurrent, common mutations in mtDNA among unrelated study subjectsonly detected in three body tissuesare "not likely being developed and maintained through purely random processes," according to Williams. They indicate "a completely different model . a decidedly non-random process that results in particular mutations, but only in specific tissues."
If our human DNA changes, or mutates, in patterns, rather than randomly; if such mutations "match" among unrelated people; or if genetic changes happen only in part of the body of one individual, what does this mean for our understanding of what it means to be human? How may it impact our medical care, cancer screening, or treatment of disease? We don't yet know, but ongoing research may help reveal the answers.
Christopher Amos, PhD, Director of the Center for Genomic Medicine and Associate Director for Population Sciences at the Cancer Center, says, "This paper identifies mutations that develop in multiple tissues, and provides novel insights that are relevant to aging. Mutations are noticed in several tissues in common across individuals, and the aging process is the most likely contributor. The theory would be that selected mutations confer a selective advantage to mitochondria, and these accumulate as we age." Amos, who is also a Professor of Community and Family Medicine at Geisel, says, "To confirm whether aging is to blame, we would need to study tissues from multiple individuals at different ages." Williams concurs, saying, "Clearly these do accumulate with age, but how and why is unknownand needs to be determined."
As more and better data become available from high-throughput genetic analyses and high-powered computers, researchers are identifying an increasing number of medical conditions that result from somatic mutations, including neurological, hematological, and immune-related disorders. Williams and colleagues are conducting further research to examine how diseases, other than cancer or even benign conditions, may result from somatic changes.5 Williams, Moore and Amos will employ iQBS's Discovery supercomputer for next-generation sequencing to process subjects' DNA data.6 Future analyses will include large, whole-genome sequencing of the data for the two individuals studied in the current report.
Williams explains, "We know that cancer is caused by mutations that cause a tumor. But in this work, we chose to study mutations in people without any cancer. Knowing how we accumulate mutations may make it easier to separate genetic signals that may cause cancer from those that accumulate normally without affecting disease. It may also allow us to see that many changes that we thought caused cancer do not in many situations, if we find the same mutations in normal tissues."
Just as our bodies' immune systems have evolved to fight disease, interestingly, they can also stave off the effects of some genetic mutations. Williams states that, "Most genetic changes don't cause disease, and if they did, we'd be in big trouble. Fortunately, it appears our systems filter a lot of that out."
Mark Israel, MD, Director of Norris Cotton Cancer Center and Professor of Pediatrics and Genetics at Geisel, says, "The fact that somatic mutation occurs in mitochondrial DNA apparently non-randomly provides a new working hypothesis for the rest of the genome. If this non-randomness is general, it may affect cancer risks in ways we could not have previously predicted. This can have real impact in understanding and changing disease susceptibility."
###
1 Williams, Scott, et al., Recurrent tissue-specific mtDNA mutations are common in humans. http://www.plosgenetics.org/doi/pgen.1003929.
2 Strain L, Dean JC, Hamilton MP, Bonthron D. A true hermaphrodite chimera resulting from embryo amalgamation after in vitro fertilization. N Engl J Med 1998;(338):166-9/
3 Norton AT and Zehner O. Project MUSE: Today's Research, Tomorrow's Inspiration. http://www.academia.edu/202539/Which_Half_Is_Mommy_Tetragametic_Chimerism_and_Trans-Subjectivity.
4 The Bradshaw Foundation [online learning resource with main areas of focus on archaeology, anthropology and genetic research]: Mitochondrial DNA: The EVE Gene. http://www.bradshawfoundation.com/journey/eve.htm.
5 Li, Chun and Williams, Scott M. Human somatic variation: It's not just for cancer anymore. Current Genetic Medicine Reporter (In Press).
6 Discovery iQBS website. http://iqbs.org/resources/discovery-supercomputer/.
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.
Now that anyone (well, anyone with an invitation) with a spare $1,500 can get their very own Google Glass, the folks in Mountain View have thoughtfully released a software update for the famous wearable. We're frankly surprised Glass owners weren't able to do this before, but you can now look up your calendar directly from the headset. Simply say "ok glass, google my agenda" or "ok glass, what am I doing next week?" to see what's up next on your busy schedule. Another new feature is the ability to customize a location as either "home" or "work" so you can easily ask directions for either of those places.
Interestingly, the update also removed a feature. After finding out that people were long-pressing their touchpads by mistake, the company has turned that functionality off. Instead, Google recommends tapping the touchpad three times to initiate a search. Other upgraded goodies include a new tutorial setup and a screencast shortcut. So if you're lucky enough to own one of these headsets, go on and download the update from the thing on your noggin. And while you're at it, maybe figure out a way to invite us onto that Google barge.
By Olivia Oran and Gerry Shih
Nov 7 (Reuters) - Twitter Inc stock soared 92
percent in their first day of trading on Thursday on the New
York Stock Exchange as investors snapped up shares in the
microblogging site, pushing its market value to a heady $25
billion.
The shares opened at $45.10 a share, up from the initial
public offering price of $26 set on Wednesday, then added to
those gains, hitting a high of $50.
Sources said the flotation had drawn strong demand, with
investors asking for 30 times the number of shares on offer as
they bet on potential growth at the money-losing social media
company.
The opening price valued the shares at about 22 times
forecast 2014 sales, nearly double that multiple at social media
rivals Facebook Inc and LinkedIn Corp.
Twitter executives including Chief Executive Dick Costolo
and founder Jack Dorsey thronged to the floor of the New York
Stock Exchange to witness the IPO. The Big Board snatched the
offering away from Nasdaq after the normally tech-focused Nasdaq
stumbled with the larger Facebook flotation last year.
"Facebook was so overhyped people felt like they couldn't
miss out," said Kenneth Polcari, a senior floor official at
O'Neil Securities Inc. "Twitter isn't like that, though you can
feel the excitement."
British actor Patrick Stewart rang the opening bell at the
exchange together with 9-year-old Vivienne Harr, who started a
charity to end childhood slavery using the microblogging site.
"I guess I represent the poster boy for Twitter," Stewart
said, adding that he had only been tweeting for about a year and
wasn't buying Twitter stock today.
Twitter's building staff opened its offices in San Francisco
extra early, at 5:30 a.m. on Thursday. By 7:30 a.m., hundreds of
employees had flocked to their 9th floor cafeteria to watch
Stewart ring the opening bell on TV.
The microblogging network priced its 70 million shares at
above the targeted range of $23 to $25, which had been raised
once before. The IPO values Twitter at $14.1 billion, with the
potential to reach $14.4 billion if underwriters exercise an
overallotment option.
If the full overallotment is exercised, as expected, Twitter
could raise $2.1 billion, making it the second largest Internet
offering in the United States behind Facebook Inc's $16
billion IPO last year and ahead of Google Inc's 2004
IPO, according to Thomson Reuters data.
Twitter boasts 230 million global users, including heads of
state and celebrities, but it lost $65 million in its most
recent quarter and questions remained about long-term prospects.
It also lacks the ubiquity of Facebook or the "stickiness"
factor that keeps people checking the No. 1 social network on a
daily basis.
A Reuters-Ipsos poll last month showed that 36 percent of
people who signed up for a Twitter account say they do not use
it.
FILE - In this Oct. 20, 2013 file photo, Chicago Bears quarterback Josh McCown talks with head coach Marc Trestman during an NFL football game against the Washington Redskins in Landover, Md. During the game, McCown led the Bears to a 24-point second half when pressed into service to replace injured Jay Cutler, but he had no preparation time in that one. Now, after a couple weeks to get ready to face the Green Bay Packers on Monday, Nov. 4, McCown expects to be ready to produce against a defense that has always given Cutler fits. (AP Photo/Alex Brandon File)
FILE - In this Oct. 20, 2013 file photo, Chicago Bears quarterback Josh McCown talks with head coach Marc Trestman during an NFL football game against the Washington Redskins in Landover, Md. During the game, McCown led the Bears to a 24-point second half when pressed into service to replace injured Jay Cutler, but he had no preparation time in that one. Now, after a couple weeks to get ready to face the Green Bay Packers on Monday, Nov. 4, McCown expects to be ready to produce against a defense that has always given Cutler fits. (AP Photo/Alex Brandon File)
Chicago Bears quarterback Josh McCown (12) talks to Jay Cutler during the first half of an NFL football game against the Green Bay Packers Monday, Nov. 4, 2013, in Green Bay, Wis. (AP Photo/Mike Roemer)
Chicago Bears quarterback Josh McCown throws past Green Bay Packers' Datone Jones during the second half of an NFL football game Monday, Nov. 4, 2013, in Green Bay, Wis. (AP Photo/Jeffrey Phelps)
LAKE FOREST, Ill. (AP) — Bears quarterback Jay Cutler will start against the Detroit Lions on Sunday after missing one game with a groin muscle tear.
Coach Marc Trestman confirmed Cutler's return Thursday following practice, saying doctors have given Cutler the clearance to play. Trestman said Cutler will not be restricted in any way due to the injury.
Cutler suffered the injury against the Washington Redskins Oct. 20 when he was sacked during the 45-41 loss. The Bears had a bye the following week, then Josh McCown started and played all of Monday night's 27-20 win at Green Bay.
Cutler has completed 146 of 225 passes for 1,658 yards and 12 touchdowns with seven interceptions. McCown completed 36 of 61 for 476 yards and did not turn the ball over as Cutler's replacement.
Associated PressSource: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2013-11-07-FBN-Bears-Quarterbacks/id-af1c59e797c24386958a8aeb70bbe23d
Episode VII may still be in the throes of pre-production, but Lucasfilm has confirmed that the Star Wars saga will continue on December 18th, 2015, with shooting officially set to start in spring 2014 and leaving just 771 days left to speculate. ...
Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/aMWIpitsqU8/
