The Obama administration official responsible for the implementation of key parts of the federal health care law apologized Wednesday for the disastrous rollout of the health insurance marketplace built by the government but vowed the problems would be fixed by the end of November.
In sworn testimony before the House Energy and Commerce Committee, Health and Human Services Secretary Kathleen Sebelius conceded that access to the federal website to buy insurance under the law "has been a miserably frustrating experience for way too many Americans."
"You deserve better. I apologize,” Sebelius said. “I'm accountable to you for fixing these problems."
Since its launch on Oct. 1, the government website has been set back with functional and accessibility problems that have prevented people seeking insurance from purchasing plans. Under the health care law passed in 2010, all Americans must be able to prove that they have insurance by March 31, 2014, and Sebelius told lawmakers that enough time will be granted to fulfill the obligation.
She conceded that before launching the site, her agency underestimated the depth of the problems with the site.
"No one indicated it could possibly go this wrong," she said, but added that private contractors who helped build the site did cite "risks" in undertaking such a massive project online.
Republicans and Democrats on the committee spent Wednesday morning grilling Sebelius during her first official testimony since the website’s launch. She spent much of her time defending the administration from questions about why thousands of private insurance plans would be canceled as a result of the law.
Republicans have seized on repeated promises from President Barack Obama that consumers could keep their health care plans, which has turned out not to be true since many plans do not meet new insurance requirements under the law, which set minimum mandates on coverage.
“They will be offered new plans,” Sebelius said when asked by Tennessee Republican Rep. Marsha Blackburn what she would say to Americans who received notices that their current coverage does not meet new requirements and will be terminated. “Insurance companies cancel individual policies year in and year out. They are a one-year contract with individuals. They are not lifetime plans.”
“I will remind you,” Blackburn replied, “some people like to drive a Ford not a Ferrari. Some people like to drink out of a red Solo cup, not a crystal stem. You’re taking away their choice.”
In her testimony, Sebeilus acknowledged that her agency did not provide enough time for final testing of the site. Last week, private contractors from companies who worked with HHS to build HealthCare.gov said they were given only two weeks for end-to-end testing.
“We did not adequately do end-to-end testing,” Sebelius said. “I don’t think anyone estimated the degree of problems.”
Jaime's sweet boy! Jaime King is smitten with her new baby boy, and decided to show him off via Instagram on Tuesday, Oct. 29. The Hart of Dixie star welcomed her first child earlier this month.
"It is a grey cotton jersey kind of day," the 34-year-old actress wrote. Alongside the caption, the former model shared an adorable photo of her son James Knight (with his face hidden!) lying on her chest as they snuggled in bed together. The mother-son duo also wore matching grey shirts.
The first-time mom looks simply blissful in the sweet snapshot, as she also showed off James' dark brunette locks. The actress shut her eyes for the photo and also gave a closeup of her stunning engagement and wedding band.
King and her director husband Kyle Newman first announced in May they were expecting and later welcomed James on Oct. 6. "Mom and Baby are happy, healthy and are doing great," a rep for the actress confirmed to Us Weekly at the time.
Two weeks later, the beaming new mom revealed her post-baby body while stepping out for coffee with her mom Nancy at Urth Caffe in Beverly Hills, Calif., on Oct. 18. That same day, she shared a picture of James -- with his face covered up once again -- wrapped in a blanket as they went for his first doctor check up.
Color everyone surprised by this one, but at the ARM developers conference Intel partner Altera has announced that the company will begin producing 64-bit ARM chips. Intel has been trying to break into the mobile space currently dominated by ARM with their own chips, so this latest news is definitely of the surprising variety. Jean-Baptiste at Forbes:
At the ARM developers’ conference today, Intel partner Altera ALTR +1.23% announced that the world’s largest semiconductor company will fabricate its ARM’s 64-bit chips starting next year. An announcement that sent shockwaves throughout the technology industry as Intel is desperately trying to break ARM’s supremacy in the mobile market.
Further still, analyst Nathan Brookwood added this:
“Intel will build Apple's A7, Qualcomm’s Snapdragon or the Nvidia Tegra for the right price. Now, the question is, are they ready to pay that premium and feed their direct competitor, except for Apple. But that would actually make business sense for everyone"
So, is this Intel's way, finally, to monetize better in the mobile space? Is this Intel's way to break into the iPhone sometime down the line? The biggest chip maker in the world appears to be out for hire. Intel's former CEO famously told the world they passed up on the opportunity to work on the original iPhone, and since Apple went all-in on the ARM architecture, perhaps this could end up being a way back in further down the road.
In this photo released by the Extraordinary Chambers in the Courts of Cambodia, Nuon Chea, left, who was the Khmer Rouge's chief ideologist and No. 2 leader, waits before his final statements at the U.N.-backed war crimes tribunal in Phnom Penh, Cambodia, Thursday, Oct. 31, 2013. Former Khmer Rouge leader Nuon Chea has denied all charges against him on the last day of a trial for leaders of the Cambodian regime widely blamed for the deaths of some 1.7 million people. (AP Photo/Extraordinary Chambers in the Courts of Cambodia, Mark Peters)
In this photo released by the Extraordinary Chambers in the Courts of Cambodia, Nuon Chea, left, who was the Khmer Rouge's chief ideologist and No. 2 leader, waits before his final statements at the U.N.-backed war crimes tribunal in Phnom Penh, Cambodia, Thursday, Oct. 31, 2013. Former Khmer Rouge leader Nuon Chea has denied all charges against him on the last day of a trial for leaders of the Cambodian regime widely blamed for the deaths of some 1.7 million people. (AP Photo/Extraordinary Chambers in the Courts of Cambodia, Mark Peters)
Nuon Chea, enter, who was the Khmer Rouge's chief ideologist and No. 2 leader, is seen on a screen at the court during a final statements at the U.N.-backed war crimes tribunal in Phnom Penh, Cambodia, Thursday, Oct. 31, 2013. Former Khmer Rouge leader Nuon Chea has denied all charges against him on the last day of a trial for leaders of the Cambodian regime widely blamed for the deaths of some 1.7 million people. (AP Photo/Heng Sinith)
In this photo released by the Extraordinary Chambers in the Courts of Cambodia, Nuon Chea, who was the Khmer Rouge's chief ideologist and No. 2 leader, waits before his final statements at the U.N.-backed war crimes tribunal in Phnom Penh, Cambodia, Thursday, Oct. 31, 2013. Former Khmer Rouge leader Nuon Chea has denied all charges against him on the last day of a trial for leaders of the Cambodian regime widely blamed for the deaths of some 1.7 million people. (AP Photo/Extraordinary Chambers in the Courts of Cambodia, Mark Peters)
Nuon Chea, who was the Khmer Rouge's chief ideologist and No. 2 leader, is seen on a screen during his final statements at the U.N.-backed war crimes tribunal in Phnom Penh, Cambodia, Thursday, Oct. 31, 2013. Former Khmer Rouge leader Nuon Chea has denied all charges against him on the last day of a trial for leaders of the Cambodian regime widely blamed for the deaths of some 1.7 million people. (AP Photo/Heng Sinith)
PHNOM PENH, Cambodia (AP) — Former Khmer Rouge leader Nuon Chea denied charges of genocide and other crimes Thursday on the last day of his trial but expressed "deepest remorse" for the deaths of some 1.7 million Cambodians during the regime's rule in the 1970s.
The ailing 87-year-old Nuon Chea, the Khmer Rouge's chief ideologist and No. 2 leader, also apologized to Cambodians and accepted "moral responsibility" for the deaths, repeating previous statements he has made in an attempt to distance himself from the actual crimes.
Along with Nuon Chea, the U.N.-backed tribunal has also charged 82-year-old Khieu Samphan, the former Khmer Rouge head of state, with genocide and crimes against humanity, including torture, enslavement and murder, for their roles in the radical communist regime nearly 40 years ago.
Khieu Samphan is also expected to deny all the charges later Thursday. A verdict is expected in the first half of 2014, more than two years after the trial began.
Nuon Chea said the Khmer Rouge was only defending itself from external and internal enemies.
Blaming "those traitors" for the tragic situation in Cambodia in the 1970s, Nuon Chea said he would nonetheless "like to sincerely apologize to the public, the victims, the families, and all Cambodian people."
"I still stand by my previously stated position that I am morally responsible for the loose and untidy control" by his party. "I wish to show my remorse and pray for the lost souls that occurred by any means" during the Khmer Rouge rule.
His words are unlikely to be any consolation for the survivors, hundreds of whom crowded the courtroom and the tribunal's grounds to hear the two aged defendants speak.
Deaths due to execution, disease, torture and starvation were widespread during the Khmer Rouge's brutal rule in the 1970s, when the communist ideologues emptied cities and forced virtually the entire population to work on farm collectives.
In his defense, Nuon Chea said he had never ordered Khmer Rouge cadres to commit any crimes.
"I never educated or instructed them to mistreat or kill people to deprive them of food or commit any genocide," said the frail former leader, speaking steadily as he read from pages of notes.
"Through this trial, it is clearly indicated that I was not engaged in any commission of the crimes as alleged by the co-prosecutors," he said. "In short, I am innocent in relation to those allegations."
"I respectfully submit to your honors to acquit me from all the charges and to subsequently release me," he said.
Death and disability have robbed the tribunal of other defendants. Khmer Rouge Foreign Minister Ieng Sary died in March, and his wife Ieng Thirith, the regime's social affairs minister, was declared unfit for trial in September 2012 after being diagnosed with dementia. The group's top leader, Pol Pot, died in 1998.
The tribunal, launched in 2006, so far has convicted only one defendant, Khmer Rouge prison director Kaing Guek Eav, who was sentenced to life imprisonment in 2011.
The present trial's focus is on the forced movement of people and excludes some of the gravest charges related to genocide, detention centers and killings. The next trial will begin as soon as possible, but the tribunal has not set a date.
Facebook’s popularity might be on the decline among some teenagers, the company signaled Wednesday.
For younger teenagers, Facebook has seen a decline in the number of daily users, the company reported during its third-quarter earnings call. Overall, usage among U.S. teens was stable between the second and third quarters, but the decrease in daily usage for some was noted early in the prepared remarks of Facebook’s chief financial officer, David Ebersman.
It was one of the first times that the social network has identified a decrease in its teenage users. Youth engagement on Facebook is hard to measure because self-reported age data is usually unreliable for younger users, the company said. But, “we wanted to share [the figure] because we get a lot of questions about teens,” Ebersman said.
Facebook didn’t disclose the size of the decline or comment on it further.
A problem?
With many rival services vying for younger users’ attention, Facebook’s ability to keep them on its site is an issue. One area of intense competition is messaging. Facebook operates its own standalone app just for messages, called Messenger, but services such as Snapchat, WhatsApp and Skype are also popular.
Part of the issue might be that everyone seems to be on Facebook now, and teens want their own place to digitally mingle. “Teens don’t want to be on the same site as their parents,” said Brian Blau, who’s an industry analyst with Gartner and a parent of a teenager himself.
Also, a study released by Pew Research Center earlier this year found that the “drama” on Facebook might be driving more teens to one of Facebook’s biggest rivals: Twitter.
Overall, on a monthly basis, Facebook grew its number of users to 1.19 billion during the quarter, an increase of 18 percent from last year. Total sales for the company, aided by mobile, were up 60 percent, to US$2.02 billion.
During the call, Facebook said it would continue to build products for people of all ages.
Zach Miners, IDG News Service , IDG News Service
Zach Miners covers social networking, search and general technology news for IDG News Service More by Zach Miners, IDG News Service
Bacteria and fat: A 'perfect storm' for inflammation, may promote diabetes
PUBLIC RELEASE DATE:
30-Oct-2013
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Contact: Jennifer Brown jennifer-l-brown@uiowa.edu 319-356-7124 University of Iowa Health Care
Bacterial toxins activate fat cells producing chronic inflammation, which in turn boosts risk of developing diabetes
Making fat cells immortal might seem like a bad idea to most people, but for a team of University of Iowa scientists it was the ideal way to study how the interaction between bacteria and fat cells might contribute to diabetes.
The connection between fat, bacteria, and diabetes is inflammation, which is the body's normal reaction to infection or injury. Inflammation is beneficial in small, controlled doses but can be extremely harmful when it persists and becomes chronic.
"The idea is that when fat cells (adipocytes) interact with environmental agents -- in this case, bacterial toxins -- they then trigger a chronic inflammatory process," says Patrick Schlievert, Ph.D., UI professor and head of microbiology and co-senior author of a new study published Oct. 30 in the journal PLOS ONE. "We know that chronic inflammation leads to insulin resistance, which can then lead to diabetes. So people are very interested in the underlying causes of chronic inflammation."
The UI researchers used immortalized fat cells to show that bacterial toxins stimulate fat cells to release molecules called cytokines, which promote inflammation. By immortalizing fat cells the UI team created a stockpile of continuously dividing, identical cells that are necessary for repeat experiments to validate results, explains Al Klingelhutz, Ph.D., UI microbiologist and co-senior author of the study.
Previous studies have shown that a toxin called lipopolysaccharide (LPS) produced by E. coli bacteria that reside in the human gut, triggers fat cells to produce pro-inflammatory cytokines, and this interaction has been proposed to contribute to the development of diabetes.
The UI team focused on a different bacterium, Staphylococcus aureus (staph), which appears to be important in the context of diabetes for two reasons. First, as people become obese and then progress into diabetes they become very heavily colonized with staph bacteria. Secondly, staph is the most common microbe isolated from diabetic foot ulcers, one of the most common and health-threatening complications of diabetes.
All staph bacteria make toxins called superantigens -- molecules that disrupt the immune system. Schlievert's research has previously shown that superantigens cause the deadly effects of various staph infections, such as toxic shock syndrome, sepsis, and endocarditis.
The new UI study shows that superantigens from staph bacteria trigger fat cells to produce pro-inflammatory molecules. Moreover, the study found that superantigens synergized with LPS from E. coli to magnify fat cells' cytokine responses, amplifying the inflammation, which could potentially boost the likelihood of developing diabetes.
"The E. coli that resides in our gut produces LPS and every day a small amount of this toxin gets into our circulation, but it is generally cleared from the circulation by the liver. However, people colonized by staph bacteria are also chronically exposed to superantigens, which shut down the LPS detoxification pathway," Schlievert explains. "That creates a synergy between the 'uncleared' LPS and the superantigen. All these two molecules do is cause inflammation and cytokine production. So in essence, their presence together creates a perfect storm for inflammation."
The findings suggest that by promoting chronic inflammation through their effect on fat cells, staph superantigens may play a role in the development of diabetes. In addition, the chronic inflammation caused by the superantigens may also hinder wound healing in diabetic foot ulcers. The ulcers, which affect 15 to 25 percent of people with diabetes, are notoriously difficult to heal and can often lead to amputation.
Why immortalize fat cells?
The UI team created immortalized fat cells for their research because primary fat cells (taken directly from fat tissue) are not very useful for lab experiments. Once the primary cells are grown in a dish, they quickly stop dividing and can't be used for repeated experiments. In contrast, the immortalized fat cells allow experiments to be repeated multiple times on identical cells ensuring consistent, reproducible results.
Klingelhutz and his team immortalized immature precursor fat cells by adding in two genes from HPV (the virus that causes cervical cancer) along with a gene for part of an enzyme that controls the length of cells' telomeres -- the pieces of DNA that protect chromosome tips from deterioration. These immortal precursor cells could then be "grown up" in petri dishes and differentiated into normal fat cells.
"The immortal fat cells are a great experimental tool that will allow us to investigate the mechanisms of the inflammation and allow us to test ways to potentially inhibit the response," says Klingelhutz. "That would be a goal in the future."
###
In addition to Schlievert and Klingelhutz, the research team included UI graduate student and study's lead author Bao Vu, and UI research assistant Francoise Gourronc; and University of Minnesota professor David Bernlohr, Ph.D.
The study was funded by a UI Department of Microbiology Development Grant and a research grant from the National Institutes of Health (Grant# AI074283).
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Bacteria and fat: A 'perfect storm' for inflammation, may promote diabetes
PUBLIC RELEASE DATE:
30-Oct-2013
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]
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Contact: Jennifer Brown jennifer-l-brown@uiowa.edu 319-356-7124 University of Iowa Health Care
Bacterial toxins activate fat cells producing chronic inflammation, which in turn boosts risk of developing diabetes
Making fat cells immortal might seem like a bad idea to most people, but for a team of University of Iowa scientists it was the ideal way to study how the interaction between bacteria and fat cells might contribute to diabetes.
The connection between fat, bacteria, and diabetes is inflammation, which is the body's normal reaction to infection or injury. Inflammation is beneficial in small, controlled doses but can be extremely harmful when it persists and becomes chronic.
"The idea is that when fat cells (adipocytes) interact with environmental agents -- in this case, bacterial toxins -- they then trigger a chronic inflammatory process," says Patrick Schlievert, Ph.D., UI professor and head of microbiology and co-senior author of a new study published Oct. 30 in the journal PLOS ONE. "We know that chronic inflammation leads to insulin resistance, which can then lead to diabetes. So people are very interested in the underlying causes of chronic inflammation."
The UI researchers used immortalized fat cells to show that bacterial toxins stimulate fat cells to release molecules called cytokines, which promote inflammation. By immortalizing fat cells the UI team created a stockpile of continuously dividing, identical cells that are necessary for repeat experiments to validate results, explains Al Klingelhutz, Ph.D., UI microbiologist and co-senior author of the study.
Previous studies have shown that a toxin called lipopolysaccharide (LPS) produced by E. coli bacteria that reside in the human gut, triggers fat cells to produce pro-inflammatory cytokines, and this interaction has been proposed to contribute to the development of diabetes.
The UI team focused on a different bacterium, Staphylococcus aureus (staph), which appears to be important in the context of diabetes for two reasons. First, as people become obese and then progress into diabetes they become very heavily colonized with staph bacteria. Secondly, staph is the most common microbe isolated from diabetic foot ulcers, one of the most common and health-threatening complications of diabetes.
All staph bacteria make toxins called superantigens -- molecules that disrupt the immune system. Schlievert's research has previously shown that superantigens cause the deadly effects of various staph infections, such as toxic shock syndrome, sepsis, and endocarditis.
The new UI study shows that superantigens from staph bacteria trigger fat cells to produce pro-inflammatory molecules. Moreover, the study found that superantigens synergized with LPS from E. coli to magnify fat cells' cytokine responses, amplifying the inflammation, which could potentially boost the likelihood of developing diabetes.
"The E. coli that resides in our gut produces LPS and every day a small amount of this toxin gets into our circulation, but it is generally cleared from the circulation by the liver. However, people colonized by staph bacteria are also chronically exposed to superantigens, which shut down the LPS detoxification pathway," Schlievert explains. "That creates a synergy between the 'uncleared' LPS and the superantigen. All these two molecules do is cause inflammation and cytokine production. So in essence, their presence together creates a perfect storm for inflammation."
The findings suggest that by promoting chronic inflammation through their effect on fat cells, staph superantigens may play a role in the development of diabetes. In addition, the chronic inflammation caused by the superantigens may also hinder wound healing in diabetic foot ulcers. The ulcers, which affect 15 to 25 percent of people with diabetes, are notoriously difficult to heal and can often lead to amputation.
Why immortalize fat cells?
The UI team created immortalized fat cells for their research because primary fat cells (taken directly from fat tissue) are not very useful for lab experiments. Once the primary cells are grown in a dish, they quickly stop dividing and can't be used for repeated experiments. In contrast, the immortalized fat cells allow experiments to be repeated multiple times on identical cells ensuring consistent, reproducible results.
Klingelhutz and his team immortalized immature precursor fat cells by adding in two genes from HPV (the virus that causes cervical cancer) along with a gene for part of an enzyme that controls the length of cells' telomeres -- the pieces of DNA that protect chromosome tips from deterioration. These immortal precursor cells could then be "grown up" in petri dishes and differentiated into normal fat cells.
"The immortal fat cells are a great experimental tool that will allow us to investigate the mechanisms of the inflammation and allow us to test ways to potentially inhibit the response," says Klingelhutz. "That would be a goal in the future."
###
In addition to Schlievert and Klingelhutz, the research team included UI graduate student and study's lead author Bao Vu, and UI research assistant Francoise Gourronc; and University of Minnesota professor David Bernlohr, Ph.D.
The study was funded by a UI Department of Microbiology Development Grant and a research grant from the National Institutes of Health (Grant# AI074283).
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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.
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