Ken Cuccinelli visits with a supporter during his campaign stop at the Courthouse Village at Spotsylvania Courthouse on Saturday Nov. 2, 2013, to campaign for the Governor's race in Virginia. (AP Photo/The Free Lance-Star, Suzanne Carr Rossi)
Ken Cuccinelli visits with a supporter during his campaign stop at the Courthouse Village at Spotsylvania Courthouse on Saturday Nov. 2, 2013, to campaign for the Governor's race in Virginia. (AP Photo/The Free Lance-Star, Suzanne Carr Rossi)
Virginia gubernatorial candidate Terry McAuliffe, center, speaks to his supporters and encourages them to make the final push by knocking on door-to-door to get more votes on Saturday, Nov. 2, 2013, in Norfolk, Va. (AP Photo/The Virginian-Pilot, The' N. Pham) MAGS OUT
ARLINGTON, Va. (AP) — President Barack Obama is telling Virginians to choose progress by voting for Democrat Terry McAuliffe in Tuesday's election for governor.
Obama spoke at a rally for McAuliffe in Arlington, just outside the nation's capital, in the final days of a bitter campaign for governor.
Obama painted Republican Ken Cuccinelli as beholden to an extreme tea party ideology that, according to the president, shut down the government and hurt Virginians.
Obama said McAuliffe knows how to push though obstacles and cares deeply about equality. The president urged McAuliffe's backers not to get complacent at the end of the race.
Cuccinelli is telling his supporters that Obama's visit highlights McAuliffe's support for Obama's unpopular health care law.
Second place finisher Tsegaye Kebede, left, of Ethiopia, and third-placed Lusapho April, right, of South Africa, flank men's winner Geoffrey Mutai of Kenya after finishing the New York City Marathon, Sunday, Nov. 3, 2013, in New York. (AP Photo/Kathy Willens)
Second place finisher Tsegaye Kebede, left, of Ethiopia, and third-placed Lusapho April, right, of South Africa, flank men's winner Geoffrey Mutai of Kenya after finishing the New York City Marathon, Sunday, Nov. 3, 2013, in New York. (AP Photo/Kathy Willens)
Women's winner Priscah Jeptoo of Kenya, center, second place finisher Buzunesh Deba of Ethiopia, left, and third place finisher Jelena Prokopcuka of Latvia pose after the New York City Marathon, Sunday, Nov. 3, 2013, in New York. (AP Photo/Kathy Willens)
Winners in the wheelchair division Tatyana McFadden of the United States, left, and Marcel Hug of Switzerland pose for a picture at the finish line of the 2013 New York City Marathon in New York, Sunday, Nov. 3, 2013. (AP Photo/Seth Wenig)
Geoffrey Mutai of Kenya holds his trophy after winning the men's division of the New York City Marathon, Sunday, Nov. 3, 2013, in New York. (AP Photo/Kathy Willens)
Geoffrey Mutai of Kenya runs along Fifth Avenue during the New York City Marathon Sunday, Nov. 3, 2013. In a double victory for Kenya, Mutai successfully defended his title and Priscah Jeptoo rallied to win the women's race. (AP Photo/Craig Ruttle)
NEW YORK (AP) — The New York City Marathon returned after a one-year absence with big crowds, heightened security and a familiar champion.
Geoffrey Mutai successfully defended his title Sunday, while fellow Kenyan Priscah Jeptoo came from behind to win the women's race. Bronx resident Buzunesh Deba finished runner-up for the second straight time in her hometown event.
Fans again packed the 26.2-mile course, undaunted by the events of the past year. The 2012 NYC Marathon was canceled because of the devastation of Superstorm Sandy, but not before many New Yorkers were enraged by initial plans to hold the race.
After the bombings at April's Boston Marathon, bomb-sniffing dogs roamed the course, and barricades limited access points to Central Park. A record 50,740 runners started the race through the five boroughs.
Mutai pulled away around Mile 22 and beat Ethiopia's Tsegaye Kebede by 52 seconds. On a windy morning, Mutai's time of 2 hours, 8 minutes, 24 seconds was well off his course record of 2:05:06 set in nearly perfect conditions two years ago. He's the first man to repeat in New York since Kenya's John Kagwe in 1997-98.
Kebede, the London Marathon champ, clinched the $500,000 bonus for the World Marathon Majors title. South Africa's Lusapho April was third.
Jeptoo trailed Deba by nearly 3½ minutes at the halfway point. But she started making her move as the race entered Manhattan and passed the Ethiopian with just over 2 miles to go.
Jeptoo, the 2012 Olympic silver medalist and 2013 London Marathon Champ, won in 2:25:07 to clinch the $500,000 World Marathon Majors bonus.
The women's race played out almost identically to the last NYC Marathon two years ago. But this time, Deba was the pursued, not the pursuer.
In 2011, Mary Keitany pulled away to a big early lead, and Deba and countrywomen Firehiwot Dado chased her down. Dado, who won that day, was 14th Sunday as the defending champ.
This time, Deba and training partner Tigist Tufa separated themselves right from the start. Deba wound up finishing 48 seconds behind Jeptoo, while Tufa fell back to eighth.
Jelena Prokopcuka of Latvia, the 2005-06 New York champ, placed third at age 37.
Security was tight from the moment the runners arrived on Staten Island. They were corralled into long bag-check lines, and officers and volunteers repeatedly reminded them to keep cellphones out.
"Security is 100 percent tougher than what I've seen at other races," said Chris Patterson of Rochester, N.Y., who was signed up for New York last year and ran Boston in April.
Elizabeth Hutchinson of Seattle recalled the joy at the starting line in Boston this year. People were handing out sunscreen, Band-Aids and energy gels with a smile.
On Staten Island, she said, "the machine guns are very visible."
"The atmosphere is so different," she said, "It kind of makes me sad."
Charles Breslin, who lost his home in the storm and was volunteering at the marathon, welcomed the race's return.
"I don't know how the rest of Staten Island feels about, but it can only be a good thing," he said. "You have to get back to normalcy."
As the professional women approached Central Park, only a sprinkling of onlookers stood at the police barricades. Ginny Smith, a Manhattan resident who comes to watch each year, said she felt "very frustrated."
Three hours after she first arrived at the park, she was finally allowed to walk in. At Columbus Circle, near the 26th and last mile of the route, police kept her waiting for two hours.
"It was difficult, it was horrible — for something that's basically for the people," she said. "It's unbelievable; you would think there was a war in the city."
Ashley O'Brien of Brooklyn was ready with a bullhorn to cheer members of her running group, the Hudson Dusters. She got teary-eyed remembering the events of the past year.
"It's a nice time to all come back together," she said. "You still remember why it was canceled last year and you remember Boston. So it's a little bittersweet."
___
Meghan Barr, Michael Casey and Verena Dobnik contributed to this report.
You might say the week is never really done in consumer technology news. Your workweek, however, hopefully draws to a close at some point. This is the Weekly Roundup on Engadget, a quick peek back at the top headlines for the past seven days -- all handpicked by the editors here at the site. Click ...
Chris Kirkpatrick married his girlfriend Karly Skladany with the his former 'N Sync bandmates as groomsmen, and Lea Michele said Kate Hudson helped her get through Cory Monteith's death: See Us Weekly's top 5 stories from the Nov. 2 weekend in the roundup!
Chris Kirkpatrick is hitched! The former 'N Sync boy bander has tied the knot with his girlfriend Karly Skladany, Us Weekly can confirm. The couple said "I do" in Orlando, Fla., at Loews Hotel on Saturday, Nov. 2.
Lea Michele continues to reflect on the death of her boyfriend Cory Monteith, and is now revealing an A-list friend who significantly helped following the tragedy -- Kate Hudson. In a new interview with Elle for its December issue, the 27-year-old actress is revealing how the Glee guest star was one of the first phone calls she made after hearing of the Canadian actor's untimely death.
Like father, like son! CaCee Cobb once again showed off an adorable photo of her son Rocco, who just so happens to look identical to his famous dad Donald Faison!
It seems the fairytale has ended! Former Once Upon a Time costars Jennifer Morrison and Sebastian Stan have officially split, multiple sources tell Us Weekly.
Sonny Bono is still a touchy subject for Cher. During a Facebook Q&A with her fans on Thursday, Oct. 31, the legendary singer answered questions for well over an hour about her professional life, her favorites movies and even about Halloween. But the most shocking answer of all just so happened to be about her late ex-husband.
WASHINGTON (AP) — The White House and the leaders of the intelligence committee in Congress are rejecting National Security Agency-contractor Edward Snowden's plea for clemency.
"Mr. Snowden violated U.S. law," White House adviser Dan Pfeiffer said Sunday about the former systems-analyst-turned-fugitive who has temporary asylum in Russia.
"He should return to the U.S. and face justice," Pfeiffer said, adding when pressed that no offers for clemency were being discussed.
Snowden made the plea in a letter given to a German politician and released Friday. In his one-page typed letter, he asks for clemency for charges over allegedly leaking classified information about the NSA to the news media. "''Speaking the truth is not a crime," Snowden wrote.
Snowden's revelations, including allegations that the U.S. has eavesdropped on allies including German Chancellor Angela Merkel, have led to calls by allies to cease such spying, and moves by Congress to overhaul U.S. surveillance laws and curb the agency's powers.
But head of the Senate Intelligence Committee said if Snowden had been a true whistle-blower, he could have reported it to her committee privately.
"That didn't happen, and now he's done this enormous disservice to our country," said Sen. Dianne Feinstein, D-Calif. "I think the answer is no clemency."
The chairman of the House Intelligence Committee, Rep. Mike Rogers, called clemency for Snowden a "terrible idea."
"He needs to come back and own up," said Rogers, R-Mich. "If he believes there's vulnerabilities in the systems he'd like to disclose, you don't do it by committing a crime that actually puts soldiers' lives at risk in places like Afghanistan."
Rogers contended that Snowden's revelations had caused three terrorist organizations to change how they communicate.
Both lawmakers addressed word that President Barack Obama did not realize Merkel's personal phone was being tapped.
Rogers implied that he didn't believe the president, or European leaders who claimed they were shocked by Snowden's allegations.
"I think there's going to be some best actor awards coming out of the White House this year and best supporting actor awards coming out of the European Union," he said "Some notion that ... some people just didn't have an understanding about how we collect information to protect the United States to me is wrong."
Feinstein said she didn't know what the president knew, but said she intended to conduct a review of all intelligence programs to see if they were going too far.
"Where allies are close, tapping private phones of theirs ... has much more political liability than probably intelligence viability," she said.
Feinstein and Rogers have taken grief for defending the NSA. Feinstein's committee produced a bill last week that she says increases congressional oversight and limits some NSA powers under the Foreign Intelligence Surveillance Act. Privacy advocates say the measure codifies the agency's rights to scoop up millions of American's telephone records.
Former NSA and CIA director Mike Hayden said it was possible Obama did not know about the alleged Merkel phone tapping.
But he said it was "impossible" that Obama's top staffers were unaware. "The fact that they didn't rush in to tell the president this was going on points out what I think is a fundamental fact: This wasn't exceptional. This is what we were expected to do."
Hayden's defense of the president comes days after he reportedly criticized the White House's handling of NSA revelations, when a former Democratic political operative tweeted snatches of Hayden's phone conversation, overheard on an Amtrak train.
Pfeiffer appeared on ABC's "This Week," while Rogers, Feinstein and Hayden were interviewed on CBS' "Face the Nation."
___
Follow Dozier at http://twitter.com/kimberlydozier
Penn researchers identify molecular link between gut microbes and intestinal health
PUBLIC RELEASE DATE:
3-Nov-2013
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Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA - It's well established that humans maintain a symbiotic relationship with the trillions of beneficial microbes that colonize their bodies. These organisms, collectively called the microbiota, help digest food, maintain the immune system, fend off pathogens, and more. There exists a long and growing list of diseases associated with changes in the composition or diversity of these bacterial populations, including cancer, diabetes, obesity, asthma, and even autism.
Inflammatory bowel disease (IBD) is one of the best-studied diseases associated with alterations in the composition of beneficial bacterial populations. However, the nature of that relationship, and how it is maintained, has yet to be clarified.
Now, researchers at the Perelman School of Medicine at the University of Pennsylvania have identified a molecule that appears to play a starring role in this process.
David Artis PhD, associate professor of Microbiology, and colleagues report in Nature that the enzyme HDAC3 is a key mediator in maintaining proper intestinal integrity and function in the presence of friendly bacteria. What's more, HDAC3 and the genetic pathways it controls appears critical to maintaining a healthy balance between intestinal microbes and their host.
"HDAC3 in intestinal epithelial cells regulates the relationship between commensal bacteria and mammalian intestine physiology," says first author Theresa Alenghat VMD PhD, instructor in the Department of Microbiology.
That humans rely on their microbial cohabitants is hardly news. Much normal human physiology is attributable to our relationship to our microbiota.
The question that Alenghat and Artis and their colleagues wanted to answer is, "What are the molecular mechanisms that control this relationship, and how is it that this relationship goes wrong and can contribute to metabolic and inflammatory diseases?"
The team focused their efforts on HDAC3, which belongs to a family of enzymes that can be responsive to environmental signals. And HDAC3 itself, an enzyme that modifies DNA and turns down gene expression, had previously been identified to have various inflammatory and metabolic roles.
Alenghat and her colleagues looked at HDAC3 expression in normal and diseased intestine from both humans and mice, finding that the enzyme is normally expressed throughout the intestinal epithelium, but that expression is reduced in tissues from subjects with inflammatory bowel disease.
The team then developed a mouse model that would mimic that observation. They created transgenic mice that lacked HDAC3 specifically in the intestinal epithelium and found that these animals exhibited altered gene expression in their intestinal epithelial cells.
The mice also showed signs of altered intestinal health. They lacked certain cells, called Paneth cells, that produce antimicrobial peptides. The mouse intestines seemed to be more porous than normal, and they showed signs of chronic intestinal inflammation, exhibiting some of the symptoms observed in patients with IBD.
When the team examined the diversity of the microbial population colonizing the mutant animal intestines, they found they were different from normal animals, with some species being overrepresented in HDAC3-deficient mice. "There's a fundamental change in the relationship between commensal bacteria and their mammalian hosts following deletion of HDAC3 in the intestine," Artis explains.
But, if the mutant animals were grown in the absence of bacteria, their intestinal symptoms largely disappeared, as did many of the observed differences in gene expression. In other words, HDAC3 was influencing the bacterial population, and the bacteria in turn were influencing the cells' behavior.
The implication, Artis says, "is that intestinal expression of HDAC3 is an essential component of how mammals regulate the relationship between commensal bacteria and normal, healthy intestinal function."
These findings, says Alenghat, suggest a role for HDAC3 in human disease, but the exact nature of that link is still being worked out. Whether dysregulation of the enzyme, or the genetic programs it oversees, actually contributes to human IBD is a question the team is currently investigating.
"Obviously more has to be done, but it is clear that this is a pathway that is of significant interest as we continue to define how mammals have co-evolved with beneficial microbes," says Artis.
###
Other Penn-based authors are Lisa C. Osborne, Steven A. Saenz, Dmytro Kobuley, Carly G. K. Ziegler, Shannon E. Mullican, Inchan Choi, Stephanie Grunberg, Rohini Sinha, Meghan Wynosky-Dolfi, Annelise Snyder, Paul R. Giacomin, Karen L. Joyce, Tram B. Hoang, Meenakshi Bewtra, Igor E. Brodsky, Gregory F. Sonnenberg, Frederic D. Bushman, Kyoung-Jae Won, and Mitchell A. Lazar.
The research was supported by the National Institute of Allergy and Infectious Disease (AI061570, AI095608, AI087990, AI074878, AI095466, AI106697, AI102942, AI097333), the Crohns and Colitis Foundation of America, the Burroughs Wellcome Fund, and the Cancer Research Institute.
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; Chester County Hospital; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Chestnut Hill Hospital and Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.
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Penn researchers identify molecular link between gut microbes and intestinal health
PUBLIC RELEASE DATE:
3-Nov-2013
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]
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Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA - It's well established that humans maintain a symbiotic relationship with the trillions of beneficial microbes that colonize their bodies. These organisms, collectively called the microbiota, help digest food, maintain the immune system, fend off pathogens, and more. There exists a long and growing list of diseases associated with changes in the composition or diversity of these bacterial populations, including cancer, diabetes, obesity, asthma, and even autism.
Inflammatory bowel disease (IBD) is one of the best-studied diseases associated with alterations in the composition of beneficial bacterial populations. However, the nature of that relationship, and how it is maintained, has yet to be clarified.
Now, researchers at the Perelman School of Medicine at the University of Pennsylvania have identified a molecule that appears to play a starring role in this process.
David Artis PhD, associate professor of Microbiology, and colleagues report in Nature that the enzyme HDAC3 is a key mediator in maintaining proper intestinal integrity and function in the presence of friendly bacteria. What's more, HDAC3 and the genetic pathways it controls appears critical to maintaining a healthy balance between intestinal microbes and their host.
"HDAC3 in intestinal epithelial cells regulates the relationship between commensal bacteria and mammalian intestine physiology," says first author Theresa Alenghat VMD PhD, instructor in the Department of Microbiology.
That humans rely on their microbial cohabitants is hardly news. Much normal human physiology is attributable to our relationship to our microbiota.
The question that Alenghat and Artis and their colleagues wanted to answer is, "What are the molecular mechanisms that control this relationship, and how is it that this relationship goes wrong and can contribute to metabolic and inflammatory diseases?"
The team focused their efforts on HDAC3, which belongs to a family of enzymes that can be responsive to environmental signals. And HDAC3 itself, an enzyme that modifies DNA and turns down gene expression, had previously been identified to have various inflammatory and metabolic roles.
Alenghat and her colleagues looked at HDAC3 expression in normal and diseased intestine from both humans and mice, finding that the enzyme is normally expressed throughout the intestinal epithelium, but that expression is reduced in tissues from subjects with inflammatory bowel disease.
The team then developed a mouse model that would mimic that observation. They created transgenic mice that lacked HDAC3 specifically in the intestinal epithelium and found that these animals exhibited altered gene expression in their intestinal epithelial cells.
The mice also showed signs of altered intestinal health. They lacked certain cells, called Paneth cells, that produce antimicrobial peptides. The mouse intestines seemed to be more porous than normal, and they showed signs of chronic intestinal inflammation, exhibiting some of the symptoms observed in patients with IBD.
When the team examined the diversity of the microbial population colonizing the mutant animal intestines, they found they were different from normal animals, with some species being overrepresented in HDAC3-deficient mice. "There's a fundamental change in the relationship between commensal bacteria and their mammalian hosts following deletion of HDAC3 in the intestine," Artis explains.
But, if the mutant animals were grown in the absence of bacteria, their intestinal symptoms largely disappeared, as did many of the observed differences in gene expression. In other words, HDAC3 was influencing the bacterial population, and the bacteria in turn were influencing the cells' behavior.
The implication, Artis says, "is that intestinal expression of HDAC3 is an essential component of how mammals regulate the relationship between commensal bacteria and normal, healthy intestinal function."
These findings, says Alenghat, suggest a role for HDAC3 in human disease, but the exact nature of that link is still being worked out. Whether dysregulation of the enzyme, or the genetic programs it oversees, actually contributes to human IBD is a question the team is currently investigating.
"Obviously more has to be done, but it is clear that this is a pathway that is of significant interest as we continue to define how mammals have co-evolved with beneficial microbes," says Artis.
###
Other Penn-based authors are Lisa C. Osborne, Steven A. Saenz, Dmytro Kobuley, Carly G. K. Ziegler, Shannon E. Mullican, Inchan Choi, Stephanie Grunberg, Rohini Sinha, Meghan Wynosky-Dolfi, Annelise Snyder, Paul R. Giacomin, Karen L. Joyce, Tram B. Hoang, Meenakshi Bewtra, Igor E. Brodsky, Gregory F. Sonnenberg, Frederic D. Bushman, Kyoung-Jae Won, and Mitchell A. Lazar.
The research was supported by the National Institute of Allergy and Infectious Disease (AI061570, AI095608, AI087990, AI074878, AI095466, AI106697, AI102942, AI097333), the Crohns and Colitis Foundation of America, the Burroughs Wellcome Fund, and the Cancer Research Institute.
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; Chester County Hospital; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Chestnut Hill Hospital and Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.
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Share
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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.
ISLAMABAD (AP) — The Pakistani Taliban leader killed in a recent U.S. drone strike was behind hotel bombings, assaults on political rallies, beheadings of policemen and suicide attacks on soldiers. But his death elicited little joy in the country where he wreaked most of his havoc and instead stirred widespread anger and suspicion.
At the time of Friday's strike targeting Hakimullah Mehsud, the Pakistani government was engaged in efforts to negotiate a peace deal with militants. Frustrated at years of military campaigns that have failed to end the bloodshed, many Pakistanis had high hopes for this latest peace effort and blame the U.S. for fouling it up.
Mehsud "should have been given the chance to negotiate, and now the consequences have to be borne by Pakistan, not the U.S.," said Syed Ahmed, a small business owner in the southern port city of Karachi.
Also contributing to the anger are fears of a bloody backlash, plus a web of complex conspiracy theories, including the idea that militants such as Mehsud are American or Indian pawns intent on weakening Pakistan.
For years, Pakistan has been fighting militants in the tribal areas that border neighboring Afghanistan, with thousands of civilians and security forces dying in bombings and shootings at the hands of militants.
Mehsud, who had a reputation as an especially ruthless warrior, was the leader of the Pakistani Taliban, or the Tehreek-e-Taliban Pakistan, as it calls itself. The TTP is an umbrella group encompassing militant organizations across the tribal areas. It has called for the overthrow of the Pakistani government, the implementation of hard-line Islamic law and an end to cooperation with the Americans in Afghanistan.
In many ways, people across Pakistan are echoing what they are hearing from politicians and top government officials. During a news conference Saturday, Interior Minister Chaudhry Nisar Ali Khan lashed out repeatedly at the U.S., which he said was trying to scuttle peace talks.
Imran Khan, the former cricket star who now leads a key opposition party, threatened to close NATO supply lines in retaliation for the drone attack.
The U.S. and Pakistan are wary allies in the war against militancy. Suspicion in Pakistan against America runs deep, fueled by a perception that Pakistan's militancy problems were foisted on it by the U.S. invasion of Afghanistan, which pushed militants into the tribal areas of northwestern Pakistan. Many Pakistanis question why Pakistan, a predominantly Muslim country, is at war with other Muslims and its own citizens.
Amir Sultan, a salesman at a garment business in Islamabad, said whenever Pakistan starts efforts to make peace with the Taliban, America sabotages it.
"It is an American agenda to destroy Pakistan," he said. "It is in America's interest to pit Muslim against Muslims."
There is also suspicion that the U.S. and neighboring India — a longtime enemy — are directly promoting and funding militants as a way to weaken the country. In the eastern city of Lahore, where that feeling is especially prevalent, lawyer Masood Wattoo blamed the U.S. and India for a recent string of bombings in the northwest, including a suicide attack on a church full of worshippers.
"It was the handiwork of America and India," he said.
In the southern port city of Karachi, Ahmad Jan suspected the U.S. and India were behind at least some of the militant groups operating across Pakistan.
"The TTP is a terrorist organization. Whoever challenges the writ of the state can't be our friends, but obviously they have the support of our enemies," he said.
Commanders from the group have been meeting to choose a successor to Mehsud, but no decision has been officially announced.
Mehsud's death has roused fears of a backlash of bombings and shootings. The militant group has already vowed to take revenge as it did after its deputy was killed in May in another drone strike.
In the northwestern city of Peshawar, which has taken the brunt of many attacks, anxiety about another wave of violence has been palpable.
"We fear more bloodshed and more destruction because these people can't attack America or shoot the drones down. Therefore only we, the poor Pakistanis, have to face the revenge, even though we had nothing to do with this," said Muhammad Tahir, a university student.
"Hakimullah's death," he added, "will make the situation more difficult for us."
___
Associated Press writers Asif Shahzad in Islamabad, Riaz Khan in Peshawar, Adil Jawad in Karachi and Zaheer Babar in Lahore contributed to this report.
You might say the week is never really done in consumer technology news. Your workweek, however, hopefully draws to a close at some point. This is the Weekly Roundup on Engadget, a quick peek back at the top headlines for the past seven days -- all handpicked by the editors here at the site. Click ...
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