More than twice as many men as women die in pedestrian-vehicle accidents. Now researchers have partly determined why.
Writing online last month in the journal Injury Prevention, investigators considered the contribution of three factors: distance walked, number of accidents and fatalities per collision.
Researchers using data from a variety of sources found that men and women walk similar distances and that men are involved in slightly more accidents per mile. Only 1 percent of the difference in death rates is attributable to distance walked, they found, and 20 percent to an increased number of accidents among men.
The rest — 79 percent of the variation — owes to the fact that when there is a collision, men die at roughly twice the rate of women. According to the National Highway Traffic Safety Administration, 4,280 pedestrians died in traffic accidents in 2010, and 2,946 — 69 percent — were men.
Why? No one knows, but the lead author, Dr. Motao Zhu, an assistant professor of epidemiology at West Virginia University, suggested two possibilities: “Maybe males are more likely to cross roads with speed limits higher than 50 miles per hour,” he said. “Also, males may be more likely to be impaired by alcohol and drugs. Most people know it’s not safe to drive drunk, but it’s not safe to walk drunk either.”
A Google e-reader is displayed at a bookstore. Sales of e-books for the devices have slowed this year.
Right about now, just as millions of e-readers and tablets are being slipped under Christmas trees, there was supposed to be a ferocious price war over e-books.
Last spring, the Justice Department sued five major publishers and Apple on e-book price-fixing charges. The case was a major victory for Amazon, and afterward there were widespread expectations — fueled by Amazon — that the price of e-books would plunge.
The most extreme outcome went like this: Digital versions of big books selling for $9.99 or less would give Amazon complete domination over the e-book market. As sales zoomed upward, even greater numbers of consumers would abandon physical books. The major publishers and traditional bookstores were contemplating a future that would pass them by.
But doomsday has not arrived, at least not yet. As four of the publishers have entered into settlements with regulators and revised the way they sell e-books, prices have selectively fallen but not as broadly or drastically as anticipated.
The $10 floor that publishers fought so hard to maintain for popular new novels is largely intact. Amazon, for instance, is selling Michael Connelly’s new mystery, “The Black Box,” for $12.74. New best sellers by David Baldacci and James Patterson cost just over $11.
One big reason for the lack of fireworks is that the triumph of e-books over their physical brethren is not happening quite as fast as forecast.
“The e-book market isn’t growing at the caffeinated level it was,” said Michael Norris, a Simba Information analyst who follows the publishing industry. “Even retailers like Amazon have to be wondering, how far can we go — or should we go — to make our prices lower than the other guys if it’s not helping us with market share?”
Adult e-book sales through August were up 34 percent from 2011, an impressive rate of growth if you forget that sales have doubled every year for the last four years. And there have been more recent signs of a market pausing for breath.
Macmillan, the only publisher that has not settled with the Justice Department, said last week as part of a statement from John Sargent, its chief executive, that “our e-book business has been softer of late, particularly for the last few weeks, even as the number of reading devices continues to grow.” His laconic conclusion: “Interesting.”
Mr. Norris said Simba, which regularly surveys e-book buyers, has been noticing what it calls “commitment to content” issues.
“A lot of these e-book consumers aren’t behaving like lab rats at a feeder bar,” the analyst said. “We have found that at any given time about a third of e-book users haven’t bought a single title in the last 12 months. I have a feeling it is the digital equivalent of the ‘overloaded night stand’ effect; someone isn’t going to buy any more books until they make a dent in reading the ones they have already acquired.”
Another, more counterintuitive possibility is that the 2011 demise of Borders, the second-biggest chain, dealt a surprising blow to the e-book industry. Readers could no longer see what they wanted to go home and order. “The print industry has been aiding and assisting the e-book industry since the beginning,” Mr. Norris said.
It is possible that Amazon, which controls about 60 percent of the e-book market, is merely holding back with price cuts for the right moment.
The next few weeks are when e-book sales traditionally take a big jump, as all those newly received devices are loaded up with content.
Amazon declined to comment beyond saying, “We have lowered prices for customers from the prices publishers set on a broad assortment of Kindle books.” Barnes & Noble declined to comment on its pricing strategy.
The question of the proper price for e-books has shadowed the industry ever since Amazon introduced the Kindle in late 2007 and created the first truly popular portable reading device. Amazon had a natural impulse to build a market and was an aggressive retailer in any case, so it took best sellers that cost $25 in independent bookstores and sold them for $9.99 as e-books. Consumers liked that. E-book adoption soared.
KABUL, Afghanistan -- Firefighters battled through the night to contain a raging fire that swept through a market in the Afghan capital.
No injuries were reported, but the blaze destroyed hundreds of stores and millions of dollars worth of merchandise, Afghan police and firefighters said at the scene.
Dealers at the neighboring currency exchange, the city’s largest, said they evacuated cash, computer equipment and records from their shops as the flames approached during the night. But in the morning, the market was jammed with people haggling over thick stacks of notes as smoke billowed overhead.
Col. Mohammed Qasem, general director of the Kabul fire department, said he suspected an electrical short was to blame for the fire.
Gas canisters used to heat the stores propelled the flames, along with the cloth and clothing sold by many of the vendors, Qasem said. “It made it very big in a short time.”
Firefighters from the Afghan defense department and NATO forces were sent to assist. But the city’s notorious traffic and the market’s narrow lanes made it difficult for responders to maneuver their vehicles, Qasem said.
Abdulrahman, who like many Afghans has only one name, squatted near a fire truck with his head in his hands as responders aimed a hose at the blackened ruins of a building still smoldering at noon Sunday, more than 12 hours after the fire broke out.
He said the building had contained three shops that he owned and a warehouse full of glassware, crockery and kitchen utensils.
“I lost everything,” he said.
Shirali Khan complained that police hadn't allowed him to remove the goods from his four clothing stores.
“They thought we were all robbers,” he said. “There’s only ashes left.”
ALSO:
Pope pardons former butler convicted of theft
Bombing kills local official, 7 other people in Pakistan
Tensions high as vote on proposed Egyptian constitution continues
Special correspondent Hashmat Baktash contributed to this report.
This Hubble telescope snapshot of MyCn18, a young planetary nebula, reveals that the object has an hourglass shape with an intricate pattern of "etchings" in its walls. A planetary nebula is the glowing relic of a dying, Sun-like star.
The results are of great interest because they shed new light on the poorly understood ejection of stellar matter that accompanies the slow death of Sun-like stars. According to one theory on the formation of planetary nebulae, the hourglass shape is produced by the expansion of a fast stellar wind within a slowly expanding cloud, which is denser near its equator than near its poles.
Image: Raghvendra Sahai and John Trauger (JPL), the WFPC2 science team, and NASA [high-resolution]
Caption: Hubble Heritage site
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(Reuters) – The big-budget “Hobbit” fantasy movie ruled movie box office charts for a second straight weekend, fending off Hollywood heavyweight Tom Cruise in new crime drama “Jack Reacher.”
“The Hobbit: An Unexpected Journey” hauled in nearly $ 37 million from theaters in the United States and Canada, according to studio estimates of Friday-through-Sunday ticket sales. The film is the first of three movies based on the classic J.R.R. Tolkien novel about a world of dwarfs, elves and dragons in the fictitious Middle Earth.
In second place, Cruise’s “Jack Reacher” about the investigation into a sniper shooting brought in just short of $ 17 million at U.S. and Canadian theaters. Distributor Paramount Pictures postponed a premiere of the film after the fatal school shooting in Newtown, Connecticut, sparked new scrutiny of violent movies.
Adult comedy “This is 40,” starring Paul Rudd and Leslie Mann as a middle-aged couple, brought in $ 12 million, finishing in third place.
“The Hobbit” was distributed by Time Warner Inc’s Warner Bros. studio. Paramount Pictures, a unit of Viacom Inc, released “Jack Reacher.” Comcast Corp’s Universal Pictures distributed “This is 40.”
(Reporting By Lisa Richwine and Andrea Burzynski)
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Title Post: “Hobbit” fever beats Tom Cruise at box office Rating: 100%
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Dr. Donald Bergstrom is a cancer specialist at Sanofi, one of three companies working on a drug to restore a tendency of damaged cells to self-destruct.
For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.
Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.
No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.
And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged.”
At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells. A large tumor was wrapped around a cord that connects the testicle to the abdomen. “I was shocked,” he said in an interview this summer.
Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi’s drug because the tumors nearly always have the exact genetic problem the drug was meant to attack — a fusion of two large proteins. If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.
“For us, this is a go/no-go situation,” said Laurent Debussche, a Sanofi scientist who leads the company’s research on the drug.
The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.
The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”
Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work.
Then, instead of going after mutated p53 genes, they went after half of cancers that used the alternative route to disable p53, blocking it by attaching it to a protein known as MDM2. When the two proteins stick together, the p53 protein no longer functions. Maybe, researchers thought, they could find a molecule to wedge itself between the two proteins and pry them apart.
The problem was that both proteins are huge and cling tightly to each other. Drug molecules are typically tiny. How could they find one that could separate these two bruisers, like a referee at a boxing match?
In 1996, researchers at Roche noticed a small pocket between the behemoths where a tiny molecule might slip in and pry them apart. It took six years, but Roche found such a molecule and named it Nutlin because the lab was in Nutley, N.J.
But Nutlins did not work as drugs because they were not absorbed into the body.
Roche, Merck and Sanofi persevered, testing thousands of molecules.
At Sanofi, the stubborn scientist leading the way, Dr. Debussche, maintained an obsession with p53 for two decades. Finally, in 2009, his team, together with Shaomeng Wang at the University of Michigan and a biotech company, Ascenta Therapeutics, found a promising compound.
The company tested the drug by pumping it each day into the stomachs of mice with sarcoma.
Dr. Donald Bergstrom is a cancer specialist at Sanofi, one of three companies working on a drug to restore a tendency of damaged cells to self-destruct.
For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.
Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.
No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.
And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged.”
At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells. A large tumor was wrapped around a cord that connects the testicle to the abdomen. “I was shocked,” he said in an interview this summer.
Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi’s drug because the tumors nearly always have the exact genetic problem the drug was meant to attack — a fusion of two large proteins. If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.
“For us, this is a go/no-go situation,” said Laurent Debussche, a Sanofi scientist who leads the company’s research on the drug.
The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.
The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”
Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work.
Then, instead of going after mutated p53 genes, they went after half of cancers that used the alternative route to disable p53, blocking it by attaching it to a protein known as MDM2. When the two proteins stick together, the p53 protein no longer functions. Maybe, researchers thought, they could find a molecule to wedge itself between the two proteins and pry them apart.
The problem was that both proteins are huge and cling tightly to each other. Drug molecules are typically tiny. How could they find one that could separate these two bruisers, like a referee at a boxing match?
In 1996, researchers at Roche noticed a small pocket between the behemoths where a tiny molecule might slip in and pry them apart. It took six years, but Roche found such a molecule and named it Nutlin because the lab was in Nutley, N.J.
But Nutlins did not work as drugs because they were not absorbed into the body.
Roche, Merck and Sanofi persevered, testing thousands of molecules.
At Sanofi, the stubborn scientist leading the way, Dr. Debussche, maintained an obsession with p53 for two decades. Finally, in 2009, his team, together with Shaomeng Wang at the University of Michigan and a biotech company, Ascenta Therapeutics, found a promising compound.
The company tested the drug by pumping it each day into the stomachs of mice with sarcoma.
Maybe you want to help others. Maybe you long to lend a hand. But you're not sure where and you're not sure how and you don't know who to call.
You could ask around. Or you could book a seat on the Do Good Bus.
You will pay $25. You will get a box lunch. You will put yourself in the hands of a stranger.
CITY BEAT: Life in the Southland
When the bus takes off, you will not know where you are going — only that when you get there, you will be put to work.
You find yourself on this weekday afternoon one of an eclectic group, gathered a little shyly on an East Hollywood curb.
There's a Yelp marketer, a grad student, an actor, a novelist, a Manhattan Beach mother with her son and daughter, who just got home from prep school and college.
You see a school bus pull up. You step on board. It feels nostalgic, like day camp or a field trip.
Rebecca Pontius welcomes you, wearing jeans and sneakers and a black fleece vest. She looks like the kind of person who would plunge her hands deep into dirt, who wouldn't be afraid of the worms, who could lead you boldly.
The bus takes off, and Pontius stands toward the front, sure-footed. She founded the Do Good Bus, she tells you, to 1) build awareness, 2) build community, 3) encourage continued engagement.
Oh, she says, and to 3a) have fun. Hence the element of mystery, the faux holly branches that decorate some of the rows of seats, the white felt reindeer antlers she's wearing on her head.
She smiles a wide, toothy smile that makes you automatically reciprocate.
So you go along when she asks you to play get-to-know-you games. Even though you're embarrassed, you don't object when she assigns you one of the 12 days of Christmas to sing and act out when it's your turn.
Everyone's singing and laughing as the bus fits-and-starts down the freeway.
Maids-a-milking, geese-a-laying, bus-a-exiting somewhere in South Los Angeles.
It stops outside a boxy blue building — the Challengers Boys and Girls Club — where, finally, Pontius tells you you'll be helping children in foster care build the bicycles that will be their Christmas gifts.
She did it last year, she says. It was great. And she's brought along some powder that turns into fake snow, which the kids will like.
You step inside a large gym, where nothing proceeds quite as expected.
It's the holiday season, so way too many volunteers have shown up. The singer Ne-Yo is coming to lead a toy giveaway. There's a whole roomful of presents the children can choose from, including pre-assembled bikes — which means no bikes will need to be built.
You stand and you sit and you wait. Then the kids come. You try to help where you can — making sure they get in the right lines, handing out raffle tickets.
You see their joy at getting gifts, which is nice. You're in a place you might not ordinarily be, which is interesting. And as the children head out, you offer them snow. You put the powder in their cupped hands. You add water. The white stuff grows and begins to look real. It's even cold.
It makes them go wide-eyed. It makes them laugh. And you feel such moments of simple happiness are something.
It's chilly as you wait to get back on the bus. You get in a group hug with your fellow bus riders, who seem like old friends.
On the trip back in the dark, Pontius plays Christmas music. She serves you eggnog in Mason jars.
And she says she's sorry your help wasn't more needed today.
She promises the January ride will be more hands-on.
Come or don't, she tells you. But whatever you do, find a way to do something.
nita.lelyveld@latimes.com
Follow City Beat @latimescitybeat on Twitter or at Los Angeles Times City Beat on Facebook.
Athey Moravetz is doing some tasty work with her 3-D printers.
The video game designer has worked on PlayStation games like Resistance Retribution and Uncharted Golden Abyss. She's also a self-described "jack-of-all-trades," skilled with 3-D modeling tools like Maya, and knows how to design compelling characters with them.
After having two children she decided to work from home, and in addition to keeping active in the computer graphics industry, she also created a wildly successful Etsy shop, where she sells 3-D printed cookie cutters based on nerd culture favorites Pokemon, Dr. Who and Super Mario Brothers.
NEW YORK (TheWrap.com) – Glen Mazzara, who led AMC‘s “The Walking Dead” to ratings highs after the exit of Frank Darabont, is leaving the show.
The announcement came with the unsurprising news of a fourth-season pickup for the series. It continues AMC’s rocky record with its showrunners, but the network said the decision was mutual.
While AMC has clashed with showrunners before over money, a person familiar with the situation told TheWrap that this time the issue is “100 percent not about money or contracts.”
Rather, it is about a difference of opinion over where the show should go in the fourth season and beyond. It involves AMC, Mazzara and the show’s writers and producers, who include Robert Kirkman, creator of the comics that provide the basis of the series.
Kirkman might be the fans’ choice to take over as showrunner, given that most of its characters were born on his pages. But he also has a busy career writing comics and novels.
In a statement, Kirkman said he believes Mazzara and AMC came to the decision “in the best interest of the future of the show.”
In an interview with TheWrap in October, Mazzara said he would love to remain with the show until the end, “if AMC and the fans would have me.”
“I would love to be the guy shutting the lights off,” he said at the time.
It didn’t work out that way, even though Mazzara has made “The Walking Dead” this season’s top-rated drama — even beating network shows. It also has a legitimate shot at ending the season as TV’s top scripted show overall.
“Both parties acknowledge that there is a difference of opinion about where the show should go moving forward, and conclude that it is best to part ways,” AMC said in a statement.
AMC also said the decision is “amicable” and that Mazzara will remain showrunner for the remainder of the third season, which resumes airing in February. The episodes have already been filmed, and Mazzara will oversee postproduction.
He is also looking for his next project.
“My time as showrunner on ‘The Walking Dead’ has been an amazing experience, but after I finish season 3, it’s time to move on,” said Mazzara. “I have told the stories I wanted to tell and connected with our fans on a level that I never imagined. It doesn’t get much better than that. Thank you to everyone who has been a part of this journey.”
Mazzara took over the show after Darabont parted ways with it after its first season. Darabont was just one of several showrunners to have issues with AMC.
Jason Horwitch left “Rubicon” during its lone season. The third season of “Hell on Wheels” was briefly put on hold last month when showrunner John Shiban left.
“Mad Men” creator Matthew Weiner nearly walked from the show during a contract dispute last year. And “Breaking Bad” briefly looked into leaving AMC before creator Vince Gilligan’s contract was renewed.
Kirkman’s full statement included his thanks to Mazzara and the show’s fans.
“I am in full support of both AMC and Glen Mazzara in the decision they have come to and believe the parties came to this decision in the best interest of the future of the show,” Kirkman said. “I thank Glen for his hard work and appreciate his many contributions to ‘The Walking Dead’ and look forward to working with him as we complete post production on Season 3. I am also excited to begin work on another spectacular season of this show that I know means so much to so many people. This show has always been the result of a wide range of extremely talented men and women working tirelessly to produce their best work collectively. I believe the future is bright for ‘The Walking Dead.’ Thank you to the fans for your continued support.”
Executive producer Gale Anne Hurd also expressed her thanks.
“I am appreciative and grateful to Glen for his hard work on ‘The Walking Dead,’” she wrote. “I am supportive of AMC and Glen’s decision and know that the series is in great hands with one of the most talented and dedicated casts and crews in the business. I look forward to the show’s continued success.”
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Title Post: ‘Walking Dead’ Showrunner Glen Mazzara Leaving Rating: 100%
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