LONDON (AP) — Tens of thousands of people have signed a petition calling for British CNN host Piers Morgan to be deported from the U.S. over his gun control views.
Morgan has taken an aggressive stand for tighter U.S. gun laws in the wake of the Newtown, Connecticut, school shooting. Last week, he called a gun advocate appearing on his “Piers Morgan Tonight” show an “unbelievably stupid man.”
Now, gun rights activists are fighting back. A petition created Dec. 21 on the White House e-petition website by a user in Texas accuses Morgan of engaging in a “hostile attack against the U.S. Constitution” by targeting the Second Amendment. It demands he be deported immediately for “exploiting his position as a national network television host to stage attacks against the rights of American citizens.”
The petition has already hit the 25,000 signature threshold to get a White House response. By Monday, it had 31,813 signatures.
Morgan seemed unfazed — and even amused — by the movement.
In a series of Twitter messages, he alternately urged his followers to sign the petition and in response to one article about the petition said “bring it on” as he appeared to track the petition’s progress.
“If I do get deported from America for wanting fewer gun murders, are there any other countries that will have me?” he wrote.
Entertainment News Headlines – Yahoo! News
Title Post: Thousands sign US petition to deport Piers Morgan Rating: 100%
based on 99998 ratings. 5 user reviews. Author: Fluser SeoLink Thanks for visiting the blog, If any criticism and suggestions please leave a comment
An internally displaced persons camp in Goma, in the Democratic Republic of Congo. In addition to recent violence in the country, a spreading measles epidemic is further endangering the lives of thousands of children there.
A large measles epidemic is spreading in Central Africa, endangering the lives of thousands of children, the medical charity Doctors Without Borders warned last week.
Since October, the charity has vaccinated more than 226,000 children in the eastern part of the Democratic Republic of Congo. The organization has also treated nearly 13,000 Congolese for the effects of the disease.
Measles is very contagious. In places where many children are malnourished and vitamin-deficient, it kills 1 percent to15 percent of those who don’t receive medical care, Doctors Without Borders estimated. (Even in the United States in the 1990s, although cases were rare, the fatality rate was 0.3 percent, according to the Centers for Disease Control and Prevention. In AIDS patients, the rate is 30 percent.)
The eastern Congo basin has serious shortages of medical workers and of drugs. While there is no treatment for measles itself, antibiotics can save those who develop pneumonia, meningitis or other secondary infections. Measles can also cause blindness by scarring the eyeball.
The outbreak is taking place despite enormous success against the disease worldwide. According to a study released earlier this year, deaths from measles have dropped by almost 75 percent since 2000.
Most of the lives saved were in Africa and India. Measles shots are often cited as one of the chief reasons that deaths of children under age 5 around the world have fallen steadily.
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
Subscribe to the Wired Science Space Photo of the Day
Follow Wired Science Space Photo of the Day on Twitter
LOS ANGELES (TheWrap.com) – “Survivor” maestro Mark Burnett‘s latest reality TV venture, “The Job,” will premiere February 8 at 8 p.m. on CBS, the network said Thursday.
The series, executive produced by Burnett and Michael Davies (of “Who Wants to Be a Millionaire” renown) and Jay Bienstock, will give contestants the chance to score jobs at prestigious American companies through several rounds of elimination challenges that will be observed by a panel of executives. As representatives from companies offer the competitors positions, the candidates will have to decide if they’ll take the jobs or continue on in pursuit of the big gig.
Former “The View” co-host Lisa Ling will host “The Job,” which is produced by Sony Pictures Television and Embassy Row.
CBS will announce the featured companies participating in the series early next year.
“The Job” will air in the time period of the network’s other work-related reality series, “Undercover Boss,” which returns April 19.
TV News Headlines – Yahoo! News
Title Post: CBS’ ”The Job” Gets Premiere Date Rating: 100%
based on 99998 ratings. 5 user reviews. Author: Fluser SeoLink Thanks for visiting the blog, If any criticism and suggestions please leave a comment
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.
LOS ANGELES (TheWrap.com) – “Django Unchained” – about a bounty hunter who partners with a freed slave to take down a plantation owner – is tracking extremely well with African Americans, the Weinstein Company said Thursday.
Quentin Tarantino wrote and directed the violent Western, which stars Christoph Waltz, Jamie Foxx and Leonardo DiCaprio, respectively. Opening on Christmas Day, it’s a front-runner in several Academy Award categories.
Despite the violence, it’s one of the few holiday offerings that would by nature of its subject matter appeal to an African-American audience.
“We think this film is going to resonate with everyone,” the Weinstein Company’s head of distribution Erik Lomis told TheWrap Thursday. And while he didn’t offer specific figures on the degree of interest among African-Americans the company’s pre-release research indicated, he did say that it is “looking very, very strong for us” with that demographic.
That’s good news for “Django,” which will open against Universal’s “Les Miserables” in a very crowded holiday box office. Analysts see a first weekend in the $ 25 million range for “Django,” and predict it ultimately will surpass $ 100 million domestically.
Last week “Django” received Golden Globes nominations for picture, director, screenplay and two supporting actors, Waltz and DiCaprio.
Movies News Headlines – Yahoo! News
Title Post: Slave-Revenge Film ‘Django Unchained’ Tracking Strongly With African-Americans Rating: 100%
based on 99998 ratings. 5 user reviews. Author: Fluser SeoLink Thanks for visiting the blog, If any criticism and suggestions please leave a comment
Subscribe to the Wired Science Space Photo of the Day
