Army Goes Goth With 'Super-Black' Materials

Get ready to break out the eyeliner and the candelabras, because the Army is going goth.

In its latest round of solicitations for small businesses, the Army is asking for proposals for super-black material. That is, material so black that it absorbs 99 percent of all light. But it isn’t really black paint, exactly. The plan is to use either an “antireflective coating or surface treatment process for metals” to absorb stray light “in the ultraviolet, visible, infrared, and far-infrared regions.” This, the Army hopes, will boost the quality of high-resolution cameras, while also cooling down sensitive electronics. Or to put it another way: The Army needs the color black to reflect its icy-cold heart.

Another curious thing is that the program is being run out of the Army’s Program Executive Office Ammunition at the Picatinny Arsenal, a main center for the Pentagon’s experiments in all sorts of weapons: from rifles and tank cannons to directed-energy weapons. But the purpose of the solicitation isn’t much more specific than described. “Simply put, it’s too early yet to speculate on where the technology(s) will go,” Frank Misurelli, an Army spokesman at Picatinny said in a statement provided to Danger Room. ”Possibly in a few months, after an contract has been awarded, more information may become available.”

But for whatever the Army wants to fade to black, it seems that regular black isn’t good enough. This is because most black paint will absorb only around 90-95 percent of light, with the other 5-10 percent reflected back outwards. For a high-resolution camera, that stray light can bounce back into the lens and interfere with the quality of an image. It’s even a problem for NASA’s ultra-deep-space sensors. In the extreme coldness of space, black paint turns a silver-y color, which increases heat and can interfere with infrared-detecting instruments.

But wait, doesn’t black get really hot when hit with light, like wearing black clothes during the summer? The answer is: sorta. Black is really good at absorbing heat, but is also really good at radiating heat away. This is why cooling fins, radiators and engines for cars and trucks are often painted black. In 2011, NASA developed a carbon-nanotube coating that absorbed between 98-99.5 percent of light, depending on the wavelength. Nor do the coating’s thin layers of nanotubes change color in extreme cold. They absorb more light, and help radiate heat away from instruments, keeping them cold.

The Army could go another route. A second option uncovered by Britain’s National Physical Laboratory involves immersing an object in a solution of nickel and sodium for several hours, which blackens the color, and then taking it out and dunking it in nitric acid for a few seconds. According to New Scientist, this creates an alloy pock-marked with tiny microscopic craters that prevent light from bouncing away.

Finally, the Army also hopes to expand the materials to “optical glass surfaces” — camera lenses, in other words — while testing to see whether “it will be able to survive in a military environment.” The material should also come in “multiple surface colors” and be able to “selectively exhibit earth color instead of broadband absorption.” And another hope is to use the materials to absorb water to cool down equipment. See, it’s tough out there being goth, but it doesn’t mean you can’t do it in comfort.

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Pro-gun rights US petition to deport Piers Morgan

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.

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N.Y.U. and Others Offer Shorter Courses Through Medical School

Training to become a doctor takes so long that just the time invested has become, to many, emblematic of the gravity and prestige of the profession.

But now one of the nation’s premier medical schools, New York University, and a few others around the United States are challenging that equation by offering a small percentage of students the chance to finish early, in three years instead of the traditional four.

Administrators at N.Y.U. say they can make the change without compromising quality, by eliminating redundancies in their science curriculum, getting students into clinical training more quickly and adding some extra class time in the summer.

Not only, they say, will those doctors be able to hang out their shingles to practice earlier, but they will save a quarter of the cost of medical school — $49,560 a year in tuition and fees at N.Y.U., and even more when room, board, books, supplies and other expenses are added in.

“We’re confident that our three-year students are going to get the same depth and core knowledge, that we’re not going to turn it into a trade school,” said Dr. Steven Abramson, vice dean for education, faculty and academic affairs at N.Y.U. School of Medicine.

At this point, the effort involves a small number of students at three medical schools: about 16 incoming students at N.Y.U., or about 10 percent of next year’s entering class; 9 at Texas Tech Health Science Center School of Medicine; and even fewer, for now, at Mercer University School of Medicine’s campus in Savannah, Ga. A similar trial at Louisiana State University has been delayed because of budget constraints.

But Dr. Steven Berk, the dean at Texas Tech, said that 10 or 15 other schools across the country had expressed interest in what his university was doing, and the deans of all three schools say that if the approach works, they will extend the option to larger numbers of students.

“You’re going to see this kind of three-year pathway become very prominent across the country,” Dr. Abramson predicted.

The deans say that getting students out the door more quickly will accomplish several goals. By speeding up production of physicians, they say, it could eventually dampen a looming doctor shortage, although the number of doctors would not increase unless the schools enrolled more students in the future.

The three-year program would also curtail student debt, which now averages $150,000 by graduation, and by doing so, persuade more students to go into shortage areas like pediatrics and internal medicine, rather than more lucrative specialties like dermatology.

The idea was supported by Dr. Ezekiel J. Emanuel, a former health adviser to President Obama, and a colleague, Victor R. Fuchs. In an editorial in the Journal of the American Medical Association in March, they said there was “substantial waste” in the nation’s medical education. “Years of training have been added without evidence that they enhance clinical skills or the quality of care,” they wrote. They suggested that the 14 years of college, medical school, residency and fellowship that it now takes to train a subspecialty physician could be reduced by 30 percent, to 10 years.

That opinion, however, is not universally held. Other experts say that a three-year medical program would deprive students of the time they need to delve deeply into their subjects, to consolidate their learning and to reach the level of maturity they need to begin practicing, while adding even more pressure to a stressful academic environment.

“The downside is that you are really tired,” said Dr. Dan Hunt, co-secretary of the Liaison Committee on Medical Education, the accrediting agency for medical schools in the United States and Canada. But because accreditation standards do not dictate the fine points of curriculum, the committee has approved N.Y.U.’s proposal, which exceeds by five weeks its requirement that schools provide at least 130 weeks of medical education.

The medical school is going ahead with its three-year program despite the damage from Hurricane Sandy, which forced NYU Langone Medical Center to evacuate more than 300 patients at the height of the storm and temporarily shut down three of its four main teaching hospitals.

Dr. Abramson of N.Y.U. said that postgraduate training, which typically includes three years in a hospital residency, and often fellowships after that, made it unnecessary to try to cram everything into the medical school years. Students in the three-year program will have to take eight weeks of class before entering medical school, and stay in the top half of their class academically. Those who do not meet the standards will revert to the four-year program.

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Raging fire guts Kabul market

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.

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Wired Science Space Photo of the Day: Hourglass Nebula

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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Disney Sets August 9 Release for ‘Cars’ Spin-off ‘Planes’

NEW YORK (TheWrap.com) – Disney will release “Planes,” a spin-off of Pixar‘s “Cars” franchise, August 9, 2013, in the United States. DisneyToon Studios is behind the film with Pixar/Disney Animation chief creative officer John Lasseter producing.

The film follows a fleet of planes, in particular Dusty. “Two and a Half Men” star Jon Cryer was to voice Dusty, but he has dropped out and the studio is now casting the part.

Disney initially intended to release “Planes” direct to video, but it will now send it into theaters domestically and overseas.

“Planes” will compete against a pair of films that summer weekend, both of which should have more adult followings. The big-ticket item will be Sony’s “Elysium,” Neill Blomkamp‘s follow-up to “District 9.” Also opening that weekend is “We’re the Millers,” a New Line drug-smuggling comedy starring Jason Sudeikis and Jennifer Aniston.

Next summer’s biggest animated movies should all be sequels save “Epic,” Fox’s story of a teenage girl caught in a forested battle. Beyonce Knowles‘ leads the voice cast. The other big openers are Despicable Me 2,” “Monsters University” and “Smurfs 2.”

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Genetic Gamble : Drugs Aim to Make Several Types of Cancer Self-Destruct

C.J. Gunther for The New York Times

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.

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Genetic Gamble : Drugs Aim to Make Several Types of Cancer Self-Destruct

C.J. Gunther for The New York Times

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.

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This bus' next stop: doing good

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.

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.

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Maker Mom Builds Cookie-Cutter Empire With 3-D Printers

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.

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