Square Feet: Moving Ahead to Update the Pier 17 Mall





Nearly two months after Hurricane Sandy devastated the South Street Seaport on the East River in Lower Manhattan, Dumpsters still line its cobblestone streets and nearly all of the stores west of the Franklin D. Roosevelt Drive remain closed.




But the storm surge largely spared Pier 17, the seaport’s long-maligned shopping mall to the east. The operators of the mall, the Howard Hughes Corporation of Dallas, say it escaped damage because it is three feet above the pier, which in turn sits well above the water. And so, the company, which holds the ground lease to the city-owned pier, is moving forward with its plans to transform its dated festival marketplace into an open and airy three-story retail and entertainment center.


The local community board voted last month to support the proposal, despite reservations about the signage and some other design features. Though the plan is still working its way through the city’s land use process, the developer’s agreement with the city Economic Development Corporation requires that construction begin on July 1. David R. Weinreb, the chief executive of Howard Hughes, said in a telephone interview that the company would meet that deadline.


After being blocked off by metal gates and closed until this month because of concerns about the stability of the pier, the mall is now open, though some stores are still closed. Inspectors from Halcrow, an international engineering company hired by Howard Hughes, recently determined that the structure was sound. The pier is south of the Brooklyn Bridge, just beyond Fulton Street.


“The pier got a solid rating,” Christopher J. Curry, a senior executive vice president at Howard Hughes, said in a recent interview at the company’s offices on Fulton Street. City officials confirmed that no problems were found at the pier.


In addition to Pier 17, the company controls 170,000 square feet of space further inland at the seaport, including stores like Brookstone, Ann Taylor and Coach, which suffered extensive storm damage.


“We’re working diligently to remediate the shops,” Mr. Weinreb said. Asked whether the closed stores would remain at the seaport, he said, “We’re in discussions with our tenants about what is in their best interests. Many of those tenants enjoy very good sales and fully expect and want to be back open.”


From the mid-1980s to the early ’90s, the seaport was a big draw, especially for young people, who crowded its bars and restaurants. But then it fell out of favor with New Yorkers, though it has remained a must-see for visitors taking in other downtown sites, retail specialists said.


The operators of the mall at Pier 17 have long wanted to give it more cachet with city residents. Shortly before the economic crisis, a previous owner, General Growth Properties, a mall developer, introduced a much more ambitious plan for the seaport, including a 42-story tower, which was unpopular with residents.


The Howard Hughes Corporation, which is primarily known for its vast master-planned communities like Summerlin, near Las Vegas, acquired the shopping center in 2010, when it was spun off from General Growth as the mall company was emerging from bankruptcy.


Completed in 1985, the Pier 17 shopping center was developed by the Rouse Company, the creator of marketplaces in Boston and Baltimore. (General Growth bought Rouse in 2004.)


But by the time the mall opened, the marketplace concept may already have been outmoded. The existing mall “has basically been a disappointment to everyone over its life,” Hardy Adasko, a senior vice president for planning at the city Economic Development Corporation, testified last week at a City Planning Commission hearing. His agency sees the redevelopment of the pier as a way of advancing its long-term investment in the waterfront, he said.


In contrast to the marketplace design, which was intended to shield visitors from the grittiness of the port, the new structure will capitalize on its waterfront location, offering abundant views of the bridge. Outdoor space on either side of the pier also will be enhanced.


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Dueling Santa trackers are off and running













Google's Santa Tracker


A screen grab from Google's Santa Tracker.
(Google / December 24, 2012)





































































All year long Santa keeps an eye on you. Now it's time to turn the tables.


One day a year, you are invited to keep an eye on Santa as he whips around the world in his sleigh, delivering a dizzying number of presents to children all over the world.


If you'd like to see where Santa is at the moment, you've got choices. Google and NORAD, which used to team up for your Santa tracking pleasure, have gone their separate ways this year and created two distinct tracking options.





Google's Santa Tracker is the slicker of the two. It takes you to Santa's Dashboard, where you can see Santa's current location, his next location, the number of miles traveled, and the number of presents delivered. Santa is also adding Twitter like status updates. The most recent one as of this writing: "Rudolph's nose just turned red." 


PHOTOS: Google Doodles of 2012


You can also click on the map and see where Santa has been, as noted by little present icons on the map. Click on the icon and you'll see how many presents Santa has delivered in each city. When Santa is on the move, you'll see him flying on the map in a sleigh. When he's stopped to deliver presents, you'll see him shoving presents down a chimney.


Over at the official NORAD Tracks Santa website you'll also find a running tally of how many presents Santa has delivered as well as what city he just left and what city he's currently headed toward. NORAD also offers Santa Cams that show animations of Santa flying around the world. 


Both Santa tracking services offer loads of extras. If you visit Santa's Village on Google's tracker you can send a message from  Santa to a friend or family member. And NORAD has more than 1,200 volunteers staffing a Santa hotline to answer all your Santa questions.  (877-HI-NORAD).


In the spirit of the season you might try them both out, but hurry up. The trackers shut down a few hours before Christmas morning. 


Happy tracking!


ALSO:


Rumored iPad 5 to be thinner -- and land in March



Battle of the Santa trackers: Google takes on NORAD


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deborah.netburn@latimes.com

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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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Thousands sign 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.


Entertainment News Headlines – Yahoo! News





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Measles: Measles Epidemic Is Spreading in Central Africa


Jehad Nga for The New York Times


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.


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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











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CBS’ ”The Job” Gets Premiere Date






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





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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.


Read More..

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.


Read More..