শুক্রবার, ৩০ নভেম্বর, ২০১২

Empire State Building surprises NY with new lights

NEW YORK (AP) ? In the middle of the night, as most of New York slept, something big and bright lit up the Manhattan skyline for just seconds ? a tightly kept secret to all but a handful of people.

It was a tiny test for the huge public surprise four days later: the flipping of a switch at the Empire State Building to turn on its dancing new LED lights. They burst from the skyscraper while synchronized with R&B star Alicia Keys singing "Empire State of Mind" on nationwide radio.

The LED system has "16.7 million color possibilities, in digital combinations of ripples, sparkles, sweeps and strobes," says Phil O'Donnell, of Burlington, Mass.-based Philips Color Kinetics that's responsible for the system and worked with a resident lighting designer. "It's the sum of all possibilities ? a huge palette."

The old lights came in only 10 colors.

From Manhattan and the Bronx to Staten Island and even New Jersey, "there were hundreds of thousands of people on the streets looking up, filming and videoing, clustered on street corners," when the new lights came on, said Anthony Malkin, whose family controls the iconic Art Deco building.

In an interview with The Associated Press at his office, he glowed with pleasure describing Monday night's inaugural light show.

Keys also sang "Girl On Fire" from her new CD.

After all, the 102-story skyscraper "has always been a symbol of what's possible in New York, and all the dreams that can come true in this city that never sleeps," Keys, a New York native, said before her performance, which was ready on tracks while she watched from a Manhattan studio.

Malkin and his technical team wanted to test the new lighting system with as few people noticing as possible and chose early Thanksgiving morning.

Good luck, in the middle of Manhattan, with people walking around even at 2:30 a.m.

That seemed the best moment, after most bars close and before dawn.

"We decided to do it facing west, in very short bursts between 2:30 a.m. and 3 a.m., because we knew we didn't have a camera trained on us from there," Malkin said.

Apparently, the secret test worked. No images of the Empire State Building alight that night appeared anywhere, as far as Malkin knows.

To stage the show, he worked with Clear Channel radio, which has 239 million monthly listeners in the United States.

The lights are part of a larger effort to modernize the 81-year-old edifice that is undergoing a more than half a billion-dollar renovation that includes making it "green." The computerized LED system will cut energy consumption by more than half, while delivering light and vibrancy superior to the old floodlights, which have huge timpani drum-size lenses that had to be changed every so often, O'Donnell said.

They may still have nostalgic value to some who watched them light up New York City for every special occasion from Christmas to the Fourth of July.

They were part of "the grande dame of the New York skyline, now state-of-the-art, but still stately," says Malkin, adding that the light show was "a gift we gave to the world, these lights. We don't get paid for this."

On a sunny Wednesday afternoon, with a spectacular view of the new World Trade Center and New York Harbor, a vacant space under reconstruction on the building's 72nd floor was filled with the retired floodlights, sitting side by side in long lines, veterans of years of New York weather. What will be done with them is also a secret ? for now.

One old light will not be discarded in favor of a 21st century novelty: a red beacon ? "half the size of a Volkswagen Beetle," as Malkin puts it ? that serves as a warning signal for aircraft constantly flying over New York City.

Source: http://news.yahoo.com/empire-state-building-surprises-ny-lights-074333318--finance.html

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Verisign's pact with ICANN gets U.S. government nod but with pricing limits

(Reuters) - Verisign Inc said the U.S. Department of Commerce approved its agreement with ICANN to run the .com internet registry, but the company will not be able to raise prices as before, sending its stock down 13 percent before the bell.

The company's current pricing of $7.85 per domain name registration will continue for the six-year term ending November 30, 2018.

Previously, the company had the right to increase prices by up to 7 percent four times in the contract period.

The company can increase prices in extraordinary circumstances, including expenses related to security threats, with approval from the Commerce Department, Verisign said.

Verisign maintains the .com domain under a license from the Internet Corp for Assigned Names and Numbers (ICANN) and charges users and corporations every time they register or renew an existing .com domain name.

Verisign's agreement with ICANN expires on Friday.

The company has been maintaining the .com domain on behalf of ICANN for over 15 years, and its contract with ICANN is reviewed every six years.

Verisign holds separate licenses for .net, .gov, .edu and a number of other domain names.

Shares of the Reston, Virginia-based company were down at $34.17 in premarket trading. They closed at $39.34 on Thursday on the Nasdaq.

(Reporting by Supantha Mukherjee in Bangalore; Editing by Maju Samuel)

Source: http://news.yahoo.com/verisigns-pact-icann-gets-u-government-nod-pricing-142455345--sector.html

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Japan Couture 2012 Singapore Fashion Show

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Source: http://www.stylebrity.co.uk/catwalk/10545/japan-couture-2012-singapore-fashion-show.html/

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Dust Bunnies Make You Sick


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Video of the Week #71, November 29th, 2012:

From: Worse Than Bedbugs, It?s the Couch Itself by Kalliopi Monoyios at Guest Blog.

Source: Audio and production: Mollie Bloudoff-Indelicato, Video: Isha Soni, Artwork: Marissa Fessenden.

Dust bunnies are seriously dangerous. Those tiny globs of grime are much more than simple household nuisances. They can contain noxious flame retardant chemicals that leak out of living room furniture like couches. Once free of the upholstery, these toxins are especially harmful to children and pets, acting as carcinogens and endocrine disruptors.

Related:

Infographic: Fire Safety Buzzkill
The Environmental Fallout of Greener Buildings

Bora ZivkovicAbout the Author: Bora Zivkovic is the Blog Editor at Scientific American, chronobiologist, biology teacher, organizer of ScienceOnline conferences and editor of Open Laboratory anthologies of best science writing on the Web. Follow on Twitter @boraz.

The views expressed are those of the author and are not necessarily those of Scientific American.

Source: http://rss.sciam.com/click.phdo?i=40b6a9afb89ea20a23f67a7a0d9f1280

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Baby named 'Hashtag' draws Internet fame, ire, skepticism

Media outlets introduced the world to Hashtag Jameson, a baby girl reportedly named after Twitter's #.

By Pamela Cyran / November 28, 2012

Meet the trending infant Hashtag Jameson.

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The mother reportedly posted a photo of her sleeping baby girl on Facebook with the caption: ?Hashtag Jameson was born at 10 oclock last nite. She weys 8pounds and i luv her so much!!!!!?

On Twitter, people use hashtags (or the #?symbol) to mark keywords and trending topics. They range from the general ? people might add #obama to Twitter posts about the president ? to the quirky and esoteric ? such as?#broncobamma?from the finals weeks of the 2012 election.

This infant?s photo is now buzzing all over the web. However, it seems that no one can confirm her name. It?s unclear if ?Hashtag? is a legitimate name from a Twitter super fan, an Internet hoax, or, as the Huffington Post put?it, "a very unfortunate typo."

Whatever the case, the photo went viral in less than 24 hours after first appearing on the website Awkward Messages, which rounds up odd Web posts and photos.

As skepticism stewed online, many people took to Twitter to argue a?parallel?question: Is "Hashtag" an appropriate name for any baby? The conversation quickly adopted a hashtag of?its own,?#babyhashtag.

?That poor girl is going to get made fun of for years to come... I'd go by my middle name instead!? wrote Nicole Pipe, who goes by @TotallyTypeA on Twitter.?(The photo, which is acting as an unofficial birth announcement to the world, doesn't say if Hashtag has a middle name.)

?I can see it now.?#babyhashtag?a few years from now playing in a sand box with her friends 'Like,' 'PTAT,' 'Tweet,' 'Share,' and '@,' " wrote Twitter users @ParisMackey.

Funny you should say that, Paris. In May of 2011, an Israeli couple gave birth to "Like," named after the?iconic Facebook button.

"I'm not worried about other children teasing Like," said Like?s mother,?Vardit Adler, in an interview with Reuters. The couple's other daughters, "Dvash and Pie, don't seem to mind their special names and nobody teases them."

Another social-media baby was born in Egypt a few months earlier, ?Facebook.? The baby girl was named after the website that played a large role in Egypt?s January uprising in 2011.

Whether you think unique baby names are clever or ridiculous, research has shown baby names have long-lasting effects well into adulthood.

Source: http://rss.csmonitor.com/~r/feeds/csm/~3/CT7I3V2bAeM/Baby-named-Hashtag-draws-Internet-fame-ire-skepticism

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Something Is Wrong With My iPad: I Still Hate My Life

I hope you Apple Geniuses are up to snuff because I'm pretty sure my iPad's busted. No matter how much I use it to check email, surf the web, or tag photos on Facebook, I'm still gnawed at by a horrifying emptiness that no amount of fiddling with your magical gadget can fill. More »


Source: http://feeds.gawker.com/~r/gizmodo/full/~3/FFp0o0w4YMo/something-is-wrong-with-my-ipad-i-still-hate-my-life

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Immune system could play a central role in age-related macular degeneration

ScienceDaily (Nov. 27, 2012) ? Changes in how genes in the immune system function may result in age-related macular degeneration (AMD), the leading cause of visual impairment in older adults, based on preliminary research conducted by National Institutes of Health (NIH) investigators.

"Our findings are epigenetic in nature, meaning that the underlying DNA is normal but gene expression has been modified, likely by environmental factors, in an adverse way," said Dr. Robert Nussenblatt, chief of the National Eye Institute (NEI) Laboratory of Immunology. Environmental factors associated with AMD include smoking, diet, and aging. "This is the first epigenetic study revealing the molecular mechanisms for any eye disease."

The study identified decreased levels of DNA methylation, a chemical reaction that switches off genes, on the interleukin-17 receptor C gene (IL17RC). The lack of DNA methylation led to increased gene activity and, in turn, increased levels of IL17RC proteins in patients with AMD. IL17RC is a protein that promotes immune responses to infections, such as fungal attacks.

The study, conducted by research teams from the NEI and other NIH institutes, including the National Heart, Lung, and Blood Institute and the National Center for Complementary and Alternative Medicine; the University of Melbourne, Australia; and Oregon Health and Science University, appears in the Nov. 29 issue of Cell Reports.

"Our study also suggests IL17- and IL17RC-mediated immune responses can be crucial in causing AMD," added Dr. Lai Wei, also of NEI's Laboratory of Immunology and first author on the paper. "By measuring IL17RC gene activity in at-risk patients, we have also potentially identified an early method to detect AMD."

AMD damages the light-sensitive cells of the macula, the central part of the retina that allows us to see fine visual detail. As the disease progresses, patients encounter great difficulty reading, driving, or performing hobbies and tasks that require hand-eye coordination. Treatments exist to prevent severe vision loss in certain types of advanced AMD but none prevent or cure the disease. Currently, 2 million Americans have advanced AMD and another 7 million have intermediate stages.

Recent studies have identified several genes with alterations that increase the risk of developing the disease. In addition, environmental risk factors have also been suggested as possible causes of the disease. One explanation may be that environmental exposures influence DNA methylation, which regulates gene expression. Changes in this process may result in the production of too much or too little of a gene's protein, leading to cellular dysfunction and disease. Changes in DNA methylation have been implicated in cancer, lupus, multiple sclerosis, and many other diseases.

To test whether changes in DNA methylation might play a role in AMD, the investigators evaluated three pairs of twins -- one pair identical and two pairs fraternal -- where only one of the siblings had AMD. Identical twins have the same genetic makeup while fraternal twins share about half of their DNA. Because of their similar genetic backgrounds, identical and fraternal twins can be helpful in studying the differences between the effects of genetics and the environment. When compared with the unaffected twins, methylation patterns were altered in 231 genes of affected twins. This finding is consistent with the hypothesis that environmental exposures may epigenetically regulate expression of many genes and lead to AMD.

Among the 231 genes, the investigators found that DNA methylation was absent in a region of the IL17RC gene in twins with AMD. The lack of methylation in the IL17RC gene led to increased gene activity and, in turn, increased levels of its protein in circulating blood. The investigators further validated these findings by comparing seven siblings with and without AMD as well as 202 AMD patients and 96 control subjects without the disease. These studies also found increased IL17RC levels in circulating blood and, most importantly, in the retina of patients with AMD but not controls.

Based on these results, the authors propose that chronic increased levels of the IL17RC protein in the retina likely promote inflammation and recruitment of immune cells that damage the retina and lead to AMD.

"This study strongly implicates epigenetic DNA methylation as another crucial biological pathway for understanding the molecular basis of AMD," according to Nussenblatt.

The investigators next plan to evaluate what environmental factors may be responsible for the regulation of IL17RC and how the epigenetic regulation leading to the chronic inflammation in AMD patients can be reversed by novel therapies. They will also evaluate the role of epigenetics in other eye diseases.

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The above story is reprinted from materials provided by NIH/National Eye Institute.

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Journal Reference:

  1. Lai Wei, Baoying Liu, Jingsheng Tuo, Defen Shen, Ping Chen, Zhiyu Li, Xunxian Liu, Jia Ni, Pradeep Dagur, H.?Nida Sen, Shayma Jawad, Diamond Ling, Stanley Park, Sagarika Chakrabarty, Catherine Meyerle, Elvira Agron, Frederick?L. Ferris, Emily?Y. Chew, J.?Philip McCoy, Emily Blum, Peter?J. Francis, Michael?L. Klein, Robyn?H. Guymer, Paul?N. Baird, Chi-Chao Chan, Robert?B. Nussenblatt. Hypomethylation of the IL17RC Promoter Associates with Age-Related Macular Degeneration. Cell Reports, 2012; DOI: 10.1016/j.celrep.2012.10.013

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/oxj41stkvaI/121128093919.htm

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