Sunday, December 2, 2012

Redray 4K Cinema Player is ready to pre-order: $1,450 for high-res, high framerate home viewing

Redray 4K Cinema Player is ready to preorder, $1,450 for highres, framerate at home

We got a peek at Red's Redray 4K Cinema Player and Projector back in April at NAB, but now you can bring the player portion of it to your own home very soon. You'll need to bring your own 4K Ultra HD display but for $1,450 you can pre-order a unit capable of native 4,096 × 2,160 or 3,840 x 2,160 video playback (in .RED file format) and upscaling. It connects to 4K displays via one HDMI 1.4 port or 4 HDMI 1.3 ports, with an additional HDMI jack needed to push 7.1 audio. It's even ready for the new high framerate 3D video that we'll see debut at theaters next week with The Hobbit. There's no mention of the Red Laser Projector yet, so you'll have to BYO 4K display, which right now would probably mean something by LG or Sony.

To get content home Red is also launching its nationwide fiber-based Odemax.com over-the-top distribution network. Red co-owner Jarred Land calls it the "only comprehensive distribution solution for 4K," with built-in DRM, sales and analytics tools. He goes on to say that the Redray player will begin shipping at the end of December, with volume shipping promised in Q1 2013. A new RRencoder plugin for the Redcine-X viewer will launch in mid-December for converting external footage to the .RED format, and finally Odemax is scheduled to come online in January in time for the Sundance film festival. Check for more details after the break, plus a few more pics and a press release with all the specs.

Continue reading Redray 4K Cinema Player is ready to pre-order: $1,450 for high-res, high framerate home viewing

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Source: Red Store, Red, Odemax.com


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New Jersey bridge collapse derails freight train; chemical leaks

PAULSBORO, New Jersey (Reuters) - A railroad bridge collapsed on Friday over a creek in southern New Jersey, causing a Conrail freight train to derail and spill hazardous chemicals into the air and water, authorities said.

Seven of the 82 cars derailed, and a tanker car that fell into Mantua Creek leaked vinyl chloride into the waterway, which feeds into the Delaware River near Philadelphia, said Deborah Hersman, chairwoman of the National Transportation Safety Board.

More than 12,000 gallons (45,425 liters) of the highly toxic and flammable industrial chemical leaked from a gash in the car's side, local officials said.

Twenty-two people were examined at a nearby hospital as a precaution and were doing fine, said Larry Ragonese, a spokesman for the New Jersey Department of Environmental Protection.

Ragonese said the health danger and environmental impact were minimal.

"Initially there was a release of gas into the air that affected some nearby residents and people working right in that area," he said.

Air quality monitors in the area did not register any problem, said Lawrence Hajna, also with the DEP. "All the levels are coming in within our safety range."

Exposure to vinyl chloride can cause a burning sensation in the eyes or respiratory discomfort, the DEP said.

The accident took place at about 7 a.m. EST (1200 GMT) in Paulsboro. Area residents initially were told to stay indoors, with windows shut, and local schools were closed.

The leak was contained and no longer posed a threat, and authorities were using booms to trap the chemical in the water, Ragonese said.

At the scene, one of the freight cars was nearly vertical, nose-down and partly submerged in the creek. Other cars lay jumbled on the collapsed bridge and the embankment.

"It's part of living in Paulsboro, with refineries and trains. We accept it," said resident John Diamond, 53, who was taking photographs.

The area is thick with chemical plants, and two refineries, PBF Energy's Paulsboro and NuStar's Asphalt, are nearby.

TANK "BREACHED"

The head of the Gloucester County, New Jersey, Office of Emergency Management, Tom Butts, said the leaking tanker car in the water had a tear in it, and the tank was "breached."

About half of its contents leaked out, he said.

The tank was carrying some 25,000 gallons (94,635 liters) of the chemical, said John Burzichelli, a state assemblyman and former mayor of Paulsboro.

"When you live between two oil refineries, you have a sense that these things can happen," he said.

Locals fish and go crabbing and jet-ski in the creek in the warm months, Diamond said.

Jeff Tittel, director of the New Jersey Sierra Club, said improved safety procedures, inspection, enforcement and oversight are needed to help prevent such accidents.

"This time it was ... vinyl chloride. What if it was chlorine?" he said, referring to a chemical that is extremely dangerous if inhaled and has the potential to explode.

Also, he said there is no mechanism to alert communities to what kinds of chemicals trains are carrying through the states.

He questioned the integrity of the bridge, which is owned and operated by Conrail, since Superstorm Sandy slammed into New Jersey on October 29, causing surges in area waterways.

The cause of the accident was undetermined. The National Transportation Safety Board is investigating, and members of the agency arrived at the scene mid-afternoon.

NTSB's chairwoman said four out of the five train cars that were on the bridge when it collapsed landed in the creek, and two other cars rolled onto the embankment.

"We have requested a great deal of information from the railroad" as part of the investigation, Hersman said.

Conrail said the train consisted of two locomotives, 82 rail cars and one caboose.

"We very much regret the impact on the local community," said Conrail spokesman John Enright, who was at the scene. "We will be working very closely with federal investigators to determine the cause."

The bridge underwent extensive repairs after getting damaged in a 2009 derailment of a coal freight train, Burzichelli said.

"That bridge is very old. It's not a good day for Conrail," Burzichelli said, adding that the bridge carries three major freight trains daily.

New Jersey State Senate President Steve Sweeney, also on the scene, said a nearby homeowner reported hearing a "loud bang" from the bridge about two days ago. Burzichelli said Conrail had come out to examine it in response.

Conrail is jointly owned by rail operators CSX Corp and Norfolk Southern Corp.

(Additional reporting by Edith Honan and Ellen Wulfhorst; Writing by Ellen Wulfhorst; Editing by Vicki Allen and Xavier Briand)

Source: http://news.yahoo.com/nj-rail-bridge-collapse-causes-derailment-chemical-leak-142136551--finance.html

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Saturday, December 1, 2012

Homes evacuated again near NJ derailment

PAULSBORO, N.J. (AP) ? Homes have been evacuated anew near the spot in southern New Jersey where a train derailed, releasing a hazardous chemical into the air and sickening dozens of people.

National Transportation Safety Board chairman Deborah Hersman said Friday night that there were evacuations in Paulsboro because of increased levels of chemicals.

Around 7 a.m., seven train cars derailed on a bridge. One tanker car was sliced open, releasing vinyl chloride. Hours later, officials gave the all-clear for residents near the site to return but warned that there could be more complications.

A 12-block radius was evacuated on Friday evening. U.S. Coast Guard Lt. Drew Madjeska tells The Philadelphia Inquirer that residents might not be allowed back for several days.

Source: http://news.yahoo.com/homes-evacuated-again-near-nj-derailment-040638391.html

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Yemen says it has arrested an Al-Qaida leader

(AP) ? Yemen's Interior Ministry says police have arrested an al-Qaida leader who is one of the country's most wanted fugitives.

The ministry, in a statement late Friday, said Suleiman Hassan Mohammed Murshed Awad was arrested in Zinjibar, the capital of southern Abyan province, once an al-Qaida hotbed. It did not say when he was arrested.

Awad, also known as Abu Osama al-Abi, was "one of the most dangerous criminal elements in al-Qaida who is involved in killing security men and joining others in terrorist attacks on foreign targets in Sanaa."

Washington, which considers Yemen's al-Qaida branch the group's most dangerous offshoot, helped Yemeni troops with airpower and advisers last summer. The offensive drove al-Qaida militants out of southern cities, including Zinjibar.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/cae69a7523db45408eeb2b3a98c0c9c5/Article_2012-12-01-Yemen/id-a458a9c7861d4522946a42538cecb4c4

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Chromatin remodeling: Activating ACL1 with a little help from 'friends'

ScienceDaily (Nov. 29, 2012) ? Chromatin remodeling -- the packaging and unpackaging of genomic DNA and its associated proteins -- regulates a host of fundamental cellular processes including gene transcription, DNA repair, programmed cell death as well as cell fate. In their latest study, scientists at the Stowers Institute for Medical Research are continuing to unravel the finicky details of how these architectural alterations are controlled.

Through a series of biochemical experiments, Stowers Investigators Ron Conaway, Ph.D., and Joan Conaway, Ph.D., and their team discovered that chromatin remodeling enzyme and suspected oncogene ALC1 (short for Amplified in Liver Cancer 1) is activated through an unusual mechanism: Its shape shifts in the presence of its activators. Their finding identifies a new instrument in cells' molecular repertoire of chromatin-remodeling tools and a potential cancer therapeutic target.

One of the main tasks of chromatin remodeling enzymes, Ron Conaway explains, is "to make DNA accessible so events like repair and gene transcription can occur." Postdoctoral research associate and first author Aaron Gottschalk, Ph.D., previously figured out that ALC1 required protein partners to activate its remodeling function. Publishing in an upcoming issue of the Journal of Biological Chemistry, he dissects the mechanism by which this occurs.

ALC1 and its ilk have a common protein domain, SNF2, that uses the energy of ATP hydrolysis to move nucleosomes -- the basic repeating units of chromatin -- around, in a process called nucleosome sliding.

"I was intrigued because ALC1 has a unique macrodomain not found on any other SNF2 family member," Gottschalk says. His interest was further piqued when he found that while most ATP-dependent chromatin remodelers function as large multi-protein complexes, ALC1 appeared to work by itself. At the same time, where most of its group-happy family members readily demonstrated nucleosome sliding activity in vitro, ALC1 was not only a lone ranger but also "completely dead on its own."

Gottschalk deduced that ALC1 may function independently, but it needs a boost from a couple of sidekicks: PARP1, an enzyme that responds to several kinds of DNA damage; and NAD+, the substrate by which PARP1 transfers chains of poly (ADP-ribose) onto itself and other target proteins, in a process called PARylation.

Only when PARP1 and NAD+ are on the scene does ALC1 spring into action, altering the accessibility of DNA by shifting nucleosomes around. Gottschalk's earlier findings were published in the Proceedings of the National Academy of Sciences in June 2009.

"We then extended this research," Conaway says, "and the upshot of our recent JBC paper is that ALC1 is likely activated through a series of physical interactions. ALC1's unique macrodomain can bind PAR, and protein-protein interactions also occur between ALC1 and PARP1." Gottschalk and coauthor Rushi Trivedi, a graduate student in the Biochemistry & Molecular Biology department at KU Medical Center, developed a novel footprinting assay that enabled this observation. Rather than merely activating ALC1 and moving on, the researchers found that the trio of PARP1, NAD+ and ALC1 hangs out in a stable complex.

"So PARylated PARP1 and NAD+ are allosteric effectors -- by binding to ALC1, they alter its state from dormant to active," Conaway says. "It's an interesting mechanism that's different from how most other chromatin remodelers work. It may also help explain other evidence that PARP1 has the ability to rearrange nucleosomes and reorganize chromatin; this could be one way by which PARP1 exerts its influence."

Apart from its role in modifying chromatin structure, not much is currently known about ALC1. It's regarded as a possible oncogene, being found in excess in hepatocellular carcinoma cells and because overexpression of ALC1 in mice induces spontaneous tumors.

PARP1, on the other hand, has attracted plenty of interest as a potential anticancer drug target, due to its importance in maintaining genomic integrity. For example, in breast cancer cells lacking BRCA1 or BRCA2 function, blocking PARP could effectively remove the cells' last line of defense against DNA-damaging chemotherapy agents. To date, no PARP inhibitor has made it past phase III clinical trials, but pharmaceutical companies continue to chip away at the challenges around optimizing this form of targeted cancer therapy.

"A better understanding of the in-depth biochemistry we're uncovering on ALC1 and PARP1 may, in the long term, ultimately lead to new or more refined therapeutic strategies," Gottschalk says.

Meanwhile, having observed that ALC1 comes to life upon interacting with friends, Gottschalk now wants to understand precisely how this activation happens. With a knockout ALC1 mouse model handy, plans are afoot to extend his studies to an in vivo characterization of a chromatin remodeler that boasts an illustrious family pedigree, yet stands apart in the crowd.

Funding for this study came from a National Institute of General Medical Sciences grant (GM41628), and a grant to the Stowers Institute from the Helen Nelson Medical Research Fund at the Greater Kansas City Community Foundation.

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The above story is reprinted from materials provided by Stowers Institute for Medical Research.

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Journal Reference:

  1. A. J. Gottschalk, R. D. Trivedi, J. W. Conaway, R. C. Conaway. Activation of the SNF2 Family ATPase ALC1 by Poly(ADP-ribose) in a Stable Nucleosome-PARP1-ALC1 Intermediate. Journal of Biological Chemistry, 2012; DOI: 10.1074/jbc.M112.401141

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.

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