Bloomberg has announced today that it will begin distributing live interbank pricing for the onshore renminbi market (CNY). The tick by tick data provided from the China Foreign Exchange Trade System will allow users to gain better control for pricing and hedging of China related business.
While not maybe not as exciting as the errant launching of Greek Drachma quotes on it terminal, the renminbi pricing will be much more useful as it fills an important gap for both on and offshore companies conducting global business with China. Demand for more Chinese currency related products has been strong in 2012 with more and more brokers providing NDFs and more recently deliverable futures this year. As such, as renminbi trading becomes more prevalent and foreign banks increase their involvement with the currency, we are seeing more an offshore market taking place.
Bloomberg First to Deliver China Interbank FX Rates Globally
New service provides investors with real-time insights into onshore renminbi market
November 28th, 2012 Hong Kong, London ? Bloomberg today announced the first global, real-time data service that provides investors access to live interbank pricing for China?s onshore renminbi (CNY) market. This service captures currency trading activity among banks and financial institutions in China, and is provided through the China Foreign Exchange Trade System (CFETS), the official interbank trading and foreign exchange (FX) division of China?s central bank.
?The addition of the CFETS data gives investors insights into real-time tick-by-tick movement, volumes and market participant information in China?s onshore interbank market,? said Tod Van Name, Bloomberg?s Global Head of FX, Economics and Commodities. ?Given the rapid internationalisation of the Chinese Yuan, this data is imperative to global markets as it provides our clients greater transparency for smarter and more timely trading, hedging and investment decisions.?
Global currency traders, corporate treasurers and institutional investors can now view executable quotes and trades on the interbank dollar-yuan spot, swap and forward markets. The CFETS data service also features the best renminbi spot prices from participating banks, historical trade sizes, and eight other renminbi currency pairs. Combined with Bloomberg?s FX suite, market participants can connect to global counterparties and liquidity, and access Bloomberg?s global FX trading community.
?The provision of real-time China interbank FX rates to international investors is yet another step in the right direction,? said Sam Phoen, head of global markets, ANZ bank (China). ?Onshore corporations and investors will benefit from real-time executable rates, while offshore players who are invested in China will have better visibility when hedging against movements of the renminbi.?
According to CFETS? publication ChinaMoney, with renminbi cross- border inflows and outflows intensifying in 2012, development of the offshore renminbi market will drive domestic financial market reform, and aid in a fair and transparent price discovery process for renminbi foreign exchange rates.
?BNP Paribas is one of the first international banks to access Bloomberg?s CFETS service,? said Julien Martin, Deputy Head of Fixed Income, BNP Paribas China. ?Offshore players can now access accurate interbank dollar-yuan rates that better reflect market conditions, providing investors with a critical edge in foreign exchange transactions amidst today?s volatile trading environment.?
This announcement follows Bloomberg?s leadership in the evolution of the offshore renminbi (CNH) market, which includes the development and adoption of the CNH code, provision of its price history and introduction of the offshore renminbi bond listing and index.
WASHINGTON (AP) ? One month before the deadline, negotiations between President Barack Obama and Republicans to save the economy from a plunge over the fiscal cliff are still in the throat-clearing stage. Serious bargaining is on hold while the two sides vie for political leverage.
Deal or no deal, nothing is likely to become clear until far closer to the year-end deadline, when the lure of getting away for the holidays will sharpen the focus of negotiators.
"There's a stalemate. Let's not kid ourselves," House Speaker John Boehner, R-Ohio, said Friday, punctuating the end of a week of political theater by divided government. "Right now we're almost nowhere."
He spoke as Obama all but called Republicans heartless louts from a Charles Dickens story. Their failure to pass an extension of middle class tax cuts would amount to a Christmas "lump of coal" for millions, Obama said in Hatfield, Pa. "That's a Scrooge Christmas," added the recently-re-elected president, who claims a voters' mandate to extend existing tax cuts for all but upper incomes.
Boehner, too, claimed a mandate after voters renewed the House Republican majority on Nov. 6. But the speaker's political hand was weakened ? witness his postelection announcement that the GOP would put revenues on the bargaining table. His control seems to have eroded further in the weeks since, as a smattering of the GOP rank and file let it be known they could support the president's tax plan under the right circumstances.
"Rate increase, if the package includes significant entitlement reform that gets you to $4 to $6 trillion (in deficit savings) over 10 years, I would vote for that," a retiring Rep. Steve LaTourette, R-Ohio, told reporters on Friday.
Rep. Charles Bass made similar comments. "If it gets us past the fiscal cliff and the president is willing to consider meaningful savings in entitlements, it's a legitimate solution," said the New Hampshire lawmaker, who was defeated for re-election this fall.
Yet the speaker also made a little-noticed move this week to shore up his bargaining position.
He issued a statement noting that Senate Democrats are threatening to weaken the Republicans' ability to block legislation in their chamber in the new Congress that convenes in January.
"Any bill that reaches a Republican-led House based on Senate Democrats' heavy-handed power play would be dead on arrival," he warned.
In the talks to date, Democrats have declined to identify a single spending cut they are willing to support, while Republicans avoid specifics on revenue increases they would swallow.
Once each side moves beyond opening gambits, Republicans will have to decide whether they are willing to raise income tax rates on upper incomes, as Obama wants, or hold fast to closing loopholes as a means of producing increased tax revenue.
For their part, Democrats will decide how much savings to pull from benefit programs like Medicare, Medicaid and possibly Social Security without cutting guaranteed benefits, a line they vowed not to cross in earlier budget negotiations.
Obama's opening proposal, delivered to Boehner and other Republicans by Treasury Secretary Tim Geithner on Thursday, calls for $1.6 trillion in higher taxes over a decade, hundreds of billions of dollars in new spending, a possible extension of the temporary Social Security payroll tax cut and enhancing the president's power to raise the national debt limit.
The new federal revenue would include $950 billion generated by raising taxes on families with incomes over $250,000 and by closing certain tax loopholes by the end of this year, according to administration officials who described the offer Friday only on condition of anonymity. The remainder would be achieved through an overhaul of the tax system next year and would not become effective until 2014, said the officials, who were not authorized to provide the details by name.
Obama is seeking new spending to help the unemployed, homeowners whose property's value is less than their mortgage, doctors who treat Medicare patients and wage-earners.
In exchange, the president would back cuts of an unspecified amount this year, and savings of as much $400 billion from Medicare and other benefit programs in 2013.
The White House plan also counts about $1 trillion in spending cuts agreed to last year, as well as about $800 billion that the administration claims as savings because of the drawdown of troops from Iraq and Afghanistan.
Republicans said they were surprised at the plan, and Democrats wondered aloud why.
"Each side said they'd submit a down payment. We have. Our preference is revenue. What is theirs?" said Sen. Chuck Schumer, D-N.Y.
Republicans have an opening offer of their own, in line with their conservative anti-tax views, much as Obama's is designed to solidify his own political position. While agreeing to new revenue, GOP lawmakers want to extend expiring income tax cuts at all levels, including the top brackets. They also want to raise the age of eligibility for Medicare and curtail future cost-of-living adjustments for Social Security and other benefit programs. The same adjustment would raise revenue for the government by making a change in annual adjustments of tax brackets.
"We're the only ones with a balanced plan to protect the economy, protect American jobs and protect the middle class from the fiscal cliff," Boehner said on Friday.
That was a jab at Obama, who campaigned for re-election advocating a balanced approach to avoiding the fiscal cliff that combines higher taxes on the wealthy with spending cuts.
Said the president: "In Washington, nothing's easy, so there is going to be some prolonged negotiations."
___
EDITOR'S NOTE ? David Espo is AP's chief congressional correspondent. Associated Press writer Alan Fram contributed to this story.
Developer kits for the Ouya were given a ship date of December 28th today, alongside news that the system's software development kit ("ODK") will be available that same day. In case it wasn't already clear how small the Android-powered console is, the folks at Ouya included the picture you see above to further illustrate that point -- the thing is really small. Ouya expects the dev kits to get into backers' hands "within a couple day" of the 28th. Final units are still intended to ship some time in March 2013, though no final date is available just yet.
How different are these dev units from the final run, though? Not that different, we'd guess, considering the company's continued promise that "every Ouya will be a dev console." The only hint given of their difference is a note in today's update calling them, "pretty special." Beyond just getting a jump on game development with the Ouya in mind, dev unit buyers will also be the first to try out Jelly Bean gaming. Of course, if you're a dev unit-level backer and you'd like to share your thoughts with us, we're all ears.
>>>weather making the news tonight as viewers on the
west coast
are well aware they're getting ready for some
heavy weather
,
heavy rain
, flood conditions that could go on for days. a huge plume of moisture that our friends at the
weather channel
say it is like a giant
fire hose
, getting ready to park itself on the
west coast
. some areas could see ten inches of rain, it could stretch south all the way to
southern california
. it could last for days and many
It's frustrated many a Drive user, and Google has taken heed, adding on-the-go spreadsheet editing to the service's iOS and Android apps. In addition to making tweaks to existing cells, users will also be able to create new spreadsheets from their iPads, iPhones or any Android device. You'll also have realtime access, letting you see changes from friends and colleagues as they're made. Other app tweaks include improved formatting reproduction for content pasted between Google documents, along with the ability to add Android home screen shortcuts to any Drive file. Hit up Google Play for the updated application today.
Like an intergalactic Swiss Army Knife, R2-D2 has an untold number of tools and accessories hidden away inside. But unless you're piloting spacecraft through asteroid fields, battling Sith Lords, or intimidating Ewoks, they're all useless compared to what this R2-D2 skinned flask is stashing away. More »
PHOENIX (Reuters) - Democratic Representative Ron Barber, a former aide to Gabrielle Giffords who was wounded alongside her in a deadly 2011 shooting, said on Tuesday he is recovering after surgery to remove a cancerous tumor from his tongue.
Barber, 67, beat Republican rival Martha McSally by a slender margin in the November 6 election to represent southeast Arizona in the state's redrawn 2nd Congressional District.
Barber's office said he learned of the tumor on November 13. He underwent surgery on Monday to remove the growth, and is expected to return to work in Washington next week.
"Congressman Barber was released from the hospital earlier today after a successful surgery," Barber's doctor, Audrey Erman, said in a statement released by the congressman's office. "He is expected to make a full recovery."
Barber was shot in the face and thigh on January 8, 2011, when Jared Loughner opened fire at an event outside a Tucson supermarket where Giffords was meeting with constituents.
Six people were killed in the shooting spree and 13 were wounded, including Giffords, who was shot through the head. She stepped down in January to focus on her recovery. Loughner was sentenced to life in prison earlier this month.
(Reporting by Tim Gaynor; Editing by Lisa Shumaker)
Protein injection points to muscular dystrophy treatmentPublic release date: 27-Nov-2012 [ | E-mail | Share ]
Contact: Paddy Moore padmoore@ohri.ca 613-737-8899 x73687 Ottawa Hospital Research Institute
November 27, 2012 Ottawa Scientists have discovered that injecting a novel human protein into muscle affected by Duchenne muscular dystrophy significantly increases its size and strength, findings that could lead to a therapy akin to the use of insulin by diabetics. These results were published today in the Proceedings of the National Academy of Sciences by Dr. Julia von Maltzahn and Dr. Michael Rudnicki, the Ottawa scientist who discovered muscle stem cells in adults.
"This is an unprecedented and dramatic restoration in muscle strength," says Dr. Rudnicki, a senior scientist and director for the Regenerative Medicine Program and Sprott Centre for Stem Cell Research at the Ottawa Hospital Research Institute. He is also a Canada Research Chair in Molecular Genetics and professor in the Faculty of Medicine at the University of Ottawa.
"We know from our previous work that this protein, called Wnt7a, promotes the growth and repair of healthy muscle tissue. In this study we show the same types of improvement in a mouse model of Duchenne muscular dystrophy. We found that Wnt7a injections increased muscle strength almost two-fold, to nearly normal levels. We also found that the size of the muscle fibre increased and there was less muscle damage, compared to mice not given Wnt7a."
Duchenne muscular dystrophy is a genetic disorder that affects one of every 3,500 newborn males. In Canada, all types of muscular dystrophy affect more than 50,000 people. The disease often progresses to a state where the muscles are so depleted that the person dies due to an inability to breath. For people with Duchenne muscular dystrophy, this usually happens in their 20s or 30s.
"This is also exciting because we think it's a therapeutic approach that could apply to other muscle-wasting diseases," says Dr. Rudnicki.
Dr. Rudnicki's lab is a world leader in research on muscle stem cells. They have contributed significantly to our understanding of how these cells work at the molecular level. This basic research, which takes place in OHRI's multidisciplinary environment of collaboration with clinicians, led to the identification of Wnt7a as a promising candidate to help people with this muscle wasting disease.
Biotechnology partner, Fate Therapeutics is currently developing Wnt7a-based therapeutic candidates for treatment of muscular dystrophy and atrophy. Preclinical assessments are ongoing and the company plans to initiate clinical trials in the near future.
###
The full article, "Wnt7a treatment ameliorates muscular dystrophy," is available online ahead of print through the Proceedings of the National Academy of Sciences site.
This research was supported by the Muscular Dystrophy Association, the Ontario Ministry of Economic Development and Innovation, the Canadian Institutes of Health Research, the National Institutes of Health, the Howard Hughes Medical Institute, Fate Therapeutics and the Canada Research Chair Program. All research at OHRI is also supported by The Ottawa Hospital Foundation.
Media Contact
Paddy Moore
Manager, Communications and Public Relations,
Ottawa Hospital Research Institute
613-798-5555 ext. 73687
613-794-6912 (cell)
padmoore@ohri.ca
Nomie Duval
Media Relations Officer
University of Ottawa
613-562-5800 x2981
613-863-7221 (cell)
neomie.duval@uOttawa.ca
About the Ottawa Hospital Research Institute (OHRI)
The Ottawa Hospital Research Institute (OHRI) is the research arm of The Ottawa Hospital and is an affiliated institute of the University of Ottawa, closely associated with the university's Faculties of Medicine and Health Sciences. OHRI includes more than 1,700 scientists, clinical investigators, graduate students, postdoctoral fellows and staff conducting research to improve the understanding, prevention, diagnosis and treatment of human disease. Research at OHRI is supported by The Ottawa Hospital Foundation. www.ohri.ca
About the University of Ottawa
The University of Ottawa is committed to research excellence and encourages an interdisciplinary approach to knowledge creation, which attracts the best academic talent from across Canada and around the world. It is an important stakeholder in the National Capital Region's economic development.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Protein injection points to muscular dystrophy treatmentPublic release date: 27-Nov-2012 [ | E-mail | Share ]
Contact: Paddy Moore padmoore@ohri.ca 613-737-8899 x73687 Ottawa Hospital Research Institute
November 27, 2012 Ottawa Scientists have discovered that injecting a novel human protein into muscle affected by Duchenne muscular dystrophy significantly increases its size and strength, findings that could lead to a therapy akin to the use of insulin by diabetics. These results were published today in the Proceedings of the National Academy of Sciences by Dr. Julia von Maltzahn and Dr. Michael Rudnicki, the Ottawa scientist who discovered muscle stem cells in adults.
"This is an unprecedented and dramatic restoration in muscle strength," says Dr. Rudnicki, a senior scientist and director for the Regenerative Medicine Program and Sprott Centre for Stem Cell Research at the Ottawa Hospital Research Institute. He is also a Canada Research Chair in Molecular Genetics and professor in the Faculty of Medicine at the University of Ottawa.
"We know from our previous work that this protein, called Wnt7a, promotes the growth and repair of healthy muscle tissue. In this study we show the same types of improvement in a mouse model of Duchenne muscular dystrophy. We found that Wnt7a injections increased muscle strength almost two-fold, to nearly normal levels. We also found that the size of the muscle fibre increased and there was less muscle damage, compared to mice not given Wnt7a."
Duchenne muscular dystrophy is a genetic disorder that affects one of every 3,500 newborn males. In Canada, all types of muscular dystrophy affect more than 50,000 people. The disease often progresses to a state where the muscles are so depleted that the person dies due to an inability to breath. For people with Duchenne muscular dystrophy, this usually happens in their 20s or 30s.
"This is also exciting because we think it's a therapeutic approach that could apply to other muscle-wasting diseases," says Dr. Rudnicki.
Dr. Rudnicki's lab is a world leader in research on muscle stem cells. They have contributed significantly to our understanding of how these cells work at the molecular level. This basic research, which takes place in OHRI's multidisciplinary environment of collaboration with clinicians, led to the identification of Wnt7a as a promising candidate to help people with this muscle wasting disease.
Biotechnology partner, Fate Therapeutics is currently developing Wnt7a-based therapeutic candidates for treatment of muscular dystrophy and atrophy. Preclinical assessments are ongoing and the company plans to initiate clinical trials in the near future.
###
The full article, "Wnt7a treatment ameliorates muscular dystrophy," is available online ahead of print through the Proceedings of the National Academy of Sciences site.
This research was supported by the Muscular Dystrophy Association, the Ontario Ministry of Economic Development and Innovation, the Canadian Institutes of Health Research, the National Institutes of Health, the Howard Hughes Medical Institute, Fate Therapeutics and the Canada Research Chair Program. All research at OHRI is also supported by The Ottawa Hospital Foundation.
Media Contact
Paddy Moore
Manager, Communications and Public Relations,
Ottawa Hospital Research Institute
613-798-5555 ext. 73687
613-794-6912 (cell)
padmoore@ohri.ca
Nomie Duval
Media Relations Officer
University of Ottawa
613-562-5800 x2981
613-863-7221 (cell)
neomie.duval@uOttawa.ca
About the Ottawa Hospital Research Institute (OHRI)
The Ottawa Hospital Research Institute (OHRI) is the research arm of The Ottawa Hospital and is an affiliated institute of the University of Ottawa, closely associated with the university's Faculties of Medicine and Health Sciences. OHRI includes more than 1,700 scientists, clinical investigators, graduate students, postdoctoral fellows and staff conducting research to improve the understanding, prevention, diagnosis and treatment of human disease. Research at OHRI is supported by The Ottawa Hospital Foundation. www.ohri.ca
About the University of Ottawa
The University of Ottawa is committed to research excellence and encourages an interdisciplinary approach to knowledge creation, which attracts the best academic talent from across Canada and around the world. It is an important stakeholder in the National Capital Region's economic development.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
This week's Tokyoflash watch will certainly tickle the fancy of those who sleep with a set square beneath their pillow. The Kisai Polygon has a ring of triangles representing the hours and the nearest 10 minutes, with the individual minute being shown as a single digit through the middle. If you'd like to indulge in some retail therapy, you can take advantage of the company's pre-sale. Available in black, mirror, blue or pink, it'll set you back $99 (€77, £61) until Thursday, after which it'll cost $129 (€100, £80). Fancy learning how to read it from the team to built it? Head down past the break for the video tutorial.
Today is the biggest online shopping day of the year, but not every deal is as good as it looks—in fact, most 50%-off-type deals are sporting inflated prices. So you don't have to spend all day parsing lists of cheap electronics, here are five deals on stuff you actually want on prices for prices are actually lower today. More »
LOS ANGELES (AP) ? Broadway superstar Audra McDonald is adding a new chapter to her long history with Lincoln Center.
The singer-actress is the new host of "Live From Lincoln Center," PBS said Tuesday.
McDonald will emcee seven broadcasts from December through spring 2013, starting Dec. 13 with "The Richard Tucker Opera Gala" and Dec. 31 with the New York Philharmonic's New Year's Eve gala.
"It's a great honor. I'm thrilled that they came to me and trusted me to do it," said McDonald, 42, whose five Tony Awards include a trophy this year for "The Gershwins' Porgy and Bess."
Her memories of the Lincoln Center performing arts complex in Manhattan run deep.
"I remember watching Beverly Sills broadcasting from the Met (the center's Metropolitan Opera House) on my PBS channel at my home in Fresno," McDonald said, adding that she was amazed at the venue's size and "inspired by the music."
As a high school student, she had the chance to visit the center and recalled thinking, "This is where I want to be some day."
That wish was fulfilled when she moved to New York to attend The Juilliard School, which has its campus there.
Stepping in as host of the PBS series "feels like it's my way of thanking Lincoln Center," she said.
"We can't imagine a more perfect match," said Elizabeth Scott, the center's executive in charge of the TV series. McDonald's passion for the performing arts is "infectious," Scott added.
McDonald, who starred in "Private Practice" as Dr. Naomi Bennett, has performed on the long-running PBS showcase several times, including programs with Elvis Costello, Patti Lupone and the New York Philharmonic.
She will be working especially hard New Year's Eve when she hosts and performs in the holiday program, "One Singular Sensation: Celebrating Marvin Hamlisch" (check local listings for time).
"We'll see if I fall down by the end of the evening, or by the middle," she said, lightly. What she'll sing is a secret for now, but McDonald said it's among Hamlisch's most famous pieces.
The composer, who died in August at age 68, created more than 40 film scores and won a Tony and the Pulitzer for Broadway's "A Chorus Line."
"Live From Lincoln Center" is in its 37th broadcast season. In recent years, artists and actors including Yo-Yo Ma and Alec Baldwin have filled the host's job that previously saw long tenures by famed opera singer Sills and TV personality Hugh Downs.
LOS ANGELES ? Dylan Royer scored 18 points and Kyle Odister came off the bench and added 15 points, including the game-winning free throws and Cal Poly upset No. 11 UCLA 70-68 on Sunday.
Chris Eversley had 15 points and 10 rebounds for the Mustangs (2-2), who erased an 18-point deficit in the second half and earned their first win against UCLA in six tries.
Down 51-33, Cal Poly went on a 34-14 run.
Eversley tipped in a miss for a 67-65 lead and Cal Poly didn't trail the rest of the way.
Odister made free throws for a 68-65 lead and 70-68 edge with 14.2 seconds remaining.
Jordan Adams missed a 3-point attempt and time expired for the Bruins (4-2), who needed overtime to defeat another Big West opponent, UC Irvine, earlier this month.
UCLA made only one field goal in the final three minutes, on Adams' layup underneath to tie it 68.
Freshman guard Shabazz Muhammad led UCLA with 15 points and 10 rebounds in his debut at Pauley Pavilion. Travis Wear had 14 points and Adams scored 13.
Cal Poly made six 3-pointers, including a career-high four by Royer, and shot 58 percent from the field in the second half as UCLA's defense struggled and its offense went stagnant.
Brian Bennett had a career-high 16 points for Cal Poly and Chris O'Brien had a career-high eight assists.
The Bruins opened the second half on a 22-6 run to take a 51-33 lead. David Wear scored seven points in that stretch, including a 3-pointer, a long jumper and a drive in the paint.
Cal Poly made only one field goal in a span of 6:07, but climbed back into the game on a 15-4 run. Odister made a pair of 3-pointers to get the Mustangs within nine points. After a UCLA timeout, Royer made a 3-pointer to make it 59-51.
Cal Poly got consecutive baskets by Odister, Eversley and Brian Bennett and, after Muhammad missed a jumper, Royer made a 3-pointer to bring the Mustangs to 61-60. Royer again made a 3 to tie it at 63.
Adams made a jumper, but the Bruins wouldn't lead again.
UCLA took a 29-27 lead into halftime after it scored the final two baskets of the first half, on a one-handed dunk by Muhammad and a driving layup by Drew.
But Cal Poly used an 11-0 run, capped by Odister's corner 3-pointer, late in the first half to lead for most the final five minutes.
Adams helped keep the Bruins in it with a 3-pointer and a three-point play following a leaping save of the ball and a block by Kyle Anderson at the other end.
UCLA went on a 9-0 run early in the game as Cal Poly went seven minutes without a making a field goal.
Earlier Sunday, UCLA announced that reserve junior guard Tyler Lamb was granted a release from the team to transfer. Lamb started 32 games last season but had knee surgery in October and hasn't played since the season opener because of swelling in the knee. Lamb averaged nine points, 3.6 rebounds and 2.8 assists per game last season. He was second on the Bruins with 43 3-pointers.
Client needs help with pin-out / wiring diagram for the Clink2 Crossover Cable to make their own version of p/n: (25 ft.) 2200-24009-001, (50 ft.) 2200-24008-001, (100 ft.) 2200-24010-001
Solution:
To build a custom Conference Link2 cable, use shielded CAT5e or better, and terminate both end connectors (P1 and P2) with standard 8P8C plugs (for example, RJ45) using the wiring connections shown below. The maximum length for this cable is 100 feet (30 m). Note that this cable provides a crossover connection between pins 1 and 2 and pins 5 and 6.
Note: HDX 6000, 7000, 8000 require the use of a Walta (M) to RJ45 (F) adapter (p/n: 2457-25646-001) on each end of this cable to connect from the HDX to the Polycom Microphone Pod.
Pair
Pins P1
Pins P2
Pair 1
1, 2
5, 6
Pair 2
3, 4
3, 4
leave out the pin 4 wire
Pair 3
5, 6
1, 2
Pair 4
7, 8
7, 8
(48 volts)
The shield drain wire should tie to pin 3
?
?
The pin 3 connection straight-thru is VERY important (one could say critical) as it sets the ground reference for the clocking signals passed on the other signal pairs (1,2 and 5,6). Without it, the cable/system stops working at lengths greater than about 25 feet.
On Polycom-supplied cables, that pin-3 is also tied to the shield of the RJ45 connector? but it?s almost impossible to do that with the drain wire and not cause an intermittent short.? So field terminations can be with the drain wire connected to the metal shield of the RJ45 connector and an unused wire pair (perhaps blue/white?)?connected to pin-3 straight thru.
?
Tagged as: clink2, HDX, microphone, Polycom
This post was written by ScanSource Communications Tech Support
You want to give your customers the best in voice and video conferencing equipment, and with ScanSource Communications, you?ll get it. With over 50 years of combined industry expertise, our Total Coverage offerings and knowledgebase can help you solve almost any communications question you can imagine. Plus, you will find articles from our savvy technical services team about key industry topics along with product support tips and tricks. You'll get it, because we get it.Contact Info: techsupport@scansourcecommunications.com 877-847-7000 x4095
KADUNA, Nigeria (AP) ? Twin suicide car bombs exploded Sunday at a church inside one of Nigeria's top military bases, killing at least 11 people and wounding another 30 in an embarrassing attack showing the continued insecurity that haunts Africa's most populous nation.
No one immediately claimed responsibility for the attacks, but suspicion immediately fell on the radical Islamist sect known as Boko Haram, whose suicide bombers target Sunday worship services in what has become a weekly macabre routine in Nigeria.
This attack in Jaji on Sunday, however, happened inside a barracks home to the Armed Forces Command and Staff College, one of the country's most important military colleges. It also showed a new dangerous sophistication as the second explosion appeared timed to target responders rushing to aid the wounded 10 minutes after the first blast, officials said.
The attack began just after noon and targeted the St. Andrew Military Protestant Church, Brig. Gen. Bola Koleoso said. A bus loaded with explosives somehow made it inside the barracks' perimeter and rammed into the church's walls before exploding, Koleoso said. The second blast came from a sedan parked nearby and struck in the chaos afterward as emergency workers, soldiers and survivors of the first blast milled around the church, he said.
"Investigation into the bombings have commenced and the area already (has been) cordoned off," Koleoso said in a text message sent to journalists after the attack. The military kept journalists away from the scene of the blast and took the wounded to military clinics, limiting independent verification of what happened in the attack. Yushau Shuaib, a spokesman for Nigeria's National Emergency Management Agency, would only say an explosion happened at the base and referred all questions to the military.
Nigerian security forces, particularly the military, routinely downplay casualty figures in attacks, so the true scope of the attack may never be known. However, this isn't the first time that a major military base has been struck during the increasingly bloody guerrilla fighting waged by Boko Haram. On New Year's Eve in 2010, a bomb allegedly planted by the sect exploded at a crowded and popular outdoor beer garden at a military barracks in Nigeria's capital, Abuja, and killed at least four people.
Sunday's attack targeted Jaji, which teaches the top military minds in Nigeria. The area sits just north of the city of Kaduna, a major city in Nigeria's north that sits on the uneasy dividing line between the country's predominantly Christian south and Muslim north. Religious violence and rioting in the city has killed thousands since Nigeria became a democracy in 1999. Most recently, a suicide car bombing in October at a Catholic church in the city killed at least seven people and wounded more than 100 others.
While several suicide car bombings in Kaduna this year have gone unclaimed, many believe them to be the work of Boko Haram, whose name means "Western education is sacrilege" in the Hausa language of Nigeria's north. Boko Haram is blamed for more than 760 killings this year alone, according to an Associated Press count. The group has said Nigeria must implement strict Shariah law and free its imprisoned members before it will stop its attacks.
Western diplomats and military officials say the sect has loose ties to both al-Qaida in the Islamic Maghreb and Somalia's al-Shabab, while also offering fighters to join Islamists now controlling northern Mali. That has led to worries the group will grow only more violent as time goes on.
Despite sending soldiers into troubled northern cities, Nigeria's military has been unable to stop the attacks and has alienated locals with heavy-handed tactics and retaliatory attacks that have seen dozens of civilians killed at a time. Sunday's attack in Jaji came only two days after a special military taskforce announced that it would offer $1.8 million in rewards for information that could lead to the arrest of top Boko Haram members.
___
Yinka Ibukun reported from Lagos, Nigeria. Associated Press writer Jon Gambrell in Johannesburg contributed to this report.
DHAKA (Reuters) - A fire swept through a garment factory on the outskirts of Bangladesh's capital, killing at least 120 people, the chief of the fire brigade said on Sunday, in the worst accident for the booming industry in recent years.
The fire at the nine-story factory in the Ashulia industrial belt started on the ground floor late on Saturday and quickly spread, trapping hundreds of workers.
"This morning we have recovered 120 dead bodies and the death toll could rise," Abu Nayeem Mohammad Shahidullah, director general of the fire brigade, told reporters.
Bangladesh has around 4,500 garment factories that make clothes for brands including Tesco, Wal-Mart, JC Penney, H&M, Marks & Spencer, Kohl's and Carrefour.
Witnesses said the workers, mostly women, ran for safety as the fire engulfed the plant, but were unable to come out through narrow exits.
"Many jumped out from the windows and were injured, or died on the spot," Milon, a resident, said
The fire leapt high into the sky and could be seen from miles (kms) away.
Bangladesh is the world's biggest exporter of clothing after China, with garments making up 80 percent of its $24 billion annual exports.
But safety standards at the factories are poor and not enforced strictly, causing scores of accidents each year.
"We are appalled to see the charred bodies coming out of the factory since last night. It was an endless stream," Milon said.
Saturday's fire was the worst in years and rescuers and police said the death count may surpass any previous toll.
Earlier this year, more than 300 factories near the capital were shut for almost a week as workers demanded higher wages and better working conditions.
(Reporting by Ruma Paul and Anis Ahmed; Editing by Sanjeev Miglani)
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FAYETTEVILLE, Ark. (AP) ? Jarvis Landry helped LSU keep the SEC championship in reach with a 20-13 win over Arkansas on Friday.
Now the receiver and the rest of the No. 8 Tigers must sit back and wait while their next destination ? perhaps next weekend's SEC championship game ? is played out elsewhere.
Landry's spectacular, reaching, one-handed touchdown catch late in the first half helped LSU (10-2, 6-2 Southeastern Conference) hold off the reeling Razorbacks. It marked the sixth time in eight seasons that the Tigers have reached double-digit wins under coach Les Miles.
LSU must now hope for an Alabama loss to Auburn (not likely) and Texas A&M victory against Missouri (very possible) on Saturday in order to win the SEC West and earn a trip to Atlanta. Even without a division crown, the Tigers could still get an at-large bid to the BCS.
"We'll take the next day and a half or so and watch TV tomorrow and be excited about it, and move forward and see how things go," Miles said.
Zach Mettenberger passed for 217 yards and hooked up with Landry for the play of the day with 1:12 left in the first half to put LSU up 10-0. The Tigers were outgained 462-306 in total yardage, but they were able to hold off record-setting performances by Arkansas quarterback Tyler Wilson and receiver Cobi Hamilton.
Wilson was 31 of 52 passing for the Razorbacks (4-8, 2-6) whose fall from preseason top 10 is now complete. The senior set the school record for career passing yards in the loss, while Hamilton set the school record for receptions in a career with 175.
The records were a bright spot in an otherwise dismal season for a Razorbacks team that struggled mightily following the April firing of former coach Bobby Petrino. Arkansas was 21-5 the last two seasons and entered the season with SEC and national championship expectations, but it was eliminated from the bowl picture following last week's loss at Mississippi State.
"We kind of stuck together (through) all the adversity," Hamilton said. "We're still brothers. We're still the same 2012 team that everybody had high expectations for. But we just stuck together."
The Tigers took at 17-3 lead early in the third quarter after a 1-yard touchdown run by Jeremy Hill, who finished with 77 yards rushing on 18 carries. The touchdown followed an 86-yard kickoff return by Michael Ford to the Arkansas 9.
It also appeared to be the clincher for LSU, though the Razorbacks rallied behind the combination of Wilson and Hamilton.
Wilson passed former Arkansas quarterback Ryan Mallet's mark of 7,493 yards passing in the second quarter, finishing with 359 yards in the game and 7,765 yards for his career, and his 28-yard touchdown pass to freshman Mekale McKay in the third quarter closed the LSU lead to 17-10.
After forcing a Tigers' punt, the Razorbacks used a key fourth-and-1 conversion to set up another scoring opportunity. Wilson found Jonathan Williams for a 37-yard completion on the fourth down at midfield, helping to set up a second-and-goal at the LSU 1.
Arkansas was unable, however, to find the end zone on its next two plays. Interim coach John L. Smith then elected to kick a 17-yard field goal, which backup kicker John Henson converted to close the Tigers' lead to 17-13.
The Razorbacks never did find the end zone again, bringing a likely end to the Arkansas career of Smith ? who was signed to a 10-month contract following Petrino's firing.
"That's the right call," Smith said of the field goal attempt. "I mean, you have to score twice to win it, don't you? At least, I think you had to score twice to win it unless my math was wrong. So do you take it there? You have to take the sure points and then come back you have to score again anyway. So that was the thought, and I think that's the right call."
The Razorbacks had one final chance in the closing seconds, but Wilson's second-down attempt from the LSU 18 was over the head of McKay as time expired.
LSU's final score came on a 27-yard field goal by Drew Alleman with 1:26 remaining, giving it a 20-13 lead. The score came after a key 47-yard third-down completion from Mettenberger to Odell Beckham, who finished with eight catches for 112 yards.
The Tigers led 10-0 at halftime in their first game in Fayetteville since 1992. They did so despite gaining the same 165 yards of total offense as the Razorbacks, whose season-long series of miscues continued in the half.
Arkansas, next to last in the SEC in red-zone offense, squandered three scoring opportunities in the half. Dennis Johnson fumbled near the LSU goal line on the game's opening drive, and kicker Zach Hocker misfired on a pair of field goal attempts before being benched in favor of Henson in the second half.
LSU's first touchdown came late in the first half when Mettenberger found Landry in the back of the end zone for a 22-yard touchdown. Landry had to reach back over his wrong shoulder to stretch out and snare the ball with his right hand, landing well in bounds.
"I felt that the throw kind of kept me in bounds," Landry said. "I felt that if he had led me any, there was a possibility I could have been out of bounds.
"It's just one of those throws where Zach trusted me, and I just went up and made it."
Hamilton finished with 10 catches for 98 yards in his final game at Arkansas, finishing his career with 175 catches. His record broke the former mark of 168 catches, set last year by Minnesota Vikings' rookie Jarius Wright.
PARKER, Texas (AP) ? Tourists and locals flocked to Southfork Ranch on Saturday, bringing flowers in memory of Larry Hagman, who played the infamous J.R. Ewing on the TV show "Dallas."
Hagman died in Dallas on Friday at age 81 due to complications from his battle with cancer.
Southfork, a ranch north of Dallas, was known to millions of viewers as the Ewing family home. Exterior shots of the house and pool were shown when the series aired from 1978 to 1991, although the show wasn't filmed there.
The ranch has been open for tours since the mid-1980s, and now sees more than 100,000 visitors each year. Each room of the house has a theme for each character.
On Saturday, J.R. Ewing's room had flowers and a card for tourists to sign.
"Today is about Larry Hagman and his family," said Janna Timm, a Southfork Ranch & Hotel spokeswoman. "He was such a wonderful person, and we will really miss him."
"Dallas" was recently revived on TNT this summer, and all of the scenes were filmed at Southfork or other places in the Dallas area. Hagman had revised his role as the scheming oilman who would even double-cross his own son.
Linda Sproule of Peterborough, Ontario, had been traveling through the U.S. the past couple of weeks and heard about Hagman's death Friday while in Dallas. She said she didn't know where Southfork was but wanted to come because she was a fan of the show in the 1980s.
"I remember on Friday nights we watched it, and J.R. was bigger than life in some ways," she said after taking the Southfork tour Saturday morning. "This ranch is beautiful. Being here is kind of emotional in a way."
Barbara Quinones and her husband were in town for their daughter's soccer tournament and had already planned to visit Southfork when they heard news of Hagman's death.
"We loved him because he was so ruthless," said Quinones, of Albuquerque, N.M. "This is a sad day, but I'm glad we're here."
Some of the show's stars, including Hagman, came to Southfork for the series' 25th anniversary. The Fort Worth-born actor also had visited several times before the show was revived.
"He was definitely a gentleman, a class act," said Jim Gomes, vice president of resorts at Southfork Ranch & Hotel. "He loved the fans as much as they loved him."
ScienceDaily: Gene Newshttp://www.sciencedaily.com/news/health_medicine/genes/ Genes and Genetics News. Read today's medical research in genetics including what can damage genes, what can protect them, and more.en-usSat, 24 Nov 2012 01:42:22 ESTSat, 24 Nov 2012 01:42:22 EST60ScienceDaily: Gene Newshttp://www.sciencedaily.com/images/logosmall.gifhttp://www.sciencedaily.com/news/health_medicine/genes/ For more science articles, visit ScienceDaily.New insights into virus proteome: Unknown proteins of the herpesvirus discoveredhttp://www.sciencedaily.com/releases/2012/11/121123092132.htm The genome encodes the complete information needed by an organism, including that required for protein production. Viruses, which are up to a thousand times smaller than human cells, have considerably smaller genomes. Using a type of herpesvirus as a model system scientists have shown that the genome of this virus contains much more information than previously assumed. The researchers identified several hundred novel proteins, many of which were surprisingly small.Fri, 23 Nov 2012 09:21:21 ESThttp://www.sciencedaily.com/releases/2012/11/121123092132.htmScientists describe elusive replication machinery of flu viruseshttp://www.sciencedaily.com/releases/2012/11/121122152928.htm Scientists have made a major advance in understanding how flu viruses replicate within infected cells. The researchers used cutting-edge molecular biology and electron-microscopy techniques to ?see? one of influenza?s essential protein complexes in unprecedented detail. The images generated in the study show flu virus proteins in the act of self-replication, highlighting the virus?s vulnerabilities that are sure to be of interest to drug developers.Thu, 22 Nov 2012 15:29:29 ESThttp://www.sciencedaily.com/releases/2012/11/121122152928.htmProtein folding: Look back on scientific advances made as result of 50-year old puzzlehttp://www.sciencedaily.com/releases/2012/11/121122152910.htm Fifty years after scientists first posed a question about protein folding, the search for answers has led to the creation of a full-fledged field of research that led to major advances in supercomputers, new materials and drug discovery, and shaped our understanding of the basic processes of life, including so-called "protein-folding diseases" such as Alzheimer's, Parkinson's and type II diabetes.Thu, 22 Nov 2012 15:29:29 ESThttp://www.sciencedaily.com/releases/2012/11/121122152910.htmStep forward in regenerating and repairing damaged nerve cellshttp://www.sciencedaily.com/releases/2012/11/121121145638.htm Researchers recently uncovered a nerve cell's internal clock, used during embryonic development. This breakthrough could lead to the development of new tools to repair and regenerate nerve cells following injuries to the central nervous system.Wed, 21 Nov 2012 14:56:56 ESThttp://www.sciencedaily.com/releases/2012/11/121121145638.htmArchitecture of rod sensory cilium disrupted by mutationhttp://www.sciencedaily.com/releases/2012/11/121121145621.htm Using a new technique called cryo-electron tomography, scientists have created a three-dimensional map that gives a better understanding of how the architecture of the rod sensory cilium (part of one type of photoreceptor in the eye) is changed by genetic mutation and how that affects its ability to transport proteins as part of the light-sensing process.Wed, 21 Nov 2012 14:56:56 ESThttp://www.sciencedaily.com/releases/2012/11/121121145621.htmAging: Scientists further unravel telomere biologyhttp://www.sciencedaily.com/releases/2012/11/121121130933.htm Researchers have resolved the structure of that allows a telomere-related protein, Cdc13, to form dimers in yeast. Mutations in this region of Cdc13 put the kibosh on the ability of telomerase and other proteins to maintain telomeres.Wed, 21 Nov 2012 13:09:09 ESThttp://www.sciencedaily.com/releases/2012/11/121121130933.htmDrug resistance biomarker could improve cancer treatmenthttp://www.sciencedaily.com/releases/2012/11/121121130811.htm Cancer therapies often have short-lived benefits due to the emergence of genetic mutations that cause drug resistance. A key gene that determines resistance to a range of cancer drugs has been reported in a new study. The study reveals a biomarker that can predict responses to cancer drugs and offers a strategy to treat drug-resistant tumors based on their genetic signature.Wed, 21 Nov 2012 13:08:08 ESThttp://www.sciencedaily.com/releases/2012/11/121121130811.htmGenome packaging: Key to breast cancer developementhttp://www.sciencedaily.com/releases/2012/11/121121130703.htm Two recent studies delve into the role of chromatin modifying enzymes and transcription factors in tumour cells. In one, it was found that the PARP1 enzyme activated by kinase CDK2 is necessary to induce the genes responsible for the proliferation of breast cancer cells in response to progesterone. In another, extensive work has been undertaken to identify those genes activated by the administration of progesterone in breast cancer, the sequences that can be recognized and how these genes are induced.Wed, 21 Nov 2012 13:07:07 ESThttp://www.sciencedaily.com/releases/2012/11/121121130703.htmShort DNA strands in genome may be key to understanding human cognition and diseaseshttp://www.sciencedaily.com/releases/2012/11/121121130643.htm Previously discarded, human-specific ?junk? DNA represents untapped resource in the study of diseases like Alzheimer?s and autism.Wed, 21 Nov 2012 13:06:06 ESThttp://www.sciencedaily.com/releases/2012/11/121121130643.htmBiomarking time: Methylome modifications offer new measure of our 'biological' agehttp://www.sciencedaily.com/releases/2012/11/121121130633.htm In a new study, researchers describe markers and a model that quantify how aging occurs at the level of genes and molecules, providing not just a more precise way to determine how old someone is, but also perhaps anticipate or treat ailments and diseases that come with the passage of time.Wed, 21 Nov 2012 13:06:06 ESThttp://www.sciencedaily.com/releases/2012/11/121121130633.htmKidney tumors have a mind of their ownhttp://www.sciencedaily.com/releases/2012/11/121121104552.htm New research has found there are several different ways that kidney tumors can achieve the same result -- namely, grow.Wed, 21 Nov 2012 10:45:45 ESThttp://www.sciencedaily.com/releases/2012/11/121121104552.htmMechanism to repair clumped proteins explainedhttp://www.sciencedaily.com/releases/2012/11/121121104416.htm Clumped proteins can be dissolved with the aid of cellular repair systems -- a process of critical importance for cell survival especially under conditions of stress. Researchers have now decrypted the fundamental mechanism for dissolving protein aggregates that involves specific molecular chaperones.Wed, 21 Nov 2012 10:44:44 ESThttp://www.sciencedaily.com/releases/2012/11/121121104416.htmNovel mechanism through which normal stromal cells become cancer-promoting stromal cells identifiedhttp://www.sciencedaily.com/releases/2012/11/121121104401.htm New understanding of molecular changes that convert harmless cells surrounding ovarian cancer cells into cells that promote tumor growth and metastasis provides potential new therapeutic targets for this deadly disease, according to new research.Wed, 21 Nov 2012 10:44:44 ESThttp://www.sciencedaily.com/releases/2012/11/121121104401.htmNew test for tuberculosis could improve treatment, prevent deaths in Southern Africahttp://www.sciencedaily.com/releases/2012/11/121120194932.htm A new rapid test for tuberculosis (TB) could substantially and cost-effectively reduce TB deaths and improve treatment in southern Africa -- a region where both HIV and tuberculosis are common.Tue, 20 Nov 2012 19:49:49 ESThttp://www.sciencedaily.com/releases/2012/11/121120194932.htmEvolution of human intellect: Human-specific regulation of neuronal geneshttp://www.sciencedaily.com/releases/2012/11/121120194926.htm A new study has identified hundreds of small regions of the genome that appear to be uniquely regulated in human neurons. These regulatory differences distinguish us from other primates, including monkeys and apes, and as neurons are at the core of our unique cognitive abilities, these features may ultimately hold the key to our intellectual prowess (and also to our potential vulnerability to a wide range of 'human-specific' diseases from autism to Alzheimer's).Tue, 20 Nov 2012 19:49:49 ESThttp://www.sciencedaily.com/releases/2012/11/121120194926.htmRibosome regulates viral protein synthesis, revealing potential therapeutic targethttp://www.sciencedaily.com/releases/2012/11/121120132906.htm Rather than target RNA viruses directly, aiming at the host cells they invade could hold promise, but any such strategy would have to be harmless to the host. Now, a surprising discovery made in ribosomes may point the way to fighting fatal viral infections such as rabies.Tue, 20 Nov 2012 13:29:29 ESThttp://www.sciencedaily.com/releases/2012/11/121120132906.htmHow does antibiotic resistance spread? Scientists find answers in the nosehttp://www.sciencedaily.com/releases/2012/11/121120121835.htm Microbiologists studying bacterial colonization in mice have discovered how the very rapid and efficient spread of antibiotic resistance works in the respiratory pathogen, Streptococcus pneumoniae (also known as the pneumococcus). The team found that resistance stems from the transfer of DNA between bacterial strains in biofilms in the nasopharynx, the area just behind the nose.Tue, 20 Nov 2012 12:18:18 ESThttp://www.sciencedaily.com/releases/2012/11/121120121835.htmScientists identify inhibitor of myelin formation in central nervous systemhttp://www.sciencedaily.com/releases/2012/11/121120100155.htm Scientists have discovered another molecule that plays an important role in regulating myelin formation in the central nervous system. Myelin promotes the conduction of nerve cell impulses by forming a sheath around their projections, the so-called axons, at specific locations -- acting like the plastic insulation around a power cord.Tue, 20 Nov 2012 10:01:01 ESThttp://www.sciencedaily.com/releases/2012/11/121120100155.htm'Obese but happy gene' challenges the common perception of link between depression and obesityhttp://www.sciencedaily.com/releases/2012/11/121120084725.htm Scientists have uncovered evidence that the gene FTO ? the major genetic contributor to obesity ? is associated with an eight per cent reduction in the risk of depression.Tue, 20 Nov 2012 08:47:47 ESThttp://www.sciencedaily.com/releases/2012/11/121120084725.htmTelomere lengths predict life expectancy in the wild, research showshttp://www.sciencedaily.com/releases/2012/11/121119213144.htm Researchers have found that biological age and life expectancy can be predicted by measuring an individual's DNA. They studied the length of chromosome caps -- known as telomeres -- in a 320-strong wild population of Seychelles Warblers on a small isolated island.Mon, 19 Nov 2012 21:31:31 ESThttp://www.sciencedaily.com/releases/2012/11/121119213144.htmCancer: Some cells don't know when to stophttp://www.sciencedaily.com/releases/2012/11/121119171403.htm Certain mutated cells keep trying to replicate their DNA -- with disastrous results -- even after medications rob them of the raw materials to do so, according to new research.Mon, 19 Nov 2012 17:14:14 ESThttp://www.sciencedaily.com/releases/2012/11/121119171403.htmMultiple sclerosis ?immune exchange? between brain and blood is uncoveredhttp://www.sciencedaily.com/releases/2012/11/121119163301.htm DNA sequences obtained from a handful of patients with multiple sclerosis have revealed the existence of an ?immune exchange? that allows the disease-causing cells to move in and out of the brain.Mon, 19 Nov 2012 16:33:33 ESThttp://www.sciencedaily.com/releases/2012/11/121119163301.htm3-D light switch for the brain: Device may help treat Parkinson's, epilepsy; aid understanding of consciousnesshttp://www.sciencedaily.com/releases/2012/11/121119114249.htm A new tool for neuroscientists delivers a thousand pinpricks of light to individual neurons in the brain. The new 3-D "light switch", created by biologists and engineers, could one day be used as a neural prosthesis that could treat conditions such as Parkinson's and epilepsy by using gene therapy to turn individual brain cells on and off with light.Mon, 19 Nov 2012 11:42:42 ESThttp://www.sciencedaily.com/releases/2012/11/121119114249.htmBlood cancer gene BCL6 identified as a key factor for differentiation of nerve cells of cerebral cortexhttp://www.sciencedaily.com/releases/2012/11/121119093848.htm The cerebral cortex is the most complex structure in our brain and the seat of consciousness, emotion, motor control and language. In order to fulfill these functions, it is composed of a diverse array of nerve cells, called cortical neurons, which are affected by many neurological and neuropsychiatric diseases. Researchers have opened new perspectives on brain development and stem cell neurobiology by discovering a gene called BCL6 as a key factor in the generation of cortical neurons during embryonic brain development.Mon, 19 Nov 2012 09:38:38 ESThttp://www.sciencedaily.com/releases/2012/11/121119093848.htmMinority report: Insight into subtle genomic differences among our own cellshttp://www.sciencedaily.com/releases/2012/11/121118141530.htm Scientists have demonstrated that induced pluripotent stem cells -- the embryonic-stem-cell look-alikes whose discovery a few years ago won this year's Nobel Prize in medicine -- are not as genetically unstable as was thought.Sun, 18 Nov 2012 14:15:15 ESThttp://www.sciencedaily.com/releases/2012/11/121118141530.htmSkin cells reveal DNA's genetic mosaichttp://www.sciencedaily.com/releases/2012/11/121118141524.htm The prevailing wisdom has been that every cell in the body contains identical DNA. However, a new study of stem cells derived from the skin has found that genetic variations are widespread in the body's tissues, a finding with profound implications for genetic screening.Sun, 18 Nov 2012 14:15:15 ESThttp://www.sciencedaily.com/releases/2012/11/121118141524.htmLikely basis of birth defect causing premature skull closure in infants identifiedhttp://www.sciencedaily.com/releases/2012/11/121118141432.htm Geneticists, pediatricians, surgeons and epidemiologists have identified two areas of the human genome associated with the most common form of non-syndromic craniosynostosis premature closure of the bony plates of the skull.Sun, 18 Nov 2012 14:14:14 ESThttp://www.sciencedaily.com/releases/2012/11/121118141432.htmDNA packaging discovery reveals principles by which CRC mutations may cause cancerhttp://www.sciencedaily.com/releases/2012/11/121117184658.htm A new discovery concerning a fundamental understanding about how DNA works will produce a "180-degree change in focus" for researchers who study how gene packaging regulates gene activity, including genes that cause cancer and other diseases.Sat, 17 Nov 2012 18:46:46 ESThttp://www.sciencedaily.com/releases/2012/11/121117184658.htmHepatitis C treatment's side effects can now be studied in the labhttp://www.sciencedaily.com/releases/2012/11/121116161059.htm Adverse side effects of certain hepatitis C medications can now be replicated in the lab, thanks to a research team. The new method aids understanding of recent failures of hepatitis C antiviral drugs in some patients, and could help to identify medications that eliminate adverse effects. The findings may aid the development of safer and more effective treatments for hepatitis C and other pathogens such as SARS and West Nile virus.Fri, 16 Nov 2012 16:10:10 ESThttp://www.sciencedaily.com/releases/2012/11/121116161059.htmReconsidering cancer's bad guyhttp://www.sciencedaily.com/releases/2012/11/121116124644.htm Researchers have found that a protein, known for causing cancer cells to spread around the body, is also one of the molecules that trigger repair processes in the brain.Fri, 16 Nov 2012 12:46:46 ESThttp://www.sciencedaily.com/releases/2012/11/121116124644.htmGene distinguishes early birds from night owls and helps predict time of deathhttp://www.sciencedaily.com/releases/2012/11/121116124551.htm New research shows that a gene is responsible for a person's tendency to be an early riser or night owl -- and helps determine the time of day a person is most likely to die.Fri, 16 Nov 2012 12:45:45 ESThttp://www.sciencedaily.com/releases/2012/11/121116124551.htmClues to cause of kids' brain tumorshttp://www.sciencedaily.com/releases/2012/11/121116091226.htm Insights from a genetic condition that causes brain cancer are helping scientists better understand the most common type of brain tumor in children.Fri, 16 Nov 2012 09:12:12 ESThttp://www.sciencedaily.com/releases/2012/11/121116091226.htmArthritis study reveals why gender bias is all in the geneshttp://www.sciencedaily.com/releases/2012/11/121115210541.htm Researchers have pieced together new genetic clues to the arthritis puzzle in a study that brings potential treatments closer to reality and could also provide insights into why more women than men succumb to the disabling condition.Thu, 15 Nov 2012 21:05:05 ESThttp://www.sciencedaily.com/releases/2012/11/121115210541.htmClass of RNA molecules protects germ cells from damagehttp://www.sciencedaily.com/releases/2012/11/121115172255.htm Passing one's genes on to the next generation is a mark of evolutionary success. So it makes sense that the body would work to ensure that the genes the next generation inherits are exact replicas of the originals. Biologists have now identified one way the body does exactly that.Thu, 15 Nov 2012 17:22:22 ESThttp://www.sciencedaily.com/releases/2012/11/121115172255.htmQuick test speeds search for Alzheimer's drugs: Compound restores motor function and longevity to fruit flieshttp://www.sciencedaily.com/releases/2012/11/121115152655.htm Researchers report that an efficient, high-volume technique for testing potential drug treatments for Alzheimer's disease uncovered an organic compound that restored motor function and longevity to fruit flies with the disease.Thu, 15 Nov 2012 15:26:26 ESThttp://www.sciencedaily.com/releases/2012/11/121115152655.htmProtein-making machinery can switch gears with a small structural change process; Implications for immunity and cancer therapyhttp://www.sciencedaily.com/releases/2012/11/121115133414.htm For the past several years, research has focused on the intricate actions of an ancient family of catalytic enzymes that play a key role in translation, the process of producing proteins. In a new study, scientists have shown that this enzyme can actually also work in another fundamental process in humans.Thu, 15 Nov 2012 13:34:34 ESThttp://www.sciencedaily.com/releases/2012/11/121115133414.htmPlant derivative, tanshinones, protects against sepsis, study suggestshttp://www.sciencedaily.com/releases/2012/11/121115133312.htm Researchers have discovered that tanshinones, which come from the plant Danshen and are highly valued in Chinese traditional medicine, protect against the life-threatening condition sepsis.Thu, 15 Nov 2012 13:33:33 ESThttp://www.sciencedaily.com/releases/2012/11/121115133312.htmStructure of enzyme topoisomerase II alpha unravelled providing basis for more accurate design of chemotherapeutic drugshttp://www.sciencedaily.com/releases/2012/11/121115132903.htm Medical researchers have for the first time described the structure of the active site core of topoisomerase II alpha, an important target for anti-cancer drugs. The type II topoisomerases are important enzymes that are involved in maintaining the structure of DNA and chromosome segregation during both replication and transcription of DNA. One of these enzymes, topoisomerase II alpha, is involved in the replication of DNA and cell proliferation, and is highly expressed in rapidly dividing cancer cells.Thu, 15 Nov 2012 13:29:29 ESThttp://www.sciencedaily.com/releases/2012/11/121115132903.htmNewly discovered enzyme important in the spreading of cancerhttp://www.sciencedaily.com/releases/2012/11/121115132901.htm Enzyme hunters at UiO have discovered the function of an enzyme that is important in the spreading of cancer. Cancer researchers now hope to inhibit the enzyme.Thu, 15 Nov 2012 13:29:29 ESThttp://www.sciencedaily.com/releases/2012/11/121115132901.htmGenetics point to serious pregnancy complication, pre-eclampsiahttp://www.sciencedaily.com/releases/2012/11/121115132613.htm New research has revealed a genetic link in pregnant moms - and their male partners - to pre-eclampsia, a life-threatening complication during pregnancy.Thu, 15 Nov 2012 13:26:26 ESThttp://www.sciencedaily.com/releases/2012/11/121115132613.htmMolecular mechanisms underlying stem cell reprogramming decodedhttp://www.sciencedaily.com/releases/2012/11/121115132344.htm Thanks to some careful detective work, scientist better understand just how iPS cells form ? and why the Yamanaka process is inefficient, an important step to work out for regenerative medicine. The findings uncover cellular impediments to iPS cell development that, if overcome, could dramatically improve the efficiency and speed of iPS cell generation.Thu, 15 Nov 2012 13:23:23 ESThttp://www.sciencedaily.com/releases/2012/11/121115132344.htmSurprising genetic link between kidney defects and neurodevelopmental disorders in kidshttp://www.sciencedaily.com/releases/2012/11/121115132342.htm About 10 percent of kids born with kidney defects have large alterations in their genomes known to be linked with neurodevelopmental delay and mental illness, a new study has shown.Thu, 15 Nov 2012 13:23:23 ESThttp://www.sciencedaily.com/releases/2012/11/121115132342.htmEven moderate drinking in pregnancy can affect a child's IQhttp://www.sciencedaily.com/releases/2012/11/121114172833.htm Relatively small levels of exposure to alcohol while in the womb can influence a child's IQ, according to a new study using data from over 4,000 mothers and their children.Wed, 14 Nov 2012 17:28:28 ESThttp://www.sciencedaily.com/releases/2012/11/121114172833.htmGene nearly triples risk of Alzheimer's, international research team findshttp://www.sciencedaily.com/releases/2012/11/121114171710.htm A gene so powerful it nearly triples the risk of Alzheimer's disease has been discovered by an international team of researchers. It is the most potent genetic risk factor for Alzheimer's identified in the past 20 years.Wed, 14 Nov 2012 17:17:17 ESThttp://www.sciencedaily.com/releases/2012/11/121114171710.htmDiscovery could lead to faster diagnosis for some chronic fatigue syndrome caseshttp://www.sciencedaily.com/releases/2012/11/121114171708.htm For the first time, researchers have landed on a potential diagnostic method to identify at least a subset of patients with chronic fatigue syndrome - testing for antibodies linked to latent Epstein-Barr virus reactivation.Wed, 14 Nov 2012 17:17:17 ESThttp://www.sciencedaily.com/releases/2012/11/121114171708.htmResearch breakthrough could halt melanoma metastasis, study suggestshttp://www.sciencedaily.com/releases/2012/11/121114153227.htm In laboratory experiments, scientists have eliminated metastasis, the spread of cancer from the original tumor to other parts of the body, in melanoma by inhibiting a protein known as melanoma differentiation associated gene-9 (mda-9)/syntenin.Wed, 14 Nov 2012 15:32:32 ESThttp://www.sciencedaily.com/releases/2012/11/121114153227.htmPig genomes provide massive amount of genomic data for human healthhttp://www.sciencedaily.com/releases/2012/11/121114134512.htm Researchers provide a whole-genome sequence and analysis of number of pig breeds, including a miniature pig that serves a model for human medical studies and therapeutic drug testing.Wed, 14 Nov 2012 13:45:45 ESThttp://www.sciencedaily.com/releases/2012/11/121114134512.htmRare parasitic fungi could have anti-flammatory benefitshttp://www.sciencedaily.com/releases/2012/11/121114134054.htm Caterpillar fungi are rare parasites found on hibernating caterpillars in the mountains of Tibet. For centuries they have been highly prized as a traditional Chinese medicine - just a small amount can fetch hundreds of dollars.Wed, 14 Nov 2012 13:40:40 ESThttp://www.sciencedaily.com/releases/2012/11/121114134054.htmCancer therapy: Nanokey opens tumors to attackhttp://www.sciencedaily.com/releases/2012/11/121114113803.htm There are plenty of effective anticancer agents around. The problem is that, very often, they cannot gain access to all the cells in solid tumors. A new gene delivery vehicle may provide a way of making tracks to the heart of the target.Wed, 14 Nov 2012 11:38:38 ESThttp://www.sciencedaily.com/releases/2012/11/121114113803.htmHigh sperm DNA damage a leading cause of 'unexplained infertility', research findshttp://www.sciencedaily.com/releases/2012/11/121114113235.htm New research has uncovered the cause of infertility for 80 per cent of couples previously diagnosed with 'unexplained infertility': high sperm DNA damage.Wed, 14 Nov 2012 11:32:32 ESThttp://www.sciencedaily.com/releases/2012/11/121114113235.htmA risk gene for cannabis psychosishttp://www.sciencedaily.com/releases/2012/11/121114083928.htm The ability of cannabis to produce psychosis has long been an important public health concern. This concern is growing in importance as there is emerging data that cannabis exposure during adolescence may increase the risk of developing schizophrenia, a serious psychotic disorder. Further, with the advent of medical marijuana, a new group of people with uncertain psychosis risk may be exposed to cannabis.Wed, 14 Nov 2012 08:39:39 ESThttp://www.sciencedaily.com/releases/2012/11/121114083928.htmBacterial DNA sequence used to map an infection outbreakhttp://www.sciencedaily.com/releases/2012/11/121113214635.htm For the first time, researchers have used DNA sequencing to help bring an infectious disease outbreak in a hospital to a close. Researchers used advanced DNA sequencing technologies to confirm the presence of an ongoing outbreak of methicillin-resistant Staphylococcus aureus (MRSA) in a Special Care Baby Unit in real time. This assisted in stopping the outbreak earlier, saving possible harm to patients. This approach is much more accurate than current methods used to detect hospital outbreaks.Tue, 13 Nov 2012 21:46:46 ESThttp://www.sciencedaily.com/releases/2012/11/121113214635.htmGenetic variation may modify associations between low vitamin D levels and adverse health outcomeshttp://www.sciencedaily.com/releases/2012/11/121113161506.htm Findings from a study suggest that certain variations in vitamin D metabolism genes may modify the association of low serum 25-hydroxyvitamin D concentrations with health outcomes such as hip fracture, heart attack, cancer, and death.Tue, 13 Nov 2012 16:15:15 ESThttp://www.sciencedaily.com/releases/2012/11/121113161506.htmNew type of bacterial protection found within cells: Novel immune system response to infections discoveredhttp://www.sciencedaily.com/releases/2012/11/121113143656.htm Biologists have discovered that fats within cells store a class of proteins with potent antibacterial activity, revealing a previously unknown type of immune system response that targets and kills bacterial infections.Tue, 13 Nov 2012 14:36:36 ESThttp://www.sciencedaily.com/releases/2012/11/121113143656.htmGlutamate neurotransmission system may be involved with depression riskhttp://www.sciencedaily.com/releases/2012/11/121113134807.htm Researchers using a new approach to identifying genes associated with depression have found that variants in a group of genes involved in transmission of signals by the neurotransmitter glutamate appear to increase the risk of depression.Tue, 13 Nov 2012 13:48:48 ESThttp://www.sciencedaily.com/releases/2012/11/121113134807.htmTargeting downstream proteins in cancer-causing pathway shows promise in cell, animal modelhttp://www.sciencedaily.com/releases/2012/11/121113134230.htm The cancer-causing form of the gene Myc alters the metabolism of mitochondria, the cell?s powerhouse, making it dependent on the amino acid glutamine for survival. Depriving cells of glutamine selectively induces programmed cell death in cells overexpressing mutant Myc. Using Myc-active neuroblastoma cells, a team three priotein executors of the glutamine-starved cell, representing a downstream target at which to aim drugs. Roughly 25 percent of all neuroblastoma cases are associated with Myc-active cells.Tue, 13 Nov 2012 13:42:42 ESThttp://www.sciencedaily.com/releases/2012/11/121113134230.htmEven low-level radioactivity is damaging, scientists concludehttp://www.sciencedaily.com/releases/2012/11/121113134224.htm Even the very lowest levels of radiation are harmful to life, scientists have concluded, reporting the results of a wide-ranging analysis of 46 peer-reviewed studies published over the past 40 years. Variation in low-level, natural background radiation was found to have small, but highly statistically significant, negative effects on DNA as well as several measures of health.Tue, 13 Nov 2012 13:42:42 ESThttp://www.sciencedaily.com/releases/2012/11/121113134224.htmLoss of essential blood cell gene leads to anemiahttp://www.sciencedaily.com/releases/2012/11/121113122220.htm Scientists have discovered a new gene that regulates heme synthesis in red blood cell formation. Heme is the deep-red, iron-containing component of hemoglobin, the protein in red blood cells responsible for transporting oxygen in the blood. The findings promise to advance the biomedical community's understanding and treatment of human anemias and mitochondrial diseases, both known and unknown.Tue, 13 Nov 2012 12:22:22 ESThttp://www.sciencedaily.com/releases/2012/11/121113122220.htmWatching the developing brain, scientists glean clues on neurological disorderhttp://www.sciencedaily.com/releases/2012/11/121113122133.htm Researchers have tracked a gene's crucial role in orchestrating the placement of neurons in the developing brain. Their findings help unravel some of the mysteries of Joubert syndrome and other neurological disorders.Tue, 13 Nov 2012 12:21:21 ESThttp://www.sciencedaily.com/releases/2012/11/121113122133.htmSolving the mystery of aging: Longevity gene makes Hydra immortal and humans grow olderhttp://www.sciencedaily.com/releases/2012/11/121113091953.htm Why do we get older? When do we die and why? Is there a life without aging? For centuries, science has been fascinated by these questions. Now researchers have examined why the polyp Hydra is immortal -- and unexpectedly discovered a link to aging in humans.Tue, 13 Nov 2012 09:19:19 ESThttp://www.sciencedaily.com/releases/2012/11/121113091953.htm
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Public release date: 27-Nov-2012
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