HBT: Wrapping up all the arbitration settlements

old TV

It?s that time of year: the time when (a) ESPN announces its Sunday Night Baseball schedule, filled with the Yankees, the Red Sox and other big market teams; and (b) people complain about ESPN?s big market and/or east coast bias. And yes, in an ideal world everyone should get a turn in the spotlight and?

Source: http://hardballtalk.nbcsports.com/

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CTS awarded accelerator pedal module production programs in Chinese market

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News Breaks

January 18, 2012

09:05 EDTCTS
theflyonthewall.com: CTS awarded accelerator pedal module production programs in Chinese market
CTS announced that CTS Automotive Products has been awarded two new production programs for its Electronic Throttle Control Accelerator Pedal Modules from Japanese and Chinese vehicle manufacturers. Both awards represent new programs for vehicles sold into the growing China market, and will result in an increase in CTS' global market share. The pedal modules will be used on both a compact car and a multi-purpose vehicle. Deliveries will begin in late 2012 and will be manufactured in CTS' Zhongshan, China facility. Total revenues from these awards are expected to reach approximately $10M over the anticipated five-year lives of the programs. These programs further strengthen CTS' position with key existing customers and continue to enhance CTS' share of the rapidly growing Asian markets. :theflyonthewall.com

News For CTS From The Last 14 Days

Check below for free stories on CTS the last two weeks.

There is 1 item on the Fly with pertinent information.
Sign up for a free trial to see the rest of the stories you've been missing.

January 18, 2012

09:05 EDTCTS

Source: http://www.theflyonthewall.com/permalinks/entry.php/CTSid1560740/CTS-CTS-awarded-accelerator-pedal-module-production-programs-in-Chinese-market

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Video: NBA Star Steven Jackson: Whats A Lockout Photoshoot

Shiite and Sunni: What are the differences?

Sectarian tensions are flaring in Iraq with the suicide bombing of a Shiite religious procession Saturday that killed at least 53 people and a ruling by an Iraqi court today that the country's Sunni vice president must stand trial in the capital. The procession was commemorating Arbaeen,?one of the major holidays in the Shiite calendar.?The festival comes at a time of stridently sectarian politics in Iraq, with the Shiite-led government of Nouri al-Maliki at loggerheads with the Sunni-backed minority in the parliament.?

We take a look at the differences ? and similarities ? between Sunni and Shiite below.

- Dan Murphy,?Staff Writer

Both sects are Muslim. They believe the Koran is the direct word of God, passed down to the prophet Muhammad in a series of revelations before his death. They pray in the direction of Mecca, and share the same dietary and general social restrictions.

Their schism lies in disputes over who would succeed Muhammad as leader of the faithful after his death in 632. The Shiites thought the prophet?s son-in-law and cousin should lead as caliph, particularly given his blood relationship to Muhammad. Their opponents, the Sunnis, thought Abu Bakr, one of Mohammad?s first converts, should be their leader.

The Shiites lost a series of wars for power in the early years of Islam and today are the clear minority in global Islam, making up about 15 percent of adherents. They are in the majority in Iraq and Iran.

Source: http://rss.csmonitor.com/~r/feeds/csm/~3/7R3X2MpKy_Q/Shiite-and-Sunni-What-are-the-differences

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Markets up on hopes IMF will get more money

Passers-by are reflected on an electronic stock board displaying the U.S. dollar's quotation against the Japanese yen at a securities firm in Tokyo, Tuesday, Jan 17, 2012. (AP Photo/Koji Sasahara)

Passers-by are reflected on an electronic stock board displaying the U.S. dollar's quotation against the Japanese yen at a securities firm in Tokyo, Tuesday, Jan 17, 2012. (AP Photo/Koji Sasahara)

(AP) ? Markets advanced further Wednesday on hopes the International Monetary Fund would get more money and as Greece resumes discussions with private creditors to get them to agree to reduce the value of their holdings of Greek debt.

Following a breakdown of talks last Friday, investors remain nervous about what may happen, though sentiment has been shored up somewhat by comments made late Tuesday from Christine Lagarde, the International Monetary Fund's managing director, that the Washington D.C.-based institution was looking at ways to increase its financial firepower, partly to deal with Europe's debt crisis.

If the IMF were to have its resources ramped up by governments raising their contributions, then it would have more money available to potentially help Europe in dealing with its debt woes.

"More resources means more liquidity which I guess is good for asset prices in the short term, or at least reduces threat of systemic risk in the interim," said Neil MacKinnon, global macro strategist at VTB Capital.

Europe's debt crisis started in Greece over two years ago and investors will be looking to see if the country can negotiate a deal with its creditors that will ease the burden of its crushing debts.

Last October, Greece's partners in the eurozone sanctioned a deal whereby Greece's creditors agree to take a cut in the value of their Greek bond holdings to help lighten the country's debt burden. The deal with private investors, known as the Private Sector Involvement, or PSI, aims to reduce Greece's debt by euro100 billion ($127.9 billion) by swapping private creditors' bonds for new ones with a lower value. It is a key part of a euro130 billion international bailout, the second one for Greece.

Without a deal with its private creditors, Greece has been told it won't get the next installment of money due from its first bailout. Without that money, Greece would be unable to pay a big bond redemption in March, potentially triggering a chain of events that could derail the global economic recovery and cause financial mayhem in Europe.

"All eyes will once again be on Greece today as talks restart with the IIF today on the voluntary restructuring of the debt with private creditors," said Michael Hewson, markets analyst at CMC Markets.

In Europe, the CAC-40 in France was up 0.4 percent at 3,284 while Germany's DAX rose 0.5 percent to 6,365. The FTSE 100 index of leading British shares was steady at 5,695.

In the currency markets, the euro remained well-supported as it rebounded off 17-month dollar lows. It was trading 0.7 percent higher at $1.2832.

Wall Street was poised for a steady open later though a run of economic data may well alter expectations ? Dow futures were up 0.4 percent at 12,469 while the broader Standard & Poor's 500 futures rose 0.5 percent to 1,295.

Earlier Asian stock markets largely continued their recent advance. Japan's Nikkei 225 index rose 1 percent to close at 8,550.58 while Hong Kong's Hang Seng added 0.3 percent to 19,686.92.

However, mainland Chinese shares fell on profit-taking after a brisk day of trade Tuesday that saw the biggest gains in 27 months. The Shanghai Composite Index lost 1.4 percent to 2,266.38, while the Shenzhen Composite Index dropped 2.7 percent to 837.40.

Investors cheered Tuesday's news out of China that the world's second-largest economy slowed less dramatically in the fourth quarter than feared ? but still enough of a slowdown to persuade investors that Beijing will pursue a pro-growth monetary policy.

"People have been buying stocks in anticipation of a relaxation in monetary policy by the Chinese government," said Derek Cheung, chief investment officer at Neutron INV Partners Ltd. in Hong Kong. "The market expects this around Chinese New Year. If China doesn't loosen around the new year, the market may come under pressure." The holiday begins Jan. 23.

With Europe seemingly sliding back toward recession and the U.S. recovery still fairly moderate by historical standards, China's performance is important to shore up the global economy and market sentiment, especially when investors are fretting about a potential Greek default that could further roil financial markets.

The World Bank was the latest organization to issue a warning about the global economy. In an economic update, the Washington D.C.-based international organization cut its growth forecast for developing countries this year to 5.4 percent from 6.2 percent and for developed countries to 1.4 percent from 2.7 percent. For the 17 countries that use the euro currency, it forecast a 0.3 percent from the previous estimate of 1.8 percent growth.

Despite the World Bank's warning, oil prices remain supported on China's positive growth news ? benchmark crude for February delivery was up 57 cents at $101.28 a barrel.

___

Pamela Sampson in Bangkok contributed to this report.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/f70471f764144b2fab526d39972d37b3/Article_2012-01-18-World-Markets/id-ff571ed39ae544f1ae3cd81071639578

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Things to read on my other blog: #scio12 preparations, truthiness at NYT, and an interview with a chloroplast.

For those of you who mostly follow my writing here on ?Doing Good Science,? I thought I should give you a pointer to some things I?ve posted so far this month (which is almost half-over already?!) on my other blog, ?Adventures in Ethics and Science?. Feel free to jump in to the discussions in the comments over there. Or, if you prefer, go ahead and discuss them here.

The month kicked off with a bunch of posts looking forward to ScienceOnline 2012, which is next week. First, on the issue of what to pack:

Packing for #scio12: plague relief.
Packing for #scio12: what are you drinking?
Packing for #scio12: sharing space with others.
Packing for #scio12: plumbing the inky depths.

Then, a discussion of what?s special about an unconference: Looking ahead to #scio12: the nature of the unconference. In this post, I put a call out for contributions to the wikis for the two sessions I?ll be helping to moderate: one (with Amy Freitag) on ?Citizens, experts, and science?, the other (with Christie Wilcox) on ?Blogging Science While Female?. Those wiki pages are just calling out for ideas, questions, or useful links. (Your ideas, questions, or useful links! What are you waiting for?)

After that, my response to a recent blog post by the New York Times?s Public Editor: Straightforward answers to questions we shouldn?t even have to ask: New York Times edition.

Finally, courtesy of my elder offspring, Friday Sprog Blogging: Interview with a Chloroplast..

Source: http://rss.sciam.com/click.phdo?i=a67d16672d01c84b0ff0f64ca8e7dac6

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Defective cell 'battery' plays central role in neurodegenerative disease

[ Back to EurekAlert! ] Public release date: 17-Jan-2012
[ | E-mail | Share Share ]

Contact: Anita Kar
anita.kar@mcgill.ca
514-398-3376
McGill University

A devastating neurodegenerative disease that first appears in toddlers just as they are beginning to walk has been traced to defects in mitochondria, the 'batteries' or energy-producing power plants of cells. This finding by a team of researchers, led by investigators from the Montreal Neurological Institute and Hospital The Neuro- at McGill University, was published in this week's issue of the Proceedings of the National Academy of Sciences of the USA (PNAS). The research, which was highlighted as "Novel & Newsworthy" by the American Society for Cell Biology (ASCB), significantly increases understanding of the disease and reveals an important common link with other neurodegenerative diseases, providing renewed hope and potential new therapeutic strategies for those affected around the world.

The disorder, Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS), primarily affects the cerebellum, a centre for movement coordination in the brain. ARSACS was first identified in the late 1970s in a large group of patients from the Charlevoix and Saguenay regions of Quebec. The incidence of ARSACS in this 'founder' population is 1 in 1,500-2,000 births, with a high carrier rate of 1 in 23. ARSACS strikes at an early age. Symptoms, which worsen over time, include poor motor coordination, spastic stiffness, muscle wasting, uncoordinated eye movements and slurred speech. Most patients with the disease are wheelchair-bound by their early 40s and have a reduced life expectancy. ARSACS is not unique to French-Canada as scientists have now found over 100 separate mutations in people worldwide including Japan, Turkey and across Western Europe.

"This finding is the first important advancement in the 10 years since the identification of the mutated gene because it gives an indication of the underlying cellular mechanism of the disease," says Dr. Bernard Brais, neurologist at The Neuro, "and is a vital first step towards developing therapeutic strategies for ARSACS." In 2000, scientists identified the gene associated with the disease, called SACS, which produces a massive 4,579 amino acid protein called sacsin, but until now the role or the function of the sacsin protein has been unknown. The multi-institutional collaborative research led by Dr. Brais and Dr. Peter McPherson at The Neuro as well as Dr. Paul Chapple at Queen Mary, University of London indicates that that the sacsin protein has a mitochondrial function, and that mutations causing ARSACS are linked to a dysfunction of mitochondria in neurons.

"By studying neurons in culture as well as in knockout mice (which do not produce sacsin), the team found that loss of the sacsin protein results in abnormally shaped and poorly functioning mitochondria," says Dr. Peter McPherson, researcher at The Neuro. This disruption led to defective changes in the neurons and eventual death of the neurons. In the knockout mice, these disruptions led to neuron death specifically in the cerebellum, suggesting that this is the basis for the neurodegenerative impairments suffered by ARSACS patients.

"Mitochondrial dysfunction has also been identified in major neurodegenerative diseases such as Parkinson, Alzheimer, and Huntington diseases," says Dr. McPherson. "This common link means that research being done on a large-scale on these other diseases may prove critically informative to rarer neurological diseases such as ARSACS, and the inverse may be true, our findings may be fundamental to the study and treatment of other neurodegenerative diseases."

###

This research was funded by the Fondation de l'Ataxie de Charlevoix-Saguenay (arsacs.com), created by Sonia Gobeil and Jean Groleau whose two children are affected by this orphan disease. The mission of the foundation is to increase public awareness of the disease and raise funds for research to find a treatment. Support for this study was also provided by the Neuromuscular Research Partnership Program of the Canadian Institutes of Health Research and the UK Medical Research Council. The study was presented at the annual meeting of the American Society for Cell Biology (ASCB) where it was selected for inclusion in the ASCB Press Book as a "Novel & Newsworthy" presentation, and was also highlighted by Nature news blog.

The Montreal Neurological Institute and Hospital

The Montreal Neurological Institute and Hospital The Neuro, is a unique academic medical centre dedicated to neuroscience. The Neuro is a research and teaching institute of McGill University and forms the basis for the Neuroscience Mission of the McGill University Health Centre. Founded in 1934 by the renowned Dr. Wilder Penfield, The Neuro is recognized internationally for integrating research, compassionate patient care and advanced training, all key to advances in science and medicine. Neuro researchers are world leaders in cellular and molecular neuroscience, brain imaging, cognitive neuroscience and the study and treatment of epilepsy, multiple sclerosis and neuromuscular disorders. The Montreal Neurological Institute was named as one of the Seven Centres of Excellence in Budget 2007, which provided the MNI with $15 million in funding to support its research and commercialization activities related to neurological disease and neuroscience



[ Back to EurekAlert! ] [ | E-mail | Share 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.


[ Back to EurekAlert! ] Public release date: 17-Jan-2012
[ | E-mail | Share Share ]

Contact: Anita Kar
anita.kar@mcgill.ca
514-398-3376
McGill University

A devastating neurodegenerative disease that first appears in toddlers just as they are beginning to walk has been traced to defects in mitochondria, the 'batteries' or energy-producing power plants of cells. This finding by a team of researchers, led by investigators from the Montreal Neurological Institute and Hospital The Neuro- at McGill University, was published in this week's issue of the Proceedings of the National Academy of Sciences of the USA (PNAS). The research, which was highlighted as "Novel & Newsworthy" by the American Society for Cell Biology (ASCB), significantly increases understanding of the disease and reveals an important common link with other neurodegenerative diseases, providing renewed hope and potential new therapeutic strategies for those affected around the world.

The disorder, Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS), primarily affects the cerebellum, a centre for movement coordination in the brain. ARSACS was first identified in the late 1970s in a large group of patients from the Charlevoix and Saguenay regions of Quebec. The incidence of ARSACS in this 'founder' population is 1 in 1,500-2,000 births, with a high carrier rate of 1 in 23. ARSACS strikes at an early age. Symptoms, which worsen over time, include poor motor coordination, spastic stiffness, muscle wasting, uncoordinated eye movements and slurred speech. Most patients with the disease are wheelchair-bound by their early 40s and have a reduced life expectancy. ARSACS is not unique to French-Canada as scientists have now found over 100 separate mutations in people worldwide including Japan, Turkey and across Western Europe.

"This finding is the first important advancement in the 10 years since the identification of the mutated gene because it gives an indication of the underlying cellular mechanism of the disease," says Dr. Bernard Brais, neurologist at The Neuro, "and is a vital first step towards developing therapeutic strategies for ARSACS." In 2000, scientists identified the gene associated with the disease, called SACS, which produces a massive 4,579 amino acid protein called sacsin, but until now the role or the function of the sacsin protein has been unknown. The multi-institutional collaborative research led by Dr. Brais and Dr. Peter McPherson at The Neuro as well as Dr. Paul Chapple at Queen Mary, University of London indicates that that the sacsin protein has a mitochondrial function, and that mutations causing ARSACS are linked to a dysfunction of mitochondria in neurons.

"By studying neurons in culture as well as in knockout mice (which do not produce sacsin), the team found that loss of the sacsin protein results in abnormally shaped and poorly functioning mitochondria," says Dr. Peter McPherson, researcher at The Neuro. This disruption led to defective changes in the neurons and eventual death of the neurons. In the knockout mice, these disruptions led to neuron death specifically in the cerebellum, suggesting that this is the basis for the neurodegenerative impairments suffered by ARSACS patients.

"Mitochondrial dysfunction has also been identified in major neurodegenerative diseases such as Parkinson, Alzheimer, and Huntington diseases," says Dr. McPherson. "This common link means that research being done on a large-scale on these other diseases may prove critically informative to rarer neurological diseases such as ARSACS, and the inverse may be true, our findings may be fundamental to the study and treatment of other neurodegenerative diseases."

###

This research was funded by the Fondation de l'Ataxie de Charlevoix-Saguenay (arsacs.com), created by Sonia Gobeil and Jean Groleau whose two children are affected by this orphan disease. The mission of the foundation is to increase public awareness of the disease and raise funds for research to find a treatment. Support for this study was also provided by the Neuromuscular Research Partnership Program of the Canadian Institutes of Health Research and the UK Medical Research Council. The study was presented at the annual meeting of the American Society for Cell Biology (ASCB) where it was selected for inclusion in the ASCB Press Book as a "Novel & Newsworthy" presentation, and was also highlighted by Nature news blog.

The Montreal Neurological Institute and Hospital

The Montreal Neurological Institute and Hospital The Neuro, is a unique academic medical centre dedicated to neuroscience. The Neuro is a research and teaching institute of McGill University and forms the basis for the Neuroscience Mission of the McGill University Health Centre. Founded in 1934 by the renowned Dr. Wilder Penfield, The Neuro is recognized internationally for integrating research, compassionate patient care and advanced training, all key to advances in science and medicine. Neuro researchers are world leaders in cellular and molecular neuroscience, brain imaging, cognitive neuroscience and the study and treatment of epilepsy, multiple sclerosis and neuromuscular disorders. The Montreal Neurological Institute was named as one of the Seven Centres of Excellence in Budget 2007, which provided the MNI with $15 million in funding to support its research and commercialization activities related to neurological disease and neuroscience



[ Back to EurekAlert! ] [ | E-mail | Share 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.


Source: http://www.eurekalert.org/pub_releases/2012-01/mu-dc011712.php

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Stop it Mr. President -- Quit Giving Our Money Away (ContributorNetwork)

COMMENTARY | When will the insanity stop? One day after President Barack Obama asked Congress for yet another increase in the debt limit so the federal government can continue to borrow money to stay solvent; he then offers to give Bangladesh another free billion dollars.

Reuters reported another $1 billion in aid was offered to the impoverished Asian country over five years to help alleviate hunger and malnutrition, as well as assist in family planning. There is little doubt Bangladesh needs help, but the U.S. has already provided nearly $6 billion in developmental assistance.

This is absolute craziness. The federal government is well over $15 trillion in debt -- all of which have been borrowed on the backs of current and future taxpayers and yet our government continues to pass it out to other countries without hardly a mere consideration for how Americans might feel about that. The people of Bangladesh need help -- they have always needed more help than any one nation can provide.

While the U.S. is a land of plenty, that "plenty" comes at a cost. The cost is too high anymore. We cannot continue to pass out aid to every cause or need. The need is too big. The wallet has run dry.

It is unconceivable that any American president would consider passing out aid with the financial conditions the U.S. is currently in. Not two months ago Congress missed a statutory deadline to strip money from the budget over a 10-year period. They couldn't do it.

Just one day ago, The Washington Post reported Obama asked for a $1.2 trillion increase in borrowing authority for the Treasury. The madness must stop and maybe it's time for ordinary Americans to cry "Enough already!" in the face of every elected official.

There are people suffering all around the world. The need is so great that no one nation -- no matter how mighty its economy may be -- can possibly meet the need. There are needs here too. Our inner cities are falling apart. Food stamp recipients are at an all time high. There has to be a time when the answer is "no."

Source: http://us.rd.yahoo.com/dailynews/rss/obama/*http%3A//news.yahoo.com/s/ac/20120115/pl_ac/10836331_stop_it_mr_president__quit_giving_our_money_away

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