Sunday, June 10, 2012

Nigeria police search for Lecce player Obodo

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Powerful quake shakes Greece's Rhodes island

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Saturday, June 9, 2012

German central bank ups growth forecast to 1 pct

BERLIN (AP) ? Germany's central bank is raising its 2012 economic growth forecast for the country to 1 percent, citing global growth and a boost to domestic demand from a healthy labor market and favorable financing conditions.

The Bundesbank's prediction Friday compared with its forecast last December of 0.6 percent growth in gross domestic product this year. It said the economy could grow by 1.6 percent in 2013, slightly below its previous prediction of 1.8 percent.

Germany's economy returned to healthy growth in this year's first quarter after a hiccup in late 2011. Its borrowing costs have sunk amid the eurozone debt crisis.

The Bundesbank cautions that its forecast comes with "exceptionally high uncertainty and risk" in view of the debt crisis and the possibility of slower growth outside Europe.

Associated Press

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Video: Wisdom from the class of 2012

Nightly?s annual commencement compilation features highlights from graduation ceremonies around the nation, and profiles students who are about to embark on the next phase of life after reaching an educational milestone. NBC?s Brian Williams reports.

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Friday, June 8, 2012

Egypt's army says ends deadlock on assembly

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GOP ignoring veto threat on medical tax repeal

WASHINGTON (AP) ? Shrugging off a veto threat, Republicans are ready to push legislation through the House repealing a tax on the producers of many medical devices sold in the United States.

GOP leaders scheduled a vote for Thursday, and with more than half the House sponsoring the measure its passage was ensured. Equally certain is its death in the Senate, where top Democrats say they won't even bring it up.

The 2.3 percent tax will be imposed on the makers of equipment used chiefly by doctors and hospitals, such as X-ray machines and replacement hips. Excluded would be goods easily bought by consumers like bandages and hearing aids. The tax takes effect in January.

Device manufacturers want to kill the tax before it kicks in. On Wednesday, more than 700 associations and companies, including AdvaMed and the Medical Device Manufacturers Association, the industry's chief trade groups, wrote to House leaders urging them to erase the tax.

"If this tax is not repealed, it will continue to force affected companies to consider cutting manufacturing operations, research and development, and employment levels to recoup the lost earnings due to the tax," they wrote.

The U.S. Chamber of Commerce also wrote to lawmakers in favor of repeal. They said the tax would "lead to increased health care costs, undercutting one of the primary goals of health care reform."

The tax was enacted in 2010 as part of President Barack Obama's health care overhaul to help pay for that law's massive expansion of coverage. Opposing the tax lets Republicans argue that they're trying to protect jobs and prevent a tax increase, while also attacking one of the financing legs of the health care law, which they oppose.

In their letter threatening a veto, White House officials argued that the health care law would give the medical device industry 30 million new potential customers who will gain health insurance. Industry officials deny that, saying the elderly patients who use many of their products are already covered by Medicare.

Repealing the tax would cost the government a projected $29 billion over the next decade.

The legislation has been combined with two other provisions. One would let people recover up to $500 from their tax-favored health flexible spending accounts if they don't use all the money for medical bills. They currently lose any unspent funds in such accounts.

The other would let people use money from some tax-advantaged health savings accounts for over-the-counter drugs.

The overall bill would cost $37 billion over 10 years.

It would be more than paid for by eliminating limits on the money the government could recover if it gives lower-earning people subsidies for buying health insurance that are higher than they ultimately qualify for. When that part of the health care law takes effect in two years, the subsidies will be paid in advance and the government estimates it will end up making billions of dollars in overpayments.

That provision would save a projected $44 billion for the government over the decade, meaning that overall the legislation would save $7 billion. White House officials say removing the limits on the subsidies the government recovers is essentially a tax increase and that it would discourage people from signing up for coverage.

In its letter, White House officials wrote that the bill "would fund tax breaks for industry by raising taxes on middle-class and low-income families."

Associated Press

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Thursday, June 7, 2012

New brain target for appetite control identified

ScienceDaily (June 7, 2012) ? Researchers at Columbia University Medical Center (CUMC) have identified a brain receptor that appears to play a central role in regulating appetite. The findings, published June 7 in the online edition of Cell, could lead to new drugs for preventing or treating obesity.

"We've identified a receptor that is intimately involved in regulating food intake," said study leader Domenico Accili, MD, professor of Medicine at CUMC. "What is especially encouraging is that this receptor is belongs to a class of receptors that turn out to be good targets for drug development, making it a highly 'druggable' target. In fact, several existing medications already seem to interact with this receptor. So, it's possible that we could have new drugs for obesity sooner rather than later."

In their search for new targets for obesity therapies, scientists have focused on the hypothalamus, a tiny brain structure that regulates appetite. Numerous studies suggest that the regulatory mechanism is concentrated in neurons that express a neuropeptide, or brain modulator, called AgRP. But the specific factors that influence AgRP expression are not known.

The CUMC researchers found new clues to appetite control by tracing the actions of insulin and leptin. Both hormones are involved in maintaining the body's energy balance, and both are known to inhibit AgRP. "Surprisingly, blocking either the insulin or leptin signaling pathway has little effect on appetite," says Dr. Accili. "We hypothesized that both pathways have to be blocked simultaneously in order to influence feeding behavior."

To test their hypothesis, the researchers created a strain of mice whose AgRP neurons lack a protein that is integral to both insulin and leptin signaling. As the researchers hypothesized, removing this protein -- Fox01 -- had a profound effect on the animals' appetite. "Mice that lack Fox01 ate less and were leaner than normal mice," said lead author Hongxia Ren, PhD, associate research scientist in Medicine. "In addition, the Fox01-deficient mice had better glucose balance and leptin and insulin sensitivity -- all signs of a healthier metabolism."

Since Fox01 is a poor drug target, the researchers searched for other ways to inhibit the action of this protein. Using gene-expression profiling, they found a gene that is highly expressed in mice with normal AgRP neurons but is effectively silenced in mice with Fox01-deficient neurons. That gene is Gpr17 (for G-protein coupled receptor 17), which produces a cell-surface receptor called Gpr17.

To confirm that the receptor is involved in appetite control, the researchers injected a Gpr17 activator into normal mice, and their appetite increased. Conversely, when the mice were given a Gpr17 inhibitor, their appetite decreased. Similar injections had no effect on Fox01-deficient mice.

According to Dr. Accili, there are several reasons why Gpr17, which is also found in humans, would be a good target for anti-obesity medications. Since Grp17 is part of the so-called G-protein-coupled receptor family, it is highly druggable. About a third of all existing drugs work through G-protein-coupled receptors. In addition, the receptor is abundant in AgRP neurons but not in other neurons, which should limit unwanted drug side effects.

Dr. Accili and Dr. Ren's paper is titled, "G protein-coupled purinergic receptor GPR17 mediates orexigenic effects of FoxO1 in AgRP neurons." The other contributors are Ian J. Orozco (CUMC), Ya Su (Albert Einstein College of Medicine, Bronx, NY), Shigetomo Suyama (Yale University School of Medicine), Roger Guti?rrez-Ju?rez (Einstein), Tamas L. Horvath (Yale), Sharon L. Wardlaw (CUMC), Leona Plum (CUMC), and Ottavio Arancio (CUMC).

The study was supported by grants from the National Institutes of Health (DK58282, DK57539, DK80003, DK45024, NS49442, and DK63608).

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Story Source:

The above story is reprinted from materials provided by Columbia University Medical Center, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Hongxia Ren, Ian?J. Orozco, Ya Su, Shigetomo Suyama, Roger Guti?rrez-Ju?rez, Tamas?L. Horvath, Sharon?L. Wardlaw, Leona Plum, Ottavio Arancio, Domenico Accili. FoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake. Cell, 2012; 149 (6): 1314 DOI: 10.1016/j.cell.2012.04.032

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

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

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