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Friday, June 29, 2012

Pinakes-zografikis Blog ? Have you considered that you might ...

Men are very sensitive about their sexual issues and usually they find it difficult to even talk to their doctors or partners about it. But if a problem does exist, then pretending to ignore it will not help. In fact it can make the situation even worse. There are many cases of men?s sex health problems becoming worse simply because they were not dealt with at the right time. To save you from all that trouble, you have the option of a male enhancement pill like Vimax. Vimax pills are developed from very natural herbs which have no side effects. The male enhancement factor in these pills improves not bring about male enhancement but also brings other effective solutions for men?s sexual health. You will have more sexual desire and a lot more strength. Your erections will become stronger and you will be relieved from erectile dysfunction problems.

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Source: http://pinakes-zografikis.info/?p=6720

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Tax, Finance, CE, CPE, EA, CPA, CFP Blog: Accounting Expertise ...

Taxpayers with rental property often turn to accountants for help in translating complex IRS rules into accurate tax reporting. Property owners usually think that any money they spend to fix a real estate unit is a tax-deductible expense. Accountants who study for CPA exam completion know better. Some fix up costs are indeed repair expenses but others are depreciable capital costs. This is the frequently confusing area of repair regulations that’s addressed in CPA study materials. The subject actually covers the tax deduction of both repairs and maintenance costs. IRS scrutiny is drawn to tax reporting that shows a substantial amount of repair costs for a single property. This is a consequence of larger outlays typically signaling capital improvements rather than repairs. The IRS has attempted to tackle this issue on several occasions. Most recently, temporary regulations were issued at the end of 2008. In addition, proposed new regulations further confront the matter by introducing new interpretations. Because the concept of expensed repair versus depreciable capital cost is common for all property owners, this topic is crucial for CPA review classes. Significant elements to define include what constitutes a property improvement and a specific property unit. Tax accountants are asked to relieve taxpayer struggles with understanding these issues. For example, one general rule is that a larger property ??" such as a commercial building ??" usually results in the likelihood of deductible repairs even when the amount is fairly high. Conversely, most CPA exam questions that refer to small units of property with high expenditures are usually describing capital improvements. The new IRS rules define a single building as a unit of property. Therefore, structural changes to one office in the building are probably repair expenses. An expenditure is treated as a capital improvement when it affects the entire building. This means that plumbing changes to one office are normally expensed while adjustments to the building’s plumbing system are capitalized improvements. The new regulations identify each system that performs a discrete and major function as a unit of property. Also clarified in the new regulations are three tests for expenditures. Costs are capitalized when they cause either “betterment”, “restoration”, or “adaptation” for a unit of property. This causes accountants to resort to the process of evaluating the facts and circumstances of each case. Consequently, a taxpayer’s detailed record of expenditures is extremely important. That is particularly true when multiple payments are made for a common project. Accountants engaged in tax work can expect to spend plenty of time investigating the specifics surrounding costs for materials, parts, and mass purchases of these items. Fortunately, they will already develop a sound foundation in this subject in order to pass CPA exam requirements. IRS Circular 230 Disclosure Pursuant to the requirements of the Internal Revenue Service Circular 230, we inform you that, to the extent any advice relating to a Federal tax issue is contained in this communication, including in any attachments, it was not written or intended to be used, and cannot be used, for the purpose of (a) avoiding any tax related penalties that may be imposed on you or any other person under the Internal Revenue Code, or (b) promoting, marketing or recommending to another person any transaction or matter addressed in this communication.

Source: http://fastforwardacademy.blogspot.com/2012/06/accounting-expertise-embodied-in.html

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GEDI chip sorts prostate cancer cells

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Posted: Jun 28th, 2012

Posted: Jun 27th, 2012

Posted: Jun 26th, 2012

Posted: Jun 27th, 2012
GEDI chip sorts prostate cancer cells
(Nanowerk News) The future of prostate cancer therapy may lie in a tiny, "sticky" silicon chip dubbed GEDI (Geometrically Enhanced Differential Immunocapture, pronounced like the "Star Wars" forces of good) that can identify and collect cancer cells from a patient's bloodstream.
A team of researchers at Weill Cornell Medical College in New York City and Cornell's College of Engineering in Ithaca has built the chip into a device that captures an unprecedentedly high concentration of rare cancer cells from metastatic prostate cancer patients for a quick, noninvasive analysis to determine the efficacy of the patients' current chemotherapy. The ability to collect a relatively pure sample of circulating tumor cells (CTCs) may also enable research to better understand the biology of metastasis and develop new treatments, the researchers said.

The "sticky" square patch (middle) of the GEDI device contains the purest collection of circulating tumor cells in the blood. The rest of the blood cells are discarded in the capsule.
Their work is described in a paper in the April 2012 issue of the journal PLoS ONE ("Functional Characterization of Circulating Tumor Cells with a Prostate-Cancer-Specific Microfluidic Device"), and was announced in a press conference at Weill by Brian Kirby, associate professor of mechanical and aerospace engineering; David Nanus, M.D., the Mark W. Pasmantier Professor of Hematology and Oncology in Medicine; and Evi Giannakakou, associate professor of pharmacology. The team includes 12 other researchers from both campuses.
Metastatic cancer is cancer that has spread from the place where it first started -- in this case, the prostate -- to another place in the body, most commonly the lungs, bones and liver. Metastasis accounts for the majority of cancer-related deaths.
"We need to be able to match the drug to the patient and the tumor," said Nanus. But tumor cells habitually mutate and develop a resistance to a previously effective therapy. In the case of prostate cancer, three drugs are in common use, but the most effective one varies with the patient and the particular cancer.
Metastasis is believed to be caused by cells that detach from the primary prostate tumor, circulate in the bloodstream and seed new tumors. Extensive clinical research shows that a reliable CTC count is a strong predictor of overall survival in metastatic prostate cancer patients. However, since the incidence of CTCs can be very small -- one CTC per 100 million blood cells -- pure CTC capture is difficult.
"This really is a needle in a haystack," Kirby emphasized.

On the GEDI chip, blood flows through an array of posts just a few millionths of a meter in diameter, coated with antibodies that stick to cancer cells. Each row of posts is offset from the one before by a distance that causes the larger cancer cells to collide with them - and stick on - more often, while other cells in the blood flow smoothly past
Cell-capture devices now in use contain antibodies that bind to an antigen found on the surface of nearly all malignant prostate cancer cells. But these antibodies also bind to other cells in the bloodstream and can collect a highly impure sample.
On the GEDI chip, a milliliter (mL, one-thousandth of a liter) of blood is pumped through a nanoscale channel filled with tiny posts just a few microns (millionths of a meter) in diameter, coated with antibodies. Successive rows of posts are offset in a carefully calculated way so that only cells larger than 15 microns will collide with the posts and stick to them, while most smaller cells flow smoothly around them.
"Most cancer cells are bigger and more rigid than normal cells, so it's about tricking these cancer cells into colliding with the sticky walls," Kirby explained.
After the test the chip is removed from the device and the captured cells extracted for analysis. In an experiment with a blood sample containing 200 mL of CTCs and 5 billion blood cells, the device captured a whopping 170mL of CTCs and only 91mL of irrelevant blood cells.
The GEDI device is scheduled to go into clinical trial this year. Meanwhile, the researchers are actively working on detectors for breast, ovarian and pancreatic cancers.
The research is one of several joint Ithaca-New York City projects associated with the Cornell Center for Microenvironment and Metastasis, a $13 million National Institutes of Health-funded Physical Sciences-Oncology Center created to use physical techniques and processes to improve understanding and care of metastatic cancer in patients.

Source: http://www.nanowerk.com/news/newsid=25741.php

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Chinese Exporters Now Cling to Dollars

BY LINGLING WEI

BEIJING?Many Chinese exporters are starting to hoard the dollars they earn, betting that the yuan is unlikely to appreciate much more, a shift in strategy that is having a ripple effect throughout the country's financial system.

Until recently, Chinese exporters like state-owned Huihong International Group and privately held Saijia Co. had rushed to sell their dollar earnings to banks as soon as they got paid, in exchange for the appreciating yuan. Now, because the Chinese currency no longer seems certain to rise, those companies are holding their dollars for as long as they can.

"In the past, we would exchange ...

BY LINGLING WEI

"In the past, we would exchange ...

Source: http://online.wsj.com/article/SB10001424052702304830704577493190295498890.html?mod=rss_asia_whats_news

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PowerA Moga Android Game Controllers Hands-On: Mount Your Tablet or Phone

With Android becoming a more powerful and popular mobile gaming platform, there?s one obvious question: where are all the controllers? Sure you could use a PC a PC game controller on an Android tablet, but they don?t always work well because they weren?t necessarily built for Android.

Enter PowerA and its upcoming line of Moga-branded controllers, which the company claims will be the first controllers built from the ground up for Google?s mobile operating system. There are other devices out there like Gamestop?s Android controller, but PowerA has a developer kit that?s made to work well with Android and the company was at Google I/O this week seeking out developers who are willing to add Moga support to their apps.

More important from a user perspective, the company has two controllers coming out that will allow you to securely mount your smartphone or tablet right on top of them. The regular Moga has two analog sticks, several buttons and dual triggers in front. Its mount supports smartphones up to five inches in size as a PowerA rep explained that the company was able to securely attach a Samsung Galaxy note.?

The slightly larger Moga Pro can mount devices up to 7-inches in size as the company demonstrated by attaching a Nexus 7 tablet. It has a much more PlayStation-like appearance with more buttons and larger analog sticks. Both Mogas will be available in the fall, with the regular Moga launching a few weeks before the Pro. PowerA has not released pricing, but says the products will be affordable.

We had a chance to watch both the regular Moga and the Moga Pro in action at PowerA?s Google I/O booth and we were impressed with how securely they mounted both a Samsung Galaxy Nexus phone and a Nexus 7 tablet. We also can imagine the Mogas working really well with Android devices that connect to your TV like the Android 4.0 Mini PC.

We look forward to reviewing the Mogas when they come, but until then, check out the video below for a closer look.

Source: http://feedproxy.google.com/~r/laptopmag/~3/1QbNpZhmrW0/powera-moga-android-game-controllers-hands-on-mount-your-tablet-or-phone

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Thursday, June 28, 2012

Google's Andy Rubin: Nexus 7 may head to retail, but we're not changing tablet app policies

We've got good news and bad news in equal measure for those pining after a Nexus 7 of their very own. If you're reluctant to spend that much hard-earned cash at the Google Play Store, Google's senior VP of mobile Andy Rubin has hinted to AllThingsD that the ASUS-made tablet could end up at retail stores before too long; the Play-only availability was just what Google had to mention at I/O. There could be some markup in other channels, given that Google is selling at what's very nearly wholesale prices. The bad news? Google won't be changing its attitude towards tablet-native apps anytime soon. Rubin sees Google Play content additions as key to driving Android tablet adoption, not the encouragement of tablet-specific app development -- he'd prefer the one-size-fits-all model. We'll see whether magazines and movie sales are enough to turn around so-so market share, but if you were hoping Rubin would address criticisms that Android tablet apps are just blown-up phone apps, you'll have to keep waiting.

Google's Andy Rubin: Nexus 7 may head to retail, but we're not changing tablet app policies originally appeared on Engadget on Wed, 27 Jun 2012 18:29:00 EDT. Please see our terms for use of feeds.

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New compound holds promise for treating Duchenne MD, other inherited diseases

ScienceDaily (June 27, 2012) ? Scientists at UCLA have identified a new compound that could treat certain types of genetic disorders in muscles. It is a big first step in what they hope will lead to human clinical trials for Duchenne muscular dystrophy.

Duchenne muscular dystrophy, or DMD, is a degenerative muscle disease that affects boys almost exclusively. It involves the progressive degeneration of voluntary and cardiac muscles, severely limiting the life span of sufferers.

In a new study, senior author Carmen Bertoni, an assistant professor in the UCLA Department of Neurology, first author Refik Kayali, a postgraduate fellow in Bertoni's lab, and their colleagues demonstrate the efficacy of a new compound known as RTC13, which suppresses so-called "nonsense" mutations in a mouse model of DMD.

The findings appear in the current online edition of the journal Human Molecular Genetics.

"We are excited about these new findings because they represent a major step toward the development of a drug that could potentially treat this devastating disease in humans," Bertoni said. "We knew that the compounds were effective in cells isolated from the mouse model for DMD, but we did not know how they would behave when administered in a living organism."

Nonsense mutations are generally caused by a single change in DNA that disrupts the normal cascade of events that changes a gene into messenger RNA, then into a protein. The result is a non-functioning protein. Approximately 13 percent of genetic defects known to cause diseases are due to such mutations. In the case of DMD, the "missing" protein is called dystrophin.

For the study, Bertoni and Kayali collaborated with the laboratory of Dr. Richard Gatti, a professor of pathology and laboratory medicine and of human genetics at UCLA. Working with the UCLA Molecular Shared Screening Resource facility at the campus's California NanoSystems Institute, the Gatti lab screened some 35,000 small molecules in the search for new compounds that could ignore nonsense mutations. Two were identified as promising candidates: RTC13 and RTC14.

The Bertoni lab tested RTC13 and RTC14 in a mouse model of DMD carrying a nonsense mutation in the dystrophin gene. While RTC14 was not found to be effective, RTC13 was able to restore significant amounts of dystrophin protein, making the compound a promising drug candidate for DMD. When RTC13 was administered to mice for five weeks, the investigators found that the compound partially restored full-length dystrophin, which resulted in a significant improvement in muscle strength. The loss of muscle strength is a hallmark of DMD.

The researchers also compared the level of dystrophin achieved to the levels seen with another experimental compound, PTC124, which has proved disappointing in clinical trials; RTC13 was found to be more effective in promoting dystrophin expression. Just as important, Bertoni noted, the study found that RTC13 was well tolerated in animals, which suggests it may also be safe to use in humans.

The next step in the research is to test whether an oral formulation of the compound would be effective in achieving therapeutically relevant amounts of dystrophin protein. If so, planning can then begin for clinical testing in patients and for expanding these studies to other diseases that may benefit from this new drug.

Other study authors included Jin-Mo Ku, Gregory Khitrov, Michael E. Jung and Olga Prikhodko, all from UCLA. The researchers report no conflicts of interest. The work has been supported in large part by the Muscular Dystrophy Association (MDA) and, more recently, by the National Institutes of Health.

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The above story is reprinted from materials provided by University of California - Los Angeles. The original article was written by Mark Wheeler.

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

Journal Reference:

R. Kayali, J.-M. Ku, G. Khitrov, M. E. Jung, O. Prikhodko, C. Bertoni. Read-through compound 13 restores dystrophin expression and improves muscle function in the mdx mouse model for Duchenne muscular dystrophy. Human Molecular Genetics, 2012; DOI: 10.1093/hmg/dds223

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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