রবিবার, ২৪ ফেব্রুয়ারী, ২০১৩

NetSuite OpenAir Mobile Comes to Android Devices

The platform allows Android OS users to update and submit time and expense reports for projects on their smartphones and tablet devices.

Cloud-based enterprise resource management (ERP) and financials software specialist NetSuite announced the availability of its OpenAir Mobile time tracking and expenses management platform for Google's Android operating system. OpenAir Mobile for Android includes a calendar to track and manage time, access to OpenAir time sheets and expense reports using the Android user interface and instantaneous synchronization with OpenAir accounts to use up-to-date customer, project and task data. "Services professionals increasingly rely on smartphones and tablets while on the road or anytime they need to access an OpenAir account," Ed Marshall, NetSuite Service Vertical general manager, said in a statement. "This new mobile app for Android puts the power of the cloud in the palm of their hand to perform more efficiently and speed time and expense reporting and approvals." The platform allows users to update and submit time and expense reports for projects. Along with entering receipt data, the app lets professionals in IT services, consulting, digital marketing and advertising, as well as media and publishing to take a photo of an expense receipt with their Android device, attach it to a record and synchronize the information with the organization's back-end NetSuite OpenAir PSA account. As an example, services organizations that bill clients based on specific time and expense reports could accelerate processes and cash flow when consultants are able to enter time and expense data through a smartphone or tablet. The application is free and only requires a customer's OpenAir credentials to sync with their account. Although an application that could run on Apple's iOS platform was a near-necessary development half a decade ago, application developers are increasingly turning to Android app development as the platform has skyrocketed in popularity. The analyst firm IDC estimates that Android commanded 75 percent of the worldwide smartphone market in the third quarter of 2012, about five times greater than the Apple iOS for the iPhone. In addition, Android's year-over-year growth rate of 91.5 percent for the 12 months ending on Sept. 30, 2012, was nearly double the 46.4 percent growth rate of the smartphone market at large, according to IDC. In the tablet market, the Android platform powered more than 44 percent of tablet shipments as of Q3 2012, second only to the Apple iOS on the iPad, which claimed a market share of 55 percent. Despite maintaining its lead for 10 straight quarters, competition from tablets powered by Android continued to eat away at Apple's success. Nearly 14 percent share was given up in the quarter to several benefactors, including Amazon, Google and Samsung.

Source: http://www.eweek.com/mobile/netsuite-openair-mobile-comes-to-android-devices/

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শনিবার, ৯ ফেব্রুয়ারী, ২০১৩

Bitter rivals Hamas, Fatah hold reconciliation talks

Mohammed Salem / Reuters

Palestinians take part in a rally marking the 48th anniversary of the founding of the Fatah movement, in Gaza City, on January 4. Hundreds of thousands of Palestinians joined a rare rally staged by President Mahmoud Abbas's Fatah group in Gaza on Friday, as tensions ease with rival Hamas.

By Lawahez Jabari, Producer, NBC News

Updated at 8:40 a.m. ET: TEL AVIV, Israel - Officials with rival factions Hamas and Fatah will this weekend seek a reconciliation deal that would potentially give Palestinians a stronger position in future peace negotiations with Israel. ??

The talks are meant to help bury years of differences that have damaged Palestinian efforts to create a separate state. Discussions began Friday and Palestinian President Mahmoud Abbas, of Fatah, and Hamas leader Khaled Meshaal were due to meet Sunday.

Salah Bardaweel, a senior official with Hamas -- which controls the Gaza Strip,?said the?negotiations between Meshaal and Abbas would cover the creation of a new government headed by Abbas.

?Reconciliation is a national necessity and all are working on achieving it," he said.

Fatah and Hamas have starkly different visions of what a future Palestinian state would consist of. ?

Fatah controls the Palestinian Authority, which represents the Palestinian cause internationally, and is pursuing a negotiated solution with Israel with the eventual establishment of a separate?state alongside Israel. Islamist Hamas, branded a terror group by the United States and other governments, does not recognize Israel as a legitimate state.?

Alaa Badarneh / EPA

Palestinians participate in a Hamas rally as part of celebrations marking the 25th anniversary of the Islamist movement's founding in the West Bank city of Qalqilya on December 15.

A recent announcement that?President Barack Obama was planning to visit?Israel and the West Bank this spring raised the prospect of a new U.S. push to restart the long-stalled Israel-Palestinian peace efforts. Success is far from certain --?Israel and the Palestinians remain deeply at odds on how to restart talks that broke down more than two years ago.

Israeli-Palestinian talks foundered in 2010 and Israeli then sped up housing construction in the occupied West Bank and East Jerusalem -- land the Palestinians claim for a future state.?

Bernard Sabella, a member of the Palestinian parliament, said reconciliation between Hamas and Fatah would give ?the Palestinian people the chance to practice its national right in electing their president, legislative council and so on.?

Ahmad Assaf, a Fatah spokesperson, said a ?transitional government would operate for three to six months until elections were held.

?The transitional government?s role is to prepare for the elections and to unify the Palestinian institutions,? he said. ?In Fatah, we are determined on achieving the reconciliation through elections.?

Divisions
While Hamas and Fatah said that they were determined to reach a reconciliation deal, signs persisted of ongoing troubles between the two sides. ?

Palestinian security forces had arrested more than 25 members of Hamas over two days, ?Agence France Presse news service cited an unnamed security source as saying on Friday. According to him, explosives were found in the possession of some of those detained in the area of Ramalah in the West Bank.

And on Thursday, Hamas accused the Fatah-controlled Palestinian Authority of escalating an arrest campaign against its supporters in the West Bank.

Hamas, which controls the Gaza Strip area, said in a press release that eight activists had been detained in the previous two days in Ramallah and Nablus districts.

A recent report by the Palestinian Independent Commission for Human Rights (ICHR?) said that human rights violations have been continuing in the West Bank and the Gaza Strip.

The report said the ICHR last month received 31 complaints about torture and mistreatment and 24 alleging unwarranted arrests.

Related:

UN panel's report: Israel must withdraw all settlers from West Bank

Rights group: Israel using deadly force against unarmed protesters

Source: http://worldnews.nbcnews.com/_news/2013/02/08/16897642-fatah-hamas-hold-reconciliation-talks-ahead-of-possible-peace-negotiations-with-israel?lite

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Delete Your Google Voice Account Without Losing Your Number

Whitson Gordon
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Delete Your Google Voice Account Without Losing Your NumberSo you made the full switch to Google Voice, but decided that it isn't for you. Want to delete your account without losing the new number you made everyone memorize? MsCassLopez points out a lesser-known feature that lets you do just that.

Google finally added the ability to delete your Voice account, but if you want to keep the number associated with your account, you can actually port your number away from Google Voice. It costs $3 to do, unless you've already ported your number to Google Voice, in which case it's free.

To do it, just head to google.com/voice/unlock and click the Unlock My Number button. Once you're done, you'll need to talk to your service provider (e.g. Verizon or AT&T) and have them port your number back. That way, you can continue using your phone without having to give anyone a new number.

Port your number out of Google Voice | via MsCassLopez

Source: http://feeds.gawker.com/~r/lifehacker/full/~3/GkiUbAFLulM/delete-your-google-voice-account-without-losing-your-number

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What Are Roots of Unity?

This blog is called ?Roots of Unity? because in 2004 I thought it would be an awesome band name.

Not the cover of my band's first album. Image courtesy of Gregory A. Moore.

I encountered the term in a college math class, and I had no illusions that I would be in a band at any time in the near future, but it seemed prudent to have some good band names in my back pocket, just in case. You never know when an awesome band will be looking for a recreational violist who already has a nerdy band name picked out.

So what is a root of unity anyway? The word ?root? in the term refers to square roots, cube roots, and any other roots you might happen to need. For any integer n, the nth root of a number k is a number that, when multiplied by itself n times, yields k. The word ?unity,? perhaps a bit anticlimactically, just means ?one.? So a root of unity is any number which, when multiplied by itself some number of times, yields 1.

At this point, the definition really seems like it?s making a mountain out of a molehill: 1 and -1 are the only numbers that seem to fit the bill. But the evocative phrase doesn?t usually come up when we?re talking about real numbers: we need to work with complex numbers to get any interesting roots of unity.

The complex numbers consist of all numbers that can be written in the form a+bi, where a and b are real numbers and i is the square root of -1. The number i doesn?t exist on the real number line because any real number multiplied by itself is positive, so the letter i, standing for ?imaginary,? is used instead. Imaginary numbers aren?t any more imaginary than the numbers 6, 8, or 27,000, but the label has stuck. The number i itself is a root of unity: i2=-1, so i4=1, making i a 4th root of unity. Any square, cube, or other roots of i are also roots of unity.

To see what makes roots of unity special, we need to delve a little bit into notation. If you don?t like notation, you should probably skip the next three paragraphs.

We can think of the set of complex numbers as a 2-dimensional plane. We specify a complex number with two coordinates the same way we would on a graph: the point (1,1) refers to the number 1+i. If we were standing on the point (0,0), we probably wouldn?t want to walk one unit over and then one unit up to get to the point (1,1). Instead, we?d take a diagonal by walking ?2 units at an angle of 45 degrees to the x-axis. Notationally, when we use this radial distance and direction, we write a complex number as rei ?, where r is the distance and ? is the direction, usually written in radians rather than degrees. There are 2? radians in a whole circle, so the number 1 is written ei 2?. The angle 45 degrees is ?/4 radians, so the point (1,1) that we found above would be written as ?2ei ?/4.

?

The complex number 1+i, written in rectangular and polar coordinates.

This method of specifying a point with a length and a direction is called using polar coordinates, and it shows up most beautifully in Euler?s identity, ei?=-1.

Polar coordinates make it really easy to multiply complex numbers. With a+bi notation, you have to FOIL (remember middle school algebra?), and you end up with a total of four terms you have to add together. But with the polar notation of rei?, it?s really easy: you multiply the distances together and add the angles. So 5ei?/6? 2ei?/3=10 ei ?/2. So multiplying involves both expansion or contraction (that?s the distance part) and rotation (that?s the angle part).

I think the most beautiful thing about roots of unity (besides the awesome name) is that they are kind of a balancing point between 0 and infinity. What I mean by that is if we have a number written rei ? which, when multiplied by itself a certain number of times, yields 1, the distance r itself must be 1. If r were larger than 1, say 2, then as we multiplied the number by itself more and more times, its distance from (0,0) would go from 2 to 4 to 8 and on and on, spiraling out to infinity. If r were smaller than 1, say 1/2, the point would spiral in to 0: 1/2, 1/4, 1/8, and so on. 1 is the only radial distance that will stay perfectly balanced, just marching around the circle as we multiply the numbers together.

To make this more concrete, I happen to know that ei2?/7 is a root of unity. When I raise it to the 7th power, I get ei2?, which is 1. Each time I multiply ei2?/7 by itself, I rotate 1/7 of the way around the circle. In fact, as I multiply ei2?/7 by itself successively, I get this picture, my blog banner.

The 7th roots of unity. Image courtesy of Gregory A. Moore.

In fact, there are seven 7th roots of unity, and each gold disc in that picture is one of them. We can get an nth root of unity for any number n by replacing the 7 in ei 2?/7 by n. The pictures for other roots of unity look a lot like that diagram above, they just have a different number of gold discs.

I?m not sure the mathematical definition of a root of unity stands up to the awesomeness of the phrase as a band name, but I do think it?s a beautiful idea, and it?s very useful in complex analysis. I?m still collecting awesome band names now that Roots of Unity is out. Two current frontrunners are ?The Butterfly Assumption,? which is related to a friend?s area of math research, and ?Premeditated Rosemary Theft,? which is just related to an unfortunate incident involving my balcony and some missing herbs.

Source: http://rss.sciam.com/click.phdo?i=d70b055dfdcb35c29a3ffb8983ede0db

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Video: Girl?s salute goes viral



>>> a still photo of a little girl is getting a lot of attention on the web, deservedly so. her name is daniella, she is 3 years old, she saluted during the anthem at ft. drummond, new york, as her dad left for afghanistan on a nine-month deployment.

Source: http://video.msnbc.msn.com/nightly-news/50749690/

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Some Sandy victims still without heat as blizzard descends on NYC

A November nor'easter dumps snow on homes in Queens, N.Y., burned in the aftermath of Superstorm Sandy. (Mario??

New York City Mayor Michael Bloomberg on Friday told residents still without heat from October's Superstorm Sandy to seek shelter elsewhere as a massive snowstorm threatens to dump up to 13 inches on the city's boroughs.

The city is under a blizzard warning until 1 p.m. Saturday, and the National Weather Service warned winds could gust up to 60 miles per hour as a potentially record-setting storm blasts through on its way to New England.

"If your house has been damaged by Sandy and still without heat, call 311 and we'll be certain to find you shelter," Bloomberg said at a press conference Friday afternoon, referencing the city's helpline. The mayor also warned that the city's coastal areas could see a storm surge, though nothing rivaling the 10-foot surge that flooded thousands of New York homes in October.

As of Feb. 7, the city was still working to restore heat, hot water, and/or power to 690 residential buildings, after completing repairs on 10,255 buildings since the storm hit. Many of these homes are clustered in hard-hit areas like the Rockaways in Queens, and in Staten Island. About a fifth of the residents in the Rockaways were still without heat in early January, according to a report released by a local nonprofit called New York Communities for Change.

Olivia Leirer, a spokeswoman for New York Communities for Change, said some of the tenants had since gotten their heat turned back on, due to a city program called Rapid Repairs.

Devon Lawrence, a homeowner in Far Rockaway, told Yahoo News his boiler was just repaired two weeks ago by Rapid Repairs, ending the nearly three-month period he lived in his home, along with his 75-year-old mother, without heat.

Lawrence stocked up on salt on Friday ahead of the blizzard and bought some extra kerosene oil as backup. "I'm only hoping that whatever happened in Sandy doesn't repeat itself this time," he said. "It was really miserable [living without heat]. Words cannot describe the feeling."

A coalition of nonprofit workers in Staten Island are trying to convince people still living in unheated homes to seek shelter as well, SILive.com reported.

Earlier this week, the Federal Emergency Management Agency (FEMA) extended hotel stays for displaced Sandy victims to Feb. 24.

For those who waited weeks or months for power after Sandy, the possibility of more outages looms. Utility companies warned on Friday that it's possible that areas with above-ground power lines will again be hit with electricity outages.

Bloomberg, who has deployed 1,700 snowplows and 450 salt spreaders to scour the city, says he hopes the impact of Sandy just 100 days ago will mean the city and its residents are prepared for the storm. "Sandy is so fresh in our minds," he said.

Source: http://news.yahoo.com/blogs/lookout/sandy-victims-still-without-heat-blizzard-descends-york-203520836.html

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শুক্রবার, ৮ ফেব্রুয়ারী, ২০১৩

Possible cause of, and treatment for, non-familial Parkinson's

Feb. 6, 2013 ? Columbia University Medical Center (CUMC) researchers have identified a protein trafficking defect within brain cells that may underlie common non-familial forms of Parkinson's disease. The defect is at a point of convergence for the action of at least three different genes that had been implicated in prior studies of Parkinson's disease. Whereas most molecular studies focus on mutations associated with rare familial forms of the disease, these findings relate directly to the common non-familial form of Parkinson's.

The study was published today in the online edition of the journal Neuron.

The defective pathway is called the "retromer" pathway, in part because it can guide the reutilization of key molecules by moving them back from the cell surface to internal stores. In this study, defects in the retromer pathway also appear to have profound effects on the cell's disposal machinery, which may explain why Parkinson's disease brain cells ultimately accumulate large protein aggregates. The trafficking defects associated with Parkinson's can be reversed by increasing retromer pathway activity, suggesting a possible therapeutic strategy. No current therapies for Parkinson's alter the progression of the disease.

The researchers also found evidence that, even in unaffected individuals who simply carry common genetic variants associated with an increased risk of Parkinson's disease, these molecular changes are at work. This supports the notion that early treatment approaches will be important in tackling Parkinson's disease.

"Taken together, the findings suggest that drugs that target the retromer pathway could help prevent or treat Parkinson's," said study leader Asa Abeliovich, MD, PhD, associate professor of pathology and cell biology and of neurology in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC.

In recent years, through genome-wide association studies (GWAS), researchers have identified about 10 common genetic variants that appear to have small effects on the risk of non-familial Parkinson's, However, it has been hard to delve deeper into the impact of these variants. "When you look at patient brain tissue at autopsy, it's usually too late -- all the critical dopamine neurons are long gone and the damage has been done," said Dr. Abeliovich.

In the current study, Dr. Abeliovich and his CUMC colleagues used an unusually broad array of approaches -- including analyses of Parkinson's disease-associated genetic variations, patient brain tissue, in vitro tissue culture studies of brain neurons, and fruit fly (Drosophila) models that harbor genetic variants related to those associated with Parkinson's disease.

The researchers found that common variants in two genes previously linked to Parkinson's disease, LRRK2 and RAB7L1, led to an unexpectedly similar impact on human brain tissue. The effects of the variants were found to be highly overlapping, pointing to a common pathway of action. Prominent cellular changes were observed in the retromer pathway, which is involved in the trafficking of proteins from the Golgi apparatus (which packages proteins for delivery to other cell components) to the lysosomes (which recycle proteins and other molecules). Mutations that affect the retromer pathway have also been found in familial Parkinson's disease. Earlier studies from Columbia's Taub Institute have shown that genetic variants in genes associated with retromer function are linked to Alzheimer's disease and retromer component levels appear altered in Alzheimer's disease brains, suggesting a broader role for retromer dysfunction in neurodegenerative diseases of aging, according to Dr. Abeliovich.

The impact of the RAB7L1 and LRRK2 variants was apparent even in individuals with no signs or symptoms of Parkinson's disease. This suggests that there is a pre-disease state in unaffected carriers of the two genetic variants that favors early disease onset and that, in theory, could be targeted therapeutically.

The CUMC researchers also demonstrated that overexpression of one of the variants, RAB7L1, can overcome the effects of the other variant. Similarly, expression of VPS35, a gene involved in the retromer pathway, can suppress LRRK2 mutant pathology. "It will be interesting to look for drugs that directly target these retromer components or that more generally promote flow through the pathway," said Dr. Abeliovich.

The title of the paper is "RAB7L1 interacts with LRRK2 to modify intraneuronal protein sorting and Parkinson's disease risk." The other contributors are David A. Macleod, Herve Rhinn, Tomoki Kuwahara, Ari Zolin, Gilbert Di Paolo, Brian D. McCabe, Lorraine N. Clark, and Scott A. Small, all at CUMC.

The study was supported by grants from the Michael J. Fox Foundation and the National Institutes of Health (NS064433, NS060876, NS060113, A6008702, AG025161, and AG08702-21.

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Story Source:

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

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


Journal Reference:

  1. David?A. MacLeod, Herve Rhinn, Tomoki Kuwahara, Ari Zolin, Gilbert Di?Paolo, Brian?D. MacCabe, Karen?S. Marder, Lawrence?S. Honig, Lorraine?N. Clark, Scott?A. Small, Asa Abeliovich. RAB7L1 Interacts with LRRK2 to Modify Intraneuronal Protein Sorting and Parkinson?s Disease Risk. Neuron, 2013; 77 (3): 425 DOI: 10.1016/j.neuron.2012.11.033

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.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/health_medicine/genes/~3/MivAmGaScak/130206130946.htm

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Here Are 10 Standout Companies From The Fifth 500 Startups Demo Day

startupsdemodayEarly stage VC fund 500 Startups today held the first of several demo day events for the fifth batch of startups graduating from its accelerator program. It was a fun event, with 32 high-energy founders pitching their companies to a room full of investors and tech press. All of the companies were compelling in their own ways, covering a wide range of technologies, geographies, and sectors -- you can check out the full list right here. It was tough, but we narrowed down a list of some of our favorites.

Source: http://feedproxy.google.com/~r/Techcrunch/~3/u5dVyAaB4hE/

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বৃহস্পতিবার, ৭ ফেব্রুয়ারী, ২০১৩

Molecular link between metabolism and breast cancer

Feb. 6, 2013 ? A protein associated with conditions of metabolic imbalance, such as diabetes and obesity, may play a role in the development of aggressive forms of breast cancer, according to new findings by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, and their colleagues. Metabolic imbalance is often caused by elevated carbohydrate intake, which can lead to over-activating a molecule called C-terminal binding protein (CtBP). This over-activation, in turn, can increase the risk of breast cancer. Results of their work appeared in Nature Communications, Feb. 5, 2013.

"Modifying diet and maintaining a healthy diet, combined with developing pharmacological ways of lessening CtBP activity, may one day lead to a way to break the link between cancer and obesity," said Kevin Gardner, M.D., Ph.D., head of NCI's Transcription Regulation Section, Genetics Branch.

It has been known, primarily through population based studies, that there is a strong link between obesity and cancer. But the mechanism behind this link has been uncertain. A previous study conceived and carried out in Gardner's laboratory found that CtBP repressed expression of a gene associated with breast cancer (BRCA1) at an early age by sensing when the cell was in a high metabolic state that, in turn, led to processing large amounts of carbohydrates in the body.

This early study suggested that obesity and weight gain may contribute to breast cancer by decreasing the level of the BRCA1 tumor suppressor gene expression in response to high carbohydrate intake. This explains, in part, why women who have hereditary mutations of BRCA1 also experience an increased risk of breast cancer if they gain weight.

Gardner's new study expands upon his past work. He analyzed prior gene expression studies to determine if gene pathways, repressed by CtBP, were diminished in breast cancer patients who suffered from more aggressive clinical outcomes. Gardner's team began first with the human breast cancer cells in the laboratory. They measured the association of CtBP and the genes it bound to in order to regulate expression. The researchers combined this approach with genome sequencing to confirm how, and where, CtBP bound to genes associated with breast cancer. Next, they integrated analyses with gene expression studies in cells in which they observed decreased the levels of CtBP by RNA interference (a process that inhibits gene expression), or by decreasing carbohydrate feeding of the cells.

The scientists found that, under conditions where they decreased the levels of CtBP, DNA repair increased and the cells developed stability and growth control. They determined that gene pathways targeted by CtBP were also disrupted in more aggressive breast cancers. Moreover, patients with high levels of CtBP in their tumors had shortened survival. And they showed that a small molecular inhibitor previously shown to bind to CtBP was able to reverse the gene-repressive effects of CtBP in breast cancer cells even under conditions of high carbohydrate feeding.

"Our new work suggests that targeting CtBP may provide a way of treating breast cancer and possibly preventing breast cancer," said Gardner. "Research should continue to focus on the link between obesity, CtBP and breast cancer. This will require more population-based studies and multi-disciplinary teams of scientist to investigate these links."

This project was funded by NCI project number 1Z01BC010847-01.

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Story Source:

The above story is reprinted from materials provided by National Cancer Institute (NCI) at NIH.

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


Journal Reference:

  1. Li-Jun Di, Jung S. Byun, Madeline M. Wong, Clay Wakano, Tara Taylor, Sven Bilke, Songjoon Baek, Kent Hunter, Howard Yang, Maxwell Lee, Cecilia Zvosec, Galina Khramtsova, Fan Cheng, Charles M. Perou, C. Ryan Miller, Rachel Raab, Olufunmilayo I. Olopade, Kevin Gardner. Genome-wide profiles of CtBP link metabolism with genome stability and epithelial reprogramming in breast cancer. Nature Communications, 2013; 4: 1449 DOI: 10.1038/ncomms2438

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.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/health_medicine/genes/~3/juNX7aqMKFQ/130206141531.htm

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