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ASUS VivoTab RT review: everything you loved about the Transformer tablets, but with Windows

ASUS VivoTab RT review everything you loved about the Transformer tablets, but with Windows

Read the comments on any of our ASUS Transformer Pad reviews. It doesn't matter if you pick the mid-range TF300 or the high-end Infinity. You'll invariably find someone saying, "That's nice, but can't it run Windows 8?" It's a perfectly sane request: sure, a tablet and optional keyboard dock make for a convenient setup, but how great would it be if you could use that keyboard to get work done in Microsoft Office? Ditto for the dock's USB port: being able to plug in a thumb drive is a good start, but it'd be even sweeter if you could drag and drop files, as you would on a PC.

Well, ladies and gents, you can quit your fantasizing. ASUS is ready to start shipping the VivoTab RT (TF600), and we're guessing it's pretty darn close to whatever Franken-tablet you've been dreaming up. Which is to say, it takes everything we loved about ASUS' Transformer Pads, and adds Windows RT. Like other tablets in ASUS' lineup, it has a 10-inch Super IPS+ display with claimed 178-degree viewing angles and a 600-nit brightness rating. Other tried-and-true specs include a quad-core Tegra 3 chip; an 8-megapixel, autofocusing rear camera capable of recording 1080p video; SonicMaster audio; and long battery life -- in this case, up to nine hours for the tablet and up to seven for the keyboard dock. At 8.3mm thick and 1.2 pounds, it's also about as thin and light as any Transformer Pad. Lastly, the VivoTab has NFC -- something you won't find on any of ASUS' older slates.

The VivoTab RT should be available beginning today, starting at $599 for the 32GB tablet with a keyboard dock included. A 64GB tablet-and-dock bundle will retail for $699. So is this as good a buy as ASUS' earlier tablets. And how does it compare to other Windows RT devices being offered at a similar price? Let's find out.

Continue reading ASUS VivoTab RT review: everything you loved about the Transformer tablets, but with Windows

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Far from random, evolution follows a predictable genetic pattern

ScienceDaily (Oct. 25, 2012) ? Evolution, often perceived as a series of random changes, might in fact be driven by a simple and repeated genetic solution to an environmental pressure that a broad range of species happen to share, according to new research.

Princeton University research published in the journal Science suggests that knowledge of a species' genes -- and how certain external conditions affect the proteins encoded by those genes -- could be used to determine a predictable evolutionary pattern driven by outside factors. Scientists could then pinpoint how the diversity of adaptations seen in the natural world developed even in distantly related animals.

"Is evolution predictable? To a surprising extent the answer is yes," said senior researcher Peter Andolfatto, an assistant professor in Princeton's Department of Ecology and Evolutionary Biology and the Lewis-Sigler Institute for Integrative Genomics. He worked with lead author and postdoctoral research associate Ying Zhen, and graduate students Matthew Aardema and Molly Schumer, all from Princeton's ecology and evolutionary biology department, as well as Edgar Medina, a biological sciences graduate student at the University of the Andes in Colombia.

The researchers carried out a survey of DNA sequences from 29 distantly related insect species, the largest sample of organisms yet examined for a single evolutionary trait. Fourteen of these species have evolved a nearly identical characteristic due to one external influence -- they feed on plants that produce cardenolides, a class of steroid-like cardiotoxins that are a natural defense for plants such as milkweed and dogbane.

Though separated by 300 million years of evolution, these diverse insects -- which include beetles, butterflies and aphids -- experienced changes to a key protein called sodium-potassium adenosine triphosphatase, or the sodium-potassium pump, which regulates a cell's crucial sodium-to-potassium ratio. The protein in these insects eventually evolved a resistance to cardenolides, which usually cripple the protein's ability to "pump" potassium into cells and excess sodium out.

Andolfatto and his co-authors first sequenced and assembled all the expressed genes in the studied species. They used these sequences to predict how the sodium-potassium pump would be encoded in each of the species' genes based on cardenolide exposure.

Scientists using similar techniques could trace protein changes in a species' DNA to understand how many diverse organisms evolved as a result of environmental factors, Andolfatto said. "To apply this approach more generally a scientist would have to know something about the genetic underpinnings of a trait and investigate how that trait evolves in large groups of species facing a common evolutionary problem," Andolfatto said.

"For instance, the sodium-potassium pump also is a candidate gene location related to salinity tolerance," he said. "Looking at changes to this protein in the right organisms could reveal how organisms have or may respond to the increasing salinization of oceans and freshwater habitats."

Jianzhi Zhang, a University of Michigan professor of ecology and evolutionary biology, said that the Princeton-based study shows that certain traits have a limited number of molecular mechanisms, and that numerous, distinct species can share the few mechanisms there are. As a result, it is likely that a cross-section of certain organisms can provide insight into the development of other creatures, he said.

"The finding of parallel evolution in not two, but numerous herbivorous insects increases the significance of the study because such frequent parallelism is extremely unlikely to have happened simply by chance," said Zhang, who is familiar with the study but had no role in it.

"It shows that a common molecular mechanism is used by many different insects to defend themselves against the toxins in their food, suggesting that perhaps the number of potential mechanisms for achieving this goal is very limited," he said. "That many different insects independently evolved the same molecular tricks to defend themselves against the same toxin suggests that studying a small number of well-chosen model organisms can teach us a lot about other species. Yes, evolution is predictable to a certain degree."

Andolfatto and his co-authors examined the sodium-potassium pump protein because of its well-known sensitivity to cardenolides. In order to function properly in a wide variety of physiological contexts, cells must be able to control levels of potassium and sodium. Situated on the cell membrane, the protein generates a desired potassium to sodium ratio by "pumping" three sodium atoms out of the cell for every two potassium atoms it brings in.

Cardenolides disrupt the exchange of potassium and sodium, essentially shutting down the protein, Andolfatto said. The human genome contains four copies of the pump protein, and it is a candidate gene for a number of human genetic disorders, including salt-sensitive hypertension and migraines. In addition, humans have long used low doses of cardenolides medicinally for purposes such as controlling heart arrhythmia and congestive heart failure.

The Princeton researchers used the DNA microarray facility in the University's Lewis-Sigler Institute for Integrative Genomics to sequence the expression of the sodium-potassium pump protein in insect species spanning three orders: butterflies and moths (Lepidoptera); beetles and weevils (Coleoptera); and aphids, bed bugs, milkweed bugs and other sucking insects (Hemiptera).

The researchers found that the genes of cardenolide-resistant insects incorporated various mutations that allowed it to resist the toxin. During the evolutionary timeframe examined, the sodium-potassium pump of insects feeding on dogbane and milkweed underwent 33 mutations at sites known to affect sensitivity to cardenolides. These mutations often involved similar or identical amino-acid changes that reduced susceptibility to the toxin. On the other hand, the sodium-potassium pump mutated just once in insects that do not feed on these plants.

Significantly, the researchers found that multiple gene duplications occurred in the ancestors of several of the resistant species. These insects essentially wound up with one conventional sodium-potassium pump protein and one "experimental" version, Andolfatto said. In these insects, the newer, hardier versions of the sodium-potassium pump are mostly expressed in gut tissue where they are likely needed most.

"These gene duplications are an elegant solution to the problem of adapting to environmental changes," Andolfatto said. "In species with these duplicates, the organism is free to experiment with one copy while keeping the other constant, avoiding the risk that the new version of the protein will not perform its primary job as well."

The researchers' findings unify the generally separate ideas of what predominately drives genetic evolution: protein evolution, the evolution of the elements that control protein expression or gene duplication. This study shows that all three mechanisms can be used to solve the same evolutionary problem, Andolfatto said.

Central to the work is the breadth of species the researchers were able to examine using modern gene sequencing equipment, Andolfatto said.

"Historically, studying genetic evolution at this level has been conducted on just a handful of 'model' organisms such as fruit flies," Andolfatto said. "Modern sequencing methods allowed us to approach evolutionary questions in a different way and come up with more comprehensive answers than had we examined one trait in any one organism.

"The power of what we've done is to survey diverse organisms facing a similar problem and find striking evidence for a limited number of possible solutions," he said. "The fact that many of these solutions are used over and over again by completely unrelated species suggests that the evolutionary path is repeatable and predictable."

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The above story is reprinted from materials provided by Princeton University. The original article was written by Morgan Kelly.

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


Journal Reference:

  1. Y. Zhen, M. L. Aardema, E. M. Medina, M. Schumer, P. Andolfatto. Parallel Molecular Evolution in an Herbivore Community. Science, 2012; 337 (6102): 1634 DOI: 10.1126/science.1226630

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

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/most_popular/~3/lVuHyQvEfGM/121025130922.htm

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I can't drive 85: Texas unveils a road with new speed limit

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Is obesity irreversible? Timing is key in weight loss

ScienceDaily (Oct. 24, 2012) ? Joint research between the University of Michigan and the Argentina-based National Council of Science and Technology (CONICET) has shed light on one of the most frustrating mysteries of weight loss -- why the weight inevitably comes back.

A novel animal model showed that the longer mice remained overweight, the more "irreversible" obesity became, according to the new study that appeared online ahead of print Oct.24 in the Journal of Clinical Investigation.

Over time, the static, obese state of the mice reset the "normal," body weight set point to become permanently elevated, despite dieting that initially worked to shed pounds, authors say.

"Our model demonstrates that obesity is in part a self-perpetuating disorder and the results further emphasize the importance of early intervention in childhood to try to prevent the condition whose effects can last a lifetime," says senior author Malcolm J. Low, M.D., Ph.D., professor of molecular and integrative physiology and internal medicine.

"Our new animal model will be useful in pinpointing the reasons why most adults find it exceedingly difficult to maintain meaningful weight loss from dieting and exercise alone."

The lead author of the study was Viviana F. Bumaschny, M.D., assistant investigator of CONICET.

Obesity affects more than 500 million adults and 43 million children younger than age 5, while related illnesses are the leading preventable cause of death.

Individuals who are overweight have a much higher risk of type 2 diabetes, hypertension, and cardiovascular diseases.

One of the major strengths of the research was a new model of obesity-programmed mice that allowed weight loss success to be tracked at different stages and ages by flipping a genetic switch that controls hunger.

Turning on the switch right after weaning prevented the mice from overeating and ever becoming obese. Similarly, mice that remained at a healthy weight into young adulthood by strict dieting alone were able to maintain normal weight without dieting after turning on the switch. However, chronically overfed mice with the earliest onset of obesity never completely returned to normal weight after flipping the switch, despite marked reduction in food intake and increased activity.

The new findings may raise questions about the long-term success rate of severe calorie restriction and strenuous exercise used later in life to lose weight, such as the extreme regimens seen in the popular reality television show "Biggest Loser."

"Somewhere along the way, if obesity is allowed to continue, the body appears to flip a switch that re-programs to a heavier set weight," Low says. "The exact mechanisms that cause this shift are still unknown and require much further study that will help us better understand why the regaining of weight seems almost unavoidable."

The findings will be published alongside a corresponding commentary "Tipping the scales early: probing the long-term effects of obesity."

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Story Source:

The above story is reprinted from materials provided by University of Michigan Health System. The original story is licensed under a Creative Commons license.

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


Journal Reference:

  1. Viviana F. Bumaschny, Miho Yamashita, Rodrigo Casas-Cordero, Ver?nica Otero-Corch?n, Fl?vio S.J. de Souza, Marcelo Rubinstein, Malcolm J. Low. Obesity-programmed mice are rescued by early genetic intervention. Journal of Clinical Investigation, 2012; DOI: 10.1172/JCI62543

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/top_news/~3/SP7IgkMBjJM/121024141635.htm

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Clarkson grand marshal for pre-Mardi Gras parade

NEW ORLEANS (AP) ? Pop star Kelly Clarkson will ride as celebrity grand marshal when the Krewe of Endymion parade rolls on the Saturday before Mardi Gras in 2013.

Clarkson was the first winner of the Fox reality show "American Idol" in 2002. Her hits include "A Moment Like This" and "Because of You."

Organizers say she'll perform at Endymion's ball at the Superdome after the parade.

Clarkson may be upstaged at the Feb. 9 parade by a float that organizers say will be the largest and most elaborate in Carnival history.

The super float will be 250 feet long and carry more than 200 riders. Its design focuses on Pontchartrain Beach, the amusement park that entertained generations on the New Orleans lakefront before closing in 1983.

Mardi Gras is Feb. 12.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/4e67281c3f754d0696fbfdee0f3f1469/Article_2012-10-25-Mardi%20Gras-Kelly%20Clarkson/id-6166350ba83642928490c34ffb78f978

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