Source: http://news.feedzilla.com/en_us/stories/politics/top-stories/270765141?client_source=feed&format=rss
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Friday, December 14, 2012
Aerobic exercise boosts brain power, review finds
Dec. 13, 2012 ? The physical benefits of regular exercise and remaining physically active, especially as we age, are well documented. However, it appears that it is not only the body which benefits from exercise, but the mind too. The evidence for this is published in a new review by Hayley Guiney and Liana Machado from the University of Otago, New Zealand, which focuses on the importance of physical activity in keeping and potentially improving cognitive function throughout life. Their review is published online in the Springer publication Psychonomic Bulletin & Review.
A certain amount of mental deterioration is expected with advancing age. However, this may not necessarily have to be the case as particular aspects of cognitive function such as task switching, selective attention and working memory among others, all appear to benefit from aerobic exercise. Studies in older adults reviewed by the authors consistently found that fitter individuals scored better in mental tests than their unfit peers. In addition, intervention studies found scores in mental tests improved in participants who were assigned to an aerobic exercise regimen compared to those assigned to stretch and tone classes.
Interestingly, these results were not replicated in children or young adults. The one area where physical fitness or regular exercise was found to have an effect on cognitive function in these age groups was for memory tasks. Both the updating of working memory and the volume of information which could be held was better in fitter individuals or those put on an aerobic exercise regime. The authors comment that despite physical fitness not affecting all areas of cognitive function in younger people, evidence is mounting that just because they are in their prime developmentally does not mean that they cannot benefit from regular exercise.
In older generations, the evidence for improvement in cognitive function is insurmountable. The types of tests of cognitive function reviewed here are important in showing that exercise may attenuate age-related decline for specific tasks. For example, it has been found to positively affect mental tasks relating to activities such as driving, an activity where age is often seen as a limiting factor.
The authors conclude that engagement in exercise can provide a simple means for people to optimize their cognitive function. They add that more research into the effects of exercise on young adults and children is required. However, they say that "the indications reported thus far -- that regular exercise can benefit brains even when they are in their prime developmentally -- warrant more rigorous investigation, particularly in the context of society becoming increasingly sedentary."
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The above story is reprinted from materials provided by Springer.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Hayley Guiney, Liana Machado. Benefits of regular aerobic exercise for executive functioning in healthy populations. Psychonomic Bulletin & Review, 2012; DOI: 10.3758/s13423-012-0345-4
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/living_well/~3/xQCHQTFXeNA/121213111830.htm
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What mechanism generates our fingers and toes? Genetic studies confirm a mathematical model
Dec. 14, 2012 ? Researchers have identified the mechanism responsible for generating our fingers and toes, and revealed the importance of gene regulation in the transition of fins to limbs during evolution.
Dr. Marie Kmita and her research team at the IRCM contributed to a multidisciplinary research project. Their scientific breakthrough is published today in the journal Science.
By combining genetic studies with mathematical modeling, the scientists provided experimental evidence supporting a theoretical model for pattern formation known as the Turing mechanism. In 1952, mathematician Alan Turing proposed mathematical equations for pattern formation, which describes how two uniformly-distributed substances, an activator and a repressor, trigger the formation of complex shapes and structures from initially-equivalent cells.
"The Turing model for pattern formation has long remained under debate, mostly due to the lack of experimental data supporting it," explains Dr. Rushikesh Sheth, postdoctoral fellow in Dr. Kmita's laboratory and co-first author of the study. "By studying the role of Hox genes during limb development, we were able to show, for the first time, that the patterning process that generates our fingers and toes relies on a Turing-like mechanism."
In humans, as in other mammals, the embryo's development is controlled, in part, by "architect" genes known as Hox genes. These genes are essential to the proper positioning of the body's architecture, and define the nature and function of cells that form organs and skeletal elements.
"Our genetic study suggested that Hox genes act as modulators of a Turing-like mechanism, which was further supported by mathematical tests performed by our collaborators, Dr. James Sharpe and his team," adds Dr. Marie Kmita, Director of the Genetics and Development research unit at the IRCM. "Moreover, we showed that drastically reducing the dose of Hox genes in mice transforms fingers into structures reminiscent of the extremities of fish fins. These findings further support the key role of Hox genes in the transition of fins to limbs during evolution, one of the most important anatomical innovations associated with the transition from aquatic to terrestrial life."
The study published in Science was a collaborative project between the teams supervised by Drs. Marie Kmita (IRCM), James Sharpe (CRG Barcelona, Spain) and Maria A. Ros (University of Cantabria, Spain). The research conducted at the IRCM was funded by the Canadian Institutes of Health Research and the Canada Research Chairs Program. The article's second first author Is Luciano Marcon from the European Molecular Biology Laboratory (EMBL) and the Pompeu Fabra University in Spain.
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The above story is reprinted from materials provided by Institut de recherches cliniques de Montreal.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- R. Sheth, L. Marcon, M. F. Bastida, M. Junco, L. Quintana, R. Dahn, M. Kmita, J. Sharpe, M. A. Ros. Hox Genes Regulate Digit Patterning by Controlling the Wavelength of a Turing-Type Mechanism. Science, 2012; 338 (6113): 1476 DOI: 10.1126/science.1226804
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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The Android Ecosystem Is Two-Faced: YotaPhone Has LCD On One Side, Electronic Paper Display On The Other
Fragmentation in the Android ecosystem can be a nightmare for developers?-- but despite all the variations between devices and operating system versions, it can remain a struggle for handset makers to produce smartphones that look distinctive from the rest of the pack. Now an enterprising Russian hardware maker is hoping its newest creation will be original and appealing enough to make some headway in the market. Yota Devices, a part of the same company that owns Russian LTE carrier Yota Mobile, has launched YotaPhone, a new Android handset that combines a full-colour touchscreen on one side, with an e-reader-style black-and-white electronic paper display on the other.Source: http://feedproxy.google.com/~r/Techcrunch/~3/KwZcvkMOTdo/
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In challenge to personalized cancer care, DNA isn't all-powerful
NEW YORK (Reuters) - The cancer cells were not behaving the way the textbooks say they should. Some of the cells in colonies that were started with colorectal tumor cells were propagating like mad; others were hardly multiplying. Some were dropping dead from chemotherapy and others were no more slowed by the drug than is a tsunami by a tissue. Yet the cells in each "clone" all had identical genomes, supposedly the all-powerful determinant of how cancer cells behave.
That finding, published online Thursday in Science, could explain why almost none of the new generation of "personalized" cancer drugs is a true cure, and suggests that drugs based on genetics alone will never achieve that holy grail.
Scientists not involved in the study praised it for correcting what Dr. Charis Eng, an oncologist and geneticist who leads the Genomic Medicine Institute at the Cleveland Clinic, called "the simple-minded" idea that tumor genomes alone explain cancer.
Calling the study "very exciting," she said the finding underlines that a tumor's behavior and, most important, its Achilles heel depend on something other than its DNA. Her own work, for instance, has shown that patients with identical mutations can have different cancers.
The core premise of the leading model of cancer therapy is that cells become malignant when they develop mutations that make them proliferate uncontrolled. Find a molecule that targets the "driver" mutation, and a pharmaceutical company will have a winner and patients will be cancer-free.
That's the basis for "molecularly targeted" drugs such as Pfizer's Xalkori for some lung cancers and Novartis's Gleevec for chronic myeloid leukemia. When those drugs stop working, the dogma says, it is because cells have developed new cancer-causing mutations that the drugs don't target.
In the new study, however, scientists found that despite having identical genetic mutations, colorectal cancer cells behaved as differently as if they were genetic strangers. The findings challenge the prevailing view that genes determine how individual cells in a solid tumor behave, including how they respond to chemotherapy and how actively they propagate.
If DNA is not the sole driver of tumors' behavior, said molecular geneticist John Dick of the Princess Margaret Cancer Centre in Toronto, who led the study, it suggests that, to vanquish a cancer entirely, drugs will have to target their non-genetic traits too, something few drug-discovery teams are doing.
Genomes are what cutting-edge clinics test for when they try to match a patient's tumor to the therapy most likely to squelch it.
For their study, Antonija Kreso, Catherine O'Brien and other scientists under Dick's direction took colorectal cancer cells from 10 patients and transplanted them into mice. They infected the cells with a special virus that let them track each cell, even after it divided and multiplied and was transplanted into another mouse, then another and another, through as many as five such "passages."
Only one in 10,000 tumor cells was responsible for keeping the cancer growing, the scientists found - in some cases for 500 days of repeated transplantation from one mouse to the next. Genetically-identical tumor cells stopped dividing within 100 days even without treatment.
Tumor cells that were not killed by chemotherapy - the scientists used oxaliplatin, a colon-cancer drug sold by Sanofi as Eloxatin - had the same mutations as cells that were. The survivors tended to be dormant, non-proliferating ones that suddenly became activated, causing the tumor to grow again. Yet the cells - dormant or active, invulnerable to chemo or susceptible - had identical genomes.
"I thought we'd be able to look at the genetics that let some cells propagate, or not be susceptible to chemotherapy, but lo and behold there was no genetic difference," said Dick. "That goes against a main dogma of the cancer enterprise: that if a tumor comes back after treatment it's because some cells acquired mutations that made them resistant."
That's true in some cases, he said, "but what our data are saying is, there are other biological properties that matter. Gene sequencing of tumors is definitely not the whole story when it comes to identifying which therapies will work."
The results were surprising enough, Dick said, that experts reviewing the paper for Science asked him to run additional tests to make sure the cells that behaved so differently were in fact genetic twins. He did, they were, and Science accepted the paper.
Other experts also praised the work, saying it supported the growing suspicion in the field that personalized cancer therapy is oversimplistic, at least in how it's sold to the public.
"It's not as simple as just sequencing mutations to tailor therapies to each tumor," said surgical oncologist Dr. Steven Libutti of the Montefiore Einstein Center for Cancer Care in New York City. "In my mind, the findings are not unexpected. Other things besides genes matter: the environment in which a tumor is growing, for instance, plays an important role in whether therapy will be effective."
Rather than targeting DNA alone, the Toronto scientists suspect, effective therapies would also take aim at what phase of its cycle a cell is in (dormant, growing or dividing, for example), which of its genes are activated, whether it sits in a region of the tumor that is starved of oxygen, and other non-genetic properties.
Nudging tumor cells out of their dormant phase and into their growth cycles, for instance, could make them more susceptible to chemotherapy, which generally targets rapidly dividing cells.
"Our findings raise questions about the resources put into sequence, sequence, sequence," said Dick. "That has led to one kind of therapeutic" - molecularly-targeted drugs - "but not the cures the public is being promised."
(Reporting by Sharon Begley; editing by Claudia Parsons)
Source: http://news.yahoo.com/challenge-personalized-cancer-care-dna-isnt-powerful-190146032--finance.html
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Thursday, December 13, 2012
CNBC's Fast Money: Stocks, Investing, Market Analysis - CNBC
A new report from the National Restaurant Association says sales will grow for the 4th straight year. Danny Meyer, CEO of Union Square Hospitality Group discusses what he's seeing in his own businesses, which include restaurants like Blue Smoke, Shake Shack and Eleven Madison Park. Also, a look at restaurant IPOs in the last year, shopping in the upscale consumer segment.
Source: http://www.cnbc.com/id/15838499/CNBCrsquos_Fast_Money_Stocks_Investing_Market_Analysis__CNBC
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Wednesday, December 12, 2012
Leaked chart appears to spill beans on Intel's Haswell desktop CPU range
The folks over at VR-Zone have snagged a chart which purports to represent Intel's plans for the Haswell architecture in 2013. If genuine, then we can expect at least 14 new desktop CPUs to arrive next year, including a range-topping 3.5GHz Core i7 with 400MHz of headroom in boost mode and a TDP of just 84W -- i.e. midway between Sandy and Ivy Bridge in terms of power consumption, but not bad when you consider this'll be a higher performance architecture with no transistor shrinkage. Integrated graphics have also apparently been tweaked, with a reference to HD 4600. Since we can't expect Intel to confirm the leak, we'll just have to file this one in the "plausible" cabinet. (What, you didn't know we had filing cabinets?)
Via: Ubergizmo
Source: VR-Zone (Translated)
Source: http://www.engadget.com/2012/12/12/haswell-leak/
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