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Wednesday, February 8, 2012

UK researchers rank best online advice for postnatal depression




(Medical Xpress) -- Researchers at the University of Sussex have identified the top five internet sites offering support for women struggling with postnatal mental illness such as depression or anxiety. Around 10-15 per cent of new mothers are diagnosed with postnatal mental illnesses, while around one in four women may have significant post-birth distress without meeting the criteria for a disorder. Many women turn to the internet to seek advice and reassurance over these conditions.
Health psychologists Donna Moore and Dr. Susan Ayers sorted through thousands of web sites and whittled down their selection to the top five sites for new mothers seeking information about postnatal depression and anxiety and the top five for healthcare professionals looking for ways to support patients.



For mums they are:
www.panda.org.au
www.hapis.org.uk
www.postpartumhealthalliance.org
www.postpartum.net
www.pndsa.co.za
And for health professionals:
www.postpartum.net
www.postpartumhealthalliance.org
 www.babybluesconnection.org
www.postpartumsupport.com
www.postpartumeducationandsupport.com
The research, published in the journal Archives of Women’s Mental Health, offers the latest systematic survey of web advice for postnatal psychological problems and serves as an authoritative guide to most reliable sites.
Women can suffer from various psychological problems after having a baby that range from mild baby blues to more severe depression, anxiety and psychosis. The researchers found that although there were thousands of sites devoted to postnatal depression (typing “postnatal depression” into Google returned more than a million results), the quality was extremely variable, with very few sites offering the full spectrum of easily accessed support, advice, information and reassurance about the different psychological problems women might encounter.
Many sites were hard to navigate, suffered from poorly edited content or had information that was out of date or just plain wrong.  Information focused on symptoms rather than risk factors or the potential negative impact of not dealing with the illness on children and families as well as the sufferer. There was some information on treatment, but it was generally superficial.
Most websites rarely had prominent information on what the users should do if they have thoughts of harming themselves or their infant.
Donna Moore says: “Most web sites did encourage women to seek medical help. However, information tended to be about depressive symptoms and largely ignored other forms of postnatal illness,namely anxiety, post traumatic stress disorder and puerperal psychosis. This could reinforce the common misconception that postnatal mental illness is solely depression or simply an extension of the ‘baby blues’.  Mothers need to know what the signs of the illness are and treatment options and health professionals need to know all the facts for effective screening. It is essential that web sites provide accurate and comprehensive information and advice for mothers and their families. Mothers need to be informed that if they get help they will get better.”
Dr. Ayers says:”The internet is often the first port of call for people worried about health issues. This is particularly the case for women suffering from depressive illness following the birth of a baby because they many find it difficult to leave the house with a young infant and, like all mental health issues, there is the fear of being stigmatised. Using the internet, therefore, provides a way of seeking reassurance, information and advice anonymously from home. Effective web sites are therefore important in directing women to the professional help they need while giving them the confidence to ask for it.”
To identify the best sites, the researchers searched for sites using the four main search engines using the terms “postnatal depression”, “postnatal illness”, “postpartum depression” and “postpartum illness”. The first 25 web sites for each key term were selected for review.
Each site had to be exclusively dedicated to postnatal mental health or have substantial information on postnatal mental illness. They were evaluated for accuracy of information, available resources and quality. A total of 114 sites were eventually surveyed.
It is hoped that through this systematic review, the top web sites will be used by healthcare professionals and help with the creation of new online resources, based on knowledge of how sufferers use web resources. Donna Moore and Susan Ayers are currently investigating how women with postnatal distress use and benefit from resources on the internet.
Accurate information on all symptoms is essential for healthcare professionals screening for postnatal mental illness and sufferers and their families deciding whether to get help.
More information: A review of postnatal mental health websites: help for healthcare professionals and patients, Archives of Women’s Mental Health.
Provided by University of Sussex
"UK researchers rank best online advice for postnatal depression." February 7th, 2012. http://medicalxpress.com/news/2012-02-uk-online-advice-postnatal-depression.html
Posted by
Robert Karl Stonjek

மனைவியைப் புரிந்து கொள்ளுங்கள்

ஒரு மனைவி, தன் கணவனிடம் அப்படி என்னதான் எதிர்பார்க்கிறாள்….? விதவிதமான பட்டுப்புடவைகளா? தங்கம், வைரம் என்று நகைக் குவியலா? பெரிய பங்களா, ஏ.சி.கார் என்று ஆடம்பர விஷயங்களா….? நிறைய சம்பளமும், ஏகப்பட்ட பேங்க் பேலன்ஸும் வேண்டுமென்றா? அல்லது தன் கணவன் மன்மதன் போல் அழகாக இருக்க வேண்டுமென்றா?

இல்லவே இல்லை…! மனைவியின் எதிர்பார்ப்பே வேறு விதமானது. அவள் அப்படி என்னதான் எதிர்பார்க்கிறாள் என்று கணவன் தெரிந்து கொண்டாலே அவர்களுடைய இல்லற வாழ்க்கை இன்னும் அன்னியோன்யம் கூடியதாக அமையும்!

கணவனிடம் ஒரு மனைவி எதிர்பார்க்கும் விசயங்கள் இவை தான்
ஆண்களே… உங்கள் மனைவியைப் புரிந்துகொள்ள இதைப் படியுங்கள்….
  • அன்பாகப் பிரியமாக இருங்கள்… அதுவே ஆயிரக்கணக்கான மதிப்புள்ள புடவைகள் தராத மகிழ்ச்சியைத் தரும்!.
  • மனது புண்படும்படி பேசாதீர்கள். அது உங்கள் மனைவிக்கு உங்கள் மேல் உள்ள பிரியத்தைக் கூடச் சில சமயங்களில் குறைத்துவிடக் கூடும். அது போல அடிக்கடி கோபப்படவும் செய்யாதீர்கள்.
  • சாப்பாட்டில் குறை சொல்லக்கூடாது. பல கணவன்மார்கள் இதைத்தான் பெரிய கடமையாகச் செய்து கொண்டிருக்கிறார்கள். உப்பு அதிகமாக இருக்கிறது என்று நீங்கள் நினைத்தீர்கள் என்றால், இன்னிக்கி சமையல் சூப்பரா இருக்கு என்று முதலில் பாராட்டிவிடுங்கள். அப்புறம் மெதுவாக கொஞ்சம் உப்பைக் குறைச்சு போட்டிருக்கலாம் என்று சொல்லிப் பாருங்கள். உங்கள் மனைவி விஷயத்தைப் புரிந்து கொண்டு அடுத்த முறை இன்னும் சூப்பராக சமைப்பார்!
  • எந்த இடத்திலும் மனைவியை விட்டுக்கொடுக்கக் கூடாது. பலர் முன்னிலையில் திட்டவோ, மரியாதைக் குறைவாகவோ பேசாதீர்கள். இது உங்கள் அன்யோன்யத்தைக் குறைத்துவிடும்.
  • உறவினர் வீட்டு விசேஷங்களுக்கு மனைவியுடன் செல்லுங்கள். அது மனைவிக்கு நீங்கள் மரியாதை கொடுப்பதாகத் தோன்றச் செய்யும்.
  • எந்த ஒரு விஷயத்தையும் மனைவியுடன் கலந்து ஆலோசிக்க வேண்டும்.
  • மனைவி சொல்வதைக் காது கொடுத்துக் கேளுங்கள். காதுக்கு வைரத்தோடு வாங்கித் தருவதைவிட சந்தோஷம் தரும் விஷயம் இது.
  • மனைவியிடம் மனம்விட்டுப் பேசுங்கள். நிறைய விஷயங்களுக்கு நல்ல தீர்வு கிடைக்கும்.
  • மனைவி வித்தியாசமாக ஏதாவது செய்தால் ரசித்துப் பாராட்டுங்கள்.
  • மாதம் ஒரு முறையாவது வெளியில் கூட்டிக் கொண்டு போங்கள். உங்கள் பேரிலுள்ள கோபம்கூட ஓடி விடும்.
  • பிள்ளைகள் படிப்பில் அக்கறை கொண்டு உதவி செய்யுங்கள். அப்படிச் செய்தால் மனைவிக்கு இன்னும் உங்கள் மீதுள்ள காதலை அதிகப்படுத்தும்.
  • இரவு விழித்து அழும் குழந்தையைப் பார்ப்பதில் உங்களுக்கு இருக்கும் அதே கஷ்டம் போலத்தான் உங்கள் மனைவிக்கும் இருக்கும். எல்லா விஷயங்களுக்கும் இது பொருந்தும்.
  • மனைவி உடல்நலம் இல்லாமல் இருக்கும் பொழுது அக்கறையுடன் உடன் இருந்து கவனியுங்கள். அவளுடைய சின்னச்சின்ன தேவைகளைப் பூர்த்தி செய்து சிறு சிறு உதவிகள் செய்தாலே அவளுக்கு மிகுந்த மகிழ்ச்சி ஏற்படும்.
  • அம்மாவிடம் காட்டும் பாசத்தை மனைவியிடமும் காட்டுங்கள். தாயளவுக்கு தாரமும் வாழ்க்கையில் முக்கியத்துவம் வாய்ந்தவர்தான்!
  • எங்கு சென்றாலும் மனைவியிடம் சொல்லி விட்டே கிளம்புங்கள். குடும்பத்தில் பல குழப்பங்களைத் தடுக்க இது உதவும்.
  • மனைவியின் பிறந்த நாளை அவரைக் கேட்காமலேயே தெரிந்து வைத்துக் கொண்டு கட்டாயம் ஏதாவது சிறு பரிசாவது வாங்கிக் கொடுங்கள். அல்லது அவளுக்கு எது பிடிக்கும் என்று தெரிந்துகொண்டு அதை இன்ப அதிர்ச்சி ஏற்படுத்தும் பரிசாகக் கொடுக்கலாம்.
  • ரொம்ப முக்கியமான விஷயம் இது… மனைவியிடம் பொய் பேசாமல் இருங்கள்.
  • கடைசியாக… கெட்ட பழக்கங்கள் எதுவும் இல்லாமல் இருக்கும் கணவனையே மனைவி கடவுள் தனக்குத் தந்த பெரும் வரமாக நினைப்பாள்.

Brilliant Painting From National Gallery Of London!!




















Green tea found to reduce disability in the elderly




green teaGreen tea. Credit: Wikimedia Commons
(Medical Xpress) -- A lot of research has been done over the past several years looking into the health benefits of green tea. As a result, scientists have found that regular consumption of the beverage leads to a reduction in several maladies often associated with aging, such as osteoporosis, stroke and cognitive impairment. But until now, according to the authors of a new study on its benefits, no such studies have been undertaken to determine if regular tea drinking provides other benefits, such as a reduction in functional disabilities. Because of this, a research project was undertaken by a team from Tokyo’s Graduate School of Medicine, and they have found that older people who drink more green tea tend to have less functional disabilities than do those who don’t. They have published their findings in The American Journal of Clinical Nutrition.
The team describes functional disabilities as those that interfere with living a normal life, such as being able to dress or bathe without assistance, or to perform household chores, or go for a walk. To find out if drinking green tea regularly helps people ward off such disabilities as they age, the team surveyed 13,998 adults age 65 and over and followed their eating, drinking and health habits over a three year period. They also accessed Japan’s Long-term Care Insurance database to help in gathering statistics.
After compiling all the data, the team found that people who drank more of the green tea, tended to have the least number of functional disabilities. Put into numbers, they found that approximately 13% of those tested that drank one cup or less of the tea every day wound up with a functional disability, whereas only 7% of those who drank five cups or more each day became so.
The research team isn’t claiming they’ve found absolute proof that drinking a lot of green tea every day will ward of functional disabilities, but that instead their research suggests that it seems likely. They say that those who drank more green tea every day also tended to live healthier lifestyles, such as eating more fish, fruits and vegetables, staying more active and maintaining a more well-rounded social life that included family. However, they note, even after discounting such factors, those that drank more tea still did better than did those who did not.
Researchers in general aren’t really clear about why green tea has health benefits, but suspect it has something to do with a compound in it called EGCG, an antioxidant that appears to ward off cell damage that can lead to disease.
More information: Green tea consumption and the risk of incident functional disability in elderly Japanese: the Ohsaki Cohort 2006 Study, Am J Clin Nutr, First published January 25, 2012, doi: 10.3945/​ajcn.111.023200
Abstract 
Background: Previous studies have reported that green tea consumption is associated with a lower risk of diseases that cause functional disability, such as stroke, cognitive impairment, and osteoporosis. Although it is expected that green tea consumption would lower the risk of incident functional disability, this has never been investigated directly. 
Objective: The objective was to determine the association between green tea consumption and incident functional disability in elderly individuals. 
Design: We conducted a prospective cohort study in 13,988 Japanese individuals aged ≥65 y. Information on daily green tea consumption and other lifestyle factors was collected via questionnaire in 2006. Data on functional disability were retrieved from the public Long-term Care Insurance database, in which subjects were followed up for 3 y. We used Cox proportional hazards regression analysis to investigate the association between green tea consumption and functional disability. 
Results: The 3-y incidence of functional disability was 9.4% (1316 cases). The multiple-adjusted HR (95% CI) of incident functional disability was 0.90 (0.77, 1.06) among respondents who consumed 1–2 cups green tea/d, 0.75 (0.64, 0.88) for those who consumed 3–4 cups/d, and 0.67 (0.57, 0.79) for those who consumed ≥5 cups/d in comparison with those who consumed <1 cup/d (P-trend < 0.001). 
Conclusion: Green tea consumption is significantly associated with a lower risk of incident functional disability, even after adjustment for possible confounding factors.
© 2011 Medical Xpress
"Green tea found to reduce disability in the elderly." February 7th, 2012. http://medicalxpress.com/news/2012-02-green-tea-disability-elderly.html
 
Posted by
Robert Karl Stonjek

Materials for First Optical Fibers With High-Speed Electronic Function Are Developed


                                                 For the first time, researchers have developed crystalline materials that allow an optical fiber to have integrated, high-speed electronic functions. The potential applications of such optical fibers include improved telecommunications and other hybrid optical and electronic technologies, improved laser technology, and more-accurate remote-sensing devices. The international team, led by John Badding, a professor of chemistry at Penn State, will publish its findings in the journal Nature Photonics. The team built an optical fiber with a high-speed electronic junction -- the active boundary where all the electronic action takes place -- integrated adjacent to the light-guiding fiber core. Light pulses (white spheres) traveling down the fiber can be converted to electrical signals (square wave) inside the fiber by the junction. The potential applications of such optical fibers include improved telecommunications and other hybrid optical and electronic technologies and improved laser technology. (Credit: John Badding lab, Penn State University)


Science Daily — For the first time, a group of chemists, physicists, and engineers has developed crystalline materials that allow an optical fiber to have integrated, high-speed electronic functions. The potential applications of such optical fibers include improved telecommunications and other hybrid optical and electronic technologies, improved laser technology, and more-accurate remote-sensing devices. The research was initiated by Rongrui He, a postdoctoral researcher in the Department of Chemistry at Penn State University.



The international team, led by John Badding, a professor of chemistry at Penn State, will publish its findings in the journal Nature Photonics.
Badding explained that one of the greatest current technological challenges is exchanging information between optics and electronics rapidly and efficiently. Existing technology has resulted in sometimes-clumsy ways of merging optical fibers with electronic chips -- silicon-based integrated circuits that serve as the building blocks for most semiconductor electronic devices such as solar cells, light-emitting diodes (LEDs), computers, and cell phones. "The optical fiber is usually a passive medium that simply transports light, while the chip is the piece that performs the electrical part of the equation," Badding said. "For example, light is transmitted from London to New York via fiber-optic cables when two people set up a video call on their computers. But the computer screens and associated electronic devices have to take that light and convert it to an image, which is an electrical process. Light and electricity are working in concert in a process called an OEO conversion, or an optical-electrical-optical conversion." Badding said that, ideally, rather than coupling the optical fiber to the chip, as is routine in existing technology, a "smart fiber" would have the electronic functions already built in.
The integration of optical fibers and chips is difficult for many reasons. First, fibers are round and cylindrical, while chips are flat, so simply shaping the connection between the two is a challenge. Another challenge is the alignment of pieces that are so small. "An optical fiber is 10 times smaller than the width of a human hair. On top of that, there are light-guiding pathways that are built onto chips that are even smaller than the fibers by as much as 100 times," Badding said. "So imagine just trying to line those two devices up. That feat is a big challenge for today's technology."
To address these challenges, the team members took a different approach. Rather than merge a flat chip with a round optical fiber, they found a way to build a new kind of optical fiber with its own integrated electronic component, thereby bypassing the need to integrate fiber-optics onto a chip. To do this, they used high-pressure chemistry techniques to deposit semiconducting materials directly, layer by layer, into tiny holes in optical fibers. "The big breakthrough here is that we don't need the whole chip as part of the finished product. We have managed to build the junction -- the active boundary where all the electronic action takes place -- right into the fiber," said Pier J. A. Sazio of the University of Southampton in the United Kingdom and one of the team's leaders. "Moreover, while conventional chip fabrication requires multimillion-dollar clean-room facilities, our process can be performed with simple equipment that costs much less."
Sazio added that one of the key goals of research in this field is to create a fast, all-fiber network. "If the signal never leaves the fiber, then it is a faster, cheaper, and more efficient technology," said Sazio. "Moving technology off the chip and directly onto the fiber, which is the more-natural place for light, opens up the potential for embedded semiconductors to carry optoelectronic applications to the next level. At present, you still have electrical switching at both ends of the optical fiber. If we can actually generate signals inside a fiber, a whole range of optoelectronic applications becomes possible."
The research also has many potential non-telecommunications applications. "For example, our work also represents a very different approach to fabricating semiconductor junctions that we are investigating for solar-cell applications," said Badding.

Preference for Fatty Foods May Have Genetic Roots


A preference for fatty foods has a genetic basis, according to researchers, who discovered that people with certain forms of the CD36 gene may like high-fat foods more than those who have other forms of this gene. (Credit: National Cancer Institute)                                                                                       Science Daily — A preference for fatty foods has a genetic basis, according to researchers, who discovered that people with certain forms of the CD36 gene may like high-fat foods more than those who have other forms of this gene.



The results help explain why some people struggle when placed on a low-fat diet and may one day assist people in selecting diets that are easier for them to follow. The results also may help food developers create new low-fat foods that taste better.
"Fat is universally palatable to humans," said Kathleen Keller, assistant professor of nutritional sciences, Penn State. "Yet we have demonstrated for the first time that people who have particular forms of the CD36 gene tend to like higher fat foods more and may be at greater risk for obesity compared to those who do not have this form of the gene. In animals, CD36 is a necessary gene for the ability to both detect and develop preferences for fat. Our study is one of the first to show this relationship in humans."
Keller and a team of scientists from Penn State, Columbia University, Cornell University and Rutgers University examined 317 African-American males and females because individuals in this ethnic group are highly vulnerable to obesity and thus are at greatest risk for obesity-related diseases.
The team gave the participants Italian salad dressings prepared with varying amounts of canola oil, which is rich in long-chain fatty acids. The participants were then asked to rate their perceptions of the dressings' oiliness, fat content and creaminess on a scale anchored on the ends with "extremely low" and "extremely high."
The team also gave participants questionnaires aimed at understanding their food preferences. Participants rated how much they liked each food on a scale anchored with "dislike extremely" and "like extremely." Foods included on the questionnaire were associated with poor dietary intake and health outcomes, such as half-and-half, sour cream, mayonnaise, bacon, fried chicken, hot dogs, French fries, cheese, chips, cake, cookies and doughnuts.
The researchers collected saliva samples from the participants to determine which forms of CD36 they had. From the saliva samples, they extracted DNA fragments and examined differences in the CD36 gene contained within the fragments.
They found that participants who had the "AA" form of the gene -- present in 21 percent of the population -- rated the salad dressings as creamier than individuals who had other forms of the gene. These individuals reported that the salad dressings were creamier regardless of how much fat was actually in them. The researchers also found that "AA" individuals liked salad dressings, half-and-half, olive oil and other cooking oils more than those who had other forms of the gene. The results are published in a recent issue of the journal Obesity.
"It is possible that the CD36 gene is associated with fat intake and therefore obesity through a mechanism of oral fat perception and preference," said Keller. "In other words, our results suggest that people with certain forms of the CD36 gene may find fat creamier and more enjoyable than others. This may increase their risk for obesity and other health problems."
According to Keller, having certain forms of a gene that help in the perception and enjoyment of fats in foods might once have been an advantage.
"Fats are essential in our diets," she said. "In our evolutionary history, people who were better able to recognize fats in foods were more likely to survive. Such forms of the gene, however, are less useful to us today as most of us no longer have to worry about getting enough fats in our diets."
In fact, she added, having such forms of a gene can be detrimental in today's world of fat-laden convenience foods.
"Our results may help explain why some people have more difficulty adhering to a low-fat diet than other people and why these same people often do better when they adopt high-fat, low-carbohydrate diets such as the Atkins diet," said Keller. "We hope these results will one day help people select diets that are easier for them to follow. We also think the results could help food developers create better tasting low-fat foods that appeal to a broader range of the population."
In the future, the team plans to expand the population they examine to include children.
"By the time we are adults it is very hard for us to change our eating behaviors," said Keller. "So if we can determine which children have forms of the CD36 gene, as well as other genes that are associated with greater liking of fats, we can help them develop healthier eating behaviors at a young age."
Keller also plans to incorporate novel techniques, such as functional magnetic resonance imaging (fMRI), to better understand why certain forms of the CD36 gene are linked to higher fat preferences.
"We plan to scan children while they are tasting high-fat foods and beverages so that we can see how their brains react to fats," she said. "By doing this, we may be able to develop foods that are perceived by the brain as palatable high-fat treats, even though in reality, they are low-fat and healthy."
Kathleen Keller was an assistant professor and research associate at Columbia University and the New York Nutrition Obesity Research Center when she conducted the research. Other authors on the paper include Columbia University graduate students Lisa Liang, Johannah Sakimura, Daniel May and Christopher van Belle; Cornell University undergraduate students Cameron Breen and Elissa Driggin; and Beverly Tepper, professor, Rutgers University. Also at Columbia were Patricia Lanzano, research coordinator; Liyong Deng, research technician; and Wendy Chung, assistant professor.
The National Institutes of Health funded this research.

Placebos and Distraction: New Study Shows How to Boost the Power of Pain Relief, Without Drugs



Placebos reduce pain by creating an expectation of relief. Distraction -- say, doing a puzzle -- relieves it by keeping the brain busy. But do they use the same brain processes? Neuromaging suggests they do. (Credit: © psdesign1 / Fotolia)

Science Daily — Placebos reduce pain by creating an expectation of relief. Distraction -- say, doing a puzzle -- relieves it by keeping the brain busy. But do they use the same brain processes? Neuromaging suggests they do. When applying a placebo, scientists see activity in the dorsolateral prefrontal cortex. That's the part of the brain that controls high-level cognitive functions like working memory and attention -- which is what you use to do that distracting puzzle.



Now a new study challenges the theory that the placebo effect is a high-level cognitive function. The authors -- Jason T. Buhle, Bradford L. Stevens, and Jonathan J. Friedman of Columbia University and Tor D. Wager of the University of Colorado Boulder -- reduced pain in two ways -- either by giving them a placebo, or a difficult memory task. lacebo. But when they put the two together, "the level of pain reduction that people experienced added up. There was no interference between them," says Buhle. "That suggests they rely on separate mechanisms." The findings, published inPsychological Science, a journal of the Association for Psychological Science, could help clinicians maximize pain relief without drugs.
In the study, 33 participants came in for three separate sessions. In the first, experimenters applied heat to the skin with a little metal plate and calibrated each individual's pain perceptions. In the second session, some of the people applied an ordinary skin cream they were told was a powerful but safe analgesic. The others put on what they were told was a regular hand cream. In the placebo-only trials, participants stared at a cross on the screen and rated the pain of numerous applications of heat -- the same level, though they were told it varied. For other trials they performed a tough memory task -- distraction and placebo simultaneously. For the third session, those who'd had the plain cream got the "analgesic" and vice versa. The procedure was the same.
The results: With either the memory task or the placebo alone, participants felt less pain than during the trials when they just stared at the cross. Together, the two effects added up; they didn't interact or interfere with each other. The data suggest that the placebo effect does not require executive attention or working memory.
So what about that neuroimaging? "Neuroimaging is great," says Buhle, "but because each brain region does many things, when you see activation in a particular area, you don't know what cognitive process is driving it." This study tested the theory about how placebos work with direct behavioral observation.
The findings are promising for pain relief. Clinicians use both placebos and distraction -- for instance, virtual reality in burn units. But they weren't sure if one might diminish the other's efficacy. "This study shows you can use them together," says Buhle, "and get the maximum bang for your buck without medications."

Why Do Cells Age? Discovery of Extremely Long-Lived Proteins May Provide Insight Into Cell Aging and Neurodegenerative Diseases



This microscope image shows extremely long-lived proteins, or ELLPs, glowing green on the outside of the nucleus of a rat brain cell. DNA inside the nucleus is pictured in blue. The Salk scientists discovered that the ELLPs, which form channels through the wall of the nucleus, lasted for more than a year without being replaced. Deterioration of these proteins may allow toxins to enter the nucleus, resulting in cellular aging. (Credit: Courtesy of Brandon Toyama, Salk Institute for Biological Studies)

Science Daily  — One of the big mysteries in biology is why cells age. Now scientists at the Salk Institute for Biological Studies report that they have discovered a weakness in a component of brain cells that may explain how the aging process occurs in the brain.



The scientists discovered that certain proteins, called extremely long-lived proteins (ELLPs), which are found on the surface of the nucleus of neurons, have a remarkably long lifespan.
While the lifespan of most proteins totals two days or less, the Salk Institute researchers identified ELLPs in the rat brain that were as old as the organism, a finding they reported February 3 in Science.
The Salk scientists are the first to discover an essential intracellular machine whose components include proteins of this age. Their results suggest the proteins last an entire lifetime, without being replaced.
ELLPs make up the transport channels on the surface of the nucleus; gates that control what materials enter and exit. Their long lifespan might be an advantage if not for the wear-and-tear that these proteins experience over time. Unlike other proteins in the body, ELLPs are not replaced when they incur aberrant chemical modifications and other damage.
Damage to the ELLPs weakens the ability of the three-dimensional transport channels that are composed of these proteins to safeguard the cell's nucleus from toxins, says Martin Hetzer, a professor in Salk's Molecular and Cell Biology Laboratory, who headed the research. These toxins may alter the cell's DNA and thereby the activity of genes, resulting in cellular aging.
Funded by the Ellison Medical Foundation and the Glenn Foundation for Medical Research, Hetzer's research group is the only lab in the world that is investigating the role of these transport channels, called the nuclear pore complex (NPC), in the aging process.
Previous studies have revealed that alterations in gene expression underlie the aging process. But, until the Hetzer lab's discovery that mammals' NPCs possess an Achilles' heel that allows DNA-damaging toxins to enter the nucleus, the scientific community has had few solid clues about how these gene alterations occur.
"The fundamental defining feature of aging is an overall decline in the functional capacity of various organs such as the heart and the brain," says Hetzer. "This decline results from deterioration of the homeostasis, or internal stability, within the constituent cells of those organs. Recent research in several laboratories has linked breakdown of protein homeostasis to declining cell function."
The results that Hetzer and his team just report suggest that declining neuron function may originate in ELLPs that deteriorate as a result of damage over time.
"Most cells, but not neurons, combat functional deterioration of their protein components through the process of protein turnover, in which the potentially impaired parts of the proteins are replaced with new functional copies," says Hetzer.
"Our results also suggest that nuclear pore deterioration might be a general aging mechanism leading to age-related defects in nuclear function, such as the loss of youthful gene expression programs," he adds.
The findings may prove relevant to understanding the molecular origins of aging and such neurodegenerative disorders as Alzheimer's disease and Parkinson's disease.
In previous studies, Hetzer and his team discovered large filaments in the nuclei of neurons of old mice and rats, whose origins they traced to the cytoplasm. Such filaments have been linked to various neurological disorders including Parkinson's disease. Whether the misplaced molecules are a cause, or a result, of the disease has not yet been determined.
Also in previous studies, Hetzer and his team documented age-dependent declines in the functioning of NPCs in the neurons of healthy aging rats, which are laboratory models of human biology.
Hetzer's team includes his colleagues at the Salk Institute as well as John Yates III, a professor in the Department of Chemical Physiology of The Scripps Research Institute.
When Hetzer decided three years ago to investigate whether the NPC plays a role in initiating or contributing to the onset of aging and certain neurodegenerative diseases, some members of the scientific community warned him that such a study was too bold and would be difficult and expensive to conduct. But Hetzer was determined despite the warnings.

Warning! Collision imminent! The brain's quick interceptions help you navigate the world




Researchers at The Neuro and the University of Maryland have figured out the mathematical calculations that specific neurons employ in order to inform us of our distance from an object and the 3-D velocities of moving objects and surfaces relative to ourselves.
When you are about to collide into something and manage to swerve away just in the nick of time, what exactly is happening in your brain? A new study from the Montreal Neurological Institute and Hospital – The Neuro, McGill University shows how the brain processes visual information to figure out when something is moving towards you or when you are about to head into a collision. The study, published in the Proceedings of the National Academy of Sciences (PNAS), provides vital insight into our sense of vision and a greater understanding of the brain.
Researchers at The Neuro and the University of Maryland have figured out the mathematical calculations that specific neurons employ in order to inform us of our distance from an object and the 3D velocities of moving objects and surfaces relative to ourselves. Highly specialized neurons located in the brain's visual cortex, in an area known as MST, respond selectively to motion patterns such as expansion, rotation, and deformation. However, the computations underlying such selectivity were unknown until now.
Using mathematical models and sophisticated recording techniques, researchers have discovered how individual MST neurons function. "Area MST is typical of high-level visual cortex, in that information about important aspects of vision can be seen in the firing patterns of single neurons. A classic example is a neuron that only fires when the subject is looking at the image of a particular face. This type of neuron has to gather information from other neurons that are selective to simpler features, like lines, colors, and textures, and combine these pieces of information in a fairly sophisticated way," says Dr. Christopher Pack, neuroscientist at The Neuro and senior author. "Similarly, for motion detection, neurons have to combine input from many other neurons earlier in the visual pathway, in order to determine whether something is moving toward you or just drifting past." The brain's visual pathway is made up of building blocks. For example, neurons in the retina respond to very simple stimuli, such as small spots of light. Further along the visual pathway, neurons respond to more complex stimulus such as straight lines, by combining inputs from neurons earlier on. Neurons further along respond to even more complex stimulus such as combinations of lines (angles), ultimately leading to neurons that can respond to, or recognize, faces and objects for example.
The research team found that a remarkably simple computation lies at the heart of this sophisticated neural selectivity: MST neurons appear to be capable of performing a multiplicative operation on their inputs. These inputs come from neurons one step earlier in the visual pathway, in a well-studied area known as MT. In other words, the inputs of MT neurons are multiplied in order to get the output of MST neurons. This turns out to be remarkably similar to what has been observed in other brain areas and in other species, suggesting it may reflect a general strategy by which brains process sensory information. "One interesting aspect of the computation is that it appears to be about the same as what other people have found in flies and beetles, suggesting that evolution solved this problem once, at least a few hundred million years ago."
"We developed a new motion stimulus with a morphing pattern flow (e.g. dots on a screen that are expansive, swirl around, circle to the right, contract etc) and recorded MST neurons responding to these stimuli," says Patrick Mineault, Ph.D. candidate at The Neuro and primary author on the study. "We circumvented the issue of increasing complexities of calculations along the various steps of the visual pathway by incorporating known data from neurons just one step earlier in the pathway - area MT, which precedes MST. As we now had measurements of the output of the MST neurons from the study's recordings, and already knew the input of MT neurons, we could calculate the math linking these two functions – and it turns out to be a multiplicative function." The mathematical models successfully account for the stimulus selectivity of some of the brain's complex motion neurons - which are vitally important in helping navigate us through the world.
Provided by McGill University
"Warning! Collision imminent! The brain's quick interceptions help you navigate the world." February 7th, 2012.http://medicalxpress.com/news/2012-02-collision-imminent-brain-quick-interceptions.html
 

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Robert Karl Stonjek

Engineers Weld Nanowires With Light



A titled, cross-sectional scanning electron microscope image of plasmonically welded nanowires of silver. (Credit: Mark Brongersma, Stanford)

Science Daily  — At the nano level, researchers at Stanford have discovered a new way to weld together meshes of tiny wires. Their work could lead to innovative electronics and solar applications. To succeed, they called upon plasmonics.



One area of intensive research at the nanoscale is the creation of electrically conductive meshes made of metal nanowires. Promising exceptional electrical throughput, low cost and easy processing, engineers foresee a day when such meshes are common in new generations of touch-screens, video displays, light-emitting diodes and thin-film solar cells.
Standing in the way, however, is a major engineering hurdle: In processing, these delicate meshes must be heated or pressed to unite the crisscross pattern of nanowires that form the mesh, damaging them in the process.
In a paper just published in the journal Nature Materials, a team of engineers at Stanford has demonstrated a promising new nanowire welding technique that harnesses plasmonics to fuse the wires with a simple blast of light.
Self-limiting
At the heart of the technique is the physics of plasmonics, the interaction of light and metal in which the light flows across the surface of the metal in waves, like water on the beach.
"When two nanowires lay crisscrossed, we know that light will generate plasmon waves at the place where the two nanowires meet, creating a hot spot. The beauty is that the hot spots exist only when the nanowires touch, not after they have fused. The welding stops itself. It's self-limiting," explained Mark Brongersma, an associate professor of materials science engineering at Stanford and an expert in plasmonics. Brongersma is one of the study's senior authors.
"The rest of the wires and, just as importantly, the underlying material are unaffected," noted Michael McGehee, a materials engineer and also senior author of the paper. "This ability to heat with precision greatly increases the control, speed and energy efficiency of nanoscale welding."
In before-and-after electron-microscope images, individual nanowires are visually distinct prior to illumination. They lay atop one another, like fallen trees in the forest. When illuminated, the top nanowire acts like an antenna of sorts, directing the plasmon waves of light into the bottom wire and creating heat that welds the wires together. Post-illumination images show X-like nanowires lying flat against the substrate with fused joints.
Transparency
In addition to making it easier to produce stronger and better performing nanowire meshes, the researchers say that the new technique could open the possibility of mesh electrodes bound to flexible or transparent plastics and polymers.
To demonstrate the possibilities, they applied their mesh on Saran wrap. They sprayed a solution containing silver nanowires in suspension on the plastic and dried it. After illumination, what was left was an ultrathin layer of welded nanowires.
"Then we balled it up like a piece of paper. When we unfurled the wrap, it maintained its electrical properties," said co-author Yi Cui, an associate professor materials science and engineering. "And when you hold it up, it's virtually transparent."
This could lead to inexpensive window coatings that generate solar power while reducing glare for those inside, the researchers said.
"In previous welding techniques that used a hotplate, this would never have been possible," said lead author, Erik C. Garnett, PhD, a post-doctoral scholar in materials science who works with Brongersma, McGehee and Cui. "The Saran wrap would have melted far sooner than the silver, destroying the device instantly."
"There are many possible applications that would not even be possible in older annealing techniques," said Brongersma. "This opens some interesting, simple and large-area processing schemes for electronic devices -- solar, LEDs and touch-screen displays, especially."
This research was supported by the Center for Advanced Molecular Photovoltaics (CAMP) at Stanford University funded by King Abdullah University of Science and Technology (KAUST).

Exercise Triggers Stem Cells in Muscle



                   Science Daily — University of Illinois researchers determined that an adult stem cell in muscle is responsive to exercise, a discovery that may link exercise and muscle health. The findings could lead to new therapeutic techniques using these cells to rehabilitate injured muscle and prevent or restore muscle loss with age.


Mesenchymal stem cells (MSCs) in skeletal muscle have been known to be important for muscle repair in response to non-physiological injury, predominantly in response to chemical injections that significantly damage muscle tissue and induce inflammation. The researchers, led by kinesiology and community health professor Marni Boppart, investigated whether MSCs also responded to strain during exercise, and if so, how.
"Since exercise can induce some injury as part of the remodeling process following mechanical strain, we wondered if MSC accumulation was a natural response to exercise and whether these cells contributed to the beneficial regeneration and growth process that occurs post-exercise," said Boppart, who also is affiliated with the Beckman Institute for Advanced Science and Technology at the U. of I.
The researchers found that MSCs in muscle are very responsive to mechanical strain. They witnessed MSC accumulation in muscle of mice after vigorous exercise. Then, they determined that although MSCs don't directly contribute to building new muscle fibers, they release growth factors that spur other cells in muscle to fuse and generate new muscle, providing the cellular basis for enhanced muscle health following exercise.
A key element to the Illinois team's method was in exercising the mice before isolating the cells to trigger secretion of beneficial growth factors. Then, they dyed the cells with a fluorescent marker and injected them into other mice to see how MSCs coordinated with other muscle-building cells.
In addition to examining the cells in vivo, the researchers studied the cells' response to strain on different substrates. They found that MSC response is very sensitive to the mechanical environment, indicating that conditions of muscle strain affect the cells' activity.
"These findings are important because we've identified an adult stem cell in muscle that may provide the basis for muscle health with exercise and enhanced muscle healing with rehabilitation/movement therapy," Boppart said. "The fact that MSCs in muscle have the potential to release high concentrations of growth factor into the circulatory system during exercise also makes us wonder if they provide a critical link between enhanced whole-body health and participation in routine physical activity."
Next, the group hopes to determine whether these cells contribute to the decline in muscle mass over a person's lifetime. Preliminary data suggest MSCs become deficient in muscle with age. The team hopes to develop a combinatorial therapy that utilizes molecular and stem-cell-based strategies to prevent age-related muscle loss.
"Although exercise is the best strategy for preserving muscle as we age, some individuals are just not able to effectively engage in physical activity," Boppart said. "Disabilities can limit opportunities for muscle growth. We're working hard to understand how we can best utilize these cells effectively to preserve muscle mass in the face of atrophy."
The team published its findings in the journal PLoS One. The Illinois Regenerative Medicine Institute, the Ellison Medical Foundation and the Mary Jane Neer Foundation supported this work.

Why Bad Immunity Genes Survive: Study Implicates Arms Race Between Genes and Germs


This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or "budding" out of an infected white blood cell known as a T-cell. By allowing the Friend virus to mutate and evolve in mice, University of Utah researchers produced new evidence that an arms race between microbes and immune-system MHC genes is responsible for maintaining an amazing diversity of those genes, even though some of them are responsible for autoimmune and infectious diseases that make us sick. (Credit: Elizabeth Fischer and Kim Hasenkrug, NIH)      Science Daily  — University of Utah biologists have found new evidence for why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs -- even though some of those genes make us susceptible to infections and to autoimmune diseases.

"Major histocompatibility complex" (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.
"This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated," says biology Professor Wayne Potts. "They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases."
By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs -- known technically as "antagonistic coevolution." The findings will be published online the week of Feb. 6, 2012, in the Proceedings of the National Academy of Sciences.
Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.
Theories for the Diversity of Immune-System MHC Genes
Most genes in humans and other vertebrate have only one or two "alleles," which are varieties or variants of a single gene. Although any given person carries no more than 12 varieties of the six human MHC genes, the human population has anywhere from hundreds to 2,300 varieties of each of the six human genes that produce MHC proteins.
"The mystery is why there are so many different versions of the same [MHC] genes in the human population," Kubinak says, especially because many people carry MHCs that make them susceptible to many pathogens (including the AIDS virus, malaria and hepatitis B and C) and autoimmune diseases (including type I diabetes, rheumatoid arthritis, lupus, multiple sclerosis, irritable bowel disease and ankylosing spondylitis).
Scientists have proposed three theories for why so many MHC gene variants exist in vertebrate animal populations (invertebrates don't have MHCs), and say all three likely are involved in maintaining the tremendous diversity of MHCs:
-- An organism with more MHC varieties has a better immune response than organisms with fewer varieties, so over time, organisms with more MHCs are more likely to survive. However, this theory cannot explain the full extent of MHC diversity.
-- Previous research indicates people and other animals are attracted to the smell of potential mates with MHCs that are "foreign" rather than "self." Parents with different MHC variants produce children with more MHCs and thus stronger immune systems.
-- Antagonistic coevolution between an organism and its pathogens. Kubinak says: "We have an organism and the microbes that infect it. Microbes evolve to better exploit the organism, and the organism evolves better defenses to fight off the infection. One theory to explain this great diversity in MHC genes is that those competing interests over time favor retaining more diversity."
The Arms Race between Germs and MHC Genes
"You naturally keep genes that fight disease," Kubinak says. "They help you survive, so those MHC genes become more common in the population over time because the people who carry them live to have offspring."
Pathogens -- disease-causing viruses, bacteria or parasites -- infect animals, which defend themselves with MHCs that recognize the invader and trigger an immune response to destroy the invading pathogen.
But over time, some pathogens mutate and evolve to become less recognizable by the MHCs and thus evade an immune response. As a result, the pathogens thrive. MHCs that lose the battle to germs become less common because they now predispose people who carry them to get sick and maybe die. It was thought such disease-susceptibility MHC genes eventually should vanish from the population, but they usually don't.
Why? While some of those MHCs do go extinct, others can persist, for two reasons. First, some of the now-rare MHCs gain an advantage because they no longer are targeted by evolving microbes, so they regain an ability to detect and fight the same germ that earlier defeated them -- after that germ mutates yet again. Second, some of the rare MHCs can mount an effective immune response against completely different microbes.
How the Study was Performed; Implications of the Findings
The researchers studied 60 mice that were genetically identical, except the mice were divided into three groups, each with a different variety of MHC genes known as b, d and k, respectively.
A mouse leukemia virus named the Friend virus was grown in tissue culture and used to infect two mice from each of the three MHC types. The fast-evolving retrovirus grew within the mice for 12 days, attacking, enlarging and replicating within the spleen and liver. Virus particles in the spleen were collected, and the severity of illness was measured by weighing the enlarged spleen.
Then, virus taken from each of the first three pairs of mice (b, d and k) was used to infect another three pair of mice with the same MHC types. The process was repeated until 10 pairs of mice in each MHC type were infected, allowing the virus time to mutate.
In this first experiment, the biologists showed they could get the Friend virus to adapt to and thus evade the MHC variants (b, d or k) in the mouse cells it attacked.
Next, the researchers showed that the virus adapted only to specific MHC proteins. For example, viruses that adapted to and sickened mice with the MHC type b protein still were attacked effectively in mice that had the type d and k MHCs.
In the third experiment, the researchers showed that pathogen fitness (measured by the number of virus particles in the spleen) correlated with pathogen virulence (as measured by spleen enlargement and thus weight). So the virus that evaded MHC type b made mice with that MHC sicker.
Together, the experiments demonstrate "the first step in the antagonistic coevolutionary dance" between a virus and MHC genes, Potts says.
Potts says the findings have some important implications:
-- The use of antibiotics to boost productivity in dairy herds and other livestock is a major reason human diseases increasingly resist antibiotics. Selective breeding for more milk and beef has reduced genetic diversity in livestock, including their MHCs. So breeding more MHCs back into herds could enhance their resistance to disease and thus reduce the need for antibiotics.
-- Because their populations are diminished, endangered species have less genetic diversity, making them an easier target for germs. Potts says it would be desirable to breed protective MHCs back into endangered species to bolster their disease defenses.
-- Genetic variation of MHCs in people and other organisms is important for limiting the evolution and spread of emerging diseases. In effect, Potts and colleagues created emerging diseases by making a virus evolve in mice. "It's a model to identify what things change in viruses to make them more virulent and thus an emerging disease."