நயினாதீவு மகா வித்தியாலயம்

இலங்கையின் இலவசக்கல்வியின் தந்தை என கூறப்படும் திரு சி.டபிள்யு.டபிள்யு கன்னங்கரா அவர்களின் பெருமுயற்சியால் கிராமங்கள் பலவற்றிலும் அரசாங்க பாடசாலைகள் நிறுவப்பட்டன. அவ்வகையில் அறுபத்து நான்கு சக்தி பீடங்களில் ஒன்றாகிய நயினை அம்மன் குடியிருந்து அருள்பாலிக்கும் நயினாதீவிலும் 1946 ஆம் ஆண்டு தைத்திங்கள் 17ஆம் நாள் 228 மாணவர்களுடன் ஒரு கனிஸ்ட ஆங்கிலப் பாடசாலை நிறுவப்பட்டது.

நயினாதீவின் கண்ணே இருந்த பல பெற்றோருடைய பெருமுயற்சிகளையும் அவவர்களுடைய முயற்சிகளுக்கு உறுதுணையாக நின்று ஊக்கமும் ஆக்கமும் அளித்த சேர். வைத்தியலிங்கம் துரைச்சாமி அவர்களுடைய தூர சிருஸ்டியையும் அப்போது வடபகுதி கல்வி அதிகாரியாக இருந்த திரு வி. கே. நாதன் அவர்களுடைய உறுதுணையையும் இப்பாடசாலையின் உருவாக்கத்திற்கும் வளர்ச்சிக்கும் அடிப்படையாயமைந்தன. சேர் வைத்தியலிங்கம் துரரைச்சாமி அவர்கள், ஊர்காவற்றுறைத் தொகுதி அரசசபை உறுப்பினராகவும் சபாநாயகராகவும் இருந்து அளப்பரிய சேவையாற்றியவர். யாழ்ப்பாணத்தை அண்டிய ஏனைய தீவுகளிலெல்லாம் தனித்தனி மகா வித்தியாலயங்கள் அமைந்திருக்க நயினாதீவு மட்டும் புறக்கணிக்கப்பட்டிருந்த வேளையில் அவர், அப்போது கல்வி அமைச்சராயிருந்த திரு. கன்னங்கரா அவர்களுடன் கலந்து நயினாதீவில் ஒரு கனிஸ்ட ஆங்கிலப் பாடசாலை நிறுவ அனுமதி பெற்றுத் தந்தார்.

பாடசாலைக்கான கட்டடமோ நிலமோ இல்லாத போதிலும் முதலாம் வட்டாரத்திலிருந்த திரு மாரிமுத்து அவர்களினால் யாத்திரிகர்களுக்கென அமைக்கப்பட்டிருந்த மடத்தில் கனிஸ்ட ஆங்கிலப் பாடசாலை நயினையிலுள்ளோர் கண்டு கண்குளிர கால் கோள் பெற்றது. ஒரு வருட காலம் வரை மேற்படி மடத்தில் இயங்கி வந்த பாடசாலை பெற்றோரின் தளராத உழைப்பினால் 1947 ஆம் ஆண்டு புதுப்பொலிவுடன் சொந்தமான ஒரு தற்காலிக அமைப்பிலே உருவாகியது. இந்தப் புதிய இருப்பிடத்திற்கு கிறிஸ்தவ சமய நிறுவனத்தார் காணியினை அன்பளிப்பாய் வழங்கினர். புதிய இருப்பிடத்தில் அமைந்த பாடசாலைக்கான தற்காலிக இருக்கையை பெற்றோர்களே அமைத்தார்கள்.

இப்பாடசாலை ஆரம்பத்தில் அரசாங்கக் கனிஸ்ட பாடசாலையாகவும் பின்னர் சிரேஸ்ட பாடசாலையாகவும் அதன் பின்னர் மகா வித்தியாலயமாகவும் தரமுயர்த்தப்பட்டது. ஆரம்பத்தில் பாடசாலையில் தற்காலிக அதிபராக திரு எஸ். அரசன் அவர்கள் கடைமையாற்றினார்கள். பின்னர் 12.02.1946 தொடக்கம் நிரந்தர அதிபராக திரு எஸ். கந்தப்பு அவர்கள் பதவியேற்று ஏழு ஆண்டுகள் கடமையாற்றினார்கள். பாடசாலை வளர்ச்சியில் கண்ணும் கருத்துமாக இருந்து பிறருக்காக வாழ்ந்து உறக்கமும் காணாது உழைத்து கருமமே கண்ணாயிருந்து நயினையின் மதிப்பிற்குரிய பெரியவராய் வாழ்ந்து சபையிலே மக்களை கவந்திழுக்கச் செய்தார் அன்று சுயமொழியில் சிரேஸ்ட பாடசாலைத் தரத்திலிருந்து பல மாணவர்களை குறுகிய காலத்தில் ஆங்கில மொழி மூலம் பயிற்றுவிக்க ஆவண செய்து ஆக்கமும் ஊக்கமும் தந்தார். ஆங்கிலக் கல்வியின் பொருட்டு அன்றைய ஆசிரியர்கள் எடுத்த முயற்சி இங்கு குறிப்பிடத்தக்கது. பாடசாலையைத் தரிசித்த மேலதிகாரிகளின் பாராட்டுக்கள் பலவற்றையும் இன்றும் பதிவுப் புத்தகங்களில் காணலாம்.

திரு. கந்தப்பு அவர்களைத் தொடர்ந்து திரு. சண்முகம் அவர்கள் நான்கரை ஆண்டுகளும், திரு. கனகரெத்தினம் அவர்கள் ஏழு ஆண்டுகளும், திரு சபா ஆனந்தா நான்கு வருடங்களும் அதிபர்களாகக் கடமையாற்றினர். முன்னைய அதிபர் விட்ட பணியை சிரமேற் கொண்டு இவர்கள் செயற்பட்டனர். இவர்களுடைய காலத்தில் நிரந்தரக் கட்டமைப்புக்களும், வகுப்பறை வசதிகளும் உண்டாயின. திரு சண்முகம் அவர்களின் காலம் தொட்டு பாடசாலை இரு நேரப் பாடசாவலயாக அமைக்கப்பட்டு நேரசூசியும் அமைக்கப்பட்டது. விஞ்ஞானக்கல்வி அவசியம் பெற்றோரினால் உணரப்பட்ட போதிலும் கனகரெத்தினம் அவர்களுடைய காலத்தில் தான் கைகூடியது. அவர் ஒரு விஞ்ஞானப் பட்டடதாரியாக இருந்தமையினால் அன்னார் பாடசாலையில் அதிபராக நியமனம் பெற்றமை விஞ்ஞானக் கல்வியைத் தொடங்குவதற்கான சாத்தியக் கூறுகளை ஏற்படுத்தியது. மாணவர்களுடைய ஆர்வமும் பெற்றோர்களுடைய ஊக்கமும் இத்துறையில் அவருக்குக் கிடைத்தமையினால் அரசிடமிருந்து உபகரணங்களையும் விஞ்ஞானக் கணித ஆசிரியர்களையும் பெறக் கூடியதாகவிருந்தது. பல மாணவர்கள் திரு கனகரெத்தினம் அவர்களுடைய காலத்திர் க.பொ.த சாதாரணப் பரீட்சையில் விஞ்ஞானப் பாடங்களில் திறமைச் சித்தியும் பெற்று இன்று அத்துறையில் முன்னோடியாகத் திகழ்கின்றனர்.

எனினும் விஞ்ஞானக் கல்வியில் நயினாதீவு மகா வித்தியாலயம் பூரண்த்துவம் அடைந்துவிட்டதென்று சொல்லுவதற்கில்லை. ஆசிரியர் பற்றாக்குறை ஆரம்ப காலந் தொடக்கமே இருந்து வருகின்றது. ஆரம்பத்தில் 1 – 10 வகுப்புக்கள் வரையும் பின்னர் 6 – 10 வகுப்புக்கள் வரையும் அதன் பின்னர் 6 – 12 ஆம் வகுப்பு வரையுமுடைய பாடசாலையாக வளர்ந்து வருகின்றது. தற்போது க.பொ. த(உயர் தர) கலை, வர்த்தக வகுப்புக்களை உள்ளடக்கிய 1C பாடசாலையாக உள்ளது. திரு கனகரெத்தினத்துக்கு பின் திரு சபானந்தா அவர்கள் 4 ஆண்டுகள் அதிபராகக் கடமையாற்றினார். இவர் பல ஆண்டுகள் அதிபராக இருந்து பெரிய கல்லூரிகளில் ஆற்றிய பணிகளை கல்வி உலகு நன்கு அறியும். இவருடைய காலத்தில் பாடசாலை எளிலும் திருவும் பெற்றதெனலாம். இன்றிருக்கின்ற அழகுத் தோற்றத்திற்கு அன்னாரே முதலில் வழிவகுத்தார். இவருடைய காலத்தில் வர்த்தகக் கல்வி ஆரம்பிக்கப்பட்டது.

திரு ஆனந்தா அவர்களுக்குப் பின் திரு. விஸ்வலிங்கம் அவர்கள் அதிபராகக் கடமையாற்றினார். பல ஆண்டுகளாக பாடசாலையில் தலைமையை ஏற்று நடத்திய அவருக்கு பல்துறை அனுபவங்கள் உண்டு. முக்கியமாக நிர்வாகத்துறை அவரின் வருகைக்குப் பின்னர் புது மெருகு பெற்றது. அத்துடன் கல்வியில் உள்ள அக்கறையும் பாடசாலையின் புனிதத்தைப் பேணுவதில் அவருக்குள்ள பற்றும் எமது பாடசாலையை ஓர் ஆலயமாக்கிவிட்டதென்றே சொல்லலாம். அவரின் வருகைக்குப் பின்னர் பலதுறைகளிலும் பாடசாலை வளர்ச்சி கண்டுள்ளது. அவர் காலத்திலும் பின்னும் நயினை மகா வித்தியாலயம் பெற்றுள்ள சிறந்த பரீட்சைப் பெறுபேறுகள் அவருடைய அயராத முயற்சிக்கு எடுத்துக்காட்டாகும்.  திரு வே. விஸ்வலிங்கம் அவர்கள் 12.07.1978 வரை அதிபராகக் கடமையாற்றினார்.

தற்போது அதிபராக திரு குணசேனன் அவர்கள் கடமையாற்றி வருகின்றார்கள்.

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இன்றைய காலத்தில் சிறுநீரகக் கற்களால் பாதிக்கப்பட்டோரின் எண்ணிக்கை அதிகமாக இருக்கிறது. அதிலும் அந்த சிறுநீரகக் கல் ஏற்பட்டால் ஆரம்பத்திலேயே அதனை சரிசெய்ய வேண்டும். அதிலும் கற்களின் அளவு 5 மிமி குறைவாக இருந்தால் அதனை கண்டிப்பாக வீட்டில் இருக்கும் ஒரு சில உணவுகளின் மூலமே சரிசெய்துவிடலாம். இல்லையென்றால் லாப்ரோஸ்கோப்பி என்ற சிகிச்சையின் மூலமே நீக்க முடியும். மேலும் சிலருக்கு அந்த கற்களின் காரணமாக வயிற்றில் அடிக்கடி வலியானது ஏற்படும். அவ்வாறு ஏற்பட்டால் உடனடியாக அதனை கரைப்பதற்கான முயற்சியில் ஈடுபட வேண்டும். அவ்வாறு அதனை ஈஸியாக வீட்டில் இருக்கும் ஒருசில உணவுகளை வைத்து கரைக்கலாம். தண்ணீர்: அனைவருக்குமே சிறுநீரகக்கல் போதிய தண்ணீரானது உடலில் இல்லாத காரணத்தினாலே வருகிறதென்று நன்கு தெரியும். ஆகவே எப்போது கற்கள் உடலில் இருக்கிறதென்று தெரிககிறதோ, அன்றிலிருந்து ஒரு நாளைக்கு 5-6 லிட்டர் தண்ணீரை குடிக்க ஆரம்பிக்க வேண்டும். இதுவே ஒரு சிறந்த எளிதான வழியாகும். வெந்தய தண்ணீர்: ஒரு டீஸ்பூன் வெந்தயத்தை ஒரு டம்ளர் தண்ணீரில் படுக்கும் முன் ஊற வைத்து, மறுநாள் காலையில் வெறும் வயிற்றில் குடிக்க வேண்டும். இதனால் சிறுநீரகக்கற்கள் கரைவதோடு மட்டுமல்லாமல், உடலில் இருக்கும் டாக்ஸின்களும் வெளியேறுகின்றன. டால் மிஸ்ரி: இது ஒரு புதுவிதமான படிகமாக்கப்பட்ட சர்க்கரை கட்டிகள். இந்த சர்க்கரைக் கட்டிகள் பனை மரத்திலிருந்து செய்யப்படுகிறது. இந்த பொருள் கிடைப்பது சற்று கடினம் தான். ஆனால் அதன் பலன் மிகவும் உயர்ந்தது. இது சிறுநீரகக்கற்களை கரைக்கும் ஒரு சிறந்த பொருள். ஆகவே அதனை இரவில் ஒரு டம்ளர் தண்ணீரில் ஊற வைத்து, மறுநாள் காலையில் அதனை குடிக்க வேண்டும். முக்கியமாக அந்த கட்டிகள் தண்ணீரில் நன்கு கரைந்திருக்க வேண்டும். வாழைத்தண்டு: சமையலில் பயன்படும் வாழைத்தண்டுகளை வாரத்திற்கு ஒரு முறை சமைத்து உண்டால், சிறுநீரகக்கற்கள் வராமல் இருக்கும். அதுவே கற்கள் இருப்பவர்கள், அதனை தினமும் ஜூஸ் போட்டு குடித்தால், கற்கள் விரைவில் கரைந்துவிடும். ஏனெனில் அதில் அதிகமான அளவு நார்ச்சத்தானது இருக்கிறது. மேலும் அதில் நீர்ச்சத்தும் அதிகம் உள்ளது. கொத்தமல்லி இலைகள்: கொத்தமல்லி ஒரு சிறந்த மூலிகைப் செடி. இதில் பல வித நன்மைகள் அடங்கியுள்ளன. அதிலும் அந்த கொத்தமல்லியை நீரில் போட்டு, கொதிக்க வைத்து, அந்த தண்ணீரை மட்டும் குடிக்க வேண்டும். இதனால் ஒரு நல்ல பலன் கிடைக்கும். எனவே சிறுநீரகக்கற்களை நீண்ட நாட்கள் வைத்து, அதனால் அறுவை சிகிச்சை செய்யுமளவு கொண்டு செல்லாமல், வீட்டிலேயே தினமும் அதற்கான உணவுகளை சரியாக உண்டு வந்தாலே, கற்கள் கரைந்துவிடும் என்று மருத்துவர்கள் கூறுகின்றனர்.

Psychology of possibilities can enhance health, happiness, research says

First-time mothers who pay attention to their emotional and physical changes during their pregnancy may feel better and have healthier newborns than new mothers who don't, according to research to be presented at American Psychological Association's 120th Annual Convention.

"These findings continue more than 40 years of research that has made clear that whether you are mindless or mindful makes a big difference in every aspect of your health and well-being -- from competence to longevity," Ellen Langer, professor of psychology at Harvard University and a pioneer in researching mindfulness, said in an interview. Langer is a past recipient of APA's Award for Distinguished Contributions to Psychology in the Public Interest.

For Langer's recent study, researchers trained women pregnant with their first child in mindfulness with instructions to notice subtle changes in their feelings and physical sensations each day, she said. When compared with two other groups of first-time pregnant mothers who did not have the mindfulness training, these women reported more well-being and positive feelings and less emotional distress. "They had higher self-esteem and life satisfaction during this period of their pregnancy and up to at least a month after birth," Langer said. "And this also had a positive impact on their deliveries and overall health of the newborns."

Teaching mindfulness through attention to variability may be helpful for many disorders, including asthma, depression and learning disabilities, to name a few, according to Langer.

"Noticing even subtle fluctuations in how you feel can counter mindlessness, or the illusion of stability. We tend to hold things still in our minds, despite the fact that all the while they are changing. If we open up our minds, a world of possibility presents itself," she said.

Author of the popular books "Mindfulness," "The Power of Mindful Learning," "On Becoming an Artist: Reinventing Yourself Through Mindful Creativity," and most recently, "Counterclockwise: Mindful Health and the Power of Possibility," Langer is known for her work on the illusion of control, aging, decision-making and mindfulness theory.

In her lecture, Langer will describe her research to test possibilities rather than find out what is typical. "Psychologists have traditionally studied the 'norm' rather than exceptions that could show that we are capable of far more than we currently realize," she said. Among other research, she will describe her work showing how a change in mindset has resulted in weight loss and improved vision and hearing, and how subtle differences in choice of words can improve health.

Langer first demonstrated the psychology of possibilities in her landmark 1981 "counterclockwise" experiment in which a group of elderly men spent time immersed in a retreat created to reflect daily life in the 1950s and where they were told to speak of the past in the present tense. Men in a comparison group reminisced for the week and were given no instructions regarding verb tense. The experimental group showed greater improvement in vision, strength, joint flexibility, finger length (their arthritis diminished and they could straighten their fingers more) and manual dexterity. On intelligence tests, 63 percent of the experimental group improved their scores, compared to 44 percent of the control group, Langer said.

BBC television recently replicated the study with British celebrities in a program that has been viewed in Great Britain, Australia, India and Hong Kong. It's currently being replicated with local celebrities in Germany and the Netherlands, Langer said.

"It is important for people to realize there can be enhanced possibilities for people of all ages and all walks of life," Langer emphasized. "My research has shown how using a different word, offering a small choice or making a subtle change in the physical environment can improve our health and well-being. Small changes can make large differences, so we should open ourselves to the impossible and embrace a psychology of possibility."

Provided by American Psychological Association

"Psychology of possibilities can enhance health, happiness, research says." August 2nd, 2012. http://medicalxpress.com/news/2012-08-psychology-possibilities-health-happiness.html

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Robert Karl Stonjek

Two effective treatments for Chronic Fatigue Syndrome / Myalgic Encephalomyelitis also cost-effective

(Medical Xpress) -- Two treatments found previously to be the most effective for patients with Chronic Fatigue Syndrome or Myalgic Encephalomyelitis (CFS/ME) have now been found to be the most cost-effective treatments according to new research led by King's College London's Institute of Psychiatry.

The latest results from the PACE trial show that both cognitive behaviour therapy (CBT) and graded exercise therapy (GET), as supplements to specialist medical care, offer good value for money for healthcare providers when the cost of treatment is weighed up against improvement in quality of life. 

CBT and GET were found to be even more cost-effective when the savings to wider society – through a reduced need for additional care by family members – were taken into account. Adaptive pacing therapy (APT) was not cost-effective. 

The research was led by King’s College London, the University of Oxford and Queen Mary, University of London, and was funded by the Medical Research Council (MRC), National Institute for Health Research (NIHR) and UK government departments.

The researchers drew their conclusions in line with healthcare cost criteria used by NICE (National Institute for Health and Clinical Excellence), which considers treatments costing less than £20,000 to £30,000 per year lived in good health (known as a quality-adjusted life years, or QALYs) to represent value for money. 

Professor Paul McCrone, Director of the Centre for the Economics of Mental and Physical Health at King’s College London’s Institute of Psychiatry and lead author of the paper, said: 'It’s very encouraging that two treatments found to help a significant number of CFS/ME patients are also cost-effective based on existing NICE criteria. There is now a strong case for the NHS to invest in providing these therapies. Our research suggests this investment would be justified in terms of improving quality of life for patients and could actually save costs to society if the impact on family members is taken into account.'

Professor Michael Sharpe from Oxford University and a co-author of the paper said: 'In the PACE trial we found that the rehabilitative treatments CBT and GET improve the fatigue and disability of people with CFS/ME. This new analysis of the trial data finds that these treatments are also cost-effective in improving patients’ quality of life. They are potentially cost-saving to society if the time of family and carers is also considered. This new evidence should encourage health service commissioners to provide these treatments to all those patients who need them.'

Professor David Lomas, Chair of the MRC Population and Systems Medicine Board, which co-funded the PACE trial, said: 'CFS/ME has a profound effect on patients and can severely impact their quality of life. These promising findings demonstrate how MRC funding can help to identify treatments that are not only effective, but are financially viable for the health service. There is still a pressing need to understand more about the underlying causes of CFS/ME and we recently announced a further £1.6m of funding for this purpose in the hope it will lead to new diagnostic tools and treatments.'

CFS/ME is a long-term, complex and debilitating condition that affects around 250,000 people in the UK, including children. Symptoms include profound physical and mental fatigue, muscle and joint pain, disturbed sleep patterns and concentration and memory problems. The combination and severity of symptoms varies from patient to patient, making it a difficult condition to diagnose and treat.

In 2011, the first findings from the PACE trial showed that CBT and GET benefit around 60 per cent of patients with CFS/ME, for whom fatigue was the main symptom. The latest study, published in the journal PLOS ONE, compared the cost-effectiveness of each treatment after one year against the criteria used by the NHS watchdog NICE. The researchers looked at the total cost of each course of treatment to the NHS and to wider society through patients requiring time off work and informal care from friends and relatives. 

Specialist medical care was the cheapest option in terms of absolute cost to provide, but when the benefit of treatment on quality of life was taken into account, CBT became the most cost-effective option (likelihood of 62.7 per cent). There was a 26.8 per cent likelihood that GET was the most cost effective, while the likelihood for APT and standard care alone were 2.6 and 7.9 per cent, respectively.

More information: McCrone, P. et al. ‘Adaptive pacing, cognitive behaviour therapy, graded exercise, and specialist medical care for chronic fatigue syndrome: A cost-effectiveness analysis’ PLoS ONE  doi:10.1371/journal.pone.0040808

Provided by King's College London

"Two effective treatments for Chronic Fatigue Syndrome / Myalgic Encephalomyelitis also cost-effective." August 2nd, 2012.http://medicalxpress.com/news/2012-08-effective-treatments-chronic-fatigue-syndrome.html

Posted by
Robert Karl Stonjek

புத்தர் ஞானம் பெற்ற போதிமரத்தை பாதுகாக்கும் முயற்சி !!!

கெளதம புத்தர் ஞானம் பெற்ற போதிமரத்தடி மிக பழமை வாய்ந்ததாக இருப்பதால், அதை பாது காக்கும் முயற்சிகள் தீவிரமாக நடந்து வருகின்றன.
புத்தர் ஞானம் பெற்ற போதிமரத்தடி கயாவில் உள்ளது. 2 500 ஆண்ட

ுகள் பழமை வாய்ந்ததாக கருதப்படும் இந்த போதிமரத்தைப் பாதுகாக்கும் முயற்சியில் பீகார் அரசு இறங்கியுள்ளது. அனைவரும் வந்து வழிபடும் தலமாக உள்ள கயாவின் போதிமரம் பட்டுப் போகாமல் இருக்க, மரத்தின் கிளைகள் முறிந்து புனிதத் தன்மை கெட்டுப்போகாமல் இருக்க, வன ஆராய்ச்சி கழக நிபுணர்களின் ஆலோசனையோடு, பழுதடைந்த கிளையில், ரசாயன விசேஷ மருந்துகள் செலுத்தப் பட்டு காப்பாற்றப் பட்டு வருவதாகத் தெரிகிறது.

மேலும் மரத்தில் பூஞ்சைகள் உருவாகா வண்ணமும் பாதுகாப்பு நடவைக்கைகள் மேற்கொள்ளப் பட்டுவருவதாகவும் வன ஆராய்ச்சிக் கழகம் தெரிவித்துள்ளது. சீன, இநதிய மக்கள் புனிதமாக கருதும் இந்த போதிமரம் உலகத்தில் உள்ள அனைத்து மக்களும் விரும்பிப் பார்க்கும் ஒரு புனிதத் தலமாகவும் மதிக்கப் படுகிறது என்பது குறிப்பிடத் தக்கது.

New malaria vaccine target found

BURNET INSTITUTE

Share on print The researchers found people who are immune to malaria develop antibodies that primarily attack a protein known as PfEMP1, which could be a target for vaccines against malaria.  Image: Henrik_L/iStockphoto Researchers at the Burnet Institute have made a major breakthrough in the quest for a vaccine against malaria, which causes up to one million deaths each year. Published in the Journal of Clinical Investigation, this research reveals a key target of the immune system’s attack against malaria. The findings show that people who are immune to malaria develop antibodies that primarily target a protein known as PfEMP1, which is produced by Plasmodium falciparum, the causative organism of most cases of malaria. Head of Burnet’s Centre for Immunology and senior author of the study, Professor James Beeson, said that these findings are a major advance towards developing an effective vaccine because they unlock the mystery of which malaria proteins, known as variant surface antigens (VSAs), an effective vaccine could target to achieve immunity to malaria. “The new findings support the idea that a vaccine could be developed that stimulates the immune system so that it specifically mounts a strong response (or attack) against the PfEMP1 protein that malaria produces,” Professor Beeson said. “A vaccine against malaria is urgently needed to reduce this disease globally and currently there is no licensed malaria vaccine available.” Co-first author, Jo-Anne Chan said the study also showed that when the immune system attacks other proteins that malaria produces, this is not as effective in protecting people. This emphasises that the immune system has to ‘get it right’ in order to fight malaria infection effectively. “Our studies of Kenyan children showed that those with antibodies to the PfEMP1 protein had a significantly reduced risk of developing malaria, whereas antibodies to other surface antigens were not associated with protective immunity” she said. Malaria is caused by a parasite that infects human red blood cells and replicates within them. While inside these cells, the malaria parasites produce specific proteins that enable infected cells to stick and clog-up blood vessels in the body. This clogging can occur in organs such as the brain and lungs, and the placenta in pregnant women, and causes severe illness and death. People who recover from malaria develop antibodies that coat the malaria-infected red blood cells so that they are destroyed by white blood cells (the body’s killer immune cells). The new studies show that the PfEMP1 protein is the major target of these protective antibodies. The research involved studies conducted at the Burnet Institute, Kenya Medical Research Institute, Walter and Eliza Hall Institute, and University of Melbourne. Researchers involved included: Jo-Anne Chan, Katherine Howell, Linda Reiling, Ricardo Ataide, Claire Mackintosh, Freya Fowkes, Michaela Petter, Joanne Chesson, Christine Langer, George Warimwe, Michael Duffy, Stephen Rogerson, Peter Bull, Alan Cowman, Kevin Marsh, and James G. Beeson. The study: ‘Targets of antibodies against Plasmodium falciparum–infected erythrocytes in malaria immunity’. Journal of Clinical Investigation, 2012 Editor's Note: Original news release can be found here.

DNA explains why women live longer

MONASH UNIVERSITY

Share on print Mitochondria (green) exist in almost all animal cells and convert food into the energy that powers the body. The researchers found mutations within mitochondrial DNA affect how long males live and the speed at which they age.  Image: Eraxion/iStockphoto Scientists are beginning to understand one of life's enduring mysteries - why women live, on average, longer than men. Published in Current Biology, research led by Monash University describes how mutations to the DNA of the mitochondria can account for differences in the life expectancy of males and females. Mitochondria, which exist in almost all animal cells, are vital for life because they convert our food into the energy that powers the body. Dr Damian Dowling and PhD student, Florencia Camus, both from the Monash School of Biological Sciences, worked with Dr David Clancy from Lancaster University to uncover differences in longevity and biological ageing across male and female fruit flies that carried mitochondria of different origins. They found that genetic variation across these mitochondria were reliable predictors of life expectancy in males, but not in females. Dr Dowling said the results point to numerous mutations within mitochondrial DNA that affect how long males live, and the speed at which they age. "Intriguingly, these same mutations have no effects on patterns of ageing in females. They only affect males,” Dr Dowling said. “All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male ageing across the animal kingdom.” The researchers said these mutations can be entirely attributed to a quirk in the way that mitochondrial genes are passed down from parents to offspring. “While children receive copies of most of their genes from both their mothers and fathers, they only receive mitochondrial genes from their mothers. This means that evolution’s quality control process, known as natural selection, only screens the quality of mitochondrial genes in mothers," Dr Dowling said. "If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed.” The study builds on previous findings by Dr Dowling and his team that investigated the consequences of maternal inheritance of mitochondria in causing male infertility. “Together, our research shows that the mitochondria are hotspots for mutations affecting male health. What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy,” Dr Dowling said. Editor's Note: Original news release can be found here.

Schizophrenic brains try to repair

NEUROSCIENCE RESEARCH AUSTRALIA

Share on print Most neurons are found in tissue near the surface of the brain, but people with schizophrenia have a high density of neurons in deeper areas. The researchers suggest this is because the neurons are migrating towards the surface, where they are lacking, in response to the disease.  Image: Sashkinw/iStockphoto New NeuRA research shows that the brains of people with schizophrenia may attempt to repair damage caused by the disease, in another example of the adult brain’s capacity to change and grow. Prof Cyndi Shannon Weickert, Dr Dipesh Joshi and colleagues from Neuroscience Research Australia studied the brains of people with schizophrenia and focussed on one of the hardest-hit regions, the orbitofrontal cortex, which is the part of the brain involved in regulating emotional and social behaviour. Most neurons – brain cells that transmit information – are found in tissue near the surface of the brain. However, in the brains of people with schizophrenia, the team found a high density of neurons in deeper areas. “For over a decade we’ve known about the high density of neurons in deeper brain tissue in people with schizophrenia. Researchers thought these neurons were simply forgotten by the brain, and somehow didn’t die off like they do during development in healthy people,” says Prof Shannon Weickert. “What we now have is evidence that suggests these neurons are derived from the part of the brain that produces new neurons, and that they may be in the process of moving. We can’t be sure where they are moving to, but given their location it is likely they are on their way to the surface of the brain, the area most affected by schizophrenia,” Prof Shannon Weickert concluded. Prof Cyndi Shannon Weickert is the Macquarie Group Foundation Chair of Schizophrenia Research, a joint venture of Neuroscience Research Australia, University of New South Wales, Schizophrenia Research Institute and Macquarie Group Foundation, and supported by NSW Health. This paper is published in the journal Biological Psychiatry.  How was this study done? - Brain tissue from the orbitofrontal cortex from 38 people with schizophrenia and 38 people without the disease were used in this study. - The density of interstitial neurons in the white matter, and the density of GABAergic neurons in the grey matter were measured. - An increased density of interstitial white matter neurons in the white matter, and decreased density of GABAergic neurons in the grey matter was found. - This pattern suggests that the migration of interstitial white matter neurons towards an area where they are lacking, because of schizophrenia, is a response to the disease. Editor's Note: Original news release can be found here.

Mohan Dhal - A Gujarati Sweet

Satisfying if not mind-blowing!


I wanted to make some sweet for one of our close friend’s babyshower(Seemantham). On the day before the babyshower, at midnight 1am (didn’t find time at all to make it during t

he day time), I made this sweet. I asked my husband to taste it. He liked it and appreciated me.
I kept the remaining sweets in the refrigerator.

After two days, my husband asked me for the sweet. When I gave him the sweet, he immediately starred at me and said this was the worst sweet he had ever had in his life. Immediately, I tasted it and did not like it at all.I felt so bad and disturbed. I was pondering how could I ever make a sweet like this and give it for a baby shower…

After few days, I tried making the same recipe with few changes to the original recipe and vahrevah….it came out well. So, now you can make this revised recipe and let me know your experience!

Ingredients

Besan Flour – 3 Cups

Vennila Essence – Few Drops

Condensed Milk – 500gm

Sugar – 4 Tablespoons

Milk – 3 Tablespoons

Chopped Cashews – 1 Tablespoon

Chopped Almonds – 1 Tablespoons

Saffron – Few Strands (Optional)

Ghee – 2 Tablespoons

Preparation

1. Warm 1 tablespoon of ghee in a nonstick pan. Fry besan flour until you get good smell. Remove besan flour and transfer it to a mixing bowl.

2. Now, when the besan flour is warm enough, add milk and stir well. Then, add desired quantity of water in such a way that the besan milk mixture becomes a thick paste.

3. In the same nonstick pan, add 1 tablespoon of remaining ghee. Fry cashews and almonds till they become golden brown. Transfer them to a bowl.

4. Now, add the besan milk mixture to the pan and fry well. Slowly, add the condensed milk,  sugar, and vennila essence and again fry well until the raw smell of the besan mixture goes off and also until there are no lumps. Put saffron strands on top. Switch off the stove.

5. Apply ghee on the bottom of the desired plate. Using a spoon, put the Mohan Dhal sweet on the plate and press well. Put some fried cashews and almonds on the sweet and gently press them. Allow the sweet to cool and then cut the sweet into desired shapes.

Now, the Mohan Dhal sweet is ready!

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(ஆசியாவில்) மிகப்பெரிய பேருந்து நிலையம்

தமிழக அரசு முத்திரை கோபுரம் – ஸ்ரீவில்லிபுத்தூர் ஆண்டாள் கோபுரம்
2. தமிழகத்தின் நுழைவாயில் – தூத்துக்குடி
3. தமிழகத்தின் மான்செஸ்டர் – கோயம்புத்தூர்
4. மக்கள் தொகை அதிகமுள்ள மாவட்டம் – கோயம்பத்தூர்
5. மக்கள் தொகை குறைந்த மாவட்டம் – பெரம்

பலூர்
6. மிக உயரமான தேசியக்கொடி மரம் – புனித ஜார்ஜ் கோட்டை (150 அடி)
7. மிகப் பெரிய பாலம் இந்தியாவின் முதல் கடல்வழி பாலம் – பாம்பன் பாலம் ( ராமேஸ்வரம் )
8. மிகப் பெரிய தேர் – திருவாரூர் தேர்
9. மிகப்பெரிய அணைக்கட்டு – மேட்டுர் அணை
10. மிகப் பழமையான அணைக்கட்டு – கல்லணை
11. மிகப்பெரிய திரையரங்கு (ஆசியாவில்) – தங்கம் (மதுரை – 2563 இருக்கைகள்)
12. மிகப்பெரிய கோயில் – தஞ்சை பிரகதீஸ்வரர் கோயில்
13. மிகப்பெரிய கோயில் பிரகாரம் – ராமேஸ்வரம் கோயில் பிரகாரம்
14. மிகப்பெரிய கோபுரம் – ஸ்ரீ ரெங்கநாதர் கோயில் கோபுரம் (திருச்சி)
15. மிகப்பெரிய தொலைநோக்கி – காவலூர் வைணுபாப்பு (700 m)
16. மிக உயர்ந்த சிகரம் – தொட்டபெட்டா [ 2,636 m (8,648 ft) ]
17. (உலகின்) மிக நீளமான கடற்கரை – மெரினா கடற்கரை (14 km )
18. மிக நீளமான ஆறு – காவிரி (760 km)
19. மக்கள் நெருக்கம் அதிகமுள்ள மாவட்டம் – சென்னை (25937/km2)
20. மக்கள் நெருக்கம் குறைவாக உள்ள மாவட்டம் – சிவகங்கை (286/km2)
21. மலைவாசல் தலங்களின் ராணி – உதகமண்டலம்
22. கோயில் நகரம் – மதுரை
23. தமிழ்நாட்டின் ஹாலந்து – திண்டுக்கல் (மலர் உற்பத்தி)
24. (ஆசியாவில்) மிகப்பெரிய பேருந்து நிலையம் – கோயம்பேடு பேருந்து நிலையம்
25. மிகப்பெரிய சிலை – திருவள்ளுவர் சிலை (133 அடி)

Sequencing of Malaria Genomes Reveals Challenges, Opportunities in Battle Against Parasite

Mosquitoes transmit malaria. Genetic variability revealed in malaria genomes newly sequenced by two multi-national research teams points to new challenges in efforts to eradicate the parasite, but also offers a clearer and more detailed picture of its genetic composition, providing an initial roadmap in the development of pharmaceuticals and vaccines to combat malaria. (Credit: © Kletr / Fotolia)                                       Science Daily  — Genetic variability revealed in malaria genomes newly sequenced by two multi-national research teams points to new challenges in efforts to eradicate the parasite, but also offers a clearer and more detailed picture of its genetic composition, providing an initial roadmap in the development of pharmaceuticals and vaccines to combat malaria.

The research appears in two studies published in the latest issue of the journal Nature Genetics. They focus on Plasmodium vivax (P. vivax), a species of malaria that afflicts humans and the most prevalent human malaria parasite outside Africa, and Plasmodium cynomolgi(P. cynomolgi), a close relative that infects Asian Old World monkeys.

"The bad news is there is significantly more genetic variation inP. vivax than we'd thought, which could make it quite adept at evading whatever arsenal of drugs and vaccines we throw at it," said Professor Jane Carlton, senior author on both studies and part of New York University's Center for Genomics and Systems Biology. "However, now that we have a better understanding of the challenges we face, we can move forward with a deeper analysis of its genomic variation in pursuing more effective remedies."

In one study, the researchers examined P. vivax strains from different geographic locations in West Africa, South America, and Asia, providing the researchers with the first genome-wide perspective of global variability within this species. Their analysis showed thatP. vivax has twice as much genetic diversity as the world-widePlasmodium falciparum (P. falciparum) strains, revealing an unexpected ability to evolve and, therefore, presenting new challenges in the search for treatments.

The second study, performed jointly with Professor Kazuyuki Tanabe at Osaka University, Japan, sequenced three genomes of P. cynomolgi. The researchers compared its genetic make-up to P. vivax and to Plasmodium knowlesi (P. knowlesi), a previously sequenced malaria parasite that affects both monkeys and humans in parts of Southeast Asia.

Their work marked the first time P. cynomolgi genomes have been sequenced, allowing researchers to identify genetic diversity in this parasite. Its similarity to P. vivax means that their results will also benefit future efforts to understand and fight against forms of malaria that afflict humans.

"We have generated a genetic map of P. cynomolgi, the sister species to P. vivax, so we can now push forward in creating a robust model system to study P. vivax," explained Tanabe. "This is important because we can't grow P. vivax in the lab, and researchers desperately need a model system to circumvent this."

Much of the work occurred under a seven-year grant from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. The funding has established 10 International Centers of Excellence for Malaria Research (ICEMR). Carlton is heading an ICEMR based in India, where malaria -- and P. vivax in particular -- is a significant public health burden. A particular aim of this Center of Excellence is to support and help train scientists in India who can then work to combat infectious diseases, such as malaria, where they are most prominent. The P. vivaxsequencing was funded by NIAID as part of the NIAID funded Genomic Sequencing Center for Infectious Diseases at the Broad Institute under Contract No. HHSN272200900018C. The Burroughs Wellcome Fund was instrumental in providing pilot funds for the P. cynomolgi sequencing.

Researchers at the following institutions were also part of theP. vivax sequencing: The Broad Institute, the National Institute of Malaria Research in India, Arizona State University, and the Centers for Disease Control and Prevention.

Researchers at the following institutions were also part of the work on P. cynomolgi: Osaka University, Dokkyo Medical University, Japan's Corporation for Production and Research of Laboratory Primates, Nagasaki University, Juntendo University's School of Medicine, the University of Tokyo, the National Institute of Biomedical Innovation, the Centers for Disease Control and Prevention, and Arizona State University.

Turning White Fat Into Energy-Burning Brown Fat: Hope for New Obesity and Diabetes Treatments

Science Daily   — Columbia University Medical Center (CUMC) researchers have identified a mechanism that can give energy-storing white fat some of the beneficial characteristics of energy-burning brown fat. The findings, based on studies of mice and of human fat tissue, could lead to new strategies for treating obesity and type 2 diabetes. The study was published August 2 in the online edition of the journal Cell.

"Turning white fat into brown fat is an appealing therapeutic approach to staunching the obesity epidemic, but it has been difficult to do so in a safe and effective way," said study leader Domenico Accili, MD, professor of Medicine and the Russell Berrie Foundation Professor at CUMC.Humans have two types of fat tissue: white fat, which stores excess energy in the form of triglycerides, and brown fat, which is highly efficient at dissipating stored energy as heat. Newborns have a relative abundance of brown fat, as protection against exposure to cold temperatures. In adults, however, almost all excess energy is stored as white fat.

White fat can be "browned" with a class of drugs called thiazolidazines (TZDs), which increase the body's sensitivity to insulin. However, TZDs have many adverse effects -- including liver toxicity, bone loss, and, ironically, weight gain -- which have limited the use of these drugs.

The current study was undertaken to learn more about the function of TZDs, with the ultimate goal of developing better ways to promote the browning of white fat.

Scientists have known that TZDs promote the browning of white fat by activating a cell receptor called peroxisome proliferator-activated receptor-gamma (ppar-gamma), but the exact mechanism was not clear. To learn more, Dr. Accili and his colleagues studied a group of enzymes called sirtuins, which are thought to affect various biological processes, including metabolism.

The researchers had previously shown in mice that when sirtuin activity increases, so does metabolic activity. In the present study, they found that sirtuins boost metabolism by promoting the browning of white fat. "When we sought to identify how sirtuins promote browning, we observed many similarities between the effect of sirtuins and that of TZDs," said lead author Li Qiang, PhD, associate research scientist in Medicine at CUMC.

Sirtuins work by severing the chemical bonds between acetyl groups and proteins, a process known as deacetylation. "So the next question was whether sirtuins remove acetyl groups from ppar-gamma and, indeed, that was what we found," said Dr. Qiang.

To confirm that the deacetylation of ppar-gamma is crucial to the browning of fat, the researchers created a mutant version of ppar-gamma, in effect mimicking the actions of sirtuins. The mutation promoted the development of brown fat-like qualities in white fat.

"Our findings have two important implications," said Dr. Accili. "First, they suggest that TZDs may not be so bad -- if you can find a way to tweak their activity. Second, one way to tweak their activity is by using sirtuin agonists -- that is, drugs that promote sirtuin activity."

"The truth is, making sirtuin agonists has proved to be a real bear -- more promise than fact," he continued. "But now, for the first time, we have a biomarker for good sirtuin activity: the deacetylation of ppar-gamma. In other words, any substance that deacetylates ppar-gamma should in turn promote the browning of white fat and have a beneficial metabolic effect."

Dr. Accili's paper is titled, "Brown Remodeling of White Adipose Tissue by SirT1-Dependent Deacetylation of Ppar-gamma." The other contributors are Ning Kon (CUMC), Wenhui Zhao (CUMC), Sangkyu Lee (University of Chicago, Chicago, Illinois), Yiying Zhang (CUMC), Michael Rosenbaum (CUMC), Yingming Zhao (University of Chicago), Wei Gu (CUMC), and Stephen R. Farmer (Boston University School of Medicine, Boston, Mass.)

This research was supported by grants from the National Institutes of Health (HL087123, DK58282, DK64773, DK063608, and RR024156).

Pranams at the feet of Shri Raghavendra

Shri Raghavendra Swami Araadhana 2012 starts today with Poorva Aradhana. Shri Raghavendra Swami Ji was a Great Saint of India and went into Jeeva Samadhi 341 years ago. The Samadhi day for 2102 falls on 4th August and is observed with due veneration and prayers all over the world by devotees.

Sri Raghavendra Swami attained Jeeva Samadhi on Dwitiya Day of Sravana Krishna Paksha in 1671. This date is celebrated each year as Sri Raghavendra Swamy Aradhana at Brindavans all over the world. The Raghavendra Swami Mutt in Mantralayam housing his Brindavan is visited by thousands of devotees every year.

Shirdi Me Ras bhar dini

Mending a Broken Heart -- With a Molecule That Turns Stem Cells Into Heart Cells

These are cardiomyocytes (heart muscle cells) generated from stem cells and expressing a green fluorescent protein. (Credit: Sanford-Burnham Medical Research Institute)                      Science Daily  — For years, scientists have been looking for a good source of heart cells that can be used to study cardiac function in the lab, or perhaps even to replace diseased or damaged tissue in heart disease patients. To do this, many are looking to stem cells. Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham), the Human BioMolecular Research Institute, and ChemRegen, Inc. have been searching for molecules that convert stem cells to heart cells for about eight years -- and now they've found one.

"Heart disease is the leading cause of death in this country. Because we can't replace lost cardiac muscle, the condition irreversibly leads to a decline in heart function and ultimately death. The only way to effectively replace lost heart muscle cells -- called cardiomyocytes -- is to transplant the entire heart," said Mark Mercola, Ph.D., director of Sanford-Burnham's Muscle Development and Regeneration Program and senior author of the study. "Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation."Writing in the August 3 issue of Cell Stem Cell, the team describes how they sifted through a large collection of drug-like chemicals and uncovered ITD-1, a molecule that can be used to generate unlimited numbers of new heart cells from stem cells.

Searching for a needle in a haystack

Stem cells are important because they do two unique things --

1) self-renew, producing more stem cells and

2) differentiate, becoming other, more specialized cell types.

To obtain a large number of a certain cell type, such as heart cells, the hard part is figuring out the signals that direct them to become the desired cell type.

Mercola's group has been hunting for heart-inducing signals for 15 years -- in embryos and in stem cells. To find a synthetic molecule that might one day lead to a drug therapy to regenerate the heart, they joined forces with a team of medicinal chemists at the Human BioMolecular Research Institute led by John Cashman, Ph.D. With funding from the California Institute for Regenerative Medicine, they used sophisticated robotic technology to methodically test a large collection of drug-like chemicals, looking for that needle in a haystack that, when added to stem cells, results in cardiomyocytes. The winning compound was ITD-1.

Therapeutic applications

There's no shortage of therapeutic possibilities for ITD-1. "This particular molecule could be useful to enhance stem cell differentiation in a damaged heart," explained Erik Willems, Ph.D., postdoctoral researcher in Mercola's lab and first author of the study. "At some point, it could become the basis for a new therapeutic drug for cardiovascular disease -- one that would likely limit scar spreading in heart failure and promote new muscle formation."

Mercola, Willems, and Cashman are now working with San Diego biotech company ChemRegen, Inc. to further develop ITD-1 into a drug that one day might be used to treat patients.

More scientific detail

The researchers discovered that ITD-1 blocks a cellular process known as TGFϐ signaling. TGFϐ (short for transforming growth factor-ϐ) is a protein produced by one cell type to influence others' behaviors, such as proliferation, scarring, and even stem cell differentiation. TGFϐ works from outside the cell, binding to a receptor on the surface of a responding cell to initiate an intracellular signaling cascade that causes genes to be switched on or off, ultimately altering cellular behavior -- in this case making heart muscle.

ITD-1 triggers degradation of the TGFϐ receptor, thus inhibiting the whole process. With TGFϐ signaling turned off, stem cells are set on a course toward cardiogenesis. ITD-1 is the first selective inhibitor of TGFϐ, meaning that it might also have applications in many other processes controlled by TGFϐ.

Embryonic Blood Vessels That Make Blood Stem Cells Can Also Make Beating Heart Muscles

UCLA stem cell researchers have found for the first time a surprising and unexpected plasticity in the embryonic endothelium, the place where blood stem cells are made in early development. Scientists found that the lack of one transcription factor, a type of gene that controls cell fate by regulating other genes, allows the precursors that normally generate blood stem and progenitor cells in blood forming tissues to become something very unexpected - beating cardiomyocytes, or heart muscle cells. (Credit: Hanna Mikkola Lab, University of California - Los Angeles Health Sciences)

Science Daily — UCLA stem cell researchers have found for the first time a surprising and unexpected plasticity in the embryonic endothelium, the place where blood stem cells are made in early development.

Scientists found that the lack of one transcription factor, a type of gene that controls cell fate by regulating other genes, allows the precursors that normally generate blood stem and progenitor cells in blood forming tissues to become something very unexpected -- beating cardiomyocytes, or heart muscle cells.

The finding is important because it suggests that the endothelium can serve as a source of heart muscle cells. The finding may provide new understanding of how to make cardiac stem cells for use in regenerative medicine, said study senior author Dr. Hanna Mikkola, an associate professor of molecular, cell and developmental biology in Life Sciences and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

"It was absolutely unbelievable. These findings went beyond anything that we could have imagined," Mikkola said. "The microenvironment in the embryonic vasculature that normally gives rise to blood cells can generate cardiac cells when only one factor, Scl, is removed, essentially converting a hematopoietic organ into a cardiogenic organ."

The two-year study is published Aug. 3, 2012 in the peer-reviewed journal Cell.

The findings were so surprising, in fact, that Mikkola and her team did not want to believe the results until all subsequent assays proved the finding to be true, said Amelie Montel-Hagen, study co-first author and a post-doctoral fellow.

"To make sure we had not switched the samples between blood forming tissues and the heart we ran the experiments again and repeatedly got the same results," Montel-Hagen said. "It turns out Scl acts as a conductor in the orchestra, telling the other genes in the endothelium who should be playing and who shouldn't be playing."

The team used microarray technology to determine which genes were "playing" in embryonic endothelium to generate blood stem and progenitor cells and found that in the absence of Scl, the genes required for making cardiomyocytes were activated instead, said study co-first author Ben Van Handel, a post-doctoral fellow.

The lone difference was that Scl was missing in the process that resulted in the fate switch between blood and heart.

"Scl has a known role as a master regulator of blood development and when we removed it from the equation, no blood cells were made," Van Handel said. "That the removal of Scl resulted in fully functional cardiomyocytes in blood forming tissues was unprecedented."

The team used the yolk sac -- the first tissue where blood cells are made -- from embryos that lacked Scl and within four hours of plating on the culture dish, the tissue had generated beating cardiomyocytes. The team also found similar cardiomyocyte potential in Scl-deficient embryos in the endocardium that lines the heart chambers. They also looked for genetic signatures that would suggest that these endothelial precursors could potentially also make other closely related tissues such as skeletal muscle, bone or kidney, but found no evidence of such plasticity. The default fate of the endothelium was to make cardiomyocytes in the absence of Scl, Mikkola said.

The findings may also have implications in cell reprogramming, which generally calls for adding factors to induce cell fate change, a process that can be problematic. It might be safer to suppress a factor like Scl to nudge cells into a cardiomyocyte fate, Mikkola said.

"This study opens new ways to think about what could be a potential source of cardiac stem cells," she said. "We now have a better understanding of how cardiac progenitor cells can be made and regulated, and this may one day lead us to a way to treat heart attacks by creating new heart muscle cells to replace those that were damaged."

Going forward, Mikkola and her team plan to investigate the developmental and regenerative potential of the endothelium-derived cardiac progenitor cells, and define the mechanisms by which Scl can at the same time activate one fate while suppressing another.

"These results call for future studies to examine the prospect of harnessing the latent cardiogenic potential in the vasculature for use in regenerative medicine, and to investigate whether similar development plasticity exists in other major cell fate decisions in the developing embryo," the study states.

Fingering the Culprit That Polluted the Solar System

The downward propagating shock wave has compressed the target cloud core and is injecting shock front material through multiple Rayleigh-Taylor (RT) fingers. (Credit: Image courtesy of Carnegie Institution)

Science Daily — For decades it has been thought that a shock wave from a supernova explosion triggered the formation of our Solar System. According to this theory, the shock wave also injected material from the exploding star into a cloud of dust and gas, and the newly polluted cloud collapsed to form the Sun and its surrounding planets. New work from Carnegie's Alan Boss and Sandra Keiser provides the first fully three-dimensional (3-D) models for how this process could have happened.

Traces of the supernova's pollution can be found in meteorites in the form of short-lived radioactive isotopes, or SLRIs. SLRIs -- versions of elements with the same number of protons, but a different number of neutrons -- found in primitive meteorites decay on time scales of millions of years and turn into different, so-called daughter, elements. A million years may sound like a long time, but it is actually considered short when compared to other radioactive isotopes studied by geochemists and cosmochemists, which have half-lives measured in billions of years.Their work will be published by The Astrophysical Journal Letters.

When scientists find the daughter elements distributed in telltale patterns in primitive meteorites, this means that the parent SLRIs had to be created just before the meteorites themselves were formed. This presents a timing problem, as the SLRIs must be formed in a supernova, injected into the presolar cloud, and trapped inside the meteoritic precursors, all in less than a million years.

The telltale patterns prove that the relevant daughter elements were not the ones that were injected. This is because the abundances of these daughters in different mineral phases in the meteorite are correlated with the abundances of a stable isotope of the parent element. Different elements have different chemical behaviors during the formation of these first solids, and the fact that the daughter elements correlate with the parent elements means that those daughters had to be derived from the decay of unstable parent elements after those solids were crystallized.

One of these SLRIs, iron-60, is only created in significant amounts by nuclear reactions in massive stars. The iron-60 must have come from a supernova, or from a giant star called an AGB star. Boss and Keiser's previous modeling showed that it was likely that a supernova triggered our Solar System's formation, as AGB star shocks are too thick to inject the iron-60 into the cloud. Supernova shocks are hundreds of times thinner, leading to more efficient injection.

Now Boss and Keiser have extended those models to 3-D, so they can see the shock wave striking the gas cloud, compressing it and forming a parabolic shock front that envelopes the cloud, creating finger-like indentations in the cloud's surface. The fingers inject the SLRI pollution from the supernova. Less than 0.1 million years later, the cloud collapses and forms the core of the protostar that became the Sun and its surrounding planets. The 3-D models show that only one or two fingers are likely to have caused the SLRI pollution found in primitive meteorites.

"The evidence leads us to believe that a supernova was indeed the culprit," said Boss. However, more detective work needs to be done: Boss and Keiser still need to find the combination of cloud and shock wave parameters that will line up perfectly with observations of exploding supernovae.

It's in Our Genes: Why Women Outlive Men

Newborn baby boy and girl. Scientists are beginning to understand one of life's enduring mysteries -- why women live, on average, longer than men. (Credit: © Barbara Helgason / Fotolia)                                                                             Science Daily  — Scientists are beginning to understand one of life's enduring mysteries -- why women live, on average, longer than men.

Published August 2 in Current Biology, research led by Monash University, describes how mutations to the DNA of the mitochondria can account for differences in the life expectancy of males and females. Mitochondria, which exist in almost all animal cells, are vital for life because they convert our food into the energy that powers the body.

Dr Damian Dowling and PhD student, Florencia Camus, both from the Monash School of Biological Sciences, worked with Dr David Clancy from Lancaster University to uncover differences in longevity and biological aging across male and female fruit flies that carried mitochondria of different origins. They found that genetic variation across these mitochondria were reliable predictors of life expectancy in males, but not in females.

Dr Dowling said the results point to numerous mutations within mitochondrial DNA that affect how long males live, and the speed at which they age.

"Intriguingly, these same mutations have no effects on patterns of aging in females. They only affect males," Dr Dowling said.

"All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male aging across the animal kingdom."

The researchers said these mutations can be entirely attributed to a quirk in the way that mitochondrial genes are passed down from parents to offspring.

"While children receive copies of most of their genes from both their mothers and fathers, they only receive mitochondrial genes from their mothers. This means that evolution's quality control process, known as natural selection, only screens the quality of mitochondrial genes in mothers," Dr Dowling said.

"If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed."

The study builds on previous findings by Dr Dowling and his team that investigated the consequences of maternal inheritance of mitochondria in causing male infertility.

"Together, our research shows that the mitochondria are hotspots for mutations affecting male health. What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy," Dr Dowling said.

Human Brain Analysis - Man vs. Woman......A MUST READ!

1. MULTI-TASKING
Women - Multiple process
Womens brains designed to concentrate multiple task at a time.
Women can Watch a TV and Talk over phone and cook.
Men - Single Process
Mens brains designed to concentrate only one work at a time. Men can not watch TV and talk over the phone at the same time. they stop the TV while Talking. They can either watch TV or talk over the phone or cook.

2. LANGUAGE
Women can easily learn many languages. But can not find solutions to problems. Men can not easily learn languages, they can easily solve problems. That's why in average a 3 years old girl has three times higher vocabulary than a 3 yeard old boy.

3. ANALYTICAL SKILLS
Mens brains has a lot of space for handling the analytical process. They can analyze and find the solution for a process and design a map of a building easily. But If a complex map is viewed by women, they can not understand it. Women can not understand the details of a map easily, For them it is just a dump of lines on a paper.

4. CAR DRIVING.
While driving a car, mans analytical spaces are used in his brain. He can drive a car fastly. If he sees an object at long distance, immediately his brain classifies the object (bus or van or car) direction and speed of the object and he drives accordingly. Where woman take a long time to recognize the object direction/ speed. Mans single process mind stops the audio in the car (if any), then concentrates only on driving.

5. LYING
When men lie to women face to face, they get caught easily. Womans super natural brain observes facial expression 70%, body language 20% and words coming from the mouth 10%. Mens brain does not have this. Women easily lie to men face to face.
So guys, do not lie face to face.

6. PROBLEMS SOLVING
If a man have a lot of problems, his brain clearly classifies the problems and puts them in individual rooms in the brain and then finds the solution one by one. You can see many guys looking at the sky for a long time. If a woman has a lot of problems, her brain can not classify the problems. she wants some one to hear that. After telling everything to a person she goes happily to bed. She does not worry about the problems being solved or not.

7. WHAT THEY WANT
Men want status, success, solutions, big process, etc... But Women want relationship, friends, family, etc...

8. UNHAPPINESS
If women are unhappy with their relations, they can not concentrate on their work. If men are unhappy with their work, they can not concentrate on the relations.

9. SPEECH
Women use indirect language in speech. But Men use direct language.


10. HANDLING EMOTION
Women talk a lot without thinking. Men act a lot without thinking.