Skull resconstruction immediately following traumatic brain injury worsens brain damage

Immediate skull reconstruction following trauma that penetrates or creates an indentation in the skull can aggravate brain damage inflicted by the initial injury, a study by a University of South Florida research team reports. Using a rat model for moderate and severe traumatic brain injury, the researchers also showed that a delay of just two days in the surgical repair of skull defects resulted in significantly less brain swelling and damage.

The study was published March 16, 2012 in the online journal PloS ONE. While further investigation is needed, the findings have implications for the acute treatment of traumatic brain injury (TBI), considered the signature wound of soldiers who have served in Iraq and Afghanistan, said the study's principal investigator Cesar Borlongan, PhD, professor and vice chair of research at the USF Health Department of Neurosurgery and Brain Repair

"A double-edged sword," is how Borlongan describes the inflammation and subsequent swelling of brain tissue that occurs immediately following TBI.

When the brain is initially penetrated -- by a bullet, shrapnel, other debris, or even the force of blast waves, for instance -- inflammation helps recruit the body's own good (glial) cells to the damaged site to limit localized injury. For a short time, the inflammation-induced edema, or swelling of the brain, is beneficial to help relieve pressure within the skull. However, chronic inflammation precipitates increases in intracranial pressure that perpetuate a vicious cycle leading to secondary cell injury and death.

Cranioplasty is an operation to repair malformations of the skull caused by TBI; the procedure may involve replacing a missing piece of the skull protecting the underlying brain and/or improving the appearance of the skull's surface. Current clinical practice emphasizes performing cranioplasty quickly upon initial hospital admission to help reduce the likelihood of infection or other complications that may arise when the brain is exposed.

"Our preclinical study indicates that reconstructing the skull too early in the brain's natural healing process may interfere with critical therapeutic benefits of brain swelling post-TBI," Dr. Borlongan said. "It's better to wait at least two days."

The USF researchers studied rats with moderate and severe TBI. Post-TBI, the animals were randomly assigned to skull bone flap replacement with or without bone wax (a sterile mixture to help control bleeding from bone surfaces); no skull reconstruction; or delayed skull reconstruction with bone wax alone, which was performed two days following TBI.

The brains of all the animals were analyzed in the laboratory five days after surgery. While immediate reconstruction provided aesthetic repair of the skull fracture, this early surgical procedure, with bone wax alone or with bone wax and skull bone flap, significantly increased cortical brain tissue damage in both moderate and severe animal models.

Overall, whether the rat model was moderate or severe TBI, delayed reconstruction limited the worsening of brain tissue damage compared to immediate reconstruction. In fact, for moderate TBI, the extent of damage observed in the brains of rats that received delayed reconstruction was on a par with that in the animals getting no reconstruction. In those with severe traumatic brain injury, the tissue damage was significantly larger. The authors suggest this may mean a two-day delay, while more beneficial than immediate reconstruction, was not sufficient to counteract the intracranial pressure generated by severe TBI.

The researchers concluded that the timing of cranioplasty warrants further evaluation in both laboratory and clinical settings.

"Our results suggest that delaying cranioplasty until the TBI-induced cerebral swelling has subsided may reduce unwanted exacerbation of cortical damage associated with skull reconstruction," Borlongan said. "We need to carefully weigh the risk of infection that comes from leaving the brain somewhat exposed with the benefit of enhancing the brain's own repair of its cells."

"Finding a safe and effective cranioplasty regimen will require determining the optimal period of time when we let the brain repair itself and balancing that with when to best introduce a regimen of surgical skull repair and other potential therapies," said co-author Harry van Loveren, MD, the David W. Cahill endowed professor and chair of the USF Health Department of Neurosurgery and Brain Repair.

More information: "Immediate, but Not Delayed, Microsurgical Skull Reconstruction Exacerbates Damage in Experimental Traumatic Brain Injury Model;" Loren E. Glover, Naoki Tajiri, Tsz Lau, Yuji Kaneko, Harry van Loveren, Cesario V. Borlongan; PloS ONE 7(3), e33646, March 16, 2012.

Provided by University of South Florida

"Skull resconstruction immediately following traumatic brain injury worsens brain damage." March 22nd, 2012.http://medicalxpress.com/news/2012-03-skull-resconstruction-immediately-traumatic-brain.html

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Robert Karl Stonjek

Prenatal exposure to combustion-related pollutants leads to anxiety, attention problems in young children

Mothers' exposure during pregnancy to a class of air pollutants called polycyclic aromatic hydrocarbons (PAH) can lead to behavioral problems in their children. PAH are released to air during incomplete combustion of fossil fuel such as diesel, gasoline, coal, and other organic material.

The study is the first report of associations between child attentional and behavioral problems among school‐age children and two complementary measures of prenatal PAH exposure: monitored air concentrations of PAH and a PAH-specific biomarker of exposure measured in maternal and umbilical cord blood. The paper, "Prenatal Polycyclic Aromatic Hydrocarbon (PAH) Exposure and Child Behavior at age 6-7," published online today in Environmental Health Perspectives, adds to rising concerns about the risks associated with exposures to air pollution during pregnancy.

The study followed the children of 253 non‐smoking inner-city women who gave birth between 1999 and 2006. Researchers led by Frederica Perera, DrPH, director of the Columbia Center for Children's Environmental Health at the Mailman School of Public Health, measured two complementary indicators of PAH exposure. One indicator was the PAH concentration in air from personal air sampling which took place during the third trimester of pregnancy. The other was a specific biological marker of exposure-- PAH–DNA adducts measured in maternal blood and newborn umbilical cord blood. When inhaled by the mother during pregnancy, PAH can be transferred across the placenta and bind to the DNA of the fetus, forming "adducts" in blood and other tissues and providing a biologic measure of pollutant exposure.

Mothers completed a detailed assessment of their child's behavior (including whether the children experienced symptoms of anxiety, depression, or attention problems. High prenatal PAH exposure, whether characterized by personal air monitoring or maternal and newborn cord adducts, was significantly associated with symptoms of Anxious/Depressed and Attention Problems.

In urban air, traffic emissions are a dominant source of the pollutants measured in the study. Illustrating widespread exposure to these pollutants, 100% of the mothers in the Columbia Center for Children's Environmental Health NYC cohort had detectable levels of PAH in prenatal personal air samples, although levels varied widely. The authors accounted for other sources of PAH such as environmental tobacco smoke and diet in their analyses. None of the mothers in the study were smokers.

"This study provides evidence that environmental levels of PAH encountered in NYC air can adversely affect child behavior. The results are of concern because attention problems and anxiety and depression have been shown to affect peer relationships and academic performance," said Dr. Perera, the study's lead author.

Provided by Columbia University

"Prenatal exposure to combustion-related pollutants leads to anxiety, attention problems in young children." March 22nd, 2012.http://medicalxpress.com/news/2012-03-prenatal-exposure-combustion-related-pollutants-anxiety.html

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Robert Karl Stonjek

My DNA, My Results

Are donors of biological material privy to research results that stem from their donation?

By Cristina Luiggi | 

Flickr, Official U.S. Navy Imagery

People who have donated biological material and data to science have a right to be informed of any significant discoveries that may arise from research down the line, according to a National Institutes of Health-funded committee. In a statement signed by 26 experts and published earlier this week, the committee concluded that biobanks housing donated materials, as well as researchers working on them, should shoulder the responsibilities of contacting and sharing any incidental findings with the original donors.

Currently, less than half of US biobanks return results to the donors of biological material, Naturereported. The NIH-funded committee, led by Susan Wolf of the University of Minnesota Law School in Minneapolis, suggested that biobanks create committees specialized for this purpose.

However, there are worries about the ethical and logistical implications of keeping track of the identities and contact information of donors, as well as the costs.

“It’s unfortunate that the authors of the consensus statement didn’t discuss the cost implications of what they’re proposing, because what they have in mind is going to be expensive and difficult, particularly at a time when funding success is as low as it’s ever been,” Ellen Wright Clayton, a pediatrician and lawyer at the Center for Biomedical Ethics and Society at Vanderbilt University in Nashville, told Nature.

Read a recent opinion piece about increasing the participation of donors in biomedical studies, and how openness can foster better research.

Source: TheScientist
http://the-scientist.com/2012/03/22/my-dna-my-results/

Posted by
Robert Karl Stonjek

Self-reflective mind: Psychologists report on continuing advances in animals

Scientists concur that when it comes to this Old World macaque: monkey see, monkey do, monkey think about what monkey do, monkey maybe do something else.

(PhysOrg.com) -- According to one of the leading scholars in the field, there is an emerging consensus among scientists that animals share functional parallels with humans' conscious metacognition -- that is, our ability to reflect on our own mental processes and guide and optimize them.

In two new contributions to this influential field of comparative psychology, David Smith, PhD, of the University at Buffalo and his fellow researchers report on continuing advances in this domain.

Smith is a professor in the Department of Psychology at UB, and a member of the university's graduate program in evolution, ecology and behavior and its Center for Cognitive Science. His co-authors on the articles are Justin J. Couchman, PhD, visiting assistant professor of psychology, State University of New York at Fredonia, and Michael J. Beran, PhD, senior research scientist, Language Research Center, Georgia State University.

In "The Highs and Lows of Theoretical Interpretation in Animal-Metacognition Research," in press at the journal Philosophical Transactions of the Royal Society, Smith, Couchman and Beran examine the theoretical and philosophical problems associated with the attribution of self-reflective, conscious mind to nonverbal animals.

Philosophical Transactions is a highly visible journal in the biological sciences and one of the oldest scientific journals published in English.

"The possibility of animal metacognition has become one of the research focal points in comparative psychology today," Smith says, "but, of course, this possibility poses difficult issues of scientific interpretation and inference." In this article, they evaluate the standards that science brings to making difficult interpretations about animal minds, describing how standards have been applied historically and as they perhaps should be applied. The article concludes that macaques do show uncertainty-monitoring capacities that are similar to those in humans.

The other contribution, "Animal Metacognition," will be published in March by Oxford University Press in the volume "Comparative Cognition: Experimental Explorations of Animal Intelligence." Smith says this volume will be one of the preeminent sources for scholarship in animal cognition for the next decade.

In this article, Smith and his colleagues provide a comprehensive review of the current state of the animal-metacognition literature. They describe how Smith inaugurated animal metacognition as a new field of study in 1995 with research on a bottlenosed dolphin. The dolphin assessed correctly when the experimenter's trials were too difficult for him, and adaptively declined to complete those trials.

The dolphin also showed his own distinctive set of hesitation, wavering and worrying behaviors when the trials were too difficult. In sharp contrast, when the trials were easy, he swam to the responses so fast that he would make a bow-wave around himself that would swamp Smith's delicate electronics. Smith says: "We finally had to buy condoms to protect the equipment."

Subsequently, Smith and many collaborators also explored the metacognitive capacities of joystick-trained macaques. These Old-World monkeys, native to Africa and Asia, can make specific responses to declare uncertainty about their memory. They can respond, "Uncertain," to gain hints from the experimenters of what to do on the first trial of new tasks. They can even respond, "Uncertain," when their memory has been erased by trans-cranial magnetic stimulation. Accordingly, this second article by Smith and colleagues also supports the consensus that animals share with humans a form of the self-reflective, metacognitive capacity.

"In all respects," says Smith, "their capacity for uncertainty monitoring, and for responding to uncertainty adaptively, show close correspondence to the same processes in humans.

"At present," he says, "members of South-American monkey species or New World monkeys have not shown the same robust capacities for uncertainty monitoring, a possible species difference that has intriguing implications regarding the emergence of reflective mind in monkeys, apes and humans."

Provided by University at Buffalo

"Self-reflective mind: Psychologists report on continuing advances in animals." March 22nd, 2012. http://www.physorg.com/news/2012-03-psychologists-advances-animals.html

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Robert Karl Stonjek

Salk scientists open new window into how cancers override cellular growth controls

 by Biomechanism 

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Worm model of back-up telomere repair strategy could speed identification of anti-cancer drugs.

Rapidly dividing cancer cells are skilled at patching up damage that would stop normal cells in their tracks, including wear and tear of telomeres, the protective caps at the end of each chromosome.

Loss of telomeres forces cells out of the dividing game and into a growth arrest state called “senescence,” but cancer cells evade this by employing an enzyme called telomerase to extend eroded telomeres.

The images in the top row each show six chromosomes found in a normal roundworm. In contrast, the bottom rows show abnormally fused chromosomes found in genetically altered roundworms created by the Salk researchers. Despite this irregularity, the Salk researchers' worms were able to reproduce, providing a new avenue for scientists to study a key pathway in the development of certain cancers. Credit: Image: Courtesy of Jan Karlseder, Professor, Molecular and Cellular Biology Laboratory and Daniel Lackner, research associate.

If telomerase fails to activate, the tumor cells of about 10 percent of all human cancers have a back-up strategy to build serviceable telomeres and keep dividing. How that pathway, called ALT for alternative lengthening of telomeres, works is unclear, because researchers have had limited options to study it experimentally. Continue reading below…

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Now scientists at the at Salk Institute for Biological Studies have created roundworms that eke out an existence, and even manage to reproduce, relying solely on ALT to maintain telomeres. That study, published March 16 in EMBO Journal, provides a valuable tool to tinker with the ALT pathway and learn how to block it, with a goal of forcing tumor cells to senesce.

“These worms are the first multicellular organisms we can study in the laboratory that maintain their telomeres through the ALT pathway and not through telomerase,” says Jan Karlseder, a professor in Salk’s Molecular and Cell Biology Laboratory and the study’s senior author. “Up to now we could only study ALT in cell lines derived from tumor cells. Now we can screen for compounds and genes that suppress or regulate ALT in a whole organism, which in worms is fairly easy to do.”

The components of telomere-building pathways are prime targets for cancer researchers. “There is a huge interest in drugs that block telomerase, since 90 percent of cancers use it for telomere maintenance,” says Daniel Lackner, a postdoctoral fellow in the Karlseder lab and one of the study’s first authors. “But these drugs won’t work for the 10 percent of cancers that use the ALT pathway. In fact, some evidence suggests that drugs targeting telomerase might actually increase ALT, making the need for ALT inhibitors more pressing.”

The new study stems from a 2008 study from the Karlseder lab that was published in Cell. In that paper, they mutated a gene encoding a telomere-binding protein in roundworms. The resulting mutants displayed functional, but slightly scruffier-looking telomeres than those built by telomerase. That was a strong hint that when forced, worm cells, like human cells, can turn on the ALT pathway.

For the new study, the team pushed the mutant worms’ survival capacity to the limit. This time they knocked out a second gene, telomerase itself, and found that these double mutants could reproduce continuously without undergoing senescence. Over the past 3 years a strain of double mutant worms has propagated for over 180 generations.

The group then used biochemistry to confirm that the worms depend totally on ALT for telomere maintenance. The telomeres of double mutants were more sloppily constructed than superior, telomerase-made caps and were similar in length and overall structure to chromosome caps displayed by human cancer cells that employ ALT.

The double mutant worms also contained wisps of telomeric DNA, called c-circles, that are unique by-products of ALT, further evidence that they were persisting via ALT.

Intriguingly, other investigators have reported that c-circles are present in the blood of human bone cancer patients and could potentially serve as a diagnostic for cancers that depend on the ALT rather than the telomerase pathway.

Although the worms are living long, species-wise, they are not quite prospering—- which is exactly what one would expect. The study reports that the double mutants have fewer offspring than normal worms, which is how roundworms exhibit “stress.” And many have fused chromosomes, a likely outcome of having barely serviceable telomeres. But what counts is that the animals are viable, rely on ALT only, and their genome reflects aberrations seen in human tumor cells. In short, they are ready for analysis.

Currently, researchers cannot predict what mechanisms a cancer will to use to maintain the telomeres. “Cancers of the bones, stomach and soft tissues may be more efficient in activating ALT than telomerase pathways,” says Karlseder, noting that indicators of ALT have also been observed in other cancer types. “We don’t know why a tumor chooses one pathway over the other. All we know is that ALT may be switched on in response to telomerase inhibition, which means we must understand this pathway.”

________

Marcela Raices, a former Salk postdoctoral fellow, now at University of California San Francisco, was co-first author with Lackner on the paper. Also contributing were Candy Haggblom of the Karlseder lab and Hugo Maruyama, a former graduate student in the lab, now at Osaka Dental University.

Funding for the study came from the National Institutes of Health, the Glenn Foundation for Medical Research, the Merieux Research Foundation, EMBO and the Blasker-Rose-Miah Fund.

சர்க்கரை நோயாளிகளுக்கு ஒரு இனிப்பான செய்தி

சர்க்கரை வியாதியால் இனிப்பை தொட்டுக் கூட பார்க்க முடியாத நிலையில் இருப்பவர்களுக்கு இது நிச்சயம் இனிப்பான செய்திதான். பராகுவேயில் பிரபலமான ஒரு செடி இப்போது உலகெங்கும் உள்ள சர்க்கரை வியாதியஸ்தர்களை பெரிதும் கவரத் தொடங்கியுள்ளது.

அதன் பெயர் ஸ்டீவியா. அதன் தாவரவியல் பெயர் ஸ்டீவியா ரிபாடியானா (Stevia rebaudiana), சுருக்கமாக ஸ்டீவியா.

இந்த செடி மகா இனிப்பானது. இதன் இலையிலிருந்து எடுக்கப்படும் சாறு அத்தனை இனிப்பு நிறைந்தது. இதை செயற்கை சர்க்கரை போல பயன்படுத்தி வருகின்றனர்- தென் அமெரிக்கா [^]வில். இத்தனை இனிப்பாக இருந்தாலும், சர்க்கரை வியாதியஸ்தர்களுக்கு இது மிகவும் பாதுகாப்பானது என்பதுதான் இதன் விசேஷமே.

இந்த செடியின் பூர்வீகம் தென் அமெரிக்காவில் உள்ள பராகுவே ஆகும். பல நூற்றாண்டுகளாக இந்த மூலிகைச் செடியை பராகுவேயில் உள்ள குவாரனி என்ற இனத்தவர் ஸ்வீடனராக பயன்படுத்தி வருகின்றனர். மிகச் சிறிய அளவிலான இந்த செடியின் இலைகளில்தான் இந்த இனிப்புத் தன்மை காணப்படுகிறது. சாதாரண சர்க்கரையை விட இதன் இனிப்பு 300 மடங்கு அதிகமாகும்.

மேலும் சர்க்கரையி்ல் உள்ளது போல அல்லாமல், இந்த ஸ்டீவியாவில் கலோரி ஒரு துளி கூட கிடையாது. மேலும் ரத்தத்தில் நமது சர்க்கரையின் அளவையும் இது அதிகரிக்காது.

உலக நாடுகளை மயக்கிக் கொண்டிருக்கும் இந்த ஸ்டீவியா தற்போது இந்தியாவுக்கும் வரவுள்ளது. நறுமணம் மிக்க ஸ்டீவியா மூலிகைச் செடி செம்மண்ணிலும் பிற வளம் நிறைந்த மண்ணிலும் நன்றாக வளரக்கூடியது. 50 முதல் 95 டிகிரி பாரன்ஹீட் வெப்பத்தில் வளரக்கூடிய இந்த செடியை பயிரிட்டு வளர்ப்பதும் பராமரிப்பதும் மிகவும் எளிது. இந்திய தட்பவெட்ப நிலையில் இந்த செடி நன்றாக வளரும். எனவே இதை இந்தியாவில் எங்கு வேண்டுமானாலும் பயிரிடலாம். வீட்டு தோட்டத்திலும் வளர்க்கலாம்.

ஸ்டீவியா செடியின் இலை, விதை, தண்டு ஆகியவற்றை காயவைத்து பொடியாக்கி சர்க்கரைக்கு பதிலாக பயன்படுத்தலாம். இது நீரிழிவு நோயாளிகளுக்கு ஒரு சிறந்த மாற்று இனிப்பு பொருள் ஆகும். ஸ்டீவியா பவுடரை தொடர்ந்து பயன்படுத்தினால் அது இன்சுலின் சுரப்பை ஊக்குவிக்க உதவும் என்பதும் கண்டு அறியப்பட்டு உள்ளது

தனியாக இருக்கும் போது மாரடைப்பு வந்தால் உங்களை நீங்களே எப்படி காப்பாற்றிக்கொள்வது ??

மாலை மணி 6:30,வழக்கம் போல் அலுவலகப் பணிகளை முடித்து விட்டு வீட்டிற்கு தனியாக சென்று கொண்டிருக்கிறீர்கள் . அலுவலகத்தில் வேலை பளுவின் காரணமாக, மற்றும் இதர சில பிரச்சனைகள் காரணமாக உங்கள் மனம் மிகவும் அழுத்தத்துடன் உள்ளது, நீங்கள் மிகவும் படபடப்பாகவும், தொய்வாகவும் உள்ளீர்கள் , திடீரென்று உங்கள் இதயத்தில் அதிக வலி ஏற்படுவதை உணர்கிறீர்கள்.

அந்த வலியானது மேல் கை முதல் தோள்பட்டை வரை பரவுவதை உணருகிறீர்கள் , உங்கள் வீட்டில் இருந்து மருத்துவமனை ஒரு ஐந்து மைல் தூரத்தில் இருப்பதாக வைத்துக்கொள்வோம், ஆனால் உங்களால் அந்த ஐந்து மையில் தூரத்தை கடக்க முடியாது என உங்கள் மூளை உங்களுக்கு சொல்கிறது இந்த நேரத்தில் நம் உயிரை நாமே காக்க என்ன செய்யலாம் ??
துரதிஷ்ட வசமாக மாரடைப்பு ஏற்படும் போதெல்லாம் இறப்பவர்கள் அதிகமாக தனியாக இருந்திருப்பவராக உள்ளனர் ! உங்கள் இதயம் தாறுமாறாக துடிக்கிறது..நீங்கள் சுயநினைவை இழக்க வெறும் 10 நொடிகள் தான் உள்ளது. இப்போது நீங்கள் செய்ய வேண்டியது தொடர்ச்சியாக மிக ஆக்ரோஷமாக இரும்ப வேண்டும், ஒவ்வொரு முறை இரும்புவதர்க்கு முன்னரும் மூச்சை இழுத்து விட வேண்டும் , இருமல் மிக ஆழமானதாக இருக்க வேண்டும்.

இருதயம் இயல்பு நிலை திரும்பும் வரையிலோ அல்லது வேறொருவர் உதவிக்கு வரும் வரையிலோ ஒவ்வொரு இரண்டு நொடிக்கும் மூச்சை இழுத்து விட்டு இரும்முக்கொண்டே இருக்க வேண்டும். மூச்சை இழுத்து விடுவதினால் நுரை ஈரலுக்கு ஆச்சிஜன் சீராக செல்ல வழி வகுக்கிறது , இருமுவதால் இருதயம் நிற்பதில் இருந்து தொடர்ச்சியாக துடித்துக்கொண்டே இருக்க உதவும், இதனால் ரத்தஓட்டம் சீரடையும்.

இருமுவதால் ஏற்படும் அதிர்வினால் இதயம் சீராக துடிக்கும்..பின்னர் இருதயம் சீரடைந்ததும் அருகில் உள்ள மருத்துவமனைக்கு செல்லலாம்..இந்த தகவலை குறைந்தது உங்களின் பத்து நண்பர்களுக்காவது பகிருங்கள்..தேவை இல்லாத விசயங்களையும், ஜோக்குகளையும் பகிர்வோர் , உயிரை காக்கும் இது போன்ற விசயங்களையும் பகிருங்கள்........ 

சத்தான காய் பாகற்காய்! எல்லா நோய்களுக்கும் அருமருந்து...

மருத்துவ குணங்கள் நிறைந்த பாகற்காய் தமிழகம் மட்டுமல்லாமல் பெரும்பாலான ஆசியா நாடுகளிலும் மிகவும் பிரபலமான ஒரு காய்.

குறிப்பாக ஜப்பான், சீனா மற்றும் வியட்நாமில் அதிக பிரபலம்.

ஆசியமற்றும் ஆப்ரிக்க நாடு மருந்துகளிலும் நிறைய பயன்படுத்தப் படுகிறது.

பிஞ்சு பாகற்காய் சமையலுக்கு உகந்தது. பாகற்காய் பொரியல், கூட்டு மற்றும் குழம்பு செய்வதற்கு நன்றாக இருக்கும்.

Bitter Gourd details in English…

மற்ற பெயர்கள்:

பிட்டர் கௌர்ட்(Bitter Gourd) - ஆங்கிலம்

கரேலா (Karela) – இந்தி

சத்து விவரம்:

வைட்டமின் A , B1, B2 மற்றும் C நிறைந்தது.

கால்சியம், இரும்பு, காப்பர், பாஸ்பரஸ் மற்றும் பொட்டசிய தாதுக்கள் நிறைந்தது.

ப்ரோகோளியை விட இருமடங்கு beta-carotene-ம், கீரையை விட இருமடங்கு கால்சியம் சத்தும், வாழைபழத்தை விட இருமடங்கு பொட்டாசியம் சத்தும் கொண்டது.

மருத்துவ பலன்கள்:

செரிமானத்திற்கும், இரத்த சுத்திகரிப்பிற்கும் மிகவும் நல்லது.

பாகற்காயில் வைட்டமின்களும் தாதுக்களும் நிறைந்திருப்பதால் இரத்த அழுத்தம், சர்க்கரை வியாதி, கண் சம்மந்தப்பட்ட நோய்களுக்கு நல்ல மருந்தாகும்.

உடல் எதிர்ப்பு சக்தியை அதிகரிக்கும்.

சர்க்கரை நோயுள்ளவர்களுக்கு நல்ல உணவு.

பாகற்காய் சாறு தொடர்ந்து அருந்தினால் சக்தியும் பலமும் அதிகமாகும்.

பல நோய்களை குணமாக்கும் வெள்ளைப் பூண்டு...

பண்டைய எகிப்திலும் பாபிலோனியாவிலும் அற்புதங்களை விளைவித் துக் குணமாக்கிய மண்ணடித் தாவரம் இது.

கிரேக்கத் தடகள வீரர்கள் விரைந்து ஓட ஊக்கம் தரும் மருந்தாக வெள் ளைப் பூண்டை கைகளில் அழுத்தித் தடவிக் கைகளைக் கழுவினார்கள். இதனால் நோய் நுண்மங்கள் அழிந்தன.

குடலில் உள்ள புழுக்களிலிருந்து மற்றும் தலைவலி முதல் புற்றுநோய் வரை பல நோய்களையும் குணமாக்க வெள்ளைப் பூண்டு பயன்படுத்தப் படுகிறது.

அறிவியல் முடிவுகளால் கூட வெள்ளைப் பூண்டின் பெருமையை மங்கச் செய்ய முடியவில்லை.

உடலில் நன்மை செய்யக்கூடிய கொலஸ்ட்ரால் உருவாக பூண்டின் பங்கு மகத்தானது.

எனவே உணவில் பூண்டினை அவசியம் சேர்த்துக் கொள்வோம்..

How bodies resist cancer drugs

DUKE-NUS

Cancer cells flowing inside a vein with blood cells. Image: adventtr/iStockphoto A multi-national research team led by scientists at Duke-NUS Graduate Medical School has identified the reason why some patients fail to respond to some of the most successful cancer drugs. Tyrosine kinase inhibitor drugs (TKIs) work effectively in most patients to fight certain blood cell cancers, such as chronic myelogenous leukemia (CML), and non-small-cell lung cancers (NSCLC) with mutations in the EGFR gene. These precisely targeted drugs shut down molecular pathways that keep these cancers flourishing and include TKIs for treating CML, and the form of NSCLC with EGFR genetic mutations. Now the team at Duke-NUS Graduate Medical School in Singapore, working with the Genome Institute of Singapore (GIS), Singapore General Hospital and the National Cancer Centre Singapore, has discovered that there is a common variation in the BIM gene in people of East Asian descent that contributes to some patients' failure to benefit from these tyrosine kinase inhibitor drugs. “Because we could determine in cells how the BIM gene variant caused TKI resistance, we were able to devise a strategy to overcome it,” said S. Tiong Ong, M.B.B. Ch.., senior author of the study and associate professor in the Cancer and Stem Cell Biology Signature Research Programme at Duke-NUS and Division of Medical Oncology, Department of Medicine, at Duke University Medical Center. “A novel class of drugs called the BH3-mimetics provided the answer,” Ong said. “When the BH3 drugs were added to the TKI therapy in experiments conducted on cancer cells with the BIM gene variant, we were able to overcome the resistance conferred by the gene. Our next step will be to bring this to clinical trials with patients.” Said Yijun Ruan, Ph.D., a co-senior author of this study and associate director for Genome Technology and Biology at GIS: “We used a genome-wide sequencing approach to specifically look for structural changes in the DNA of patient samples. This helped in the discovery of the East Asian BIM gene variant.  What’s more gratifying is that this collaboration validates the use of basic genomic technology to make clinically important discoveries.” The study was published online in Nature Medicine on March 18. If the drug combination does override TKI resistance in people, this will be good news for those with the BIM gene variant, which occurs in about 15 percent of the typical East Asian population. By contrast, no people of European or African ancestry were found to have this gene variant. “While it’s interesting to learn about this ethnic difference for the mutation, the greater significance of the finding is that the same principle may apply for other populations,” said Patrick Casey, Ph.D., senior vice dean for research at Duke-NUS and James B. Duke Professor of Pharmacology and Cancer Biology. “There may well be other, yet to be discovered gene variations that account for drug resistance in different world populations. These findings underscore the importance of learning all we can about cancer pathways, mutations, and treatments that work for different types of individuals. This is how we can personalize cancer treatment and, ultimately, control cancer.” “We estimate that about 14,000 newly diagnosed East Asian CML and EGFR non-small-cell lung cancer patients per year will carry the gene variant,” Ong said. “Notably, EGFR NSCLC is much more common in East Asia, and accounts for about 50 percent of all non-small-cell lung cancers in East Asia, compared to only 10 percent in the West.” The researchers found that drug resistance occurred because of impaired production of BH3-containing forms of the BIM protein. They confirmed that restoring BIM gene function with the BH3 drugs worked to overcome TKI resistance in both types of cancer. “BH3-mimetic drugs are already being studied in clinical trials in combination with chemotherapy, and we are hopeful that BH3 drugs in combination with TKIs can actually overcome this form of TKI resistance in patients with CML and EGFR non-small-cell lung cancer,” Ong said. “We are working closely with GIS and the commercialization arm of the Agency for Science, Technology & Research (A*STAR), to develop a clinical test for the BIM gene variant, so that we can take our discovery quickly to the patient.” The major contributors to the study include additional researchers and teams from the Duke-NUS Graduate Medical School, Genome Institute of Singapore (Dr. Yijun Ruan and Dr. Axel Hillmer), Singapore General Hospital (Dr. Charles Chuah), and National Cancer Centre Singapore (Dr. Darren Wan-Teck Lim).   In addition, the investigators also received important contributions from Akita University Graduate School of Medicine, Japan (Dr. Naoto Takahashi), the Cancer Science Institute of Singapore (Dr. Ross Soo), the National University Cancer Institute of Singapore (Drs. Liang Piu Koh and Tan Min Chin), the Yong Loo Lin School of Medicine, National University of Singapore (Dr. Seet Ju Ee), the University of Bonn, Germany (Dr. Markus Nöthen), the University of Malaya (Dr. Veera Nadarajan), and the University of Tokyo, Japan (Dr. Hiroyuki Mano). Editor's Note: Original news release can be found here.

Lying brings more satisfaction

THE UNIVERSITY OF SYDNEY

Honesty may be the best policy, but new research from the University of Sydney suggests that consumers feel more satisfied if they lie and get what they want than if they tell the truth. The study, to be published in the Journal of Consumer Research by Dr Christina Anthony and Professor Elizabeth Cowley of the University of Sydney Business School, found that people who lie during a service encounter have more extreme reactions to the outcome than their honest peers. The research raises interesting questions about the way marketers and businesses respond to dishonest customers and train their staff, particularly given the volume of lies people tell every day - previous research shows that people tell on average one to two lies a day, which equates to about 42,000 lies before the age of 60. "Lying is hard work. When people lie, they're so preoccupied with telling the lie and not revealing the truth that they aren't able to monitor cues from the listener, which are important for updating expectations about the likely outcome of the conversation. This means that they are more surprised by the outcome and so have a stronger reaction to it," says Dr Anthony. "So when you lie to get a refund or to file an insurance claim and get away with it, you will have a much more polarised reaction than if you had told the truth. People who lie are more satisfied than truth tellers if they get a favourable outcome and more dissatisfied if they get an unfavourable outcome." The researchers conducted a series of lab experiments in which participants either told the truth or lied during a conversation with a service provider in order to get a material reward. This included lying to a salesperson about better competitor offers to secure a more favourable deal and lying to obtain a refund that fell outside the terms of the refund policy. In one experiment, participants were asked to answer some questions about a consumer product and told that some of them would receive the product as a prize if they met some pre-determined criteria. Half of the participants were then informed that they were eligible for the prize, even though their responses did not match the specified eligibility criteria - and they knew it. Participants therefore had a choice: to lie and get the prize, or to correct the error and miss out. "We found that about 50 percent of participants in this situation chose to lie. They were more thrilled with the outcome when they got the prize and more disappointed when they missed out," says Dr Anthony. The fact that customers who lie have more extreme reactions to service encounters also has important consequences for businesses and marketers, says Dr Anthony. "Because a successful lie may boost satisfaction with a transaction, it may be wise in some instances to turn a blind eye if the company doesn't have too much to lose financially." "If marketers are overly cautious of dishonest consumers, they also run the risk of wrongly accusing and alienating people who are telling the truth." Editor's Note: Original news release can be found here.

Arsenic in soil ups cancer risk

THE UNIVERSITY OF MELBOURNE

Exposure to arsenic in soil and mine waste may have contributed to a slight increase in past cancer risk in socio-economically disadvantaged areas in the Goldfields region of Victoria, according to new research published in theJournal of Exposure Science and Environmental Epidemiology. Researchers from the University of Ballarat have released findings showing that the incidence of some cancers between 1984 and 2003 was slightly higher in areas with higher arsenic levels.  Dr Dora Pearce, now at the Melbourne School of Population Health, University of Melbourne, explored how soil arsenic levels and cancer rates varied across central Victoria.  By using 20 years of data from the Victorian Cancer Registry and a measure of soil arsenic derived from geochemical data provided by the University of Ballarat and GeoScience Victoria, Dr Pearce has concluded that ongoing recorded monitoring of environmental sources of arsenic is needed.  “Arsenic is naturally occurring around gold mineralisation and is even used as an indicator in gold exploration, so it can be concentrated in soil and mine waste dumps that are still scattered across our landscape,” Dr Dora Pearce said. In the Goldfields region, many residential communities have grown up around historical gold mining areas.  “Our previous research detected small traces of arsenic in toenail clippings from children living in this region, showing that exposure to arsenic in soil could be an ongoing problem and that we should not be too complacent.  “We hope that by raising community awareness of this issue, childhood exposures to arsenic in soil, and future cancer risk, will be reduced in the Goldfields region of Victoria,” Dr Pearce said. Editor's Note: Original news release can be found here.

How HIV remains a puzzle

THE UNIVERSITY OF ADELAIDE

"Even in early infection when the virus population is low, HIV rapidly evolves to evade immune defences and treatments." Image: skodonnell/iStockphoto New research from the University of Adelaide shows why the development of a cure and new treatments for HIV have been so difficult for scientists to crack. Dr Jack da Silva from the University's School of Molecular & Biomedical Science has used computer simulations to discover that even in early infection when the virus population is low, HIV rapidly evolves to evade immune defences and treatments. These results - published in this month's issue of the prestigious journal GENETICS - challenge the commonly held belief that evolution of the virus under these circumstances is very slow. "I believe the search for a cure for AIDS has failed so far because we do not fully understand how HIV evolves," Dr da Silva said. To make this discovery, Dr da Silva used computer simulations to determine whether, under realistic conditions, the virus could evolve rapidly if an infection started from a single virus. This was done by constructing a model of the virus population, then simulating the killing of virus-infected cells by the immune system, along with mutation, recombination (the process by which genetic material is broken and joined to other genetic material), and random genetic changes. Results show that for realistic rates of cell killing, mutation and recombination, and a realistic population size, the virus could evolve very rapidly even if the initial population size is one. "At low population levels, viruses have reduced genetic variation and therefore it should be harder for them to evolve rapidly. However, it appears that the evolution of HIV goes against conventional wisdom," Dr da Silva said. "We now need further insight into the precise genetic mechanisms that enable the virus to so readily adapt to all the challenges we throw at it. Such knowledge will, hopefully, lead to novel strategies for vaccines and other control measures." Mark Johnston, Editor-in-Chief of GENETICS, said: "Now that we know HIV rapidly evolves, even when its population size is small, we may be able to interfere with its ability to evolve so we can get the most out of the treatments that are developed." The full report from Dr Jack da Silva can be read online. Editor's Note: Original news release can be found here.