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	<title>Biology News, Latest Health News, Biology Articles and Headlines</title>
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	<pubDate>Tue, 15 Apr 2008 12:09:37 +0000</pubDate>
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		<title>String of genetic mutations cause aggressive form of leukaemia</title>
		<link>http://www.ebiologynews.com/4264.html</link>
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		<pubDate>Tue, 15 Apr 2008 12:09:37 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Cancer Research]]></category>

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		<description><![CDATA[April 15 : Experts at St. Jude Children&#8217;s Research Hospital have unearthed evidence that a combination of genetic mutations is to blame for most cases of acute lymphoblastic leukemia (ALL),  which often proves fatal.
Given that a series of genetic mutations work together cause the disease, the researchers have named these defects ‘cooperating oncogenic lesions’.
The]]></description>
			<content:encoded><![CDATA[<p>April 15 : Experts at St. Jude Children&#8217;s Research Hospital have unearthed evidence that a combination of genetic mutations is to blame for most cases of acute lymphoblastic leukemia (ALL),<span id="more-4264"></span>  which often proves fatal.</p>
<p>Given that a series of genetic mutations work together cause the disease, the researchers have named these defects ‘cooperating oncogenic lesions’.</p>
<p>The researchers have revealed that these defects include the deletion of a gene called IKZF1, whose protein Ikaros normally helps guide the development of a blood stem cell into a lymphocyte.</p>
<p>They have also discovered that the loss of the same gene accompanied the transformation of chronic myelogenous leukaemias (CMLs) to a life-threatening acute stage.</p>
<p>&#8220;These findings provide new avenues to pursue to gain a better understanding of these disease processes and, ultimately, to develop better therapies,&#8221; Nature magazine quoted Dr. James R. Downing, St. Jude scientific director and chair of the Department of Pathology, as saying.</p>
<p>He says that his team’s findings lend further support to the idea that malignancies frenquently require mutations in multiple genes in order to develop.</p>
<p>Dr. Downing says that cells contain oncogenes, which exist harmlessly until something triggers them to turn the cells malignant.</p>
<p>&#8220;It really takes a series of genetic lesions to lead to cancer. You may get activation of an oncogene, but you may also need activation of a tumor suppressor gene and an alteration in a cell-death pathway,&#8221; he said.</p>
<p>In a previous study, the researchers tried to identify genetic differences between CML and a form of acute leukaemia known as BCR-ABL1 ALL.</p>
<p>Both diseases are characterized by the Philadelphia chromosome, which results from the translocation (joining) of parts of two different chromosomes, and the result of this translocation is the expression of BCR-ABL1, an oncogene.</p>
<p>&#8220;It appears from our study, and other work published previously, that all you need to get CML is that chromosomal translocation and BCR-ABL1 expression,&#8221; Dr. Downing said.</p>
<p>In their latest study, the researchers re-examined the genetic makeup of 304 ALL patients who had been studied earlier, including 43 paediatric and adult BCR-ABL1 ALL patients and 23 adults with CML.</p>
<p>The number of genetic mutations found in the original gene survey was increased using a more sensitive technology.</p>
<p>In the first study, the gene most commonly altered was one called PAX5, followed by a gene designated IKZF1, whose protein Ikaros is involved in the development and differentiation of B lymphocyte cells, which are part of the immune system.</p>
<p>&#8220;The vast majority of pediatric acute lymphoblastic leukemias are of B-cell lineage,&#8221; Downing said.</p>
<p>The researchers said that among the ALL patients, they found an average of 8.79 copy number alterations, a form of genetic change linked to the development and progression of cancer. The most common change was deletion of the gene for Ikaros, they added.</p>
<p>The gene was deleted in 83.7 per cent of the BCR-ABL1 ALL patients, including 76.2 per cent of the paediatric and 90.9 per cent of the adult cases.</p>
<p>&#8220;The loss of the Ikaros gene is a nearly obligatory lesion for the development of BCR-ABL1 ALL, and clearly must be a genetic lesion that is cooperating with BCR-ABL1,&#8221; Dr. Downing said.</p>
<p>In their study report, the researchers wrote that a gene known as CDKN2A was deleted in 53.5 per cent of the BCR-ABL1 ALL patients, 87.5 per cent of whom also had lost the gene for Ikaros.</p>
<p>The PAX5 deletion occurred in 51 per cent of the BCR-ABL1 ALL patients, and 95 per cent of such people were missing the Ikaros gene.</p>
<p>Among the CML patients, whose disease converted to ALL, two out of three had the deletion of the Ikaros gene. A lower percentage of those who converted to acute myeloblastic leukemia had the same gene deleted.</p>
<p>The researchers said that those findings suggested that the deletion of Ikaros was cooperating with BCR-ABL1 to cause ALL.</p>
<p>&#8220;That is an important finding that may give insight into how that transformation occurs, or it may give insight into a better way to treat the disease, if one can figure out how the Ikaros deletion is working,&#8221; Dr. Downing said. (ANI)</p>
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		<coop:keyword><![CDATA[Cancer Research]]></coop:keyword>
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		<title>Children’s Everest trek paves way for lung research</title>
		<link>http://www.ebiologynews.com/4263.html</link>
		<comments>http://www.ebiologynews.com/4263.html#comments</comments>
		<pubDate>Tue, 15 Apr 2008 11:09:34 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Health News]]></category>

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		<description><![CDATA[April 15 : A study of nine British children who trekked towards Everest Base Camp has furnished data that can form the basis for future research into potent strategies to prevent premature babies from blindness and lung damage.
The results of the Smiths Medical Young Everest Study may also pave the way for children with chronic]]></description>
			<content:encoded><![CDATA[<p>April 15 : A study of nine British children who trekked towards Everest Base Camp has furnished data that can form the basis for future research into potent strategies to prevent premature babies<span id="more-4263"></span> from blindness and lung damage.</p>
<p>The results of the Smiths Medical Young Everest Study may also pave the way for children with chronic lung diseases to be monitored at home rather than in hospital, say the researchers associated with the project.</p>
<p>While trekking, the children were breathing far less oxygen than they would at sea level. It was as debilitating as a critical illness, and similar to the conditions experienced by premature babies.</p>
<p>The study’s results showed that the children coped better than would be expected with the low levels of oxygen saturation in the blood.</p>
<p>Doctors generally administer oxygen to premature babies or children with chronic breathing difficulties. But administering too much of oxygen to children may cause damage to their lungs, and it may lead to blindness in premature babies.</p>
<p>Experts believe that the information on the nine children who ascended mountain pathways may help study whether doctors can lower the doses of oxygen administered.</p>
<p>According to them, the study’s results indicate that the human body copes with lower oxygen levels by reverting to techniques used in the womb.</p>
<p>“A child in the womb uses less oxygen, about the amount that someone would have at 8,500 m (27,900ft),” Times Online quoted Monty Mythen, Smiths Medical Professor of Anaesthesia and Critical Care at University College London, who volunteered his own four children for the study, as saying.</p>
<p>Medical experts, including intensive care doctors and doctors who specialise in foetal growth, will meet next week to discuss whether there is a link between people experiencing high altitudes, foetuses in the womb and diving mammals.</p>
<p>“Younger children may actually be better than people who have gone through puberty. Being closer to the womb, they have more of their adaptive processes still switched on,” said Professor Mythen.</p>
<p>He revealed that, though all the children participants in the study coped well with lower levels of oxygen in their blood, some coped far better than others.</p>
<p>He added that that observation suggested that such children had a genetic predisposition to adapt to low oxygen levels.</p>
<p>According to him, this information might be helpful in developing tailored treatments for children in intensive care.</p>
<p>Janet Stocks, Professor of Respiratory Physiology at University College London, who led the study, said: “The children all kept diaries recording how they were feeling, and this really didn’t reflect how their bodies were coping. I think it’s fairly clear that there is a genetic determinant.”</p>
<p>Professor Mythen now plans to take 100 British children to the Himalayas in 2011 for a study. (ANI)</p>
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		<coop:keyword><![CDATA[Health News]]></coop:keyword>
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		<title>Brain study may pave way for better epilepsy treatments</title>
		<link>http://www.ebiologynews.com/4262.html</link>
		<comments>http://www.ebiologynews.com/4262.html#comments</comments>
		<pubDate>Tue, 15 Apr 2008 08:55:03 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Neurobiology]]></category>

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		<description><![CDATA[April 15 : Scientists have discovered in a study on mice how a neurotransmitter that the body releases during epilepsy seizures, known as glutamate, leads to an increased production of a protein that may reduce medication entry into the brain.
The finding attains significance as it may help discern why about 30 per cent of patients]]></description>
			<content:encoded><![CDATA[<p>April 15 : Scientists have discovered in a study on mice how a neurotransmitter that the body releases during epilepsy seizures, known as glutamate, leads to an increased production of a protein <span id="more-4262"></span>that may reduce medication entry into the brain.</p>
<p>The finding attains significance as it may help discern why about 30 per cent of patients with epilepsy do not respond to anti-epileptic medications.</p>
<p>“Our work identifies the mechanism by which seizures increase production of a drug transport protein in the blood brain barrier, known as P-glycoprotein, and suggests new therapeutic targets that could reduce resistance,” said Dr. David Miller, a principal investigator in the Laboratory of Pharmacology at the National Institute of Environmental Health Sciences (NIEHS).</p>
<p>The blood-brain barrier (BBB), which resides in brain capillaries, is a limiting factor in treatment of many central nervous system disorders. It is altered in epilepsy so that it no longer permits free passage of administered anti-epileptic drugs into the brain.</p>
<p>In their study report, available in the online edition of Molecular Pharmacology, the researchers write that P-glycoprotein forms a functional barrier in the BBB that protects the brain by limiting access of foreign chemicals.</p>
<p>“The problem is that the protein does not distinguish well between neurotoxicants and therapeutic drugs, so it can often be an obstacle to the treatment of a number of diseases, including brain cancer,” Miller said.</p>
<p>The researcher writes in the study report that increased levels of P-glycoprotein in the BBB has been suggested as one probable cause of drug resistance in epilepsy.</p>
<p>The researcher studied isolated brain capillaries from mice and rats and an animal model of epilepsy during the study.</p>
<p>They observed that glutamate turns on a signalling pathway that activates cyclooxygenase-2 (COX-2), causing increased synthesis of P-glycoprotein.</p>
<p>When COX-2 was knocked out in mice, the increased expression of P-glycoprotein was abolished.</p>
<p>The researchers, however, insist that it has yet to be shown in animals or patients that targeting COX-2 will reduce seizure frequency or increase the effectiveness of anti-epileptic drugs.</p>
<p>&#8220;These findings provide insight into one mechanism that underlies drug resistance in epilepsy and possibly other central nervous system disorders,&#8221; said Dr. Bjoern Bauer, lead author on the publication.</p>
<p>&#8220;Targeting blood-brain barrier signals that increase P-glycoprotein expression rather than the transporter itself suggests a promising way to improve the effectiveness of drugs that are used to treat epilepsy, though more research is needed before new therapies can be developed,” Bauer added. (ANI)</p>
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		<coop:keyword><![CDATA[Neurobiology]]></coop:keyword>
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		<title>Scientists mimic bacteria to produce magnetic nanoparticles</title>
		<link>http://www.ebiologynews.com/4261.html</link>
		<comments>http://www.ebiologynews.com/4261.html#comments</comments>
		<pubDate>Tue, 15 Apr 2008 08:53:23 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Nanobiotechnology]]></category>

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		<description><![CDATA[April 15 : Scientists have mimicked bacteria to produce magnetic nanoparticles that could be used for drug targeting and delivery in magnetic inks and high-density memory devices, or as magnetic seals in motors. 
The procedure was carried out by a group of researchers at the US Department of Energy’s Ames Laboratory.
Commercial room-temperature synthesis of ferromagnetic]]></description>
			<content:encoded><![CDATA[<p>April 15 : Scientists have mimicked bacteria to produce magnetic nanoparticles that could be used for drug targeting and delivery in magnetic inks and high-density memory devices, or as magnetic seals in motors. <span id="more-4261"></span></p>
<p>The procedure was carried out by a group of researchers at the US Department of Energy’s Ames Laboratory.</p>
<p>Commercial room-temperature synthesis of ferromagnetic nanoparticles is difficult because the particles form rapidly, resulting in agglomerated clusters of particles with less than ideal crystalline and magnetic properties. </p>
<p>Also, as particles get smaller, their magnetic properties, particularly with regard to temperature, also diminish.</p>
<p>However, several strains of bacteria produce magnetite (Fe3O4) –  fine, uniform nanoparticles that have desirable magnetic properties. </p>
<p>These magnetotactic bacteria use a protein to form crystalline particles about 50 nanometers in size. These crystals are bound by membranes to form chains of particles which the bacteria use like a compass needle to orient themselves with the Earth’s magnetic field.</p>
<p>To see if researchers could learn from the bacteria, Surya Mallapragada, Ames Laboratory Materials Chemistry and Biomolecular Materials program director, pulled together a team that included microbiologists, biochemists, material chemists, chemical engineers, materials scientists and physicists from Ames Laboratory and Iowa State University.</p>
<p>As a starting point, from the University of Nevada-Las Vegas, isolated several strains of magnetotactic bacteria for use in the study.</p>
<p>Based on earlier work by a Japanese research team, Ames Laboratory biochemist Marit Nilsen-Hamilton looked at several proteins known to bind iron, including Mms6 found in magnetotactic bacteria, which she cloned from the bacteria. </p>
<p>“This protein is associated with the membranes that surround the magnetite crystals, and each bacterium appears to make particles with their own unique crystal structure,” said Nilsen-Hamilton.</p>
<p>Ames Lab chemist Tanya Prozorov tried synthesizing crystals, using the proteins with various concentrations of reagents in an aqueous solution, but the particles formed quickly, were small and lacked specific crystal morphology.</p>
<p>At the suggestion of Ames Lab senior physicist Paul Canfield, the team used polymer gels developed by Mallapragada and Balaji Narasimhan, to slow down the reaction and help control formation of the nanocrystals and minimize aggregation.</p>
<p>Prozorov also conducted electron microscopy analysis of the synthetic nanoparticles which showed that Mms6 produced well-formed, faceted crystals resembling those produced naturally by the bacteria. </p>
<p>Powder X-ray diffraction studies verified the crystal structure of the particles.</p>
<p>Ames Lab physicist Ruslan Prozorov, tested the magnetic properties of the synthetic crystals which also showed striking similarities to the bacteria-produced crystals and bulk magnetite. </p>
<p>The magnetic studies also showed that the “chains” of particles formed by the bacteria had a much sharper magnetic transition definition at a higher temperature than single crystals. (ANI)</p>
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		<coop:keyword><![CDATA[Nanobiotechnology]]></coop:keyword>
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		<title>Blood pressure drugs may help prevent pancreatic cancer spread</title>
		<link>http://www.ebiologynews.com/4260.html</link>
		<comments>http://www.ebiologynews.com/4260.html#comments</comments>
		<pubDate>Tue, 15 Apr 2008 07:22:36 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Cancer Research]]></category>

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		<description><![CDATA[April 15 : Researchers at the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia have found that a blood pressure-lowering drug called an angiotensin receptor blocker inhibits pancreatic cancer cell growth and causes cell death.
In previous studies, Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at Jefferson Medical College, and her colleagues showed that]]></description>
			<content:encoded><![CDATA[<p>April 15 : Researchers at the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia have found that a blood pressure-lowering drug called an angiotensin receptor blocker inhibits <span id="more-4260"></span>pancreatic cancer cell growth and causes cell death.</p>
<p>In previous studies, Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at Jefferson Medical College, and her colleagues showed that angiotensin receptor blockers might help reduce the development of tumour-feeding blood vessels, a process called angiogenesis.</p>
<p>Other studies have associated a lower incidence of cancer with the use of angiotensin blocking therapies. Arafat said that theses drugs might become part of a novel strategy to control the growth and spread of cancer.</p>
<p>One such drug, AT1R (Ang II type 1 receptor) blockers, inhibits the function of the hormone angiotensin II (Ang II) in the pancreas.</p>
<p>The receptor is expressed in pancreatic cancer cells. Ang II boosts the production of VEGF, a vascular factor that promotes blood vessel growth in a number of cancers.</p>
<p>High levels of VEGF have been linked to poor cancer prognosis and early recurrence after surgery. Dr. Arafat and her team have shown that AngII indirectly causes VEGF expression by boosting AT1R expression.</p>
<p>Researchers investigated the effects of blocking AT1R on the pancreatic cancer cell reproductive cycle and programmed cell death, or apoptosis, and the mechanisms involved.</p>
<p>They found that blocking AT1R inhibited pancreatic cancer cell growth and promoted cell death.</p>
<p>“This happens through inducing the activity of the gene p53, which controls programmed cell death, and also by inhibiting anti-cell death pathways such as those involving the gene bcl-2,” Dr. Arafat said.</p>
<p>The researchers also found that blocking AT1R affects p21, a gene that regulates the cell cycle.</p>
<p>“We found that blocking this receptor can cause cell cycle arrest. This is really exciting because the role of this receptor has never been known,” Dr. Arafat said.</p>
<p>“It’s never been connected to cell division or apoptosis. We’re also now further exploring the mechanisms involved. The exciting thing is that this receptor already has so many available pharmaceutical blockers on the market,” she added.</p>
<p>She further said that the group hopes to be able to test these agents in human trials.</p>
<p>The findings have been reported on April 14, 2008 at the annual meeting of the American Association for Cancer Research in San Diego. (ANI)</p>
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		<coop:keyword><![CDATA[Cancer Research]]></coop:keyword>
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		<title>Staying aerobically fit through middle age can delay ageing by 12 years</title>
		<link>http://www.ebiologynews.com/4259.html</link>
		<comments>http://www.ebiologynews.com/4259.html#comments</comments>
		<pubDate>Thu, 10 Apr 2008 09:28:04 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Health News]]></category>

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		<description><![CDATA[April 10 : A new study has found that staying aerobically fit, especially through middle age and beyond, can delay biological aging by up to 12 years and prolong independence during old age.
Aerobic exercise, such as jogging, swimming, cycling or walking - improves a person&#8217;s oxygen consumption and boosts their metabolism.
But maximal aerobic power starts]]></description>
			<content:encoded><![CDATA[<p>April 10 : A new study has found that staying aerobically fit, especially through middle age and beyond, can delay biological aging by up to 12 years and prolong independence during old age.<span id="more-4259"></span></p>
<p>Aerobic exercise, such as jogging, swimming, cycling or walking - improves a person&#8217;s oxygen consumption and boosts their metabolism.</p>
<p>But maximal aerobic power starts to fall steadily from middle age, decreasing by around 5 ml/[kg.min] every decade.</p>
<p>When it falls below around 18 ml in men and 15 ml in women, it becomes difficult to do very much at all without severe fatigue.</p>
<p>In a typical sedentary man, the maximal aerobic power will have fallen to around 25 mil/[kg.min] by the age of 60, almost half of what it was at the age of 20.</p>
<p>But the evidence shows that regular aerobic exercise can slow or reverse the inexorable decline, even in later life.</p>
<p>Research by scientists at the University of Toronto in Canada has shown that high-intensity exercise, taken regularly for more than a year, can boost maximal aerobic power by 25 percent, equivalent to a gain of 6 ml/ [kg.min], or 10 to 12 biological years.</p>
<p>&#8220;There seems good evidence that the conservation of maximal oxygen intake increases the likelihood that the healthy elderly person will retain functional independence,&#8221; an author said.</p>
<p>The other positive spin-offs of aerobic exercise are reduced risks of serious disease, faster recovery after injury or illness, and reduced risks of falls because of the maintenance of muscle power, balance, and coordination.</p>
<p>The results are published in the British Journal of Sports Medicine. (ANI)</p>
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		<coop:keyword><![CDATA[Health News]]></coop:keyword>
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		<title>Preeclampsia during pregnancy puts babies at cardiovascular risk</title>
		<link>http://www.ebiologynews.com/4250.html</link>
		<comments>http://www.ebiologynews.com/4250.html#comments</comments>
		<pubDate>Wed, 09 Apr 2008 09:14:46 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Developmental Biology]]></category>

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		<description><![CDATA[Apr 9 : Researchers at the University of Cambridge have revealed that babies whose mothers have preeclampsia during pregnancy are at an increased risk of developing cardiovascular problems later in life.
Pre-eclampsia is a medical condition in which hypertension arises in pregnancy along with other problems that can lower the amount of oxygen the foetus receives.
The]]></description>
			<content:encoded><![CDATA[<p>Apr 9 : Researchers at the University of Cambridge have revealed that babies whose mothers have preeclampsia during pregnancy are at an increased risk of developing <span id="more-4250"></span>cardiovascular problems later in life.</p>
<p>Pre-eclampsia is a medical condition in which hypertension arises in pregnancy along with other problems that can lower the amount of oxygen the foetus receives.</p>
<p>The lack of oxygen may impede growth and damage the baby&#8217;s cardiovascular, metabolic and endocrine systems.</p>
<p>The researchers conducted the study on pregnant animals and examined the pregnancies at high altitude, where oxygen is restricted.</p>
<p>The findings showed changes in the way the foetus grew when oxygen was restricted, and significant variations in the way key systems in the body developed.</p>
<p>According to the research team, this can put the baby at the risk of developing heart disease later in life.</p>
<p>&#8220;We have known for a while that changes in maternal nutrition can affect foetal development and influence disease susceptibility later in life, but relatively little work has investigated how low oxygen levels in the womb may affect infant development,&#8221; BBC quoted Dr Dino Giussani, lead researcher, as saying. </p>
<p>&#8220;Our research shows that changes to the amount of oxygen available in the womb can have a profound influence on the development of the foetus in both the short - and long - term, and trigger an early origin of heart disease,&#8221; he added. </p>
<p>The researchers suggest that damage caused by lack of oxygen could be compensated by increasing mother’s diet with nutrients such as Vitamins C and E, selenium and lycopen.</p>
<p>“This may halt the development of heart disease at its very origin, bringing preventative medicine back into the womb,&#8221; said Giussani.</p>
<p>The study is to be presented at a Society for Endocrinology meeting. (ANI)</p>
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		<coop:keyword><![CDATA[Developmental Biology]]></coop:keyword>
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		<title>Positive experiences reduce depression symptoms in MS patients</title>
		<link>http://www.ebiologynews.com/4249.html</link>
		<comments>http://www.ebiologynews.com/4249.html#comments</comments>
		<pubDate>Wed, 09 Apr 2008 08:13:21 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Health News]]></category>

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		<description><![CDATA[Apr 9 : A new study has revealed that positive experiences can significantly reduce emotional and psychological stress or depression among people with multiple sclerosis (MS).  
The study conducted by Alexa Stuifbergen, professor of nursing and associate dean of research at The University of Texas at Austin, and Lorraine Phillips, assistant professor in the]]></description>
			<content:encoded><![CDATA[<p>Apr 9 : A new study has revealed that positive experiences can significantly reduce emotional and psychological stress or depression among people with multiple sclerosis (MS). <span id="more-4249"></span> </p>
<p>The study conducted by Alexa Stuifbergen, professor of nursing and associate dean of research at The University of Texas at Austin, and Lorraine Phillips, assistant professor in the University of Missouri Sinclair School of Nursing has found that increasing positive experiences can decrease depression symptoms in MS patients.</p>
<p>“Positive experiences significantly affected the participants’ perceptions of the quality of their lives and symptoms of depression, even when taking into account age, education and disease-related factors, such as mobility, vision and cognition,” said Phillips.</p>
<p>“People with MS typically rate the quality of their lives lower than that of the general population, so it is important for people with MS and clinicians involved in their care to understand what factors may improve the quality of their lives.</p>
<p>“The participants were asked to record the frequency of positive experiences in their lives, such as “I said ‘thank you’ and meant it,” “I said something pleasant to someone who didn’t expect it,” and “I exercised and felt good about doing it,” she added.</p>
<p>Phillips found that participants who reported a higher number of positive experiences had lowered depression symptoms.</p>
<p>“By incorporating positive experiences or behaviours into their lives, people with MS may be able to limit the additional risks and costs of medical treatments for depression,” she said.</p>
<p>“Health care providers should encourage people with MS to participate in positive activities every day.</p>
<p>“Previous research found that people with MS benefit more from frequent smaller activities like smelling fresh flowers, talking with neighbours or writing letters, than they do from larger activities like taking a week-long vacation or buying an expensive outfit that they can only do once in a while,” she added.</p>
<p>The study, “The Influence of Positive Experiences on Depression and Quality of Life in Persons with Multiple Sclerosis,” was published in the March 2008 issue of The Journal of Holistic Nursing. (ANI)</p>
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		<coop:keyword><![CDATA[Health News]]></coop:keyword>
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		<title>Sea salt worsens coastal air pollution</title>
		<link>http://www.ebiologynews.com/4248.html</link>
		<comments>http://www.ebiologynews.com/4248.html#comments</comments>
		<pubDate>Wed, 09 Apr 2008 07:13:15 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Ecology]]></category>

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		<description><![CDATA[April 9 : A new study has indicated that sea salt worsens coastal air pollution, showing that industrial and shipping pollution is aggravated when it combines with sunshine and salty sea  air.
A team of researchers that included University of Calgary chemistry professor Hans Osthoff, carried out the study.
The team reported that the disturbing phenomenon]]></description>
			<content:encoded><![CDATA[<p>April 9 : A new study has indicated that sea salt worsens coastal air pollution, showing that industrial and shipping pollution is aggravated when it combines with sunshine and salty sea <span id="more-4248"></span> air.</p>
<p>A team of researchers that included University of Calgary chemistry professor Hans Osthoff, carried out the study.</p>
<p>The team reported that the disturbing phenomenon of sea salt combining with air pollution substantially raises the levels of ground-level ozone and other pollutants in coastal areas.</p>
<p>“We found unexpectedly high levels of certain air pollutants where pollution from cities and ships meets salt in the ocean air along the southeast coast of the United States,” said Osthoff.</p>
<p>“It only makes sense that this is a problem everywhere industrial pollution meets the ocean, as is the case in many of the largest cities around the world,” he added.</p>
<p>Osthoff was part of a National Oceanic and Atmospheric Administration (NOAA) team that spent six weeks monitoring air quality in busy shipping areas off the southeastern coast of the United States between Charleston, South Carolina and Houston, Texas, in the summer of 2006.</p>
<p>The researchers found unexpectedly high levels of nitryl chloride (ClNO2), a chemical long suspected to be involved in ground-level ozone production along the coast.</p>
<p>They then determined that the compound is efficiently produced at night by the reaction of the nitrogen oxide N2O5 in polluted air with chloride from sea salt.</p>
<p>With the help of sunlight, the chemical then splits into radicals that accelerate production of ozone and, potentially, fine particulate matter, which are the main components of air pollution.</p>
<p>Their findings also show that up to 30 per cent of the ground-level ozone present in seaside cities such as Houston may be the result of pollution mixing with salt from ocean mist.</p>
<p>According to Osthoff, “It also changes our view of the chemical transformations that occur in ship engine exhaust plumes, and tells us that emissions from marine vessels may be polluting the globe to a greater extent than currently estimated.” (ANI)</p>
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		<coop:keyword><![CDATA[Ecology]]></coop:keyword>
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		<title>Study shows genes drive children’s changing fears</title>
		<link>http://www.ebiologynews.com/4244.html</link>
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		<pubDate>Tue, 08 Apr 2008 22:50:33 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Genetics]]></category>

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		<description><![CDATA[Apr 8 : A new study has shown that common fears in humans are linked to genetic factors, which keep changing as children and adolescents age. 
The study found that genetic factors linked with fears appear to change as children and adolescents age, with some familial factors losing their importance over time while other genetic]]></description>
			<content:encoded><![CDATA[<p>Apr 8 : A new study has shown that common fears in humans are linked to genetic factors, which keep changing as children and adolescents age. <span id="more-4244"></span></p>
<p>The study found that genetic factors linked with fears appear to change as children and adolescents age, with some familial factors losing their importance over time while other genetic risk factors arising in adolescence and adulthood.</p>
<p>The study by Kenneth S. Kendler, M.D., of the Virginia Commonwealth University School of Medicine, Richmond, has recommended two hypotheses regarding genetic risk factors for these fears.</p>
<p>“The ‘developmentally stable’ hypothesis predicts that a single set of genetic risk factors impacts the level of fears at age 8 years and these same genes constitute the only genetic influences on fear-proneness throughout development. By contrast, the ‘developmentally dynamic’ hypothesis predicts that genetic effects on fear-proneness will vary over time,” wrote the authors.</p>
<p>For the study, the researchers examined 2,490 twins born in Sweden between 1985 and 1986, who were later assessed for their level of fear four times: at age 8 to 9 by a questionnaire mailed to parents, at ages 13 to 14 and 16 to 17 with questionnaires mailed to twins and parents and at age 19 to 20 with questionnaires only to the twins.</p>
<p>The researchers naturally divided fears into three categories: situational fears (such as fear of closed spaces, flying or the dark), animal fears (including rats, dogs and snakes) and blood or injury fears (fears of dentists, injections and blood). On the whole, genetic factors influenced all three types of fears, but did not remain stable over time.</p>
<p>“We identified one set of genetic risk factors that act in childhood and have a steep decline in influence with age. Furthermore, we see evidence for new sets of genetic risk factors ‘coming on line’ in early adolescence, late adolescence and early adulthood,” the authors stated.</p>
<p>It was found that with increase in age, effects of the twins’ shared environment on their fears diminished and the influence of their individual environment increased.</p>
<p>“This is an expected pattern given that adolescence is a time of declining influence of the home environment as individuals spend less time with family and progressively make their own world, spending more time with friends,” the authors wrote.</p>
<p>The study is published in the latest issue of Archives of General Psychiatry, one of the JAMA/Archives journals. (ANI)</p>
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		<coop:keyword><![CDATA[Genetics]]></coop:keyword>
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		<title>Biologists find first lungless frog</title>
		<link>http://www.ebiologynews.com/4247.html</link>
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		<pubDate>Tue, 08 Apr 2008 22:12:44 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Biology News]]></category>

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		<description><![CDATA[April 8 : Biologists have found the first recorded species of frog that breathes without lungs in a clear, cold-water stream on the island of Borneo in Indonesia.
According to a report in National Geographic News, the frog, named “Barbourula kalimantanensis”, gets all its oxygen through its skin.
“Nobody knew about the lunglessness before we accidentally discovered]]></description>
			<content:encoded><![CDATA[<p>April 8 : Biologists have found the first recorded species of frog that breathes without lungs in a clear, cold-water stream on the island of Borneo in Indonesia.<span id="more-4247"></span></p>
<p>According to a report in National Geographic News, the frog, named “Barbourula kalimantanensis”, gets all its oxygen through its skin.</p>
<p>“Nobody knew about the lunglessness before we accidentally discovered it doing routine dissections,” said David Bickford, a biologist at the National University of Singapore.</p>
<p>Though two specimens of the frog were discovered in 1978 by Djoko Iskandar at the Bandung Institute of Technology in Indonesia, they were not dissected as scientists deemed them as valuable.</p>
<p>But Bickford immediately partially dissected several frogs when he found the species on a recent expedition to Borneo.</p>
<p>According to Bickford and colleagues, tetrapods, or four-limbed creatures, that develop without lungs are rare evolutionary events.</p>
<p>The trait in amphibians is likely an adaptation to life between water and land and their ability to respire through the skin, they added.</p>
<p>The researchers suggest lunglessness in B. kalimantanensis may be an adaptation to the higher oxygen content in fast-flowing, cold water.</p>
<p>“Cold water can hold more dissolved oxygen than warm water,” Bickford explained.</p>
<p>The frog also has a low metabolic rate, which means it needs less oxygen.</p>
<p>What’s more, the species is severely flat compared to other frogs, which increases the surface area of the skin.</p>
<p>“Along with the fact that having lungs makes you more likely to be swept away in a fast-flowing stream—because you would float—this is a very strong context for the evolution of loss of lungs,” said Bickford.</p>
<p>But, biologists are unsure why a few species have entirely gotten rid of the organs.</p>
<p>“This species is so rare that we know next to nothing concerning its biology. But, it is aquatic and lives in cold streams and doubtless has low basal metabolic rate,” said David Wake, a biologist and expert in amphibian evolution at the University of California, Berkeley.</p>
<p>“Thus, loss of lungs as an adaptation to the cold, fast-flowing water seems like a rational hypothesis to me,” he said. (ANI)</p>
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		<coop:keyword><![CDATA[Biology News]]></coop:keyword>
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		<title>TV in bedroom linked to unhealthy habits in teens</title>
		<link>http://www.ebiologynews.com/4245.html</link>
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		<pubDate>Tue, 08 Apr 2008 21:53:10 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Health News]]></category>

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		<description><![CDATA[Apr 8 : Teens who watch TV in their bedrooms are less likely to engage in healthy habits such as exercising, eating fruits or vegetables, and enjoying family meals, according to a new study. 
Apart from this, the study by researchers at the University of Minnesota School of Public Health, also revealed that such children]]></description>
			<content:encoded><![CDATA[<p>Apr 8 : Teens who watch TV in their bedrooms are less likely to engage in healthy habits such as exercising, eating fruits or vegetables, and enjoying family meals, according to a new study. <span id="more-4245"></span></p>
<p>Apart from this, the study by researchers at the University of Minnesota School of Public Health, also revealed that such children also consumed larger quantities of sweetened beverages and fast food, were categorized as heavy TV watchers, and read or studied less than teens without TVs in their bedrooms.</p>
<p>“The American Academy of Pediatrics recommends that parents remove television sets from their children’s bedrooms. Despite this recommendation, almost two-thirds of our sample had a bedroom TV, which appears to be a factor for less than optimal behaviour,” said Daheia Barr-Anderson, Ph.D., M.S.P.H., lead author of the study.</p>
<p>The researchers examined a group of 781 socio-economically and ethnically diverse teens as part of the School of Public Health Project Eating Among Teens (EAT) study on the basis of their television viewing habits, study habits, grades, diet, exercise habits, and family connectedness.</p>
<p>Almost two-thirds of the participants had a television in their bedroom or sleeping area, and those who did watched four to five more hours of television every week.</p>
<p>The results indicated that girls having a TV in their bedrooms tended to spend less time in vigorous activity each week than girls without TVs in their rooms (1.8 versus 2.5 hours). Also, they consumed fewer vegetables (1.7 versus 2 servings per day), and had fewer family meals (2.9 versus 3.7 meals per week).</p>
<p>On the other hand, boys having TVs in their rooms not only had lower fruit intake (1.7 versus 2.2) and fewer family meals (2.9 versus 3.6), they also scored low on the grade point average compared with those who did not have TVs in the bedroom (2.6 versus 2.9).</p>
<p>Barr-Anderson suggests that the first step parents can take to help their teens decrease unhealthy behaviours is to keep, or remove, a TV from the bedroom of their teen.</p>
<p>Dianne Neumark-Sztainer, Ph.D., principal investigator of Project EAT noted: &#8220;Our findings suggest the importance of not having a television in a child&#8217;s bedroom. When families upgrade their living room television, they may want to resist the temptation to put the older television set in their children&#8217;s bedroom.&#8221;</p>
<p>The study, “Characteristics Associated With Older Adolescents Who Have a Television in Their Bedrooms,” will be published in the May edition of Pediatrics, the official journal of the American Academy of Pediatrics. (ANI)</p>
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		<coop:keyword><![CDATA[Health News]]></coop:keyword>
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		<title>Shiny lip balms, glosses linked to skin cancer risk</title>
		<link>http://www.ebiologynews.com/4242.html</link>
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		<pubDate>Tue, 08 Apr 2008 21:50:32 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Cancer Research]]></category>

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		<description><![CDATA[Apr 8 : Can’t get enough of the daily dose of sunscreen, shiny lip balm, and gloss to protect your skin and add that dash of shine to your face? Well, then here’s a new flash for you – these so-called beauty enhancing products can actually increase your chances of developing a skin cancer.
According to]]></description>
			<content:encoded><![CDATA[<p>Apr 8 : Can’t get enough of the daily dose of sunscreen, shiny lip balm, and gloss to protect your skin and add that dash of shine to your face? Well, then here’s a new flash for you – these so-called beauty enhancing products can actually increase your <span id="more-4242"></span>chances of developing a skin cancer.</p>
<p>According to a new research, which was led by Christine Brown, M.D., dermatologist on the medical staff at Baylor University Medical Center at Dallas, less than one-in-four Americans wear some form of lip protection.</p>
<p>Experts say this is concerning since the lips are not only more susceptible to aging from chronic sun damage, but are also more prone to developing serious cancers.</p>
<p>“Many people do use sunscreen; however they tend to forget their lips. When skin cancer occurs on the lower lip it has the potential to be much more aggressive and metastasize to surrounding lymph nodes,” said Brown.</p>
<p>“What most people don’t realize is they’re actually increasing light penetration through the lip surface by applying something clear and shiny to them,” she added.</p>
<p>In fact, dermatologists advise that women should avoid wearing glossy lipsticks in the sun altogether unless they have a layer of sun protection on underneath.</p>
<p>“For people who are planning to be outdoors for more than 20 minutes at a time—they really should have a specific lip sun block with an SPF of 30 ideally,” said Brown.</p>
<p>In order to protect lips, Brown said that the first thing you need to do is get a lip balm or a lip sunscreen that has an SPF of 30. You should apply it in the morning under any lipsticks or lip-glosses and then reapply throughout the day just as you would a lip color. (ANI)</p>
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		<coop:keyword><![CDATA[Cancer Research]]></coop:keyword>
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		<title>Son-to-father avian flu transmission worries health experts</title>
		<link>http://www.ebiologynews.com/4241.html</link>
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		<pubDate>Tue, 08 Apr 2008 21:48:36 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Virology]]></category>

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		<description><![CDATA[April 8 : Two cases of avian flu in a Chinese family have given rise to speculations that the H5N1 virus may have acquired mutations that let it pass from one person to another.
Dr. Yu Wang of the Beijing-based Chinese Centre for Disease Control and Prevention says that a father was probably infected by his]]></description>
			<content:encoded><![CDATA[<p>April 8 : Two cases of avian flu in a Chinese family have given rise to speculations that the H5N1 virus may have acquired mutations that let it pass from one person to another.<span id="more-4241"></span></p>
<p>Dr. Yu Wang of the Beijing-based Chinese Centre for Disease Control and Prevention says that a father was probably infected by his dying son in Jiangsu Province last December.</p>
<p>The son was a salesman who was infected by H5N1 avian flu virus when he went to a poultry market six days before falling ill. He was admitted to hospital owing to his constantly worsening condition, where he died five days later.</p>
<p>The doctors believe that his father probably caught the infection while taking care of him at the hospital, for samples of H5N1 virus taken from them were genetically identical, except for one small change.</p>
<p>The father, however, saved survived after being treated with antiviral drugs and blood plasma from a woman who had been deliberately infected with inactive H5N1 in a clinical trial. He spent 22 days in hospital.</p>
<p>Given the rapidity with which flu virus mutates, the researchers believe that the fact that the strains that infected the two men were identical is strong evidence of direct son-to-father infection.</p>
<p>“If we continue to experience widespread, uncontrolled outbreaks of H5N1 in poultry, the appearance of strains well-adapted to human beings might be just a matter of time,” Times Online quoted Jeremy Farrar, a doctor at the Hospital for Tropical Diseases in Vietnam, as saying.</p>
<p>A team of doctors identified and followed up 100 close contacts of the father and son for 10 days. Eight of them had been exposed to both men, but none developed H5N1 flu.</p>
<p>The team came to the conclusion that the son passed the infection to his father, probably at the hospital.</p>
<p>They also explored the possibility of the father catching the infection when he visited another market to buy vegetables, where poultry were being slaughtered.</p>
<p>However, the father’s insistence that he did not go anywhere near them gives further support to the proposition that he caught avian flu from his son.</p>
<p>In their study report, appearing in the journal Lancet, the researchers have revealed that other cases of suspected person-to-person transmission have also been between blood relations, suggesting that there may be a genetic susceptibility to H5N1 infection.</p>
<p>However, Wendy Barclay, Chair in Influenza Virology at Imperial College London, said: “Although it is possible that the father did catch H5N1 influenza from his son, there is no virological evidence to support the idea that this strain of H5N1 virus has acquired mutations that allow it to pass readily from one person to another.” (ANI)</p>
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		<coop:keyword><![CDATA[Virology]]></coop:keyword>
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		<title>Leaky blood vessels may play key role in Lou Gehrig&#8217;s progression</title>
		<link>http://www.ebiologynews.com/4237.html</link>
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		<pubDate>Tue, 08 Apr 2008 21:42:07 +0000</pubDate>
		<dc:creator>BioNews</dc:creator>
		
		<category><![CDATA[Neurobiology]]></category>

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		<description><![CDATA[Apr 8 : A new study from University of Rochester Medical Centre has found that leaky blood vessels that are unable to protect the spinal cord from toxins may play a crucial role in amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease  progression.
Lou Gehrig’s or ALS is a progressive and fatal, neurodegenerative disease caused]]></description>
			<content:encoded><![CDATA[<p>Apr 8 : A new study from University of Rochester Medical Centre has found that leaky blood vessels that are unable to protect the spinal cord from toxins may play a crucial role in amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease <span id="more-4237"></span> progression.</p>
<p>Lou Gehrig’s or ALS is a progressive and fatal, neurodegenerative disease caused by the degeneration of motor neurons, the nerve cells in the central nervous system that control voluntary muscle movement thereby causing muscle weakness.</p>
<p>“We believe these changes contribute to or possibly initiate the onset of ALS,” Nature quoted Dr Berislav Zlokovic lead author, of the University of Rochester Medical Centre, as saying. </p>
<p>“It’s clear that these changes occur before the loss of neurons, and it’s well known that the types of changes we are seeing certainly injure or kill these types of cells, which are extremely sensitive to their biochemical environment,” he added.</p>
<p>The researchers conducted their study over mice mutant in a gene for superoxide dismutase 1 (SOD-1). SOD-1 plays a crucial role in keeping cells safe from damaging molecules known as free radicals in healthy people and mice. </p>
<p>They found that the mice intended to get ALS displayed a breakdown in the natural barrier between the blood and the spinal cord long before nerve cells appear sick or die, thereby permitting toxic substances to flood into the spinal cord and directly influence neurons.</p>
<p>Researchers also found that a SOD-1 mutation interrupted chief building blocks in the barrier.</p>
<p>With the weakened barrier the neurons were exposed directly to biochemical by-products of haemoglobin that formed reactive oxygen molecules that injure neurons, even diminutive hemorrhages appeared on the spinal column.</p>
<p>“The vascular system is crucial to health – it’s how oxygen and other nutrients are delivered to cells, and how toxins are removed,” said Zlokovic</p>
<p>“Any damage to the vascular system is a serious threat to the organism. It’s clear now that the vascular system is certainly involved in the development of ALS,” he added.</p>
<p>The study is published in the April issue of Nature Neuroscience. (ANI)</p>
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		<coop:keyword><![CDATA[Neurobiology]]></coop:keyword>
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