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Thursday, 14 August 2014

9/11 dust cloud may have caused widespread pregnancy issues

Pregnant women living near the World Trade Center during 9/11 experienced higher-than-normal negative birth outcomes, according to a new working paper by Princeton University's Woodrow Wilson School of Public and International Affairs.
These mothers were more likely to give birth prematurely and deliver babies with low birth weights. Their babies - especially baby boys - were also more likely to be admitted to neonatal intensive care units after birth. The study, led by the Wilson School's Janet Currie and Hannes Schwandt, was released by the National Bureau of Labor Economics in August.
"Previous research into the health impacts of in utero exposure to the 9/11 dust cloud on birth outcomes has shown little evidence of consistent effects. This is a puzzle given that 9/11 was one of the worst environmental catastrophes to have ever befallen New York City," said Currie, Henry Putnam Professor of Economics and Public Affairs, director of the economics department and director of the Wilson School's Center for Health and Wellbeing. "Our work suggests a simple resolution of this puzzle, which is that the women who lived in neighborhoods exposed to the 9/11 dust cloud had very different experiences than women in other parts of New York City."
The collapse of the two towers created a zone of negative air pressure that pushed dust and smoke into the avenues surrounding the World Trade Center site. Other past studies have shown that environmental exposure to the World Trade Center dust cloud was associated with significant adverse effects on the health of adult community residents and emergency workers.
Using data on all births that were in utero on Sept. 11, 2001 in New York City and comparing those babies to their siblings, the researchers found that, for mothers in their first trimester during 9/11, exposure to this catastrophe more than doubled their chances of delivering a baby prematurely. Of the babies born, boys were more likely to have birth complications and very low birth weights. They were also more likely to be admitted to the NICU.
The neighborhoods most affected by the 9/11 dust cloud included Lower Manhattan, Battery Park City, SoHo, TriBeCa, Civic Center, Little Italy, Chinatown and the Lower East Side. Previous studies analyzing the aftermath of 9/11 on health failed to account for many women living in Lower Manhattan, who were generally less likely to have poor birth outcomes than women living in other neighborhoods.
Source:Princeton University, Woodrow Wilson School of Public and International Affairs

Single enzyme is necessary for development of diabetes

An enzyme called 12-LO promotes the obesity-induced oxidative stress in the pancreatic cells that leads to pre-diabetes, and diabetes. 12-LO's enzymatic action is the last step in the production of certain small molecules that harm the cell, according to a team from Indiana University School of Medicine, Indianapolis. The findings will enable the development of drugs that can interfere with this enzyme, preventing or even reversing diabetes. The research is published ahead of print in the journal Molecular and Cellular Biology.
Nearly 40 percent of Americans—more than 120 million people—have diabetes or pre-diabetes. Diabetes results when the pancreas fails to produce sufficient insulin to remove sugar from the blood.
"We surmised that when individuals eat high fat foods and become overweight, the beta cells of their pancreases fail to produce sufficient insulin," says principal investigator Raghavendra Mirmira. In earlier studies, these researchers and their collaborators at Eastern Virginia Medical School showed that 12-LO (which stands for 12-lipoxygenase) is present in these cells only in people who become overweight.
The harmful small molecules resulting from 12-LO's enzymatic action are known as HETEs, short for hydroxyeicosatetraenoic acid. HETEs harm the mitochondria, which then fail to produce sufficient energy to enable the pancreatic cells to manufacture the necessary quantities of insulin.
For the study, the investigators genetically engineered mice that lacked the gene for 12-LO exclusively in their pancreas cells. Mice were either fed a low-fat or high-fat diet.
Both the control mice and the knockout mice on the high fat diet developed obesity and insulin resistance. The investigators also examined the pancreatic beta cells of both knockout and control mice, using both microscopic studies and molecular analysis. Those from the knockout mice were intact and healthy, while those from the control mice showed oxidative damage, demonstrating that 12-LO and the resulting HETEs caused the beta cell failure.
Mirmira notes that fatty diet used in the study was the Western Diet, which comprises mostly saturated—"bad"—fats. Based partly on a recent study of related metabolic pathways, he says that the unsaturated and mono-unsaturated fats—which comprise most fats in the healthy, relatively high fat Mediterranean diet—are unlikely to have the same effects.
"Our research is the first to show that 12-LO in the beta cell is the culprit in the development of pre-diabetes, following high fat diets," says Mirmira. "Our work also lends important credence to the notion that the beta cell is the primary defective cell in virtually all forms of diabetes and pre-diabetes."
Source:journal Molecular and Cellular Biology.

Human milk fat improves growth in premature infants

For premature infants, adequate growth while in the neonatal intensive care unit is an indicator of better long-term health and developmental outcomes. Researchers at the USDA/ARS Children's Nutrition Research Center at Baylor College of Medicine and Texas Children's Hospital have now successfully incorporated a cream supplement into premature infants' diets that improved their growth outcomes in the NICU. The report appears today in the Journal of Pediatrics.
"For premature babies who weigh less than 1,000 grams (about 2 pounds, 2 ounces), one of the problems is that their lungs and other organs are still developing when they are born. If the infant gains weight and increases in length at a good rate while in the NICU, this helps improve their outcomes," said Dr. Amy Hair, assistant professor of pediatrics at Baylor, neonatologist at Texas Children's Hospital and first author of the study.
Previous research has shown that an exclusive human milk diet protects the intestines of premature infants and supports their growth. This diet consists of mothers' own breast milk or donor human milk, as well as a fortifier consisting of protein and minerals made from the donor milk.
In this study, researchers sought a way to optimize this growth in very small infants (those who weigh between 750 and 1,250 grams) who need additional calories. Because infants are already receiving enough protein from the fortifier, another way to help them grow is by giving them fat. One of the byproducts of pasteurizing donor milk is milk fat, also referred to as a cream supplement.
In this study, researchers compared the growth outcomes of infants who received the exclusive human milk diet and the cream supplement to infants who received just the exclusive human milk diet. They found that infants in the cream group had better growth outcomes in terms of weight and length than infants in the control group.
"This is a natural way to give them fat. Previously, we would add oils or infant formula to help premature babies grow, but we can now use a natural source from donor milk," said Hair.
Hair noted that because the growth was both in weight and length, this growth is likely lean mass, consisting of bone and muscle growth.
"You want to see babies growing in both weight and length," said Hair.
She also noted that the volume of milk given to these infants cannot change to help them grow because their stomach and intestine can only tolerate a certain amount of feedings.
"You cannot give them more volumes of milk. Especially if they have lung problems, they have to have a certain volume of milk. This is a way to add calories but not change the volume of milk," she said.
Since November 2013, the NICU at Texas Children's Hospital has changed its protocol to add this cream supplement to the diet of infants who weigh less than 1,500 grams.
"This also emphasizes the importance of donating excess breast milk that your baby doesn't need to a milk bank. It can help nourish our tiniest and most vulnerable infants," said Hair.
Texas Children's was the first hospital in the world to add human milk-based cream to the diets of very low birth weight infants.
In addition to adding cream to the diets of premature infants, since 2009, Texas Children's has significantly reduced its rates of necrotizing enterocolitis, one of the most devastating and potentially fatal diseases a neonate can face, by implementing a human milk feeding protocol for all infants weighing less than 3.3 pounds.

"Texas Children's strives to be a leader in human milk feeding, because we know it impacts outcomes," said Hair.
Source:Journal of Pediatrics.

Brain 'Switchboard' Important in Attention and Sleep Discovered

Scientists have discovered a new brain switchboard which is important in attention and sleep.
 Brain 'Switchboard' Important in Attention and Sleep Discovered

In experiments with alert mice, Dr. Halassa's group found that sensory TRN cells fired very little. This suggested that while these neurons block the flow of external information during sleep, they facilitate the flow of information when an animal is awake and alert. 

By contrast, TRN cells that control the flow of internal signals behaved in an opposite fashion, firing very little in sleep. This lowered level of activity, Dr. Halassa suspects, may allow memories to form, which is known to occur during sleep. The thalamus has nerve connections to the hippocampus, which plays an important role in learning and memory. 

In a second part of the study, Dr. Halassa's group employed a technique called optogenetics, which uses light to turn nerve cells on and off, to test whether altering TRN nerve cell firing affected attention behavior in the mice. 

In one experiment, mice learned to associate a visual stimulus with food. Well-rested mice took just a second or two to find food when a stimulus was presented, while sleep-deprived mice took much longer. By turning on TRN cells that specifically controlled the visual part of the thalamus, as would happen normally in sleep, the rested mice behaved like they were sleep deprived. On the other hand, when the researchers turned off these TRN cells, sleep-deprived mice quickly found the food. 

"With a flick of a light switch, we seemed able to alter the mental status of the mice, changing the speed at which information can travel in the brain," says Dr. Halassa. Mapping brain circuits and disrupting their pathways will hopefully lead to new treatment targets for a range of neuropsychiatric disorders, he adds. 

Mechanism That Stops Progression of Abnormal Cells into Cancer Identified

A tumor suppressor pathway, called the Hippo pathway, is responsible for sensing abnormal chromosome numbers in cells and triggering cell cycle arrest, thus preventing progression into cancer, researchers from Boston University School of Medicine (BUSM) reveal.Although the link between abnormal cells and tumor suppressor pathways—like that mediated by the well known p53 gene—has been firmly established, the critical steps in between are not well understood. According to the authors, whose work appears in Cell, this work completes at least one of the missing links. 

Normal human cells contain 23 pairs of chromosomes, but this number doubles to 46 pairs as a cell prepares to divide. At the end of a normal cell division cycle, these chromosomes evenly divide to produce two identical cells with 23 pairs of chromosomes each. Sometimes, however, errors occur during division and cells fail to divide properly, resulting in giant cells with double the number of chromosomes, known as a tetraploid cells. Normally, p53 dependent pathways stop these tetraploid cells from proliferating. This response is critical because those tetraploid cells that escape detection can facilitate cancer development: Recent studies suggest that as many as 40% of all solid tumors have passed through a tetraploid stage at some point during their development. Thus, there has been great interest in understanding how a cell "knows" it has a tetraploid complement of chromosomes and is in need of tumor suppression. 

Using a technique known as genome-wide screening, the scientists systematically depleted every human gene from tetraploid cells in order to discover which ones were important to prevent proliferation. They found that when one specific gene, LATS2, was eliminated, the arrested tetraploid cells resumed proliferation, thus demonstrating that LATS2 was an upstream gene responsible for halting abnormal cell division. The LATS2 gene is known to activate the Hippo tumor suppressor pathway, which is the same pathway our bodies use to ensure our vital organs don't grow out of control. Now, the authors demonstrate that the Hippo pathway also represents the underlying pathway that prevents tetraploid cells from proliferating and causing tumors. "Although more studies are needed to further clarify this critical pathway, this work may help guide the development of new therapies that specifically target tumor cells with abnormal numbers of chromosomes, while sparing the normal healthy cells from which they originated," explained corresponding author Neil J. Ganem, PhD, Assistant Professor of Pharmacology and Medicine in the Shamim and Ashraf Dahod Breast Cancer Research Laboratories at BUSM. 
Source:University School of Medicine (BUSM)

Tuesday, 12 August 2014

DBT, MRC to collaborate with DFID of UK to begin global health research programme

Aiming to address the health needs of women and children in the most disadvantaged populations across the world, the Medical Research Council (MRC), UK and the Department of Biotechnology (DBT) in collaboration with UK Department of International Development (DFID) will soon begin 'global health research programme'.

The purpose of this global health research programme is to fund global health research projects which will bring together researchers from the UK, India and low income countries. It also aims to fund work which addresses health needs of the most disadvantaged populations globally.  

The scope of the programme is research proposals that address major health needs of women and children in low resource settings, with a focus on issues relating to one or combinations of the topics such as maternal, new born and child health (including women’s and girls’ sexual health); nutrition; and infectious diseases (e.g. malaria).

The programme will fund high quality biomedical and health research with a focus on translational and implementation science of relevance to low income countries. They include development and testing of health interventions, including clinical trials (early and later phases); prevention, diagnosis, management and treatment of health problems; biomedical, nutritional, public health, behavioural, structural, community, health services and health systems interventions; operational and implementation science research to deliver health interventions, including research that leads to better knowledge and understanding of service integration; and population health sciences, clinical studies and epidemiological research which will provide data needed to conduct future interventions development work.

The MRC, DBT and the DFID have called for collaborative proposals which will require applicants based in India, low income countries (LIC) and the UK to work together in partnership within cross national teams on research projects. Proposals must include at least one institution from each of India, UK and an LIC.


Is Sugar The New Tobacco? Watch this News Video

“This generation of children will lead shorter lifespans of their parents, sugar has been pumped into so many low fat foods, the USDA has an inherent conflict of interest when it comes to US agriculture and setting dietary guidelines, big food doesn’t necessarily want us to know what we are eating, labels don’t tell the whole story, marketing to children is basically coopting their brains and wiring them at a very early age and we can actually do something about all of these things.” – Katic Couric (1a)
Katie Couric  journalist, author and talk-show host is executive producer of her recent documentary ‘Fed Up,’ directed written and produced by Stephanie Soechtig a documentary which illustrates how sugar is impacting the health and well-being of American society.  America is not alone, with obesity rates in Australia tipping near 30%, 31% in New Zealand, Canada is pushing near 25%, in Europe 23% of women and 20% of men are obese. These figures do not include the percentage of overweight people within these countries which pushes these numbers significantly higher. In some cases the combined percentage of populations that are either overweight or obese is almost 70%. For example in the UK 67% of men and 57% of women are either overweight or obese. Sarah Wilson’s I Quit Sugar website outlines some of the health risks of high sugar diets and has links to some of the studies and research undertaken around sugar and high fructose corn syrup. Some of these include: sugar ages the body and causes wrinkles, increased risk of heart disease, increasing the risk of cancer and sugar increases your risk of diabetes A retrospective, worldwide study found small increases in sugar can lead to significant increases in diabetes rates. The white stuff makes you fat, a meta-analysis study published in the British Medical Journal shows increased sugar intake is significantly associated with weight gain and an increased risk of obesity in children having just one sweetened drink per day.
‘Fed Up’ premiered at the Sundance Film Festival this year which suggested Sugar may be the New Cigarettes?  Fed Uptraces back the last 35 years and makes a convincing case that big business is to blame. (When isn’t it?) The food industry responded to the McGovern Report by flooding the grocery aisles with “healthy” chips, cookies, drinks and cereals that cut fat while quietly upping the sugar. Since then, sugar consumption has doubled. It’s not because we’re pounding down the pound cakes — a breakfast of orange juice and a bowl of processed cereal maxes out our ideal sugar intake for the rest of the day. Sugar increases insulin, insulin increases fat storage. And it’s addictive. In a study Soechtig quotes, 93 percent of lab rats chose sugar water over cocaine. At this rate, in twenty years, 95 percent of the population will be obese, a crisis that affects every aspect of our country’s stability from health care spending to national defense. A group of retired military leaders is so alarmed by our out-of-shape society that they’ve issued a warning study called “Too Fat to Fight.” At that point in the screening, the slender actresses to the right of me tsk-tsked, but then Fed Up dropped a bomb: 40 percent of thin people are also fat, their internal organs padded with enough damaging blubber that they may as well be clinically obese. Behold, our new national paranoia: TOFI, or Thin Outside, Fat Inside. 
“The Government is subsidizing the obesity epidemic.” – Michael Pollan
Fed Up shows how the first dietary guidelines issued by the U.S. government 30 years ago overlooked the role of dietary sugar in increasing risks of obesitydiabetes, and associated ill-health outcomes, particularly in children. Since these guidelines effectively condoned unlimited addition of sugar to foods consumed by children, sugar consumption has greatly increased, obesity has skyrocketed, and generations of children have grown up far fatter than their parents. These children face impaired health and shorter lifespans as a result. The film upends the conventional wisdom of why we gain weight and lays bare the misinformation put forth on how to lose it. It reveals that far more of the American public gets sick from what they eat than anyone realized. The film traces the history of processed foods adding dangerous levels of sugar and sweeteners to their roster of ingredients. (It began in the late 1970s with the rise of low-fat foods and has intensified since then.) Doctors bemoan the rise of adult-onset diabetes in young children, as well as children suffering strokes and heart attacks at a very young age, due to their excessive intake of sugar.
“There are 600,000 food items in America, 80% of them have added sugar.” – Dr Robert Lustig
“Fed Up” is a mixture of in-the-life coverage and a roster of talking heads that include former President Bill Clinton. Soechtig spent two years with a group of kids, documenting their efforts to improve their health through dieting and exercise. The tragedy, her film argues, is that the pervasiveness of the food industry and the misinformation it disseminates has stacked all the odds against them. Personal responsibility and freedom of choice has always been Big Food’s counter to accusations of public endangerment, but if the American people has been so intricately misled, where is the personal freedom to make the right decision for one’s health? If “Fed Up” is persuasive and passionate enough in making its argument, it could lead to a huge difference in how we view healthy consumption. 

A gene linked to disease found to play a critical role in normal memory development

It has been more than 20 years since scientists discovered that mutations in the genehuntingtin cause the devastating progressive neurological condition Huntington's disease, which involves involuntary movements, emotional disturbance and cognitive impairment. Surprisingly little, however, has been known about the gene's role in normal brain activity.
Now, a study from The Scripps Research Institute's (TSRI's) Florida campus and Columbia University shows it plays a critical role in long-term memory.
"We found that huntingtin expression levels are necessary for what is known as long-term synaptic plasticity—the ability of the synapses to grow and change—which is critical to the formation of long-term memory," said TSRI Assistant Professor Sathyanarayanan V. Puthanveettil, who led the study with Nobel laureate Eric Kandel of Columbia University.
In the study, published recently by the journal PLOS ONE, the team identified an equivalent of the human huntingtin protein in the marine snail Aplysia, a widely used animal model in genetic studies, and found that, just like its human counterpart, the protein inAplysia is widely expressed in neurons throughout the central nervous system.
Using cellular models, the scientists studied what is known as the sensory-to-motor neuron synapse of Aplysia—in this case, gill withdrawal, a defensive move that occurs when the animal is disturbed.
The study found that the expression of messenger RNAs of huntingtin—messenger RNAs are used to produce proteins from instructions coded in genes—is increased by serotonin, a neurotransmitter released during learning in Aplysia. After knocking down production of the huntingtin protein, neurons failed to function normally.
"During the learning, production of the huntingtin mRNAs is increased both in pre- and post-synaptic neurons—that is a new finding," Puthanveettil said. "And if you block production of the protein either in pre- or post-synaptic neuron, you block formation of memory."
The findings could have implications for the development of future treatments of Huntington's disease. While the full biological functions of the huntingtin protein are not yet fully understood, the results caution against a therapeutic approach that attempts to eliminate the protein entirely.

Anxiety and Amen: Prayer Doesn’t Ease Symptoms of Anxiety-Related Disorders for Everyone, Baylor Study Finds.

Whether the problem is health, enemies, poverty or difficulty with aging, “Take your burden to the Lord and leave it there,” suggested the late gospel musician Charles A. Tindley. But when it comes to easing symptoms of anxiety-related disorders, prayer doesn’t have the same effect for everybody, according to Baylor University research.
Prayer and anxietyWhat seemed to matter more was the type of attachment the praying individual felt toward God. According to the Baylor study, those who prayed to a loving and supportive God whom they thought would be there to comfort and protect them in times of need were less likely to show symptoms of anxiety-related disorders — symptoms such as irrational worry, fear, self-consciousness, dread in social situations and obsessive-compulsive behavior — than those who prayed but did not expect God to comfort or protect them.
An article about the research — “Prayer, Attachment to God, and Symptoms of Anxiety-Related Disorders among U.S. Adults” — is published in the journal Sociology of Religion and was funded by the John Templeton Foundation.
While previous research has shown that people who have a secure attachment to God are more satisfied with life and less depressed and lonely, little attention has been paid to psychiatric symptoms, said researcher Matt Bradshaw, Ph.D., assistant professor of sociology in Baylor’s College of Arts & Sciences.
“For many individuals, God is a major source of comfort and strength that makes the world seem less threatening and dangerous. Through prayer, individuals seek to develop an intimate relationship with God,” Bradshaw said. “Those who achieve this goal, and believe that God will be there to protect and support them during times of need, develop a secure attachment to God. In this context, prayer appears to confer emotional comfort, which results in fewer symptoms of anxiety-related disorders.
“Other people, however, form avoidant or insecure attachments to God — meaning that they do not necessarily believe God will be there when they need Him,” he said. “For these individuals, prayer may feel like an unsuccessful attempt to cultivate and maintain an intimate relationship with God. Rejected, unanswered or otherwise unsuccessful experiences of prayer may be disturbing and debilitating — and may therefore lead to more frequent and severe symptoms of anxiety-related disorders.”
Researchers analyzed data from 1,714 of the individuals who participated in the most recent wave of the Baylor Religion Survey, completed in November 2010 by the Gallup Organization and analyzed by sociologist researchers at Baylor. The study focused on general anxiety, social anxiety, obsession and compulsion.
Teachings of Christianity and some other faiths use the parent-child imagery to depict the relationship between God and an individual, with one researcher describing God as “the ultimate attachment figure.” The Baylor study findings are consistent with a growing body of research indicating that a person’s perceived relationship with God can play an important role in shaping mental health.
In theory, people who pray regularly may be inclined to live out their religion more faithfully, which may lead to less stress, such as marriage and family conflicts, researchers wrote. People who pray often may have more of a sense of purpose in life or have more supportive personal relations. And many people use prayer as a coping strategy.
When it comes to personal prayer outside of religious organizations, however, findings by previous researchers have been inconsistent — and puzzling. Some studies indicate frequent praying has positive effects on mental health; others report no effect — or even that people who pray more often have poorer mental health than those who pray less frequently.
“At the present, we don’t know exactly why the findings have been so inconsistent,” Bradshaw said. “Prayer is complex.”
Some possible explanations for varying findings:
• Individual expectations. Some scholars suggest that “if you expect prayer to matter, it just might,” Bradshaw said. In several studies of older adults, people who believe that only God knows when and how to respond to prayer fare well when it comes to mental health; those who think their prayers are not being answered do not.
• Style of prayer. In general, meditative and colloquial prayers have been linked with desirable outcomes, including emotional well-being, while ritualistic prayer actually has been associated with poor mental health outcomes. Meditative praye.r is concerned with closeness and intimacy during reflection and communication with a loving, supportive God; colloquial prayer takes that a step further by also asking for help, such as guidance in decision-making, blessings for the world or less widespread suffering. “These requests tend to be broad, however, and are aimed at making the world a better place instead of personal enrichment,” Bradshaw said. Ritualistic prayer, in contrast, is less intimate and usually involves reciting common prayers or lines from sacred texts.
• Perceived characteristics of God — such as loving, remote or judgmental — affect the relationship between prayer and mental health. “Our previous work has found that prayer is associated with desirable mental health outcomes among individuals who believe that they are praying to a God who is close as opposed to remote, and the results from the current study are largely consistent with this finding,” Bradshaw said.
• Differences in study design and sampling.
“These are all important considerations, but a comprehensive understanding of the connection between prayer and mental health remains elusive,” he said. “We still have a lot of work to do in this area.”
Co-researchers were Christopher Ellison, Ph.D., Dean’s Distinguished Professor in the department of sociology at The University of Texas at San Antonio; Kevin J. Flannelly, Ph.D., Senior Researcher at the Center for Psychosocial Research in Massapequa, N.Y.; and Kathleen C. Galek, Ph.D., Research Associate with The HealthCare Chaplaincy in New York City
Source:Baylor University research

Blueberry Preferred for Taste, Not for Health

Blueberries are preferred by consumers more for its taste than for its health benefits, revealed a study.
University of Florida researchers suggest that about 61 percent of the blueberry consumers prefers flavor over health, while 39 percent believe the fruit, which contains antioxidants, provides health benefits. 

Jim Olmstead, assistant professor, who will use the data to breed new types of blueberries, said that they were trying to determine what the consumers' perception of the ideal blueberry was. 

Thomas Colquhoun, study's co-author, said that historically, many blueberry traits had been selected with producers in mind, including climate adaptation, yield, harvest potential and disease resistance. 

He added that developing a new blueberry variety could take more than 10 years, so before investing that time, scientists and growers need to know what consumers want. 

Source:The study is published in the journal HortScience.


Making Nuts Safer for Those With Allergies

For the millions of children and adults in the U.S. who have to shun nuts to avoid an allergic reaction, help could be on the way.
Scientists are now developing a method to process cashews — and potentially other nuts — that could make them safer to eat for people who are allergic to them. 

The researchers are presenting their work at the 248th National Meeting & Exposition of the American Chemical Society (ACS), the world's largest scientific society. The meeting, being held here through Thursday, features nearly 12,000 presentations on a wide range of science topics. 

"The only widely accepted practice for preventing an allergic reaction to nuts is strict avoidance — stay away from the food," notes Chris Mattison, Ph.D. "Clinical trials to test immunotherapy are underway, but we're approaching it from an agricultural perspective rather than medical. Can we change the food, instead of treating the person, so we can eliminate or reduce severe reactions?" 

For those with food allergies, responses to offending products can range from mild itching in the mouth or skin to life-threatening anaphylaxis, which makes it hard to breathe. Once every three minutes, someone in the U.S. ends up in the emergency room due to a food allergy reaction — that adds up to about 200,000 visits a year. 

To try to reduce those numbers, Mattison's team is looking at ways to modify proteins in tree nuts and peanuts (which are legumes) that trigger an immune response in people who are allergic. The response is launched by antibodies called immunoglobulin E (IgE), which recognize and latch onto the proteins. Mattison explains that changing the shape of the proteins makes it harder for IgE to find them. 

But past research taking this approach has involved harsh chemicals. Mattison, a researcher with the Agricultural Research Service branch of the U.S. Department of Agriculture, wanted to see if his team could achieve the same results, but using compounds that are "generally regarded as safe," or GRAS. These are substances that are accepted by the Food and Drug Administration for use in food and pharmaceuticals. 

"We found that the GRAS compound sodium sulfite can effectively disrupt the structure of a couple of the cashew allergens," Mattison says. "And we've done a couple of different tests to show we reduced IgE binding to the proteins when they've been treated with sodium sulfite." 

Next, they plan to conduct experiments on whole nuts and test the modified proteins on cells in the lab to see how they respond. They're also looking at enzymes, which are molecules that can cut up proteins, as candidates to disrupt the allergens. 

And, although this particular report focuses on cashew proteins, Mattison says the work could have broader implications. The kinds of allergenic proteins the GRAS compound and enzymes affect are not exclusive to one kind of nut. 

"One of our goals is to apply our knowledge from the cashew experiments to other tree nuts and to peanuts," he says. 
Source: American Chemical Society (ACS)

Sunday, 10 August 2014

News Video:How Cumulative Sleep Debt Is Impacting Your Brain Functioning & Alertness

Sleep is at the core of so much of what we do. Whether you regularly monitor and ensure that you are always fully rested, or you just get what your life allows you to  get, we all spend a lot of time sleeping. On a microcosmic scale it’s quite easy to quantify the effects of not getting a good night’s rest, as we’ve all experienced some mixture of: fogginess, fatigue, burning eyes and a lack of alertness amongst other things. But what happens when we apply sleep deprivation to a macrocosmic scale?

Cumulative Sleep Debt

To help explain a lack of sleep over an extended period of time, scientists have coined the term ‘Cumulative Sleep Debt’ (CSD). CSD accounts for the lasting effects on brain functionality when we do not receive an adequate amount of sleep. The following video put together by asap Science fully explains the concept of CSD and shows why we should all ensure we regularly receive a proper amount of sleep.
Watch this Video

MAC Pune offers common branding & marketing platform for Ayurveda MSMEs

Aimed at implementing the concept of Health for All through the concept of Ayurveda, the second Ayurveda industry cluster namely Maharashtra Ayurved Centre Pvt Ltd (MAC) at Pune under the Centre's Ayush scheme has launched an online e-commerce portal - to offer a common marketing platform for farmers, traders,  doctors, researchers, pharmacists and other stakeholders across the state.

The project will benefit around 900 Micro, Small and Medium Enterprises (MSMEs) through interventions like exhibition, production, contract manufacturing, raw material processing and will translate into 50 per cent cost saving in the respective businesses of the stakeholders.

Says Dr Sunita Belgamwar, chairperson of MAC, "The online business platform will not only help 49 members of MAC Pune but will also serve as a common interface for our distribution channels like Ayurveda Healthstore, Cafetaria, Exhibition and Pharmacy which will facilitate display of over 700 ayurvedic products under different brands."

The project cost of MAC Pune cluster which is the second Ayurveda cluster after Konkan in the state is Rs.17 crore of which an installment of Rs.4 crore is being awaited from the central government. Pune cluster will house a ayurvedic cafe for the development of Ayurveda cuisine, a dedicated raw material processing centre for supply of standardised, graded, certified and processed raw materials in bulk to the ayurvedic manufacturers.

The procurement of the raw materials will be done by the cluster from the farmers growing herbal and medicinal plants across the country by setting up backward linkages. 
Spanning an area of 45,000 square feet built up facility, the cluster will have a common facility centre at Kolewadi with its corporate office at Pune. The project is also estimated to give employment to 108 people directly and 1000 people indirectly. It is also envisaged to establish EU/USA FDA approved manufacturing facilities in three years, setting up advanced teaching institutes, create exclusive exports division in five years, establish 15 exclusive herbal and Ayurveda products distribution centres (Ayurways stores) by 2015 across Maharashtra. 

Scientists unravel mystery of brain cell growth

In the developing brain, special proteins that act like molecular tugboats push or pull on growing nerve cells, or neurons, helping them navigate to their assigned places amidst the brain’s wiring.
How a single protein can exert both a push and a pull force to nudge a neuron in the desired direction is a longstanding mystery that has now been solved by scientists from Dana-Farber Cancer Institute and collaborators in Europe and China.
Jia-huai Wang, PhD, who led the work at Dana-Farber and Peking University in Beijing, is a corresponding author of a report published in the August 7 online edition of Neuron that explains how one guidance protein, netrin-1, can either attract or repel a brain cell to steer it along its course. Wang and co-authors at the European Molecular Biology Laboratory (EMBL) in Hamburg, Germany, used X-ray crystallography to reveal the three-dimensional atomic structure of netrin-1 as it bound to a docking molecule, called DCC, on the axon of a neuron. The axon is the long, thin extension of a neuron that connects to other neurons or to muscle cells.
As connections between neurons are established – in the developing brain and throughout life – axons grow out from a neuron and extend through the brain until they reach the neuron they are connecting to. To choose its path, a growing axon senses and reacts to different molecules it encounters along the way. One of these molecules, netrin-1, posed an interesting puzzle: an axon can be both attracted to and repelled from this cue. The axon’s behavior is determined by two types of receptors on its tip: DCC drives attraction, while UNC5 in combination with DCC drives repulsion.
“How netrin works at the molecular level has long been a puzzle in neuroscience field,” said Wang, “We now provide structure evidences that reveal a novel mechanism of this important guidance cue molecule.” The structure showed that netrin-1 binds not to one, but to two DCC molecules. And most surprisingly, it binds those two molecules in different ways.
“Normally a receptor and a signal are like lock-and-key, they have evolved to bind each other and are highly specific – and that’s what we see in one netrin site,” said Meijers. “But the second binding site is a very unusual one, which is not specific for DCC.”
Not all of the second binding site connects directly to a receptor. Instead, in a large portion of the binding interface, it requires small molecules that act as middle-men. These intermediary molecules seem to have a preference for UNC5, so if the axon has both UNC5 and DCC receptors, netrin-1 will bind to one copy of UNC5 via those molecules and the other copy of DCC at the DCC-specific site. This triggers a cascade of events inside the cell that ultimately drives the axon away from the source of netrin-1, author Yan Zhang’s lab at Peking University found. The researchers surmised that, if an axon has only DCC receptors, each netrin-1 molecule binds two DCC molecules, which results in the axon being attracted to netrin-1. “By controlling whether or not UNC5 is present on its tip, an axon can switch from moving toward netrin to moving away from it, weaving through the brain to establish the right connection,” said Zhang.
Knowing how neurons switch from being attracted to netrin to being repelled opens the door to devise ways of activating that switch in other cells that respond to netrin cues, too. For instance, many cancer cells produce netrin to attract growing blood vessels that bring them nourishment and allow the tumor to grow, so switching off that attraction could starve the tumor, or at least prevent it from growing.
On the other hand, when cancers metastasize they often stop being responsive to netrin. In fact, the DCC receptor was first identified as a marker for an aggressive form of colon cancer, and DCC stands for "deleted in colorectal cancer." Since colorectal cancer cells have no DCC, they are ‘immune’ to the programmed cell death that would normally follow once they move away from the lining of the gut and no longer have access to netrin. As a result, these tumor cells continue to move into the bloodstream, and metastasize to other tissues. “Therefore, to understand the molecular mechanism of how netrin works should also have a good impact in cancer biology,” said Wang.
The guidance issue is a very complicated cell biology problem. Meijers, Zhang, Wang and their colleagues are now investigating how other receptors bind to netrin-1, exactly how the intermediary molecules ‘choose’ their preferred receptor, how other guidance molecule binds to DCC, and how the system is regulated. The answers could one day enable researchers to steer a cell’s response to netrin and other guidance cues, ultimately changing its fate.
The international collaborative project was co-initiated by Wang and Meijers. Wang’s postdoctoral fellow, Lorenzo Finici at Peking University is the first author on the paper. The work was funded by an NIH grant HL103526 and the Ministry of Education of China among other sources.

New culprit identified in metabolic syndrome

A new study suggests uric acid may play a role in causing metabolic syndrome, a cluster of risk factors that increases the risk of heart disease and type 2 diabetes.
Uric acid is a normal waste product removed from the body by the kidneys and intestines and released in urine and stool. Elevated levels of uric acid are known to cause gout, an accumulation of the acid in the joints. High levels also are associated with the markers of metabolic syndrome, which is characterized by obesity, high blood pressure, elevated blood sugar and high cholesterol. But it has been unclear whether uric acid itself is causing damage or is simply a byproduct of other processes that lead to dysfunctional metabolism.
Published Aug. 7 in Nature Communications, the new research atWashington University School of Medicine in St. Louis suggests excess uric acid in the blood is no innocent bystander. Rather, it appears to be a culprit in disrupting normal metabolism.
“Uric acid may play a direct, causative role in the development of metabolic syndrome,” said first author Brian J. DeBosch, MD, PhD, an instructor in pediatrics. “Our work showed that the gut is an important clearance mechanism for uric acid, opening the door to new potential therapies for preventing or treating type 2 diabetes and metabolic syndrome.”
Recent research by the paper’s senior author, Kelle H. Moley, MD, the James P. Crane Professor of Obstetrics and Gynecology, and her collaborators has shown that a protein called GLUT9 is an important transporter of uric acid.
DeBosch, a pediatric gastroenterologist who treats patients at St. Louis Children’s Hospital, studied mice to learn what happens when GLUT9 stops working in the gut, essentially blocking the body’s ability to remove uric acid from the intestine. In this study, the kidney’s ability to remove uric acid remained normal.
Eating regular chow, mice missing GLUT9 only in the gut quickly developed elevated uric acid in the blood and urine compared with control mice. And at only 6-8 weeks of age, they developed hallmarks of metabolic syndrome: high blood pressure, elevated cholesterol, high blood insulin and fatty liver deposits, among other symptoms.
The researchers also found that the drug allopurinol, which reduces uric acid production in the body and has long been used to treat gout, improved some, but not all, of the measures of metabolic health. Treatment with the drug lowered blood pressure and total cholesterol levels.
Exposure to uric acid is impossible to avoid because it is a normal byproduct of cell turnover in the body. But there is evidence that diet may contribute to uric acid levels. Many foods contain compounds called purines that break down into uric acid. And adding to growing concerns about fructose in the diet, evidence suggests that fructose metabolism in the liver also drives uric acid production.
“Switching so heavily to fructose in foods over the past 30 years has been devastating,” Moley said. “There’s a growing feeling that uric acid is a cause, not a consequence, of metabolic syndrome. And now we know fructose directly makes uric acid in the liver. With that in mind, we are doing further research to study what happens to these mice on a high-fructose diet.”
Source:Nature Communications

Pregnant women and fetuses exposed to antibacterial compounds face potential health risks

As the Food and Drug Administration (FDA) mulls over whether to rein in the use of common antibacterial compounds that are causing growing concern among environmental health experts, scientists are reporting today that many pregnant women and their fetuses are being exposed to these substances. They will present their work at the 248th National Meeting & Exposition of the American Chemical Society (ACS), the world's largest scientific society.
The meeting, which takes place here through Thursday, features nearly 12,000 presentations on a wide range of science topics.
"We looked at the exposure of pregnant women and their fetuses to triclosan and triclocarban, two of the most commonly used germ-killers in soaps and other everyday products," says Benny Pycke, Ph.D. "We found triclosan in all of the urine samples from the pregnant women that we screened. We also detected it in about half of the umbilical cord blood samples we took, which means it transfers to fetuses. Triclocarban was also in many of the samples."
The problem with this, explains Pycke, a research scientist at Arizona State University (ASU), is that there is a growing body of evidence showing that the compounds can lead to developmental and reproductive problems in animals and potentially in humans. Also, some research suggests that the additives could contribute to antibiotic resistance, a growing public health problem.
Although the human body is efficient at flushing out triclosan and triclocarban, a person's exposure to them can potentially be constant.
"If you cut off the source of exposure, eventually triclosan and triclocarban would quickly be diluted out, but the truth is that we have universal use of these chemicals, and therefore also universal exposure," says Rolf Halden, Ph.D., the lead investigator of the study at ASU.
The compounds are used in more than 2,000 everyday products marketed as antimicrobial, including toothpastes, soaps, detergents, carpets, paints, school supplies and toys, the researchers say.
Showing what effect antimicrobials have on people is a challenge. But Halden and Pycke's colleague Laura Geer, Ph.D., of the State University of New York, found at least one interesting result. Geer says the study yielded a link between women with higher levels of another ubiquitous antimicrobial, butyl paraben, which is commonly used in cosmetics, and shorter newborn lengths. The long-term consequences of this are not clear, but Geer adds that, if this finding is confirmed in larger studies, it could mean that widespread exposure to these compounds could cause a subtle but large-scale shift in birth sizes.

State policymakers, the FDA and industry have taken notice of the mounting evidence against triclosan. Minnesota became the first state to pass a ban on the antimicrobial's use in certain products, and it will take effect in January 2017. Some companies, such as Johnson & Johnson and Procter & Gamble, have announced that they are phasing out the compound from some products. At the federal level, the FDA and Environmental Protection Agency are reviewing the use and effects of the compounds.
Source:American Chemical Society (ACS)

Target identified for rare inherited neurological disease in men

 Scientists show bad androgen receptor impairs body's ability to dispose of damaged cells

Researchers at University of California, San Diego School of Medicine have identified the mechanism by which a rare, inherited neurodegenerative disease causes often crippling muscle weakness in men, in addition to reduced fertility.
The study, published August 10 in the journal Nature Neuroscience, shows that a gene mutation long recognized as a key to the development of Kennedy's disease impairs the body's ability to degrade, remove and recycle clumps of "trash" proteins that may otherwise build up on neurons, progressively impairing their ability to control muscle contraction. This mechanism, called autophagy, is akin to a garbage disposal system and is the only way for the body to purge itself of non-working, misshapen trash proteins.
"We've known since the mid-1990s that Alzheimer's disease, Parkinson's disease and Huntington's disease are caused by the accumulation of misfolded proteins that should have been degraded, but cannot be turned over," said senior author Albert La Spada, MD, PhD and professor of pediatrics, cellular and molecular medicine, and neurosciences. "The value of this study is that it identifies a target for halting the progression of protein build-up, not just in this rare disease, but in many other diseases that are associated with impaired autophagy pathway function."
Of the 400 to 500 men in the U.S. with Kennedy's disease, the slow but progressive loss of motor function results in about 15 to 20 percent of those with the disease becoming wheel-chair bound during later stages of the disease.
Kennedy's disease, also known as spinal and bulbar muscular atrophy, is a recessive X-linked disease men inherit from their mother. Women don't get the disease because they have two copies of the X chromosome. The genetic abnormality causes men to produce a mutant androgen receptor protein, which impairs the body's sensitivity and response to male sex hormones, sometimes resulting in testicular atrophy and enlargement of male breasts.
In experiments with mice, scientists discovered that the mutant androgen receptor protein besides disrupting male reproductive biology also deactivates a protein called transcription factor EB (TFEB) that is believed to be a master regulator of autophagy in nerve and other cell types.
Specifically, the mutant androgen receptor protein in Kennedy's disease binds to TFEB and blocks its ability to mediate the break-down and removal of non-working proteins and aggregated proteins.
"Our study tells us that if we can find a way to keep TFEB working, we likely can prevent this disease and others like it from progressing," La Spada said. "We now have a target for new therapies to treat not only Kennedy's disease, but also many more common neurological disorders."
Source:Nature Neuroscience

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