>O2 HEALTH > IF YOUR KIDS ARE IN FRONT OF A SCREEN LONGER THAN USUAL THEN YOU SHOULD BE REALLY CONCERNED

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Family watching television, c. 1958

 

Kids’ ‘screen time’ linked to early markers for cardiovascular disease

Six-year-olds who spent the most time watching television, using a computer or playing video games had narrower arteries in the back of their eyes — a marker of future cardiovascular risk, in a first-of-its-kind study reported in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association.

Australian researchers found that more sedentary behavior such as “screen time” was associated with an average narrowing of 2.3 microns in the retinal arteriolar caliber. A micron is one thousandth of a millimeter or one-25th of a thousandth of an inch.
In the study, 6- to 7-year-olds who regularly participated in outdoor had 2.2 microns wider average retinal arteriolar compared to those children with the lowest level of activity.
The magnitude of the narrowing associated with each hour of television/computer viewing was similar to that associated with 10 millimeters of mercury (mm HG) increase in systolic in children, researchers said.
“We found that children with a high level of physical activity had a more beneficial microvascular profile compared to those with the lowest levels of physical activity,” said Bamini Gopinath, Ph.D., lead author and senior research fellow at the Center for Vision Research at the University of Sydney. “This suggests that unhealthy lifestyle factors may influence microcirculation early in life and increase the risk of cardiovascular disease and hypertension later in life.”
Retinal microvascular caliber is a marker for cardiovascular disease and high blood pressure in adults. But this is the first time that a sedentary lifestyle in childhood showed a narrowing of the vessels in the retina that could be a subclinical marker for in the future.
The study included 1,492 children in 34 primary schools in Sydney, Australia. Parents answered a 193-item questionnaire, providing the number of hours spent each week in indoor and outdoor physical activity and sedentary activity such as , videogames, computer time and reading.
Researchers took digital photographs of the vasculature in the back of each child’s eye, then calculated average retinal vascular calibers. Height, weight, body mass index (BMI) and three separate blood pressure measurements were taken and averaged.

On average, the children spent 1.9 hours per day in screen time and 36 minutes a day in total physical activity. Children in the highest levels of physical activity at just over an hour or more had significantly wider average retinal arteriolar caliber than those spending just under half an hour or less per day.
Increased screen time was associated with narrower average retinal arteriolar diameter after adjusting for age, sex, ethnicity, iris color, length of the eyeball, BMI, birth weight and blood pressure. Each hour per day of TV viewing time was associated on average with 1.53 microns narrower retinal arteriolar caliber.
“Excessive screen time leads to less physical activity, unhealthy dietary habits and weight gain,” Gopinath said. “Replacing one hour a day of screen time with physical activity could be effective in buffering the effects of sedentariness on the retinal microvasculature in children. Free play should be promoted and schools should have a mandatory two hours a week in physical activity for children.”
Physical activity enhances endothelial function and increases blood flow resulting in enhanced nitric oxide production, which has a positive effect on the linings of blood vessels.
The researchers said their findings might not be applicable to other regions of the world because of the temperate climate in Australia, where children are more apt to play outdoors. Study limitations included the use of parental rather than objective measurement of the children’s time spent in physical and sedentary activities.
“Parents need to get their up and moving and off the couch,” Gopinath said. “Parents can also lead the way by being more physically active themselves.”

Provided by American Heart Association (news : web)

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>O2 HEALTH > Does sugar feed cancer??

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Chain form: ball-and-stick model

Researchers at Huntsman Cancer Institute at the University of Utah have uncovered new information on the notion that sugar “feeds” tumors. The findings may also have implications for other diseases such as diabetes. The research is published in the journal Proceedings of the National Academy of Sciences.

“It’s been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth,” says Don Ayer, Ph.D., a Huntsman Cancer Institute investigator and professor in the Department of Oncological Sciences at the University of Utah.
During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). Glucose and glutamine are both essential for cell growth, and it was long assumed they operated independently, but Ayer’s research shows they are inter-dependent. He discovered that by restricting glutamine availability, glucose utilization is also stopped. “Essentially, if you don’t have glutamine, the cell is short circuited due to a lack of glucose, which halts the growth of the tumor cell” Ayer says.
The research, spearheaded by Mohan Kaadige, Ph.D., a postdoctoral fellow in Ayer’s lab, focused on MondoA, a protein that is responsible for turning genes on and off. In the presence of glutamine, MondoA blocks the expression of a gene called TXNIP. TXNIP is thought to be a , but when it’s blocked by MondoA , it allows cells to take up glucose, which in turn drives tumor growth. Ayer’s research could lead to new drugs that would target glutamine utilization, or target MondoA or TXNIP.
Ayer says the next step in his research is to develop animal models to test his ideas about how MondoA and TXNIP control . “If we can understand that, we can break the cycle of glucose utilization which could be beneficial in the treatment of cancer,” Ayer says.

Source: University of Utah Health Sciences (news : web)

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>O2 HEALTH > NEW link between brain molecule and obesity& diabetes

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None - This image is in the public domain and ...

Researchers find link between brain molecule and obesity and diabetes

The brain’s hypothalamus plays a key role in obesity and one of its major complications – type 2 diabetes. Nerve cells in the hypothalamus detect nutrients and hormones circulating in the blood and then coordinate a complex series of behavioral and physiological responses to maintain a balance between calories eaten and calories burned. Obesity and diabetes can result when this regulatory mechanism goes awry.

Now, research by postdoctoral fellow Clémence Blouet, Ph.D., and Gary Schwartz, Ph.D., professor in the Dominick P. Purpura Department of Neuroscience and of medicine at Albert Einstein College of Medicine of Yeshiva University, has revealed a molecule in the brain that may contribute to those health problems, both of which are reaching epidemic proportions. A 2008 study in the journal predicted that 86 percent of U.S. adults will be overweight or obese by 2030 if current trends continue. And last October the U.S. Centers for Disease Control and Prevention estimated that the prevalence of among American adults could rise from the current 1 in 10 to as many as 1 in 3 by 2050.
In work involving mouse models of obesity and diabetes, Drs. Blouet and Schwartz have shown that excess nutrient availability leads to an overabundance of a protein found in nutrient-sensing nerve cells of the . They concluded that increased levels of this protein, known as thioredoxin-interacting protein, or TXNIP, contribute to the onset of obesity and the impaired control of blood sugar levels that characterizes type 2 diabetes. Their findings were published in the April 20 online edition of the Journal of Neuroscience.
“Our study indicates that TXNIP in hypothalamic nerve cells provides a crucial link between nutrient sensing and the increases in body weight and fat mass that lead to obesity and diabetes,” said Dr. Schwartz. “Hyperglycemia—pathologically elevated glucose levels—causes an excess of TXNIP in hypothalamic neurons, which in turn may contribute in several ways to a breakdown in energy homeostasis—the balance between calories taken in and calories burned. For example, we’ve found that elevated TXNIP in contributes to obesity by decreasing energy expenditure, as evidenced by decreased physical activity, and by reducing the rate at which fat is burned to produce energy. In addition to increasing fat mass, hypothalamic TXNIP overabundance also impairs glucose tolerance and insulin sensitivity—two of the hallmarks of diabetes.”
Dr. Schwartz notes that these findings regarding TXNIP could eventually lead to therapies. “Interventions that can suppress TXNIP production or selectively inactivate this protein might help in preventing weight gain and the obesity and diabetes that result from it,” he said.
The title of the paper is “Nutrient-sensing hypothalamic TXNIP links nutrient excess to energy imbalance in mice.” The research was funded by the Skirball Institute for Nutrient Sensing and the National Institutes of Health through the Albert Einstein Diabetes Research and Training Center and the New York Obesity Research Center. Albert Einstein College of Medicine is actively seeking licensing partners interested in pursuing clinical application of this patent-pending technology.

Provided by Albert Einstein College of Medicine (news : web)

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>O2 TECH > NEW INTERACTION BETWEEN YOU TUBE & BLOGGER

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Better YouTube Support in Blogger

Blogger allows you to upload your own videos via the Blogger Post Editor. It also allows you to embed YouTube videos into your posts(by copy pasting the YouTube embed code into your post editor). Now Blogger has made this process even more simpler by providing a better interface for adding YouTube videos.
This YouTube integration is available only in the updated Post Editor. So if you are still using the old editor, it’s a good time for an upgrade.
This feature is currently available in the draft version of blogger. So, to test this new feature,you should login to your Draft Dashboard(http://draft.blogger.com) instead of the regular one(http://www.blogger.com)

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Search for some video using some keywords, select the video and click the select button
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Now you should see the video in your post Editor. You can continue editing the post using the WYSIWYG Editor and publish it. If you are trying to embed your own YouTube videos(The ones uploaded to YouTube by you), then you can use the “My YouTube videos” Tab.
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Sharing a  video from YouTube.

YouTube has  got a Blogger Share Button which will enable you to quickly post the video onto your blog.This might be very useful when you suddenly stumble upon some interesting video and want to post it onto your blog.
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If you have multiple blogs, select the appropriate one from the Popup Post Editor and you can quickly publish the video to your blog.

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>O2 HEALTH > How fear and anxiety are formed in the brain?

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Regions of the brain affected by PTSD and stress.

Study to investigate how fear and anxiety are formed in the brain

About 25 per cent of us will experience the effects of anxiety disorders at some point in our lives, with sometimes dire repercussions for friends, family and our own well-being. Yet little is known about the molecular mechanisms in the brain which contribute to stress-induced anxiety.

A neuroscientist at the University of Leicester has recently been awarded major EU funding amounting to €1.7m over four years to investigate how fear and anxiety are formed in the brain, in a project that could lead to more efficient ways of treating stress-related conditions.
Dr Robert Pawlak, a researcher in the University’s Department of Cell Physiology and Pharmacology, has received the prestigious Marie Curie Excellence Grant to support his research project which will look at the mechanisms in the brain that lead to anxiety.
Fear memories are encoded as changes in neuronal connections called synapses, in a process known as plasticity. Dr Pawlak and his colleagues have recently shown that proteases (proteins that cut other proteins) play a critical role in this process and significantly contribute to fear and anxiety related to stress.
Dr Pawlak commented: “Understanding neural bases of stress, fear and anxiety is of immense importance to modern society. The most dramatic form, posttraumatic stress disorder (PTSD) is characterised by cognitive impairment, depression, fear, anxiety, and may eventually lead to suicide.
“Understanding the neural mechanisms of PTSD, depression and anxiety disorders could reduce the personal and societal impact through development of more efficient therapies. This project looks at cellular mechanisms involved in experience-induced neuronal plasticity underlying learning, fear and anxiety.”
Dr Blair Grubb, Head of the Department of Cell Physiology and Pharmacology, added: “EU Marie Curie Excellence Grants are extremely competitive and it is a major achievement that Robert Pawlak has made a successful application so early on in his independent research career.
“Robert is one of a number of neuroscientists working in this department and this grant award adds significantly to our research profile in this general area. The proposed research programme will make a major contribution to our understanding of how stress leads to fear and anxiety.”
Source: University of Leicester

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>O2 HEALTH > new Chemical Pathway’ in the BRAIN for STRESS

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Neuroscientists discover new ‘chemical pathway’ in the brain for stress

Neuroscientists discover new 'chemical pathway' in the brain for stress

Nerve cells (red) reach out and communicate with each other at junctions called synapses (green) that release chemicals to promote anxiety. Credit: University of Leicester
A team of neuroscientists at the University of Leicester, UK, in collaboration with researchers from Poland and Japan, has announced a breakthrough in the understanding of the ‘brain chemistry’ that triggers our response to highly stressful and traumatic events.

The discovery of a critical and previously unknown pathway in the that is linked to our response to stress is announced today in the journal Nature. The advance offers new hope for targeted treatment, or even prevention, of stress-related psychiatric disorders.
About 20% of the population experience some form of anxiety disorder at least once in their lives. The cumulative lifetime prevalence of all stress-related disorders is difficult to estimate but is probably higher than 30%.
Dr Robert Pawlak, from the University of Leicester who led the UK team, said: “Stress-related disorders affect a large percentage of the population and generate an enormous personal, social and economic impact. It was previously known that certain individuals are more susceptible to detrimental effects of stress than others. Although the majority of us experience traumatic events, only some develop stress-associated psychiatric disorders such as depression, anxiety or posttraumatic . The reasons for this were not clear.”
Dr Pawlak added that a lack of correspondence between the commonness of exposure to psychological trauma and the development of pathological anxiety prompted the researchers to look for factors that may make some individuals more vulnerable to stress than others.
“We asked: What is the molecular basis of anxiety in response to noxious stimuli? How are stress-related environmental signals translated into proper behavioural responses? To investigate these problems we used a combination of genetic, molecular, electrophysiological and behavioural approaches. This resulted in the discovery of a critical, previously unknown pathway mediating anxiety in response to stress.”
The study found that the emotional centre of the brain – the amygdala – reacts to stress by increasing production of a protein called neuropsin. This triggers a series of chemical events which in turn cause the amygdala to increase its activity. As a consequence, a gene is turned on that determines the stress response at a cellular level.

“We then examined behavioural consequences of the above series of cellular events caused by stress in the amygdala,” said Dr Pawlak. “Studies in mice revealed that upon feeling stressed, they stayed away from zones in a maze where they felt unsafe. These were open and illuminated spaces they avoid when they are anxious.”
Neuroscientists discover new 'chemical pathway' in the brain for stress
 


Newly discovered neurochemical cascade promoting stress-induced anxiety. Neuropsin interacts with cell membrane proteins NMDA and EphB2 to induce expression of the Fkbp5 gene. Credit: University of Leicester

“However when the proteins produced by the amygdala were blocked – either pharmacologically or by gene therapy – the mice did not exhibit the same traits. The behavioural consequences of stress were no longer present. We conclude that the activity of neuropsin and its partners may determine vulnerability to stress.” Neuropsin was previously discovered by Professor Sadao Shiosaka, a co-author of the paper. This research, for which the bioinformatics modelling was done by Professor Ryszard Przewlocki and his team, has for the first time characterized its mechanism of action in controlling anxiety in the amygdala.
The study took four years to complete, during which scientists from the Department of Cell Physiology and Pharmacology collaborated with colleagues from the Medical Research Council Toxicology Unit at the University of Leicester, the Department of Molecular Neuropharmacology, Polish Academy of Sciences in Krakow, Poland and Nara Institute of Science and Technology in Japan. The work was supported by the European Union, the Medical Research Council and Medisearch – the Leicestershire Medical Research Foundation. The first author, Benjamin Attwood, sponsored by Medisearch, took 3 years off from his medical studies curriculum to complete the necessary experiments. He commented: “It has been a thoroughly absorbing project to uncover how our experiences can change the way we behave. Hopefully this will lead to help for people that have to live with the damaging consequences of traumatic experiences.”
Dr Pawlak added: “We are tremendously excited about these findings. We know that all members of the neuropsin pathway are present in the human brain. They may play a similar role in humans and further research will be necessary to examine the potential of intervention therapies for controlling stress-induced behaviours.”
“Although research is now needed to translate our findings to the clinical situation, our discovery opens new possibilities for prevention and treatment of stress-related psychiatric disorders such as depression and posttraumatic disorder.”

More information: Neuropsin cleaves EphB2 in the amygdala to control anxiety, DOI: 10.1038/nature09938
Provided by University of Leicester (news : web)

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