November 7, 2007, 7:41 PM CT

Why poor kids may make sicker adults

Researchers have known for years that people living in poverty have poorer health and shorter life spans than the more affluent. Now, Cornell University scientists have identified several key mechanisms in 13-year-olds that may help explain how low socio-economic status takes its toll on health.

In the first longitudinal study on the physiological effects of poverty in young children, the Cornell scientists report that the longer 13-year-olds have lived in poverty, the less efficient their bodies become in handling environmental demands.

We believe that these mechanisms may be correlation to the fact that children who grow up in poverty have a steeper life trajectory of premature health problems than other children, regardless of their socio-economic status in adulthood, said Gary Evans, the Elizabeth Lee Vincent Professor of Human Ecology and professor of human development and of design and environmental analysis in Cornells College of Human Ecology.

His study, co-authored with graduate student Pilyoung Kim, is reported in the recent issue of Psychological Science.

These muted responses of stress regulatory mechanisms, which are part of the cardiovascular system, not only compromise the ability of the adolescents' bodies to respond to such stressors as noise, poor housing and family turmoil but also indicate they are suffering from more stress-induced physiological strain on their organs and tissues than other young people, said Evans......... Posted by: Rose      Read more         Source

November 1, 2007, 10:03 PM CT

High-fat diet makes mice susceptible to liver injury

A high fat diet may kill regulatory T cells in the liver, allowing steatosis (simple fatty liver) to develop into steatohepatitis (fatty liver with inflammation), as per the results of a new study in the recent issue of Hepatology, a journal published by John Wiley & Sons on behalf of the American Association for the Study of Liver Diseases (AASLD). The article is also available online at Wiley Interscience

Nonalcoholic fatty liver disease (NAFLD), a condition correlation to obesity, can range in severity from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis which can lead to death. However, the progression of the disease is not well understood. The prevailing hypothesis suggests two-hits are necessary. The first is prolonged over-nutrition which causes the accumulation of fat in the liver. The second hit has been hypothesized to involve oxidative stress, mitochondrial injury or inflammatory cytokine production involving regulatory T cells (Tregs).

Tregs have recently emerged as a key player in hepatic immune regulation, so researchers, led by Xiong Ma of Johns Hopkins University in Baltimore, sought to determine their role in the pathogenesis of NASH. They hypothesized that regulation by Tregs is decreased in a fatty liver, which makes inflammation worse when the organ is exposed to secondary injury......... Posted by: Rose      Read more         Source

October 29, 2007, 10:06 PM CT

Brain circuits that control hunger

Scientists at UCLA have determined the brain circuits involved in hunger that are influenced by a hormone called leptin. In prior clinical trials, supplementation of leptin, the signaling molecule produced by fat cells, produced moderate weight loss in some obese patients, purportedly by inhibiting hunger and promoting feelings of being full. Thus, this new work suggests possible new targets for treating obesity.

Reporting in the Oct. 29 online edition of the Proceedings of the National Academy of Science, Edythe London, a professor of psychiatry in the UCLA Semel Institute for Neuroscience and Human Behavior; Kate Baicy, a graduate student in Londons lab, and his colleagues report that leptin reduces activation in regions of the brain associated with hunger while enhancing activation in regions associated with inhibition and satiety. The findings suggest possible new therapeutic targets for human obesity, an increasing problem in adults as well as children.

The scientists used functional magnetic resonance imaging (fMRI) to measure brain activity before and after leptin supplementation in three adults from a Turkish family who lacked the leptin (ob) hormone due to a mutation. Such a mutation in the ob gene causes leptin deficiency and morbid obesity.

The reason the study only involved three subjects, said London, is because having a genetic deficiency in leptin is extremely rare, so we were fortunate in finding them. Indeed, research published in 2005 by Julio Licinio, then at UCLA, used the same three family members to show that when leptin replacement was provided to them, body weight and eating behavior was normalized (Also in 2005, London and her team showed that leptin produced sustained changes in the tissue composition of the cerebral cortex in the same individuals.)......... Posted by: Rose      Read more         Source

October 29, 2007, 7:32 PM CT

Structure of Molecular Target of Many Drugs

More than 40 years after beta blockers were first used clinically, researchers can finally get a detailed, three-dimensional look at the drugs' molecular target-the beta2-adrenergic receptor. This receptor hails from a family of proteins called G protein-coupled receptors (GPCRs) that control critical bodily functions, several of our senses, and the action of about half of today's pharmaceuticals. Because this is the first known structure of a human GPCR, the work promises not only to speed the discovery of new and improved drugs, but also to broaden our understanding of human health and disease.

Published online in the October 25 issue of Science Express, the research was supported by two major initiatives of the National Institutes of Health-the NIH Roadmap for Medical Research and the Protein Structure Initiative (PSI), which is led by the National Institute of General Medical Sciences. Additional funding came from a Javits Neuroscience Award from the National Institute of Neurological Disorders and Stroke.

To solve the new structure, the scientists overcame daunting scientific obstacles. A number of of these difficulties arise because GPCRs are membrane proteins-some of the trickiest molecules to capture in three-dimensional detail because they resist forming crystals, which are needed for structure determination......... Posted by: Rose      Read more         Source

October 28, 2007, 4:20 PM CT

Therapeutic gene expression can be sustainable for 1 year

Scientists at the Board of Governors Gene Therapeutics Research Institute at Cedars-Sinai Medical Center have demonstrated for the first time that it is possible to sustain therapeutic gene expression in the central nervous system for up to a year, even in the presence of an anti-viral immune response mechanism that is normally present in humans.

The scientists demonstrated in an animal model that the delivery system for the gene, a novel gutted adenoviral vector called HC-Adv, is completely invisible to the immune system. Vectors previously used to deliver genes carried minute amounts of viral proteins that were detected by the immune system, triggering an immune response that rendered the therapeutic gene inactive after a period of weeks.

As per the researchers, this delivery system is safer and more effective than what is currently available, and should therefore advance clinical gene treatment trials for people suffering from central nervous system disorders such as Parkinsons, Alzheimers, and Multiple Sclerosis. The research was sponsored in part by The National Institutes of Health......... Posted by: Rose      Read more         Source

Sun, 28 Oct 2007 14:05:59 GMT

Brain Regions Responsible for Optimism

Via Slashdot user TaeKwonDood - Quoted - The brain region responsible for believing you can seduce Giselle Bundchen or make a YouTube clone for bobble-head doll movies successful has been located. Surprisingly, it is not in a bottle of Jager, it's in the rostral anterior cingulate and amygdala.Read More Posted by: Zinzi      Read more     Source

Thu, 18 Oct 2007 00:04:41 GMT

Why We Don't Help Others: Bystander Apathy

In the next nomination for the best social psychology study I need your help as I'm in two minds. On one hand this study, inspired by the highly publicised murder of Kitty Genovese in 1964, is mentioned in every textbook and often dubbed 'seminal'. On the other, I'm not sure how original it is. So I'll explain the study then ask you to vote on whether it should be included in my top ten social psychology studies. Get your critical faculties into gear!

The study investigates the 'bystander effect'. In social psychology this is the surprising finding that the mere presence of other people inhibits our own helping behaviours in an emergency. John Darley and Bibb Latane were inspired to investigate emergency helping behaviours after the murder of Kitty Genovese in 1964.

The newspaper report of the murder stated that 38 people had heard and seen the attack, which lasted an hour, yet they did nothing. Subsequent reports, however, suggest the number of witnesses was much lower and few, perhaps none, had witnessed the whole attack.

Epileptic seizure
Whatever the status of this incident the facts of the study are well-known. Participants were invited into the lab under the pretext they were taking part in a discussion about 'personal problems' (Darley & Latane, 1968). Participants were talking to a number of unknown others, varying from just one up to four in each of the experimental trials.

Because of the sensitive nature of the discussion they were told the discussion would take place over an intercom. In fact this was just a ruse to ensure the participants couldn't physically see the other people they were talking to.

During the discussion one member of the group would suddenly appear to be having an epileptic seizure. Here is the script:
"I-er-um-I think I-I need-er-if-if could-er-er-somebody er-er-er-er-er-er-er give me a little-er-give me a little help here because-er-I-er-I'm-er-erh-h-having a-a-a real problem-er-right now and I-er-if somebody could help me out it would-it would-er-er s-s-sure be-sure be good . . . because-there-er-er-a cause I-er-I-uh-I've got a-a one of the-er-sei er-er-things coming on and-and-and I could really-er-use some help so if somebody would-er-give me a little h-help-uh-er-er-er-er-er c-could somebody-er-er-help-er-uh-uh-uh (choking sounds). . . . I'm gonna die-er-er-I'm . . . gonna die-er-help-er-er-seizure-er-[chokes, then quiet]."
The experimenters then measured how long it took for participants to go the person's aid. They clearly found that the more people were involved in the group discussion, the slower participants were to respond to the apparent emergency. It seems that the presence of others inhibits people's helping behaviours.

Don't you care?
Some participants made no move to intervene in the apparent emergency. What was going on? Darley and Latane (1968) report that those who did not act were far from uncaring about the seizure victim. Quite the reverse in fact, compared to those who did report the emergency, they appeared to be in a more heightened state of arousal. Many were sweating, had trembling hands and looked to be in considerable discomfort.

The non-helpers appeared to be caught in a double bind that locked them up. One part of them felt shame and guilt for not helping. Another part of them didn't want to expose themselves to embarrassment or to ruin the experiment which, they had been told depended on each conversant remaining anonymous from the others.

More than Milgram?
It's here that I wonder about the originality of the finding. Certainly Milgram's study of obedience casts a long shadow over this experiment. Similar to the Milgram situation, participants here were put under pressure to continue with the experiment by authority figures (the psychologists). Again, someone was suffering discomfort and participants felt conflicted about whether or not to intervene. In this case in an epileptic seizure, in Milgram's study, it was the electrical shocks participants themselves were administering.

This study's originality comes from the finding that the more people are present, the longer participants take to help. And this is certainly an important insight in social psychological terms. Because of the way the experiment was set up participants had no way of knowing how the other people who heard the seizure had responded. This meant that the only variable was how many other people they knew to be present. Posted by: Jerry      Read more     Source

October 10, 2007, 4:56 PM CT

How stem cells decide

Scientists have discovered a key protein that controls how stem cells choose to become either skeletal muscle cells that move limbs, or smooth muscle cells that support blood vessels, as per a research studypublished recently in the Proceedings of the National Academy of Sciences (PNAS). The results not only provide insight into the development of muscle types in the human fetus, but also suggest new ways to treat atherosclerosis and cancer, diseases that involve the creation of new blood vessels from stem cell reserves that would otherwise replace worn out skeletal muscle. The newly discovered mechanism also suggests that some current cancer therapys may weaken muscle, and that doctor scientists should start watching to see if a previously undetected side effect exists.

Thanks to stem cells, humans develop from a single cell into a complex being with as a number of as 400 cell types in millions of combinations. The original, single human stem cell, the fertilized embryo, has the potential to develop into every kind of human cell. As we develop in the womb, successive generations of stem cells specialize (differentiate), with each group able to become fewer and fewer cell types. One set of mostly differentiated stem cells has the ability to become bone, blood, skeletal muscle or smooth muscle. A number of human tissues keep a reserve of stem cells on hand in adulthood, ready to differentiate into replacement parts depending on the stimuli they receive. If body signals that skeletal muscle needs replacing, the stem cells take that route. If tissues signal for more blood vessels, the same stem cells may become smooth muscle that supports the lining of blood vessels......... Posted by: Rose      Read more         Source

October 4, 2007, 9:41 PM CT

What emotional memories are made of

Both extensive psychological research and personal experiences confirm that events that happen during heightened states of emotion such as fear, anger and joy are far more memorable than less dramatic occurrences. In a report this week in Cell, Johns Hopkins scientists and their collaborators at Cold Spring Harbor and New York University have identified the likely biological basis for this: a hormone released during emotional arousal primes nerve cells to remember events by increasing their chemical sensitivity at sites where nerves rewire to form new memory circuits.

Describing the brain as a big circuit board in which each new experience creates a new circuit, Hopkins neuroscience professor Richard Huganir, Ph.D. says that he and his team observed that during emotional peaks, the hormone norepinephrine dramatically sensitizes synapses the site where nerve cells make an electro-chemical connection to enhance the sculpting of a memory into the big board.

Norepinephrine, more widely known as a fight or flight hormone, energizes the process by adding phosphate molecules to a nerve cell receptor called GluR1. The phosphates help guide the receptors to insert themselves adjacent to a synapse. Now when the brain needs to form a memory, the nerves have plenty of available receptors to quickly adjust the strength of the connection and lock that memory into place, Huganir says......... Posted by: Rose      Read more         Source

September 18, 2007, 5:28 AM CT

Women more depressed and men more impulsive

Women and men appear to respond differently to the same biochemical manipulation. Major depressive disorder (MDD) is one of the most common mental disorders, and it is also one of the most studied. It is already known that reduced serotonin transmission contributes to the pathophysiology, or functional changes, linked to MDD and most of todays most popular antidepressants block the serotonin uptake site, also known as the transporter, in the brain. It is also known that people with MDD are frequently found to have impaired impulse control. A new study being reported in the September 15th issue of Biological Psychiatry now reports on important sex and genetic differences in the way that men and women react to reductions in serotonin function, specifically in terms of their mood and impulsivity.

Using a technique in healthy participants called acute tryptophan depletion, which decreases serotonin levels in the brain, Walderhaug and his colleagues observed that men became more impulsive, but did not experience any mood changes in response to the induced chemical changes. However, women in this study reported a worsening of their mood and they became more cautious, a response usually linked to depression. The scientists also discovered that the mood lowering effect in women was influenced by variation in the promotor region of the serotonin transporter gene (5-HTTLPR)......... Posted by: Rose      Read more         Source