Our eyes are in constant motion. Even when we attempt to stare straight at a stationary target, our eyes jump and jiggle imperceptibly. Although these unconscious flicks, also known as microsaccades, had long been considered mere "motor noise," researchers at the Salk Institute for Biological Studies found that they are instead actively controlled by the same brain region that instructs our eyes to scan the lines in a newspaper or follow a moving object.

Their findings, published in the Feb. 13, 2009 issue of Science, provide new insights into the importance of these movements in generating normal vision.

"For several decades, scientists have debated the function, if any, of these fixational eye movements," says Richard Krauzlis, Ph.D., an associate professor in the Salk Institute's Systems Neurobiology Laboratory, who led the current study. "Our results show that the neural circuit for generating microsaccades is essentially the same as that for voluntary eye movements. This implies that they are caused by the minute fluctuations in how the brain represents where you want to look."

"There was a lot of past effort to figure out what fixational eye movements contribute to our vision," adds lead author Ziad Hafed, Ph.D., Sloan-Swartz Fellow in the Systems Neurobiology Laboratory, "but nobody had looked at the neural mechanism that generates these movements. Without such knowledge, one could only go so far in evaluating microsaccades' significance and why they actually exist."

Wondering whether the command center responsible for generating fixational eye movements resides within the same brain structure that is in charge of initiating and directing large voluntary eye movements, Hafed decided to measure neural activity in the superior colliculus before and during microsaccades.

He not only discovered that the superior colliculus is an integral part of the neural mechanism that controls microsaccades, but he also found that individual neurons in the superior colliculus are highly specific about which particular microsaccade directions and amplitudes they command - whether they be, say, rightward or downward or even oblique movements. "Data from the population of neurons we analyzed shows that the superior colliculus contains a remarkably precise representation of amplitude and direction down to the tiniest of eye movements," says Krauzlis.

The Salk researchers, in collaboration with Laurent Goffart, Ph.D., a professor at the Institut de Neurosciences Cognitives de la Méditerranée in Marseille, France, also temporarily inactivated a subset of superior colliculus neurons and analyzed the resulting changes in microsaccades. They discovered that a fully functional superior colliculus is required to generate normal microsaccades.

"Because images on the retina fade from view if they are perfectly stabilized, the active generation of fixational eye movements by the central nervous system allows these movements to constantly shift the scene ever so slightly, thus refreshing the images on our retina and preventing us from going 'blind,'" explains Hafed. "When images begin to fade, the uncertainty about where to look increases the fluctuations in superior colliculus activity, triggering a microsaccade," adds Krauzlis.

Microsaccades may, however, do more than prevent the world around us from fading when we stare at it for too long. Even when our gaze is fixed, our attention can shift to an object at the periphery that attracts our interest. In an earlier study, Hafed discovered that although we may avert our eyes from an attractive man or woman, microsaccades will reveal such objects of attraction because their direction is biased toward objects to which we are unconsciously attracted.

Peripheral neuropathy, which causes pain and numbness in the hands and feet, affects about one-third of persons with diabetes mellitus. It may also cause balance problems and unsteadiness when walking. According to a study in Volume 45, Issue 9 of the Journal of Rehabilitation Research and Development (JRRD), vibrating insoles improved standing in persons with peripheral neuropathy when attention was distracted and vision was occluded.

For the study, vibrating insoles were designed to apply random vibrations to the plantar surface of the feet by piezoelectric elements. Piezoelectric elements are thin and relatively cheap and therefore ideal for application in an insole.

The study assessed participating subjects, ranging in age from 40 to 60, in four different conditions (i.e., eyes open or closed and with or without an attention-demanding task). The findings demonstrate that nondisabled subjects were unaffected by the vibrations. The use of vibrating insoles in which the vibration is applied by piezoelectric elements seems to be an option for increasing stability in persons with neuropathy when compensatory strategies to control balance are limited.

Terminally ill rodents with type 1 diabetes have been restored to full health with a single injection of a substance other than insulin by UT Southwestern Medical Center scientists.

Since the discovery of insulin in 1922, type 1 diabetes (insulin-dependent diabetes) in humans has been treated by injecting insulin to lower high blood sugar levels and prevent diabetic coma. New findings by UT Southwestern researchers, which appears in the Proceedings of the National Academy of Sciences, suggest that insulin isn't the only agent that is effective. Leptin, a hormone produced by the body's fat cells, also lowers blood glucose levels and maintains them in a normal range for extended periods, they found.

"The fact that these animals don't die and are restored to normal health despite a total lack of insulin is hard for many researchers and clinicians to believe," said Dr. Roger Unger, professor of internal medicine and senior author of the study. "Many scientists, including us, thought it would be a waste of time to give leptin in the absence of insulin. We've been brainwashed into thinking that insulin is the only substance that can correct the consequences of insulin deficiency."

The mechanism of leptin's glucose-lowering action appears to involve the suppression of glucagon, a hormone produced by the pancreas that raises glucose levels. Normally, glucagon is released when the glucose, or sugar, level in the blood is low. In insulin deficiency, however, glucagon levels are inappropriately high and cause the liver to release excessive amounts of glucose into the bloodstream. This action is opposed by insulin, which tells the body's cells to remove sugar from the bloodstream.

In type 1 diabetes, which affects about 1 million people in the U.S., the pancreatic islet cells that produce insulin are destroyed. Type 1 diabetics must take insulin multiple times a day to metabolize blood glucose and regiment their diets. In comparison, patients with non-insulin dependent, or type 2, diabetes make insulin, but their bodies don't respond well to it. Type 2 diabetes affects between 18 million and 20 million people in this country.

In the current study, researchers tested for the first time whether a single injection of the leptin gene given to insulin-deficient mice and rats on the verge of death from diabetic coma could reverse the severe condition and prevent the animals from dying. The animals that received the leptin gene began producing excessive amounts of leptin, which reversed all the measurable consequences of type 1 diabetes including weight loss, hyperglycemia and ketoacidosis, a potentially fatal condition that develops when the body doesn't have enough insulin to meet basic metabolic requirements. Much of the effect was mediated by complete suppression of the high glucagon levels, said Dr. Xinxin Yu, assistant instructor of internal medicine and lead author of the study.

"These animals were actually dying," Dr. Yu said. "But if we gave them the leptin gene, within two weeks, the terminally ill rodents were restored to full health without any other treatment."

Dr. Unger said it's too premature to know whether leptin might someday replace insulin as a treatment for diabetic patients, but this study demonstrates that leptin could at least handle some of insulin's job requirements and do it for longer periods of time. Injected insulin is biologically active for only three to four hours.

"My hope is that you could give leptin for one type of action glucagon's suppression, for example and insulin for another. Or perhaps give a substance other than insulin entirely," Dr. Unger said. "What would be a tremendous advance would be the ability to give an oral agent that suppresses glucagon without injections."

Dr. Yu said the research team hypothesizes that leptin combats diabetes not only be suppressing glucagon's action on the liver, but also by boosting the insulin-like actions of IGF-1 (insulin-like growth factor-1), a hormone that promotes growth and mimics insulin.

"One of the things that happens when a child gets type 1 diabetes is their growth is stunted until they're given insulin," Dr. Unger said. "The same is true with mice. However, we found if you take a diabetic rat that's not receiving insulin and make it hyperleptinemic, it almost catches up growthwise."

While the treated animals' blood glucose levels inched back up over time, their hyperglycemia (high blood sugar) consistently remained well below the elevated pre-treatment levels. The untreated rodents, on the other hand, died within two or three days. The researchers tracked the treated rodents for 25 weeks.

The next step is to study other potential glucagon suppressants and begin leptin clinical trials within the next year.

Other UT Southwestern researchers involved in the study were Dr. May-Yun Wang, assistant professor of internal medicine; Dr. Zhao Wang, postdoctoral researcher in internal medicine; and former postdoctoral fellow Dr. Byung-Hyun Park.

The work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the Department of Veterans Affairs, and the Juvenile Diabetes Research Foundation.

MUMBAI: Obesity problem in India was bad enough, but it just got larger. According to Dr Ramen Goel,of the All India Association for Advancing
Research (AIAARO) in Obesity, about 15% more Indians now have the dubious distinction of being considered overweight or obese. This is the upshot of new scientific definitions of obesity for Indians announced by Dr. Anoop Misra and Dr Makkar at the Asia-Oceana Conference on Obesity organized for the first time in India recently by the AIAARO.

The findings were a part of a Consensus Statement published in February 2009 issue of the Journal of the Association of Physicians of India (JAPI). The statement was published by a prestigious consensus group of medical professionals representing numerous medical disciplines from reputed medical institutions, hospitals, government-funded medical research institutions and policy making bodies.

Several years of excellent research provided the basis for redefining obesity for Indians. Current definitions for obesity and for predicting associated adverse health effects are largely adapted from the criteria developed in the Western countries for the Caucasian population.

Increased body fat, is associated with many health conditions associated with obesity such as diabetes and high blood pressure. Particularly, central fat – the fat deposited around waist and the internal organs such as intestines and liver is the worse offender.

Higher body fat or the central fat dramatically increases obesity-related health risks. Body mass index (BMI) is a convenient surrogate marker for estimating body fat content. BMI is calculated by dividing your weight in kg twice by your height in meters. Western standards consider a BMI of 20 – 24.9 as “normal”, 25 – 29.9 as overweight and 30 and above as obesity. Overweight and obesity cut-off points indicate a sharp increase in obesity-related health risks.

However, research showed a peculiar phenomenon. At similar BMI, Asian Indians have much greater central or total body fat compared to Caucasians, indicating that Asian Indians are more predisposed to health risks at a BMI that may be considered normal for Caucasians.

Moreover, Asians with body fat and central fat distribution similar to that of Caucasians, had greater health risks compared to Caucasians. Thus, Indians appear to get obesity-related diseases at a lower body fat levels compared to Caucasians. This contributed to reconsidering the validity of the cut-off points for Asian Indians.

Those with BMI between 23 – 25 will now be considered overweight and above 25 will be considered obese. Similarly, new lowered cut-off points suggest that Indian men with waist circumference above 78 and women above 72 cm should be alerted against further weight gain and active treatment be initiated for weight management for waist circumferences above 90 and 80 cms for Indian men and women, respectively.

Redefining overweight or obesity has more than academic significance. By recognizing possible health risks in a population segment hitherto considered “normal”, more Indians are likely to receive medical attention needed for prevention and treatment of obesity-related conditions.

The new consensus guidelines also make specific treatment recommendations for Indians including physical activity, and for initiating drugs or surgical therapy. Overall, the recognition of a peculiar health situations in Indians, which is different from that of the West is a very welcome sign and is hoped to lead to appropriate corrective actions in this country.


Source : Times of India

WASHINGTON: Researchers who mapped the DNA of more than 100 different cold viruses said they discovered a shortcut in their life cycle, which which may explain why they can inflict misery so quickly
They also believe they may find ways to design drugs to fight the rhinoviruses, which use their single gene to move rapidly from person to person, causing symptoms that range from irritating sniffles to pneumonia.

Instead of designing one drug to cure the common cold, several may be needed because the virus mutates so efficiently, said Dr. Stephen Liggett of the University of Maryland medical school, who led the study published in the journal Science.

"We may end up having four or five drugs," Liggett said in a telephone interview on Thursday.
The hope had been that it might be easy to fight the viruses, which sicken children on average 10 times a year and adults at least twice a year on average.

This is because any rhinovirus has just one gene, which in turn makes a giant protein that appears to do little or nothing until it gets chopped up into 11 smaller pieces by an enzyme called a protease.

Researchers tried to attack this big, clumsy protein before. "The first drug, the virus mutated around it," Liggett said. "But now that we have all the pieces we can begin to understand what areas are not so flexible. We can begin to do some more rational drug design."

For example it might be possible to attack the protease - an approach that has worked in fighting AIDS. "If we could inhibit that protease from cleaving that protein, maybe we could render all rhinoviruses ineffective," Liggett said.

Liggett's team also found the viruses take a shortcut in making the proteins, which probably speeds up their ability to make a person feel sick soon after infection.

Claire Fraser-Liggett, who directs the Institute for Genome Sciences and also worked on the study, called this a "new insight."

The viruses also swap genes promiscuously in the equivalent of viral sex, a process known as recombination. This helps them constantly change and adapt.

"We generally think of colds as a nuisance, but they can be debilitating in the very young and in older individuals, and can trigger asthma attacks at any age," Liggett said.

Common colds and related complications cost an estimated $60 billion a year in direct and indirect costs in the United States, the researchers wrote.


Source: Times Of India