New Study Helps Explain

Decompression Sickness

Science(June 28, 2010) — As you go about your day-to-day activities, tiny bubbles of nitrogen come and go inside your tissues. This is not a problem unless you happen to experience large changes in ambient pressure, such as those encountered by scuba divers and astronauts. During large, fast pressure drops, these bubbles can grow and lead to decompression sickness, popularly known as “the bends.”

A study in the Journal of Chemical Physics, which is published by the American Institute of Physics (AIP), may provide a physical basis for the existence of these bubbles, and could be useful in understanding decompression sickness.

A physiological model that accounts for these bubbles is needed both to protect against and to treat decompression sickness. There is a problem though. “These bubbles should not exist,” says author Saul Goldman of the University of Guelph in Ontario, Canada.

Because they are believed to be composed mostly of nitrogen, while the surrounding atmosphere consists of both nitrogen and oxygen, the pressure of the bubbles should be less than that of the surrounding atmosphere. But if this were so, they would collapse.

“We need to account for their apparent continuous existence in tissues in spite of this putative pressure imbalance,” says Goldman.

If, as is widely believed, decompression sickness is the result of the growth of pre-existing gas bubbles in tissues, those bubbles must be sufficiently stable to have non-negligible half-lives. The proposed explanation involves modeling body tissues as soft elastic materials that have some degree of rigidity. Previous models have focused on bubble formation in simple liquids, which differ from elastic materials in having no rigidity.

Using the soft-elastic tissue model, Goldman finds pockets of reduced pressure in which nitrogen bubbles can form and have enough stability to account for a continuous presence of tiny bubbles that can expand when the ambient pressure drops. Tribonucleation, the phenomenon of formation of new gas bubbles when submerged surfaces separate rapidly, provides the physical mechanism for formation of new gas bubbles in solution. The rapid separation of adhering surfaces results in momentary negative pressures at the plane of separation. Therefore, while these tiny bubbles in elastic media are metastable, and do not last indefinitely, they are replaced periodically. According to this picture, tribonucleation is the source, and finite half-lives the sink, for the continuous generation and loss small gas bubbles in tissues.

Sourced & published by Henry Sapiecha

Pressure, Research Finds

Science (June 28, 2010) — For people with hypertension, eating dark chocolate can significantly reduce blood pressure. Researchers writing in the open access journal BMC Medicine combined the results of 15 studies into the effects of flavanols, the compounds in chocolate which cause dilation of blood vessels, on blood pressure.

Dr Karin Ried worked with a team of researchers from the University of Adelaide, Australia, to conduct the analysis. She said, “Flavanols have been shown to increase the formation of endothelial nitric oxide, which promotes vasodilation and consequently may lower blood pressure. There have, however, been conflicting results as to the real-life effects of eating chocolate. We’ve found that consumption can significantly, albeit modestly, reduce blood pressure for people with high blood pressure but not for people with normal blood pressure.”

The pressure reduction seen in the combined results for people with hypertension, 5mm Hg systolic, may be clinically relevant — it is comparable to the known effects of 30 daily minutes of physical activity (4-9mm Hg) and could theoretically reduce the risk of a cardiovascular event by about 20% over five years.

The researchers are cautious, however, “The practicability of chocolate or cocoa drinks as long-term treatment is questionable,” said Dr Ried.

Sourced and published by Henry Sapiecha

in Living Animals

Science (June 11, 2010) — Scientists are reporting the first evidence that a plastic antibody — an artificial version of the proteins produced by the body’s immune system to recognize and fight infections and foreign substances — works in the bloodstream of a living animal.

The discovery, they suggest in a report in the Journal of the American Chemical Society, is an advance toward medical use of simple plastic particles custom tailored to fight an array of troublesome “antigens.”

Those antigens include everything from disease-causing viruses and bacteria to the troublesome proteins that cause allergic reactions to plant pollen, house dust, certain foods, poison ivy, bee stings and other substances.

In the report, Kenneth Shea, Yu Hosino, and colleagues refer to previous research in which they developed a method for making plastic nanoparticles, barely 1/50,000th the width of a human hair, that mimic natural antibodies in their ability to latch onto an antigen. That antigen was melittin, the main toxin in bee venom. They make the antibody with molecular imprinting, a process similar to leaving a footprint in wet concrete. The scientists mixed melittin with small molecules called monomers, and then started a chemical reaction that links those building blocks into long chains, and makes them solidify. When the plastic dots hardened, the researchers leached the poison out. That left the nanoparticles with tiny toxin-shaped craters.

Their new research, together with Naoto Oku’s group of the University Shizuoka Japan, established that the plastic melittin antibodies worked like natural antibodies. The scientists gave lab mice lethal injections of melittin, which breaks open and kills cells. Animals that then immediately received an injection of the melittin-targeting plastic antibody showed a significantly higher survival rate than those that did not receive the nanoparticles. Such nanoparticles could be fabricated for a variety of targets, Shea says. “This opens the door to serious consideration for these nanoparticles in all applications where antibodies are used,” he adds.

Sourced and published by Henry Sapiecha 12th June 2010

Research Targets Lethal Chagas’

Disease Spread by Insect

That Bites Lips

Science (Apr. 29, 2010) — It makes your skin crawl — a bug that crawls onto your lips while you sleep, drawn by the exhaled carbon dioxide, numbs your skin, bites, then gorges on your blood. And if that’s not insult enough, it promptly defecates on the wound-and passes on a potentially deadly disease.

Now Jean-Paul Paluzzi, a PhD candidate in biology at the University of Toronto Mississauga, believes that manipulating physiology to prevent the insects from leaving their messy calling card represents the best hope for stopping the transmission of the illness, known as Chagas’ disease.

“This is a disease of the poor,” says Paluzzi, who has visited parts of the world affected by the illness. “The bugs are found in makeshift homes with mud walls and palm tree-like ceilings. Unfortunately, the people of Central and South America that this affects don’t have sufficient voice to get help. Given that there are roughly 15 to 19 million people that are infected-a substantial proportion of that area’s population-it’s a disease that’s been neglected.”

Chagas’ disease is one of the major health problems in South and Central America and is spread by reduvid bugs, also known as “kissing bugs” because of their fondness for lips. The disease they transmit is caused by Trypanosoma cruzi, a parasite that lives in their gut. In the initial acute stage, symptoms are relatively mild, but as the disease progresses over several years, serious chronic symptoms can appear, such as heart disease and malformation of the intestines. Without treatment, it can be fatal. Currently, insecticide sprays are used to control insect populations, and anti-parasitic drugs are somewhat successful at treating acute infections.

Once the disease is chronic, it cannot be cured.

To make matters worse, kissing bugs are particularly “bloodthirsty.” In mosquitoes, which go through four distinct stages of development, only adult females feed on blood (and potentially transmit disease). This means that pest control methods need to target only one out of eight stages (when you include both sexes). But in kissing bugs, each sex feeds on blood through all fives stages of development. “So you have about a ten-fold greater chance of infection just because of the number of times that these insects have to feed,” says Paluzzi.

His research focuses on insect diuresis-more specifically, the genes and peptides that control how the kissing bug eliminates excess fluid in its gut after it gorges on blood. For the insect, the real prize in its meal is the red blood cells, while the water and salt is “excess baggage.” After they feed, the bugs are bloated and sluggish, and must jettison the waste so they can make their escape.

Here’s how it happens: when the kissing bug finds a snoozing victim and feeds, its levels of serotonin and diuretic hormones rise sharply, targeting the insect’s midgut and Malpighian tubules (the equivalent of kidneys), and triggering the release of waste. About four hours later, a peptide named CAP2b is released in the insect’s gut, abolishing the effect of the diuretic hormones.

Paluzzi has identified two genes (RhoprCAPA-alpha and RhoprCAPA-beta) that carry the chemical recipe for the peptides that stop diuresis. With that information, he hopes to create a peptide “agonist”-something that would enhance the activity of the CAP2B peptide and prevent the insect from leaving waste (and the parasite) on the wound. In theory, says Paluzzi, this might be an insecticide-like room spray or topical lotion that is biologically stable and has no effect on humans or other insects. Paluzzi is collaborating with a structural biochemist at the U.S. Food and Drug Administration in Texas, with the ultimate goal of creating a pest control solution, but he cautions that a market-ready product is many years away.

The research was funded by the Natural Sciences and Engineering Research Council of Canada, through a discovery grant to Professor Ian Orchard of the Department of Biology and a Canada Graduate Scholarship to Paluzzi.

Sourced and published by Henry Sapiecha 2nd May 2010

REMOTELY REPORTS THEIR CONDITION TO HOSPITALS

This idea aims to provide medical attention to old incapacitated people who cannot intimate the hospitals about their health in case of a serious heart attack.

All such old peoples would be provided with an E-Band which would consist of  pulse rate detecting equipment.

This equipment would consist of a pulse rate detecting sensor and a microprocessor. The sensor would constantly monitor the pulse rate of the patient and at regular intervals send the pulse rate as input to the microprocessor.

The microprocessor would be so programmed so that it generates a high output if appreciable fall or rise in the pulse rate is observed.

This output would be in turn connected to the transmitter attached to the walking stick used by the patient. As soon as the transmitter receives a high signal, it would transmit data signals consisting of a certain bit combination which would be unique for each patient, to the nearest hospital.

The hospital would be provided with the receiver in order to receive the signals and depending bit pattern in the signal, the location of the victim can be easily identified and in this way immediate medical attention can be given to the patient.

For power supply, Batteries and a switch connection is provided in the walking stick. Whenever the switch is switched on the entire circuitry would perform the above mentioned functionality. The market acquiring capacity of this product would be immense as this only requires a normal pulse detecting sensor and a microprocessor which are quite easily available and a small interface circuit between them.

Again the transmitter also is an easily available component and connection also does not require a lot of hardware. Apart from this the idea involves the usage of some minor hardware such as wiring to provide dc power and to send the microprocessor output to the transmitter and a battery and switch connection.

In the hospital a receiver is required in order to receive the transmitted signals and determine the location of the patient depending on bit pattern. And the cost involved surely is worth saving a life.

Sourced and published by Henry Sapiecha 8th Sept 2009

The Electromagnetic Rail Motor (ERM) can power anything from aircraft and cars, to artificial human limbs. The ERM is based on the modern rail gun. By taking the two rails and forming a ring, a continuous rotational force is created that is easily managed and controlled. The speed of rotation can be directly controlled by adjusting the voltage, similar to a gas pedal. Once the ERM powers up, the motor rotation will accelerate to its terminal speed. The blades act as both rotational shafts and as propeller blades to help cool the motor during extremely high speeds. The rail housing holds the assembly together and keeps the rails in place to counter the immense separation force.

Sourced and published by Henry Sapiecha 8th Sept 2009

MINNEAPOLIS (UPI) – Healthy middle-aged women with feelings of hopelessness may develop neck artery thickening, a risk factor for stroke, U.S. researchers said.

Researchers at the University of Minnesota Medical School looked at 559 women — average age 50, 62 percent white, 38 percent African-American — who were generally healthy and did not show signs of clinical cardiovascular disease.

Susan A. Everson-Rose and colleagues measured hopelessness with a questionnaire assessing expectancies regarding future and personal goals. Depressive symptoms were measured with a 20-item Center for Epidemiologic Studies Depression Scale. Thickness of neck arteries was assessed using ultrasound.

The study, published online in Stroke: Journal of the American Heart Association, found hopelessness — negative thinking and feelings of uselessness — affects arteries independent of clinical depression and before women develop clinically relevant cardiovascular disease.

The researchers found a consistent, progressive and linear association between increasing neck artery thickness and rising levels of hopelessness.

Copyright 2009 by United Press International

Sourced and published by Henry Sapiecha 8th Sept 2009

HEIDELBERG, Germany (UPI) — German researchers suggest some infusion solutions in a common intravenous treatment may cause life-threatening inflammation.

The study, published in the Journal of Leukocyte Biology, found a common intravenous treatment used to boost blood pressure in critical patients contains substances called “advanced glycation end products.”

This reaction among various proteins occurring after the fluid has been formulated for use is called “post-translational modification.”

The researchers suggest screening infusion solutions for post-translational protein modifications and then removing the compounds.

“Improving the quality of infusion solutions by accounting for post-translational modification of proteins could lead to better clinical outcomes for patients, such as those treated solutions containing albumin,” study co-author Angelika Bierhaus of the University of Heidelberg in Germany said in a statement.

Bierhaus and colleagues injected advanced glycation end products detected in several currently available albumin infusion solutions into mice. The mice receiving the high levels of advanced glycation end products experienced significantly higher inflammation and death rates than the mice receiving low levels.

Copyright 2009 by United Press International

Sourced and published by Henry Sapiecha 8th Sept 2009