What is swine flu (novel H1N1 influenza A swine flu)?

Swine flu (swine influenza) is a respiratory disease caused by viruses (influenza viruses) that infect the respiratory tract of pigs and result in nasal secretions, a barking-like cough, decreased appetite, and listless behavior. Swine flu produces most of the same symptoms in pigs as human flu produces in people. Swine flu can last about one to two weeks in pigs that survive. Swine influenza virus was first isolated from pigs in 1930 in the U.S. and has been recognized by pork producers and veterinarians to cause infections in pigs worldwide. In a number of instances, people have developed the swine flu infection when they are closely associated with pigs (for example, farmers, pork processors), and likewise, pig populations have occasionally been infected with the human flu infection. In most instances, the cross-species infections (swine virus to man; human flu virus to pigs) have remained in local areas and have not caused national or worldwide infections in either pigs or humans. Unfortunately, this cross-species situation with influenza viruses has had the potential to change. Investigators think the 2009 swine flu strain, first seen in Mexico, should be termed novel H1N1 flu since it is mainly found infecting people and exhibits two main surface antigens, H1 (hemagglutinin type 1) and N1 (neuraminidase type1). Recent investigations show the eight RNA strands from novel H1N1 flu have one strand derived from human flu strains, two from avian (bird) strains, and five from swine strains.

Tai chi soothes pain in arthritis sufferers

CM NEWS – The results of a new analysis have provided good evidence to suggest that Tai Chi is beneficial for arthritis. Specifically, it was shown to decrease pain with trends towards improving overall physical health, level of tension and satisfaction with health status.

Musculoskeletal pain, such as that experienced by people with arthritis, places a severe burden on the patient and community and is recognized as an international health priority. Exercise therapy including such as strengthening, stretching and aerobic programs, have been shown to be effective for arthritic pain. Tai Chi, is a form of exercise that is regularly practiced in China to improve overall health and well-being. It is usually preformed in a group but is also practiced individually at one’s leisure, which differs from traditional exercise therapy approaches used in the clinic.

Recently, a new study examined the effectiveness of Tai Chi in decreasing pain and disability and improving physical function and quality of life in people with chronic musculoskeletal pain. The study is published in the June issue of Arthritis Care & Research. Led by Amanda Hall of The George Institute in Sydney, Australia, researchers conducted a systematic review and meta-analysis. They analyzed seven eligible randomized controlled trials that used Tai Chi as the main intervention for patients with musculoskeletal pain. The results demonstrate that Tai Chi improves pain and disability in patients suffering arthritis.

The authors state, “The fact that Tai Chi is inexpensive, convenient, and enjoyable and conveys other psychological and social benefits supports the use this type of intervention for pain conditions such as arthritis.”

“It is of importance to note that the results reported in this systematic review are indicative of the effect of Tai Chi versus minimal intervention (usual health care or health education) or wait list control,” the authors note. Establishing the specific effects of Tai Chi would require a placebo-controlled trial, which has not yet been undertaken.

Alternative To Open Heart Surgery Interventional Cardiologists Help The Faint Of Heart Without Surgery

January 1, 2009 — Interventional cardiologists created an alternative to open heart surgery by developing a mitral valve clip. To alleviate mitral valve regurgitation–a condition where the heart’s mitral valve does not close properly, allowing blood to leak back into the heart–cardiologists insert a catheter into the patient’s groin that travels up into the mitral valve. The clip is fed through this catheter, where it finally grasps and tightens the valves’ leaflets–effectively preventing blood from leaking. The clip remains in place while the catheter is removed, the entire procedure taking approximately two hours and recovery a few weeks. The procedure is good for those with weaker hearts, when traditional surgery is more dangerous.
ABOUT MITRA CLIP: The Mitra Clip is a device inserted into the heart by a catheter. It is used to gather and fasten the leaflets of the mitral valve of the heart, which can become loose enough to allow blood to leak when the valve is closed. Doctors insert the catheter into the femoral artery, and then work it through the body to the heart. Using this technique can help patients recover more quickly from mitral valve repairs.

HAVE A HEART: The heart pumps 5.6 liters of blood through the entire body in roughly 20 seconds; each day your blood travels some 12,000 miles, and your heart beats about 100,000 times. This delivers oxygen and other essential nutrients to the body’s cells and organs. A heart attack occurs when the blood supply to the heart muscle is cut off, either because part of the heart is damaged (such as the valves to the chambers), or because plaque has built up inside the arteries, narrowing them and severely restricting blood flow. Symptoms of a heart attack include a squeezing discomfort in the center of the chest, pain or tingling in the left arm, shortness of breath and sometimes a cold sweat, nausea, or dizziness.

ABOUT HEART DISEASE: Most heart diseases arise from hardening of the arteries, especially from the buildup of fatty material along the inner lining of the arteries. Coronary arteries supply blood to the heart. When a blockage occurs, this flow is decreased. Heart medications target these blockages in several different ways. Nitrates dilate the veins, decreasing the oxygen requirements of the heart. They also dilate the coronary arteries to increase blood flow to the heart. Beta-blockers decrease the heart rate and the force of the heart’s contractions. Aspirin prevents platelets in the blood from clotting and clumping on blood vessel walls.

Damaging Inflammatory Response Could Hinder Spinal Cord Repair

ScienceDaily (Oct. 22, 2009) — The inflammatory response following a spinal cord injury appears to be set up to cause extra tissue damage instead of promoting healing, new research suggests.
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Scientists analyzing this inflammatory response in mice discovered that the types of cells recruited to the site of the injury are dominated within a week by those that promote inflammation. When chronic, inflammation can prevent healing, and these inflammatory cells are believed to remain at the injury site indefinitely.

Meanwhile, similar cells that are typically involved in a later phase of injury repair and that are anti-inflammatory were found to promote effective growth of axons that connect nerve cells. However, these cells disappear shortly after an injury, making it unlikely that they get a chance to complete their work under naturally occurring circumstances.

All of the responding cells in question are macrophages, but the study revealed that they have slightly different characteristics that define their functions. The research suggests that changing the balance of how these cells are activated in favor of the anti-inflammatory macrophages could be a potential treatment strategy for spinal cord injury.

Currently, no Food and Drug Administration-approved treatment exists for spinal cord injury, and scientists have not discovered a way to repair nerve cells that are damaged or killed when the spinal cord is injured. An estimated 1.3 million people in the United States are living with a spinal cord injury, experiencing paralysis and complications that include bladder, bowel and sexual dysfunction and chronic pain.

“If these pro-inflammatory macrophages are a big part of the reason cells are dying, and we can figure out how to shut off that death cascade that they start, we might be able to minimize the amount of tissue damage,” said senior study author Phillip Popovich, a professor of neuroscience and molecular virology, immunology and medical genetics at Ohio State University.

“If that could be achieved by injecting a drug or giving a patient a pill for a set number of days after injury, that could improve a lot of function and quality of life for people who suffer a spinal cord injury.”

The research was presented Wednesday during a poster session at the Society for Neuroscience annual meeting in Chicago.

Popovich has known about the presence of macrophages after spinal cord injury for a long time. What he didn’t know was exactly what they did, or how they did it, or whether there could be more than one function among these cells.

“I’ve always been of the mind that if nature requires these cells to be there, we must figure out if it’s advantageous or disadvantageous for spinal cord function,” said Popovich, also director of Ohio State’s Center for Brain and Spinal Cord Repair.

“If what they do is disadvantageous, how can we change that without completely removing them? Because if we remove them, it will probably change a lot of other things and that is not going to be beneficial.”

In this study, he and colleagues compared the spinal cords of mice with injury to the spinal cords of uninjured mice. The mouse injuries resembled the most common contusion/compression spinal cord damage in humans that occurs when a vertebral bone or a disc bumps into the cord, causing a lesion and bleeding.

The researchers used chemicals to stain the spinal cords with markers that would indicate what types of cells were active at the injury site. They named the pro-inflammatory macrophages M1 cells and anti-inflammatory macrophages M2 cells.

Immediately after the injury, the researchers observed an intermingling of M1 and M2 cells at the site of the spinal cord injury. In just a few days, all of the anti-inflammatory M2 cells had disappeared. The pro-inflammatory M1 population persisted for a month after injury — the longest period scientists have ever observed.

Popovich said he and colleagues used recent principles learned by others in models of repair of injured heart muscle to predict how the inflammatory response to spinal cord injury would occur. After the heart is damaged, macrophages migrate to the site to clean up debris and protect against any invading bacteria or other pathogens. Signals are eventually sent out to initiate a next phase, which prepares the site for repair. Then new cells are recruited, blood vessels grow and other macrophages facilitate closure of the wound.

In the spinal cord, the long-term presence of pro-inflammatory M1 cells appears to prevent the shift into a repair phase.

“What we’ve done is overly simplistic, but it’s an advance conceptually from where we were because we’re saying that even though it looks like a homogeneous response, not all macrophages are created equal,” Popovich said.

Once they knew how M1 and M2 cells were distributed at an injury site, the researchers sought to determine what those two types of macrophages could do.

They created in vitro models — essentially, test tube experiments — in which they examined the effects of M1 and M2 macrophages on neurons, the cells that make up most of the spinal cord and brain.

The M1 macrophages killed neurons or stimulated a sprouting type of growth among their axons, which function as arms on neurons that reach out to connect with other cells or to send and receive signals. This type of sprouting of axons is associated with misguided circuits and can actually cause chronic pain.

The M2 cells, on the other hand, promoted long-distance axon growth without causing toxicity. This is the kind of axon growth required to regenerate spinal cord tissue and is the type of axon growth that is normally inhibited by proteins and cells that accumulate in the spinal cord after injury.

Popovich speculates that the immune system normally inhibits axon regeneration because its primary goal is to keep the injured spinal cord free from infection.

“The injury opens tissue to the external environment, increasing the potential to be exposed to pathogens. The immune system doesn’t care that the spinal cord is damaged — it just wants to keep the organism alive,” he said. “And neurons want to regrow, but when they try to grow their axons, they hit a wall of inflammatory cells that they can’t get past or that are working against them.”

One class of drugs — PPARgamma agonists, used to treat diabetes — is known to promote recruitment of M2 macrophages and has appeared in previous research to protect neurons in models of spinal cord injury, Popovich said. But before pursuing drug therapies, researchers must determine whether changing the balance of macrophages in an injured spinal cord to favor the activation of M2 cells would actually be beneficial in a human body.

“The only benefits we’ve shown so far were in vitro,” he said. “There’s a chance we’ll never be able to figure out how to regenerate an axon. But if we could minimize damage caused by inflammation, that would be helpful. Each axon that dies gets you closer to a threshold where you lose function. If we could just keep axons and neurons alive, we may have a better chance at promoting recovery.”

The National Institutes of Health and the National Institute of Neurological Disorders and Stroke supported this research.

Popovich conducted the work with postdoctoral researchers Kristina Kigerl and John Gensel, and research scientist Daniel Ankeny, all of Ohio State’s Department of Molecular Virology, Immunology and Medical Genetics; Jessica Alexander of the Neuroscience Graduate Studies Program; and graduate student Dustin Donnelly of the Medical Scientist Program. All of the co-authors also are also investigators in the Center for Brain and Spinal Cord Repair.

Clock Molecule’s Sensitivity To Lithium Sheds Light On Bipolar Disorder

ScienceDaily (Feb. 21, 2006) — Researchers at the University of Pennsylvania School of Medicine discovered that a key receptor protein is a critical component of the internal molecular clock in mammals. What’s more, this molecule — called Rev-erb — is sensitive to lithium and may help shed light on circadian rhythm disorders, including bipolar disorder. The findings, which also provide insight into clock-controlled aspects of metabolism, are reported in this week’s issue of Science.
See also:
Health & Medicine

* Sleep Disorder Research
* Insomnia Research
* Obesity

Mind & Brain

* Insomnia
* Psychiatry
* Depression

Reference

* Circadian rhythm sleep disorder
* Circadian rhythm
* Jet lag
* Appetite

“We’re interested in the internal control of metabolism because feeding behavior is on a daily cycle, and hormonal activities that regulate this are circadian,” says senior author Mitch Lazar, MD, PhD, Director of the Institute for Diabetes, Obesity, and Metabolism at Penn. “Many studies, including those here at Penn, suggest a relationship between the human circadian clock and metabolism. Proteins are the gears of the clock, and not much is known about what regulates protein levels within the cell.”

Rev-erb was known to be a key component of the clock that exists in most cells of the body. Rev-erb inhibits clock genes called bmal and clock, but within a normal 24-hour circadian cycle the Rev-erb protein is destroyed within the cell, allowing bmal and other clock proteins to increase. Among other actions, these clock genes cause Rev-erb to increase, which again inhibits bmal and clock. “The time it takes for that to happen determines the length of the cycle — roughly 24 hours — and keeps the clock going,” explains Lazar.

Penn colleague and coauthor Peter Klein, MD, PhD, Assistant Professor of Medicine, discovered a few years ago that the drug lithium, used to treat biopolar illness, inhibits GSK3, an enzyme known to regulate circadian rhythm in several animal species. In the present study, the researchers showed that the destruction of Rev-erb, a receptor shown previously by Lazar and others to play a role in maintaining normal metabolism, is prevented by GSK3 in mouse and human cells. “It’s like pulling a pin out of the gears of the clock, to allow them to turn in a synchronized manner,” says Lazar.

Lithium blocks this action of GSK3, tagging Rev-erb for destruction, which leads to activation of clock genes such as bmal1. “We suggest that just as our cells in the incubator need to have their internal clocks reset, maybe this is what happens in some people with circadian disorders,” says Lazar. “One effect of lithium may be to reset clocks that become stuck when Rev-erb levels build up.”

These results point to Rev-erb as a lithium-sensitive component of the human clock and therefore a possible target for developing new circadian-disorder drugs. Some patients taking lithium have developed kidney toxicity and other problems. Lazar surmises that new treatments that lead to the destruction of Rev-erb would have the potential of providing another point of entry into the circadian pathway.

Noting that Rev-erb is present in metabolically active tissues, Lazar and his team at the Institute for Diabetes, Obesity, and Metabolism are also interested in the relationship between the control of the circadian clock and metabolic diseases such as obesity and diabetes. “There is a dynamic interplay between circadian rhythms and metabolism,” Lazar says. “You don’t eat while you are sleeping, and the body needs to take this into account.”

Study co-authors are Lei Yin and Jing Wang, both from Penn. The research was funded by the National Institute of Diabetes & Digestive & Kidney Diseases and the National Institute of Mental Health.

Inner Workings Of Molecular Thermostat Point To Pathways To Fight Diabetes, Obesity

ScienceDaily (Sep. 13, 2009) — Best known as the oxygen-carrying component of hemoglobin, the protein that makes blood red, heme also plays a role in chemical detoxification and energy metabolism within the cell. Heme levels are tightly maintained, and with good reason: Too little heme prevents cell growth and division; excessive amounts of heme are toxic.
Researchers at the University of Pennsylvania School of Medicine have discovered a molecular circuit involving heme that helps maintain proper metabolism in the body, providing new insights into metabolic disorders such as obesity and diabetes.

The work builds on 2007 findings from the same team, led by Mitchell Lazar, MD, PhD, Director of Penn’s Institute for Diabetes, Obesity, and Metabolism, showing that a protein called Rev-erbα coordinates the daily cycles of heme. The new research, published online in Genes & Development, makes it clear that Rev-erbα, by controlling the production of heme, also plays a key role in maintaining the body’s correct metabolism. This happens through a molecular pathway that allows the cell to monitor and adjust internal heme levels, creating more when heme levels fall, and slowing it down when levels rise.

The circuit is a negative feedback loop, with Rev-erbα as its central component, explains Lazar. “Rev-erbα is a thermostat for heme.” When heme levels are high, Rev-erbα is activated, reducing heme, which leads the cell back towards a normal state. On the other hand, when heme levels are low, Rev-erbα activity is low, and this permits the cell to make more heme, again leading back toward a normal state. Maintaining this stasis allows energy metabolism to occur but avoids harm to the cell due to excessive levels of heme.

Understanding the control of heme levels is likely to be relevant to several diseases. For example, obesity is a condition where fat tissue builds up due to low energy expenditure relative to energy intake. Proteins such as Rev-erbα that help maintain a cell’s proper metabolism and energy balance point to their role in such metabolic disorders as obesity and diabetes and suggest ways to intervene.

Rev-erbα is a transcription factor, a protein that binds to DNA in front of, or within, genes to alter their expression. Rev-erbα acts as repressor of gene expression, that is, gene expression goes down when it binds to DNA.

Lazar has been studying the protein for nearly 20 years, yet he never really knew how it worked. What he did know was that, as a member of a family of nuclear receptor proteins, Rev-erbα could bind DNA and likely had an intracellular binding partner.

Typical nuclear receptor proteins are like sensors, registering a specific molecular event and responding accordingly, generally by altering gene expression patterns. So, Lazar asked, “What is the purpose of having a system that responds to changes in cellular heme levels?” He hypothesized that the sensor could act to regulate heme itself.

Working with cultured human and mouse cells his team, led by first author, graduate student Nan Wu, monitored heme levels as Rev-erbα abundance changed. What they found confirmed the protein’s role in heme regulation: when overexpressed, heme levels dropped; when suppressed, heme levels rose.

“That was consistent with the hypothesis,” says Lazar. “The question was, how does heme do this?”

To figure that out, the team looked for Rev-erbα binding sites within the sequences of genes known to control heme biosynthesis and found one in PGC-1α, a transcription factor that stimulates the production of heme. Since Rev-erb activity is controlled by heme itself, the net effect is that, as heme levels rise, PGC-1α gets repressed, and heme synthesis drops off.

The team also demonstrated the physiological consequence of disrupting this pathway. “We reasoned, if heme levels get too low, cells won’t like it,” Lazar says, “and they don’t: They stop growing, and they reduce their oxygen consumption in a manner consistent with the role of heme being used to make ATP,” a form of cellular energy.

Lazar states that, “Up until now, no one knew there even was a mechanism for keeping heme levels in this narrow range. We’ve shown that it exists and have defined molecular players that make it work.”

In so doing, he and his team have linked heme biosynthesis with both energy metabolism and the body’s internal clock. Rev-erbα is a negative regulator of genes involved in energy metabolism. It also, along with PGC-1α and heme, rises and falls over a 24-hour period and even regulates some of the cogs within the clock itself.

Now the question is, can this pathway be exploited in the clinic. Lazar’s team showed that downregulating heme stifled cell division and metabolism, while upregulating heme enhanced them. It therefore is possible, Lazar says, that by pharmacologically “tickling” Rev-erbα or its other cellular partners to believe the cell has more or less heme than it actually does, researchers may be able to either boost or suppress metabolism accordingly, opening the door to potential therapies for cancer and obesity.

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. Lei Yin, Elyisha A. Hanniman, and Shree Joshi, all from Penn, are co-authors.

Infertility And The Battle Of The Sexes: Evolutionary Explanation For Today’s Fertility Problems?

Electronic Cigarette Known as ecig Helps You Quit Smoking

Washington, USA (PRWEB) September 8, 2009 — An electronic cigarette or “e-cigarette”,”e-cig”, is a battery-powered device that provides inhaled doses of nicotine by delivering a vaporized liquid nicotine solution. It is an alternative to smoked tobacco products, such as cigarettes, cigars, or pipes. In addition to nicotine delivery, this vapor also provides a flavor and physical sensation similar to that of inhaled tobacco smoke, while no tobacco, smoke, or combustion is actually involved in its operation.

An electronic cigarette usually takes the form of some manner of elongated tube, though many are designed to resemble the outward appearance of real smoking products, like cigarettes, cigars, and pipes. A common design is also the “pen-style”, so named for its visual resemblance to a ballpoint pen.

Most electronic cigarettes are reusable devices with replaceable and refillable parts. A number of disposable electronic cigarettes have also been developed.

National Health Interview Survey (NHIS) reported in 2006 the statistics of cigarette smokers. In the United States alone, an estimated 26.2 million men (23.5 percent) and 20.9 million women (18.1 percent) are smokers. These people are at higher risk of heart attack and stroke. The latest estimates for persons age

Groundbreaking Treatment for Oxygen-Deprived Newborns

A new treatment for newborns suffering from oxygen deprivation during delivery involves a two-week course of injections of erythropoietin that can be started as late as two days after birth.

Researchers from Sahlgrenska Academy (Gothenburg, Sweden), in collaboration with Zhengzhou University (China) conducted a study involving a total of 167 full-term infants with moderate to severe neonatal hypoxic-ischemic encephalopathy (HIE), who were assigned randomly to receive either erythropoietin (83 newborns) or conventional treatment (84 newborns). Recombinant human erythropoietin, at either 300 U/kg or 500 U/kg, was administered every other day for two weeks, starting at most at 48 hours after birth. The primary outcome was death or disability, and neurodevelopmental outcomes were assessed at 18 months of age. Of the 167 patients, 9 dropped out during treatment, and 5 patients were lost to follow-up monitoring.

The researchers found that death or moderate-to-severe disability occurred in 35 (43.8%) of 80 infants in the control group and 18 (24.6%) of 73 infants in the erythropoietin group at 18 months. The primary outcomes were similar between the two erythropoietin doses. Subgroup analyses indicated that erythropoietin improved long-term outcomes only for infants with moderate HIE, and not those with severe HIE. No negative hematopoietic side effects were observed. The study was published in the August 2009 issue of the journal Pediatrics.

“For the first time we can demonstrate that it is possible to influence the brain damage occurring as a result of oxygen deprivation during delivery considerably later than the six-hour window of opportunity for treating with cooling,” said lead author Klas Blomgren, M.D., Ph.D., a professor of pediatrics at the Sahlgrenska Academy. “This appears to be a safe treatment, almost without side effects, and it is also cheaper and technically simpler to administer in comparison with cooling.”

Erythropoietin is a glycoprotein hormone that controls erythropoiesis, or red blood cell (RBC) production; it is a cytokine for erythrocyte precursors in the bone marrow. Also called hematopoietin or hemopoietin, it is produced by the peritubular capillary endothelial cells in the kidney. Besides regulating RBC production, it has other known biological functions, including an important role in the brain’s response to neuronal injury and in the wound healing process.

Monkey brains signal the desire to explore

DURHAM, N.C. Sticking with what you know often comes at the price of learning about more favorable alternatives.

Managing this trade-off is easy for many, but not for those with conditions such as Alzheimer’s disease or obsessive-compulsive disorder who are trapped in simple routines.

Using brain scans in monkeys, Duke University Medical Center researchers are now able to predict when monkeys will switch from exploiting a known resource to exploring their options.

“Humans aren’t the only animals who wonder if the grass is greener elsewhere, but it’s hard to abandon what we know in hopes of finding something better,” said John Pearson, Ph.D., research associate in the Duke Department of Neurobiology and lead author of a study published in this week’s Current Biology.

“Studies like this one help reveal how the brain weighs costs and benefits in making that kind of decision,” Pearson said. “We suspect that such a fundamental question engages many areas of the brain, but this is one of the first studies to show how individual neurons can carry signals for these kinds of strategic decisions.”

The researchers looked at how nerve cells fired in a part of the brain known as the posterior cingulate cortex as the monkeys were offered a selection of rewards. Generally, these neurons fired more strongly when monkeys decided to explore new alternatives.

The monkeys started with four rewards to choose from, each a 200 microliter cup of juice. After that, the four targets began to slowly change in value, becoming larger or smaller. The monkeys were free to explore the other targets or stay with the initial target, whose value they knew for certain. Monkeys had to select an option to learn its current value and integrate this information with their knowledge of the chances of getting more juice at a different target.

By studying the individual neurons, the researchers could predict which strategy the mo

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