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Malaysia has been declared free from avian influenza, three months after the deadly virus was detected in poultry from a village in the central Selangor state, a minister announced Monday.In June, the H5N1 strain of bird flu was discovered after a poultry rearer from the Paya Jaras Hilir village in Selangor, next to the capital Kuala Lumpur, reported that 60 of his chickens had suddenly died over three days.

Health ministry officials immediately screened villagers and conducted checks on all birds and poultry.

“The prompt action by the Veterinary Services Department to stamp out the bird flu outbreak according to the protocol had been effective,” said agriculture minister Muhyiddin Yassin.

Following three months of surveillance and laboratory tests that have not shown any traces of the virus, the country had fulfilled conditions set by the World Organisation for Animal Health and has been “declared free from the disease”, Muhyiddin was quoted as saying by the official Bernama news agency.

Following the outbreak in June, a total of 4,226 chicken, ducks and other birds were culled, incurring a cost of 39,939 ringgit ($11,735) in compensation paid out to the livestock owners, he said.

Muhyiddin said the government was still taking preventive measures against the virus, such as conducting checks on poultry farms, prohibiting the import of chicken, ducks and other birds from countries affected by the disease and intensifying checks at border checkpoints to curb smuggling.

“The government has so far spent almost 10 million ringgit ($2.9 million dollars) in compensation to the affected poultry rearers.

“Almost 80,000 birds were culled since the first bird flu case was detected in 2004,” he said.

Following news of June’s outbreak, neighbouring Singapore stopped import of poultry and eggs from the affected area.

Malaysia has suffered no known human infections from the deadly virus.(DPA)

A new study has added to the list of health problems posed by smoking, by finding that it also contributes to atherosclerosis, or hardening of the arteries.Researchers from Weill Cornell Medical College in New York City pinpoint their evidence to the addictive chemical in cigarettes - nicotine.

By comparing reduced-nicotine cigarettes like Quest 3 and Eclipse with regular cigarettes, researchers discovered that the degree of cigarette-smoke induced atherosclerosis in mice correlated with the levels of nicotine — the higher the nicotine, the more disease.

“Right now, the general consensus is that the problem with cigarettes is tar and that nicotine is safe. That’s why you can buy nicotine gum or patches to help you stop smoking. Our study presents new evidence that nicotine may not be safe at all, especially for your heart,” says Dr. Daniel F. Catanzaro, principal investigator of the study.

The new study looked at two so-called “potentially reduced exposure products” (PREPs) — Eclipse and Quest.

The study found that mice exposed to smoke from low-nicotine cigarettes had significantly smaller atherosclerotic lesions, compared to those exposed to regular cigarettes but still larger than lesions in control mice not exposed to cigarette smoke, which showed the least evidence of atherosclerosis.

“While our study seems to suggest that low-nicotine cigarettes are safer, we also know that smokers adjust their smoking habits to maintain their level of nicotine. In other words, if you switch to a low-nicotine product, you will probably increase the number of cigarettes you smoke, or change the way you smoke to get more nicotine out of each cigarette. The best thing to do is quit,” says Dr. Catanzaro.

Researchers also found that iPF2alphaV, a marker for oxidative stress that has been linked with atherosclerosis in humans, increased proportionately with the level of nicotine. This finding may signify that nicotine promotes atherosclerosis, partially, by blocking production of nitric oxide, a chemical that mediates the protective functions of the lining of blood vessels.

“These findings are preliminary. Going forward we will want to look at whether doping cigarettes with extra nicotine increases their atherogenic potential; whether blockers of nicotine reduce atherosclerosis; and if oral administration of nicotine has the same effects,” says Dr. Catanzaro.

The study is published in the journal Cardiovascular Toxicology.

Researchers have discovered a new application for tropical and popular aquarium fish, Zebrafish - it can now be used to study COX deficiencies in humans.Researchers at the University of Oregon claim that their finding has opened an unparalleled pathway to examine the earliest stages of mitochondrial impairments that lead to potentially fatal metabolic disorders.

COX deficiencies refer to a breakdown of cytochrome coxidase, an enzyme located in the mitochondrion of every cell. Mitochondria are crucial cellular workhorses that provide chemical energy. Research of the deficiency has been foiled by a lack of model organisms, with mice being introduced as the first model by Japanese researchers just seven years ago.

COX involves multiple proteins and assembly factors, and deficiencies of any one of them can negatively affect metabolic tissues, including the brain, muscle and eyes. Deficiencies during the prenatal period are considered to be a potential cause of miscarriages and have been led to prenatal screenings.

The comprehensive study, led by doctoral student Katrina N. Baden, could speed research and point to specific targets to test potential drug therapies, said co-author Karen Guillemin, a professor of molecular biology and member of the UO Institute of Molecular Biology.

“Mitochondrial impairments are emerging as important in many human diseases, but there have been few models for understanding exactly what is happening during the early development of the diseases. The use of mice is limited, because knocking out protein expression in mice mitochondria to mimic human-disease states results in large numbers of deaths in utero. Therefore, the symptoms that researchers have wanted to study have not been assessable in mice,” Guillemin said.

Baden, a veterinarian, performed several experiments, using RNA-blocking reagents known as morpholinos to reduce gene expression of both a critical COX subunit and Surf1, an assembly-factor protein that when mutated can lead to Leigh syndrome, a severe neurological disorder.

She targeted a variety of proteins, alone and in combination, and then added back components to rescue each deficiency. Normal COX activity declined as much as 50 percent in the experimental conditions and resulted in developmental defects in endodermal tissue, cardiac function and swimming behaviour in the zebrafish.

“The unique characteristics of zebrafish make them an ideal model for studying the effects of mitochondrial deficiencies on early development. Because they develop outside of a uterus and are transparent in early stages, I was able to visualize the effects that molecular alterations have on cell biology, nervous system development, cardiac function and fish behaviour,” said Baden.

The external and transparent embryo, Guillemin said, will allow scientists to create specific deficits that mirror those in humans.

“The transparency of the embryo will let us see primary defects, what happens in the earliest stages, rather than having to settle for seeing secondary downstream defects later in the disease state. Different tissues respond differently to specific losses in mitochondria,” she said.

Baden and Guillemin said that the use of zebrafish will improve scientific understanding of the mechanisms of mitochondrial associated pathology in people and speed the identification of new treatments for mitochondrial diseases.

The study has been published online ahead of regular publication by the Journal of Biological Chemistry.

Researchers have identified a blood formation gene, which, if lost, results in early bone marrow failure.Dartmouth Medical School cancer geneticists have found that all blood cell production in adults depends on the steady work of this vital gene that if lost can lead to premature bone marrow failure.

Their research reveals an unforeseen role for the gene in sustaining the adult blood-forming system, and opens novel strategies for targeting the gene, which is often involved in a type of childhood leukemia.

“We have identified a new pathway that is essential for blood stem cell turnover,” said team leader Dr. Patricia Ernst, adding that the pathway could be exploited for treating a rare but aggressive infant leukaemia.

For the study, the investigators created a mouse model to track the function of a gene called MLL, which stands for Mixed Lineage Leukemia. The gene acts in bone marrow stem cells and controls key aspects of their growth to generate all the mature blood cells. If disrupted, it cannot work properly, and thus allows leukemia to develop.

“MLL is the most commonly affected gene in childhood leukemia in children under a year of age; this particular type of leukemia has one of the worst success rates with the existing cancer therapies,” said Ernst.

Previous studies indicated that MLL is crucial for embryonic blood stem cell development, but its role for the adult system was unknown. In their mouse model, the researchers found that bone marrow failure occurred as early as 14 days after they induced the experimental loss of MLL, demonstrating the crucial role of MLL as “necessary for both the development and maintenance of the body’s blood supply,” according to the researchers.

“We have shown that the adult blood-forming system depends on the continuous actions of MLL,” Ernst said.

In addition, with the mouse model, they can begin exploring how to craft new anti-cancer treatments, she pointed out.

“We and other groups can start designing targeted therapies that inhibit cancerous forms of MLL that occur in childhood leukemia and do not affect normal MLL function, which, based on our studies in mice, would be fatal for the patient,” she said.

The study is published in the September issue of Cell Stem Cell.

McMaster researchers have found that a major class of cells called glial cells contain the fragile X mental retardation protein (FMRP), a discovery that has strong implications for the cellular causes of Fragile X Syndrome (FXS), the most common genetic disorder associated with mental impairment.According to the background information in a report, brain development in the absence of FMRP leads to cognitive effects, learning and memory problems, attention deficit, hyperactivity, and autistic behaviours.

The researchers say that their discovery attains significance as the neuro-glial cells (astrocytes) play important roles in the development and maintenance of normal communication between neurons in the brain and spinal cord.

They say that the absence of FMRP in astrocytes may contribute to the abnormal neuronal structures seen in the brains of Fragile X patients.

“This is an unexpected finding. Like fitting a piece of a puzzle that suddenly paints the main picture in a different perspective. We have another major cell type as a focus in Fragile X research. It will supply needed insight on the biology causing Fragile X and help to strengthen the potential for treatment strategies,” says Laurie Doering, associate professor in the Department of Pathology and Molecular Medicine.

Until now, FMRP was thought to be found only in neurons.

But while studying the development of adult stem cells from the mouse brain, Laura Pacey, a Ph.D. student in Prof. Doering’s laboratory, realised that cells also produced the FMRP in addition to neurons. (ANI)