Research has shown that varenicline tartrate - a novel new drug specifically developed for smoking cessation - allows smokers to abstain from cigarettes significantly longer and more effectively than smokers using a placebo.

A paper in Respirology, published by Wiley-Blackwell, compared the efficacy of a standard 12-week regimen of varenicline for smoking cessation with a placebo on 333 subjects in 15 test sites across China, Singapore and Thailand.

"The smoking cessation rate achieved after the treatment period and the follow-up period was significantly higher with varenicline than with placebo. Likewise, the long-term quit rate for smokers treated with varenicline was also significantly higher", said Dr. Chen Wang from the Beijing Institute of Respiratory Medicine.

More than half of the smokers from the varenicline group abstained from cigarettes within the treatment period while 38% continued to abstain for the next 12 weeks after the treatment. The abstinence rate for the placebo group was significantly lower with only 31% of the participants managing to abstain during the treatment period and 25 % for the non-treatment period.

Varenicline tartrate is a selective nicotinic acetylcholine receptor which is licensed in Europe, the USA and Japan. This study further evaluates and establishes the efficacy, tolerability and safety profiles of varenicline in Asian smokers.

A US study that reviewed the available evidence on bed bugs found that while they are highly resistant to various ways of getting rid of them, they seem to be more of a nuisance than a serious health problem, but the possibility that they could one day serve as a vehicle for disease has not been well researched.

The study was the work of Drs Jerome Goddard and Richard deShazo from the Department of Medicine, University of Mississippi Medical Center, Jackson, and is published online on 1 April in the Journal of the American Medical Association, JAMA. Goddard also works at the Department of Entomology and Plant Pathology, Mississippi State University.

The bed bug (Cimex lectularius) has been a human parasite for thousands of years, and infestations are rising fast, more so in developed countries, probably due to international travel, immigration, changes in how pests are controlled and insecticide resistance, wrote the authors.

Bed bugs prefer to hide within a few feet of their hosts, in places like mattress seams, crevices in the bed, behind the headboard and loose wallpaper.

From what we know, bed bug bites tend to be more of a nuisance than anything, although they can cause some skin reactions. However, their potential to serve as "disease vectors" and how best to control and eradicate them is not well understood.

For the study, Goddard and deShazo searched databases for medical and pest control articles from 1960 to 2008. They also did manual searches for older texts in journals, textbooks, trade journals and newspapers. This covered the period 1892 to 2008.

In their review they only included articles that met certain criteria in terms of clinical evidence for the medical articles and measured reductions of infestations for the pest control articles.

For instance, for the clinical studies, they included only original accounts of bed bug investigations that had enough detail of cause and effect between the insect bites and clinical effects and enough evidence that bed bugs were the source of the bites. On the pest control side, they only included articles that showed evidence that eradication led to a measured reduction in bed bugs.

They found 53 articles that met these criteria and included them in their summary review. They only found 2 clinical trials on bed bugs that " tested the ability of pest control interventions to eradicate bed bugs".

They found that a variety of clinical reactions to bed bugs have been reported, mostly skin reactions and rarely systemic reactions.

Also, although bed bugs have been blamed for transmitting over 40 human diseases, they found little evidence that "they are vectors of communicable diseases".

They also found that several kinds of treatment have been used for bed bug bites, with varying results. These include: antibiotics, antihistamines, corticosteroids (as creams and tablets), and epinephrine (adrenaline).

The researchers found no reports of evidence-based attempts to eradicate bed bugs or prevent bites.

A majority of the human population has been exposed to newly discovered KI (KIV), WU (WUV), and Merkel cell (MCV) human polyomaviruses, according to a new study by researchers at the University of Colorado. Published March 27 in the open-access journal PLoS Pathogens, the results, based on antibody measurements in serum samples, also suggest that infection with these viruses occurs early in childhood.

For over 30 years, scientists have known about two human polyomaviruses, BKV and JCV. Within the past two years, however, three new viruses have been described that belong to this same virus family. KIV and WUV were detected in nasal secretions, and may be respiratory viruses. MCV was discovered in Merkel Cell carcinomas, a rare skin cancer. Further studies are needed to determine what fraction of the human population has been infected with these viruses and when initial exposure occurs.

In this study, Kean and colleagues tested over 2220 anonymous donor blood samples (more than1500 adult and more than 700 pediatric [< 21 years of age]) They measured antibodies that reacted with specific viral proteins. In addition to KIV, WUV, MCV, BKV, and JCV, two monkey polyomaviruses, SV40 and lymphotropic polyomavirus (LPV), were also studied. Antibodies to LPV were detected in a fraction of people (15%), confirming previous studies suggesting that a relative of this virus may infect humans. The majority of antibodies against SV40 proteins may be attributed to the immune response to BKV. The diseases caused by these viruses remain to be fully described.

The samples and results reported are likely representative of infection in the Denver metropolitan area where they were collected. Future studies will be important to help determine differences in the prevalence of these infections in other geographic areas.

Using aquatic microbes as their "canary-in-a-cage," scientists from Ohio have reported that nanoparticles now being added to cosmetics, sunscreens, and hundreds of other personal care products may be harmful to the environment.

Their report was part of symposia that included almost two dozen papers at the 237th National Meeting of the American Chemical Society where scientists grappled to understand the environmental and human health effects of nanotechnology. Hundreds of products utilizing these microscopic particles - 1/5,000th the diameter of a human hair - already are on the market. With many more poised for debut, scientists are seeking to avoid unwanted health and environmental effects in advance.

The study by Cyndee Gruden, Ph.D. and Olga Mileyeva-Biebesheimer focused on nano-titanium dioxide (nano-TiO2) particles found in cosmetics, sunscreens, and other personal care products. The particles are added to those products for their highly beneficial effects in blocking ultraviolet light in sunlight. Excess exposure can cause premature aging of the skin and skin cancer.

Gruden, who is with the University of Toledo, explained that the particles are washed down the drain in homes as people bathe and end up in municipal sewage treatment plants. From there, they can enter lakes, rivers, and other water sources where microorganisms serve essential roles in maintaining a healthy environment.

"When they enter a lake, what happens?" Gruden asked. "Would they enter an organism or bind to it? Maybe they kill it - or have nothing to do with it at all. These are important questions for determining the effects that nanoparticles may have on the environment. Right now, we're not really sure of the answers."

Gruden studied survival of Escherichia coli (E. coli) bacteria when exposed in laboratory cultures to various amounts of nano-TiO2. She found surprisingly large reductions in survival in samples exposed to small concentrations of the nanoparticles for less than an hour. "How fast the impact was surprised me," she said. The findings open the door to future research, including studies to determine whether the same effects occur in the natural environment.

Gruden's method for pinpointing damage from nanoparticles uses fluorescence to identify when the cell membrane in microbes undergo damage. When membranes - a crucial part of the microbe - are damaged, the cells emit a faint red glow. "Methods based upon fluorescence allow us to obtain results faster, maybe with greater sensitivity," she said, adding that this approach could speed scientific efforts to understand the threshold at which nanoparticles become toxic to microbes.

In a second study on nanotoxicity at the ACS National Meeting, scientists from Utah described development of a new biosensor that flashes like a beacon upon detecting nanoparticles in the environment.

Anne Anderson and colleagues at Utah State University and the University of Utah have inserted genes into a strain of Pseudomonas putida (P. putida) - a beneficial soil microbe - so that it emits light upon contact with nanoparticles of heavy metals. They are with Utah State University. The bacteria glow brightly when it is in its normal healthy state. The glow dims upon exposure to toxic substances.

"The novelty of the biosensor is we're able to get responses very, very quickly," she said, "and we can get those answers in the absence of other factors that could bind the challenging compounds." Anderson noted that traditional approaches in measuring bacterial cell growth may take two days. "At the snap of your finger you can see some of these things take place."

Anderson's group discovered that P. putida cannot tolerate silver, copper oxide and zinc oxide nanoparticles. Toxicity occurred at levels as low as micrograms per liter. That's equivalent to two or three drops of water in an Olympic-sized swimming pool. Anderson warns it could spell danger for aquatic life. "If you look up the Environmental Protection Agency's risk level of Copper to fish and other aquatic organisms, you are at that point of toxicity."

There's much debate in the science community about nanoparticle toxicity, Anderson said. Some scientists believe that nanoparticles in nature will aggregate together or bind onto silt and/or other organic matter, greatly reducing their toxicity. "We don't know if that's true or not," she said. So other members of this Utah research group currently are investigating that aspect of the issue.

Although the public is ultimately responsible for understanding the risks of consumer products, Gruden said, science plays a large role in highlighting possible hazards. "It is the scientist's job to perform good research and let the findings speak for themselves," she said. And so far the promises of nanotechnology need more evaluation. "To date, it's unclear whether the benefits of nanotech outweigh the risks associated with environmental release and exposure to nanoparticles."

A tiny variation within a single gene can determine not only how quickly and well lungs grow and function in children and adolescents, but how susceptible those children will be to exposure to second-hand tobacco smoke, even in utero, according to researchers from the University of Southern California.

"Many factors can affect lung function and growth, including genetic variation and environmental exposures such as tobacco smoke and air pollutants," said Carrie Breton, Sc.D., lead author of the study conducted at the University of Southern California. "We wanted to determine whether specific gene variations would have measurable and predictable effects on lung function growth and susceptibility to environmental insults. We looked at a class of genes known to be involved in antioxidant defense, the glutathione-s transferase (GST) genes. Overall, we found that variation in several of the GST genes was important. This was particularly true for children of mothers who had smoked during pregnancy."

The researchers analyzed eight years' worth of lung function metrics and genotyping data from more than 2,100 children from two cohorts of fourth-graders. The lung function measurements used were maximal mid expiratory flow rate (MMEF), forced vital capacity (FVC) and forced expiratory volume in one second (FEV1).

"FEV1 is a measure of large airways, FVC of total lung volume and MMEF of smaller airways, so they measure slightly different things and we wouldn't necessarily expect to see all outcomes behaving the same," said Dr. Breton.

They found that for three of the specific haplotypes (patterns of genetic variation within genes) they investigated, each had a significant effect on lung function.

For one gene, GSTM2, two variant patterns were analyzed. These patterns occurred in 30-35 percent of the white population. One was found to promote stronger lung function, while the other variant was correlated with poorer lung function and greater susceptibility to damage caused by maternal cigarette smoking during pregnancy. Moreover, the reduction in lung function was greater in children who had two copies of the variant pattern that reduced lung function, compared to children with only one copy.

For a relatively rarer haplotype in GSTM3, occurring in only 6-8 percent of the white population, they found a strong negative effect on MMEF.

Finally, another haplotype in GSTM4, occurring in 16-22% of the population, showed significantly decreased rates of growth for FEV1, FVC and MMEF. Like GSTM2, the reduction in lung function was greatest in children who had two copies of the variant pattern that reduced lung function.

The researchers suggest that the gene variants may not alter the development of the lung, but its ability to defend itself against damage caused by free radicals. "The GST genes are important to the detoxification of reactive oxygen species, including carcinogens and environmental exposures, such as cigarette smoke. We speculate that the patterns of genetic variation we investigated may alter this process, thereby reducing the lung's ability to detoxify harmful agents and causing a cascade of other events that promote inflammation, bronchial constriction, airway hyperresponsiveness and asthma-like symptoms," said Dr. Breton.

"The next step would be to investigate how these genes interact with one another to jointly effect lung development. Future studies should also investigate the timing and quantity of tobacco smoke exposure during pregnancy in combination with variation in these genes to further understand how they jointly affect fetal lung development," said Dr. Breton.