Significant uncertainty remains about the precise vectors th

Significant uncertainty remains about the precise vectors, the plasticity of vector host-selection (ie, monkey human) and the exact location of vector exposure that results in human transmission of especially across different parts of Asia. In particular, uncertainty exists as to whether transmission is occurring predominately in the forest, farms at the forest-fringe, or villages, and the degree of transmission that is peri-domestic or domestic. Grigg and colleagues noted that having long grass around the house, and having open eaves or gaps in walls are associated with increased risk of . Similarly the use of indoor residual spraying, which was only implemented in 94 (41%) of the 229 cases, was associated with a significant urokinase in risk. They also found that the use of bednets by 177 (78%) cases, seemed to have only a marginal effect on risk. These findings are generally supportive of those of Manin and colleagues who identified peri-domestic transmission as being a more greater problem than domestic transmission. Together these studies show that greater benefits might result from improving housing and cutting back peri-domestic vegetation than from intensifying indoor residual spraying and bednet distribution. Wong and colleagues have described higher densities of in villages than in farming areas and forests, but that mosquito longevity, which is crucial for development, was higher in farming areas and forests. Brant and colleagues have also described a preference of to bite humans at ground level rather than high in the forest canopy. Thus, the likelihood that the main place of transmission occurs outdoors at ground level in forested areas was strongly supported by the findings of Grigg and colleagues, who showed that recent clearing of vegetation was a high-risk activity, as was sleeping outside the house, even though this was relatively infrequent; only 33 (15%) of cases. Recent awareness of the presence of monkeys was also a strong predictor of risk, further suggesting a high likelihood of monkey-to-human transmission as the predominant transmission pathway, rather than human-to-human transmission. This study by Grigg and colleagues provides quantifiable risk estimates for a wide range of variables relevant to the transmission of to humans. There are now a series of studies shedding light on the transmission dynamics of in Sabah, but further research is needed in this area and in other parts of southeast Asia where humans live in the forest or on the forest fringe, sharing their habitat with -infected macaques and their Anopheline vectors. In particular, further research is needed to better understand the ecological interactions that place people at risk of and the measures that can be implemented to minimise these risks. This will also be greatly aided by improving diagnostics and surveillance for this infection so that hot spots of transmission can be rapidly and precisely identified.
Bisphenols are used in the polymerisation of polycarbonate plastics and production of epoxy resins. Bisphenol A (BPA) was first synthesised by Alexander Dianin in 1891, and was considered for use as a pharmaceutical oestrogen for pregnant women, but was not sufficiently potent, and eventually diethylstilbestrol was used instead. Increasing evidence from the past two decades suggest that synthetic chemicals represent an underrecognised third key factor in the obesity epidemic worldwide, alongside diet and physical activity. Bisphenols are one major category of chemicals now recognised as obesogens. Laboratory studies have documented that BPA makes fat cells bigger and inhibits function of adiponectin. Cross-sectional and longitudinal human studies have also associated BPA exposure with obesity in children and adults. Notably, human studies have not consistently identified the key periods of susceptibility. Differences in results between studies might be the result of leveraging a limited number of spot urine samples in pregnancy as a proxy of exposure. Given that the half-life of BPA is generally 24–48 h, use of a modest number of spot samples introduces exposure imprecision that can influence statistical results.