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Malaria has been a heavy social and health burden in the remote and poor areas in southern China. Analyses of malaria epidemic patterns can uncover important features of malaria transmission. This study identified spatial clusters, seasonal patterns, and geographic variations of malaria deaths at a county level in Yunnan, China, during 1991–2010. A discrete Poisson model was used to identify purely spatial clusters of malaria deaths. Logistic regression analysis was performed to detect changes in geographic patterns. The results show that malaria mortality had declined in Yunnan over the study period and the most likely spatial clusters (relative risk [RR] = 23.03–32.06, P < 0.001) of malaria deaths were identified in western Yunnan along the China–Myanmar border. The highest risk of malaria deaths occurred in autumn (RR = 58.91, P < 0.001) and summer (RR = 31.91, P < 0.001). The results suggested that the geographic distribution of malaria deaths was significantly changed with longitude, which indicated there was decreased mortality of malaria in eastern areas over the last two decades, although there was no significant change in latitude during the same period. Public health interventions should target populations in western Yunnan along border areas, especially focusing on floating populations crossing international borders.

BACKGROUND Malaria remains a public health problem in the remote and poor area of Yunnan Province, China. Yunnan faces an increasing risk of imported malaria infections from Mekong river neighboring countries. This study aimed to identify the high risk area of malaria transmission in Yunnan Province, and to estimate the effects of climatic variability on the transmission of Plasmodium vivax and Plasmodium falciparum in the identified area. METHODS We identified spatial clusters of malaria cases using spatial cluster analysis at a county level in Yunnan Province, 2005-2010, and estimated the weekly effects of climatic factors on P. vivax and P. falciparum based on a dataset of daily malaria cases and climatic variables. A distributed lag nonlinear model was used to estimate the impact of temperature, relative humidity and rainfall up to 10-week lags on both types of malaria parasite after adjusting for seasonal and long-term effects. RESULTS The primary cluster area was identified along the China-Myanmar border in western Yunnan. A 1°C increase in minimum temperature was associated with a lag 4 to 9 weeks relative risk (RR), with the highest effect at lag 7 weeks for P. vivax (RR = 1.03; 95% CI, 1.01, 1.05) and 6 weeks for P. falciparum (RR = 1.07; 95% CI, 1.04, 1.11); a 10-mm increment in rainfall was associated with RRs of lags 2-4 weeks and 9-10 weeks, with the highest effect at 3 weeks for both P. vivax (RR = 1.03; 95% CI, 1.01, 1.04) and P. falciparum (RR = 1.04; 95% CI, 1.01, 1.06); and the RRs with a 10% rise in relative humidity were significant from lag 3 to 8 weeks with the highest RR of 1.24 (95% CI, 1.10, 1.41) for P. vivax at 5-week lag. CONCLUSIONS Our findings suggest that the China-Myanmar border is a high risk area for malaria transmission. Climatic factors appeared to be among major determinants of malaria transmission in this area. The estimated lag effects for the association between temperature and malaria are consistent with the life cycles of b

Climate change is affecting and will increasingly influence human health and wellbeing. Children are particularly vulnerable to the impact of climate change. An extensive literature review regarding the impact of climate change on children’s health was conducted in April 2012 by searching electronic databases PubMed, Scopus, ProQuest, ScienceDirect, and Web of Science, as well as relevant websites, such as IPCC and WHO. Climate change affects children’s health through increased air pollution, more weather-related disasters, more frequent and intense heat waves, decreased water quality and quantity, food shortage and greater exposure to toxicants. As a result, children experience greater risk of mental disorders, malnutrition, infectious diseases, allergic diseases and respiratory diseases. Mitigation measures like reducing carbon pollution emissions, and adaptation measures such as early warning systems and post-disaster counseling are strongly needed. Future health research directions should focus on: (1) identifying whether climate change impacts on children will be modified by gender, age and socioeconomic status; (2) refining outcome measures of children’s vulnerability to climate change; (3) projecting children’s disease burden under climate change scenarios; (4) exploring children’s disease burden related to climate change in low-income countries, and ; (5) identifying the most cost-effective mitigation and adaptation actions from a children’s health perspective.

Objectives Heatwaves can have significant health consequences resulting in increased mortality and morbidity. However, their impact on people living in tropical/subtropical regions remains largely unknown. This study assessed the impact of heatwaves on mortality and emergency hospital admissions (EHAs) from non-external causes (NEC) in Brisbane, a subtropical city in Australia. Methods We acquired daily data on weather, air pollution and EHAs for patients aged 15 years and over in Brisbane between January 1996 and December 2005, and on mortality between January 1996 and November 2004. A locally derived definition of heatwave (daily maximum ≥37°C for 2 or more consecutive days) was adopted. Case–crossover analyses were used to assess the impact of heatwaves on cause-specific mortality and EHAs. Results During heatwaves, there was a statistically significant increase in NEC mortality (OR 1.46; 95% CI 1.21 to 1.77), cardiovascular mortality (OR 1.89; 95% CI 1.44 to 2.48), diabetes mortality in those aged 75+ (OR 9.96; 95% CI 1.02 to 96.85), NEC EHAs (OR 1.15; 95% CI 1.07 to 1.23) and EHAs from renal diseases (OR 1.41; 95% CI 1.09 to 1.83). The elderly were found to be particularly vulnerable to heatwaves (eg, for NEC EHAs, OR 1.24 for 65–74-year-olds and 1.39 for those aged 75+). Conclusions Significant increases in NEC mortality and EHAs were observed during heatwaves in Brisbane where people are well accustomed to hot summer weather. The most vulnerable were the elderly and people with cardiovascular, renal or diabetic disease.

OBJECTIVE: This paper reviews the epidemiological evidence on the relationship between ambient temperature and morbidity. It assesses the methodological issues in previous studies, and proposes future research directions. DATA SOURCES AND DATA EXTRACTION: We searched the PubMed database for epidemiological studies on ambient temperature and morbidity of non-communicable diseases published in refereed English journals prior to June 2010. 40 relevant studies were identified. Of these, 24 examined the relationship between ambient temperature and morbidity, 15 investigated the short-term effects of heatwave on morbidity, and 1 assessed both temperature and heatwave effects. DATA SYNTHESIS: Descriptive and time-series studies were the two main research designs used to investigate the temperature–morbidity relationship. Measurements of temperature exposure and health outcomes used in these studies differed widely. The majority of studies reported a significant relationship between ambient temperature and total or cause-specific morbidities. However, there were some inconsistencies in the direction and magnitude of non-linear lag effects. The lag effect of hot temperature on morbidity was shorter (several days) compared to that of cold temperature (up to a few weeks). The temperature–morbidity relationship may be confounded and/or modified by socio-demographic factors and air pollution. CONCLUSIONS: There is a significant short-term effect of ambient temperature on total and cause-specific morbidities. However, further research is needed to determine an appropriate temperature measure, consider a diverse range of morbidities, and to use consistent methodology to make different studies more comparable.

In this communication, we report a newly developed cell pattering methodology by a silicon-based stencil, which exhibited advantages such as easy handling, reusability, hydrophilic surface and mature fabrication technologies. Cell arrays obtained by this method were used to investigate cell growth under a temperature gradient, which demonstrated the possibility of studying cell behavior in a high-throughput assay.

The relationship between temperature and mortality is non-linear and the effect estimates depend on the threshold temperatures selected. However, little is known about whether threshold temperatures differ with age or cause of deaths in the Southern Hemisphere. We conducted polynomial distributed lag non-linear models to assess the threshold temperatures for mortality from all ages (Dall), aged from 15 to 64 (D15-64), 65- 84(D65-84), ≥85 years (D85+), respiratory (RD) and cardiovascular diseases (CVD) in Brisbane, Australia, 1996–2004. We examined both hot and cold thresholds, and the lags of up to 15 days for cold effects and 3 days for hot effects. Results show that for the current day, the cold threshold was 20°C and the hot threshold was 28°C for the groups of Dall, D15-64 and D85+. The cold threshold was higher (23°C) for the group of D65-84 and lower (21°C) for the group of CVD. The hot threshold was higher (29°C) for the group of D65-84 and lower (27°C) for the group of RD. Compared to the current day, for the cold effects of up to 15-day lags, the threshold was lower for the group of D15-64, and the thresholds were higher for the groups of D65-84, D85+, RD and CVD; while for the hot effects of 3-day lags, the threshold was higher for the group of D15-64 and the thresholds were lower for the groups of D65-84 and RD. Temperature thresholds appeared to differ with age and death categories. The elderly and deaths from RD and CVD were more sensitive to temperature stress than the adult group. These findings may have implications in the assessment of temperature-related mortality and development of weather/health warning systems.

BACKGROUND: The relationship between temperature and mortality has been explored for decades and many temperature indicators have been applied separately. However, few data are available to show how the effects of different temperature indicators on different mortality categories, particularly in a typical subtropical climate. OBJECTIVE: To assess the associations between various temperature indicators and different mortality categories in Brisbane, Australia during 1996-2004. METHODS: We applied two methods to assess the threshold and temperature indicator for each age and death groups: mean temperature and the threshold assessed from all cause mortality was used for all mortality categories; the specific temperature indicator and the threshold for each mortality category were identified separately according to the minimisation of AIC. We conducted polynomial distributed lag non-linear model to identify effect estimates in mortality with one degree of temperature increase (or decrease) above (or below) the threshold on current days and lagged effects using both methods. RESULTS: Akaike's Information Criterion was minimized when mean temperature was used for all non-external deaths and deaths from 75 to 84 years; when minimum temperature was used for deaths from 0 to 64 years, 65-74 years, ≥ 85 years, and from the respiratory diseases; when maximum temperature was used for deaths from cardiovascular diseases. The effect estimates using certain temperature indicators were similar as mean temperature both for current day and lag effects. CONCLUSION: Different age groups and death categories were sensitive to different temperature indicators. However, the effect estimates from certain temperature indicators did not significantly differ from those of mean temperature.

Objective To quantify the lagged effects of mean temperature on deaths from cardiovascular diseases in Brisbane, Australia. Design Polynomial distributed lag models were used to assess the percentage increase in mortality up to 30 days associated with an increase (or decrease) of 1°C above (or below) the threshold temperature. Setting Brisbane, Australia. Patients 22 805 cardiovascular deaths registered between 1996 and 2004. Main outcome measures Deaths from cardiovascular diseases. Results The results show a longer lagged effect in cold days and a shorter lagged effect in hot days. For the hot effect, a statistically significant association was observed only for lag 0–1 days. The percentage increase in mortality was found to be 3.7% (95% CI 0.4% to 7.1%) for people aged ≥65 years and 3.5% (95% CI 0.4% to 6.7%) for all ages associated with an increase of 1°C above the threshold temperature of 24°C. For the cold effect, a significant effect of temperature was found for 10–15 lag days. The percentage estimates for older people and all ages were 3.1% (95% CI 0.7% to 5.7%) and 2.8% (95% CI 0.5% to 5.1%), respectively, with a decrease of 1°C below the threshold temperature of 24°C. Conclusions The lagged effects lasted longer for cold temperatures but were apparently shorter for hot temperatures. There was no substantial difference in the lag effect of temperature on mortality between all ages and those aged ≥65 years in Brisbane, Australia.

Background There has been increasing interest in assessing the impacts of temperature on mortality. However, few studies have used a case–crossover design to examine non-linear and distributed lag effects of temperature on mortality. Additionally, little evidence is available on the temperature-mortality relationship in China, or what temperature measure is the best predictor of mortality. Objectives To use a distributed lag non-linear model (DLNM) as a part of case–crossover design. To examine the non-linear and distributed lag effects of temperature on mortality in Tianjin, China. To explore which temperature measure is the best predictor of mortality; Methods: The DLNM was applied to a case¬−crossover design to assess the non-linear and delayed effects of temperatures (maximum, mean and minimum) on deaths (non-accidental, cardiopulmonary, cardiovascular and respiratory). Results A U-shaped relationship was consistently found between temperature and mortality. Cold effects (significantly increased mortality associated with low temperatures) were delayed by 3 days, and persisted for 10 days. Hot effects (significantly increased mortality associated with high temperatures) were acute and lasted for three days, and were followed by mortality displacement for non-accidental, cardiopulmonary, and cardiovascular deaths. Mean temperature was a better predictor of mortality (based on model fit) than maximum or minimum temperature. Conclusions In Tianjin, extreme cold and hot temperatures increased the risk of mortality. Results suggest that the effects of cold last longer than the effects of heat. It is possible to combine the case−crossover design with DLNMs. This allows the case−crossover design to flexibly estimate the non-linear and delayed effects of temperature (or air pollution) whilst controlling for season.

Although interests in assessing the relationship between temperature and mortality have arisen due to climate change, relatively few data are available on lag structure of temperature-mortality relationship, particularly in the Southern Hemisphere. This study identified the lag effects of mean temperature on mortality among age groups and death categories using polynomial distributed lag models in Brisbane, Australia, a subtropical city, 1996-2004. For a 1 °C increase above the threshold, the highest percent increase in mortality on the current day occurred among people over 85 years (7.2% (95% CI: 4.3%, 10.2%)). The effect estimates among cardiovascular deaths were higher than those among all-cause mortality. For a 1 °C decrease below the threshold, the percent increases in mortality at 21 lag days were 3.9% (95% CI: 1.9%, 6.0%) and 3.4% (95% CI: 0.9%, 6.0%) for people aged over 85 years and with cardiovascular diseases, respectively. These findings may have implications for developing intervention strategies to reduce and prevent temperature-related mortality.

Background: A number of studies have examined the relationship between high ambient temperature and mortality. Recently, concern has arisen about whether this relationship is modified by socio-demographic factors. However, data for this type of study is relatively scarce in subtropical/tropical regions where people are well accustomed to warm temperatures. Objective: To investigate whether the relationship between daily mean temperature and daily all-cause mortality is modified by age, gender and socio-economic status (SES) in Brisbane, Australia. Methods: We obtained daily mean temperature and all-cause mortality data for Brisbane, Australia during 1996–2004. A generalised additive model was fitted to assess the percentage increase in all deaths with every one degree increment above the threshold temperature. Different age, gender and SES groups were included in the model as categorical variables and their modification effects were estimated separately. Results: A total of 53,316 non-external deaths were included during the study period. There was a clear increasing trend in the harmful effect of high temperature on mortality with age. The effect estimate among women was more than 20 times that among men. We did not find an SES effect on the percent increase associated with temperature. Conclusions: The effects of high temperature on all deaths were modified by age and gender but not by SES in Brisbane, Australia.

Background: Many studies have illustrated that ambient air pollution negatively impacts on health. However, little evidence is available for the effects of air pollution on cardiovascular mortality (CVM) in Tianjin, China. Also, no study has examined which strata length for the time-stratified case–crossover analysis gives estimates that most closely match the estimates from time series analysis. Objectives: The purpose of this study was to estimate the effects of air pollutants on CVM in Tianjin, China, and compare time-stratified case–crossover and time series analyses. Method: A time-stratified case–crossover and generalized additive model (time series) were applied to examine the impact of air pollution on CVM from 2005 to 2007. Four time-stratified case–crossover analyses were used by varying the stratum length (Calendar month, 28, 21 or 14 days). Jackknifing was used to compare the methods. Residual analysis was used to check whether the models fitted well. Results: Both case–crossover and time series analyses show that air pollutants (PM10, SO2 and NO2) were positively associated with CVM. The estimates from the time-stratified case–crossover varied greatly with changing strata length. The estimates from the time series analyses varied slightly with changing degrees of freedom per year for time. The residuals from the time series analyses had less autocorrelation than those from the case–crossover analyses indicating a better fit. Conclusion: Air pollution was associated with an increased risk of CVM in Tianjin, China. Time series analyses performed better than the time-stratified case–crossover analyses in terms of residual checking.

We report evidence suggesting that methyltransferase SET8 plays a novel role in regulating cell cycle by suppressing DNA replication through histone binding. First, the distribution of SET8 is strongly cell cycle-dependent. SET8 was concentrated in the nucleus during G(1) and G(2) phases, and was excluded from the nucleus during S phase. Second, at G(1)/S transition, SET8 was degraded through ubiquitination via SCF/Skp2. Third, it was evident that the SET8 binds to the H4 N-terminal tail (H4NT) and blocks the acetylation of lysine residues K5, K8 and K12 of histone H4 during G1. Such a blockage can hinder DNA replication. Fourth, SET8 binds to hypoacetylated but not hyperacetylated H4NT. Finally, overexpressing the histone-binding domain of SET8 appeared to suppress DNA replication and arrest the cell cycle before the G(1)/S transition. Taken together, these findings suggest that SET8 can be a negative regulator of DNA replication and the destruction of SET8 is required for the onset of S phase.

The orienting reflex (OR) may involve the locus coeruleus - norepinephrine pathway (LC-NE). For example, a role for the LC-NE in attention and vigilance has been hypothesized, and neurons in the LC-NE of awake animals respond best to salient sensory stimuli. Stimulation of the LC-NE slows heart rate and desynchronizes electroencephalogram (EEG) (Miyawaki, 1993; Berridge & Foote, 1991), which are two components of the orienting reflex . Rats were chronically implanted for electrocardiogram (EKG) and EEG recordings. The OR was elicited in rats by taped rat vocalizations or continuous tone stimuli in a sound attenuating chamber. Norepinephrine was depleted by single N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP4) injections (50 mg/kg, i. p.), a selective neurotoxin for the LC-NE, and tested for an OR 11 to 17 days after injection. Central NE levels in control and DSP4 treated animals were determined by HPLC with electrochemical detection. NE concentrations were significantly reduced by DSP4 lesions by 60.9% (p < 0.005) in hippocampus and 49.1% (p < 0.05) in parietal cortex. Reduction of NE concentrations in hypothalamus (47.1%) and frontal cortex (42.7%) were not significant. In control animals (n=10) there was a 7% decrease (p < 0.05) during the 60-second rat vocalizations and a 6.1% decrease (p < 0.05) during the 60-second continuous tone within ten seconds after the onset of these orienting stimuli, as compared to baseline heart rate (10 seconds before stimuli), and heart rate remained significantly decreased (p < 0.05) for 40 seconds. Some habituation was seen in both cases. In addition, log absolute power of alpha frequencies (8 and 9 Hz) in the EEG were also suppressed significantly (p < 0.05) after onset of rat vocalizations in control animals (n=8), comparing five seconds of post-stimulus activity to five seconds of pre-stimulus baseline activity. In contrast, in the DSP4 treated rats (n=10), showed a small, non-significant decrease in heart r