996 resultados para Hot temperature


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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.

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The impact of climate change on the health of vulnerable groups such as the elderly has been of increasing concern. However, to date there has been no meta-analysis of current literature relating to the effects of temperature fluctuations upon mortality amongst the elderly. We synthesised risk estimates of the overall impact of daily mean temperature on elderly mortality across different continents. A comprehensive literature search was conducted using MEDLINE and PubMed to identify papers published up to December 2010. Selection criteria including suitable temperature indicators, endpoints, study-designs and identification of threshold were used. A two-stage Bayesian hierarchical model was performed to summarise the percent increase in mortality with a 1°C temperature increase (or decrease) with 95% confidence intervals in hot (or cold) days, with lagged effects also measured. Fifteen studies met the eligibility criteria and almost 13 million elderly deaths were included in this meta-analysis. In total, there was a 2-5% increase for a 1°C increment during hot temperature intervals, and a 1-2 % increase in all-cause mortality for a 1°C decrease during cold temperature intervals. Lags of up to 9 days in exposure to cold temperature intervals were substantially associated with all-cause mortality, but no substantial lagged effects were observed for hot intervals. Thus, both hot and cold temperatures substantially increased mortality among the elderly, but the magnitude of heat-related effects seemed to be larger than that of cold effects within a global context.

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The relationship between weather and mortality has been observed for centuries. Recently, studies on temperature-related mortality have become a popular topic as climate change continues. Most of the previous studies found that exposure to hot or cold temperature affects mortality. This study aims to address three research questions: 1. What is the overall effect of daily mean temperature variation on the elderly mortality in the published literature using a meta-analysis approach? 2. Does the association between temperature and mortality differ with age, sex, or socio-economic status in Brisbane? 3. How is the magnitude of the lag effects of the daily mean temperature on mortality varied by age and cause-of-death groups in Brisbane? In the meta-analysis, there was a 1-2 % increase in all-cause mortality for a 1ºC decrease during cold temperature intervals and a 2-5% increase for a 1ºC increment during hot temperature intervals among the elderly. Lags of up to 9 days in exposure to cold temperature intervals were statistically significantly associated with all-cause mortality, but no significant lag effects were observed for hot temperature intervals. In Brisbane, the harmful effect of high temperature (over 24ºC) on mortality appeared to be greater among the elderly than other age groups. The effect estimate among women was greater than among men. However, No evidence was found that socio-economic status modified the temperature-mortality relationship. The results of this research also show longer lag effects in cold days and shorter lag effects in hot days. For 3-day hot effects associated with 1°C increase above the threshold, the highest percent increases in mortality occurred among people aged 85 years or over (5.4% (95% CI: 1.4%, 9.5%)) compared with all age group (3.2% (95% CI: 0.9%, 5.6%)). The effect estimate among cardiovascular deaths was slightly higher than those among all-cause mortality. For overall 21-day cold effects associated with a 1°C decrease below the threshold, the percent estimates in mortality for people aged 85 years or over, and from cardiovascular diseases were 3.9% (95% CI: 1.9%, 6.0%) and 3.4% (95% CI: 0.9%, 6.0%), respectively compared with all age group (2.0% (95% CI: 0.7%, 3.3%)). Little research of this kind has been conducted in the Southern Hemisphere. This PhD research may contribute to the quantitative assessment of the overall impact, effect modification and lag effects of temperature variation on mortality in Australia and The findings may provide useful information for the development and implementation of public health policies to reduce and prevent temperature-related health problems.

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Objective: To examine the effects of extremely cold and hot temperatures on ischaemic heart disease (IHD) mortality in five cities (Beijing, Tianjin, Shanghai, Wuhan and Guangzhou) in China; and to examine the time relationships between cold and hot temperatures and IHD mortality for each city. Design: A negative binomial regression model combined with a distributed lag non-linear model was used to examine city-specific temperature effects on IHD mortality up to 20 lag days. A meta-analysis was used to pool the cold effects and hot effects across the five cities. Patients: 16 559 IHD deaths were monitored by a sentinel surveillance system in five cities during 2004–2008. Results: The relationships between temperature and IHD mortality were non-linear in all five cities. The minimum-mortality temperatures in northern cities were lower than in southern cities. In Beijing, Tianjin and Guangzhou, the effects of extremely cold temperatures were delayed, while Shanghai and Wuhan had immediate cold effects. The effects of extremely hot temperatures appeared immediately in all the cities except Wuhan. Meta-analysis showed that IHD mortality increased 48% at the 1st percentile of temperature (extremely cold temperature) compared with the 10th percentile, while IHD mortality increased 18% at the 99th percentile of temperature (extremely hot temperature) compared with the 90th percentile. Conclusions: Results indicate that both extremely cold and hot temperatures increase IHD mortality in China. Each city has its characteristics of heat effects on IHD mortality. The policy for response to climate change should consider local climate–IHD mortality relationships.

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As Earth's climate is rapidly changing, the impact of ambient temperature on health outcomes has attracted increasing attention in the recent time. Considerable number of excess deaths has been reported because of exposure to ambient hot and cold temperatures. However, relatively little research has been conducted on the relation between temperature and morbidity. The aim of this study was to characterize the relationship between both hot and cold temperatures and emergency hospital admissions in Brisbane, Australia, and to examine whether the relation varied by age and socioeconomic factors. It aimed to explore lag structures of temperature–morbidity association for respiratory causes, and to estimate the magnitude of emergency hospital admissions for cardiovascular diseases attributable to hot and cold temperatures for the large contribution of both diseases to the total emergency hospital admissions. A time series study design was applied using routinely collected data of daily emergency hospital admissions, weather and air pollution variables in Brisbane during 1996–2005. Poisson regression model with a distributed lag non-linear structure was adopted to assess the impact of temperature on emergency hospital admissions after adjustment for confounding factors. Both hot and cold effects were found, with higher risk of hot temperatures than that of cold temperatures. Increases in mean temperature above 24.2oC were associated with increased morbidity, especially for the elderly ≥ 75 years old with the largest effect. The magnitude of the risk estimates of hot temperature varied by age and socioeconomic factors. High population density, low household income, and unemployment appeared to modify the temperature–morbidity relation. There were different lag structures for hot and cold temperatures, with the acute hot effect within 3 days after hot exposure and about 2-week lagged cold effect on respiratory diseases. A strong harvesting effect after 3 days was evident for respiratory diseases. People suffering from cardiovascular diseases were found to be more vulnerable to hot temperatures than cold temperatures. However, more patients admitted for cardiovascular diseases were attributable to cold temperatures in Brisbane compared with hot temperatures. This study contributes to the knowledge base about the association between temperature and morbidity. It is vitally important in the context of ongoing climate change. The findings of this study may provide useful information for the development and implementation of public health policy and strategic initiatives designed to reduce and prevent the burden of disease due to the impact of climate change.

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To study the relation between temperature and mortality by estimating the temperature-related mortality in Beijing, Shanghai, and Guangzhou. METHODS: Data of daily mortality, weather and air pollution in the three cities were collected. A distributed lag nonlinear model was established and used in analyzing the effects of temperature on mortality. Current and future net temperature-related mortality was estimated. RESULTS: The association between temperature and mortality was J-shaped, with an increased death risk of both hot and cold temperature in these cities. The effects of cold temperature on health lasted longer than those of hot temperature. The projected temperature-related mortality increased with the decreased cold-related mortality. The mortality was higher in Guangzhou than in Beijing and Shanghai. CONCLUSION: The impact of temperature on health varies in the 3 cities of China, which may have implications for climate policy making in China.

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Colon-residing bacteria, such as vancomycin-resistant Enterococcus faecalis and Bacteroides fragilis, can cause a range of serious clinical infections. Photodynamic antimicrobial chemotherapy (PACT) may be a novel treatment option for these multidrug resistant organisms. The aim of this study was to formulate a Eudragit®-based drug delivery system, via hot melt extrusion (HME), for targeting colonic release of photosensitizer. The susceptibility of E. faecalis and B. fragilis to PACT mediated by methylene blue (MB), meso-tetra(N-methyl-4-pyridyl)porphine tetra-tosylate (TMP), or 5-aminolevulinic acid hexyl-ester (h-ALA) was determined, with tetrachlorodecaoxide (TCDO), an oxygen-releasing compound, added in some studies. Results show that, for MB, an average of 30% of the total drug load was released over a 6-h period. For TMP and h-ALA, these values were 50% and 16% respectively. No drug was released in the acidic media. Levels of E. faecalis and B. fragilis were reduced by up to 4.67 and 7.73 logs, respectively, on PACT exposure under anaerobic conditions, with increased kill associated with TCDO. With these formulations, photosensitizer release could potentially be targeted to the colon, and colon-residing pathogens killed by PACT. TCDO could be used in vivo to generate oxygen, which could significantly impact on the success of PACT in the clinic.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Maximal amounts of prodigiosin were synthesized in either minimal or complete medium after incubation of cultures at 27 C for 7 days. Biosynthesis of prodigiosin began earlier and the range of temperature for formation was greater in complete medium. No prodigiosin was formed in either medium when cultures were incubated at 38 C; however, after a shift to 27 C, pigmentation ensued, provided the period of incubation at 38 C was not longer than 36 hr for minimal medium or 48 hr for complete medium. Washed, nonpigmented cells grown in either medium at 38 C for 72 hr could synthesize prodigiosin when suspended in saline at 27 C when casein hydrolysate was added. These suspensions produced less prodigiosin at a slower rate than did cultures growing in casein hydrolysate at 27 C without prior incubation at 38 C. Optimal concentration of casein hydrolysate for pigment formation by suspensions was 0.4%; optimal temperature was 27 C. Anaerobic incubation, shift back to 38 C, killing cells by heating, or chloramphenicol (25 mug/ml) inhibited pigmentation. Suspensions of washed cells forming pigment reached pH 8.0 to 8.3 rapidly and maintained this pH throughout incubation for 7 days. Measurements of viable count and of protein, plus other data, indicated that cellular multiplication did not occur in suspensions of washed cells during pigment formation. By this procedure utilizing a shift down in temperature, biosynthesis of prodigiosin by washed cells could be separated from multiplication of bacteria.

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Silicon substrates coated with a bromide-terminated silane are transformed into highly reactive, cyclopentadiene covered analogues. These surfaces undergo rapid cycloaddition reactions with various dienophile-capped polymers. Mild heating of the substrates causes the retro-Diels-Alder reaction to occur, thus reforming the reactive cyclopentadiene surface, generating an efficiently switchable surface.

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OBJECTIVES: To examine the effect of thermal agents on the range of movement (ROM) and mechanical properties in soft tissue and to discuss their clinical relevance. DATA SOURCES: Electronic databases (Cochrane Central Register of Controlled Trials, MEDLINE, and EMBASE) were searched from their earliest available record up to May 2011 using Medical Subjects Headings and key words. We also undertook related articles searches and read reference lists of all incoming articles. STUDY SELECTION: Studies involving human participants describing the effects of thermal interventions on ROM and/or mechanical properties in soft tissue. Two reviewers independently screened studies against eligibility criteria. DATA EXTRACTION: Data were extracted independently by 2 review authors using a customized form. Methodologic quality was also assessed by 2 authors independently, using the Cochrane risk of bias tool. DATA SYNTHESIS: Thirty-six studies, comprising a total of 1301 healthy participants, satisfied the inclusion criteria. There was a high risk of bias across all studies. Meta-analyses were not undertaken because of clinical heterogeneity; however, effect sizes were calculated. There were conflicting data on the effect of cold on joint ROM, accessory joint movement, and passive stiffness. There was limited evidence to determine whether acute cold applications enhance the effects of stretching, and further evidence is required. There was evidence that heat increases ROM, and a combination of heat and stretching is more effective than stretching alone. CONCLUSIONS: Heat is an effective adjunct to developmental and therapeutic stretching techniques and should be the treatment of choice for enhancing ROM in a clinical or sporting setting. The effects of heat or ice on other important mechanical properties (eg, passive stiffness) remain equivocal and should be the focus of future study.

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Objectives To review the existing research on the effectiveness of heat warning systems (HWSs) in saving lives and reducing harm. Methods A systematic search of major databases was conducted, using “heat, heatwave, high temperature, hot temperature, OR hot climate” AND “warning system”. Results Fifteen articles were retrieved. Six studies asserted that fewer people died of excessive heat after HWS implementation. HWS was associated with reduction in ambulance use. One study estimated the benefits of HWS to be 468millionforsaving117livescomparedto210,000 costs of running the system. Eight studies showed that mere availability of HWS did not lead to behavioral changes. Perceived threat of heat dangers to self/others was the main factor related to heeding warnings and taking proper actions. However, costs and barriers associated with taking protective actions, such as costs of running air conditioners, were of significant concern particularly to the poor. Conclusions Research in this area is limited. Prospective designs applying health behavior theories should establish whether HWS can produce the health benefits they are purported to achieve by identifying the target vulnerable groups.

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Background Heatwaves have a significant impact on population health including both morbidity and mortality. In this study we examined the association between heatwaves and emergency hospital admissions (EHAs) for renal diseases in children (aged 0–14 years) in Brisbane, Australia. Methods Daily data on EHAs for renal diseases in children and exposure to temperature and air pollution were obtained for Brisbane city from January 1, 1996 to December 31, 2005. A time-stratified case-crossover design was used to compare the risks for renal diseases between heatwave and non-heatwave periods. Results There were 1565 EHAs for renal diseases in children during the study period. Heatwaves exhibited a significant impact on EHAs for renal diseases in children after adjusting for confounding factors (odds ratio: 3.6; 95% confidence interval: 1.4–9.5). The risk estimates differed with lags and the use of different heatwave definitions. Conclusions There was a significant increase in EHAs for renal diseases in children during heatwaves in Brisbane, a subtropical city where people are well accustomed to warm weather. This finding may have significant implications for pediatric renal care, particularly in subtropical and tropical regions.

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Os efeitos das temperaturas elevadas na saúde humana representam um problema de grande magnitude na saúde pública. A temperatura atmosférica e a poluição do ar são fatores de risco para as doenças crônicas não transmissíveis, em particular as doenças isquêmicas do coração. O estudo teve como objetivo analisar a associação entre a temperatura atmosférica e internações hospitalares por doenças cardíacas isquêmicas no município do Rio de Janeiro entre os anos de 2009 e 2013. Utilizaram-se modelos de séries temporais, via modelos aditivos generalizados, em regressão de Poisson, para testar a hipótese de associação. Como variáveis de controle de confusão foram utilizadas as concentrações de poluentes atmosféricos (ozônio e material particulado) e umidade relativa o ar; utilizou-se método de defasagem simples e distribuída para avaliar o impacto da variação de 1oC nas internações hospitalares diárias. No modelo de defasagem simples foram encontradas associações estatisticamente significativas para as internações por DIC no dia concorrente a exposição ao calor, tanto para a temperatura média quanto para a máxima. No modelo de defasagem distribuída polinomial, essa associação foi observada com 1 e 2 dias de defasagem e no efeito acumulado tanto para a temperatura média quanto para a máxima. Ao estratificarmos por faixa etária, as associações para as internações por DIC e exposição ao calor não foram estatisticamente significativas no modelo de defasagem simples para as temperaturas média e máxima. Em contrapartida, no modelo de defasagem distribuída polinomial, a correlação entre internações por DIC e exposição ao calor foi observada na faixa de 30 a 60 anos no efeito acumulado para a temperatura média; e com defasagem de 1 e 2 dias para 60 anos ou mais de idade para a temperatura média. Estes resultados sugerem associação positiva entre as internações hospitalares por doença cardíaca isquêmica e temperatura na cidade do Rio de Janeiro. Os resultados do presente estudo fornecem informações para o planejamento de investimentos de áreas urbanas climatizadas e para a preparação dos hospitais para receber emergências relacionadas aos efeitos de calor que é uma das consequências mais importantes das mudanças climáticas.

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Morphine induces antinociception by activating mu opioid receptors (muORs) in spinal and supraspinal regions of the CNS. (Beta)arrestin-2 (beta)arr2), a G-protein-coupled receptor-regulating protein, regulates the muOR in vivo. We have shown previously that mice lacking (beta)arr2 experience enhanced morphine-induced analgesia and do not become tolerant to morphine as determined in the hot-plate test, a paradigm that primarily assesses supraspinal pain responsiveness. To determine the general applicability of the (beta)arr2-muOR interaction in other neuronal systems, we have, in the present study, tested (beta)arr2 knock-out ((beta)arr2-KO) mice using the warm water tail-immersion paradigm, which primarily assesses spinal reflexes to painful thermal stimuli. In this test, the (beta)arr2-KO mice have greater basal nociceptive thresholds and markedly enhanced sensitivity to morphine. Interestingly, however, after a delayed onset, they do ultimately develop morphine tolerance, although to a lesser degree than the wild-type (WT) controls. In the (beta)arr2-KO but not WT mice, morphine tolerance can be completely reversed with a low dose of the classical protein kinase C (PKC) inhibitor chelerythrine. These findings provide in vivo evidence that the muOR is differentially regulated in diverse regions of the CNS. Furthermore, although (beta)arr2 appears to be the most prominent and proximal determinant of muOR desensitization and morphine tolerance, in the absence of this mechanism, the contributions of a PKC-dependent regulatory system become readily apparent.