The seasonality of acute coronary syndrome and its relations with climatic parameters.

BACKGROUND: Most research on the seasonality of acute coronary syndrome (ACS) has been were reported from hospital-based data. We aimed to investigate the seasonal distribution of ACS in Beijing and to elucidate the relations between ACS occurrence and climatic parameters in a prehospital setting. METHODS: We retrospectively reviewed the electronic prehospital medical records from the Beijing's emergency medical service system spanning August 1, 2005, to July 31, 2007. Case data were analyzed by month and season with χ² test. The effects of climatic factors on the occurrence of ACS were analyzed by Poisson regression with generalized linear model. RESULTS: During the 2-year study period, a total of 7037 ACS events were identified, including 4135 male patients (58.8%) and 2902 female patients (41.2%). Significant variations were observed in the monthly (P < .001) and seasonal (P < .001) distribution of ACS. The highest seasonal incidence occurred in winter and lowest in autumn. Significant negative correlations were noticed between the number of ACS events and daily mean temperature (P < .001) and between the number of ACS events and barometric pressure (P < .001). Comparing to the baseline level (temperature of 25°C to approximately 31°C; barometric pressure of 1026 to approximately 1048 hectopascal (hPa)), an increase of 41.3% of daily ACS incidence was associated with temperature lower than 2°C (-10.0°C to approximately 2.0°C), and an increase of 19.8% was associated with barometric pressure under 1006 hPa (991.0 to approximately 1006 hPa). CONCLUSIONS: There are clear monthly and seasonal rhythms of ACS in Beijing metropolitan area. Temperature and barometric pressure are negatively related with the occurrence of ACS.

Domicile-related carbon monoxide poisoning in cold months and its relation with climatic factors.

BACKGROUND: Many studies have identified strong correlations between winter months and acute, unintentional carbon monoxide (CO) poisoning. In this study, we aimed to investigate the incidence pattern of acute domicile-related CO poisoning in Beijing and its relation with climatic factors. METHODS: Data on CO poisoning were collected from the emergency medical service system during August 1, 2005, to July 31, 2007, in Beijing. Variations of the monthly and seasonal distribution of CO poisoning occurrences were examined with χ(2) testing. Climatic data including temperature, barometric pressure, humidity, wind speed, and visibility were obtained from the Beijing Meteorological Bureau. Correlations between the occurrence of CO poisoning and mean of each meteorological parameter spanning 3 days were analyzed with partial correlation test, with related parameters controlled. RESULTS: Significant differences were found among the cases occurring each month of the year (P < .001). The monthly caseload reached the peak and the nadir in January and in September, respectively. During the cold period, 3331 patients were recorded, accounting for 88.4% of the total cases of the 2-year study period. Among the 5 climatic parameters, only temperature had a significant inverse correlation with the occurrence of CO poisoning (P < .001, r = -0.467). CONCLUSIONS: The incidences of CO poisoning were highest during winter, particularly during the time period when charcoal or coal use for indoor heating would be most prevalent in Beijing.

Neurotensin stimulates IL-8 expression in human colonic epithelial cells through Rho GTPase-mediated NF-kappa B pathways.

Neurotensin (NT), a neuropeptide highly expressed in the gastrointestinal tract, participates in the pathophysiology of intestinal inflammation. We recently showed that NT stimulates interleukin-8 (IL-8) expression in NCM460 nontransformed human colonic epithelial cells via both mitogen-activating protein kinase (MAPK)- and NF-kappaB-dependent pathways. However, the molecular mechanism by which NT induces expression of proinflammatory cytokines such as IL-8 has not been investigated. In this study we show that inhibition of endogenous Rho family proteins (RhoA, Rac1, and Cdc42) by their respective dominant negative mutants inhibits NT-induced IL-8 protein production and promoter activity. Western blot experiments demonstrated that NT strongly activated RhoA, Rac1, and Cdc42. Overexpression of the dominant negative mutants of RhoA, Rac1, and Cdc42 significantly inhibited NT-induced NF-kappaB-dependent reporter gene expression and NF-kappaB DNA binding activity. NT also stimulated p38 MAPK phosphorylation, and overexpression of dominant negative mutants of RhoA, Rac1, and Cdc42 did not significantly alter p38 and ERK1/2 phosphorylation in response to NT. Together, our findings indicate that NT-stimulated IL-8 expression is mediated via a Rho-dependent NF-kappaB-mediated pathway.

Substance P-stimulated interleukin-8 expression in human colonic epithelial cells involves Rho family small GTPases.

Interaction of the neuropeptide substance P (SP) and its neurokinin-1 receptor (NK-1R) plays an important role in the pathophysiology of intestinal inflammation. SP is known to stimulate production of interleukin (IL)-6 and IL-8 in the U-373-MG human astrocytoma cell line via activation of p38 MAPK (mitogen-activated protein kinase) and nuclear factor (NF)-kappaB, respectively. However, the signalling mechanisms by which SP-NK-1R interaction induces NF-kappaB activation and IL-8 expression are still not clear. In this study we demonstrate that SP stimulates IL-8 secretion and IL-8 promoter activity in the NCM460 non-transformed human colonic epithelial cell line transfected with NK-1R cDNA. Our results indicate that inhibition of endogenous Rho family proteins (RhoA, Rac1 and Cdc42) by their respective dominant negative mutants significantly decreases SP-induced IL-8 secretion and IL-8 promoter activity. We also demonstrate that SP rapidly activates RhoA, Rac1 and Cdc42 and that co-expression of the dominant negative mutants of RhoA, Rac1 and Cdc42 in NK-1R cDNA-transfected NCM460 cells significantly inhibits SP-induced NF-kappaB-dependent gene expression. These results demonstrate that Rho family small GTPases RhoA, Rac1 and Cdc42 are novel signal transducers for SP-stimulated IL-8 expression.