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Background Previous studies using meta-analysis to explore the relationship between air pollution exposure and ischemic stroke (IS) mostly focus on particulate matter-related themes, few include gaseous pollutants in the study, and subgroup analyses of factors such as different lag days, seasons, and genders are rarely been reported. Objective To quantitatively evaluate the relationships between short-term exposures to 6 common air pollutants, including fine particulate matter (PM2.5), inhalable particulate matter (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3), and the incidence of IS. Methods A systematic search was conducted to collect literature studying the 6 common air pollutants and IS published up to May 1, 2022 in 6 databases (China Journal Full-text Database, China Biology Medicine Disc, PubMed, Cochrane Library, Web of Science, and Embase). Literature quality evaluation was performed using the Newcastle-Ottawa Scale. Stata 16.0 software was used to conduct meta-analysis including heterogeneity test, combined effect size, meta-regression, subgroup analysis, sensitivity analysis, and publication bias test. Results A total of 33 articles were qualified for inclusion. The total number of samples included in the literature was 7195631. The meta-analysis results showed that short-term exposures to PM2.5 (OR=1.0082, 95%CI: 1.0049−1.0116), PM10 (OR=1.0017, 95%CI: 1.0008−1.0026), CO (OR=1.0328, 95%CI: 1.0231−1.0426), NO2 (OR=1.0150, 95%CI: 1.0079−1.0222), SO2 (OR=1.0158, 95%CI: 1.0078-1.0238), and O3 (OR=1.0017, 95%CI: 1.0003−1.0032) were associated with an increased risk of IS. PM10 and O3 increased the risk of IS in both lag0 and lag1, while PM2.5, CO, NO2, and SO2 all showed an associated increased risk of IS only in lag0. The results of sensitivity analysis showed stable results for all pollutants studied, and there was no publication bias in the literature on the association of the remaining five pollutants with IS incidence except for the PM2.5-related literature. Conclusion Short-term exposures to PM2.5, PM10, CO, NO2, SO2, and O3 may increase the incidence of IS, with this risk showing the most significant level on the day of IS onset.
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In recent years, the incidence of stroke increased year by year and the research on post-stroke epilepsy (PSD) is also increasing.In addition to the type, location, and severity of stroke, the occurrence of PSD is also associated with small vessel disease and genetic factors;however, the exact pathophysiological mechanisms are not very clear.This article reviews the risk factors and pathophysiological mechanisms of PSD.
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Objective To study the effect of allicin on the growth and radiosensitivity of human pancreatic carcinoma BXPC3 cells.Methods BXPC3 cells were exposed to X-rays in the presence or absence of allicin.Cell proliferation was measured by MTT assay.Cell cycle distribution and apoptosis were detected by flow cytometry assay.Cell radiosensitivity and the influence of allicin on it was evaluated by colony formation assay.The expressions of Bax and Bcl-2 proteins were assayed by RT-PCR and Western blot.Results IC50 values of allicin on cell growth were 76.24,58.34 and 43.58 μmol/L under 12,24 and 48 h treatment,respectively.Treatment of cells with allicin obviously inhibited cell growth after irradiation and hence increased radiosensitivity (t =2.74,P ＜ 0.05).This treament also enhanced radiation-induced cell cycle arrest at G2/M phase (t =11.41,P ＜0.05),apoptosis induction (t =12.36,P ＜ 0.05),and Bax expression (t =4.83,P ＜ 0.05),but it decreased Bcl-2 expression (t =3.69,P ＜ 0.05).Conclusions Allicin could inhibit cell growth,induce cell cycle arrest and apoptosis via Bax/Bcl-2 pathway and hence increases radiosensitivity of BXPC3 cells.
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Objective To observe the expression of peroxisome proliferator-activated receptor γ (PPARγ) in hippocampus neurons in rats after different time of neuron oxygen deprivation/oxygen supply, and to investigate the role of PPARγ in neuron ischemia reperfusion injury.Methods One day old newborn SD rats were chosen. Primary cultured hippocampus neurons were used to establish neuron ischemic reperfusion model in vitro by oxygen and glucose depriving 15 minutes and supplying again, and then the neuron structure was observed by transmission electron microscope of JEM-200EX.The expression of PPARγ mRNA and protein were detected by RT-PCR and Western blot, respectively.Results Neuron structure was damaged after neuron oxygen deprivation/oxygen supply. There was no significant difference between 0 h oxygen supply group and the control group.The expression of PPARγ was decreased both at mRNA and protein level after 6 h of oxygen supply. The difference between 6 h oxygen supply group and the control group was significant(P<0.01), which decreased with the length of reperfusion and the lowest was at 48 h after the reperfusion. The difference among the different reperfusion groups and the control group was significant(P<0.01). Conclusion PPARγ may participate in the pathological damage course of neuron ischemical reperfusion injury, and may become a new intervention target of treatment for ischemic cerebrovascular disease.