Effects of short-term air pollution exposure and physical activity on neural damage in the elderly / 环境与职业医学

Background Emerging evidence has shown the damage of air pollution and the benefits of physical activity to human health, and the effects of air pollution and physical activity on the nervous system need more research. Objective To explore the effects of short-term air pollution exposure and physical activity on neural damage biomarkers in healthy elderly. Methods Using a design of panel study, physically and mentally healthy retired employees were recruited from Xinxiang Medical University, and were followed up five times regularly from December 2018 to April 2019. The demographic characteristics and physical activity information were obtained by questionnaire, and the weekly physical activity level was calculated according to intensity and duration of physical activity. Biomarkers of neural damage in serum were measured, including brain-derived neurotrophic factor (BDNF), neurofilament light chain (NF-L), neuron specific enolase (NSE), protein gene product 9.5 (PGP9.5), and S100 calcium-binding protein B (S100B). Air pollution data (including PM2.5, PM10, O3, SO2, CO, and NO2) of the follow-up period were collected. Generalized estimation equation was used to analyze the association of air pollution concentration and physical activity level with the concentration of neural damage biomarkers. Results A total of 29 volunteers were included in the study, with an average age of (63.5±5.9) years; there were 11 men accounting for 37.93%; more than half of them (62.07%) received above junior middle school education; the mean physical activity level was (80.23±54.51) MET-h·week−1. The daily average concentrations of PM2.5, PM10, O3, SO2, CO, and NO2 during the study period were (68.27±60.98) μg·m−3, (130.57±58.71) μg·m−3, (36.86±13.89) μg·m−3, (17.86±10.59) μg·m−3, (4.94±1.34) mg·m−3, and (50.83±8.03) μg·m−3, respectively. The average serum concentrations of BDNF, NF-L, NSE, PGP9.5, and S100B were (139.12±46.71) μg·L−1, (402.60±183.31) ng·L−1, (11.26±10.32) ng·L−1, (14.32±13.57) ng·L−1, and (127.57±41.74) ng·L−1, respectively. The results of generalized estimation equation showed that a higher concentration of PM2.5 or O3 was associated with increased serum NSE (OR=1.359, 95%CI: 1.224-1.509, P<0.001; OR=1.286, 95%CI: 1.076-1.537, P=0.006), while a higher concentration of NO2 was associated with decreased serum NSE (OR=0.692, 95%CI: 0.549-0.873, P=0.002); a higher concentration of O3 or SO2 was related to the reduction of serum NF-L concentration (OR=0.855, 95%CI: 0.740-0.989, P=0.035; OR=0.813, 95%CI: 0.700-0.946, P=0.007); a higher concentration of NO2 was associated with decreased PGP9.5 in serum (OR=0.866, 95%CI: 0.777-0.965, P=0.009); a higher level of physical activity was associated with increased serum S100B (OR=1.038, 95%CI: 1.003-1.074, P=0.034); and no significant association of physical activity level or air pollution with BDNF (P>0.05). Conclusion Acute exposure to air pollution and high-level physical activity might affect the neural damage of elderly populations. Specifically, particulate matter (PM2.5) could increase NSE, while gaseous pollutants (O3, NO2, and SO2) could decrease NF-L and PGP9.5.

Effects of methamphetamine acute exposure on neural damage / 中华急诊医学杂志

Objective To explore the neural damage induced by acute exposure to methamphetamine (METH).Methods The mice were administrated with METH,then the stereotyped behavior of mice was evaluated,and spatial recognition memory was analyzed by Y-maze test.In addition,nitric oxide synthase (NOS) activity was detected by kit,and the apoptotic proteins including Bax,Bcl-2,Caspase-3 were assayed by using Western blot.The DNA injury induced by METH was observed by using the comet assay.Moreover,mitochondrial membrane potential was detected to assess the toxic effects of METH on mitochondria by JC-1.With the Western blot assay,the phosphorylation of MAPK signaling pathways were also investigated.Results Acute METH exposure significantly increased the stereotyped behavior in mice,and spatial recognition ability of mice was obviously decreased.On the molecular level,total nitric oxide synthase (TNOS) and induced nitric oxide synthase (iNOS) were increased,and the apoptotic proteins,such as Bax and cleaved caspase-3 were markedly enhanced.With the comet assay,it showed that METH exposure resulted in DNA damage.In parallel,mitochondrial membrane was damaged which manifested as mitochondrial membrane potential decreased.With the western blot,It was further found that METH enhanced the activation of MAPKs.However,p38 MAPK signahng pathway was demonstrated to be the only one factor involved in METH-induced neural damage.Conclusion METH induced neural damage,and MAPK signaling pathways might be involved in this process,since inhibition of p38 MAPK signaling pathway significantly ameliorated METH-induced neural damage.

Ototoxicity of dihydrostreptomycin and combined preparations

This paper is a study of the ototoxicity or sensory-neural damage produced by dihydrostreptomycin and the combined preparation on 500 patients treated for pulmonary tuberculosis for a period of observation extending from 3 months to four years. The dose employed was 1 gm. once daily for 1 month, subsequently reduced to twice a week. (Summary)