Objective To explore the mechanism of SH?SY5Y mitochondrial dysfunction treated by manganese to find a new potential therapeutic target. Methods Transmission Electron Microscopy(TEM)to observe the morphology of mitochondria. Cell treated with 250μmol/L for periods of time(2 h, 4 h, 6 h)while mitochondrial membrane potential(MMP)and ROS can be detected by FCM and fluorescence microplate reader. Results After treating with MnCl2 in 6 h, TEM images showed early vacuoles, lamellar structures of SH?SY5Y cells. Then test the mitochondrial membrane potential and showed that MMP would be decreased gradually. Meanwhile, analysis showed that in comparison with control, treatment group had a higher ROS level respectively (P < 0.05). Conclusion MnCl2 can cause mitochondrial damage through a mechanism closely related to disrupt the MMP or generate abundant ROS.

Aiming at the continuous advancement and deepening of curriculum ideological and political education in medical courses, taking the recent outbreak of public health emergency as an example, this paper expounds the feasibility of taking public health emergencies as typical cases of ideological and political education in public health courses in medical colleges from medical ethics, national spirit, policy guidelines, medical and health administrative system, social benefits and economic evaluation, scientific research collaboration, international cooperation and other aspects, in order to realize the simultaneous development of professional education and ideological and political education, and cultivate more high-quality medical talents with both merit and talent.

The circadian rhythm is commonly present in mammals, and its maintenance is regulated by clock genes. In recent years, an increasing number of studies have shown that the polymorphism and expression of clock genes are abnormal in patients with Parkinson's disease. This article reviews the research progress of clock genes, CLOCK, BMAL1, PER, REV-ERBα, and CRY, as well as the pathogenesis of Parkinson's disease, which is helpful to further explore the role of clock genes and circadian rhythm disorders in the pathogenesis of Parkinson's disease. It provides ideas for further research on the mechanism of Parkinson's disease.

Background Manganese (Mn) is one of the environmental factors of Parkinson's disease (PD), and long-term exposure to Mn can cause nerve damage. It is important to explore the common mechanism of neurotoxic effects of Mn and neurodegenerative diseases (NDD), especially PD, for early diagnosis of the disease. Objective To comprehensively analyze the core messenger RNA (mRNA)-microRNAs (miRNAs) co-expressed in frontal cortex of NDD patients and neuronal cells exposed to Mn via bioinformatics, and to reveal the potential common mechanism between Mn-induced neurotoxicity and NDD, especially PD. Methods Difference of the mRNAs from frontal cortex of NDD patients (GSE150696) and human neuroblastoma (SH-SY5Y) cells exposed to Mn were analyzed by R software; Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed on the overlapping differentially expressed genes (DEGs). The miRNAs were predicted using the miRNet database, mRNA-miRNA interactions were identified by the starBase and miRTarBase databases, and mRNA-miRNA regulatory networks were constructed with Cytoscape software. The core miRNAs associated with PD (GSE77667) were incorporated into Weighted Gene Co-Expression Network Analysis (WGCNA) and the mRNA-miRNA regulatory network was comparatively analyzed. Results A total of 34 overlapping DEGs were identified in the frontal cortical of NDD patients and the neuronal cells exposed to Mn, mainly enriched in interleukin-17 (IL-17) signaling pathway, cyclic adenosine monophosphate (cAMP) signaling pathway, and primary immunodeficiency. Based on the results of database prediction, 52 miRNAs with 71 pairs of interaction relationships were finally included to construct the miRNA-mRNA regulatory network. Six core miRNAs were screened by WGCNA: hsa-let-7i-5p, hsa-mir-155-5p, hsa-mir-219-2-3p, hsa-mir-221-3p, hsa-mir-485-3p, and hsa-mir-509-3-5p, among which hsa-let-7i-5p interacted with the target gene FBXW2 and hsa-mir-155-5p interacted with the target gene CCL2. The results of the KEGG analysis indicated that CCL2 was closely related to the IL-17 signaling pathway. Conclusion There are similar molecular regulatory mechanisms involved in the neurotoxicity of Mn and NDD, and the IL-17 signaling pathway may play a role in Mn-related NDD through CCL2 and hsa-mir-155-5p.

Objective:To evaluate the effects of fine particle matter(PM2.5)and ozone(O3)com-bined exposure on adenosine triphosphate(ATP)amount and ATPase activities in nasal mucosa of Spra-gue Dawley(SD)rats.Methods:Twenty male SD rats were divided into control group(n=10)and exposure group(n=10)by random number table method.The rats were fed in the conventional clean environment and the air pollutant exposure system established by our team,respectively,and exposed for 208 d.During the exposure period,the concentrations of PM2 5 and O3 in the exposure system were moni-tored,and a comprehensive assessment of PM2 5 and O3 in the exposure system was conducted by combi-ning self-measurement and site data.On the 208 d of exposure,the core,liver,spleen,kidney,testis and other major organs and nasal mucosal tissues of the rats were harvested.Each organ was weighed and the organ coefficient calculated.The total amount of ATP was measured by bioluminescence,and the ac-tivities of Na+-K+-ATPase and Ca2+-ATPase were detected by spectrophotometry.The t test of two inde-pendent samples was used to compare the differences among the indicator groups.Results:From the 3rd week to the end of exposure duration,the body weight of the rats in the exposure group was higher than that in the control group(P＜0.05),and there was no significant difference in organ coefficients be-tween the two groups.The average daily PM2 5 concentration in the exposure group was(30.68±19.23)μg/m3,and the maximum 8 h ozone concentration(O3-8 h)was(82.45±35.81)μg/m3.The chemi-luminescence value(792.4±274.1)IU/L of ATP in nasal mucosa of the rats in the exposure group was lower than that in the control group(1 126.8±218.1)IU/L.The Na+-K+-ATPase activity(1.53±0.85)U/mg in nasal mucosa of the rats in the exposure group was lower than that in the control group(4.31±1.60)U/mg(P＜0.05).The protein content of nasal mucosa in the control group and the exposure group were(302.14±52.51)mg/L and(234.58±53.49)mg/L,respectively,and the ac-tivity of Ca2+-ATPase was(0.81±0.27)U/mg and(0.99±0.73)U/mg,respectively.There was no significant difference between the groups.Conclusion:The ability of power capacity decreased in the rat nasal mucossa under the sub-chronic low-concentration exposure of PM2 5 and O3.