Background: Glioma characterized by the high degree of drug resistance and the poor prognosis is the most common primary malignant tumors of the brain. And miRNA is involved in a variety of biological behaviors of tumors, enhancing or inhibiting the occurrence and development of tumors. Therefore, the present study aims to explore whether miR-155-5p can regulate autophagy and apoptosis of glioma through RICTOR. Methods: The significantly differential gene miR-155-5p was identified from the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo) databases GSE165937 and GSE138764 using bioinformatics analysis, and its expression was validated by quantitative real-time polymerase chain reaction (qRT-PCR). The putative target genes of miR-155-5p were predicted through interrogation of relevant databases, followed by identification of key target genes. Subsequently, core target genes were selected for functional enrichment analysis. The U87MG cell line was utilized as the experimental model and divided into Negative Control1 (NC1) group, Mimic group, Negative Control2 (NC2) group, Inhibitor group, and NC + 3-methyladenine (3-MA) group. The expression levels of miR-155-5p, RICTOR, P62, LC-3, Bax, Bcl-2, and Caspase-3 were assessed using qRT-PCR, cellular fluorescence imaging, and Western blotting; while apoptosis in the U87MG cell line was evaluated via flow cytometry. Results: The results showed that miR-155-5P was highly expressed in glioma cells, which could inhibit the expression of Bax, Caspase-3, LCII/LCI and Beclin-1, and increase the expression of Bcl2 and P62. Flow cytometry and cell fluorescence were used to verify the above results. Moreover, when U87MG cells treated with miR-155-5p inhibitor were inhibited by 3-MA, the results showed that miR-155-5p enhanced the anti-apoptotic ability of U87MG cells by regulating autophagy. In addition, the bioinformatics results show that miR-155-5p survival prognosis in glioma into a strong negative correlation, while the survival prognosis of RICTOR in glioma showed a strong positive correlation. The core target genes Kyoto Encyclopedia of Genes and Genomes (KEGG) mainly occurred in PI3K-AKT signaling pathway; in addition, qRT-PCR and Western blot confirmed the regulatory effect of miR-155-5P on RICTOR. Conclusions: MiR-155-5p regulates autophagy and apoptosis-related proteins in glioma cells through RICTOR, affecting the occurrence and development of glioma.

Recently, a growing body of research has shown that microRNAs (miRNAs) are crucial in the pathophysiological mechanisms of brain disorders, miR-210 is one of the significant miRNAs implicated in these disorders, and its function in intracerebral hemorrhage (ICH) is not yet fully understood. Research the impact of miR-210 on intracerebral hemorrhage and probe into its working mechanism. The ICH model was established by injecting collagenase into the basal ganglia of male C57/BL6 mice (n = 142). Firstly, the mice were divided into sham group (n = 6) and ICH group (n = 30) (3 h, 6 h, 12 h, 24 h, 72 h), the samples of the sham group were collected at 48 h after operation, the brain tissues of the left and right basal ganglia were collected in each groupand. qPCR was used to detect the level of miR-210 in each group. Then, LV-miR-210 was injected into the lateral ventricle to establish a model of miR-210 overexpression, and NS injection was set as a comparison, which was divided into sham group (n = 15), ICH group (n = 15), ICH + NS group (n = 15), and ICH + LV-miR-210 group (n = 15). Water maze training was started on the 2 d after surgery. qPCR was used to detect the levels of miR-210, iNOS, IL-1β, IL-6, TNF-α, and IL-10 in each group at 3 d after operation. Western blotting was used to detect the levels of p-AMPK/AMPK, p-mTOR/mTOR, Beclin 1, Bax, Bcl-2, and LC3 II/I in each group. Immunofluorescence was used to detect the expression of lentivirus-mediated miR-210 in mouse brain. Water maze was used to evaluate the learning and memory function of the mice. The dry-wet method was used to evaluate brain edema, TUNEL was used to detect the apoptosis of brain cells in each group. Then, Rapamycin and AICAR were used to intervene p-AMPK/AMPK and p-mTOR/mTOR, and they were divided into sham group (n = 6), ICH group (n = 6), ICH + LV-miR-210 group (n = 6), ICH + LV-miR-210 + AICAR group (n = 6), and ICH + LV-miR-210 + Rapamycin group (n = 6). The levels of miR-210 in each group were detected by qPCR at 3 d after operation, and the levels of p-AMPK/AMPK, p-mTOR/mTOR, Beclin 1, Bax, Bcl-2, and LC3 II/I in each group were detected by WB. Finally, HT22 cells were stimulated with Hemin to construct an in vitro intracerebral hemorrhage model, and the time gradient was set (control group, 3 h, 6 h, 12 h, and 24 h). qPCR was used to detect the expression of miR-210 in each group. Then HT22 cells were transfected with lentivirus, and rapamycin and AICAR were used to interfere with p-AMPK/AMPK and p-mTOR/mTOR. Control group, Hemin group, Hemin + LV-miR-210 group, Hemin + LV-miR-210 + AICAR group, and Hemin + LV-miR-210 + Rapamycin group. qPCR was used to detect the level of miR-210 in each group. The levels of p-AMPK/AMPK, p-mTOR/mTOR, Beclin 1, Bax, Bcl-2, and LC3 II/I in each group were detected by Western blotting. miR-210 is significantly increased in a short time after intracerebral hemorrhage in mice. miR-210 can alleviate secondary injury of ICH by improving neurological deficit and reducing brain edema. In addition, upregulation of miR-210 expression inhibited autophagy and alleviated apoptosis and inflammation. In our study, we found that miR-210 significantly inhibited the activation of AMPK/ mTOR pathway triggered by ICH, and the neuroprotective effect of miR-210 was partially reversed when Rapamycin and AICAR reversed this inhibition. At the mechanistic level, miR-210 exerts its function by regulating AMPK/mTOR signaling pathway, thereby inhibiting autophagy and reducing apoptosis and inflammation. Further studies at the cellular level were basically consistent with the above results. miR-210 is up-regulated after ICH and can play a neuroprotective role by regulating the AMPK/mTOR signaling pathway mediated by autophagy, suggesting that it may become a therapeutic target for reducing nerve injury after ICH.

To studied epidemiological characteristics of 493 cases of acute poisoning in Nantong city, Jiangsu province. Based on the analysis platform of poisoning treatment, adopted single center and prospective investigation method, analyzed data of acute poisoning patients from May 2015 to December 2018 in the second affiliated hospital of Nantong University. Among 493 patients with acute poisoning, men 227 (46.04%), women 266 (53.96%). Age ranged from 12 to 89 years old, average age 41.6 years. In the occupational distribution, farmers were 30.02%; 351 cases (71.20%) visited the hospital within 6 hours after exposure. Oral exposure poisoning 415 cases (84.18%). Pesticide poisoning accounted for 45.45% of deaths. Using the poisoning treatment platform to analyze the clinical characteristic had accurately and reliably in Nantong. The fatality rate of pesticide poisoning in cases of acute poisoning is high. Management of highly toxic pesticides should be continued and effective health education on pesticide use should be carried out.

Introduction: In the occurrence and development of heat stroke (HS), factors such as hyperthermia, ischemia and hypoxia are essential to the central nervous system (CNS) inflammatory response, but the main mechanism underlying CNS inflammation remains unclear. The aim of the study was to observe the polarization of microglia in response to heat-induced early nerve injury and to explore its possible mechanism of action.Material and methods: To establish a heatstroke animal model in Beagle dogs, 18 Beagle dogs were divided into control (group A) and experimental groups (group B, group C and group D) according to a random numbers table. The animals in the experimental groups were placed on an electric blanket of an animal body temperature maintaining apparatus. The temperature was set at 40 ±0.5°C, and the rectal temperature was monitored every 5 min until the target body temperature was reached. Once the target temperature was reached, the dogs were transferred to an environment of 26 ±0.5°C and 60 ±0.5% humidity. Western blot analysis was used to detect the expression of microglia-specific markers CD45, iNOS, arginase, and CD206 in normal and heat-damaged brain tissues at different time points (1 h, 6 h, 24 h). The expression of CD45 and arginase was further determined by co-localization with immunofluorescence.Results: CD45 and iNOS protein expression was detected in group A. The two protein markers in group B were significantly higher than those in group A (p < 0.05), and the protein markers in group C were still higher than those in group A (p < 0.05). There was no statistically significant difference among the animals in group A (p > 0.05). Arginase and CD206 protein expression was also detected in group A. Levels of the two protein markers in group B were higher than those in group A (p < 0.05), and the protein marker levels in group C were even higher than those in group A (p < 0.05). Further analysis of the two groups of protein markers in group D showed significantly higher levels than those in group A (p < 0.001). Immunofluorescence co-loca­lization of CD45 and arginase showed significantly increased fluorescence density at 6 h and 24 h after thermal injury (p < 0.001).Conclusions: After heat-induced disease, microglia were found to be active in the brain tissues of dogs. The microglia activated in the early 1-6 h of CNS injury were mainly the M1 type, which were then converted to the M2 type after 6 h. The 24 h M2 type was dominant. The relationship between M1/M2 polarization trends and early brain injury in heat-induced disease may be a key to understanding CNS injury in heat-induced disease.

Background: Circular RNAs play an important regulatory role in the occurrence and development of nerve damage and related diseases, but there is little research on non-coding RNAs in heat sickness, especially circRNAs, and there has been no report on the mechanism of fever progression.Methods: 1. Mice were randomly divided into a control group, a heat radiation disease 0.8 h group (HS 0.8), 8 h group (HS 8), 24 h group (HS 24). By establishing a mouse model of heat shock (HS), heat-damaged brain tissue was obtained, microglia were isolated. 2. QPCR was used to detect M1 and M2 marker molecules in microglia, and to evaluate the polarization direction and type of microglia. 3. The expression level of circhipk3 in microglial cells, and the effect of circhipk3 on microglial polarization was determined by determining the expression of circhipk3 in microglial cells.Results: The expressions of CD45 and CD11-b in the HS 8 group were significantly higher than those in the normal group, while the expressions of CD45 and CD11-b in the HS 24 group were significantly lower than those in the HS 8 group. At the same time, the expression of CD206, FIZZ, and Arg1 in the HS 8 group began to increase compared with the normal group, while CD206, FIZZ, and Arg1 in the HS 24 group significantly increased when compared with the normal group. Circhipk3 mimics significantly increased the expression of Arg1 and inhibited the expressions of CD45 and HO-1, while the circhipk3 inhibitor promoted the expressions of CD45 and HO-1 and inhibited the expression of Arg1. Conclusion: Microglial cells were the main M1-type in early neurological injury of heat radiation disease. HO-1 may be one of the microglial M1-type markers. The high expression of circhipk3 in microglial cells mainly promoted its transformation to the M2 type.