Effect of intensive education on stroke prevention and management ability of community doctors: a cross-sectional study.

BACKGROUND: Prevention and treatment of stroke are extremely important to reduce the incidence of stroke-related disability and the associated death. This study aimed to investigate the current ability of community doctors in stroke management in the Jinjiang district of Chengdu, China, and the effect of intensive education on stroke prevention and management ability of these doctors. METHODS: A self-designed questionnaire was used to investigate the current status of stroke management by community doctors in the Jinjiang district. Subsequently, a series of intensive stroke management education courses for community doctors was designed according to the relevant guidelines for cerebrovascular accident prevention and treatment in China. All community doctors were trained, and their ability to treat and prevent stroke was reassessed using the self-designed questionnaire. RESULTS: Of the 450 questionnaires issued, 370 (82.2%) and 389 (86.4%) community doctors were enrolled before and after intensive education, respectively. The results showed that only 37.8% of the community doctors in the Jinjiang district knew the guidelines for the prevention and treatment of cerebrovascular diseases, and only 45.9% thought they had stroke management ability. The stroke management ability of community doctors improved after intensive education (p < 0.05), including pre-hospital identification and management of stroke, and management of its risk factors. CONCLUSIONS: The capacity of community doctors in the Jinjiang district of Chengdu is far from meeting the requirements of stroke prevention and treatment. However, the stroke management ability of the community doctors was greatly improved by promoting intensive education.

Role of Stat3 in NLRP3/caspase-1-mediated hippocampal neuronal pyroptosis in epileptic mice.

Epilepsy, a fairly common neurological disorder, is linked to various sequelae and greatly impairs the quality of life. Meanwhile, there is evidence to suggest an association between pyroptosis and epilepsy. Accordingly, the current study sought to determine the role of signal transduction activator of transcription 3 (Stat3) in pyroptosis in epileptic mice. First, epileptic mouse models were induced by lithium chloride, atropine, and pilocarpine, and HT22 cells were treated with lipopolysaccharide (LPS) to establish in vitro hippocampal neuronal inflammation models. Subsequently, Stat3, NOD-like receptor protein 3 (NLRP3), cleaved-caspase-1, gasdermin D (GSDMD)-N, activated Stat3 (p-Stat3), and H3K9Ac levels were detected in the mouse hippocampus and HT22 cells. Morris water maze test was further performed to detect changes in the learning and memory abilities of epileptic mice, and hematoxylin-eosin staining and Nissl staining were conducted to detect the pathological injury. HT22 cell proliferation and apoptosis were also detected using a cell counting kit-8 assay and flow cytometry. An enzyme-linked immunosorbent assay was adopted to detect Interleukin (IL)-1ß and IL-18 concentrations in the mouse hippocampus and HT22 cells. Furthermore, the enrichment of H3K9Ac and p-Stat3 in the NLRP3 promoter region was detected with the help of a chromatin immunoprecipitation assay. The obtained findings revealed that Stat3 was highly expressed in the hippocampus of epileptic mice and LPS-treated HT22 cells. Meanwhile, Stat3 silencing brought about improvements in the learning and memory abilities of the mice, in addition to alleviation of hippocampal neuronal damage and pyroptosis-related factors in hippocampal tissue and HT22 cells. We also observed that Stat3 bound to the NLRP3 promoter to promote H3K9 acetylation and NLRP3 transcription. Moreover, increasing H3K9Ac in cells annulled the inhibition of silencing Stat3 on neuronal pyroptosis. To conclude, our findings revealed that Stat3 bound to the NLRP3 promoter to augment H3K9 acetylation, NLRP3 transcription, and NLRP3/caspase-1-mediated neuronal pyroptosis, resulting in aggravation of neuronal damage in epileptic mice.