Non-alcoholic fatty liver disease (NAFLD) is one of the common chronic liver diseases with increasing incidence and prevalence. Given the current lack of effective therapeutic drugs, NAFLD has emerged as a focal point in hepatology research. The pathogenesis of NAFLD is complex, and immune cells play an important role in this process. Immune cells can release extracellular vesicles (EVs), which carry bioactive cargo such as proteins and microRNAs, thereby influencing the progression of NAFLD. Moreover, EVs are characterized by the advantages of good biocompatibility and low immunogenicity, making them widely explored as drug carriers. Exploring the application of immune cell-derived EVs in NAFLD may provide new directions for the treatment of NAFLD.

AIM:To explore the role and mechanism of calcium-sensing receptor(CaSR)in regulating macro-phage polarization in hypertensive rats.METHODS:Male spontaneously hypertensive rats(SHR)and Wistar-Kyoto(WKY)rats were categorized into WKY group,SHR group,SHR+R568(CaSR agonist)group,and SHR+NPS2143(CaSR inhibitor)group.The thoracic aorta was isolated,and the expression of CaSR and macrophage polarization markers in the aorta was observed through immunofluorescence staining.The primary peritoneal macrophages of SHR and WKY rats were aseptically extracted following anesthesia.After intervention with R568 and NPS2143,the expression levels of M1 and M2 markers of peritoneal macrophages were observed by Western blot and immunofluorescence staining.The levels of interleukin(IL)-1β and IL-10 were measured by ELISA.The concentration of Ca2+in peritoneal macrophages was mea-sured by immunofluorescence.Western blot was employed to identify the expression of CaSR and nucleotide-binding oligo-merization domain-like receptor protein 3(NLRP3)inflammasome components.Following anesthesia,vascular smooth muscle cells(VSMCs)were isolated from SHR using an adherent method.Subsequently,a co-culture system was estab-lished with macrophage supernatant.The optimal action time for this co-culture system was determined through CCK-8 as-say.RESULTS:Compared with SHR group,activation of CaSR resulted in a significant decrease in the protein expres-sion of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers in the aorta(P<0.05).Compared with SHR group,administration of R568 led to a significant decrease in the protein ex-pression of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers(P<0.05)in peritoneal macrophages.Additionally,there was a notable reduction in the protein levels of NLRP3 inflammasome components(P<0.05).Furthermore,the fluorescence intensity of intracellular Ca2+was significantly en-hanced following R568 treatment(P<0.05).After administration of MCC950,an NLRP3 inflammasome inhibitor,the re-sults were consistent with those observed following R568 treatment,demonstrating statistical significance(P<0.05).This effect was reversed by the combined intervention of U73122,a phospholipase C(PLC)inhibitor(P<0.05).Compared with the control(0 h),the 24-h peritoneal macrophage supernatant exhibited the strongest capacity to enhance the viabili-ty of VSMCs after 24 h of culture(P<0.05).CONCLUSION:In hypertensive rats,the CaSR inhibits NLRP3 inflamma-some activation via the PLC-Ca2+signaling pathway,thereby mediating an increase in macrophage polarization towards the M2 phenotype and a decrease towards the M1 phenotype.

AIM:To explore the role and mechanism of calcium-sensing receptor(CaSR)in regulating macro-phage polarization in hypertensive rats.METHODS:Male spontaneously hypertensive rats(SHR)and Wistar-Kyoto(WKY)rats were categorized into WKY group,SHR group,SHR+R568(CaSR agonist)group,and SHR+NPS2143(CaSR inhibitor)group.The thoracic aorta was isolated,and the expression of CaSR and macrophage polarization markers in the aorta was observed through immunofluorescence staining.The primary peritoneal macrophages of SHR and WKY rats were aseptically extracted following anesthesia.After intervention with R568 and NPS2143,the expression levels of M1 and M2 markers of peritoneal macrophages were observed by Western blot and immunofluorescence staining.The levels of interleukin(IL)-1β and IL-10 were measured by ELISA.The concentration of Ca2+in peritoneal macrophages was mea-sured by immunofluorescence.Western blot was employed to identify the expression of CaSR and nucleotide-binding oligo-merization domain-like receptor protein 3(NLRP3)inflammasome components.Following anesthesia,vascular smooth muscle cells(VSMCs)were isolated from SHR using an adherent method.Subsequently,a co-culture system was estab-lished with macrophage supernatant.The optimal action time for this co-culture system was determined through CCK-8 as-say.RESULTS:Compared with SHR group,activation of CaSR resulted in a significant decrease in the protein expres-sion of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers in the aorta(P<0.05).Compared with SHR group,administration of R568 led to a significant decrease in the protein ex-pression of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers(P<0.05)in peritoneal macrophages.Additionally,there was a notable reduction in the protein levels of NLRP3 inflammasome components(P<0.05).Furthermore,the fluorescence intensity of intracellular Ca2+was significantly en-hanced following R568 treatment(P<0.05).After administration of MCC950,an NLRP3 inflammasome inhibitor,the re-sults were consistent with those observed following R568 treatment,demonstrating statistical significance(P<0.05).This effect was reversed by the combined intervention of U73122,a phospholipase C(PLC)inhibitor(P<0.05).Compared with the control(0 h),the 24-h peritoneal macrophage supernatant exhibited the strongest capacity to enhance the viabili-ty of VSMCs after 24 h of culture(P<0.05).CONCLUSION:In hypertensive rats,the CaSR inhibits NLRP3 inflamma-some activation via the PLC-Ca2+signaling pathway,thereby mediating an increase in macrophage polarization towards the M2 phenotype and a decrease towards the M1 phenotype.

Non-alcoholic fatty liver disease (NAFLD) is one of the common chronic liver diseases with increasing incidence and prevalence. Given the current lack of effective therapeutic drugs, NAFLD has emerged as a focal point in hepatology research. The pathogenesis of NAFLD is complex, and immune cells play an important role in this process. Immune cells can release extracellular vesicles (EVs), which carry bioactive cargo such as proteins and microRNAs, thereby influencing the progression of NAFLD. Moreover, EVs are characterized by the advantages of good biocompatibility and low immunogenicity, making them widely explored as drug carriers. Exploring the application of immune cell-derived EVs in NAFLD may provide new directions for the treatment of NAFLD.

At present,the AIDS epidemic situation in college students is becoming more and more serious.In view of the particularity of colleges students and the lack of professional team for AIDS prevention and control in colleges and universities,there exists ethical issues when carry out the prevention and control for AIDS in colleges and universities such as the ethical issue in publicity and education,the ethical issue in AIDS behavioral intervention,the ethical issue in the consultation and detection for AIDS.This paper suggests that it should confront the current situation of AIDS prevention and control,improve the professional level of carrying out AIDS prevention and control,adhere to the necessary principles of AIDS prevention and control,and explore a new mode to construct AIDS prevention and control in colleges and universities.

Objective:To investigate the difference of CD3+CD4+and CD3+CD8+T cells between patients with advanced small cell lung cancer and with non-small cell lung cancer, and provide available reference for treatment.Methods: Peripheral blood was taken from 65 patients with advanced lung cancer which was included 14 cases of small cell lung cancer and 51 cases of non-small cell lung cancer, 20 cases normal controls.The expression of CD3+CD4+ and CD3+CD8+ on lymphocytes was analyzed with flow cytometry.Results:We found that the percentage of CD3+CD4+T cells in small cell and non-small cell lung cancer patients were both much less than that of normal controls.There was no significant variation in the percentage of CD3+CD8+T cells between advanced lung cancer patients and normal controls.CD4+/CD8+in patients with advanced small cell lung cancer were a lot less than those in normal controls.Conclusion:Both of the percentage of CD3+CD4+T cells in small cell and non-small cell advanced lung cancer patients were significantly decreased than that in normal controls.Patients who attacked with advanced lung cancer were severely injured in cellular immunity.