ObjectiveTo explore the regulatory effect of Ganluqingwen prescription on inflammation and immunity by observing the clinical efficacy of Ganluqingwen prescription in the treatment of community-acquired pneumonia （CAP）， so as to provide a clinical basis for the treatment of CAP by traditional Chinese medicine （TCM）. MethodsA randomized controlled trial was conducted by selecting patients who were diagnosed with CAP and identified as wind-heat attacking lungs in Xinjiang Uygur Autonomous Region Hospital of TCM from January 2024 to May 2024 and assigning the patients to a control group （treated by western medicine treatment） or an experimental group （treated by Ganluqingwen prescription combined with western medicine）. The data of the enrolled patients before treatment， for three-day treatment， for seven-day treatment， and for 14-day treatment were collected， including basic information， medical history， pneumonia severity index （PSI） classification， and distribution and difference of laboratory and imaging information indexes. The peripheral blood specimens were collected from the patients. and the changes of inflammatory factors in peripheral blood were detected by using enzyme-linked immunosorbent assay （ELISA） reagent kits and flow-type multifactor microarrays to evaluate the clinical safety and efficacy of Ganluqingwen prescription in CAP. ResultsCompared with those in the groups before treatment， the total scores of TCM syndromes significantly decreased in both groups （P<0.05）. Compared with those in the control group after treatment， the total scores of TCM syndromes decreased more significantly in the experimental group （P<0.05）. Compared with the control group after treatment， the experimental group displayed a significantly reduced number of days of fever in patients （P<0.05）. Compared with those in the groups before treatment， the leukocyte， neutrophil counts， C-reactive protein （CRP）， procalcitonin （PCT）， interleukin （IL）-6， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， creatinine （Cr）， creatine kinase （CK）， and creatine kinase isoenzymes （CK-MB） in both groups decreased （P<0.05） after treatment. Compared with that in the control group after treatment， the decrease of leukocyte， neutrophil counts， CRP， PCT， IL-6， ALT， AST， Cr， CK， and CK-MB was more pronounced in the experimental group （P<0.05）. Compared with those in the group before treatment， the partial pressure of carbon dioxide increased in the experimental group for 3 d of treatment （P<0.05）， and the standard alkali residual， actual alkali residual， standard bicarbonate concentration， and actual bicarbonate concentration increased in the experimental group for 7 d of treatment （P<0.05）. Compared with that in the group before treatment， D-dimer decreased in the control group for 7 d of treatment （P<0.05）. D-dimer and activated partial thromboplastin time （APTT） decreased in the experimental group for 3 d of treatment （P<0.05）， and D-dimer， fibrinogen （FIB）， and APTI significantly decreased in the group for 7 d of treatment （P<0.05）. Compared with the group for 3 d of treatment， the experimental group for 7 d of treatment showed decreased FIB （P<0.05）. Compared with those in the groups before treatment， the levels of inflammatory factors IL-4， IL-10， and IL-13 were elevated in the peripheral blood of the two groups after treatment， and the levels of B lymphocyte chemoattractant （BLC）， interferon gamma-induced protein 10 （IP-10）， tumor necrosis factor-alpha （TNF-α）， interferon-gamma （IFN-γ）， monocyte chemoattractant protein-1 （MCP-1）， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 were significantly reduced （P<0.01）. Compared with the control group after treatment， the experimental group exhibited more significant improvement in indexes above （P<0.01）. ConclusionThe group treated by Ganluqingwen prescription combined with western medicine shows more significant effects on reducing total scores of TCM syndromes， lowering the ability of leukocyte and neutrophil counts， decreasing BLC， IP-10， TNF-α， IFN-γ， MCP-1， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 in the peripheral blood of the patients， and elevating levels of IL-4， IL-10， and IL-13 than the group treated by western drugs alone.

ObjectiveTo explore the regulatory effect of Ganluqingwen prescription on inflammation and immunity by observing the clinical efficacy of Ganluqingwen prescription in the treatment of community-acquired pneumonia （CAP）， so as to provide a clinical basis for the treatment of CAP by traditional Chinese medicine （TCM）. MethodsA randomized controlled trial was conducted by selecting patients who were diagnosed with CAP and identified as wind-heat attacking lungs in Xinjiang Uygur Autonomous Region Hospital of TCM from January 2024 to May 2024 and assigning the patients to a control group （treated by western medicine treatment） or an experimental group （treated by Ganluqingwen prescription combined with western medicine）. The data of the enrolled patients before treatment， for three-day treatment， for seven-day treatment， and for 14-day treatment were collected， including basic information， medical history， pneumonia severity index （PSI） classification， and distribution and difference of laboratory and imaging information indexes. The peripheral blood specimens were collected from the patients. and the changes of inflammatory factors in peripheral blood were detected by using enzyme-linked immunosorbent assay （ELISA） reagent kits and flow-type multifactor microarrays to evaluate the clinical safety and efficacy of Ganluqingwen prescription in CAP. ResultsCompared with those in the groups before treatment， the total scores of TCM syndromes significantly decreased in both groups （P<0.05）. Compared with those in the control group after treatment， the total scores of TCM syndromes decreased more significantly in the experimental group （P<0.05）. Compared with the control group after treatment， the experimental group displayed a significantly reduced number of days of fever in patients （P<0.05）. Compared with those in the groups before treatment， the leukocyte， neutrophil counts， C-reactive protein （CRP）， procalcitonin （PCT）， interleukin （IL）-6， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， creatinine （Cr）， creatine kinase （CK）， and creatine kinase isoenzymes （CK-MB） in both groups decreased （P<0.05） after treatment. Compared with that in the control group after treatment， the decrease of leukocyte， neutrophil counts， CRP， PCT， IL-6， ALT， AST， Cr， CK， and CK-MB was more pronounced in the experimental group （P<0.05）. Compared with those in the group before treatment， the partial pressure of carbon dioxide increased in the experimental group for 3 d of treatment （P<0.05）， and the standard alkali residual， actual alkali residual， standard bicarbonate concentration， and actual bicarbonate concentration increased in the experimental group for 7 d of treatment （P<0.05）. Compared with that in the group before treatment， D-dimer decreased in the control group for 7 d of treatment （P<0.05）. D-dimer and activated partial thromboplastin time （APTT） decreased in the experimental group for 3 d of treatment （P<0.05）， and D-dimer， fibrinogen （FIB）， and APTI significantly decreased in the group for 7 d of treatment （P<0.05）. Compared with the group for 3 d of treatment， the experimental group for 7 d of treatment showed decreased FIB （P<0.05）. Compared with those in the groups before treatment， the levels of inflammatory factors IL-4， IL-10， and IL-13 were elevated in the peripheral blood of the two groups after treatment， and the levels of B lymphocyte chemoattractant （BLC）， interferon gamma-induced protein 10 （IP-10）， tumor necrosis factor-alpha （TNF-α）， interferon-gamma （IFN-γ）， monocyte chemoattractant protein-1 （MCP-1）， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 were significantly reduced （P<0.01）. Compared with the control group after treatment， the experimental group exhibited more significant improvement in indexes above （P<0.01）. ConclusionThe group treated by Ganluqingwen prescription combined with western medicine shows more significant effects on reducing total scores of TCM syndromes， lowering the ability of leukocyte and neutrophil counts， decreasing BLC， IP-10， TNF-α， IFN-γ， MCP-1， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 in the peripheral blood of the patients， and elevating levels of IL-4， IL-10， and IL-13 than the group treated by western drugs alone.

Cell death is a fundamental phenomenon for organisms to maintain their basic morphology.When a pathogen infects a cell,the process of programmed cell death is activated,the lysed cells carrying the pathogen ac-tivate the immune response of the organism in the process of removing infected cells,thus exerting immune de-fense.The molecular mechanisms of the 4 types of cell death modes apoptosis,pyroptosis,necroptosis and pan-apoptosis as well as their effects on innate immune defense against microbial infections were mainly elaborated in the article,the interactions among the different programmed cell death pathways were briefly interpreted so as to provide new ideas for further study of pathogenic mechanisms of infectious diseases.

Objective To analyze the occurrence and clinical characteristics of bleeding adverse reactions induced by apixaban,and to provide reference for clinical therapy.Methods From the marking of apixaban to May 2024,cases of adverse reactions to hemorrhage caused by apixaban were searched in the database of CNKI,Wanfang,VIP,PubMed and Web of Science.Statistical analysis was performed on the collected data.Results A total of thirty-nine cases of hemorrhagic adverse reactions induced by apixaban were documented.Therewere thirty-three patients(84.62%)over 60 years old.Twenty-two patients had bleeding within 30 days of treatment(56.41%).Intracranial hemorrhage occurred in nine patients(23.08%).Twenty-two patients improved after conventional treatment(56.41%).Twenty-three patients(58.97%)stopped bleeding within 30 days,and two patients(5.13%)died,all of whom died within 1 month after taking apixaban.Conclusions Physician and pharmacists should pay close attention to the adverse reactions of hemorrhage caused by apixaban,and do a good job in drug monitoring and patient education to ensure the safety of clinical medication.

Objective To preliminarily describe the current situation of chronic disease drug continuity between community hospitals and the Affiliated Hospital of Qingdao University in the medical alliance,to explore the key points for further improving the connection between upper and lower-level hospitals in the medical alliance,and to improve the drug supply guarantee and the ability of pharmaceutical services of primary medical institutions.Methods The nine community hospitals within the medical alliance centered on the Affiliated Hospital of Qingdao University were taken as the research subjects to investigate the medication continuity between the community hospitals and the core hospital in terms of cardiovascular diseases,diabetes,and respiratory system diseases before and after the medical alliance.Results Before the integration of medical alliances,the drug linkage rate for cardiovascular diseases,diabetes,and respiratory system diseases in community hospitals and core hospitals was relatively low.After the integration of medical alliances,the average drug linkage rate for the three chronic diseases significantly increased,all exceeding 60%.At the same time,the drug catalog in community hospitals was streamlined,reducing the phenomenon of one drug having multiple specifications.There is a significant difference in the number of drug varieties provided by different community hospitals for the three chronic diseases.Conclusion The medical alliance with the Affiliated Hospital of Qingdao University as the core promotes the up-down linkage of drug treatment in community hospitals,simplifies the drug catalog of primary medical structure,and facilitates the treatment and prescription of chronic patients.

This study established an indirect ELISA method for antibody detection based on human rotavirus group A(RVA)VP6 protein,to provide technical support for RVA antibody detection.An ELISA method for detecting RVA antibodies was established through a checkerboard assay for optimization of the reaction conditions with VP6 protein of RVA as the diagnostic antigen.Serum samples from healthy children and patients infected with RVA were collected and detected with the ELISA method.The optimal work-ing conditions for ELISA involved coating the ELISA plate with VP6 protein at a concentration of 2 μg/mL and diluting the serum at a ratio of 1∶250.The critical value of negative and positive samples was 0.137.The ELISA method had good specificity,sensitivity,and repeatability,and showed a 95%consistency rate with the western blotting antibody detection method.We tested 370 serum samples collected from children,which showed an antibody positivity rate of 81.1%.We additionally tested the acute and recovery phase sera from 15 patients infected with RVA,and observed a significantly higher RVA antibody titer in the recovery phase serum than the acute infection phase serum.The ELISA antibody detection method showed good specificity,sensitivity,and reproducibility,and therefore can be used for RVA antibody detection and auxiliary diagnosis of RVA infection.

This study expressed the VP6 protein of human group A rotavirus in a prokaryotic expression system and prepared mouse polyclonal antibodies to this protein.The human rotavirus VP6 gene was amplified through RT-PCR from fecal samples infected with group A rotavirus and cloned into the pET-32a vector to construct the recombinant pET-32a-VP6 prokaryotic expression plas-mid.The recombinant plasmid was transformed into Escherichia coli BL21(DE3).VP6 protein was expressed through induction with isopropyl-β-D-thiopyranoside(IPTG),purified with nickel nitrilotriacetic acid(Ni-NTA)affinity chromatography,and identified through SDS-PAGE and western blotting.Polyclonal antibodies to the VP6 protein were obtained by immunization of BALB/c mice with VP6 protein.Antibody titers were determined through indirect ELISA.The recombinant expression plasmid pET-32a-VP6 was con-structed,and VP6 protein was expressed primarily in inclusion bodies.Polyclonal antibodies to VP6 protein with a titer of 1∶32 000 were obtained by immunization of mice with VP6 protein purified by affinity chromatography.The antibodies specifically reacted with VP6 protein.The VP6 protein of human group A rotavirus was expressed and purified,and mouse polyclonal antibodies to this protein were prepared,thus providing a foundation for the preparation of a diagnostic antigen for human group A rotavirus and the establishment of serological detection methods.

This study established an indirect ELISA method for antibody detection based on human rotavirus group A(RVA)VP6 protein,to provide technical support for RVA antibody detection.An ELISA method for detecting RVA antibodies was established through a checkerboard assay for optimization of the reaction conditions with VP6 protein of RVA as the diagnostic antigen.Serum samples from healthy children and patients infected with RVA were collected and detected with the ELISA method.The optimal work-ing conditions for ELISA involved coating the ELISA plate with VP6 protein at a concentration of 2 μg/mL and diluting the serum at a ratio of 1∶250.The critical value of negative and positive samples was 0.137.The ELISA method had good specificity,sensitivity,and repeatability,and showed a 95%consistency rate with the western blotting antibody detection method.We tested 370 serum samples collected from children,which showed an antibody positivity rate of 81.1%.We additionally tested the acute and recovery phase sera from 15 patients infected with RVA,and observed a significantly higher RVA antibody titer in the recovery phase serum than the acute infection phase serum.The ELISA antibody detection method showed good specificity,sensitivity,and reproducibility,and therefore can be used for RVA antibody detection and auxiliary diagnosis of RVA infection.

This study expressed the VP6 protein of human group A rotavirus in a prokaryotic expression system and prepared mouse polyclonal antibodies to this protein.The human rotavirus VP6 gene was amplified through RT-PCR from fecal samples infected with group A rotavirus and cloned into the pET-32a vector to construct the recombinant pET-32a-VP6 prokaryotic expression plas-mid.The recombinant plasmid was transformed into Escherichia coli BL21(DE3).VP6 protein was expressed through induction with isopropyl-β-D-thiopyranoside(IPTG),purified with nickel nitrilotriacetic acid(Ni-NTA)affinity chromatography,and identified through SDS-PAGE and western blotting.Polyclonal antibodies to the VP6 protein were obtained by immunization of BALB/c mice with VP6 protein.Antibody titers were determined through indirect ELISA.The recombinant expression plasmid pET-32a-VP6 was con-structed,and VP6 protein was expressed primarily in inclusion bodies.Polyclonal antibodies to VP6 protein with a titer of 1∶32 000 were obtained by immunization of mice with VP6 protein purified by affinity chromatography.The antibodies specifically reacted with VP6 protein.The VP6 protein of human group A rotavirus was expressed and purified,and mouse polyclonal antibodies to this protein were prepared,thus providing a foundation for the preparation of a diagnostic antigen for human group A rotavirus and the establishment of serological detection methods.

Cell death is a fundamental phenomenon for organisms to maintain their basic morphology.When a pathogen infects a cell,the process of programmed cell death is activated,the lysed cells carrying the pathogen ac-tivate the immune response of the organism in the process of removing infected cells,thus exerting immune de-fense.The molecular mechanisms of the 4 types of cell death modes apoptosis,pyroptosis,necroptosis and pan-apoptosis as well as their effects on innate immune defense against microbial infections were mainly elaborated in the article,the interactions among the different programmed cell death pathways were briefly interpreted so as to provide new ideas for further study of pathogenic mechanisms of infectious diseases.