Objective To investigate the epidemiological trends,temporal and spatial distribution characteristics of pulmonary tuberculosis in Lanping County.Methods Based on tuberculosis management data and basic information systems from the"China Disease Prevention and Control Information System,"pulmonary tuberculosis data from Lanping County for 2018-2023 were obtained.Descriptive epidemiology,concentration method,circular distribution method,and spatial autocorrelation analysis were used to conduct epidemiological and spatial analyses of the pulmonary tuberculosis data.Results A total of 2836 TB cases were reported in Lanping County from 2018 to 2023,with an average annual incidence rate of 233.26 per 100000,showing a declining trend.The male-to-female ratio was 1.95∶1,with the highest incidence among individuals aged 60 and above(932 cases,32.86%).Cases were predominantly among farmers(91.01%)and the Lisu ethnic group(52.68%).TB incidence showed weak seasonality with a bimodal distribution,with primary peak occurring from October to March and secondary peak from June to August.Tu'e Township(324.74 per 100,000),Shideng Township(307.42 per 100000),and Jinding Town(260.98 per 100,000)had the highest incidence rates,accounting for 1,284 cases or 45.28%of the county's total cases.In 2020,the incidence of pulmonary tuberculosis in Lanping County showed a spatial clustering distribution(global Morans's I value<0,P value<0.05),with Shideng Township consistently showing high-low aggregation characteristics.Conclusion Between 2018-2023,while the tuberculosis incidence rate in Lanping County has declined,it still falls short of Yunnan Province's tuberculosis prevention and control targets,and the prevention and control work continues to face significant challenges.Strengthening screening of high-risk populations and providing medical support to remote areas will be key measures for future prevention and treatment.

Objective:To explore the molecular mechanism of miR-4508 regulating the inflammatory response of human bronchial epithelial cells induced by representative chrysotile asbestos.Methods:The chrysotile asbestos was ground into ultrafine dust using a horizontal planetary instrument, and human bronchial epithelium (16HBE) cells were taken as the object of infection. Cell survival rate was detected by cell counting kit-8 method, cytotoxicity was detected by lactate dehydrogenase (LDH) kit. The released of inflammatory factor IL-6 was detected by electrochemical luminescence. The released inflammatory factor IL-8 was detected by enzyme-linked immunosorbent assay. The expression level of miR-4508 was screened and verified by reverse transcription-quantitative real-time polymerase chain reaction. After 16HBE cells were treated with AKT inhibitor MK2206, the phosphorylation levels of AKT and PTEN were detected by western blot. The expression levels of AKT and PTEN and the contents of IL-6 and IL-8 were detected in miR-4508 overexpression and interference experiments.Results:With the increase of chrysotile asbestos exposure concentration, the cell survival rate decreased in a concentration-dependent manner, and the LDH content gradually increased. The secretion of IL-6 and IL-8 in chrysotile 25, 50 and 75 μg/ml groups were (325.92±8.61) pg/ml, (331.51±4.96) pg/ml, (378.74±13.77) pg/ml, and (94.95±3.11) pg/ml, (357.60±1.80) pg/ml, (537.19±3.11) pg/ml, respectively, while the group with 0 μg/ml chrysotile was (95.85±1.20) pg/ml and (7.81±0.00) pg/ml ( P＜0.05). In addition, chrysotile asbestos exposure to 16HBE could induce the high expression of miR-4508 . After pretreatment with MK2206, the phosphorylation levels of AKT and PTEN were decreased, the contents of IL-6 and IL-8 were significantly decreased, and the expression level of miR-4508 was significantly reduced. Overexpression of miR-4508 significantly increased the expressions of AKT and PTEN, and the contents of IL-6 and IL-8 ( P＜0.01). After interfering with miR-4508, the expressions of AKT and PTEN were significantly decreased, and the contents of IL-6 and IL-8 were significantly decreased ( P＜0.01). Conclusions:Chrysotile asbestos can induce the inflammatory response of 16HBE cells and up-regulate the expression level of miR-4508. The up-regulation of miR-4508 promotes the 16HBE inflammatory response induced by chrysotile asbestos through the PI3K/AKT pathway.

The liver is one of the important metabolic organs in the body, and liver diseases are also one of the major public health issues globally. Currently, the lack of models that accurately simulating human physiology and pathology is the key challenge in liver disease research, and the emerging of organoid technology is an excellent solution to this challenge. Organoids are three-dimensional cellular structures cultured in vitro that can mimic the structure and function of real organs while maintaining genetic stability. The development of organoids has provided possibilities for personalized medicine and precision therapy and has become a key tool in the research and treatment of liver diseases. The authors focuse on the application and development of organoids in liver disease research, while also emphasizing their limitations and future prospects.

Objective:To elucidate the mechanism by which Clostridium butyricum alleviates atopic dermatitis (AD) from three aspects: immune cells, gut microbiota, and the metabolites of gut microbiota, short-chain fatty acids (SCFAs), and provide a theoretical reference for clinical probiotic-assisted treatment of AD. Methods:A model of 2, 4-dinitrochlorobenzene (DNCB)-induced AD was established using BALB/c mice. Three groups including control group, AD group, and Clostridium butyricum intervention group were set up with 20 mice in each group. The dermatitis score, scratching score, pathological conditions and mast cell infiltration at the lesion site, and the levels of cytokines related to Th1/Th2 and Th17/Treg as well as IgE levels in serum samples were analyzed. Gut microbiota was detected by 16S rRNA gene sequencing. The contents of SCFAs in mouse fecal samples were detected by gas chromatography-mass spectrometry. Spearman correlation analysis was performed to investigate the correlation between the cytokines related to Th1/Th2 and Th17/Treg, gut microbiota, and SCFAs. Comparisons between groups were performed using one-way analysis of variance with Turkey post hoc test correction. Results:Clostridium butyricum intervention down-regulated various inflammatory indexes and alleviated pathological changes in AD mice, elevated the levels of IFN-γ ( P<0.05) and IL-10 ( P<0.01), reduced the levels of IL-4, IL-17 and IgE ( P<0.01), and maintained the balance of Th1/Th2 ( P<0.01) and Th17/Treg ( P<0.001). Besides, the intervention improved intestinal dysbiosis by decreasing the abundance of conditionally pathogenic bacteria such as Prevotellaceae_ UCG-001 ( P<0.01) and increasing the abundance of beneficial bacteria such as Lachnospiraceae_ NK4A136_ group and norank_ f_ Oscillospiraceae ( P<0.05), and enhanced the production of SCFAs ( P<0.05). Correlation analysis showed that allergy-associated immune cytokines were strongly correlated with the composition of gut microbiota and the content of SCFAs. Conclusions:Clostridium butyricum may regulate the microbiota-SCFAs signaling response by inhibiting the colonization of harmful bacteria and increasing the abundance of beneficial bacteria. This, in turn, increases the level of SCFAs, decreases the number of pro-inflammatory cytokines, and maintains the balance of Th1/Th2 and Th17/Treg in the body. Therefore, Clostridium butyricum may alleviate allergic diseases.

Objective:To elucidate the mechanism by which Clostridium butyricum alleviates atopic dermatitis (AD) from three aspects: immune cells, gut microbiota, and the metabolites of gut microbiota, short-chain fatty acids (SCFAs), and provide a theoretical reference for clinical probiotic-assisted treatment of AD. Methods:A model of 2, 4-dinitrochlorobenzene (DNCB)-induced AD was established using BALB/c mice. Three groups including control group, AD group, and Clostridium butyricum intervention group were set up with 20 mice in each group. The dermatitis score, scratching score, pathological conditions and mast cell infiltration at the lesion site, and the levels of cytokines related to Th1/Th2 and Th17/Treg as well as IgE levels in serum samples were analyzed. Gut microbiota was detected by 16S rRNA gene sequencing. The contents of SCFAs in mouse fecal samples were detected by gas chromatography-mass spectrometry. Spearman correlation analysis was performed to investigate the correlation between the cytokines related to Th1/Th2 and Th17/Treg, gut microbiota, and SCFAs. Comparisons between groups were performed using one-way analysis of variance with Turkey post hoc test correction. Results:Clostridium butyricum intervention down-regulated various inflammatory indexes and alleviated pathological changes in AD mice, elevated the levels of IFN-γ ( P<0.05) and IL-10 ( P<0.01), reduced the levels of IL-4, IL-17 and IgE ( P<0.01), and maintained the balance of Th1/Th2 ( P<0.01) and Th17/Treg ( P<0.001). Besides, the intervention improved intestinal dysbiosis by decreasing the abundance of conditionally pathogenic bacteria such as Prevotellaceae_ UCG-001 ( P<0.01) and increasing the abundance of beneficial bacteria such as Lachnospiraceae_ NK4A136_ group and norank_ f_ Oscillospiraceae ( P<0.05), and enhanced the production of SCFAs ( P<0.05). Correlation analysis showed that allergy-associated immune cytokines were strongly correlated with the composition of gut microbiota and the content of SCFAs. Conclusions:Clostridium butyricum may regulate the microbiota-SCFAs signaling response by inhibiting the colonization of harmful bacteria and increasing the abundance of beneficial bacteria. This, in turn, increases the level of SCFAs, decreases the number of pro-inflammatory cytokines, and maintains the balance of Th1/Th2 and Th17/Treg in the body. Therefore, Clostridium butyricum may alleviate allergic diseases.

The liver is one of the important metabolic organs in the body, and liver diseases are also one of the major public health issues globally. Currently, the lack of models that accurately simulating human physiology and pathology is the key challenge in liver disease research, and the emerging of organoid technology is an excellent solution to this challenge. Organoids are three-dimensional cellular structures cultured in vitro that can mimic the structure and function of real organs while maintaining genetic stability. The development of organoids has provided possibilities for personalized medicine and precision therapy and has become a key tool in the research and treatment of liver diseases. The authors focuse on the application and development of organoids in liver disease research, while also emphasizing their limitations and future prospects.

Objective:To explore the molecular mechanism of miR-4508 regulating the inflammatory response of human bronchial epithelial cells induced by representative chrysotile asbestos.Methods:The chrysotile asbestos was ground into ultrafine dust using a horizontal planetary instrument, and human bronchial epithelium (16HBE) cells were taken as the object of infection. Cell survival rate was detected by cell counting kit-8 method, cytotoxicity was detected by lactate dehydrogenase (LDH) kit. The released of inflammatory factor IL-6 was detected by electrochemical luminescence. The released inflammatory factor IL-8 was detected by enzyme-linked immunosorbent assay. The expression level of miR-4508 was screened and verified by reverse transcription-quantitative real-time polymerase chain reaction. After 16HBE cells were treated with AKT inhibitor MK2206, the phosphorylation levels of AKT and PTEN were detected by western blot. The expression levels of AKT and PTEN and the contents of IL-6 and IL-8 were detected in miR-4508 overexpression and interference experiments.Results:With the increase of chrysotile asbestos exposure concentration, the cell survival rate decreased in a concentration-dependent manner, and the LDH content gradually increased. The secretion of IL-6 and IL-8 in chrysotile 25, 50 and 75 μg/ml groups were (325.92±8.61) pg/ml, (331.51±4.96) pg/ml, (378.74±13.77) pg/ml, and (94.95±3.11) pg/ml, (357.60±1.80) pg/ml, (537.19±3.11) pg/ml, respectively, while the group with 0 μg/ml chrysotile was (95.85±1.20) pg/ml and (7.81±0.00) pg/ml ( P＜0.05). In addition, chrysotile asbestos exposure to 16HBE could induce the high expression of miR-4508 . After pretreatment with MK2206, the phosphorylation levels of AKT and PTEN were decreased, the contents of IL-6 and IL-8 were significantly decreased, and the expression level of miR-4508 was significantly reduced. Overexpression of miR-4508 significantly increased the expressions of AKT and PTEN, and the contents of IL-6 and IL-8 ( P＜0.01). After interfering with miR-4508, the expressions of AKT and PTEN were significantly decreased, and the contents of IL-6 and IL-8 were significantly decreased ( P＜0.01). Conclusions:Chrysotile asbestos can induce the inflammatory response of 16HBE cells and up-regulate the expression level of miR-4508. The up-regulation of miR-4508 promotes the 16HBE inflammatory response induced by chrysotile asbestos through the PI3K/AKT pathway.

Objective To analyze the implementation effect of quality control on the homepage of inpatient medical re-cords based on the background of Disease Diagnosis Related Groups(DRG).Methods A retrospective study was conducted,including a total of 20,000 medical records from Dongguan People's Hospital from 2018 to 2022.Among them,10,000 medical records from January to December 2018,before the implementation of DRG-based quality control,were included as the control group;10,000 medical records from January to December 2022,after the implementation of DRG-based quality control,were in-cluded as the observation group.The implementation effect of quality control of hospital admission medical records among different groups based on DRG was explored.Results In the control group,there were 1,943 medical records with defects,accounting for 19.43％,which affected DRG grouping in 1,000 cases(51.47％)and did not affect DRG grouping in 943 cases(48.53％).In the observation group,there were 1,316 medical records with defects,accounting for 13.16％,among which 643 cases(48.86％)affected DRG grouping and 673 cases(51.14％)did not affect DRG grouping.The difference in the number of defective medical records between the groups was statistically significant(χ2=144.11,P<0.05).The missing rates of diagnos-tic and treatment information and cost information in the observation group were lower than those in the control group(P<0.05).The completeness and accuracy rates of diagnosis and surgical information in the observation group were higher than those in the control group(P<0.05).Conclusion The implementation of quality control of hospital admission medical records based on DRG can significantly improve the quality of medical records,increase the accuracy of diagnosis and surgical information in medi-cal records,and have higher comprehensive quality control value.It is recommended for clinical promotion and use.

Objective To investigate the involvement of calmodulin(CaM)in the pathogenesis of Alzheimer disease(AD)and the mechanism by which CaM binds to amyloid-β(Aβ).Methods The hub genes expressed in AD and predicted to be the target proteins for AD prevention and treatment were obtained using bioinformatics methods.The GST-Aβ1-42 recombinant plasmid was constructed through genetic recombination and was then sequenced.The recombinant plasmids were identified using agarose gel electrophoresis,while the extracted and purified GST-Aβ1-42 fusion protein was confirmed using SDS-PAGE gel electrophoresis.GST pull-down assay was used to detect the interaction between GST-Aβ1-42 protein and CaM,expressed in the plasmid.Results The top 20 hub genes in degree ranking were obtained.The DNA sequencing results of the plasmid proved that the recombinant plasmid was successfully constructed.The agarose gel electrophoresis results indicated that the fragment digested by the enzyme was similar to the molecular weight of the Aβ1-42 gene seg-ments,further proving the successful construction of the recombinant plasmid.Binding of GST-Aβ1-42 protein to CaM in a concentration dependent manner was revealed through the GST pull down experiment.Conclusion The GST-Aβ1-42 recombinant plasmid is success-fully constructed and is shown to bind to CaM.