ObjectiveTo establish and validate a new prediction model for the risk of death in patients with acute-on-chronic liver failure （ACLF） based on sarcopenia and other clinical indicators， and to improve the accuracy of prognostic assessment for ACLF patients. MethodsA total of 380 patients with ACLF who were admitted to Beijing YouAn Hospital， Capital Medical University， from January 2019 to January 2022 were enrolled， and they were divided into training group with 228 patients and testing group with 152 patients in a ratio of 6∶4 using the stratified random sampling method. For the training group， CT images were used to measure the cross-sectional area of the skeletal muscle at the third lumbar vertebra （L3）， and L3 skeletal muscle index （L3-SMI） was calculated. Sarcopenia was diagnosed based on the previously established L3-SMI reference values for healthy adults in northern China. Univariate and multivariable Cox regression analyses were used to establish a sarcopenia-ACLF model which integrated sarcopenia and clinical risk factors， and a nomogram was developed for presentation. The area under the ROC curve （AUC） was used to assess the predictive performance of the model， the calibration curve was used to assess the degree of calibration， and a decision curve analysis was used to investigate the clinical application value of the model. The independent-samples t test or the Mann-Whitney U test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between two groups. The Kaplan-Meier method was used to plot survival curves， and the Log-rank test was used for comparison between groups. The DeLong test was used for comparison of AUC between different models. ResultsThe multivariate Cox regression analysis showed that sarcopenia （hazard ratio ［HR］=1.962， 95% confidence interval ［CI］： 1.185‍ ‍—‍ ‍3.250， P=0.009）， total bilirubin （HR=1.003， 95%CI： 1.002‍ ‍—‍ ‍1.005， P<0.001）， international normalized ratio （HR=1.997， 95%CI： 1.674‍ ‍—‍ ‍2.382， P<0.001）， and lactic acid （HR=1.382， 95%CI： 1.170‍ ‍—‍ ‍1.632， P<0.001） were included in the sarcopenia-ACLF model. In the training cohort， the sarcopenia-ACLF model had a larger AUC than MELD-Na score in predicting 90-day mortality in patients with ACLF （0.80 vs 0.73， Z=1.97， P=0.049）. In the test cohort， the sarcopenia-ACLF model had a significantly larger AUC than MELD score （0.79 vs 0.69， Z=2.70， P=0.007） and MELD-Na score （0.79 vs 0.68， Z=2.92， P=0.004）. The calibration curve showed that the model had good calibration ability， with a relatively good consistency between the predicted risk of mortality and the observed results. The DCA results showed that within a reasonable range of threshold probabilities， the sarcopenia-ACLF model showed a greater net benefit than MELD and MELD-Na scores in both the training cohort and the test cohort. ConclusionThe sarcopenia-ACLF model developed in this study provides a more accurate tool for predicting the risk of 90-day mortality in ACLF patients， which provides support for clinical decision-making and helps to optimize treatment strategies.

Background Existing studies have confirmed that fine particulate matter (PM_2.5)is one of the important factors inducing pulmonary fibrosis. Pulmonary fibrosis is the terminal stage of a major category of lung diseases characterized by the destruction of tissue structure, and eventually leading lung ventilation and ventilation dysfunction. No effective pulmonary fibrosis treatment is available yet. Objective To investigate the protective effect of salidroside on pulmonary fibrosis induced by the exposure of PM_2.5 and its molecular mechanism. Methods Seventy 7-week-old male C57BL/6 mice were randomly divided into four groups: control group (intratracheal instillation of normal saline + saline by gavage, n=25), Sal group (intratracheal instillation of normal saline + Sal 60 mg·kg⁻¹ by gavage, n=10), PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ + saline by gavage, n=10), and Sal + PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ +Sal 60 mg·kg⁻¹ by gavage, n=10). The mice were administered by gavage once daily, intratracheal instillation once every 3 d, and every 3 d constituted an experimental cycle. At the end of the 26-30th cycles, 3 mice in the control group and 3 mice in the PM_2.5 group were randomly sacrificed, and the lung tissues were collected for Masson staining to verify whether the pulmonary fibrosis model was successfully established. After 30 cycles, the model was successfully constructed. After 1 week of continuous observation, the mice were sacrificed, and the blood and lung tissues of the mice were collected to make lung tissue sections. Assay kits were correspondingly employed to detect oxidative stress indicators such as serum malondialdehyde (MDA) and superoxide dismutase (SOD). Western blotting was used to detect the expression of fibrosis-related proteins (Collagen-III, α-SMA), mitochondrial dynamics-related proteins (MFN1, Drp1), and mitophagy-related proteins (PINK1, Parkin, and LC3). Results Compared with the control group, the weight gain rate of the PM_2.5 group was slowed down (P<0.05), which was alleviated by the Sal intervention (P<0.05). The lung coefficient increased after the PM_2.5 exposure (P<0.05), which was alleviated by Sal intervention. Compared with the control group, the PM_2.5 group showed severe alveolar structure damage, inflammatory cell infiltration, and blue collagen deposition, and significantly increased the lung injury score, collagen volume fraction (CVF), Szapiel score, and Ashcroft score (P<0.05), as well as serum oxidative stress levels (P<0.05). The protein expression levels of Collagen-III, α-SMA, Drp1, PINK1, Parkin, and LC3 II/I were increased (P<0.05), and the expression of MFN1 was decreased (P<0.05). Compared with the PM_2.5 group, the Sal intervention alleviated lung injury, reduced inflammatory cell infiltration and collagen deposition, showing decreased lung injury score, CVF, Szapiel score, and Ashcroft score (P<0.05), and decreased serum oxidative stress levels (P<0.05); the protein expression levels of Collagen-III, α-SMA, PINK1, Parkin, and LC3 II/I were decreased (P<0.05), the expression level of Drp1 was decreased, and the expression level of MFN1 was increased. Conclusion In the process of pulmonary fibrosis induced by PM_2.5 exposure in mice, Sal may affect mitochondrial autophagy through PINK1/Parkin pathway and play a protective role. The specific mechanism needs to be further verified.

Objective:To evaluate the effect of electroacupuncture on liver regeneration after partial hepatectomy in mice and the role of the Notch signaling pathway.Methods:Thirty-six SPF healthy male C57BL/6 mice, aged 6 weeks, weighing 20-22 g, were divided into 6 groups ( n=6 each) using a random number table method: sham operation group (group S), partial hepatectomy group (group PH), non-acupoint electroacupuncture+ partial hepatectomy group (group NPH), partial hepatectomy+ Fli-06 group (group PH+ F), acupoint electroacupuncture+ partial hepatectomy group (group EPH), and acupoint electroacupuncture+ partial hepatectomy+ Fli-06 group (group EPH+ F). All the mice except for group S underwent partial hepatectomy. Fli-06 4.8 mg/kg was intraperitoneally injected starting from 2 days before surgery, once a day, until the mice were sacrificed in group PH+ F and group EPH+ F, while the equal volume of 0.9% sodium chloride solution was injected in the other groups. In EPH group, electroacupuncture of bilateral " Zusanli" acupoints lasting for 15 min was performed using continuous waves with a frequency of 2 Hz and an intensity of 1 mA once a day starting from the time point immediately after surgery for 3 consecutive days. Mice were anesthetized at day 2 after partial hepatectomy, and blood samples were taken from the eyeball for determination of the serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations (using a fully automated biochemical analyzer) and concentrations of serum epidermal growth factor (EGF) and hepatocyte growth factor (HGF) (by enzyme-linked immunosorbent assay). The mice were subsequently sacrificed and liver tissues were taken for calculation of the liver mass to body mass ratio and for determination of the expression of liver proliferation marker Ki-67 (by immunohistochemical staining), proliferating cell nuclear antigen (PCNA), cyclin D1 (CCND1), Notch Intracellular Domain (NICD), and hypoxia-inducible factor-1alpha (HIF-1α) (using Western blot) and Notch1, jagged canonical Notch ligand 1 (Jagged1) and hairy and enhancer of split 1 (Hes1) mRNA (by real-time polymerase chain reaction). Results:Compared with group S, the serum ALT, AST, EGF and HGF concentrations were significantly increased, and the expression of hepatic Notch1, Jagged1 and Hes1 mRNA and Ki-67, PCNA, CCND1 and NICD was up-regulated in group PH ( P<0.05 or 0.01). Compared with group PH, the liver mass to body mass ratio and serum EGF and HGF concentrations were significantly increased, the serum ALT and AST concentrations were decreased, and the expression of hepatic Notch1, Jagged1, Hes1 mRNA and Ki-67, PCNA, CCND1, NICD and HIF-1α was up-regulated in group EPH, and the liver mass to body mass ratio and the serum HGF concentrations were significantly decreased, the serum ALT and AST concentrations were increased, and the expression of hepatic Jagged1 and Hes1 mRNA and Ki-67, PCNA, CCND1, NICD, and HIF-1α was down-regulated in group PH+ F ( P<0.05 or 0.01). Compared with group EPH, the liver mass to body mass ratio and serum EGF and HGF concentrations were significantly decreased, the serum ALT and AST concentrations were increased, and the expression of hepatic Notch1, Jagged1, Hes1 mRNA and Ki-67, PCNA, CCND1, NICD and HIF-1α was down-regulated in group EPH+ F ( P<0.01). Conclusions:Electroacupuncture at Zusanli acupoint promotes liver regeneration after partial hepatectomy in mice, and the mechanism may be related to the activation of the Notch signaling pathway.

Objective:To assess the association between diabetes mellitus and the risk of sudden cardiac death (SCD), and to identify potential contributing factors.Methods:This meta-analysis was an updated version of the original study Diabetes mellitus and the risk of sudden cardiac death： a systematic review and meta-analysis of prospective studies. The original review included all eligible case-control and cohort studies published in PubMed and Embase up to 2017 that investigated the association between diabetes and SCD risk. In this updated study, newly published studies were added, including those available in PubMed, Embase, China National Knowledge Infrastructure (CNKI), and WANFANG MED ONLINE up to December 3, 2023. Search terms included "diabetes""glucose""sudden cardiac death" "cardiac arrest" and their Chinese equivalent. The primary outcome was the risk of SCD, while factors such as country, ethnicity, skin color, follow-up duration, left ventricular ejection fraction (LVEF), baseline comorbidities, and other relevant variables were analyzed as potential influencing factors. Relative risk ( RR) was used as the summary measure. A random-effects model was used when significant heterogeneity was detected, otherwise a fixed-effects model was used. Cochran′s Q test was used for subgroup analysis to assess the influence of factors such as region, baseline diseases, LVEF, and ethnicity (based on skin color) on the outcomes. Results:A total of 32 cohort/case-control studies with a combined sample size of 3 252 954 individuals were included. The meta-analysis showed that the risk of SCD in patients with diabetes was double that of non-diabetics ( RR=2.00, 95% CI: 1.83-2.19, P<0.001). In Asian populations, the risk of SCD in diabetic patients was 1.78 times that of non-diabetic individuals ( RR=1.78, 95% CI: 1.51-2.10), 2.05 times that of in European populations ( RR=2.05, 95% CI: 1.79-2.34), and 2.12 times that of in American populations ( RR=2.12, 95% CI: 1.82-2.47), with no statistically significant heterogeneity between regions ( P=0.287). Among individuals without other baseline comorbidities, the risk of SCD was 2.12 times higher in diabetic patients than in those without diabetes ( RR=2.12, 95% CI: 1.89-2.38). In patients with baseline coronary heart disease, the risk was 1.75 times that of non-diabetics ( RR=1.75, 95% CI: 1.45-2.11). In those with baseline heart failure, the risk was 1.92 times that of non-diabetics ( RR=1.92, 95% CI: 1.51-2.43). In patients with baseline atrial fibrillation, the risk was 4.00 times that of non-diabetic individuals ( RR=4.00, 95% CI: 1.38-11.56). In patients undergoing hemodialysis due to renal failure, the risk was 1.76 times that of non-diabetic individuals ( RR=1.76, 95% CI: 1.25-2.48), with no statistically significant heterogeneity between groups ( P=0.262). In cardiac patients with LVEF>50%, the risk of SCD in diabetic patients was 2.08 times that of non-diabetic individuals ( RR=2.08, 95% CI: 1.57-2.75), and in those with LVEF<50%, the risk was 1.69 times that of non-diabetic individuals ( RR=1.69, 95% CI: 1.30-2.18), with no statistically significant heterogeneity between groups ( P=0.277). In yellow-skinned populations, the risk of SCD in diabetic patients was 1.80 times that of healthy individuals ( RR=1.80, 95% CI: 1.73-1.87), and in white-skinned populations, it was 2.18 times that of healthy individuals ( RR=2.18, 95% CI: 1.88-2.54), with statistically significant heterogeneity between groups ( P=0.014). Conclusions:Diabetes mellitus significantly increased the risk of SCD, and this effect may be more pronounced in white-skinned populations, while region, baseline comorbidities, and LVEF had no further effect.

Asthma is a chronic inflammatory disorder of the lungs that results in airway inflammation and narrowing. BS012 is an herbal remedy containing Asarum sieboldii, Platycodon grandiflorum, and Cinnamomum cassia extracts. To elucidate the anti-asthma effect of BS012, this study analyzed the immune response, respiratory protection, and changes in metabolic mechanisms in an ovalbumininduced allergic asthma mouse model. Female BALB/c mice were exposed to ovalbumin to induce allergic asthma. Bronchoalveolar lavage fluid and plasma were analyzed for interleukin and immunoglobulin E levels. Histological analyses of the lungs were performed to measure morphological changes. Apoptosis-related mediators were assayed by western blotting. Plasma and lung tissue metabolomic analyses were performed to investigate the metabolic changes. A T-helper-2-like differentiated cell model was used to identify the active components of BS012. BS012 treatment improved inflammatory cell infiltration, mucus production, and goblet cell hyperplasia in lung tissues. BS012 also significantly downregulated ovalbumin-specific immunoglobulin E in plasma and T-helper-2-specific cytokines, interleukin-4 and -5, in bronchoalveolar lavage fluid. The lungs of ovalbumin-inhaled mice exhibited nerve growth factor-mediated apoptotic protein expression, which was significantly attenuated by BS012 treatment. Ovalbumin-induced abnormalities in amino acid and lipid metabolism were improved by BS012 in correlation with its anti-inflammatory properties and normalization of energy metabolism. Additionally, the differentiated cell model revealed that N-isobutyl-dodecatetraenamide is an active component that contributes to the anti-allergic properties of BS012. The current findings demonstrate the anti-allergic and respiratory protective functions of BS012 against allergic asthma, which can be considered a therapeutic candidate.

Asthma is a chronic inflammatory disorder of the lungs that results in airway inflammation and narrowing. BS012 is an herbal remedy containing Asarum sieboldii, Platycodon grandiflorum, and Cinnamomum cassia extracts. To elucidate the anti-asthma effect of BS012, this study analyzed the immune response, respiratory protection, and changes in metabolic mechanisms in an ovalbumininduced allergic asthma mouse model. Female BALB/c mice were exposed to ovalbumin to induce allergic asthma. Bronchoalveolar lavage fluid and plasma were analyzed for interleukin and immunoglobulin E levels. Histological analyses of the lungs were performed to measure morphological changes. Apoptosis-related mediators were assayed by western blotting. Plasma and lung tissue metabolomic analyses were performed to investigate the metabolic changes. A T-helper-2-like differentiated cell model was used to identify the active components of BS012. BS012 treatment improved inflammatory cell infiltration, mucus production, and goblet cell hyperplasia in lung tissues. BS012 also significantly downregulated ovalbumin-specific immunoglobulin E in plasma and T-helper-2-specific cytokines, interleukin-4 and -5, in bronchoalveolar lavage fluid. The lungs of ovalbumin-inhaled mice exhibited nerve growth factor-mediated apoptotic protein expression, which was significantly attenuated by BS012 treatment. Ovalbumin-induced abnormalities in amino acid and lipid metabolism were improved by BS012 in correlation with its anti-inflammatory properties and normalization of energy metabolism. Additionally, the differentiated cell model revealed that N-isobutyl-dodecatetraenamide is an active component that contributes to the anti-allergic properties of BS012. The current findings demonstrate the anti-allergic and respiratory protective functions of BS012 against allergic asthma, which can be considered a therapeutic candidate.

Objectives:To understand the differences in clinical characteristics, treatment status, and prognosis between outpatient and inpatient heart failure patients in the real world.Methods:A prospective, multicenter registration study was conducted to select 972 outpatient or inpatient heart failure patients from 24 different regions and levels of hospitals in China from December 2012 to November 2014. Demographic and clinical data, as well as treatment status, were collected and followed up at 1 year. The difference in medication treatment status between baseline and 1-year follow-up was compared using McNemar paired χ 2 test. Pearson χ 2 test was used to compare the differences in clinical data, treatment status, and outcomes between outpatient and inpatient patients. Results:There were 610 outpatient patients (62.8%), and the proportion of outpatient patients under 65 years old was higher than that of hospitalized patients [44.9%(274/610) vs 35.1%(127/362), P<0.05]. The proportion of NYHA grade Ⅲ/Ⅳ patients was as high as 50.8%(310/610), and 92.5%(564/610) of outpatient patients had difficulty breathing while walking uphill. 27.9%(170/610) of outpatient patients had jugular vein pressure greater than 6 cmH 2O, and 24.3%(148/610) of outpatient patients had pulmonary moist rales. There was no significant difference in the main causes of heart failure between outpatient and inpatient patients ( P=0.063), with ischemic cardiomyopathy being the main cause. At baseline, the use of beta blockers in outpatient patients was higher than that in hospitalized patients [63.0%(384/610) vs 54.4%(197/362), P<0.05], while the use of diuretics and aldosterone receptor antagonists was lower than that in hospitalized patients [53.1%(324/610) vs 72.1%(261/362), 49.5%(302/610) vs 61.3%(222/362), P<0.05]. There was no statistically significant difference in the use of ACEI/ARB between the two groups [67.4%(411/610) vs 62.4%(226/362), P>0.05]. At one-year follow-up, the use of ACEI/ARB in outpatient patients decreased [63.5%(360/567) vs 67.4%(411/610), P<0.05], the usage rate of aldosterone receptor antagonists in hospitalized patients decreased by [50.3%(165/328) vs 61.3%(222/362), P<0.05]. The one-year all-cause mortality rate of the two groups of patients was close to [6.7%(41/610) vs 9.4%(34/362), P=0.124], The hospitalization rate for heart failure in the outpatient group was lower than that of hospitalized patients [25.4%(155/610) vs 36.5%(132/362), P<0.05], but still>25.0%. Conclusions:Outpatient heart failure patients still have obvious symptoms and signs, and the prognosis is poor. The standardized management of outpatient heart failure patients cannot be ignored.

Objective To explore the targets and mechanism of Jiegengbai Powder in the treatment of lung adenocarcinoma based on network pharmacology and animal experiments.Methods The targets of effective components of Jiegengbai Powder were obtained from TCMSP,the targets of lung adenocarcinoma were screened from GeneCards,PharmGKB,DrugBank,TTD,OMIM databases,and the intersection targets were obtained.The protein-protein interaction(PPI)network and active components of Chinese materia medica-target network were constructed by using Cytoscape 3.8.0 software,and the key components and core targets were screened out.The intersection targets were analyzed by GO and KEGG enrichment analysis.PyMOL and AutoDockTools 1.5.6 software were used to verify the molecular docking between the key components and core targets.The lung cancer mice model was established.The mice were randomly divided into blank group,model group,cisplatin group,Jiegengbai Powder combined with cisplatin group,Jiegengbai Powder low-,medium-and high-dosage groups.After 14 days of intervention,the tumor inhibition rate was calculated,and the morphology of tumor tissues was observed by HE staining.The gene and protein expressions of PI3K,PTEN,Akt and mTOR in tumor tissues were detected by RT-qPCR and Western blot.Results The core targets of Jiegengbai Powder in the treatment of lung adenocarcinoma such as TP53,CASP3,BCL2L1 and AKT1 were screened by network pharmacology.The key pathways of enrichment were PI3K-Akt signaling pathway and so on.Jiegengbai Powder can inhibit the growth of tumor effectively.Compared with the model group,the mRNA expressions of PI3K,Akt and mTOR decreased in the Jiegengbai Powder medium-and high-dosage groups,and PTEN mRNA expression increased,the ratio of p-PI3K/PI3K,p-Akt/Akt and p-mTOR/mTOR decreased,and the expression of PTEN protein increased(P<0.05,P<0.01).Conclusion Jiegengbai Powder has the characteristics of multi-level and multi-target in the treatment of lung adenocarcinoma.It may promote tumor cell apoptosis and autophagy by regulating PI3K/Akt/mTOR signaling pathway,so as to achieve the anti-tumor effect of inhibiting tumor cell growth.

Background Salidroside (SAL) has a protective effect on multiple organ systems. Exposure to fine particulate matter (PM_2.5) in the atmosphere may lead to disruptions in gut microbiota and impact intestinal health. The regulatory effect of SAL on the gut microbiota of mice exposed to PM_2.5 requires further investigation. Objective To evaluate gut microbiota disruption in mice after being exposed to PM_2.5 and the potential effect of SAL. Methods Forty male C57BL/6 mice, aged 6 to 8 weeks, were randomly divided into four groups: a control group, an SAL group, a PM_2.5 group, and an SAL+PM_2.5 group, each containing 10 mice. In the SAL group and the SAL+PM_2.5 group, the mice were administered SAL (60 mg·kg⁻¹) by gavage, while in the control group and the PM_2.5 group, sterile saline (10 mL·kg⁻¹) was administered by gavage. In the PM_2.5 group and the SAL+PM_2.5 group, PM_2.5 suspension (8 mg·kg⁻¹) was intratracheally instilled, and in the control group and SAL group, sterile saline (1.5 mL·kg⁻¹) was intratracheally administered. Each experiment cycle spanned 2 d, with a total of 10 cycles conducted over 20 d. Histopathological changes in the ileum tissue of the mice were observed after HE staining. Colon contents were collected for gut microbiota sequencing and short-chain fatty acids (SCFAs) measurements. Results The PM_2.5 group showed infiltration of inflammatory cells in the ileum tissue, while the SAL+PM_2.5 group exhibited only a small amount of inflammatory cell infiltration. Compared to the control group, the PM_2.5 group showed decreased Shannon index (P<0.05) and increased Simpson index (P<0.05), indicating that the diversity of gut microbiota in this group was decreased; the SAL+PM_2.5 group showed increased Shannon index compared to the PM_2.5 group (P<0.05) and decreased Simpson index (P<0.05), indicating that the diversity of gut microbiota in mice intervened with SAL was increased. The principal coordinates analysis (PCoA) revealed a significant separation between the PM_2.5 group and the control group, while the separation trend was less evident among the control group, the SAL group, and the SAL+PM_2.5 group. The unweighted pair-group method with arithmetic means (UPGMA) clustering tree results showed that the control group and the SAL group clustered together first, followed by clustering with the SAL+PM_2.5 group, and finally, the three groups clustered with the PM_2.5 group. The PCoA and UPGMA clustering results indicated that the uniformity and similarity of the microbiota in the PM_2.5 group were significantly decreased. Compared to the control group, the PM_2.5 group showed decreased abundance of phylum Bacteroidetes and Candidatus_Saccharimonas (P<0.05) and increased abundance of phylum Proteobacteria, genus Escherichia, genus Bacteroides, genus Prevotella, genus Enterococcus, and genus Proteus (P<0.05). Compared to the PM_2.5 group, the SAL+PM_2.5 group showed decreased abundance of phylum Proteobacteria, phylum Actinobacteria, genus Prevotella, and genus Proteus (P<0.05), and increased abundance of Candidatus_Saccharimonas (P<0.05). The PM_2.5 group showed reduced levels of propionic acid, valeric acid, and hexanoic acid compared to the control group (P<0.05), while the SAL+PM_2.5 group showed increased levels of propionic acid, isobutyric acid, butyric acid, valeric acid, and hexanoic acid compared to the PM_2.5 group (P<0.05). Conclusion Exposure to PM_2.5 can cause pathological alterations, microbial dysbiosis, and disturbing production of SCFAs in intestinal tissue in mice. However, SAL can provide a certain degree of protective effect against these changes.

Objective To understand the molecular characteristics of Streptomycin(SM)resistance in multidrug-resistant tuberculosis(MDR-TB)in Jiangxi Province,and to explore the relationship between SM resistant genes(rpsL,rrs and gidB)mutations and SM resistant phenotypes in Beijing genotype TB.Methods 106 non-replicated MDR-TB isolates were collected from Gaoxin Branch of The First Affiliated Hospital of Nanchang University and Jiangxi Provincial Chest Hospital from January to December 2021,and tested for drug-resistance phenotypes,whether they were Beijing genotype or not and the characteristics of rpsL,rrs and gidB gene mutations.Chi-square test was performed to determine whether rpsL,rrs and gidB mutations were related to genotypes and drug-resistance phenotypes.Results Among 106 cases of MDR-TB,76 cases were resistant to SM.A total of 58 cases had rpsL 43A>G mutation,8 cases had 88A>G mutation,5 cases had rrs mutation,and 3 cases had gidB mutation.Statistical analysis showed that the coincidence rate of gene mutation and phenotypic drug-resistance detection was 89.6%,and the specificity and sensitivity were 86.7%and 90.8%,respectively.The isolated rate of Beijing genotype TB was 88.7%,and the drug-resistant gene mutations were mainly concentrated in rpsL and rrs,while the drug-resistant mutations of non-Beijing genotype were mainly concentrated in gidB;in addition,Beijing genotype bacteria were more prone to gene mutations(P = 0.013),but there was no difference in phenotypic drug-resistance.Conclusions Mutations in rpsL,rrs,and gidB genes have a good coincidence rate with phenotypic drug-resistance,and molecular biology can be used to detect directly drug-resistance genes to predict bacterial resistance;TB genotypes are strongly associated with streptomycin resistance characteristics.