Objective:To detect the expression levels of long non-coding RNAs(lncRNA)in elderly patients with pulmonary tuberculosis(PTB)and those with non-tuberculous lung diseases(non-TB), and to assess the performance of these lncRNA in the differential diagnosis of PTB.Methods:A total of 300 elderly patients with suspected PTB were recruited from Beijing Chest Hospital between January 2024 and September 2024, and were further divided into the PTB group and the non-TB lung disease group based on the results of mycobacterium tuberculosis(MTB)pathogenicity testing.Peripheral blood mononuclear cells were isolated using a lymphocyte separation solution, and RNA was extracted using the TRIzol method.Nine lncRNAs, previously identified as differentially expressed in PTB through our group's microarray analysis, were selected and detected by real-time fluorescence quantitative polymerase chain reaction to evaluate the expression levels of these lncRNAs between the PTB and non-TB lung disease groups.The overall patients were randomly divided into training and validation sets in a 7∶3 ratio.Lasso regression was employed to select the characteristic variables, and a random forest algorithm was then used to construct the lncRNA diagnostic portfolio.Receiver operating characteristic(ROC)curves were generated to evaluate the diagnostic performance of individual lncRNAs and the combined panel in differentiating elderly patients with PTB from those with other non-TB lung diseases.Results:A total of 201 cases were included, with 105 confirmed elderly patients diagnosed with PTB(52.2%)and 96 elderly patients suffering from non-TB lung disease(47.8%).Compared to the elderly patients with non-TB lung disease, the expression levels of ENST00000417346.1, ENST00000620744.1, lncRNA PWP1, ENST00000583184.1, lncRNA ABHD17B, ENST00000607464.1, ENST00000516057.1, and NR_003000 were significantly downregulated in the PTB patients, whereas the expression level of lncRNA BCL2L10 was significantly upregulated in the PTB patients.ROC analysis revealed that the area under the curve(AUC)for each lncRNA ranged from 0.659 to 0.848.The diagnostic panel, which included NR_003000, ENST00000607464.1, ENST00000583184.1, and ENST00000620744.1 as determined by Lasso analysis, exhibited AUC values of 0.917 and 0.906 in the training and validation sets, respectively.The performance of this panel was superior to that of each individual lncRNA.Conclusions:The random forest model, which incorporates NR_003000, ENST00000607464.1, ENST00000583184.1, and ENST00000620744.1, demonstrates potential in differentiating between PTB and non-TB lung diseases.

Objective:To analyze the correlation between 24-hour urinary sodium excretion and early renal function impairment in patients with primary hypertension.Methods:This cross-sectional study included patients with primary hypertension who were admitted to the Department of Cardiology of the Chinese People′s Liberation Army General Hospital between January 2021 and October 2024. Patients were divided into low-sodium, medium-sodium, and high-sodium groups based on their 24-hour urinary sodium excretion. General clinical data were collected using the electronic medical record system. Urinary sodium, protein, and microalbumin excretion were analyzed from 24-hour urine samples. Spearman correlation analysis was used to explore the relationship between 24-hour urinary sodium excretion and urinary microalbumin excretion. A multiple linear regression model was used to further assess the independent association between these variables. Subgroup analyses were conducted based on age were performed to determine whether age influenced the relationship between urinary sodium excretion and renal function impairment.Results:A total of 1 065 patients with primary hypertension were included, with a mean age of (55.26±14.06) years, including 568(53.33%) males. The low-sodium, medium-sodium, and high-sodium groups included 223, 579, and 263 patients, respectively. The 24-hour urinary microalbumin excretion in the high-sodium group was significantly higher than in the medium-sodium and low-sodium groups, and this trend remained consistent across different age groups (all P<0.05). Spearman correlation analysis showed a positive correlation between 24-hour urinary sodium excretion and urinary microalbumin excretion ( r=0.220, P<0.001), and this relationship was observed in all age groups (all P<0.05). Multiple linear regression analysis confirmed an independent association between 24-hour urinary sodium excretion and urinary microalbumin excretion (all P<0.001), which persisted across different age groups (all P<0.05). Conclusion:In patients with primary hypertension, 24-hour urinary sodium excretion is closely associated with microalbumin excretion, suggesting a potential link to early renal function impairment.

Objective : To analyze the current status of anti-PD-1 combined with chemotherapy in advanced gastric cancer. Methods: The clinical data of 120 patients with advanced gastric cancer treated with chemotherapy or anti-PD-1 plus chemotherapy were retrospectively analyzed. The efficacy [measures include objective response rate(ORR), disease control rate(DCR), and progression-free survival(PFS)]and the occurrence of adverse reactions in patients was monitored. Univariate and multivariate Cox were used to analyze the relationship between clinicopathologic data [including age, gender, body mass index(BMI), differentiation degree, and related hematological indexes], specific treatment conditions and PFS, and to analyze the influence of treatment plan and line number on the curative effect. Results : The PFS of chemotherapy plus immunotherapy was significantly better than that of chemotherapy alone(P<0.05), and the median PFS of the two was 7.17 months(95%CI5.85-8.49) and 5.33 months(95%CI3.96-5.70), respectively. In the combination group, the overall ORR was 27.5% and DCR was 94.8%. In the chemotherapy group alone, the overall ORR was 9.7% and DCR was 69.4%.In the chemotherapy plus anti-PD-1 group, a high prognostic nutritional index(PNI) level also provided superior PFS in patients with a 47% reduction in the risk of progression versus a low PNI level [HR0.53(95%CI0.30-0.96);P<0.05]. The median PFS was 7.47 months(95%CI5.83-9.11) with a high PNI level versus 6.00 months(95%CI4.45-7.55) with a low PNI level. The overall incidence of adverse reactions of chemotherapy combined with anti-PD-1 was slightly higher than that of chemotherapy alone, and the incidence of adverse reactions of grade 3-4 was similar, within a controllable range, and could be improved after clinical treatment. Conclusion The efficacy of anti-PD-1 combined with chemotherapy in patients with advanced gastric cancer is better than that of chemotherapy, and the adverse reactions are controllable. In the chemotherapy plus anti-PD-1 group, patients with high PNI levels achieved a higher PFS.

Objective To explore the repair effect and mechanism of human amniotic mesenchymal stem cells(hAMSCs)on endometrial injury.Methods hAMSCs were isolated using a two-enzyme digestion and then cultured.The third-passage(P3)cells were harvested to detect the surface markers by flow cytometry and to identify their trilineage differentiation potentials.Eighteen nulliparous female SD rats(8～9 weeks old,weighing 250～280 g)were randomly divided into 3 groups(n=6):normal control group,model group,and hAMSCs group.A rat model of intrauterine adhesions(IUA)was established in SD rats by using curettage combined with lipopolysaccharide(LPS)infection.In 2 weeks after modeling,the hAMSCs group received a bilateral uterine horn transplantation of 0.2 mL hAMSCs(1.0×10? cells/mL),while the model group received a same volume of PBS into both uterine horns.All rats were sacrificed in 2 weeks after transplantation.HE and Masson staining was used to observe endometrial thickness and gland number as well as endometrial fibrosis area.RT-qPCR and Western blotting were performed to detect the mRNA and protein levels of TGF-β1,Smad3,Smad7,epithelial-mesenchymal transition(EMT)markers(E-cadherin,Vimentin),fibrosis factor α-SMA,and endometrial estrogen receptor(ER)and progesterone receptor(PR)in endometrial tissues.Results The obtained cells were identified as hAMSCs due to the characteristics of surface markers and differentiation potentials.Compared with the normal control group,the model group showed decreased endometrial thickness,reduced gland number,increased fibrosis area,and enhanced mRNA and protein levels of fibrosis-related factors TGF-β1,Smad3,Vimentin,and α-SMA(P<0.01),while down-regulation of fibrosis-inhibiting molecule Smad7,the EMT marker E-cadherin,and endometrial receptors ER and PR at both mRNA and protein levels(P<0.01).hAMSCs transplantation increased endometrial thickness and gland number,decreased fibrosis area,and down-regulated mRNA expression of the aforementioned fibrosis-related factors(P<0.01),and up-regulated the mRNA expression levels of Smad7,E-cadherin,ER,and PR(P<0.01).The hAMSCs group also exhibited obviously down-regulated protein levels of TGF-β1,Smad3,and α-SMA(P<0.05),while enhanced protein levels of Smad7 and PR(P<0.05).Conclusion Intrauterine transplantation of hAMSCs can promote the repair of endometrial injury,and inhibits endometrial EMT and fibrosis through the TGF-β1/Smad7 signaling pathway.

Objective:To investigate the influence of four preoperative CT image characteristics on the outcome of thoracoscopic surgery for chronic tuberculous empyema.Methods:This is a retrospective cohort study. Two hundred and eleven patients of tuberculous empyema who underwent video-assisted thoracic surgery(VATS) decortication at the First Department of Surgery , Wuhan Pulmonary Hospital from June 2020 to June 2023 were retrospectively analyzed. There were 162 male cases and 49 female cases, with an age ( M (IQR)) of 33 (27) years (range: 8 to 76 years). Patients were divided into two groups according to whether low-density lines, mass-patchy density, pleural fusion were observed, and the lesion size. Compare the clinical indicators of two groups of cases. Using the rapeutic efficacy as the dependent variable and four CT features as covariates, cases with cure or improve were included in Logistic regression analysis to calculate OR (95% CI) values. Results:Preoperative chest CT images showed that 127 cases (60.2%) had low-density lines, 102 cases (48.3%) had mass-patchy density, and 88 cases (47.7%) had pleural fusion. The lesions spanned 2 to 11 intercostal spaces, with a median of 7 intercostal spaces. The lesion size was divided into two groups according to <7 intercostal spaces and ≥7 intercostal spaces, with 101 cases (47.9%) and 110 cases (52.1%), respectively. In the intra-group comparison, there were no difference in age, lesion location and pulmonary tuberculosis. In the comparison of gender, except that the proportion of female patients in the group with lesion size <7 intercostal spaces ( χ2=6.064, P=0.010) was higher than ≥7 intercostal spaces, there were no significant difference between other groups. In low-density lines group, there was no difference in the incidence of anemia and hypoproteinemia between the two groups. Compared with the non low-density line group, patients with low-density line group exhibited fewer cases of abnormal elevation in ESR and CRP was lower(all P<0.01), the period of preoperative treatment ( U=7 281.00, P<0.01) was longer than the non low-density line group, while the operation time, intraoperative hemorrhage, postoperative drainage at 72 hours, postoperative drainage duration, lung re-expansion duration, and therapeutic efficacy were all better than the non low-density line group(all P<0.05). In the comparison between the mass-patchy density group, there were fewer cases of anemia, hypoproteinemia, abnormal elevation of ESR and CRP in the without mass-patchy density group(all P<0.05), and the period of preoperative treatmentwas shorter ( U=4 581.50, P=0.026), and the operation time, intraoperative hemorrhage, postoperative drainage at 72 hours, postoperative drainage duration, lung re-expansion duration and therapeutic effect were better too(all P<0.05). In the grouping comparison of pleural fusion, there were no difference in cases of anemia, hypoproteinemia, abnormal elevation of ESR and CRP, and the period of preoperative treatment between the two groups; the operation time, intraoperative hemorrhage, postoperative drainage at 72 hours, postoperative drainage duration, lung re-expansion duration, and therapeutic efficacy of the group without pleural fusion were better than the group with pleural fusion(all P<0.05). The group with <7 intercostal spaces had fewer cases of anemia, hypoproteinemia, abnormal elevation of ESR and CRP (all P<0.05), the period of preoperative treatment was longer ( U=4 295.00, P=0.004), the operation time, intraoperative hemorrhage, postoperative drainage at 72 hours,postoperative drainage duration, lung re-expansion duration and complications were less (all P<0.05), the therapeutic efficacy was better than the group with ≥7 intercostal spaces ( χ2=27.912, P<0.01). The Logistic regression analysis of cured and improved cases showed that mass-patchy density and lesion size were independent risk factors affecting the therapeutic efficacy (all P<0.05). Conclusions:For patients with CT images showing mass-patchy density, pleural fusion, and a large lesion size, the difficulty and risk of surgery may be relatively high.The preoperative CT images can provide objective reference for clinical preoperative evaluation.

Objective:To investigate the role and mechanism of TrxR1 in reprogramming tumor-associated macrophage in breast cancer,providing novel insights and theoretical foundations for clinical breast cancer treatment.Methods:TISIDB database was used to analyze the relationship between TXNRD1(encoding TrxR1)and tumor immunity.Mouse breast cancer 4T1 cells conditioned medium was collected and co-cultured with bone marrow-derived macrophage(BMDM)cells for 48 h to detect the expression of macrophage immunosuppression-related factors.TrxR1 secretion by tumor cells was measured using ELISA kits.TXNRD1 knockdown efficiency was verified via Western blot.Fluorescence quantitative PCR(qPCR)and flow cytometry were used to detect the expression levels of macrophage immunosuppressive factors after TXNRD1 knockdown in tumor cells.JASPAR database was used to analyze the potential regulatory factors,and Western blot was used to verify the expression of pathway-related proteins.Results:Database analysis found that TXNRD1 expression positively correlated with survival risk indices across multiple cancers,with the strongest association observed in breast cancer.Further analysis found that elevated TXNRD1 expression correlated with reduced infiltration of M1 macrophages and natural killer(NK)cells,but increased M2 macrophage infiltration.qPCR and flow cytometry demonstrated that tumor-conditioned medium enhanced macrophage immunosuppression,whereas medium from TXNRD1-knockdown tumor cells suppressed this effect.And TrxR1-neutralizing antibodies could also reversed this effect.JASPAR database analysis identified STAT3 and STAT6 as potential transcriptional regulators,and Western blot confirmed that TXNRD1-knockdown tumor cells conditioned medium inhibited STAT6 pathway activation in macrophages.Conclusion:In the tumor microenvironment,breast tumor-derived TrxR1 promotes macrophage immunosuppression,potentially through activation of the STAT6 signaling pathway.

Objective·To investigate the effects of rutin on proliferation,apoptosis,migration and invasion of osteosarcoma cells and its possible molecular mechanisms.Methods·Human osteosarcoma MG63 and U2OS cells were treated with rutin at concentrations of 10,20 and 40 μmol/L,respectively.The effects of rutin on proliferation,apoptosis,migration,and invasion of MG63 and U2OS cells were assessed by using CCK-8 assay,colony formation assay,flow cytometry,scratch closure assay,and Transwell assay.The expression levels of cell proliferation antigen Ki67,B-cell lymphoma-2(Bcl-2),and Bcl-2 associated X protein(Bax)proteins were detected by Western blotting.Twelve BALB/c nude mice were subcutaneously injected with osteosarcoma MG63 cells to establish a subcutaneous transplant tumor model.The mice were randomly divided into two groups:a control group and a rutin 40 mg/kg group(6 mice in each group).The rutin 40 mg/kg group was intraperitoneally injected with rutin(40 mg/kg),and the control group was intraperitoneally injected with an equal volume of saline,once every other day for 4 weeks.The tumor volume was measured every week.After 4 weeks,the mice were euthanized,and the tumors were excised and weighed.Immunohistochemistry was used to detect the expression of Ki67 and vascular endothelial growth factor(VEGF)in tumor tissues.TUNEL was used to detect tumor cell apoptosis.Results·Compared with MG63 and U2OS cells not treated with rutin,MG63 and U2OS cells treated with rutin at 20 and 40 μmol/L showed a significant decrease in proliferation rate,an increase in apoptotic rate,a decrease in migration and invasion abilities,a significant downregulation of Ki67 protein,and a significant increase in Bax/Bcl-2 ratio,with statistically significant differences(all P＜0.05).In addition,rutin significantly inhibited the in vivo growth of osteosarcoma cells,reduced the expression of Ki67 and VEGF in tumor tissues,and promoted cell apoptosis(all P＜0.05).Conclusion·Rutin can inhibit the proliferation,migration,and invasion of osteosarcoma cells,and promote apoptosis.

Objective To investigate the anti-tumor effect of Job's tears oral solution on lung cancer mice.Methods Observe the histopathological morphology of the tumor;Flow cytometry detected the changes in the levels of CD4+T and CD8+T in splenic lymphocytes;Elisa detected the contents of immunoglobulins IgA,IgG,IL-2 and IFN-γ;Blood routine was detected;the kit determined the levels of liver and kidney glutathione peroxidase(GSH-Px),superoxide dismutase(SOD)and malondialdehyde(MDA)content;Serum alanine aminotransferase(ALT),alkaline phosphatase(ALB),azelaic transaminase(AST),urea nitrogen(BUN),and blood creatinine(CRE)were measured in each group of mice.The transcriptome was found differential genes and pathway enrichment was performed.Western blot was used to detect the expression of proteins related to IL-17 signaling pathway(STAT3,NF-κB,VEGF)and TNF signaling pathway(PI3K/AKT,MAPK,JNK).Results Tumor histopathological and morphological changes were obvious in each administration group,and the heterogeneity was gradually reduced.Compared with the cisplatin group,the levels of CD4+T,CD8+T,CD4+T/CD8+T,IL-2,IFN-γ,and IgG in the Job's tears group were significantly increased(P<0.01).The blood routine results:compared with the model group,WBC,RBC,HGB,PLT,Lym%and GR%in the Job's tears group decreased significantly(P<0.01);Compared with the cisplatin group,WBC,RBC,PLT,HGB and Lym%in the Job's tears group increased significantly(P<0.01).The antioxidant indexes of liver and kidney showed that the levels of GSH and SOD in the liver and kidney tissues of the Job's tears group increased significantly(P<0.01),and the level of MDA decreased significantly(P<0.01).Effects on liver and kidney function indexes in mice AST,ALT,BUN and CRE decreased significantly in the Job's tears group(P<0.01),and ALB level increased significantly in the Job's tears group(P<0.01).Transcriptome results,Job's tears high-dose group mainly exerted anti-tumor effects by affecting TNF signaling pathway and IL-17 signaling pathway.Western blot results,in the IL-17 signaling pathway,S-TAT3 and VEGF decreased in the cisplatin group and the Job's tears group compared with the model group(P<0.01),and NF-κB decreased in the Job's tears high-dose group(P<0.01);Compared with the cisplatin group,STAT3 and NF-κB were decreased in the Job's tears group(P<0.01);VEGF was decreased in the Job's tears low-dose group(P<0.01);In the TNF signaling pathway,PI3K and MAPK were decreased in the cisplatin group and Job's tears group(P<0.01);AKT and P-AKT were decreased in the Job's tears group(P<0.01).Compared with the cisplatin group,the Job's tears group AKT,PI3K,and MAPK decreased(P<0.01);P-AKT decreased in the high dose group of Job's tears(P<0.01).Conclusion High-dose Job's tears oral solution inhibits tumor proliferation,attenuates inflammatory response,enhances immunity,improves blood routine and reduces liver and kidney injury in lung cancer mice mainly by inhibiting IL-17 and TNF signaling pathway.

Objective:To investigate the role and mechanism of TrxR1 in reprogramming tumor-associated macrophage in breast cancer,providing novel insights and theoretical foundations for clinical breast cancer treatment.Methods:TISIDB database was used to analyze the relationship between TXNRD1(encoding TrxR1)and tumor immunity.Mouse breast cancer 4T1 cells conditioned medium was collected and co-cultured with bone marrow-derived macrophage(BMDM)cells for 48 h to detect the expression of macrophage immunosuppression-related factors.TrxR1 secretion by tumor cells was measured using ELISA kits.TXNRD1 knockdown efficiency was verified via Western blot.Fluorescence quantitative PCR(qPCR)and flow cytometry were used to detect the expression levels of macrophage immunosuppressive factors after TXNRD1 knockdown in tumor cells.JASPAR database was used to analyze the potential regulatory factors,and Western blot was used to verify the expression of pathway-related proteins.Results:Database analysis found that TXNRD1 expression positively correlated with survival risk indices across multiple cancers,with the strongest association observed in breast cancer.Further analysis found that elevated TXNRD1 expression correlated with reduced infiltration of M1 macrophages and natural killer(NK)cells,but increased M2 macrophage infiltration.qPCR and flow cytometry demonstrated that tumor-conditioned medium enhanced macrophage immunosuppression,whereas medium from TXNRD1-knockdown tumor cells suppressed this effect.And TrxR1-neutralizing antibodies could also reversed this effect.JASPAR database analysis identified STAT3 and STAT6 as potential transcriptional regulators,and Western blot confirmed that TXNRD1-knockdown tumor cells conditioned medium inhibited STAT6 pathway activation in macrophages.Conclusion:In the tumor microenvironment,breast tumor-derived TrxR1 promotes macrophage immunosuppression,potentially through activation of the STAT6 signaling pathway.