Objective To construct and validate the efficacy of a risk prediction model for pneumothorax after CT-guided percutaneous pulmonary puncture biopsy(CT-PCNB)based on nomograms.Methods A total of 246 patients who underwent CT-PCNB examination in the hospital from October 2020 to October 2023 were selected and divided into training set(n=144)and validation set(n=102)using a random sampling method.In the training set,univariate and multivariate logistic regression analyses were performed to identify risk factors for pneumothorax after CT-PCNB.A nomogram model was constructed based on the identified risk factors,and its accuracy was validated using the validation set.Results Multifactorial logistic regression analysis showed that age≥60 years,concomitant underlying lung disease,lesion diameter<2 cm,distance from lesion to pleura≥10 mm,puncture through interlobular pleura,and≥2 pleural punctures were the risk factors for pneumothorax after CT-PCNB in the training set(P<0.05).A nomogram model was constructed based on these six factors.The ROC curve results for the training set showed an AUC of 0.852,sensitivity of 84.50%,and specificity of 67.50%.The nomogram model was validated using the validation set,with ROC curve results showing an AUC of 0.845,sensitivity of 83.00%,and specificity of 69.50%.There was no statistically significant difference between the predicted and actual values in both the training and validation sets(χ2=1.803,1.225;P>0.05),indicating clinical validity.Conclusion The nomogram model constructed based on the risk factors for pneumothorax after CT-PCNB has high predictive efficacy and is clinically meaningful.

Objective To investigate the impact of aortic valve calcification on ascending aortic elasticity.Methods A total of 103 patients with aortic valve calcification indicated by coronary computed tomography angiography(CCTA)(calcification group),and 101 patients without aortic valve calcification(non calcification group)were selected.The calcification group was subdivided into group A,group B,and group C based on the number of calcified leaflets.The original data was automatically reconstructed at 5％R-R intervals throughout the cardiac cycle.Cross-sectional area and diameter of the ascending aorta were measured at 45 mm above the annulus,and four ascending aortic elasticity indicators aortic(％A),aortic distensibility(AD),aortic compliance(AC)and aortic stiffness index(ASI)were calculated.Agatston method was used to calculate the aortic valve calcification score.The effect of aortic valve calcification on the elasticity of the ascending aortic and its correlation were analyzed.Results The％A,AD,and AC of the calcification group were lower than those of the non calcification group,but the ASI was higher than that of the non calcification group,the difference was statistically significant(P＜0.05).The number of calcified leaflets affected ascending aortic elasticity,with comparisons between groups A and B,the difference was no statistically significant(P＞0.05),groups A and C,and groups B and C,the difference was statistically significant(P＜0.05).Calcification score was negatively correlated with％A,AD,and AC,and positively correlated with ASI.Conclusion Aortic valve calcification can affect the elasticity of the ascending aortic,and more than two calcified leaflets have more significant effects on the elasticity of the ascending aortic.

Objective To construct and validate the efficacy of a risk prediction model for pneumothorax after CT-guided percutaneous pulmonary puncture biopsy(CT-PCNB)based on nomograms.Methods A total of 246 patients who underwent CT-PCNB examination in the hospital from October 2020 to October 2023 were selected and divided into training set(n=144)and validation set(n=102)using a random sampling method.In the training set,univariate and multivariate logistic regression analyses were performed to identify risk factors for pneumothorax after CT-PCNB.A nomogram model was constructed based on the identified risk factors,and its accuracy was validated using the validation set.Results Multifactorial logistic regression analysis showed that age≥60 years,concomitant underlying lung disease,lesion diameter<2 cm,distance from lesion to pleura≥10 mm,puncture through interlobular pleura,and≥2 pleural punctures were the risk factors for pneumothorax after CT-PCNB in the training set(P<0.05).A nomogram model was constructed based on these six factors.The ROC curve results for the training set showed an AUC of 0.852,sensitivity of 84.50%,and specificity of 67.50%.The nomogram model was validated using the validation set,with ROC curve results showing an AUC of 0.845,sensitivity of 83.00%,and specificity of 69.50%.There was no statistically significant difference between the predicted and actual values in both the training and validation sets(χ2=1.803,1.225;P>0.05),indicating clinical validity.Conclusion The nomogram model constructed based on the risk factors for pneumothorax after CT-PCNB has high predictive efficacy and is clinically meaningful.

Objective To investigate the impact of aortic valve calcification on ascending aortic elasticity.Methods A total of 103 patients with aortic valve calcification indicated by coronary computed tomography angiography(CCTA)(calcification group),and 101 patients without aortic valve calcification(non calcification group)were selected.The calcification group was subdivided into group A,group B,and group C based on the number of calcified leaflets.The original data was automatically reconstructed at 5％R-R intervals throughout the cardiac cycle.Cross-sectional area and diameter of the ascending aorta were measured at 45 mm above the annulus,and four ascending aortic elasticity indicators aortic(％A),aortic distensibility(AD),aortic compliance(AC)and aortic stiffness index(ASI)were calculated.Agatston method was used to calculate the aortic valve calcification score.The effect of aortic valve calcification on the elasticity of the ascending aortic and its correlation were analyzed.Results The％A,AD,and AC of the calcification group were lower than those of the non calcification group,but the ASI was higher than that of the non calcification group,the difference was statistically significant(P＜0.05).The number of calcified leaflets affected ascending aortic elasticity,with comparisons between groups A and B,the difference was no statistically significant(P＞0.05),groups A and C,and groups B and C,the difference was statistically significant(P＜0.05).Calcification score was negatively correlated with％A,AD,and AC,and positively correlated with ASI.Conclusion Aortic valve calcification can affect the elasticity of the ascending aortic,and more than two calcified leaflets have more significant effects on the elasticity of the ascending aortic.

Trihelix transcription factors play important roles in plant light responses, growth and development, and stress responses. However, Trihelix has not yet been reported in Eucommia ulmoides. In this study, bioinformatics methods were used to comprehensively identify and analyze the expression patterns of the Trihelix gene family in E. ulmoides, aiming to provide a basis for further functional studies of EuGTs genes. A total of 9 Trihelix gene family members were identified in E. ulmoides, encoding proteins with 339 to 883 amino acids, with isoelectric points ranging from 5.13 to 9.39 and relative molecular weights between 36 992.06 and 97 871.61. Subcellular localization results showed that only EuGT-2 was localized in chloroplasts, while the others were located in the nucleus. The Trihelix gene family was categorized into six subfamilies: GT-1, GT-2, SH4, SIP1, GTγ, and GTδ. EuGTs were distributed among three subfamilies: SH4, GT-1, and GT-2, containing 1, 6, and 2 Trihelix proteins, respectively, with 2 to 17 exons. The promoters of EuGTs contained various cis-acting elements related to hormones, stress, photoperiod, and growth and development. Collinearity analysis revealed 5 collinear gene pairs between E. ulmoides and Arabidopsis thaliana, and 14 collinear gene pairs between E. ulmoides and Populus. Expression pattern analysis showed that EuGTs exhibited tissue-specific expression: EuGT-1, EuGT-2 had the highest expression levels in leaves, EuGT-4, EuGT-6, EuGT-9 had the highest transcriptional levels in marginal peel, and EuGT-5、EuGT-8 were predominantly expressed in the xylem. As leaves developed, EuGTs showed a trend of asynchronous changes. No significant differences in EuGTs expression were observed between male and female flowers, with high expression levels mainly during the induction stage of flowering. The qRT-PCR analysis indicated that most EuGTs genes were most highly expressed in the leaves of E. ulmoides, while EuGT-5 was highly expressed in the stems. Under 200 mmol·L~(-1) NaCl treatment, most EuGTs genes exhibited an initial increase followed by a decrease in expression, significantly responding to salt stress. This study provides important genetic resources for further exploration of EuGTs gene functions and germplasm innovation in E. ulmoides.
Plant Proteins/metabolism* ; Gene Expression Regulation, Plant ; Eucommiaceae/chemistry* ; Phylogeny ; Multigene Family/genetics* ; Gene Expression Profiling ; Transcription Factors/metabolism* ; Genome, Plant/genetics*

Objective:To explore the role of cathepsin S(CTSS) in diabetic vascular injury-induced restenosis.Methods:(1) Dendritic cells(DCs) were stimulated with different concentrations of glucose, and CTSS was either knocked down or upregulated in dendritic cells using adenovirus transfection. The mRNA and protein expression levels of CTSS were detected by RT-qPCR and Western blot, and the changes of interleukin(IL)-6 levels were assessed using RT-qPCR and ELISA in response to CTSS. (2) The extent of Th17 cell differentiation was evaluated with Flow cytometry when CTSS was downregulated or overexpressed. Levels of ROR-γt, IL-17A, IL-17F, IL-22, and IL-23 were measured. (3) Streptozomycin(STZ, 60 mg/kg) was injected into the intraperitoneal cavity of rats fasted for 12 h to obtain a diabetic rat model, and the restenosis model was obtained by balloon catheter and carotid guidewire injury, and the differentiation degree of Th17 cells in different groups of rats was compared when CTSS was up-regulated and down-regulated.Results:(1) DC viability decreased when stimulated with 35 mmol/L glucose for 48 hours. Compared to the control group, glucose treatment led to a concentration-dependent increase in CTSS and IL-6 levels in DCs( P<0.05). Inhibition of CTSS reduced IL-6 protein levels, while its overexpression increased IL-6 protein levels( P<0.05). (2) Compared with the control group, CTSS inhibition in DC decreased the percentage of Th17 cells in T cells, with decreased protein levels of ROR-γt, IL-17A, IL-17F, IL-22, and IL-23, and vice versa ( P<0.050). (3) After carotid artery injury, CTSS expression was increased in perivascular adipose tissue(PVAT) of rats, and levels of ROR-γt, IL-17A, IL-17F, IL-22, and IL-23 in PVAT were significantly elevated. Down-regulation of CTSS eliminated the glucose-induced enhancement. Conclusion:Inhibition of CTSS in DC reduces Th17 cell differentiation and thereby suppresses restenosis following diabetic vascular injury.

Benign prostatic hyperplasia(BPH)is one of the major chronic complications of type 2 diabetes mellitus(T2DM),and sex steroid hormones are common risk factors for the occurrence of T2DM and BPH.The profiles of sex steroid hormones are simultaneously quantified by LC-MS/MS in the clinical serum of patients,including simple BPH patients,newly diagnosed T2DM patients,T2DM complicated with BPH patients and matched healthy individuals.The G protein-coupled estrogen receptor(GPER)inhibitor G15,GPER knockdown lentivirus,the YAP1 inhibitor verteporfin,YAP1 knockdown/overexpression lentivirus,targeted metabolomics analysis,and Co-IP assays are used to investigate the molecular mechanisms of the disrupted sex steroid hormones homeostasis in the pathological process of T2DM complicated with BPH.The homeostasis of sex steroid hormone is disrupted in the serum of patients,accompanying with the proliferated prostatic epithelial cells(PECs).The sex steroid hormone metabolic profiles of T2DM patients complicated with BPH have the greatest degrees of separation from those of healthy individuals.Elevated 17β-estradiol(E2)is the key contributor to the disrupted sex steroid hormone homeostasis,and is significantly positively related to the clinical characteristics of T2DM patients complicated with BPH.Activating GPER by E2 via Hippo-YAP1 signaling exacerbates high glucose(HG)-induced PECs prolifer-ation through the formation of the YAP1-TEAD4 heterodimer.Knockdown or inhibition of GPER-mediated Hippo-YAP1 signaling suppresses PECs proliferation in HG and E2 co-treated BPH-1 cells.The anti-proliferative effects of verteporfin,an inhibitor of YAP1,are blocked by YAP1 overexpression in HG and E2 co-treated BPH-1 cells.Inactivating E2/GPER/Hippo/YAP1 signaling may be effective at delaying the progression of T2DM complicated with BPH by inhibiting PECs proliferation.

Mismatch repair-deficient/microsatellite instability-high(dMMR/MSI-H)gastric cancer represents a distinct molecular subtype of tumors characterized by pronounced sensitivity to immune checkpoint inhibitors(ICIs)attributed to its unique immune microenvironment and elevated mutation burden.Various clinical studies underscore the efficacy of ICIs in treating dMMR/MSI-H gastric cancer;however,chal-lenges such as primary and acquired resistance persist.Overcoming resistance and identifying optimal ICIs for its treatment remain critical clinical issues.This review delineates the mechanisms of ICIs,recent advances in their therapeutic application for dMMR/MSI-H gastric can-cer,and ongoing challenges in combating resistance,aiming to guide clinical practice effectively.

Objective To investigate the effect of glycine N-methyl transferase (GNMT)on intrauterine adhesion (IUA)fibrosis and its related mechanism.Methods In vivo experiment:A total of 36 healthy female SD rats (SPF grade,6～8 weeks old and weighing from 180～220 g)were subjected in this study.IUA model of SD rats and IUA model of GNMT overexpressed rats were established.RT-qPCR and immunofluorescence assay were applied to detect GNMT expression level in normal uterus and model group.RT-qPCR and Western blotting were used to detect the mRNA and protein levels of fibrosis-related molecules and the activation of TGF-β1/Smad3 signaling pathway in each group.The number of endometrial glands in each group was observed by HE staining.Masson staining was used to analyze the severity of endometrial fibrosis in each group.In vitro experiment:transformed human endometrial stromal cells (THESCs)fibrotic phenotype model was constructed using TGF-β1,and THESCs stably transfected with GNMT overexpression lentvirus were treated with TGF-β1.RT-qPCR and Western blotting were used to detect the mRNA and protein expression of fibrosis-related molecules.The expression of TGF-β1/Smad3 signaling pathway was detected by Western blotting.TGF-β1/Smad3 signaling pathway was activated by TGF-β1/Smad signaling pathway activator (SRI-011381),and the expression of TGF-β1/Smad3 signaling pathway and key molecular proteins of fibrosis phenotype was measured with Western blotting.Results In vivo experiment,the mRNA and protein expression levels of GNMT were significantly decreased in the IUA rats than the control rats (P<0.05).Overexpression of GNMT decreased the mRNA and protein levels of fibrosis related molecules,Collagen Ⅰ,Collagen Ⅲ and FN in the IUA rats (P<0.05),and decreased the phosphorylation levels of TGF-β1 and its downstream Smad3 protein (P<0.05).HE and Masson staining showed that overexpression of GNMT could increase the number of endometrial glands and reduce the severity of fibrosis in the IUA rats (P<0.05).In vitro experiments:overexpression of GNMT decreased the mRNA and protein levels of Collagen Ⅰ,Collagen Ⅲ and FN associated with fibrotic phenotype of THESCs (P<0.05),and reduced the phosphorylation level of Smad3 protein,downstream of TGF-β1 (P<0.05).After activation of TGF-β1/Smad3 signaling pathway,the protein levels of TGF-β1/Smad3 signaling pathway and downstream fibrosis phenotype molecules,Collagen Ⅲ and FN,were significantly decreased in the LV-GNMT+SRI-011381 group.Conclusion Overexpression of GNMT can inhibit endometrial fibrosis by regulating TGF-β1/Smad3 signaling pathway,thus achieving therapeutic effect on IUA.

Objective To explore the intrinsic steady-state electrophysiological properties of mouse heart under physiological conditions by high-resolution quantitative analysis.Methods Twenty-two young adult C57BL/6 mice with a 1:1 male-to-female ratio were used.The limbs of the mice were fixed without anesthesia,and electrocardiographic waveforms,including characteristic P-waves,R-waves,and ST-waves,were recorded using a sensitive 12-lead electrophysiological recorder(ECGsqa)under spontaneous breathing.LabScribe software was used to extract and quantify high-resolution time course and amplitude parameters within a single cardiac cycle from the V3 precordial lead.Pearson correlation test combined with simple linear regression was used to generate a scatter plot of ECG parameter fitting.The common and unique correlation parameters were separately identified by joint associations for profiling the quantitative association network.Results ECGsqa analysis identified and quantified 14 characteristic ECG parameters,28.6%of which showed statistical differences between the groups.Compared to male mice,female mice exhibited higher amplitudes and velocities of R and ST waves.Among the 51 association pairs identified in primary association analysis,47.1%were positively correlated,including shared(29.2%),male-specific(29.2%),and female-specific(41.7%)association groups.Second-order clustering of the association pairs revealed that the amplitude-rate association pairs of each waveform voltage in both male and female mouse hearts were strongly correlated.The male mice showed an atrioventricular interconnection pattern,while the female mice showed a unique atrial conduction system quality dependence.The distribution network characteristics of the association groups showed that sex-specific and common correlation sets formed a certain series pattern.Conclusion We discovered a novel intrinsic correlation network of cardiac electrophysiological traits in male and female mice,which reveals the key internal quantitative characteristics and gender difference of both atrial and ventricular conduction systems.