Objective:This study aimed to analyze the prognostic risk factors for hepatoid adenocarcinoma of the stomach (HAS) and construct two nomogram-based clinical prediction models to predict overall survival (OS) and recurrence-free survival (RFS) in patients with HAS.Methods:Data were retrospectively collected from 82 patients (64 males, 18 females; mean age 60.3 ± 9.4 years) who underwent radical gastrectomy and were pathologically diagnosed with gastric hepatoid adenocarcinoma at the First Medical Center of the PLA General Hospital between February 2006 and September 2023. Statistical analyses were conducted using SPSS 25.0 and R 4.3.2. Survival analyses were performed using the Kaplan-Meier method, and univariate analyses were used to identify clinical and pathological factors associated with prognosis. Variables with P<0.05 in the univariate analysis were included in multivariate Cox regression models to identify independent risk factors for OS and RFS. These factors were incorporated into the prediction models to construct nomograms. The discriminatory power of the models was assessed using the area under the curve (AUC) of receiver operating characteristic (ROC) analyses, while calibration curves, decision curve analysis (DCA), and comparisons with the 8th edition of the TNM staging system of the American Joint Committee on Cancer (AJCC) were employed to evaluate model performance. Results:Among the 82 patients, 36 (43.9%) exhibited vascular infiltration, 61 (74.4%) had nerve infiltration, and lymph node metastasis was observed in 60 cases (73.2%). Pathological stages I, II, III, and IV were distributed as 11 (13.4%), 26 (31.7%), 44 (53.7%), and 1 (1.2%) cases, respectively. Inflammatory markers included neutrophil-to-lymphocyte ratio (NLR) ≥ 4.33 in 22 cases (26.8%), platelet-to-lymphocyte ratio (PLR) ≥ 142.2 in 50 cases (61.0%), monocyte-to-lymphocyte ratio (MLR) ≥ 0.411 in 22 cases (26.8%), α-fetoprotein (AFP) ≥ 2.48 μg/L in 64 cases (78.0%), and C-reactive protein (CRP) ≥ 7.506 mg/L in 12 cases (14.6%). Among the 82 patients, 3 cases (3.6%) were lost to follow-up. The median follow-up time was 52 (range: 8–147) months, with a median OS of 61(2–147) months. The 1-year and 3-year OS rates were 78.5% and 58.5%, respectively, while the 1-year and 3-year RFS rates were 77.3% and 60.3%, respectively. Multivariate analysis identified several independent risk factors influencing OS in patients with HAS: advanced pathological stage, MLR ≥ 0.411, AFP ≥ 2.545 μg/L, and CRP ≥ 7.51 mg/L. The hazard ratios (HRs) and 95% confidence intervals (CIs) were as follows: 5.218 (1.230–22.143), 2.610 (1.287–5.294), 2.950 (1.013–8.589), and 2.594 (1.145–5.877), respectively (all P < 0.05). For RFS, advanced pathological stage, PLR ≥ 152.0, and MLR ≥ 0.411 were independent risk factors, with HRs (95% CIs) of 4.735 (1.080–20.760), 3.759 (1.259–11.226), and 2.714 (1.218–6.048), respectively (all P < 0.05). The AUC values for OS prediction at 1 year, 3 years, and 5 years were 0.7765, 0.7525, and 0.7702, respectively. For RFS, the AUC values were 0.7304, 0.8137, and 0.8307 at 1 year, 3 years, and 5 years, respectively. The calibration curves demonstrated strong agreement between nomogram- predicted outcomes and observed survival data. DCA indicated that both TNM staging and the nomogram-based clinical prediction models provided a net positive benefit in predicting OS and RFS in HAS patients, with the nomogram model demonstrating superior performance. Conclusion:The nomogram-based clinical prediction models developed in this study demonstrated robust performance in predicting long-term OS and RFS in patients with HAS.

Objectives:This study aims to investigate the association between Chinese visceral adiposity index(CVAI)and the risk of cardiovascular disease(CVD),and explore the sex differences.Methods:Participants were screened from the three sub-cohorts of Prediction for Atherosclerotic Cardiovascular Disease Risk in China(China-PAR)project,baseline information on body measure and biochemistry examinations were collected from 1998,2000-2001,and 2007-2008,separately.Participants were followed up to 2015.Cohort-stratified Cox proportional risk models were used to analyze the relationship between CVAI,both in continuous(per standard deviation increase)and categorical(quartiles,with Q1 as reference)scales,and CVD risk in the total population,men and women.The multiplicative interaction between sex and CVAI on CVD risk were calculated.Restricted cubic spline regression was employed to investigate the dose-response relationship.Results:A total of 98 464 participants without CVD at baseline were included.During the 723 508 person-years of follow-up,3 605 CVD events were recorded.After multivariate adjustment,the HRs(95％CIs)of CVD were 1.25(1.20-1.29),1.09(1.04-1.15),and 1.54(1.46-1.64)for per standard deviation increment in CVAI in the general population,men and women,respectively.Besides,compared with Q1 group,the HRs(95％CIs)in Q4 group were 1.87(1.67-2.10),1.33(1.14-1.54)and 3.84(3.09-4.78),correspondingly,and the effect of CVAI on the risk of CVD was significantly higher in women than in men(Pinteraction<0.05).Additionally,there was a positive dose-response relationship between CVAI and the risk of CVD.Conclusions:Elevated CVAI is an independent risk factor for CVD,especially in women.

Objective:This study aimed to analyze the prognostic risk factors for hepatoid adenocarcinoma of the stomach (HAS) and construct two nomogram-based clinical prediction models to predict overall survival (OS) and recurrence-free survival (RFS) in patients with HAS.Methods:Data were retrospectively collected from 82 patients (64 males, 18 females; mean age 60.3 ± 9.4 years) who underwent radical gastrectomy and were pathologically diagnosed with gastric hepatoid adenocarcinoma at the First Medical Center of the PLA General Hospital between February 2006 and September 2023. Statistical analyses were conducted using SPSS 25.0 and R 4.3.2. Survival analyses were performed using the Kaplan-Meier method, and univariate analyses were used to identify clinical and pathological factors associated with prognosis. Variables with P<0.05 in the univariate analysis were included in multivariate Cox regression models to identify independent risk factors for OS and RFS. These factors were incorporated into the prediction models to construct nomograms. The discriminatory power of the models was assessed using the area under the curve (AUC) of receiver operating characteristic (ROC) analyses, while calibration curves, decision curve analysis (DCA), and comparisons with the 8th edition of the TNM staging system of the American Joint Committee on Cancer (AJCC) were employed to evaluate model performance. Results:Among the 82 patients, 36 (43.9%) exhibited vascular infiltration, 61 (74.4%) had nerve infiltration, and lymph node metastasis was observed in 60 cases (73.2%). Pathological stages I, II, III, and IV were distributed as 11 (13.4%), 26 (31.7%), 44 (53.7%), and 1 (1.2%) cases, respectively. Inflammatory markers included neutrophil-to-lymphocyte ratio (NLR) ≥ 4.33 in 22 cases (26.8%), platelet-to-lymphocyte ratio (PLR) ≥ 142.2 in 50 cases (61.0%), monocyte-to-lymphocyte ratio (MLR) ≥ 0.411 in 22 cases (26.8%), α-fetoprotein (AFP) ≥ 2.48 μg/L in 64 cases (78.0%), and C-reactive protein (CRP) ≥ 7.506 mg/L in 12 cases (14.6%). Among the 82 patients, 3 cases (3.6%) were lost to follow-up. The median follow-up time was 52 (range: 8–147) months, with a median OS of 61(2–147) months. The 1-year and 3-year OS rates were 78.5% and 58.5%, respectively, while the 1-year and 3-year RFS rates were 77.3% and 60.3%, respectively. Multivariate analysis identified several independent risk factors influencing OS in patients with HAS: advanced pathological stage, MLR ≥ 0.411, AFP ≥ 2.545 μg/L, and CRP ≥ 7.51 mg/L. The hazard ratios (HRs) and 95% confidence intervals (CIs) were as follows: 5.218 (1.230–22.143), 2.610 (1.287–5.294), 2.950 (1.013–8.589), and 2.594 (1.145–5.877), respectively (all P < 0.05). For RFS, advanced pathological stage, PLR ≥ 152.0, and MLR ≥ 0.411 were independent risk factors, with HRs (95% CIs) of 4.735 (1.080–20.760), 3.759 (1.259–11.226), and 2.714 (1.218–6.048), respectively (all P < 0.05). The AUC values for OS prediction at 1 year, 3 years, and 5 years were 0.7765, 0.7525, and 0.7702, respectively. For RFS, the AUC values were 0.7304, 0.8137, and 0.8307 at 1 year, 3 years, and 5 years, respectively. The calibration curves demonstrated strong agreement between nomogram- predicted outcomes and observed survival data. DCA indicated that both TNM staging and the nomogram-based clinical prediction models provided a net positive benefit in predicting OS and RFS in HAS patients, with the nomogram model demonstrating superior performance. Conclusion:The nomogram-based clinical prediction models developed in this study demonstrated robust performance in predicting long-term OS and RFS in patients with HAS.

OBJECTIVE To investigate the anti-inflammatory mechanisms of demethylzeylasteral(Dem)in ulcerative colitis(UC)and collagen-induced arthritis(CIA),focusing on its regulation of Th17 cell differentiation and associated signaling pathways.METHODS UC was induced in C57BL/6 mice using dextran sulfate sodium(DSS),and Dem was administered by gavage at low(1 mg·kg-1)or high(2 mg·kg-1)doses.Disease severity was assessed by body weight loss,colon length,and stool consisten-cy.Serum cytokines(TNF-α,IL-1β,IL-6)were quantified by ELISA,and Th17 cell ratio in mesenteric lymph nodes was deter-mined by flow cytometry.The anti-inflammatory efficacy of Dem was further validated using a CIA mouse model.The efficacy of Dem was further verified in the CIA model,and the expression of JAK2 and STAT3 was intervened by siRNA to investigate its mechanism of action in Th17 differentiation.RESULTS Dem-treated mice showed reduced weight loss and colon shortening,and decreases in ser-um TNF-α,IL-1β,and IL-6 levels(P<0.01)and Th17 cell proportion(P<0.01).Western blot and siRNA assays showed that Dem significantly inhibited the differentiation and activation of Th17 cells by suppressing the phosphorylation of the JAK2-STAT3 path-way.Dem also significantly alleviated arthritis symptoms and related markers in the CIA model,confirming its anti-inflammatory effects.CONCLUSION Dem improves UC and rheumatoid arthritis by downregulating the JAK2-STAT3 signaling pathway,inhibi-ting Th17 cell differentiation and pro-inflammatory cytokine expression,suggesting its potential therapeutic value in immune-related diseases.

OBJECTIVE To investigate the anti-inflammatory mechanisms of demethylzeylasteral(Dem)in ulcerative colitis(UC)and collagen-induced arthritis(CIA),focusing on its regulation of Th17 cell differentiation and associated signaling pathways.METHODS UC was induced in C57BL/6 mice using dextran sulfate sodium(DSS),and Dem was administered by gavage at low(1 mg·kg-1)or high(2 mg·kg-1)doses.Disease severity was assessed by body weight loss,colon length,and stool consisten-cy.Serum cytokines(TNF-α,IL-1β,IL-6)were quantified by ELISA,and Th17 cell ratio in mesenteric lymph nodes was deter-mined by flow cytometry.The anti-inflammatory efficacy of Dem was further validated using a CIA mouse model.The efficacy of Dem was further verified in the CIA model,and the expression of JAK2 and STAT3 was intervened by siRNA to investigate its mechanism of action in Th17 differentiation.RESULTS Dem-treated mice showed reduced weight loss and colon shortening,and decreases in ser-um TNF-α,IL-1β,and IL-6 levels(P<0.01)and Th17 cell proportion(P<0.01).Western blot and siRNA assays showed that Dem significantly inhibited the differentiation and activation of Th17 cells by suppressing the phosphorylation of the JAK2-STAT3 path-way.Dem also significantly alleviated arthritis symptoms and related markers in the CIA model,confirming its anti-inflammatory effects.CONCLUSION Dem improves UC and rheumatoid arthritis by downregulating the JAK2-STAT3 signaling pathway,inhibi-ting Th17 cell differentiation and pro-inflammatory cytokine expression,suggesting its potential therapeutic value in immune-related diseases.

Objectives:This study aims to investigate the association between Chinese visceral adiposity index(CVAI)and the risk of cardiovascular disease(CVD),and explore the sex differences.Methods:Participants were screened from the three sub-cohorts of Prediction for Atherosclerotic Cardiovascular Disease Risk in China(China-PAR)project,baseline information on body measure and biochemistry examinations were collected from 1998,2000-2001,and 2007-2008,separately.Participants were followed up to 2015.Cohort-stratified Cox proportional risk models were used to analyze the relationship between CVAI,both in continuous(per standard deviation increase)and categorical(quartiles,with Q1 as reference)scales,and CVD risk in the total population,men and women.The multiplicative interaction between sex and CVAI on CVD risk were calculated.Restricted cubic spline regression was employed to investigate the dose-response relationship.Results:A total of 98 464 participants without CVD at baseline were included.During the 723 508 person-years of follow-up,3 605 CVD events were recorded.After multivariate adjustment,the HRs(95％CIs)of CVD were 1.25(1.20-1.29),1.09(1.04-1.15),and 1.54(1.46-1.64)for per standard deviation increment in CVAI in the general population,men and women,respectively.Besides,compared with Q1 group,the HRs(95％CIs)in Q4 group were 1.87(1.67-2.10),1.33(1.14-1.54)and 3.84(3.09-4.78),correspondingly,and the effect of CVAI on the risk of CVD was significantly higher in women than in men(Pinteraction<0.05).Additionally,there was a positive dose-response relationship between CVAI and the risk of CVD.Conclusions:Elevated CVAI is an independent risk factor for CVD,especially in women.

Background::Despite the adverse effects of ambient fine particulate matter (PM 2.5) on type 2 diabetes and the beneficial role of physical activity (PA), the influence of PM 2.5 on the relationship between PA and type 2 diabetes remains unclear. Methods::In this prospective study with 71,689 participants, PA was assessed by a questionnaire and was categorized into quartiles for volume and three groups for intensity. Long-term PM 2.5 exposure was calculated using 1-km resolution satellite-based PM 2.5 estimates. PM 2.5 exposure and PA's effect on type 2 diabetes were assessed by cohort-stratified Cox proportional hazards models, individually and in combination. Results::In 488,166 person-years of follow-up, 5487 incident type 2 diabetes cases were observed. The association between PA and type 2 diabetes was modified by PM 2.5. Compared with the lowest quartile of PA volume, the highest quartile was associated with reduced type 2 diabetes risk in low PM 2.5 stratification (≤65.02 μg/m 3) other than in high PM 2.5 stratification (>65.02 μg/m 3), with the hazard ratio (HR) of 0.75 (95% confidence interval [CI]: 0.66-0.85) and 1.10 (95% CI: 0.99-1.22), respectively. Similar results were observed for PA intensity. High PM 2.5 exposure combined with the highest PA levels increased the risk of type 2 diabetes the most (HR= 1.79, 95% CI: 1.59-2.01 for PA volume; HR = 1.82, 95% CI: 1.64-2.02 for PA intensity). Conclusion::PA could reduce type 2 diabetes risk in low-pollution areas, but high PM 2.5 exposure may weaken or even reverse the protective effects of PA. Safety and health benefits of PA should be thoroughly assessed for long-term polluted residents.

AIM: To evaluate the effect of remimazolam on early postoperative cognitive function in elderly patients with hip fracture based on a randomized controlled trial. METHODS: A total of 106 elderly patients, aged 65-90 years, ASA grade Ⅱ or III, who underwent hip fracture surgery under combined spinal-epidural anesthesia in the Sixth Affiliated Hospital of Wenzhou Medical University from December 2022 to June 2023 and met the inclusion criteria, were selected and randomized into remimazolam group (group R) and propofol group (group P) according to the random number table, with 53 cases in each group. Patients in group P received a slow intravenous injection of propofol at a dose of 0.3-0.5 mg / kg (injection time of 1min), followed by a pump infusion at 0.5-3 mg · kg