Background Ambient air pollution is a major environmental risk factor for cardiovascular disease (CVD). However, epidemiological evidence regarding the modifying effect of a healthy lifestyle on the association between air pollution and CVD remains inconsistent. Objective To investigate the modifying effect of a healthy lifestyle on the association between exposure to air pollutants and CVD risk, to provide evidence for targeted prevention strategies. Methods Databases including PubMed, Web of Science, Embase, the Cochrane Library, CNKI, and Wanfang were systematically searched for epidemiological studies published from January 2011 to August 2025. The quality of included studies was assessed, and relevant data were extracted. A meta-analysis was performed to examine the association between air pollutant exposure and CVD outcomes, as well as the modifying effect of a healthy lifestyle. Results A total of 24 studies were included. The meta-analysis demonstrated that each 10 μg·m⁻³ increase in the concentration of ultrafine particulate matter (PM₁), fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), and ozone (O₃) was associated with pooled relative risks (RRs) for CVD morbidity of 1.176 (95%CI: 1.007, 1.373), 1.167 (95%CI: 1.035, 1.315), 1.030 (95%CI: 1.012, 1.048), 1.093 (95%CI: 1.039, 1.150), 1.014 (95%CI: 0.996, 1.032), and 1.216 (95%CI: 0.901, 1.641), respectively; each 10 mg·m⁻³ increase in the concentration of carbon monoxide (CO) was associated with a pooled RR for CVD morbidity of 1.005 (95%CI: 1.005, 1.006). For CVD mortality, each 10 μg·m⁻³ increase in PM_2.5, PM₁₀, and NO₂ yielded pooled RRs of 1.188 (95%CI: 1.032, 1.367), 1.137 (95%CI: 0.953, 1.357), and 1.038 (95%CI: 1.011, 1.066), respectively; for SO₂ and O₃, where only a single study was available, RRs were 1.068 (95%CI: 1.030, 1.108) and 1.010 (95%CI: 0.996, 1.024) per 10 μg·m⁻³ increase, respectively; for CO, where also only a single study was available, the RR was 1.002 (95%CI: 1.001, 1.003) per 10 mg·m⁻³ increase. Adherence to a healthy lifestyle significantly modified the PM_2.5-associated CVD risk. Specifically, compared to healthy behaviors, unhealthy factors including smoking, low-quality diet, and physical inactivity exacerbated this risk, with relative effect sizes (RES; ratio of hazard ratios of the unhealthy group to the healthy group) of 1.016 (95%CI: 1.013, 1.020), 1.008 (95%CI: 1.003, 1.013), and 1.058 (95%CI: 1.055, 1.062), respectively. Furthermore, a combined healthy lifestyle demonstrated a superior modifying effect compared to any single lifestyle factor, which significantly attenuated the PM_2.5-associated CVD risk (P for interaction < 0.05). Conclusion Long-term exposure to ambient PM_2.5 significantly increases CVD risk. However, adherence to a combined healthy lifestyle can effectively mitigate these adverse effects, offering substantially greater cardiovascular protection than maintaining any single healthy habit.

Background: and Purpose Vertebrobasilar fusiform aneurysms (VBFAs) carry substantial morbidity and mortality, but optimal management for unruptured VBFAs remains unclear. We compared the safety and efficacy of conservative management (CM), stent-assisted coiling (SAC), and flow diverters (FDs) in patients with unruptured VBFAs, focusing on long-term prognosis. Methods: This study included data from a nationwide Chinese cohort of patients with vertebrobasilar dissecting aneurysms. Inverse probability of treatment weighting (IPTW) balanced confounders across groups. The primary outcome was poor prognosis (modified Rankin Scale score >2). Secondary outcomes included aneurysm rupture, ischemic stroke, compression symptoms, and VBFA-related deaths. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup and sensitivity analyses were performed. Results: Among 1,115 patients with unruptured VBFAs, 838 (median age, 54 years; 655 men) were included. After IPTW, baseline characteristics were balanced. Median follow-up was 54 months. FD was associated with a lower risk of poor prognosis than CM (OR, 0.48 [95% CI, 0.30 to 0.77]; p=0.002), with no difference between CM and SAC. FD also reduced aneurysm rupture (OR, 0.20 [95% CI, 0.07 to 0.60]; p=0.004) and compression symptoms (OR, 0.30 [95% CI, 0.13 to 0.68]; p=0.004) versus CM. Time-to-event analyses further revealed significant differences in vertebral artery lesions and Type I–II VBFAs, whereas no significant differences were observed in basilar or vertebrobasilar junction lesions or in Type III–IV VBFAs. Conclusions Compared with CM, FD was associated with improved long-term outcomes in unruptured VBFAs, particularly in vertebral artery lesions and Type I–II VBFAs, although residual confounding cannot be excluded.

ObjectiveTo investigate the protective effect of Xielitang on dextran sulfate sodium （DSS）-induced ulcerative colitis （UC） mice and its possible mechanism. MethodsDSS was used to establish UC model. Sixty mice were randomly divided into a normal group， a model group， a sulfasalazine group （0.6 g·kg^-1）， and low-， medium-， and high-dose Xielitang groups （1.67， 3.34， 6.68 g·kg^-1）. After treatment for 42 d， the colon length was recorded， and the disease activity index （DAI） score was calculated. Enzyme-linked immunosorbent assay （ELISA） was used to detect the serum levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-10 （IL-10）. Hematoxylin-eosin （HE） staining was used to observe the pathomorphological changes of colon. Western blot was used to detect the protein expression of farnesoid X receptor （FXR）， small heterodimer partner （SHP）， liver receptor homolog-1 （LRH-1）， cholesterol 7α-hydroxylase （CYP7A1）， and fibroblast growth factor receptor 4 （FGFR4） in liver and FXR， sodium-dependent bile acid transporter （ASBT）， and fibroblast growth factor 15 （FGF15） in ileum. 16S rRNA sequencing was used to analyze the intestinal flora. Moreover， ultra-high performance liquid chromatography–tandem mass spectrometry was used to detect the bile acid content. ResultsCompared with the normal group， the model group showed significantly decreased colon length， IL-10 content， α-diversity index， abundance of Firmicutes and Lactobacillus， and content of deoxycholic acid （DCA） and lithocholic acid （LCA） （P<0.01）， significantly increased DAI score， IL-6 and TNF-α content， abundance of Bacteroidetes， and the content of cholic acid （CA）， chenodeoxycholic acid （CDCA）， and taurocholic acid （TCA） （P<0.05， P<0.01）， significantly down-regulated protein expression of FXR， SHP， and FGFR4 in liver and FXR， ASBT， and FGF15 in ileum （P<0.01）， and significantly up-regulated protein expression of LRH-1 and CYP7A1 in liver （P<0.01）. In addition， the structure of colonic mucosa was destroyed， and inflammatory cells infiltrated in the model group. Compared with the model group， Xielitang could significantly increase the colon length， IL-10 content， α-diversity index， the abundance of Firmicutes and Lactobacillus， and DCA and LCA content （P<0.05， P<0.01）， decrease DAI score， abundance of Bacteroidetes， and the content of IL-6， TNF-α， CA， CDCA， and TCA （P<0.01）， up-regulate the protein expression of FXR， SHP， and FGFR4 in liver and FXR， ASBT， and FGF15 in ileum （P<0.01）， and down-regulate the protein expression of LRH-1 and CYP7A1 in liver （P<0.01）. The pathological damage of colonic mucosa was obviously alleviated. ConclusionXielitang protects against UC probably by regulating the "intestinal microbiota-bile acid" axis， regulating intestinal flora imbalance， and maintaining bile acid homeostasis.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Objective:To evaluate the role of ferroptosis in reduction of intestinal ischemia-reperfusion injury (IRI) by sodium butyrate pretreatment in mice.Methods:Thirty SPF healthy male C57BL/6 mice, aged 6-8 weeks, weighing 20-23 g, were divided into 5 groups ( n=6 each) using a random number table method: sham operation group (S group), intestinal IRI group (IR group), intestinal IRI + sodium butyrate pretreatment group (IN group), intestinal IRI + sodium butyrate pretreatment+ FER-1 group (INF group), and intestinal IRI + sodium butyrate pretreatment + Erastin group (INE group). The intestinal IRI model was established by occluding the superior mesenteric artery for 45 min followed by reperfusion for 30 min in S group. In IN, INF and INE groups, sodium butyrate was administered by gavage at a dose of 500 mg/kg daily at 1 week before developing the model, while the equal volume of normal saline was given by gavage in the other two groups. The ferroptosis inhibitor FER-1 5 mg/kg and ferroptosis agonist Erastin 30 mg/kg were intraperitoneally injected at 1 h prior to ischemia in INF and INE groups. Mice were sacrificed after anesthesia at the end of reperfusion to obtain small intestinal tissues for examination of the pathological changes (using light microscopy) which were scored according to Chiu and for determination of the contents of Fe 2+, malondialdehyde (MDA), glutathione (GSH) and glutathione disulfide(GSSG) (by enzyme-linked immunosorbent assay), expression of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and ferritin heavy chain 1 (FTH1) (by Western blot). The ratio of GSH to GSSG was calculated. Results:Compared to S group, Chiu′s scores and contents of MDA and Fe 2+ were significantly increased, the expression of GSH, GPX4, FTH1 and SLC7A11 was down-regulated, and the GSH/GSSG ratio was decreased in IR group ( P<0.001). Compared to IR group, Chiu′s scores and contents of MDA and Fe 2+ were significantly decreased, the expression of GSH, GPX4, FTH1 and SLC7A11 was up-regulated, and the GSH/GSSG ratio was increased in IN and INF groups ( P<0.001). Compared to IN group, Chiu′s scores and contents of MDA and Fe 2+ were significantly increased, the expression of GSH, GPX4, FTH1 and SLC7A11 was down-regulated, and the GSH/GSSG ratio was decreased in INE group ( P<0.001). Conclusions:Ferroptosis is involved in sodium butyrate pretreatment-induced reduction of intestinal I/RI in mice.

The new era imposes heightened demands on medical professionals,who must not only possess a solid theoretical foundation but also exhibit strong practical skills and innovative capabilities.The quality of medical func-tional laboratory construction is crucial for cultivating high-caliber medical talents.In light of the current developmental status and trends regarding functional experiment teaching within Chinese higher education institutions,particularly the disparities in development across various regions and institutions,the Functional Experiment Teaching Committee of the Chinese Pathophysiology Society has developed an expert consensus on laboratory construction standards.This consensus was established through comprehensive investigations,research,and extensive discussions to provide a reference for di-verse institutions to continuously enhance their levels of laboratory construction.

Objective To evaluate the protective effects of the traditional Chinese medicine formula Shenxiankang on renal injury and fibrosis,and to explore its potential mechanisms of action.Methods Chronic kidney disease(CKD)model was established in mice using unilateral ureteral obstruction(UUO).The mice were randomly divided into four groups:sham,UUO,and Shenxiankang(SXK)Low/High dose groups(1500,4500 mg/(kg·d)),each comprising eight mice.The each SXK groups received daily oral administration of Shenxiankang,and the remaining mice were gavaged equivalent volumes of saline for 7 d.After the experiment,renal tissues were collected for assessment of renal injury and fibrosis using HE and Masson staining.The expression levels of fibrosis markers and proteins involved in the epithelial membrane protein 3(Emp3)and Tgf-β/Smad3 signaling pathway were determined by Real-time PCR,immunohistochemistry,and Western Blot.In cell-based experiments,the effects of Shenxiankang on the Emp3/Tgf-β/Smad3 pathway and its interaction with TGF-beta receptor R2(Tgfβ2)were further analyzed using an Emp3 knockdown and Co-IP assays.Results Shenxiankang significantly reduced immune cell infiltration and tubular atrophy in the UUO model group and decreased the expression of kidney injury markers kidney injury molecule 1(Kim1)and Lipocalin 2(Lcn2),confirming its efficacy in alleviating renal injury.Masson staining and analysis of fibrosis markers Fibronectin(Fn)and α-smooth muscle actin(α-SMA)indicated that Shenxiankang effectively suppressed fibrosis induced by UUO.Mechanistic studies revealed that Shenxiankang exerted its effects by selectively downregulating the abnormal activation of the Emp3/Tgf-β/Smad3 signaling pathway,a finding further supported by cellular experiments showing that Shenxiankang modulates Tgf-β/Smad3 signaling through Emp3 regulation.Moreover,the Co-IP experiment result indicate that Shenxiankang exerts its effects by regulating the interaction between Emp3 and Tgfβ2.Conclusions Shenxiankang exhibits significant protective effects in a mouse model of chronic kidney disease,effectively reducing renal injury and fibrosis.These effects are likely mediated through the downregulation of the Emp3/Tgf-β/Smad3 signaling pathway,suggesting Shenxiankang's potential therapeutic value in renal protection.

Objective To explore the dietary nutrition status and nutritional intervention strategy of patients with Alzheimer’s disease (AD). Methods Among the 1 332 patients with AD diagnosed at Xijing Hospital from January 2021 to December 2023 were enrolled as the study subjects. The dietary intake data of patients were collected through questionnaire surveys and dietary reviews. During the study period, 30 patients did not complete the intervention due to withdrawal or loss of follow-up. Based on the actual number of people who completed the intervention, AD patients were randomly divided into intervention group (n=651, individualized nutritional intervention strategy) and control group (n=651, routine nutritional intervention), and both groups were intervened for 3 months. The cognitive function (MMSE score and MoCA score), nutritional status (MNA scale, NRS-2002 scale), and quality of life (GQOL-74) of the two groups of AD patients were compared to evaluate the effectiveness of the intervention strategies. Results A total of 1 332 questionnaires were distributed, and 1 302 valid questionnaires were finally recovered, with an effective recovery rate of 97.75% (1 302/1 332). The survey results showed that there were no statistical differences in baseline characteristics and dietary nutrition status between the two groups of AD patients before intervention (P>0.05). After nutritional intervention, the cognitive function, quality of life, and nutritional status of patients in the intervention group were significantly improved. The MMSE score, MoCA score, MNA score, and GQOL-74 score of the intervention group were significantly higher than those of the control group, while the NRS-2002 score was lower than that of the control group (P<0.05). Conclusion Nutritional intervention strategy has a significant effect on improving nutritional status, cognitive function, and quality of life of AD patients.

This study aimed to comprehensively examine the association of gallstones, cholecystectomy, and cancer risk. Multivariable logistic regressions were performed to estimate the observational associations of gallstones and cholecystectomy with cancer risk, using data from a nationwide cohort involving 239 799 participants. General and gender-specific two-sample Mendelian randomization (MR) analysis was further conducted to assess the causalities of the observed associations. Observationally, a history of gallstones without cholecystectomy was associated with a high risk of stomach cancer (adjusted odds ratio (aOR)=2.54, 95% confidence interval (CI) 1.50-4.28), liver and bile duct cancer (aOR=2.46, 95% CI 1.17-5.16), kidney cancer (aOR=2.04, 95% CI 1.05-3.94), and bladder cancer (aOR=2.23, 95% CI 1.01-5.13) in the general population, as well as cervical cancer (aOR=1.69, 95% CI 1.12-2.56) in women. Moreover, cholecystectomy was associated with high odds of stomach cancer (aOR=2.41, 95% CI 1.29-4.49), colorectal cancer (aOR=1.83, 95% CI 1.18-2.85), and cancer of liver and bile duct (aOR=2.58, 95% CI 1.11-6.02). MR analysis only supported the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer. This study added evidence to the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer, highlighting the importance of cancer screening in individuals with gallstones.
Humans ; Mendelian Randomization Analysis ; Gallstones/complications* ; Female ; Male ; Cholecystectomy/statistics & numerical data* ; Middle Aged ; Risk Factors ; Aged ; Adult ; Neoplasms/etiology* ; Stomach Neoplasms/epidemiology*

Objective:To retrospectively analyze the changes in the proportion of refined lymphocyte subsets in peripheral blood of patients with Graves disease (GD), and their correlation with the clinical characteristics and efficacy of GD, and to explore the immunological pathogenesis of Graves disease for seeking new therapeutic targets.Methods:A total of 97 newly diagnosed GD patients (GD group), 27 patients after treatment (treatment group), and 31 healthy individuals (control group) who visited the Fifth Medical Center of the PLA General Hospital from 2018 to 2021 were included in this study. The data of refined lymphocyte subsets, thyroid function, blood routine and clinical treatment of the three groups were compared and analyzed. The t-test and rank sum test were used to compare the proportions of lymphocyte subsets among different groups, and Pearson correlation analysis was used to analyze the correlation between the proportions of lymphocyte subsets and thyroid function indicators.Results:The proportion of B cells in GD group was higher than that in the control group [16.2%(11.8%, 21.8%) vs 10.2%(8.1%,13.6%)], while the proportion of natural killer (NK) cells was lower [9.4%(4.9%, 13.6%) vs 14.6%(12.1%,18.8%)], and the differences were statistically significant ( P<0.05). Abnormal T cell differentiation: the proportions of functional cells, including activated T cells, memory T cells, clustering antigen(CD)4+memory T cells, Th1 cells, and Tc1 cells, were lower than that in the control group [3.2%(2.1%, 5.7%) vs 5.8%(3.0%, 9.3%), P<0.05; 36.7% (29.9%, 48.1%) vs 48.0%(39.2%,57.7%), P<0.05; 23.1%(17.4%, 30.1%) vs 28.9%(23.3%,34.6%), P<0.05; 16.4% (11.8%, 23.6%) vs 24.3%(16.9%,28.5%), P<0.05; 28.5% (14.7%, 39.2%) vs 46.3%(21.6%,69.2%), P<0.05]. The proportion of activated T cells in the treatment group was higher than that in the GD group [6.5% (4.6%, 13.6%) vs 3.2% (2.1%, 5.7%), P<0.05]. The total triiodothyronine results showed positive correlations with B cells ( r=0.356, P<0.01) and negative correlations with NK cells ( r=?0.416, P<0.01), while the total thyroxine values showed negative correlations with NK cells and activated T cells ( r=?0.318,?0.335; P<0.01). Thyroid stimulating hormone and CD8+initial T cells were positively correlated ( r=0.382, P<0.01). The proportion of B cells, cytotoxic T cells and suppressor T cells in CD8+cells of patients with complications [such as Graves orbitopathy (GO), thyroid toxic cardiomyopathy, etc.] was significantly different from that of the simple GD patients [18.3% (14.1%, 27.1%) vs 14.6% (10.8%, 21.4%), Z=2.54, P<0.05; 73.4%(65.6%,83.6%)vs 65.0%(50.3%,79.3%), Z=2.93, P<0.05; 26.6%(16.4%, 37.5%)vs 35.0%(20.7%,49.7%), Z=?2.74, P<0.05]. The proportion of suppressor T cells in GO patients was lower than that in non-GO patients [6.1% (3.4%, 8.1%) vs 8.5% (4.9%, 13.6%), Z=?3.20 P<0.05]. Conclusion:There are significant alterations in the circulating immune cells of GD patients, suggesting that immunological abnormalities play a crucial role in the onset and progression of the disease.