Irritable bowel syndrome （IBS） is a functional bowel disorder characterized primarily by abdominal pain and altered defecation habits. In recent years， traditional Chinese medicine （TCM） has made progress in multiple aspects of IBS research and treatment， including syndrome distribution， development of TCM formulas， clinical efficacy evaluation， external therapies， and psychosocial regulation. However， it still faces challenges such as over-reliance on symptomatic manifestations rather than biomarkers for diagnostic criteria， and the lack of high-quality evidence-based data supporting the efficacy of TCM formulas in treating IBS. This paper proposed that TCM diagnosis and treatment of IBS should adhere to the strategy of integrating the holistic concept with syndrome differentiation and treatment， combining TCM external therapies such as acupuncture， moxibustion and acupoint application）， and emphasizing individualized diagnosis and treatment for psychosomatic abnormalities. Future research should integrate multi-omics technologies， artificial intelligence and other methods to deepen the understanding of the pathogenesis of IBS and the mechanisms of TCM formulas， so as to promote the standardization and internationalization of TCM in the diagnosis and treatment of IBS.

Objective To investigate the causal relationship between metabolic syndrome and breast cancer by using a bidirectional two-sample Mendelian randomization (MR) approach. Methods Genome-wide association study (GWAS) summary statistics for metabolic syndrome and breast cancer were acquired from the Integrative Epidemiology Unit GWAS database and the GWAS Catalog, with populations encompassing the United States and East Asia. A bidirectional causal design was employed: a forward analysis with metabolic syndrome as the exposure and breast cancer as the outcome, followed by a reverse analysis wherein their roles were interchanged. The inverse-variance weighting (IVW) method was primarily used for effect estimation, supplemented by MR-Egger regression, the weighted median method, the simple mode method, and the weighted mode method. Instrument variable strength was screened using the F-statistic (F>10). Robustness of the results was assessed through heterogeneity tests, horizontal pleiotropy tests, forest plots, and leave-one-out sensitivity analyses. Results The IVW analysis indicated no significant causal relationship between metabolic syndrome and breast cancer (OR=1.00, 95%CI: 0.97-1.03), P>0.05). Sensitivity analyses yielded consistent results, suggesting the good robustness of the study findings. Conclusion This study found no evidence to support a causal relationship, either positive or negative, between metabolic syndrome and breast cancer.

Objective: To develop a RHCE genotyping assay based on kompetitive allele-specific PCR (KASP) and assess its clinical accuracy for RhCE blood group determination. Methods: KASP primers were designed to interrogate three RHCE loci: the 109 bp insertion/deletion in intron 2, c. 307T>C, and c. 676C>G. A total of 1 194 RhD-positive inpatients from Chengdu were typed by both KASP genotyping and manual tube serology. Discordant samples (n=10) were retested by both methods and further resolved by Sanger sequencing. An additional 377 cases were tested for the c. 48C>G locus to evaluate the predictive accuracy of individual loci and combined locus testing for RhC antigen. Results: Genotyping concordance with serology was 100.0% for both the c. 676C>G locus (RhE/Rhe) and the c. 307T>C locus (Rhc). For RhC prediction using the 109 bp insertion, overall accuracy was 99.7% (1 191/1 194); the 3 discordant cases were confirmed by Sanger sequencing to be false negatives attributable to 109 bp deletion in intron 2. Testing the c. 48C>G allele for RhC prediction yielded 7 false positives, with an accuracy of 98.1% (370/377). RhC antigen status was determined by combining the 109 bp insertion and the c. 48C allele. After excluding 10 samples with inconsistent results between the two loci, the accuracy reached 100% in the remaining 367 samples. When both loci were applied in combination, accuracy reached 100% in the 367 cases with concordant results. Among the 1 194 patients, CCee (45.8%) and CcEe (31.7%) were the most common RhCE phenotypes. The e antigen had the highest positivity rate (92.2%), and the Ce haplotype was the most frequent (66.9%). Conclusion: The KASP-based RHCE genotyping method achieves high accuracy for clinical RhCE typing. Combining the 109 bp insertion/deletion with the c. 48C allele significantly improves RhC antigen prediction compared with either locus alone. This method was applied to RhCE genotyping of 1 194 RhD-positive inpatients in Chengdu, providing local RhCE phenotype and haplotype distribution data to support RhCE-matched transfusion practice.

Objective: To develop and validate a clinically actionable prediction model for postoperative pulmonary complications (PPCs) in cardiac surgery patients, focusing on modifiable preoperative risk factors amenable to targeted optimization. Methods: In this prospective observational cohort study, 492 adults undergoing open-chest cardiac surgery between August 15, 2023 and December 31, 2023 were analyzed. Prespecified predictors included gas exchange variables, pulmonary function, inspiratory muscle strength, and physical performance. Univariable and multivariable logistic regression analyses were used to develop the prediction model. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC). Results: A total of 90 patients (14.1%) developed PPCs after surgery. Five independent predictors were identified: elevated arterial PaCO2 (odds ratio [OR] 1.12, 95% confidence interval [CI] 1.00–1.26), oxygen desaturation (SpO2<93%) (OR 12.47, 95% CI 3.51–48.13), reduced gait speed (OR 0.17, 95% CI 0.04–0.71), lower FEV1/FVC ratio (OR 0.96, 95% CI 0.92–1.00), and diminished inspiratory muscle strength (MIP % predicted) (OR 0.96, 95% CI 0.92–0.99). The model demonstrated good discriminative ability with an AUC of 0.86 (95% CI 0.80–0.93) in the training cohort and 0.87 (95% CI 0.74–0.93) in the validation cohort. Conclusion This parsimonious model achieved high predictive accuracy using five modifiable physiological variables. By targeting abnormalities in gas exchange, pulmonary mechanics, muscle strength, and functional reserve, the model offers a practical tool to guide individualized prehabilitation strategies for reducing PPC risk in cardiac surgery patients.

Juvenile dermatomyositis(JDM) is the most common idiopathic inflammatory myopathy in children, characterized by symmetric proximal muscle weakness and characteristic skin rashes, which may be accompanied by involvement of major organs. Aberrant upregulation of the interferon signaling pathway has been confirmed as the core pathological mechanism of JDM, and is closely associated with mitochondrial dysfunction, peripheral blood immune cell dysregulation, muscle damage and repair dysfunction, as well as cutaneous and pulmonary lesions. Interferon-related biomarkers and interferon scores can serve as evaluation indicators for disease activity. Type Ⅰ interferon inhibitors and Janus kinase inhibitors provide new therapeutic options for refractory JDM. This review systematically summarizes the role of the interferon signaling pathway in the pathogenesis of JDM and its potential therapeutic targets, aiming to provide references for the mechanistic research and precise treatment of JDM.

BackgroundCurrent studies on the relationship between depressive symptoms and the risks of stroke and all-cause mortality mostly focus on the elderly population or high-risk groups with chronic diseases. The long-term impact of depressive symptoms in young and middle-aged people on the risks of stroke and all-cause mortality still lacks systematic assessment， and the relevant evidence is insufficient. ObjectiveTo explore the association between depressive symptoms and the risks of stroke and all-cause mortality in young and middle-aged adults， thereby expanding the risk evidence in this age group and providing epidemiological basis for early identification of high-risk individuals and the development of targeted intervention strategies. MethodsBased on data from the National Health and Nutrition Examination Survey （NHANES） database （2009–2018）， a total of 14 947 young and middle-aged respondents aged 18 to 64 were included as the research subjects. Logistic regression and restricted cubic spline （RCS） models were employed to examine the association between depressive symptoms and stroke. Cox proportional hazards model， RCS model， and Kaplan-Meier （K-M） survival curves were used to clarify the relationship between depressive symptoms and all-cause mortality risk. To verify the robustness of main findings， sensitivity analysis was conducted stratified by gender， hypertension， diabetes， hyperlipidemia， body mass index （BMI）， and age. ResultsLogistic regression analysis revealed that compared with the non-depressed group， the risk of stroke in the mild depression group increased by 53.50% （OR=1.535， 95% CI： 1.147–2.053）， while the moderate-to-severe depression group showed the highest risk with a 132.90% increase （OR=2.329， 95% CI： 1.733–3.129）. RCS analysis indicated an approximately linear dose-response relationship between PHQ-9 score and the risk of stroke （P_{for non-linearity}=0.089）， with stroke risk increasing as PHQ-9 scores rose. As the PHQ-9 score increased， the risk of stroke also showed an upward trend. Cox regression analysis demonstrated that compared with the non-depressed group， the risk of all-cause mortality in the mild depression group increased by 48.80% （HR=1.488， 95% CI： 1.164–1.902）， and the moderate-to-severe depression group had a 70.60% increased risk （HR=1.706， 95% CI： 1.310–2.221）. RCS analysis showed a linear dose-response relationship between PHQ-9 scores and all-cause mortality risk （P_{for non-linearity}=0.440）. K-M curves indicated that as the severity of depressive symptoms increases， the risk of all-cause mortality gradually rises （P<0.05）. Sensitivity analysis confirmed that the associations between depression symptoms and risks of stroke and all-cause mortality were not modified by gender， hypertension， diabetes， hyperlipidemia， BMI， or age， demonstrating robust findings. ConclusionAmong the young and middle-aged population， both mild and moderate-to-severe depression were associated with increased risks of stroke and all-cause mortality， with the moderate-to-severe depression group showed more pronounced risk elevations. A positive dose-response relationship was observed between depressive symptoms and these risks.

Objective: To evaluate the methodological quality and reporting quality of clinical practice guidelines or expert consensus on blood transfusion and blood use (BTBU) in China (hereinafter referred to as "guidelines/consensus"), providing reference for the development and updating of future BTBU guidelines/consensus. Methods: A systematic search was conducted in Chinese databases such as China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP Data-base, relevant guideline release platforms, and professional association websites. BTBU-related guidelines/consensus published between January 2006 and December 2025 were included. According to the inclusion and exclusion criteria, after completing literature screening and data extraction, three evaluators independently assessed the quality of the included literature using the Scientificity, Transparency, and Applicability of Guidelines Rating Tool (STAR), the Appraisal of Guidelines for Research and Evaluation Ⅱ (AGREE Ⅱ), and the International Practice Guideline Reporting Standards (RIGHT). Results: A total of 29 documents were included, including 5 guidelines, 22 consensus statements, and 2 protocols. The results of the STAR assessment showed that the total score was (21.7±8.8)%. The domain score ratios for registration, research protocol, funding, working group, conflict of interest, clinical question, evidence, consensus method, recommendation, accessibility and other domains were (2.2±12.1)%, 0, (36.7±25.1)%, (18.3±7.6)%, (19.2±15.3)%, (16.6±23.1)%, (15.1±6.3)%, (9.6±21.2)%, (54.3±18.4)%, (31.7±10.4)% and (10.3±31.0)%, respectively. For the AGREE Ⅱ assessment, the methodological quality of 26 articles was rated Grade B and 3 articles Grade C. The results of the RIGHT assessment indicated that the overall reporting rate of all guidelines/consensuses was (65.3±4.0)%. Conclusion: The methodological and reporting quality of current expert guidelines/consensus on BTBU in China still need improvement, and guidelines and consensus should be strictly formulated and standardized according to the standards of STAR, AGREE II and RIGHT.

ObjectiveTo explore the therapeutic effect and mechanism of Huangqi Xiayuxue decoction against hepatocellular carcinoma based on network pharmacology， animal experiments， and cell experiments. MethodsThe active ingredients and corresponding targets of Huangqi Xiayuxue decoction were screened via databases including the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine （BATMAN-TCM）. Hepatocellular carcinoma-related targets were retrieved from the GeneCards database. The common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were subjected to Gene Ontology （GO） functional annotation and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses. Huangqi Xiayuxue decoction-containing plasma was prepared. The cell counting kit-8 （CCK-8） assay was adopted to observe the effects of different volume fractions （5%， 10%， 15%， and 20%） of Huangqi Xiayuxue decoction-containing plasma on the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells， and the concentration for subsequent experiments was determined. Flow cytometry was adopted to detect the effects of Huangqi Xiayuxue decoction-containing plasma （5%， 10%， 15%， and 20%） on the apoptosis of MHCC-97H cells. A mouse model of subcutaneous xenograft hepatocellular carcinoma was established. The model mice were assigned into low-， medium-， and high-dose （4.63， 9.25， 18.5 g·kg^-1） Huangqi Xiayuxue decoction and sorafenib （20 mg·kg^-1） groups. Body mass and tumor volume of mice were dynamically monitored during the intervention period. After 3 weeks of intervention， hematoxylin-eosin （HE） staining was performed to observe tumor morphology. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） assay was employed to detect cell apoptosis. Immunohistochemistry （IHC） was adopted to examine the expression of cysteinyl aspartate-specific proteinase-3 （Caspase-3）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the tumor tissue. Real-time PCR and Western blot were employed to verify the changes in apoptosis-related factors and the phosphatidylinositol 3-kinase/protein kinase B/forkhead box O1 （PI3K/Akt/FoxO1） signaling pathway. ResultsA total of 220 common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were screened out by network pharmacology， among which tumor protein p53 （TP53）， Akt1， and signal transducer and activator of transcription 3 （STAT3） were the core targets. Pathway enrichment analysis indicated that the common targets were involved in cell apoptosis and proliferation， as well as the PI3K/Akt and FoxO signaling pathways. Cell experiments showed that compared with the blank plasma group， all volume fractions of Huangqi Xiayuxue decoction-containing plasma inhibited the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells （P<0.01）. The proportion of early apoptotic cells in MHCC-97H cells was increased after treatment with different volume fractions of Huangqi Xiayuxue decoction-containing plasma （P<0.01）. Animal experiments revealed that Huangqi Xiayuxue decoction inhibited the growth of tumor volume， promoted tumor cell apoptosis in the high-dose group， up-regulated the protein and mRNA levels of Bax and Caspase-3， down-regulated the protein and mRNA levels of Bcl-2， and reduced the phosphorylation level of the PI3K/Akt/FoxO1 signaling pathway （P<0.05， P<0.01）. ConclusionHuangqi Xiayuxue decoction exerts anti-hepatocellular carcinoma effects by inhibiting the activation of the PI3K/Akt/FoxO1 signaling pathway and promoting hepatocellular carcinoma cell apoptosis.

ObjectiveTo explore the therapeutic effect and mechanism of Huangqi Xiayuxue decoction against hepatocellular carcinoma based on network pharmacology， animal experiments， and cell experiments. MethodsThe active ingredients and corresponding targets of Huangqi Xiayuxue decoction were screened via databases including the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine （BATMAN-TCM）. Hepatocellular carcinoma-related targets were retrieved from the GeneCards database. The common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were subjected to Gene Ontology （GO） functional annotation and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses. Huangqi Xiayuxue decoction-containing plasma was prepared. The cell counting kit-8 （CCK-8） assay was adopted to observe the effects of different volume fractions （5%， 10%， 15%， and 20%） of Huangqi Xiayuxue decoction-containing plasma on the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells， and the concentration for subsequent experiments was determined. Flow cytometry was adopted to detect the effects of Huangqi Xiayuxue decoction-containing plasma （5%， 10%， 15%， and 20%） on the apoptosis of MHCC-97H cells. A mouse model of subcutaneous xenograft hepatocellular carcinoma was established. The model mice were assigned into low-， medium-， and high-dose （4.63， 9.25， 18.5 g·kg^-1） Huangqi Xiayuxue decoction and sorafenib （20 mg·kg^-1） groups. Body mass and tumor volume of mice were dynamically monitored during the intervention period. After 3 weeks of intervention， hematoxylin-eosin （HE） staining was performed to observe tumor morphology. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） assay was employed to detect cell apoptosis. Immunohistochemistry （IHC） was adopted to examine the expression of cysteinyl aspartate-specific proteinase-3 （Caspase-3）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the tumor tissue. Real-time PCR and Western blot were employed to verify the changes in apoptosis-related factors and the phosphatidylinositol 3-kinase/protein kinase B/forkhead box O1 （PI3K/Akt/FoxO1） signaling pathway. ResultsA total of 220 common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were screened out by network pharmacology， among which tumor protein p53 （TP53）， Akt1， and signal transducer and activator of transcription 3 （STAT3） were the core targets. Pathway enrichment analysis indicated that the common targets were involved in cell apoptosis and proliferation， as well as the PI3K/Akt and FoxO signaling pathways. Cell experiments showed that compared with the blank plasma group， all volume fractions of Huangqi Xiayuxue decoction-containing plasma inhibited the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells （P<0.01）. The proportion of early apoptotic cells in MHCC-97H cells was increased after treatment with different volume fractions of Huangqi Xiayuxue decoction-containing plasma （P<0.01）. Animal experiments revealed that Huangqi Xiayuxue decoction inhibited the growth of tumor volume， promoted tumor cell apoptosis in the high-dose group， up-regulated the protein and mRNA levels of Bax and Caspase-3， down-regulated the protein and mRNA levels of Bcl-2， and reduced the phosphorylation level of the PI3K/Akt/FoxO1 signaling pathway （P<0.05， P<0.01）. ConclusionHuangqi Xiayuxue decoction exerts anti-hepatocellular carcinoma effects by inhibiting the activation of the PI3K/Akt/FoxO1 signaling pathway and promoting hepatocellular carcinoma cell apoptosis.

OBJECTIVE To investigate the mechanism by which aloin （ALO） ameliorates atherosclerosis （AS）. METHODS Eight C57BL/6J mice were assigned to the control group （CON group） and fed a standard diet； thirty-two apolipoprotein E-knockout （APOE－/－） mice were randomly divided into model group （MOD group）， ALO low-dose and high-dose groups [ALO-L group， ALO-H group， 20， 40 mg/（kg·d）]， and atorvastatin positive control group [ATO group， 4 mg/（kg·d）]， with 8 mice in each group， establishing the AS model through feeding with a high-fat diet. The mice were administered the drug via gavage or given an equal volume of deionized water for 8 consecutive weeks. The lipid levels in the serum of mice were measured， and the pathological structural changes in their aortas were observed. The expressions of macrophage polarization markers （CD86+ ， CD206+） in the aorta were determined， along with the mRNA expressions of inducible nitric oxide synthase （iNOS）， tumor necrosis factor-α （TNF-α）， arginase-1 （Arg-1）， and interleukin-10 （IL-10）， as well as the protein expressions of iNOS and Arg- 1， and the phosphorylation levels of nuclear factor κB p65 （NF-κB p65） and signal transduction and activator of transcription 3 （STAT3） proteins. Additionally， a macrophage polarization model was established using lipopolysaccharide （LPS）-induced RAW264.7 cells， and the effect of ALO （400 μmol/L） on the cellular polarization phenotype was investigated. RESULTS Compared with the MOD group， administration groups all showed significant improvement in dyslipidemia （except for high-density lipoprotein cholesterol in the serum of ALO-L group） （P＜0.05）； aortic intimal structure improved significantly， plaque area was reduced significantly （P＜0.01）； the CD86+ relative fluorescence intensity in the aorta decreased significantly， the CD206+relative fluorescence intensity increased significantly （P＜0.01）， while the expressions of iNOS and TNF-α mRNA were down-regulated significantly （P＜0.05）； mRNA expressions of Arg-1 and IL-10， and protein expression of Arg-1 were increased significantly in ALO-H group and ATO group （P＜0.05）； the protein expressions of iNOS， and the phosphorylation levels of NF-κB p65 and STAT3 protein were decreased significantly （P＜0.05）. In vitro experiments further confirmed that ALO significantly reduced the proportion of LPS-induced M1-type macrophages but increased the proportion of M2-type macrophages （P＜0.01）. CONCLUSIONS ALO inhibits M1-type macrophage polarization and promotes M2-type polarization， ameliorates dyslipidemia and reduces arterial plaque formation in AS model mice， improve the structure of the aortic intima potentially through suppression of the NF-κB/STAT3 signaling pathway.