AIM:To analyze the characteristics and correlation of phacoemulsification parameters and anterior segment parameters in cataract patients with different blood glucose levels.METHODS:A total of 45 type 2 diabetic cataract patients(45 eyes)treated in our hospital from March 2023 to April 2024 were stratified into two groups based on glycosylated hemoglobin(HbA1c)levels: group A: HbA1c <7%(n=18)and group B: 7%≤HbA1c<8.5%(n=27); a total of 94 age-matched age-related cataract patients(94 eyes)were enrolled as the control group(group C). All underwent phacoemulsification with intraocular lens implantation. Anterior segment parameters, including corneal, lens and anterior chamber measurements, were recorded. Correlations between phacoemulsification parameters and anterior segment parameters were analyzed, and differences among groups were compared.RESULTS: In groups A and B, effective phacoemulsification time(EPT)negatively correlated with corneal endothelial cell density(CECD)(r=-0.315, P=0.035). Average phacoemulsification time(APT)positively correlated with the anterior corneal surface radius of curvature(Rm; r=0.402, P=0.006)and negatively correlated with the flat axis meridian curvature(K1), steep axis meridian curvature(K2), mean curvature(Km)of the anterior corneal surface, and lens density at 6 mm zones(PDZ3; all P<0.05). Average phacoemulsification energy(AVE)positively correlated with mean lens density(LD-mean), lens density at 2 mm zones(PDZ1), lens density at 4 mm zones(PDZ2), and PDZ3(all P<0.05), and negatively with pupil diameter(r=-0.385, P=0.009). In the group C, EPT showed a positive correlation with Pentacam nucleus staging(PNS)density grade, PDZ1, PDZ2, and PDZ3(all P<0.05). A positive correlation was observed between AVE and PNS classification(r=0.246, P=0.018). Conversely, AVE exhibited a negative correlation with CECD(r=-0.245, P=0.018). EPT in groups A and B was higher than that in the group C(P<0.05). Both EPT and APT in the group B were higher than those in the group A(P<0.05). In diabetic cataract patients, CECD, corneal density(CD), and posterior corneal surface height positively correlated with diabetes duration(P<0.05). Posterior corneal surface K1 and Rm positively correlated with 7%≤HbA1c<8.5%(P<0.05). Total corneal astigmatism negatively correlated with HbA1c, 2-hour post-breakfast blood glucose(2hPBG), and fasting insulin(FINS; P<0.05). CD and lens thickness(LT)positively correlated with FINS(P<0.05).CONCLUSION: Phacoemulsification parameters and blood glucose-related indices exhibited varying degrees of correlation with anterior segment parameters in cataract patients with different blood glucose levels. EPT in diabetic cataract patients was higher than that in age-related cataract patients, while EPT and APT in diabetic cataract patients with poor glycemic control were higher than those with good glycemic control.

In maintaining normal function and activation processes, glycolysis, lipid metabolism, and amino acid metabolism play key roles in the energy demand of platelets. In the resting state, platelets primarily rely on glycolysis and aerobic oxidation to generate energy. Upon activation, platelets preferentially utilize glycolysis, as it can more rapidly provide the required ATP. In addition to glycolysis, platelets can also utilize glycogen and fatty acids as additional energy sources. The ATP provided by fatty acid oxidation is crucial for platelet activation. Additionally, during platelet storage, distinctive changes in energy metabolism occur. In the early stages of storage, platelets primarily rely on glycolysis and the pentose phosphate pathway (PPP) to generate energy. In the mid-storage phase, there is an increase in tricarboxylic acid cycle (TCA) metabolism. In the later stages of storage, cellular metabolism gradually declines. The regulation and flexibility of these metabolic pathways play a critical role in the survival and function of platelets in different states.

Depression, a prevalent mental disorder with significant socioeconomic burdens, underscores the urgent need for safe and effective non-pharmacological interventions. Recent advances in microbiome research have revealed the pivotal role of gut microbiota dysbiosis in the pathogenesis of depression. Concurrently, exercise, as a cost-effective and accessible intervention, has demonstrated remarkable efficacy in alleviating depressive symptoms. This comprehensive review synthesizes current evidence on the interplay among exercise, gut microbiota modulation, and depression, elucidating the mechanistic pathways through which exercise ameliorates depressive symptoms via the microbiota-gut-brain (MGB) axis. Depression is characterized by gut microbiota alterations, including reduced alpha and beta diversity, depletion of beneficial taxa (e.g., Bifidobacterium, Lactobacillus, and Coprococcus), and overgrowth of pro-inflammatory and pathogenic bacteria (e.g., Morganella, Klebsiella, and Enterobacteriaceae). Metagenomic analyses reveal disrupted metabolic functions in depressive patients, such as diminished synthesis of short-chain fatty acids (SCFAs), impaired tryptophan metabolism, and dysregulated bile acid conversion. For instance, Bifidobacterium longum deficiency correlates with reduced synthesis of neuroactive metabolites like homovanillic acid, while decreased Coprococcus abundance limits butyrate production, exacerbating neuroinflammation. Furthermore, elevated levels of indole derivatives from Clostridium species inhibit serotonin (5-HT) synthesis, contributing to depressive phenotypes. These dysbiotic profiles disrupt the MGB axis, triggering systemic inflammation, neurotransmitter imbalances, and hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. Exercise exerts profound effects on gut microbiota composition, diversity, and metabolic activity. Longitudinal studies demonstrate that sustained aerobic exercise increases alpha diversity, enriches SCFA-producing genera (e.g., Faecalibacterium prausnitzii, Roseburia, and Akkermansia), and suppresses pathobionts (e.g., Desulfovibrio and Streptococcus). For example, a meta-analysis of 25 trials involving 1 044 participants confirmed that exercise enhances microbial richness and restores the Firmicutes/Bacteroidetes ratio, a biomarker of metabolic health. Notably, endurance training promotes Veillonella proliferation, which converts lactate into propionate, enhancing energy metabolism and delaying fatigue. Exercise also strengthens intestinal barrier integrity by upregulating tight junction proteins (e.g., ZO-1, occludin), thereby reducing lipopolysaccharide (LPS) translocation and systemic inflammation. However, excessive exercise may paradoxically diminish microbial diversity and exacerbate intestinal permeability, highlighting the importance of moderate intensity and duration. Exercise ameliorates depressive symptoms through multifaceted interactions with the gut microbiota, primarily via 4 interconnected pathways. First, exercise mitigates neuroinflammation by elevating anti-inflammatory SCFAs such as butyrate, which suppresses NF-κB signaling to attenuate microglial activation and oxidative stress in the hippocampus. Animal studies demonstrate that voluntary wheel running reduces hippocampal TNF‑α and IL-17 levels in stress-induced depression models, while fecal microbiota transplantation (FMT) from exercised mice reverses depressive behaviors by modulating the TLR4/NF‑κB pathway. Second, exercise regulates neurotransmitter dynamics by enriching GABA-producing Lactobacillus and Bifidobacterium, thereby counteracting neuronal hyperexcitability. Aerobic exercise also enhances the abundance of Lactobacillus plantarum and Streptococcus thermophilus, which facilitate 5-HT and dopamine synthesis. Clinical trials reveal that 12 weeks of moderate exercise increases fecal Coprococcus and Blautia abundance, correlating with improved 5-HT bioavailability and reduced depression scores. Third, exercise normalizes HPA axis hyperactivity by reducing cortisol levels and restoring glucocorticoid receptor sensitivity. In rodent models, chronic stress-induced corticosterone elevation is reversed by probiotic supplementation (e.g., Lactobacillus), which enhances endocannabinoid signaling and hippocampal neurogenesis. Furthermore, exercise upregulates brain-derived neurotrophic factor (BDNF) via microbial metabolites like butyrate, promoting histone acetylation and synaptic plasticity. FMT experiments confirm that exercise-induced microbiota elevates prefrontal BDNF expression, reversing stress-induced neuronal atrophy. Fourth, exercise reshapes microbial metabolic crosstalk, diverting tryptophan metabolism toward 5-HT synthesis instead of neurotoxic kynurenine derivatives. Butyrate inhibits indoleamine 2,3-dioxygenase (IDO), a key enzyme in the kynurenine pathway linked to depression. Concurrently, exercise-induced Akkermansia enrichment enhances mucin production, fortifies the gut barrier, and reduces LPS-driven neuroinflammation. Collectively, these mechanisms underscore exercise as a potent modulator of the microbiota-gut-brain axis, offering a holistic approach to alleviating depression through microbial and neurophysiological synergy. Current evidence supports exercise as a potent adjunct therapy for depression, with personalized regimens (e.g., aerobic, resistance, or yoga) tailored to individual microbiota profiles. However, challenges remain in optimizing exercise prescriptions (intensity, duration, and type) and integrating them with probiotics, prebiotics, or FMT for synergistic effects. Future research should prioritize large-scale randomized controlled trials to validate causality, multi-omics approaches to decipher MGB axis dynamics, and mechanistic studies exploring microbial metabolites as therapeutic targets. The authors advocate for a paradigm shift toward microbiota-centric interventions, emphasizing the bidirectional relationship between physical activity and gut ecosystem resilience in mental health management. In conclusion, this review underscores exercise as a multifaceted modulator of the gut-brain axis, offering novel insights into non-pharmacological strategies for depression. By bridging microbial ecology, neuroimmunology, and exercise physiology, this work lays a foundation for precision medicine approaches targeting the gut microbiota to alleviate depressive disorders.

Objective: To accurately determine the ABO blood group of samples exhibiting forward/reverse grouping discrepancies by combining first-generation (Sanger) and third-generation (long-read) sequencing technologies. Methods: Five samples with ABO forward/reverse grouping discrepancies were selected. Serological testing was conducted using automated blood typing instruments and the tube method. Genotyping was conducted using both Sanger and long-read sequencing technologies. Results: Sanger sequencing identified specific genetic mutations in two samples, with genotypes of ABO BA. 04/ABO O.01.01 and ABO B3.05/ABO O.01.02. Further analysis with long-read sequencing revealed specific mutations in the +5.8kb region of intron 1 (c.28+5885C>T and c.28+5861T>G) in three samples where mutations were not detected by Sanger sequencing. These mutations affect the expression of the ABO antigens and are likely responsible for the ABO subgroup phenotypes. Conclusion: The integration of Sanger and long-read sequencing technologies effectively identifies genetic variations causing ABO subtypes, providing a scientific basis for enhancing clinical transfusion safety and ensuring accurate blood group determination.

Objective: To accurately determine the ABO blood group of samples exhibiting forward/reverse grouping discrepancies by combining first-generation (Sanger) and third-generation (long-read) sequencing technologies. Methods: Five samples with ABO forward/reverse grouping discrepancies were selected. Serological testing was conducted using automated blood typing instruments and the tube method. Genotyping was conducted using both Sanger and long-read sequencing technologies. Results: Sanger sequencing identified specific genetic mutations in two samples, with genotypes of ABO BA. 04/ABO O.01.01 and ABO B3.05/ABO O.01.02. Further analysis with long-read sequencing revealed specific mutations in the +5.8kb region of intron 1 (c.28+5885C>T and c.28+5861T>G) in three samples where mutations were not detected by Sanger sequencing. These mutations affect the expression of the ABO antigens and are likely responsible for the ABO subgroup phenotypes. Conclusion: The integration of Sanger and long-read sequencing technologies effectively identifies genetic variations causing ABO subtypes, providing a scientific basis for enhancing clinical transfusion safety and ensuring accurate blood group determination.

The Consolidated Standards of Reporting Trials (CONSORT) statement aims to enhance the quality of reporting for randomized controlled trial (RCT) by providing a minimum item checklist. It was first published in 1996, and updated in 2001 and 2010, respectively. The latest version was released in April 2025, continuously reflecting new evidence, methodological advancements, and user feedback. CONSORT 2025 includes 30 essential checklist items and a template for a participant flow diagram. The main changes to the checklist include the addition of 7 items, revision of 3 items, and deletion of 1 item, as well as the integration of multiple key extensions. This article provides a comprehensive interpretation of the statement, aiming to help clinical trial staff, journal editors, and reviewers fully understand the essence of CONSORT 2025, correctly apply it in writing RCT reports and evaluating RCT quality, and provide guidance for conducting high-level RCT research in China.

Objective: To investigate the correlation among α2, 6-sialyltransferase (ST6Gal-Ⅰ), CD36 desialylation, and caveolin-1 (Cav-1) in phorbol ester (PMA)-induced MEG-01 cell model, as well as their potential mechanism in immune thrombocytopenia (ITP). Methods: MEG-01 cells were treated with 10 ng/mL PMA for 48 hours (control group: 0.1% DMSO). Flow cytometry was used to detect cell surface markers: desialylation (CD41 RCA ) and α2, 6-sialylation (CD41 SNA ). Western blot was performed to analyze the protein expressions of ST6Gal-Ⅰ, CD36, and Cav-1. Results: Flow cytometry analysis revealed that, compared with the control group (set as 100%), the proportion of CD41 RCA positive cells in the MEG-01 cells after PMA intervention significantly increased to (127.79±2.01)%, while the proportion of CD41 SNA positive cells significantly decreased to (78.09±1.76)% (both P<0.05). Western blot analysis results showed that, compared with the control group, PMA intervention significantly downregulated the expression of ST6Gal-Ⅰ protein (0.602±0.023 vs 0.768±0.068) and Cav-1 protein (1.012±0.028 vs 1.253±0.068) (both P<0.05), while significantly upregulating the expression of CD36 protein (0.936±0.033 vs 0.694±0.070, P<0.05). Conclusion: PMA can significantly inhibit the expression of ST6Gal-Ⅰ, accompanied by increased desialylation (β-galactose exposure), elevated CD36, and downregulated Cav-1. These changes suggest that the increased exposure of CD36 antigen and the disorder of membrane microenvironment may be involved in the pathological process of ITP, providing a new direction for mechanism research.

Objective To explore the longitudinal associations of body roundness index (BRI), visceral adiposity index (VAI), and metabolic score for visceral fat (METS-VF) with the risk of new-onset atrial fibrillation (AF). Methods This study included participants from the UK Biobank who were free of AF or pregnancy at baseline and completed the first and second assessments of BRI, VAI, and METS-VF. The changes in BRI, VAI, and METS-VF were classified using K-means clustering analyses, and the cumulative adiposity indices were also calculated. The primary outcome was new-onset AF. Three Cox regression models were employed to investigate the longitudinal associations of the BRI, VAI, and METS-VF changes with the risk of incident new-onset AF. The results were presented as hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs). Restricted cubic spline analyses were performed to explore potential non-linear associations between baseline or cumulative adiposity indices and the risk of new-onset AF. C-index analyses were conducted to evaluate the predictive value of BRI, VAI, and METS-VF for new-onset AF. Subgroup analyses were performed according to age, gender, race, smoking status, alcohol consumption, and physical activity. Polygenic risk scores were applied to account for genetic susceptibility and investigate potential interactions between adiposity indices and genetic risk. Univariate linear regression analyses were performed to evaluate the relationships of cumulative adiposity indices and magnetic resonance imaging and dual X-ray absorptiometry parameters, including visceral adipose tissue (VAT) volume, VAT mass, trunk fat volume, and trunk fat mass. We further applied the eXtreme Gradient Boosting (XGBoost) algorithm, with the feature importance being measured to evaluate the predictive value of each adiposity index for imaging parameters. Mendelian randomization analysis was further conducted to investigate the potential causal relationship between trunk fat mass and AF. Results A total of 12 776 participants were included. Over a median follow-up of 9.60 years, 761 (5.96%) new-onset AF events were recorded. Participants were divided into four classes based on the changes in adiposity indices. In the fully adjusted model, compared to participants in Class 1 of BRI, those in Class 3 (HR＝1.30, 95%CI 1.04-1.63, P＝0.023) and Class 4 (HR＝2.17, 95%CI 1.61-2.93, P＜0.001) were associated with significantly higher risks of new-onset AF. Regarding METS-VF, participants in Class 4 of METS-VF also demonstrated a significantly higher risk of new-onset AF compared to those in Class 1 (HR＝1.66, 95%CI 1.15-2.39, P＝0.007). However, no significant association was observed between different classes of VAI and the risk of new-onset AF. For every 1 standard deviation increase in cumulative BRI, VAI, and METS-VF, the fully adjusted HRs of new-onset AF were 1.23 (95%CI 1.13-1.35), 1.02 (95%CI 0.94-1.10), and 1.23 (95%CI 1.12-1.35), respectively. Cumulative adiposity indices (BRI, VAI, and METS-VF) were divided into quartiles. Using the first quartile as reference, participants in the highest quartiles of BRI (HR＝1.40, 95%CI 1.10-1.79, P＝0.007) and METS-VF (HR＝1.44, 95%CI 1.13-1.83, P＝0.003) both exerted a significantly higher risk of new-onset AF. Regarding VAI, no significant association was observed (HR＝1.00, 95%CI 0.81-1.23, P＝0.988). Restricted cubic spline analyses revealed non-linear relationships between cumulative BRI, baseline/cumulative VAI, and baseline/cumulative METS-VF with new-onset AF risk (all P_overall＜0.05, P_non-linear＜0.05). In the C-index analysis, BRI demonstrated the highest predictive performance for new-onset AF, followed by METS-VF and VAI. Subgroup analysis indicated a stronger association between METS-VF and the risk of new-onset AF amongst participants younger than 60 years (P_interaction＝0.008). Polygenic risk score analysis stratified by genetic risk demonstrated a synergistic effect between BRI and genetic risk with new-onset AF, with the overall risk of new-onset AF increasing as both BRI and genetic risk increased. Linear regression analysis revealed a positive correlation between cumulative BRI with VAT volume, VAT mass, trunk fat volume, and trunk fat mass. The feature importance plot derived from the XGBoost algorithm indicated that cumulative BRI had the greatest predictive value on VAT volume, VAT mass, trunk fat volume, and trunk fat mass. Mendelian randomization analysis confirmed a significant causal relationship between trunk fat mass and AF. Conclusions There are significant non-linear associations between BRI, METS-VF, and VAI with new-onset AF. Higher BRI and METS-VF are significantly associated with a higher risk of new-onset AF, whereas no significant association is observed for the VAI. BRI exhibits a positive correlation with VAT and trunk fat, and demonstrates superior performance in predicting new-onset AF compared to VAI and METS-VF. Monitoring and managing BRI may be important in the early detection and intervention of AF.

Background::Intrauterine valvuloplasty is an innovative therapy, which promotes ventricular growth and function in some congenital heart diseases (CHDs). The technique remains challenging and can only be performed in a few centers. This study aimed to assess the feasibility and mid-term outcomes of fetal cardiac intervention (FCI) in fetuses with critical CHD in an experienced tertiary center.Methods::Five fetal aortic valvuloplasty (FAV) or fetal pulmonary valvuloplasty (FPV) procedures were performed in our fetal heart center between August 2018 and May 2022. Technical success was defined as crossing the aortic or pulmonary valve and balloon inflation, followed by evidence of increased blood flow across the valve and/or new regurgitation. Follow-up clinical records and echocardiography were obtained during the prenatal and postnatal periods.Results::Five fetuses received FAV or FPV, including critical aortic stenosis ( n = 2) and pulmonary atresia with intact ventricular septum ( n = 3). The mean maternal age was 33.0 ± 2.6 years. The median gestational age (GA) at diagnosis was 24 weeks (range, 22-26 weeks). The median GA at intervention was 29 weeks (range, 28-32 weeks). All five cases underwent successful or partially successful procedures. One patient had pulmonary valve perforation without balloon dilation. No procedure-related deaths or significant complications occurred. However, one neonatal death occurred due to heart and renal failure. The median follow-up period was 29.5 months (range, 8.0-48.0 months). The four surviving patients had achieved biventricular circulation, exhibited improved valve, and ventricular development at the last follow-up visit. Conclusion::Intrauterine FCI could be performed safely with good prognosis in critical CHD.

Background::Evaluating the impact of digestive system diseases is vital for devising effective prevention strategies. However, comprehensive reports on the burden of digestive system diseases in China are lacking. Our study aimed to provide an overview of the burden and trends of digestive system diseases from 1990 to 2019 in China and its provinces.Methods::This cross-sectional study utilized the Global Disease Burden Study 2019 to estimate the incidence, mortality rate, disability-adjusted life years (DALYs), years of life disability, years of life lost, and changes in the burden of digestive diseases across Chinese provinces from 1990 to 2019. The analysis of disease burden primarily examines the characteristics of sub-disease distribution, time trends, age distribution, and sex distribution. Additionally, we compared provincial age-standardized DALYs for digestive diseases with the expected rates based on the socio-demographic index (SDI).Results::In 2019, there were 499.2 million cases of digestive system diseases in China, resulting in 1,557,310 deaths. Stomach cancer, colon and rectal cancer, and esophageal cancer are the top three diseases associated with mortality and DALY related to digestive system diseases. Meanwhile, cirrhosis and other chronic liver diseases, gastroesophageal reflux disease, and gallbladder and biliary diseases are the top three kinds of diseases with the highest prevalence among digestive system diseases. The risk of gastric cancer sharply increases among men after the age of 40 years, leading to a significant disparity in burden between men and women. As the SDI increased, the DALYs associated with digestive system diseases in China and its provinces showed a downward trend.Conclusion::Our study highlights the inverse correlation between DALYs associated with digestive system diseases and the SDI.