AIM: To investigate the features of retinal peripheral defocus and its associated variables in unilateral myopia. METHODS: This cross-sectional study included consecutive anisometropic myopic patients who visited Center for Optometry and Visual Science from August 2023 to March 2025 in Guangxi Zhuang Autonomous Region. Eyes were classified based on spherical equivalent(SE)and uncorrected visual acuity(UCVA): myopic eyes(SE ≤-0.50 D, UCVA <0.2 LogMAR)and contralateral normal eyes(SE ≥-0.25, UCVA ≥0 LogMAR). Total relative defocus value(TRDV)across the visual field, RDV at 15°, 30°, and 45°(RDV-15, RDV-30, RDV-45), and quadrant-specific RDV(superior/RDV-S, inferior/RDV-I, temporal/RDV-T, nasal/RDV-N)were compared between groups.RESULTS: This study enrolled 81 anisometropic patients(81 myopic eyes, 81 contralateral normal eyes). The cohort comprised 42 males and 39 females, 47 patients aged 8-12 y and 34 patients aged 13-17 y(mean age: 11.8±2.4 y). Myopic eyes demonstrated significantly higher values in TRDV, RDV-30, RDV-45, RDV-I, RDV-S, RDV-N, and RDV-T versus contralateral normal eyes(all P<0.001). RDV-15 showed no significant difference between groups in either 8-12-year-olds or 13-17-year-olds(both P>0.05). Among 13-17-year-olds, RDV-S also exhibited no intergroup difference(P>0.05). All other parameters differed significantly across both age strata(all P<0.05). In myopic eyes, age positively correlated with TRDV(r=0.31, P=0.005), RDV-30(r=0.33, P=0.002), RDV-45(r=0.32, P=0.004), and RDV-N(r=0.37, P<0.001). In contralateral eyes, scotopic pupil diameter negatively correlated with TRDV(r=-0.25, P=0.03), RDV-45(r=-0.25, P=0.02), RDV-S(r=-0.29, P=0.008), and RDV-N(r=-0.27, P=0.014). And age positively correlated with RDV-N(r=0.30, P= 0.006), axial length positively correlated with RDV-T(r=0.30, P=0.006). CONCLUSION: The peripheral defocus of unilateral myopic eyes varies from that of their contralateral normal counterparts. The former presents hyperopic defocus, which augments with age, while the latter displays myopic defocus, which accentuates with the increase of the scotopic pupil size.

Esophageal cancer is a prevalent malignant tumor of the digestive tract in China, and radical surgery remains the cornerstone of its comprehensive treatment. However, multifactorial challenges such as postoperative gastrointestinal tract reconstruction, traumatic stress, and tumor-related metabolic disturbances render esophageal cancer patients highly susceptible to malnutrition. Perioperative nutritional support therapy plays a crucial role in enhancing surgical safety, improving clinical outcomes, and elevating patients' quality of life by regulating metabolic homeostasis, preserving organ function, and optimizing the immune microenvironment. This article reviews the mechanisms underlying malnutrition in esophageal cancer, methods for nutritional status assessment, and precision intervention pathways based on multi-omics evaluations. The aim is to strengthen clinicians' awareness of standardized perioperative nutritional management for esophageal cancer patients and promote its clinical implementation, thereby facilitating postoperative recovery and improving long-term quality of life.

OBJECTIVE To evaluate the clinical efficacy of Chaihu anxin capsules in the treatment of mild-to-moderate depression， analyze the influencing factors of its efficacy, construct a nomogram prediction model.METHODS Patients with mild-to-moderate depression treated at The First Hospital of Hebei Medical University from May 1， 2023 to March 10， 2025 were retrospectively included and categorized into Chaihu anxin capsules group and milnacipran group according to treatment regimen. Propensity score matching （PSM） was used to balance baseline characteristics， and treatment efficacy was compared after 8 weeks， including 24 Hamilton Depression Scale （HAMD-24） scores and changes， Hamilton Anxiety Scale （HAMA） scores and changes， and treatment response rate after 8 weeks of treatment. Patients receiving Chaihu anxin capsules were further classified as responders or non-responders based on the occurrence of treatment response. Univariate and multivariate Logistic regression analyses were conducted to identify the influencing factors of treatment response， and a nomogram model was constructed to predict the probability of treatment response， its predictive performance was evaluated using receiver operating characteristic （ROC） curves， calibration curves， and decision curve analysis.RESULTS A total of 297 patients were included before PSM， including 196 patients in the Chaihu anxin capsules group and 101 patients in the milnacipran group. After PSM， each group included 44 patients. After PSM， the HAMD-24 scores and HAMA scores at 8 weeks after treatment in the Chaihu anxin capsules group， as well as the HAMD-24 scores in the milnacipran group， were significantly lower than their respective baseline values （ P ＜0.05）； the change in HAMA score in the Chaihu anxin capsules group was significantly greater than that in the milnacipran group （ P ＝0.04）. Multivariable Logistic regression identified age， total bilirubin， and baseline HAMD-24 score as independent predictors of treatment response （ P ＜0.05）. The area under the ROC curve of the constructed nomogram prediction model was 0.72 （95% confidence interval： 0.637-0.799）， and the corrected Brier score was 0.143 （95% confidence interval： 0.112-0.176）； compared with the “all intervention” and “all non intervention” strategies， applying this nomogram prediction model could achieve higher net benefits within the threshold probability range of 8% to 37%.CONCLUSIONS The efficacy of Chaihu anxin capsules in improving mild-to-moderate depression is comparable to that of milnacipran， and it has certain advantages in improving anxiety symptoms； age， total bilirubin， and baseline HAMD-24 score are independent influencing factors for the treatment response of Chaihu anxin capsules. The nomogram prediction model constructed based on these factors has good discrimination， calibration， and clinical applicability.

Objective:To unveil the dynamic molecular characteristics of colorectal cancer (CRC) progression, identify key molecules and signaling pathways driving disease development, and provide a theoretical basis for precision diagnosis and treatment.Methods:Differentially expressed genes (DEGs) were identified using DESeq2 based on the TCGA-CRC dataset (556 colorectal cancer samples) and three independent validation cohorts from the GEO database (GSE39582, GSE68468, GSE41258). Mfuzz time-series analysiswas applied to identify gene clusters with continuously upregulated expression during tumor progression. Functional enrichment analysis was performed using clusterProfiler, and protein-protein interaction (PPI) networks were constructed via the STRING online platform to pinpoint hub genes. Single-cell sequencing data (GSE132465/GSE144735) were integrated to resolve the cellular origins and intercellular communication of key genes. The prognostic value of genes was assessed using a univariate Cox proportional hazards model (likelihood ratio test), and single-cell sequencing data were analyzed using the Seurat pipeline with Wilcoxon rank-sum test to identify DEGs.Results:Time-series analysis identified Gene Cluster 4 (containing 186 genes) with a sustained upregulation trend across CRC stages from Ⅰ to Ⅳ. Functional enrichment revealed these genes were significantly involved in extracellular matrix (ECM) remodeling and pathways such as PI3K-Akt and MAPK signaling. PPI network analysis screened 10 hub genes ( COL10A1, THBS2, SPP1, etc.), whose high expression correlated significantly with poor patient prognosis. Single-cell sequencing demonstrated that these hub genes were predominantly expressed in fibroblast subpopulations, while SPP1 was enriched in macrophages. Cell-cell communication analysis confirmed that THBS2-CD47 and SPP1-CD44 were the primary pathways mediating fibroblast-immune/endothelial cell interactions. Conclusion:ECM-related genes are closely associated with the progression of CRC, in which the key molecules THBS2 and SPP1 may drive stromal-immune cell communication in the tumor microenvironment by mediating the THBS2-CD47 and SPP1-CD44 interaction pathways, thereby promoting the progression of CRC.

Objective To identify the risk factors and investigate etiological spectrum of pulmonary fungal infections(PFIs)in patients with end-stage liver disease(ESLD).Methods A retrospective analysis was performed on the clinical data of 211 ESLD patients.Based on pulmonary imaging,clinical manifestations,and microbiological test results,patients were categorized into three groups,including the PFI group(or the case group),the non-fungal pneumonia group(or the control group 1),and the group without pneumonia(or the control group 2).The clinical characteristics of patients in the the case group were then compared with those of patients in the two control groups.Taking patients without pneumonia as the control,univariate and multivariate logistic regression analyses were performed to identify independent risk factors for PFI,and a nomogram prediction model was constructed based on these risk factors.Results Among the 211 patients,76(36.1%)had PFIs,46(21.8%)had non-fungal pneumonia,and 89(42.2%)did not have pneumonia.According to findings from the multivariate logistic regression,elevated white blood cell count upon admission(OR=1.211;95%CI,1.011-1.460),higher Model for End-Stage Liver Disease-Sodium(MELD-Na)score(OR=1.140;95%CI,1.021-1.282),concomitant hepatorenal syndrome(OR=4.150;95%CI,1.050-17.300),cumulative glucocorticoid use for more than seven days(OR=26.832;95%CI,6.361-113.221),and the administration of broad-spectrum antibiotics at the time of hospital admission(OR=6.601;95%CI,1.951-22.362)were identified as independent risk factors for PFI.A predictive nomogram model named TJLFPFI was constructed based on these risk factors.The area under the receiver operating characteristic(AUC)curve of the model was 0.899(95%CI,0.853-0.945).Etiologic analysis of the 76 PFI cases revealed that 36(47.4%)had positive results for culture,while 40(52.6%)had negative results for sputum culture but tested positive by the 1,3-β-D-glucan test and/or galactomannan test.Aspergillus was the most frequently identified pathogen,detected in 25 of the 36 cases(59.5%).Conclusion PFI in ESLD patients is closely associated with disease severity at admission,early use of broad-spectrum antibiotics,and prolonged glucocorticoid therapy.Aspergillus is the predominant pathogen.The TJLFPFI model shows potential value in identifying high-risk patients,but prospective validation is still warranted.

Objective To explore the relationship between plasma trimethylamine N-oxide(TMAO)level and atrial fibrillation(AF)by a clinical trial.Methods Totally 257 patients with AF were enrolled including 114 patients with paroxysmal AF and 143 with persistent AF.The control group had 122 non-AF patients;Plasma TMAO level,the demographic characteristics and clinical data of patients were collected.Regression analysis was performed to identify the association between TMAO and presence of AF.Results Plasma TMAO level of patients with AF was higher than that of patients without AF(3.9[2.4-5.9]vs.2.4[1.6-3.7]μmol/L,P＜0.001);Even after adjust-ment of confounding factors including age,hypertension,diabetes,heart failure and body mass index;Plasma TMAO level was still related to presence of AF(OR:1.290,95％CI:1.151-1.445;P＜0.001).The plasma TMAO level of patients with persistent AF was higher than that of patients with paroxysmal AF(4.4[2.8-6.8]vs.3.2[2.2-5.0]μmol/L,P＜0.01);Even after adjustment of confounding factors including age,hypertension,diabetes and heart failure and coronary heart disease;Plasma TMAO level was still related to persistent AF(OR:1.092,95％CI:1.009-1.182;P=0.029).Conclusions The level of plasma TMAO of patients with AF is higher than that of patients without AF.Elevated plasma TMAO level is related to an increased risk of AF.Elevated plasma TMAO level in patients with AF is related to an increased risk of persistent AF.

Knee osteoarthritis(KOA)is a common chronic degenerative bone and joint disease characterized by degeneration and wear of knee cartilage.It is commonly found in middle-aged and elderly people and seriously impacts on their lower limb activity and quality of life.At present,the treatment of early and middle stage KOA mainly relies on the conservative methods such as oral medication,joint injection,topical patches and traditional Chinese medicine.Platelet rich plasma(PRP),as an autologous platelet concentrate,is rich in various growth factors and has no risk of immune rejection.In recent years,it has been widely used in the repair of bone,joint,and soft tissue injuries.However,the short biological half-life of growth factors in PRP and the fluidity of injection sites can result in insufficient binding force,short action time,poor target therapy efficacy,and the need for repeated injections in the joint cavity,which will increase the risk of iatrogenic infections.Hydrogels are cross-linked polymer networks containing water,and their high histocompatibility and drug release have attracted much attention.The slow and continuous release of drug is achieved by loading PRP onto hydrogel.Its unique adhesion reduces the flow of drug in the joint,thus extending the local action time of PRP and reducing the need for repeated injection.This article reviews the biological characteristics of PRP and hydrogel,the mechanism of action and clinical application of PRP loaded hydrogel in the treatment of KOA,and analyzes the existing problems and challenges,aiming to provide more effective treatment options for KOA patients through the in-depth discussion of this new treatment method.

Acute respiratory distress syndrome(ARDS)is a common respiratory emergency,but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures.Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS,but the application of hydrogen has flammable and explosive safety concerns.Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance,thus improving ARDS in patients and animal models.Coral calcium hydrogenation(CCH)is a new solid molecular hydrogen carrier prepared from coral calcium(CC).Whether and how CCH affects acute lung injury in ARDS re-mains unstudied.In this study,we observed the therapeutic effect of CCH on lipopolysaccharide(LPS)induced acute lung injury in ARDS mice.The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable,demonstrating a significant improvement compared to the untreated ARDS model group.CCH treatment significantly reduced pulmonary hemorrhage and edema,and improved pulmonary function and local microcirculation in ARDS mice.CCH promoted mitochon-drial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2),improved lung mitochondrial dysfunction induced by LPS,and reduced oxidative stress damage.The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Objective:To assess the efficacy and safety profile of antaitasvir phosphate combined with yiqibuvir in the treatment of chronic hepatitis C (CHC) of various genotypes, without cirrhosis or with compensated cirrhosis.Methods:394 cases with CHC from 22 centers were collected from October 2021 to April 2023. They were randomly assigned to receive either the experimental drugs (antaitasvir phosphate 100 mg+yiqibuvir 600 mg) or placebo treatment in a 3∶1 ratio. The patients were administered drugs once a day for 12 consecutive weeks, and then followed up for 24 weeks after treatment cessation. All subjects were unblinded at the four-week follow-up following drug discontinuation, with the experimental drug group continuing to complete subsequent post-discontinuation follow-up. The placebo group was switched to receive the experimental drugs for a repeated 12-week treatment period and followed up for another 24 weeks after discontinuation of the drug (placebo delayed treatment phase).The sustained virologic response rate (SVR12) was observed for subjects in the double-blind phase and the placebo delayed-treatment phase at 12 weeks after treatment cessation.Virological resistance analysis was performed on subjects who failed treatment. The primary efficacy endpoint was SVR12. The number and percentage of subjects who achieved "HCV RNA

Pristimerin, which is one of the compounds present in Celastraceae and Hippocrateaceae, has antitumor effects. However, its mechanism of action in esophageal squamous cell carcinoma (ESCC) remains unclear. This study aims to investigate the efficacy and mechanism of pristimerin on ESCC in vitro and in vivo. The inhibitory effect of pristimerin on cell growth was assessed using trypan blue exclusion and colony formation assays. Cell apoptosis was evaluated by flow cytometry. Gene and protein expressions were analyzed through quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry. RNA sequencing (RNA-Seq) was employed to identify significantly differentially expressed genes (DEGs). Cell transfection and RNA interference assays were utilized to examine the role of key proteins in pristimerin?s effect. Xenograft models were established to evaluate the antitumor efficiency of pristimerin in vivo. Pristimerin inhibited cell growth and induced apoptosis in ESCC cells. Upregulation of Noxa was crucial for pristimerin-induced apoptosis. Pristimerin activated the Forkhead box O3a (FoxO3a) signaling pathway and triggered FoxO3a recruitment to the Noxa promoter, leading to Noxa transcription. Blocking FoxO3a reversed pristimerin-induced Noxa upregulation and cell apoptosis. Pristimerin treatment suppressed xenograft tumors in nude mice, but these effects were largely negated in Noxa-KO tumors. Furthermore, the chemosensitization effects of pristimerin in vitro and in vivo were mediated by Noxa. This study demonstrates that pristimerin exerts an antitumor effect on ESCC by inducing AKT/FoxO3a-mediated Noxa upregulation. These findings suggest that pristimerin may serve as a potent anticancer agent for ESCC treatment.
Forkhead Box Protein O3/genetics* ; Humans ; Apoptosis/drug effects* ; Esophageal Squamous Cell Carcinoma/physiopathology* ; Esophageal Neoplasms/physiopathology* ; Pentacyclic Triterpenes ; Animals ; Cell Line, Tumor ; Proto-Oncogene Proteins c-bcl-2/genetics* ; Mice ; Signal Transduction/drug effects* ; Mice, Nude ; Cell Proliferation/drug effects* ; Triterpenes/pharmacology* ; Xenograft Model Antitumor Assays ; Mice, Inbred BALB C ; Male ; Gene Expression Regulation, Neoplastic/drug effects*