ObjectiveTo establish a new noninvasive， simple， and convenient clinical predictive model by identifying independent predictive factors for rebleeding after endoscopic therapy in cirrhotic patients with esophagogastric variceal bleeding （EGVB）， and to provide a basis for individualized risk assessment and development of clinical intervention strategies. MethodsCirrhotic patients with EGVB who were diagnosed and treated in The First Affiliated Hospital of Xi’an Medical University from September 2018 to October 2023 were enrolled as subjects， and according to whether the patient experienced rebleeding within 1 year after endoscopic therapy， they were divided into rebleeding group with 93 patients and non-rebleeding group with 84 patients. Clinical data were collected and analyzed. The independent samples t-test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups； the chi-square test was used for comparison of categorical data between two groups. A Logistic model was established based on the results of the univariate and multivariate analyses， and the receiver operating characteristic （ROC） curve and the area under the ROC curve （AUC） were used to assess the accuracy of the model. R software was used to visualize the model by plotting a nomogram， and the Bootstrap method was used for internal validation of the model. ResultsThe multivariate analysis showed that red blood cell count （RBC）， cholinesterase （ChE）， alkaline phosphatase （ALP）， albumin （Alb）， thrombin time （TT）， portal vein trunk diameter， sequential therapy， and primary prevention were independent predictive factors for rebleeding. Based on the results of the multivariate analysis， a logistic model was established as logit（P）=-0.805-1.978×（RBC）+0.001×（ChE）-0.020×（ALP）-0.314×（Alb）+0.567×（TT）+0.428×（portal vein trunk diameter）-2.303×［sequential therapy （yes=1， no=0）］-2.368×［primary prevention （yes=1， no=0）］. The logistic model （AUC=0.928， 95% confidence interval ［CI］： 0.893—0.964， P<0.001） had a better performance in predicting rebleeding than MELD score （AUC=0.603， 95%CI： 0.520—0.687， P=0.003）， Child-Pugh class （AUC=0.650， 95%CI： 0.578—0.722， P=0.001）， and FIB-4 index （AUC=0.587， 95%CI： 0.503—0.671， P=0.045）. The model had an optimal cut-off value of 0.607， a sensitivity of 0.817， and a specificity of 0.817. Internal validation confirmed that the model had good predictive performance and accuracy. ConclusionSequential therapy， implementation of primary prevention， an increase in RBC， and an increase in Alb are protective factors against rebleeding， while prolonged TT and widened main portal vein diameter are risk factors. The logistic model based on these independent predictive factors can predict rebleeding and thus holds promise for clinical application.

ObjectiveTo investigate the expression level of mammalian sterile 20-like kinase 1 （MST1） in prostate cancer （PCa） tissues， its biological functions， and its regulatory effects on androgen receptor （AR） and vascular endothelial growth factor （VEGF） expression. MethodsImmunohistochemistry was performed to detect MST1 expression in 77 prostate cancer tissues and 34 benign prostatic hyperplasia （BPH） tissues， and the relationship between MST1 expression and clinicopathological parameters was analyzed. MST1-overexpressing C4-2 and LNCaP cell lines were constructed. CCK-8 assay， Transwell migration assay， and angiogenesis assay were conducted to evaluate the effects of MST1 on cell proliferation， migration， and angiogenesis. The expression changes of AR and VEGF were detected by qRT-PCR and Western blot. ResultsMST1 expression was significantly lower in PCa tissues compared with BPH tissues （P=0.012）. Low MST1 expression was significantly associated with tumor metastasis （P=0.033）. MST1 overexpression inhibited C4-2 cell proliferation and migration， with transmembrane migrated cells reduced by 53.6% （P<0.01）. MST1 overexpression decreased the mRNA and protein expression levels of AR and VEGF （P<0.05）. Angiogenesis assay demonstrated that the length of new vessel structure was significantly reduced （P<0.05）. ConclusionMST1 shows a low expression level in PCa tissues and is associated with tumor metastasis. MST1 exerts tumor-suppressive effects in prostate cancer by inhibiting cell proliferation， migration， and angiogenesis， as well as downregulating the expression of AR and VEGF， indicating its potential as a therapeutic target for prostate cancer.

Objective: To analyze the implementation status of the “Three-Exemptions” policy for voluntary blood donation in China by taking Shandong Province as a case study, explore the sociodemographic characteristics of policy beneficiaries and the distribution differences in blood donation frequencies, so as to provide practical references for improving the honor incentive system of voluntary blood donation and stabilizing the blood donation team. Methods: Excel was used to sort out and summarize the policy documents from 31 provincial-level administrative regions of China (excluding Hong Kong, Macao and Taiwan), and its implementation models, temporal characteristics and implementation basis were analyzed. Using 238 193 policy beneficiaries in Shandong Province as the research objects, Stata was adopted for descriptive statistical analysis of sociodemographic characteristics including gender, age, educational background and occupation. The Mann-Whitney U test and Kruskal-Wallis H test were performed to compare the distribution differences of blood donation frequencies among populations with different characteristics. Results: The “Three Exemption” policy has been implemented in 29 provinces nationwide, forming five differentiated implementation models. Specifically, 45.16% of the regions adopted province-wide unified implementation, 32.26% adopted partial prefecture-level city implementation, 12.90% adopted partial clause implementation, 3.23% adopted encouraging implementation, and 6.45% had not implemented the policy. The period from 2023 to 2026 witnessed the concentrated promotion of the policy. In Shandong Province, the beneficiaries were mainly males (82.08%), middle-aged individuals aged 40-60 years (71.78%), groups with junior and senior high school education (56.57%), and staff employees (30.60%). The distribution of blood donation frequencies showed that nearly 60% (56.95%) of the beneficiaries had donated blood 20 to 29 times. Statistically significant differences in donation frequency distributions were observed across genders, age groups, educational backgrounds, and occupations (all P<0.05). Further analysis revealed that the proportion of males with 40 or more blood donations was higher than that of females (24.32% vs 15.60%), while females had a higher proportion of 20-29 blood donations than males (65.98% vs 54.99%). With the increase of age, the proportion of those with 20-29 blood donations gradually decreased, whereas the proportion of those with≥40 blood donations gradually increased. Conclusion: The coverage of the “Three Exemptions” policy for voluntary blood donation in China continues to expand. However, there is still room for optimization in terms of policy implementation standards, population structure adaptation and incentive gradient design. Future efforts should strengthen national top-level design to balance regional development gaps. Moreover, hierarchical and targeted incentive and publicity strategies combined with population structural characteristics should be implemented to enhance public enthusiasm for voluntary blood donation.

Alzheimer’s disease (AD) is pathologically characterized by cerebral amyloid β‑protein (Aβ) aggregation, neurofibrillary tangles and progressive cognitive deterioration. There is an urgent clinical demand for targeted therapeutic agents against AD, whereas the blood-brain barrier (BBB) acts as a critical physical barrier that blocks over 98% small-molecule drugs and nearly all biomacromolecules from entering brain parenchyma. Nanomedicine-based drug delivery systems (NDDSs) with tunable physicochemical properties can cross the BBB via multiple transcytosis pathways including adsorptive-mediated, receptor-mediated and transporter-mediated routes, opening a promising avenue for targeted AD treatment. A core academic viewpoint proposed herein is that robust in vitro endothelial penetration of nanocarriers cannot guarantee effective accumulation in brain target cells. Comprehensive evaluation of BBB-crossing delivery efficiency should not merely rely on in vitro permeability tests, but cover the full multi-step transcytosis cascade, cellular tropism in brain tissues and in vivo therapeutic outcomes. This review systematically sorts out diverse nanoplatforms applicable to BBB penetration for AD intervention. Inorganic nanomaterials such as gold and ceria nanoparticles possess large specific surface areas and intrinsic antioxidant capacity, which eliminate reactive oxygen species and hinder Aβ fibrillization. Liposomal formulations and solid lipid nanoparticles exhibit superior biocompatibility with biomimetic phospholipid bilayer architectures, capable of co-loading hydrophilic nucleic acids for Tau regulation and lipophilic Aβ inhibitors; relying on receptor-mediated transcytosis, they achieve sustained drug retention in the brain. Polymeric nanocarriers including nanogels and polyamidoamine dendrimers enable multi-target combinatorial therapy, and can be engineered to release cargo in response to inflammatory microenvironments, thereby suppressing excessive microglial activation and protecting neuronal mitochondria. Beyond conventional nanocarriers, this work elaborates two cutting-edge BBB-crossing delivery platforms: biomimetic nanosystems and metal-organic frameworks (MOFs). Biomimetic nanoparticles camouflaged with erythrocyte, platelet or macrophage membranes, as well as natural exosomes, evade immune clearance, prolong systemic circulation and inherently home to inflammatory lesions. Serving as “nano-decoys”, they neutralize Aβ neurotoxins and remodel cerebral inflammatory microenvironments simultaneously. MOFs feature high porosity and customizable pore channels for co-delivery of multiple therapeutics, and can be integrated with near-infrared photothermal and photooxidation modalities to facilitate focal brain lesion therapy. This review highlights a transformative paradigm shift in the field of BBB-targeted AD therapy: research focus has shifted from simply maximizing cerebral drug penetration toward active modulation and functional restoration of the BBB. Impaired BBB transporters intrinsically impede endogenous Aβ clearance. Accordingly, BBB-regulating nanocarriers are designed to remodel the low-density lipoprotein receptor-related protein 1 (LRP1) trafficking cascade, redirecting endocytic vesicles from lysosomal degradation to non-degradable transcytosis and restoring the intrinsic Aβ efflux capacity of the BBB. Distinct from conventional strategies that only exert local lesion inhibition, this systemic clearance strategy eliminates cerebral Aβ deposits by accelerating peripheral excretion.

ObjectiveCurrently， evidence regarding whether the left or right nostril should be preferentially selected for nasotracheal intubation （NTI） in children remains insufficient， particularly under continuous visualization conditions. This study aimed to compare the efficiency and safety of NTI via the left versus right nostril in children under flexible intubation video endoscope （FIVE） guidance. MethodsA total of 100 children aged 3-7 years with American Society of Anesthesiologists physical status I-II， who were scheduled for elective dental caries treatment under general anesthesia， were randomly assigned to undergo FIVE-guided NTI via either the left nostril （group L） or the right nostril （group R）. The primary outcome was intubation time. Secondary outcomes included first-attempt success rate， number of intubation attempts， incidence and severity of epistaxis， peri-intubation hemodynamic and respiratory parameters， and postoperative procedure-related complications （nasal blockage， sore throat， and hoarseness）. ResultsNo statistically significant between-group difference was found in intubation time （L group： 36.86 ± 6.04 s vs. R group： 37.96 ± 6.20 s； P=0.371） or first-attempt success rate （96% vs. 92%， respectively； P=0.400）. The incidence and severity of epistaxis were comparable between groups （10% vs. 12%； P=0.749）. No statistically significant between-group differences were observed in hemodynamic and respiratory parameters at all measured time points （all P>0.05）. The incidences of postoperative nasal congestion， sore throat， and hoarseness were low in both groups. ConclusionIn children undergoing FIVE-guided NTI， tracheal catheter insertion via the left or right nostril yields comparable efficacy and safety. When using visualization-guided techniques in routine pediatric clinical practice， nostril laterality does not need to be prioritized when selecting the insertion side for NTI.

Objective To investigate the effect of miR-185-5p-mediated targeted negative regulation of transmembrane 9 superfamily member 1(TM9SF1)on proliferation,migration and autophagy in lung adenocarcinoma cells.Methods The expression of miR-185-5p in lung adenocarcinoma tissues was analyzed using dataset GSE51853 downloaded from the Gene Expression Omnibus(GEO)database.Potential target proteins of miR-185-5p were predicted using online databases(miRTargetLink,miRTarbase,and DIANA-microT-CD),and autophagy-related proteins were obtained from HADb.The intersected results from these four databases was identified,and survival curves of vascular endothelial growth factor A(VEGFA)and TM9SF1 within the overlapping candidates were analyzed using the StarBase database.TM9SF1 3'UTR wild-type(WT)or TM9SF1 3'UTR mutant(MUT)reporter plasmids were separately co-transfected with miR-185-5p control plasmid(CON)or miR-185-5p overexpression plasmid(over-miR-185-5p)into HEK-293T cells.A dual-luciferase reporter gene assay was employed to assess the binding interaction between miR-185-5p and TM9SF1 and quantify the subsequent luciferase activity.Western blotting was used to assess TM9SF1 protein expression levels in A549 cells transfected with over-miR-185-5p.A549 cells were divided into three groups:(1)CON+NC group,co-transfected with miR-185-5p control plasmid and TM9SF1 control plasmid;(2)over-miR-185-5p+NC group,co-transfected with over-miR-185-5p and TM9SF1 control plasmid;(3)over-miR-185-5p+over-TM9SF1 group,co-transfected with both miR-185-5p and TM9SF1 overexpression plasmids.EdU cell proliferation assay,wound healing assay,and Transwell migration assay were performed to validate the effects of miR-185-5p targeted binding to TM9SF1 on proliferation and migration capacities in lung adenocarcinoma.Changes in autophagic flux and mitochondrial membrane potential(MMP)of lung adenocarcinoma cells were detected using stubRFP-sensGFP-LC3 lentivirus and JC-1 assays,respectively.Results In the GSE51853 dataset,miR-185-5p expression level was significantly lower in lung adenocarcinoma tissues compared with normal lung tissues(P<0.01).qRT-PCR analysis revealed that miR-185-5p expression was downregulated in lung adenocarcinoma cell lines NCI-H1299 and A549 compared with normal lung epithelial cells BEAS-2B(P<0.01).Bioinformatics predictions using miRTargetLink,miRTarbase,DIANA-microT-CD,and HADb databases indicated that miR-185-5p could target and regulate the autophagy-related protein TM9SF1.Dual-luciferase reporter assays and Western blotting demonstrated that miR-185-5p directly bound to the 3'UTR region of TM9SF1 mRNA,and overexpression of miR-185-5p significantly reduced the expression of target protein TM9SF1(P<0.05).EdU cell proliferation,wound healing,and Transwell migration assays demonstrated that miR-185-5p overexpression inhibited proliferation and migration capacities of lung adenocarcinoma cells,whereas TM9SF1 overexpression could attenuate this inhibition effect(P<0.05).Results of stubRFP-sensGFP-LC3 for autophagic flux analysis demonstrated that overexpression of miR-185-5p enhanced autophagic flux in A549 cells,whereas co-overexpression of miR-185-5p and TM9SF1 suppressed autophagic flux.JC-1 assays showed a decreased MMP level in A549 cells after miR-185-5p overexpression,with higher MMP level observed when miR-185-5p and TM9SF1 were co-overexpressed.Conclusion miR-185-5p may suppress proliferation,migration,and autophagy capacities in lung adenocarcinoma cells by targeting TM9SF1 through negative regulation.

Breast cancer(BRCA)remains one of the leading causes of cancer-related deaths worldwide due to its high rates of metastasis and recurrence,making it crucial to explore its underlying molecular mechanisms.Our previous study demonstrated that miR-326 inhibits BRCA progression by targeting EPH receptor B3(EPHB3).This study further explores the molecular mechanism by which long non-coding RNAs(LncRNAs)regulates BRCA progression via the competing endogenous RNA(ceRNA)mecha-nism,in which it competes with EPHB3 for miR-326 binding.Bioinformatics analysis identified LncRNA Small Nucleolar RNA Host Gene 12(SNHG12)as a potential miR-326-binding molecule.SNHG12 was found to be significantly upregulated in BRCA tissues,exhibiting a negative correlation trend with miR-326 and a positive correlation trend with EPHB3,suggesting its potential involvement in the ceRNA regu-latory network.Nuclear-cytoplasmic fractionation assays revealed cytoplasmic localization of SNHG12,while dual-luciferase reporter assays confirmed its direct binding to miR-326.Functional experiments demonstrated that SNHG12 knockdown significantly suppressed BRCA cell proliferation,invasion,and migration,while miR-326 inhibition reversed these effects.Furthermore,miRNA pulldown assay re-vealed significant enrichment of SNHG12 and EPHB3 in the miR-326 pulldown products,indicating di-rect binding between them.Western blotting and rescue experiments revealed that SNHG12 upregulates EPHB3 expression by sponging miR-326,thereby promoting the malignant behaviors of BRCA cells.Col-lectively,this study revealed that LncRNA SNHG12 promotes BRCA progression by regulating the miR-326/EPHB3 axis through a ceRNA mechanism.The SNHG12/miR-326/EPHB3 pathway may represent a promising target for the molecular diagnosis and targeted therapy of BRCA.

Objective To investigate the analgesic effect of ultrasound-guided quadratus lumborum block combined with patient-controlled intravenous analgesia after lower abdominal surgery.Methods A total of 134 patients who underwent lower abdominal surgery in General Hospital of Central Theater Command from April 2021 to April 2024 were prospectively selected and randomly divided into the observation group and the control group,with 67 patients in each group.Patients in the observation group received ultrasound-guided quadratus lumborum block combined with patient-controlled intravenous analgesia.Patients in the control group underwent only patient-controlled intravenous analgesia.The number of analgesic pump compressions and the cumulative sufentanil consumption 4 hours,6 hours,12 hours,and 24 hours after surgery,the visual analogue score(VAS)of pain at rest and exercise,and the incidence of adverse reactions during postoperative analgesia were compared between the two groups.Results Compared with the control group,the number of analgesic pump compressions and the cumulative sufentanil consumption of patients were fewer/less at 6 hours,12 hours and 24 hours after surgery in the observation group(P<0.05).The VAS scores of patients at exercise 4 hours,6 hours,12 hours and 24 hours after surgery in the observation group were significantly lower than those in the control group(P<0.05).The incidence of nausea,vomiting and vertigo in the observation group was significantly lower than that in the control group(P<0.05).Conclusion Compared with patient-controlled intravenous analgesia,ultrasound-guided quadratus lumborum block combined with patient-controlled intravenous analgesia can significantly reduce the number of analgesia pump compressions and the cumulative sufentanil consumption in postoperative analgesia of lower abdominal surgery,and has a better effect in relieving exercise pain,it can also reduce the occurrence of adverse reactions such as nausea and vomiting.

AIM To investigate the impact of varying dosages of Supplemented Wendan Decoction on the PI3K/Akt/FOXO1 glycolipid metabolic pathway in 3T3-L1 adipocytes.METHODS The CCK-8 assay was used to determine the concentration of Supplemented Wendan Decoction-medicated serum.The mature adipocytes differentiated from 3T3-L1 preadipocytes after induction were further divided into the blank control group,the model group,the rosiglitazone group(10 mg/L),and the Supplemented Wendan Decoction groups(5％,10％,and 20％),followed by the sample collections after 48 hours of treatment.Oil red O staining quantified lipid accumulation in 3T3-L1 adipocytes;extracellular glucose levels were measured using glucose oxidase(GOD)assay;RT-qPCR analyzed mRNA expressions of IRS-1,PI3K,Akt,GLUT4,IL-6,TNF-α and IL-1β;Western blot assessed protein expressions of INSR,IRS-1,PI3K-p85,Akt,FOXO1 and GLUT4.RESULTS No significant changes in cell viability(P＞0.05)were observed in 3T3-L1 preadipocytes exposed to serum containing supplemented Wendan Decoction at different concentrations for 24,48,or 72 hours.The 3T3-L1 preadipocytes held the capacity to differentiate into mature adipocytes within a 14-day induction period.Compared to the model group,all supplemented Wendan Decoction groups exhibited reduced lipid accumulation in adipocytes and downregulated mRNA expression of IRS-1,IL-6,TNF-α and IL-1β(P＜0.01);the low-dose group demonstrated increased mRNA expressions of PI3K and GLUT4(P＜0.05,P＜0.01),alongside elevated protein expressions of INSR,IRS-1,PI3K-p85,Akt and GLUT4(P＜0.05,P＜0.01);the medium-dose group showed enhanced GLUT4 mRNA expression,and upregulated protein expressions of INSR and FOXO1(P＜0.01).After 24 hours intervention,the high-dose Supplemented Wendan Decoction group exhibited increased glucose consumption in adipocytes(P＜0.01),and elevated protein expression of INSR,Akt and FOXO1(P＜0.05,P＜0.01).CONCLUSION Supplemented Wendan Decoction reduces lipid accumulation in adipocytes,regulates glucose and lipid metabolism,and promotes metabolic homeostasis through PI3K/Akt/FOXO1 signaling pathway.