OBJECTIVE To investigate the influence of CYP2C19 gene polymorphism on platelet function and inflammatory cytokines in elderly patients with ischemic stroke， and to analyze potential factors associated with poor prognosis. METHODS A retrospective study was conducted on elderly patients with ischemic stroke admitted to our hospital from June 2024 to June 2025， wh o underwent CYP2C19 genotype testing and received antiplatelet therapy with clopidogrel. The levels of platelet function indicators and inflammatory cytokines before and after treatment were compared among patients with different metabolic phenotypes. Based on the prognosis at 6 months post-treatment， patients were divided into poor prognosis group and good prognosis group. Univariate analysis was performed on general data， metabolic phenotype， the levels of platelet function indicators and inflammatory cytokines. Variables with P ＜0.05 and the levels of inflammatory cytokines before treatment were included in a multivariate Logistic regression analysis to identify independent risk factors for poor prognosis. Multiple linear regression was used to further analyze the relationship between metabolic phenotypes and inflammatory cytokines. RESULTS A total of 448 elderly patients with ischemic stroke were included； among them， 162 cases were normal metabolic phenotype， 218 were intermediate metabolic phenotype， and 68 were poor metabolic phenotype. No rapid or ultrarapid metabolic phenotypes were observed. After treatment， platelet aggregation rate， the levels of P-selectin and platelet activated complex-1 （PAC-1）， high-sensitivity C-reactive Protein （hs-CRP）， interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α （TNF-α） in the normal metabolic phenotype group， intermediate metabolic phenotype group， and poor metabolic phenotype group （except for platelet aggregation rate， and the levels of P-selectin and PAC-1 in the poor metabolic phenotype group） were significantly lower than those before treatment in the same group. Moreover， the above indicators in the normal metabolic phenotype group were significantly lower than those in the intermediate and poor metabolic phenotype groups at the corresponding time， and the levels of platelet function indicators in the intermediate metabolic phenotype group were significantly lower than those in the poor metabol ic phenotype group at the corresponding time （ P ＜0.05）. Univariate and multivariate Logistic regression analyses showed that combined with hypertension， combined with diabetes mellitus， and intermediate or poor metabolic genotypes were independent risk factors for poor prognosis in elderly patients with ischemic stroke （ P ＜0.05）. Multiple linear regression analysis showed that serum levels of hs-CRP， IL-1β， IL-6 and TNF-α before treatment were significantly higher in patients with intermediate and poor metabolic genotypes compared to those with normal metabolic genotype （ P ＜0.05）， with a greater magnitude of increase in inflammatory cytokines observed in the patients with poor metabolic genotype. CONCLUSIONS The elderly ischemic stroke patients with CYP2C19 intermediate and poor metabolic genotypes have poor inhibition effect on platelet and higher levels of inflammatory cytokines than normal metabolic genotype； CYP2C19 gene polymorphism， and in combination with hypertension and diabetes， can be used as independent predictors of poor prognosis.

AIM:To automatically identify and quantitatively assess myopia-related fundus structural changes by combining non-mydriatic color fundus photography with an artificial intelligence(AI)-powered quantitative fundus analysis system and to further analyze the correlations between these fundus parameters and spherical equivalent(SE), axial length(AL), and age, providing the objective basis for monitoring myopia progression and supporting the formulation of personalized myopia prevention and control strategies. METHODS:A cross-sectional study was conducted enrolling myopic patients aged 18-50 y who underwent myopia screening from March 2023 to December 2023. Patients were stratified into three groups based on SE: the -3.00 D

Objective To analyze the impact of chronic obstructive pulmonary disease(COPD)on coronary plaque burden in elderly patients.Methods A total of 120 COPD patients admitted to the Hongqi Hospital Affiliated to Mudanjiang Medical University from January 2022 to December 2024 were prospectively enrolled and served as the COPD group.Another 120 healthy volunteers were recruited as the control group during the same period.The general clinical data and coronary plaque burden were compared between the two groups.Pearson linear correlation analysis was used to investigate the correlation between forced expiratory volume in the first second(FEV1)and coronary plaque burden as well as left ventricular ejection fraction(LVEF).Multiple linear regression analysis was employed to identify the influencing factors of total coronary plaque bur-den and calcified plaque burden.Results The COPD group had significantly larger smoking ratio and higher levels of high-sensitivity C-reactive protein(hs-CRP)and IL-6,but obviously lower LVEF and FEV1 levels than the control group(P＜0.01).Notably increased total coronary plaque burden(38.30±8.22 vs 24.61±5.56,P＜0.01),calcified plaque burden(21.11±6.57 vs 12.54±3.65,P＜0.01)and non-calcified plaque burden(17.19±5.39 vs 12.07±3.92,P＜0.01)were observed in the COPD group than the control group.FEV1 was negatively correlated with coro-nary plaque burden,calcified plaque burden,and non-calcified plaque burden,and positively corre-lated with LVEF(P＜0.01).Multiple linear regression analysis showed that FEV1 and IL-6 were influencing factors for both total coronary plaque burden(P＜0.01)and coronary calcified plaque burden(P＜0.01),and FEV1 was an influencing factor of non-calcified plaque burden in coronary arteries(P＜0.01).Conclusion COPD promotes the development of coronary plaque burden.So,for COPD patients,it is necessary to strengthen the monitoring and early prevention of coronary plaque burden.

Objective To investigate the effect and mechanism of melatonin in alleviating hypoxia-induced apoptosis in ovarian gra-nulosa cells.Methods Rat ovarian granulosa cells were isolated and divided into normoxic,hypoxic,and melatonin groups.Hypoxia-induced injury models were established in the hypoxic and melatonin groups,and granulosa cells in the melatonin group were treated with melatonin.A total of 24 rats were randomized into the control,model,and intervention groups(n=8 per group).Rat models of declining ovarian function induced by long-term hypoxia were established in the model and intervention groups.The rats in the intervention group were intraperitoneally injected with melatonin.Cell proliferation was measured using a CCK-8 assay,and lactate secretion and HIF-1αprotein with a specific kit,respectively.The levels of estradiol and progesterone in the cell supernatant and rat serum were detected using ELISA.Granulosa cell apoptosis was detected by flow cytometry,ovarian morphology by HE staining,and Bax and caspase-3 expression by Western blotting.Results Compared with the normoxic group,the hypoxic group exhibited decreased granulosa cell proliferation,increased apoptosis,elevated lactate and HIF-1α levels,and reduced estradiol and progesterone levels(P＜0.05).Compared with hypoxic group,these changes were significantly reversed in the molatonin group(P＜0.05).Compared with the control group,the model group showed increased lactate,HIF-1α,Bax,and caspase-3 levels,decreased estradiol and progesterone levels,and reduced follicles.Compared with the model group,all the indicators were ameliorated in the intervention group(P＜0.05).Conclusion Melatonin alleviated hypoxia-induced granulosa cell apoptosis and promoted the recovery of ovarian function.

Objective To investigate the effects of miR-23c and its target gene OCT1 on the proliferation,migration and apoptosis of hepatocellular liver cancer.Methods The expression level of miR-23c in normal liver cell line LO2 and hepatocel-lular carcinoma cell lines(including Huh7,HepG2,Hep-3B,SK-HEP1,HCCLM3 and MHCC97H)was detected by real-time flu-orescence quantitative PCR(qRT-PCR).The miR-23c mimics were designed to measure the proliferation status,migration abili-ty and apoptosis level of cells in the hepatocellular carcinoma cell line Huh7 using CCK-8 assay,cell migration assay and flow cytometric analysis.The target relationship between miR-23c and OCT1 was verified by predictive site prediction and dual lucif-erase assay,and the effect of miR-23c overexpression on OCT1 level was analyzed by Western blotting.The effect of miR-23c targeting OCT1 on the proliferation,migration and apoptosis of hepatocellular carcinoma was investigated by rescue as-say.Results Compared with the normal liver cell line LO2,the expression of miR-23c was significantly downregulated in liver cancer cell lines.In comparison with the NC group,Huh7 cells transfected with miR-23c mimics showed reduced proliferation and migration,while apoptosis was significantly enhanced.The interaction between miR-23c and OCT1 was verified.OCT1 pro-tein expression in Huh7 cells was reduced after miR-23c overexpression.The proliferation and migration of Huh7 cells were in-hibited,and apoptosis was promoted after transfection of miR-23c mimics.These effects were reversed by overexpression of OCT1.Conclusion miR-23c can downregulate OCT1,thereby inhibiting proliferation and migration,and promoting apoptosis in hepatocellular liver cancer cells.

Hemodynamic monitoring in shock is one of the core challenges in sepsis management.This article systematically explores how to optimize hemodynamic management in septic shock from three perspectives:assessment of fluid responsiveness and tolerance,monitoring of arterial and venous blood pressure,and macro- and microcirculatory monitoring.Firstly,fluid responsiveness assessment is the foundation of fluid therapy,but it must be combined with fluid tolerance to avoid fluid overload.Secondly,the refined evaluation of arterial and venous pressure changes,from macrocirculation to microcirculation,provides a more comprehensive perspective for hemodynamic management.Thirdly,the transition from cardiac output to microcirculatory flow is critical for optimizing oxygen delivery,requiring dynamic adjustment of treatment through both invasive and non-invasive techniques,while also considering the relationship between cardiac output and oxygen delivery and their impact on tissue oxygenation.By integrating these monitoring approaches,individualized and precise treatment for septic shock patients can be achieved,thereby improving outcomes.

BACKGROUND:Research has shown that endoplasmic reticulum stress-induced autophagy of neurons in the ischemic penumbra is a key link in cerebral ischemia-reperfusion injury.Autophagy mediated by the dissociation and activation of endoplasmic reticulum transmembrane proteins PERK,IRE1 α,ATF6,and GRP78/BIP plays an important role in neuronal outcomes.Traditional Chinese medicine can regulate endoplasmic reticulum stress-autophagy,reduce neuronal damage or death,and exert neuroprotective effects.OBJECTIVE:To explore the role of endoplasmic reticulum stress-autophagy in cerebral ischemia-reperfusion injury and the research progress in the regulatory mechanisms of traditional Chinese medicine.METHODS:A literature retrieval was conducted in CNKI and PubMed for relevant literature related to endoplasmic reticulum stress,autophagy,cerebral ischemia-reperfusion injury,and regulation by traditional Chinese Medicine published from January 2015 to May 2024.The search terms were"cerebral ischemia-reperfusion injury,ischemic stroke,brain injury,endoplasmic reticulum stress,autophagy,traditional Chinese medicine,compounds,signaling pathways,saponins,polyphenols,alkaloids"in Chinese and English,respectively.Any literature that is inconsistent with the research content,outdated,or duplicated was excluded.A total of 1197 relevant literature were retrieved,and 71 articles were ultimately included.RESULTS AND CONCLUSION:(1)Numerous studies have suggested that endoplasmic reticulum stress-autophagy is closely related with cerebral ischemia-reperfusion injury.(2)The active ingredients and compound formulas of traditional Chinese medicine monomers can regulate the expression of endoplasmic reticulum stress-autophagy related proteins,alleviate neuronal damage,and exert neuroprotective effects by regulating signal pathways such as PERK-eIF2α-ATF4,IRE1α-ASK1-JNK,and IRE1α-XBP.

To construct a recombinant fowl adenovirus 4(FAdV-4)expressing the Cap protein of goose astrovirus genotype 2(GoAstV-2),the expression cassette of Cap gene was inserted into the natural 1 966 bp deletion region of the FAdV-4 genome in the infectious clone p15A-cm-FAdV4-HNJZ.The resulted recombinant plasmid p15A-cm-FAdV4-HNJZ-Cap/GoAstV-2 was linearized with restriction enzyme and transfected into chicken hepatoma cell line(LMH)to rescue the recombinant FAdV-4 expressing the Cap protein of GoAstV-2,rF Ad V4-Cap/GoAstV-2.After 15 passages in LMH cells,the recombinant rFAdV4-Cap/GoAstV-2 was identified by PCR using primers flanking the insertion site of the Cap gene expression cassette and using viral genome DNA extracted from rFAdV4-Cap/GoAstV-2 infected LMH cells as template.LMH cells were in-fected with 15th passage rFAdV4-Cap/GoAstV-2 and indirect immunofluorescence was performed with a polyclonal antibody against Cap protein as the primary antibody.Western blot was carried out with lysates of rFAdV4-Cap/GoAstV-2 infected LMH cells.The in vitro replication dynamic of the 15th passage of the rFAdV4-Cap/GoAstV-2 was also investigated in LMH cells.The results demonstrated that the Cap gene of GoAstV-2 was presented in the genome of the recombinant vi-rus rF AdV4-Cap/Go Ast V-2,and could be expressed stably.The prepared recombinant virus in this study will lay a foundation for developing inactivated bivalent vaccine candidate against co-in-fection of FAdV-4 and GoAstV-2 in goose.

Objective To explore the application value of three-dimensional T1-weighted multi-echo DIXON(3D-T1W-mDIXON)with three-dimensional T2-weighted driven imaging with variable excitation(3D-T2W-DRIVE)in unilateral vascular compressive hemifacial spasm(HFS),and to improve the accuracy of preoperative imaging diagnosis of microvascular decompression(MVD).Methods The clinical and imaging data of 235 patients with unilateral vascular compressive HFS treated with MVD from July 2018 to August 2024 in Xuzhou City Hospital of Traditional Chinese Medicine were analyzed retrospectively.Before MVD,3D-T1W-mDIXON and 3D-T2W-DRIVE sequence image,multiplanar reconstruction were used to analyze the spatial walking relationship between facial nerve and offending vessels.The differences between the affected side and the healthy side were compared,and then compared with the MVD;By using paired chi square test,image result of 3D-T1W-mDIXON combined with 3D-T2W-DRIVE sequence with either sequence alone were compared to evaluate the superiority of two combined sequences in the diagnosis of vascular compressive HFS.Results Among 235 cases HFS on the affected side,there were 149 cases of vascular compression and 68 cases with specific neurovascular contacts,and 15 cases with dubious contacts,with a positive rate of 92.34％;In the 235 cases HFS of the healthy side,there were 21 cases of vascular compression and 25 cases with specific neurovascular contacts,and 77 cases with dubious contacts,with a positive rate of 19.57％.By using the findings during facial nerve MVD procedure as the gold standard,the positive rate of diagnosing HFS using 3D-T1W-mDIXON combined with 3D-T2W-DRIVE sequence was 92.34％.The ability of 3D-T1W-mDIXON combined with 3D-T2W-DRIVE sequence to identify offending vessels(92.34％)is superior to using 3D-T1W-mDIXON sequence alone(83.00％,x2=9.52,P＜0.05)or using 3D-T2W-DRIVE sequence alone(86.38％,x2=4.30,P＜0.05).Conclusion 3D-T1W-mDIXON combined with 3D-T2W-DRIVE sequence image can clearly show the relationship between facial nerve and peripheral blood vessels,and the diagnostic efficacy is higher than that of any sequence alone,can provide better imaging evidence for clinical diagnosis and treatment of HFS.

Objective To analyze the impact of chronic obstructive pulmonary disease(COPD)on coronary plaque burden in elderly patients.Methods A total of 120 COPD patients admitted to the Hongqi Hospital Affiliated to Mudanjiang Medical University from January 2022 to December 2024 were prospectively enrolled and served as the COPD group.Another 120 healthy volunteers were recruited as the control group during the same period.The general clinical data and coronary plaque burden were compared between the two groups.Pearson linear correlation analysis was used to investigate the correlation between forced expiratory volume in the first second(FEV1)and coronary plaque burden as well as left ventricular ejection fraction(LVEF).Multiple linear regression analysis was employed to identify the influencing factors of total coronary plaque bur-den and calcified plaque burden.Results The COPD group had significantly larger smoking ratio and higher levels of high-sensitivity C-reactive protein(hs-CRP)and IL-6,but obviously lower LVEF and FEV1 levels than the control group(P＜0.01).Notably increased total coronary plaque burden(38.30±8.22 vs 24.61±5.56,P＜0.01),calcified plaque burden(21.11±6.57 vs 12.54±3.65,P＜0.01)and non-calcified plaque burden(17.19±5.39 vs 12.07±3.92,P＜0.01)were observed in the COPD group than the control group.FEV1 was negatively correlated with coro-nary plaque burden,calcified plaque burden,and non-calcified plaque burden,and positively corre-lated with LVEF(P＜0.01).Multiple linear regression analysis showed that FEV1 and IL-6 were influencing factors for both total coronary plaque burden(P＜0.01)and coronary calcified plaque burden(P＜0.01),and FEV1 was an influencing factor of non-calcified plaque burden in coronary arteries(P＜0.01).Conclusion COPD promotes the development of coronary plaque burden.So,for COPD patients,it is necessary to strengthen the monitoring and early prevention of coronary plaque burden.