Post-stroke cognitive impairment （PSCI） is a common and severe complication in stroke patients， significantly affecting their quality of life and social function. Despite increasing research on PSCI in recent years， effective therapeutic methods remain limited. The Wnt/β-catenin signaling pathway has emerged as a critical research focus in neuroscience due to its essential role in neuroprotection， neurorepair， and cognitive recovery. Dysregulation of the Wnt/β-catenin pathway is considered one of the key mechanisms in the onset and progression of PSCI. Traditional Chinese medicine （TCM）， with its multi-component， multi-target， and synergistic properties， has shown unique advantages in modulating the Wnt/β-catenin signaling pathway， providing a potential novel approach for PSCI treatment. TCM regulates the Wnt/β-catenin pathway through various mechanisms and exerts effects such as inhibiting cell apoptosis， maintaining blood-brain barrier integrity， reducing neuroinflammation， promoting neuroplasticity， and enhancing neurorepair， thereby improving post-stroke cognitive function. This review summarized the latest research progress on the regulation of the Wnt/β-catenin signaling pathway by TCM in intervening PSCI. It analyzed the mechanisms of action of various TCM components and compound formulas within this pathway， aiming to provide a theoretical basis for innovative strategies for PSCI treatment in the future and offer new research insights and practical guidance for the application of TCM in cerebrovascular diseases.

Post-stroke cognitive impairment （PSCI） is a common and severe complication in stroke patients， significantly affecting their quality of life and social function. Despite increasing research on PSCI in recent years， effective therapeutic methods remain limited. The Wnt/β-catenin signaling pathway has emerged as a critical research focus in neuroscience due to its essential role in neuroprotection， neurorepair， and cognitive recovery. Dysregulation of the Wnt/β-catenin pathway is considered one of the key mechanisms in the onset and progression of PSCI. Traditional Chinese medicine （TCM）， with its multi-component， multi-target， and synergistic properties， has shown unique advantages in modulating the Wnt/β-catenin signaling pathway， providing a potential novel approach for PSCI treatment. TCM regulates the Wnt/β-catenin pathway through various mechanisms and exerts effects such as inhibiting cell apoptosis， maintaining blood-brain barrier integrity， reducing neuroinflammation， promoting neuroplasticity， and enhancing neurorepair， thereby improving post-stroke cognitive function. This review summarized the latest research progress on the regulation of the Wnt/β-catenin signaling pathway by TCM in intervening PSCI. It analyzed the mechanisms of action of various TCM components and compound formulas within this pathway， aiming to provide a theoretical basis for innovative strategies for PSCI treatment in the future and offer new research insights and practical guidance for the application of TCM in cerebrovascular diseases.

AIM: To explore the factors affecting the whole-eye astigmatism after pterygium excision combined with autologous limbal stem cell transplantation.METHODS: A retrospective analysis was conducted on the medical records of 42 patients(42 eyes)with primary pterygium admitted in the ophthalmology department of Xijing Hospital from January 2023 to October 2023. They underwent pterygium excision combined with autologous limbal stem cell transplantation. The maximum invasion depth of pterygium into the cornea was measured with anterior segment optical coherence tomography(AS-OCT)before operation, the length of the pterygium invading cornea, the width of the limbus and the area of the invading cornea were measured during the operation, and three-dimensional values of corneal astigmatism of anterior segment, index of surface variance(ISV), index of vertical asymmetry(IVA), best corrected visual acuity(BCVA)and whole-eye astigmatism were collected before and at 1 mo after surgery. Patients with astigmatism ≤0.50 D or >0.50 D of the whole eye at 1 mo after surgery were assigned to group A and B, respectively. The differences of clinical data before and at 1 mo after surgery between the two groups, and the correlation between pre-operative clinical indicators and whole-eye astigmatism were analyzed. The decision tree algorithm was performed to explore the influencing factors of whole-eye astigmatism at 1 mo postoperatively.RESULTS: The maximum invasion depth of pterygium in the group A was significantly less than that in the group B [80.00(40.00, 180.00)μm vs 175.00(123.00, 190.00)μm, P=0.002]. Preoperative BCVA(LogMAR), whole-eye astigmatism, cornea astigmatism, ISV, IVA and maximum invasion depth of pterygium were positively correlated with whole-eye astigmatism at 1 mo after surgery(rs=0.317, P=0.041; rs=0.545, P<0.001; rs=0.448, P=0.003; rs=0.389, P=0.011; rs=0.382, P=0.013; rs=0.391, P=0.010). The decision tree algorithm screened out two influential factors: the maximum invasion depth of pterygium into the cornea and preoperative whole-eye astigmatism. The risk of whole-eye astigmatism >0.50 D at 1 mo after operation was higher with maximum invasion depth of pterygium into the cornea >95 μm than that with ≤95 μm. Among the patients with whole-eye astigmatism >2.63 D before operation, the probability of residual whole-eye astigmatism >0.50 D was 88.9%, and the predictive model AUC was 0.804.CONCLUSION: The whole-eye astigmatism after pterygium resection is mainly affected by the maximum invasion depth of pterygium into the cornea and preoperative whole-eye astigmatism. When the maximum invasion depth of pterygium into the corneal is >95 μm and the whole-eye stigmatism is >2.63 D before surgery, the patient should receive surgical treatment as soon as possible in order to obtain good clinical benefits.

Maternal obesity has been shown to exert adverse transgenerational effects on offspring ovarian function,characterized by reduced ovarian follicle reserve,impaired granulosa cell function,and disrupted reproductive cycles.The underlying mechanisms involve cellular stress-induced damage characterized by mitochondrial dysfunction,oxidative stress,and apoptosis,as well as dysregulation in key regulatory pathways such as ovarian hormone secretion,gene expression,and epigenetic modifications.This review synthesizes existing evidence on how maternal obesity-induced acute stress and chronic genetic/epigenetic alterations jointly contribute to offspring ovarian impairment.The findings elu-cidate the complex relationship between maternal metabolic status and offspring reproductive health,providing a robust theoretical foundation for refining prenatal management and developing targeted intervention strategies.

AIM:To investigate the effect of plasmin on epithelial sodium channel γ-subunit(γ-ENaC)acti-vation in mouse M-1 cells and the role of nuclear factor-κB(NF-κB).METHODS:Mouse M-1 cells were divided into three experimental parts.In the first part,the cells were divided into a control group,a plasmin group,and a plasmin+BAY 11-7082(NF-κB inhibitor)group to explore the effects of plasmin on inflammatory factors and γ-ENaC.In the sec-ond part,the cells were divided into a control group,a BAY 11-7082 group and a BAY 11-7082+plasmin group.M-1 cells were pretreated with BAY 11-7082 to explore the role of NF-κB in the regulation of γ-ENaC expression by plasmin.In the third part,the cells were divided into a control group,a plasmin group and an interleukin-6(IL-6)group.M-1 cells were treated with plasmin or IL-6 to explore the regulatory effect of IL-6 downstream of NF-κB on γ-ENaC.After drug interven-tion,the levels of IL-6,tumor necrosis factor-α(TNF-α),monocyte chemoattractant protein-1(MCP-1)and IL-1β in cell culture supernatants were detected by ELISA.The protein levels of phosphorylated inhibitor of nuclear factor-κB α(p-IκBα)/IκBα,p-NF-κB p65/NF-κB p65,and γ-ENaC was detected by Western blot.The distribution of γ-ENaC on the membrane was detected by immunofluorescence staining.RESULTS:Compared with control group,the levels of IL-6,TNF-α,MCP-1 and IL-1β in the supernatants of cells treated with 10 mg/L plasmin for 24 h were increased(n=3,P<0.01),the protein levels of p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC were increased(n=5,P<0.01),and the distribution of γ-ENaC on the membrane was increased.Compared with plasmin group,the levels of IL-6,TNF-α,MCP-1,IL-1β,p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC,and the γ-ENaC distribution on the membrane were lowered in plasmin and BAY 11-7082 coculture group(n=3,P<0.05 or P<0.01).Compared with control group,the ratio of p-NF-κB p65/NF-κB p65 decreased in BAY 11-7082 group(n=5,P<0.05),whereas there was no significant change in γ-ENaC.After stimulation with plasmin,the levels of p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC in-creased(n=5,P<0.05 or P<0.01),and the γ-ENaC distribution on the membrane increased.Treatment with IL-6,downstream of NF-κB,increased the protein expression of γ-ENaC(n=5,P<0.05)and the distribution of γ-ENaC on the membrane after 24 h of intervention.CONCLUSION:The regulation of γ-ENaC expression by plasmin in mouse M-1 cells is related to the abnormal increase in inflammatory factors after NF-κB activation.

Maternal obesity has been shown to exert adverse transgenerational effects on offspring ovarian function,characterized by reduced ovarian follicle reserve,impaired granulosa cell function,and disrupted reproductive cycles.The underlying mechanisms involve cellular stress-induced damage characterized by mitochondrial dysfunction,oxidative stress,and apoptosis,as well as dysregulation in key regulatory pathways such as ovarian hormone secretion,gene expression,and epigenetic modifications.This review synthesizes existing evidence on how maternal obesity-induced acute stress and chronic genetic/epigenetic alterations jointly contribute to offspring ovarian impairment.The findings elu-cidate the complex relationship between maternal metabolic status and offspring reproductive health,providing a robust theoretical foundation for refining prenatal management and developing targeted intervention strategies.

OBJECTIVE To understand the disinfectant-resistant genes in the gram-negative bacteria isolated from the dirt retention on air recure filters of air conditioners and observe the drug resistance.METHODS The dirt re-tention samples were collected from the air return filters of air conditioners of some wards in 3 hospitals of Wuhan(Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology,Wuhan Central Hospital,and Hubei Provincial Maternal and Child Health Hospital)from 2018 to 2024.The gram-negative bac-teria were screened out,the disinfectant-resistant genes in the strains were detected by polymerase chain reaction(PCR),and the results of drug susceptibility test were analyzed.RESULTS Of 354 dirt retention samples that were collected from the air return filers of air conditioners,77 were detected with 138 strains of gram-negative bacteria,87 of which were Acinetobacter baumannii,50 were Enterobacteriaceae,and 1 was Pseudomonas aerug-inosa.The detection rates of qacEΔ1,qacEΔ1-sul1,aceI and qacA/B were 73.19％,82.61％,69.57％and 2.90％,respectively.None of the strains were detected with qacC,qacH or qacJ.The result of drug susceptibility test showed that 76.81％of the gram-negative bacteria were resistant to at least 1 type of antibiotic;93 strains of multidrug-resistant gram-negative bacteria were isolated,most of which were isolated from intensive care unit(ICU).The detection rates of qacEΔ1 and qacEΔ1-sul1 were higher in the drug-resistant strains than those in the non-drug-resistant strains;there were significant differences in the drug resistance rates to carbapenems,quin-olones and β-lactams between the qacEΔ1-sul 1-positive strains and the qacEΔ1-sul1-negative strains(P＜0.05).CONCLUSIONS There are drug-resistant gram-negative bacteria contaminations in some wards of the 3 hospitals in Wuhan.The carrying rates of disinfectant-resistant genes of the strains are high,and the strains show varying degree of resistance to the commonly used antibiotics;the strains carrying the qacEΔ1-sul1 have certain statistical association with the drug resistance.It is suggested that the hospital should take targeted disinfec-tion measures for the environment and reasonably use antibiotics.

OBJECTIVE To understand the disinfectant-resistant genes in the gram-negative bacteria isolated from the dirt retention on air recure filters of air conditioners and observe the drug resistance.METHODS The dirt re-tention samples were collected from the air return filters of air conditioners of some wards in 3 hospitals of Wuhan(Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology,Wuhan Central Hospital,and Hubei Provincial Maternal and Child Health Hospital)from 2018 to 2024.The gram-negative bac-teria were screened out,the disinfectant-resistant genes in the strains were detected by polymerase chain reaction(PCR),and the results of drug susceptibility test were analyzed.RESULTS Of 354 dirt retention samples that were collected from the air return filers of air conditioners,77 were detected with 138 strains of gram-negative bacteria,87 of which were Acinetobacter baumannii,50 were Enterobacteriaceae,and 1 was Pseudomonas aerug-inosa.The detection rates of qacEΔ1,qacEΔ1-sul1,aceI and qacA/B were 73.19％,82.61％,69.57％and 2.90％,respectively.None of the strains were detected with qacC,qacH or qacJ.The result of drug susceptibility test showed that 76.81％of the gram-negative bacteria were resistant to at least 1 type of antibiotic;93 strains of multidrug-resistant gram-negative bacteria were isolated,most of which were isolated from intensive care unit(ICU).The detection rates of qacEΔ1 and qacEΔ1-sul1 were higher in the drug-resistant strains than those in the non-drug-resistant strains;there were significant differences in the drug resistance rates to carbapenems,quin-olones and β-lactams between the qacEΔ1-sul 1-positive strains and the qacEΔ1-sul1-negative strains(P＜0.05).CONCLUSIONS There are drug-resistant gram-negative bacteria contaminations in some wards of the 3 hospitals in Wuhan.The carrying rates of disinfectant-resistant genes of the strains are high,and the strains show varying degree of resistance to the commonly used antibiotics;the strains carrying the qacEΔ1-sul1 have certain statistical association with the drug resistance.It is suggested that the hospital should take targeted disinfec-tion measures for the environment and reasonably use antibiotics.

AIM:To investigate the effect of plasmin on epithelial sodium channel γ-subunit(γ-ENaC)acti-vation in mouse M-1 cells and the role of nuclear factor-κB(NF-κB).METHODS:Mouse M-1 cells were divided into three experimental parts.In the first part,the cells were divided into a control group,a plasmin group,and a plasmin+BAY 11-7082(NF-κB inhibitor)group to explore the effects of plasmin on inflammatory factors and γ-ENaC.In the sec-ond part,the cells were divided into a control group,a BAY 11-7082 group and a BAY 11-7082+plasmin group.M-1 cells were pretreated with BAY 11-7082 to explore the role of NF-κB in the regulation of γ-ENaC expression by plasmin.In the third part,the cells were divided into a control group,a plasmin group and an interleukin-6(IL-6)group.M-1 cells were treated with plasmin or IL-6 to explore the regulatory effect of IL-6 downstream of NF-κB on γ-ENaC.After drug interven-tion,the levels of IL-6,tumor necrosis factor-α(TNF-α),monocyte chemoattractant protein-1(MCP-1)and IL-1β in cell culture supernatants were detected by ELISA.The protein levels of phosphorylated inhibitor of nuclear factor-κB α(p-IκBα)/IκBα,p-NF-κB p65/NF-κB p65,and γ-ENaC was detected by Western blot.The distribution of γ-ENaC on the membrane was detected by immunofluorescence staining.RESULTS:Compared with control group,the levels of IL-6,TNF-α,MCP-1 and IL-1β in the supernatants of cells treated with 10 mg/L plasmin for 24 h were increased(n=3,P<0.01),the protein levels of p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC were increased(n=5,P<0.01),and the distribution of γ-ENaC on the membrane was increased.Compared with plasmin group,the levels of IL-6,TNF-α,MCP-1,IL-1β,p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC,and the γ-ENaC distribution on the membrane were lowered in plasmin and BAY 11-7082 coculture group(n=3,P<0.05 or P<0.01).Compared with control group,the ratio of p-NF-κB p65/NF-κB p65 decreased in BAY 11-7082 group(n=5,P<0.05),whereas there was no significant change in γ-ENaC.After stimulation with plasmin,the levels of p-IκBα/IκBα,p-NF-κB p65/NF-κB p65 and γ-ENaC in-creased(n=5,P<0.05 or P<0.01),and the γ-ENaC distribution on the membrane increased.Treatment with IL-6,downstream of NF-κB,increased the protein expression of γ-ENaC(n=5,P<0.05)and the distribution of γ-ENaC on the membrane after 24 h of intervention.CONCLUSION:The regulation of γ-ENaC expression by plasmin in mouse M-1 cells is related to the abnormal increase in inflammatory factors after NF-κB activation.