AIM: To investigate the influence of relevant inflammatory markers in peripheral blood on the progression of neovascular glaucoma(NVG)secondary to diabetic retinopathy(DR)patients.METHODS: Retrospective case-control study. Patients were categorized into two groups based on the presence or absence of NVG: those with proliferative diabetic retinopathy(PDR)alone(PDR group, n=148)and those with NVG secondary to PDR(NVG secondary to PDR group, n=142). Peripheral blood inflammatory markers were evaluated, including white blood cell-related indices, neutrophil-to-lymphocyte ratio(NLR), platelet-to-lymphocyte ratio(PLR), monocyte-to-lymphocyte ratio(MLR), and systemic immune-inflammation index(SII). The distinctions in peripheral blood inflammatory markers between the two groups of patients and their relationships with NVG secondary to PDR were analyzed.RESULTS:No statistically significant differences were observed in basic characteristics between the two groups, confirming their comparability. However, significant differences were found in eosinophil percentage and MLR between the PDR group and the NVG secondary to PDR group(all P<0.05), with both values being significantly higher in the NVG secondary to PDR group. Multivariate Logistic regression analysis revealed that the eosinophil percentage and the MLR were factors influencing the development of patients with NVG secondary to PDR.CONCLUSION: Eosinophil percentage and MLR may be associated with the progression of PDR to NVG, and could serve as potential predictive markers for NVG development in PDR patients.

With the continuous advancement and innovation in medical equipment technology, the transition between high-flow oxygen therapy, non-invasive ventilation, and invasive ventilation can be easily achieved by adjusting the ventilation mode of ventilators. During the weaning phase for tracheotomized patients, it is necessary to disconnect the ventilator circuit, change the ventilator mode, and gradually extend the weaning time to achieve complete ventilator liberation. During the weaning process, due to patients' excessive dependence on the ventilator, there may be situations where respiratory endpoints and Y-connectors of the ventilator are reconnected for invasive ventilation. However, during the weaning process, the Y-connector and expiratory end connectors are exposed to the air, which cannot ensure the tightness of the ventilator circuit, easily increasing the probability of ventilator circuit contamination and subsequently the risk of ventilator-associated pneumonia (VAP). To overcome these issues, the research team of department of critical care medicine of Zhongda Hospital Southeast University has designed a ventilator circuit interface protective device for weaning and has obtained a National Utility Model Patent of China (ZL 2023 2 1453385.8). The main body of the protective device is a Y-connector plug, consisting of multiple components, including a sealing piece, a protective cover, a sealing plug, an interface 1 (connects with the patient's tracheal tube), an interface 2 (connects with the respiratory branch of the ventilator), and an interface 3 (connects with the expiratory branch of the ventilator), featuring a unique design and easy operation. During the patient's weaning training process, the interface 1 and interface 2 is disconnected from the patient's tracheal tube and respiratory branch, respectively. The interface 1 is plugged with a stopper, and the interface 2 is covered with a protective cover to ensure the tightness of the expiratory branch and Y-connector of the ventilator. During the period when the patient is using the ventilator, the protective cover and plug are removed, and connecting them together ensures the tightness of the device itself, reducing the incidence of VAP caused by ventilator circuit contamination, avoiding nosocomial infections, and shortening the prolonged use of invasive ventilation, increased complication rate, extended hospital stay, and increased medical cost associated with weaning.
Humans ; Ventilator Weaning/methods* ; Equipment Design ; Ventilators, Mechanical ; Respiration, Artificial/instrumentation* ; Pneumonia, Ventilator-Associated/prevention & control*

Objective:To investigate the influencing factors for microvascular invasion (MVI) in hepatocellular carcinoma based on three-dimensional visualization and the construction of its nomogram model.Methods:The retrospective cohort study method was conducted. The clinico-pathological data of 190 patients with hepatocellular carcinoma who were admitted to Henan University People′s Hospital from May 2018 to May 2021 were collected. There were 148 males and 42 females, aged (58±12)years. The 190 patients were randomly divided into the training set of 133 cases and the validation set of 57 cases by the method of random number table in the ratio of 7:3. The abdominal three-dimensional visualization system was used to characterize the tumor morphology and other imaging features. Observation indicators: (1) analysis of influencing factors for MVI in hepatocellular carcinoma; (2) construction and evaluation of nomogram model of MVI in hepatocellular carcinoma. Measurement data with normal distribution were expressed as Mean± SD, and independent sample t test was used for comparison between groups. Measurement data with skewed distribution were expressed as M( Q1, Q3), and non-parametric rank sum test was used for comparison between groups. Count data were expressed as absolute numbers, and the chi-square test was used for comparison between groups. Corresponding statistical methods were used for univariate analysis. Binary Logistic regression model was used for multivariate analysis. Receiver operator characteristic (ROC) curves were plotted, and the nomogram model was assessed by area under the curve (AUC), calibration curve, and decision curve. Results:(1) Analysis of influencing factors for MVI in hepatocellular carcinoma. Among 190 patients with hepatocellular carcinoma, there were 97 cases of positive MVI (including 63 cases in the training set and 34 cases in the validation set) and 93 cases of negative MVI (including 70 cases in the training set and 23 cases in the validation set). Results of multivariate analysis showed that alpha-fetoprotein, vascular endothelial growth factor, tumor volume, the number of tumors, and tumor morphology were independent factors affecting the MVI of patients with hepatocellular carcinoma ( odds ratio=5.06, 3.62, 1.00, 2.02, 2.59, 95% confidence interval as 1.61-15.90, 1.28-10.20, 1.00-1.01, 1.02-3.98, 1.03-6.52, P<0.05). (2) Construction and evaluation of nomogram model of MVI in hepatocellular carcinoma. The results of multivariate analysis were incorporated to construct a nomogram prediction model for MVI of hepatocellular carcinoma. ROC curves showed that the AUC of the training set of nomogram model was 0.85 (95% confidence interval as 0.79-0.92), the optimal fractional cutoff based on the Jordon′s index was 0.51, the sensitivity was 0.71, and the specificity was 0.84. The above indicators of validation set were 0.92 (95% confidence interval as 0.85-0.99), 0.50, 0.90, and 0.82, respectively. The higher total score of the training set suggested a higher risk of MVI in hepatocellular carcinoma. The calibration curves of both training and validation sets of nomogram model fitted well with the standard curves and have a high degree of calibration. The decision curve showed a high net gain of nomogram model. Conclusions:Alpha-fetoprotein, vascular endothelial growth factor, tumor volume, the number of tumors, and tumor morphology are independent influencing factors for MVI in patients with hepatocellular carcinoma. A nomogram model constructed based on three-dimensional visualized imaging features can predict MVI in hepatocellular carcinoma.

Objective To study the epidemiological characteristics of chronic obstructive pulmonary disease (COPD) in Ma'anshan area and analyze the influencing factors of acute exacerbation. Methods The clinical data of 1 676 patients with COPD who visited the Department of Respiratory Medicine of Deyu Medical Ma'anshan General Hospital from 2020 to 2022 were retrospectively analyzed. The patients were divided into acute exacerbation group and stable group according to whether they had acute exacerbation or not，and the general information, severity of COPD, previous pulmonary infection and combined hypoproteinemia were compared between the two groups. Logistic regression was used to analyze the influencing factors of acute exacerbation. Results A total of 1 676 COPD patients were mainly male (58.17%) and ≥ 46 years old (82.58%), of which the incidence of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) was 78.82%. Logistic regression analysis showed that male sex , ≥46 years of age, smoking >400 cigarettes/year, occupational exposure to dust, severe and very severe COPD, recurrent new coronavirus infections, combined cardiovascular disease, or hypoproteinemia were risk factors for acute exacerbations in COPD patients. Conclusion Nearly 80% of COPD patients in Ma'anshan area have previously experienced acute exacerbations, and prevention and treatment cannot be ignored. Strengthening the education and prevention of key populations can effectively reduce the incidence of AECOPD and improve the overall prognosis of COPD patients.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.