Objective:To investigate the influences of long non-coding RNA metastasis-associated lung adenocarcinoma tran-script 1(lncRNA MALAT1)/miR-876-5p/forkhead box protein M1(FOXM1)axis on TNF-α-induced proliferation,apoptosis and in-flammatory response of HaCaT cells.Methods:HaCaT cells were grouped into Ct group,Model group,si-NC group,si-MALAT1 group,mimic NC group,miR-876-5p mimic group,si-MALAT1+inhibitor NC group,and si-MALAT1+miR-876-5p inhibitor group.Except for the Ct group,cells in other groups were treated with 25 μg/L TNF-α to induce the in vitro cell model of psoriasis,and after 24 hours of TNF-α induction,the corresponding transfectants were transfected for 48 hours for subsequent experiments.qRT-PCR was applied to detect the expression of MALAT1 and miR-876-5p in cells;CCK-8 method and EdU staining were applied to detect cell pro-liferation;flow cytometry was applied to detect apoptosis;ELISA method was applied to detect the levels of IL-6,TNF-α,and IL-1β in cell supernatant;Western blot was applied to detect the protein expressions of FOXM1,proliferating cell nuclear antigen(PCNA),Bcl-2-associated X protein(Bax)and B-lymphocytoma-2(Bcl-2);dual-luciferase reporter gene assay was applied to verify the rela-tionship between MALAT1 and miR-876-5p,miR-876-5p and FOXM1;and RNA pull down experiments were applied to verify the re-lationship between MALAT1 and miR-876-5p.Results:Compared with the control group,the expressions of MALAT1 and FOXM1 protein expression in the experimental group were increased,and the expression of miR-876-5p was decreased(P<0.05);compared with Ct group,the expressions of MALAT1 and FOXM1 protein expression in HaCaT cells,A450 value,EdU positive rate,the levels of IL-6,TNF-α,IL-1β,and the protein expressions of PCNA and Bcl-2 in cell supernatant in Model group increased,the expression of miR-876-5p,apoptosis rate and the protein expression of Bax were decreased(P<0.05);silencing MALAT1 or overexpressing miR-876-5p could inhibit the proliferation and inflammatory response of HaCaT cells induced by TNF-α,and promote cell apoptosis;miR-876-5p inhibitor attenuated the inhibitory effects of silencing MALAT1 on TNF-α-induced HaCaT cell proliferation and inflammatory response,and the promotion on cell apoptosis;MALAT1 targeted and regulated the miR-876-5p/FOXM1 axis.Conclusion:Silencing MALAT1 may inhibit the expression of FOXM1 by up-regulating miR-876-5p,thereby inhibiting the proliferation and inflammatory re-sponse of HaCaT cells induced by TNF-α,and promoting cell apoptosis.

Objective:To investigate the influences of long non-coding RNA metastasis-associated lung adenocarcinoma tran-script 1(lncRNA MALAT1)/miR-876-5p/forkhead box protein M1(FOXM1)axis on TNF-α-induced proliferation,apoptosis and in-flammatory response of HaCaT cells.Methods:HaCaT cells were grouped into Ct group,Model group,si-NC group,si-MALAT1 group,mimic NC group,miR-876-5p mimic group,si-MALAT1+inhibitor NC group,and si-MALAT1+miR-876-5p inhibitor group.Except for the Ct group,cells in other groups were treated with 25 μg/L TNF-α to induce the in vitro cell model of psoriasis,and after 24 hours of TNF-α induction,the corresponding transfectants were transfected for 48 hours for subsequent experiments.qRT-PCR was applied to detect the expression of MALAT1 and miR-876-5p in cells;CCK-8 method and EdU staining were applied to detect cell pro-liferation;flow cytometry was applied to detect apoptosis;ELISA method was applied to detect the levels of IL-6,TNF-α,and IL-1β in cell supernatant;Western blot was applied to detect the protein expressions of FOXM1,proliferating cell nuclear antigen(PCNA),Bcl-2-associated X protein(Bax)and B-lymphocytoma-2(Bcl-2);dual-luciferase reporter gene assay was applied to verify the rela-tionship between MALAT1 and miR-876-5p,miR-876-5p and FOXM1;and RNA pull down experiments were applied to verify the re-lationship between MALAT1 and miR-876-5p.Results:Compared with the control group,the expressions of MALAT1 and FOXM1 protein expression in the experimental group were increased,and the expression of miR-876-5p was decreased(P<0.05);compared with Ct group,the expressions of MALAT1 and FOXM1 protein expression in HaCaT cells,A450 value,EdU positive rate,the levels of IL-6,TNF-α,IL-1β,and the protein expressions of PCNA and Bcl-2 in cell supernatant in Model group increased,the expression of miR-876-5p,apoptosis rate and the protein expression of Bax were decreased(P<0.05);silencing MALAT1 or overexpressing miR-876-5p could inhibit the proliferation and inflammatory response of HaCaT cells induced by TNF-α,and promote cell apoptosis;miR-876-5p inhibitor attenuated the inhibitory effects of silencing MALAT1 on TNF-α-induced HaCaT cell proliferation and inflammatory response,and the promotion on cell apoptosis;MALAT1 targeted and regulated the miR-876-5p/FOXM1 axis.Conclusion:Silencing MALAT1 may inhibit the expression of FOXM1 by up-regulating miR-876-5p,thereby inhibiting the proliferation and inflammatory re-sponse of HaCaT cells induced by TNF-α,and promoting cell apoptosis.

Objective:To understand the usage situation of e-cigarettes among residents aged 18-65 in Beijing, explore the relationship between e-cigarette use and cigarette smoking as well as smoking cessation behaviors, and provide scientific support for the developing and improving policies and measures related to e-cigarettes.Methods:Using 19 684 residents data from the Beijing Non-communication Chronic Disease and Risk Factors Surveillance in 2022, complex sampling weighted methods were used to estimate proportions, and complex sampling logistic regression analysis was applied to explore the relationship between e-cigarette use, cigarette smoking, and smoking cessation.Results:Among all study participants, the proportion of those who had ever used e-cigarettes was 3.36%, with the current e-cigarette use at 1.26%. The proportion of current e-cigarette users (1.87%) and the former e-cigarette users (3.47%) were higher ( χ2=64.70, P<0.001) among males compared to females (0.60% and 0.64% respectively). The top three reasons for using e-cigarettes were wanting to quit smoking, perceiving e-cigarettes as less harmful, and enjoying the flavors of e-cigarettes. 83.54% of e-cigarette users started with cigarettes. The results of the complex sampling multivariable logistic regression analysis showed that current smoking ( OR=61.35, 95% CI: 36.98-101.76) and former smoking ( OR=31.20, 95% CI: 15.52-62.71) were positively associated with e-cigarette, while current e-cigarette use ( OR=0.13, 95% CI: 0.04-0.39) was negatively associated with quitting cigarette smoking. Conclusions:The proportion of e-cigarette use in Beijing was relatively low. E-cigarette use was associated with cigarette use and was not conducive to smoking cessation. Therefore, stronger regulatory measures and health education campaigns regarding the risks of e-cigarettes should be implemented.

This narrative review examines the challenges, strategies, and future directions in the development of young teachers within the pathophysiology departments of Chinese medical colleges. A thorough review of 49 studies published between 2013 and 2024 was carried out using PubMed, Web of Science, and various Chinese databases. The primary challenges identified include teaching innovation (cited in 84.2% of the studies), research pressure (91.2%), disciplinary characteristics (87.7%), and career development (80.7%). Medical schools have responded by enhancing training systems (94.7%), innovating teaching methods (93.0%), and bolstering research support (96.5%). Looking ahead, trends are shifting toward the application of new technologies, interdisciplinary integration, and international collaboration. The focus on cultivating young teachers is increasingly geared towards personalization and diversification, which are essential for advancing education in pathophysiology. High-quality young teachers are pivotal in raising teaching standards, fostering research innovation, and facilitating interdisciplinary exchanges. Based on these insights, we recommend several practical measures to enhance the quality of pathophysiology education in China. These include establishing comprehensive training programs that integrate teaching innovation and research skills; developing structured mentorship systems with clear pathways for career advancement; creating platforms that support technology-enhanced teaching and international collaboration; and implementing systematic evaluation mechanisms to assess teaching effectiveness. These targeted interventions will require a coordinated effort from department heads, educational institutions, and policymakers to ensure a sustained improvement in the quality of pathophysiology education.

This narrative review examines the challenges, strategies, and future directions in the development of young teachers within the pathophysiology departments of Chinese medical colleges. A thorough review of 49 studies published between 2013 and 2024 was carried out using PubMed, Web of Science, and various Chinese databases. The primary challenges identified include teaching innovation (cited in 84.2% of the studies), research pressure (91.2%), disciplinary characteristics (87.7%), and career development (80.7%). Medical schools have responded by enhancing training systems (94.7%), innovating teaching methods (93.0%), and bolstering research support (96.5%). Looking ahead, trends are shifting toward the application of new technologies, interdisciplinary integration, and international collaboration. The focus on cultivating young teachers is increasingly geared towards personalization and diversification, which are essential for advancing education in pathophysiology. High-quality young teachers are pivotal in raising teaching standards, fostering research innovation, and facilitating interdisciplinary exchanges. Based on these insights, we recommend several practical measures to enhance the quality of pathophysiology education in China. These include establishing comprehensive training programs that integrate teaching innovation and research skills; developing structured mentorship systems with clear pathways for career advancement; creating platforms that support technology-enhanced teaching and international collaboration; and implementing systematic evaluation mechanisms to assess teaching effectiveness. These targeted interventions will require a coordinated effort from department heads, educational institutions, and policymakers to ensure a sustained improvement in the quality of pathophysiology education.

Alzheimer's disease(AD)is an age-related neurodegenerative disease with an increasing incidence worldwide.A large number of studies have shown that the incidence rates of hearing loss is high in patients with mild cognitive impairment and Alzheimer's disease,and may be a risk factor for the occurrence and development of cognitive impairment.There is an interaction between the two,but the causal mechanism is still unclear.Early screening and management of hearing impairment may play an important role in the early diagnosis,symptom im-provement and disease progression of Alzheimer's disease.This paper reviews relevant clinical and basic research to discuss the correlation between hearing loss and Alzheimer's disease,and the possible causal mechanism between them.

This study aims to explore the specific mechanism by which puerarin inhibits ferroptosis and improves the myocardial contractile function in myocardial hypertrophy through the nuclear factor erythroid 2-related factor 2(Nrf2)/antioxidant response element(ARE)/heme oxygenase-1(HO-1) signaling pathway. The hypertrophic cardiomyocyte model was established using phenylephrine, and H9c2 cells were divided into control group, model group, puerarin group, and puerarin+ML385 group. Cell viability and surface area were detected by cell counting kit-8(CCK-8) and immunofluorescence experiments. The mitochondrial membrane potential and Ca~(2+) concentration were measured. The ferroptosis-related indicators were detected by biochemical and fluorescence staining methods. The expression of proteins related to ferroptosis and the Nrf2/ARE/HO-1 signaling pathway was detected by Western blot. A myocardial hypertrophy model was established, and 40 rats were randomly divided into sham group, model group, puerarin group, and puerarin+Nrf2 inhibitor(ML385) group, with 10 rats in each group. Echocardiogram, hemodynamic parameters, and myocardial hypertrophy parameters were measured. Histopathological changes of myocardial tissues were observed by hematoxylin and eosin(HE) staining and Masson staining. Biochemical methods, enzyme-linked immunosorbent assay(ELISA), and fluorescence staining were used to detect inflammatory factors and ferroptosis-related indicators. Immunohistochemistry was used to detect the expression of proteins related to ferroptosis and the Nrf2/ARE/HO-1 signaling pathway. Cell experiments showed that puerarin intervention significantly enhanced the viability of hypertrophic cardiomyocytes, reduced their surface area, and restored mitochondrial membrane potential and Ca~(2+) homeostasis. Mechanism studies revealed that puerarin promoted Nrf2 nuclear translocation, upregulated the expression of HO-1, solute carrier family 7 member 11(SLC7A11), and glutathione peroxidase 4(GPX4), and decreased malondialdehyde(MDA), reactive oxygen species(ROS), and iron levels. These protective effects were reversed by ML385. In animal experiments, puerarin improved cardiac function in rats with myocardial hypertrophy, alleviated myocardial hypertrophy and fibrosis, inhibited inflammatory responses and ferroptosis, and promoted nuclear Nrf2 translocation and HO-1 expression. However, combined intervention with ML385 led to deterioration of hemodynamics and a rebound in ferroptosis marker levels. In conclusion, puerarin may inhibit cardiomyocyte ferroptosis through the Nrf2/ARE/HO-1 signaling pathway, thereby improving myocardial contractile function in myocardial hypertrophy.
Animals ; NF-E2-Related Factor 2/genetics* ; Rats ; Ferroptosis/drug effects* ; Signal Transduction/drug effects* ; Isoflavones/pharmacology* ; Male ; Rats, Sprague-Dawley ; Cardiomegaly/genetics* ; Myocytes, Cardiac/metabolism* ; Antioxidant Response Elements/drug effects* ; Myocardial Contraction/drug effects* ; Heme Oxygenase-1/genetics* ; Cell Line

This narrative review examines the challenges, strategies, and future directions in the development of young teachers within the pathophysiology departments of Chinese medical colleges. A thorough review of 49 studies published between 2013 and 2024 was carried out using PubMed, Web of Science, and various Chinese databases. The primary challenges identified include teaching innovation (cited in 84.2% of the studies), research pressure (91.2%), disciplinary characteristics (87.7%), and career development (80.7%). Medical schools have responded by enhancing training systems (94.7%), innovating teaching methods (93.0%), and bolstering research support (96.5%). Looking ahead, trends are shifting toward the application of new technologies, interdisciplinary integration, and international collaboration. The focus on cultivating young teachers is increasingly geared towards personalization and diversification, which are essential for advancing education in pathophysiology. High-quality young teachers are pivotal in raising teaching standards, fostering research innovation, and facilitating interdisciplinary exchanges. Based on these insights, we recommend several practical measures to enhance the quality of pathophysiology education in China. These include establishing comprehensive training programs that integrate teaching innovation and research skills; developing structured mentorship systems with clear pathways for career advancement; creating platforms that support technology-enhanced teaching and international collaboration; and implementing systematic evaluation mechanisms to assess teaching effectiveness. These targeted interventions will require a coordinated effort from department heads, educational institutions, and policymakers to ensure a sustained improvement in the quality of pathophysiology education.

This narrative review examines the challenges, strategies, and future directions in the development of young teachers within the pathophysiology departments of Chinese medical colleges. A thorough review of 49 studies published between 2013 and 2024 was carried out using PubMed, Web of Science, and various Chinese databases. The primary challenges identified include teaching innovation (cited in 84.2% of the studies), research pressure (91.2%), disciplinary characteristics (87.7%), and career development (80.7%). Medical schools have responded by enhancing training systems (94.7%), innovating teaching methods (93.0%), and bolstering research support (96.5%). Looking ahead, trends are shifting toward the application of new technologies, interdisciplinary integration, and international collaboration. The focus on cultivating young teachers is increasingly geared towards personalization and diversification, which are essential for advancing education in pathophysiology. High-quality young teachers are pivotal in raising teaching standards, fostering research innovation, and facilitating interdisciplinary exchanges. Based on these insights, we recommend several practical measures to enhance the quality of pathophysiology education in China. These include establishing comprehensive training programs that integrate teaching innovation and research skills; developing structured mentorship systems with clear pathways for career advancement; creating platforms that support technology-enhanced teaching and international collaboration; and implementing systematic evaluation mechanisms to assess teaching effectiveness. These targeted interventions will require a coordinated effort from department heads, educational institutions, and policymakers to ensure a sustained improvement in the quality of pathophysiology education.

This narrative review examines the challenges, strategies, and future directions in the development of young teachers within the pathophysiology departments of Chinese medical colleges. A thorough review of 49 studies published between 2013 and 2024 was carried out using PubMed, Web of Science, and various Chinese databases. The primary challenges identified include teaching innovation (cited in 84.2% of the studies), research pressure (91.2%), disciplinary characteristics (87.7%), and career development (80.7%). Medical schools have responded by enhancing training systems (94.7%), innovating teaching methods (93.0%), and bolstering research support (96.5%). Looking ahead, trends are shifting toward the application of new technologies, interdisciplinary integration, and international collaboration. The focus on cultivating young teachers is increasingly geared towards personalization and diversification, which are essential for advancing education in pathophysiology. High-quality young teachers are pivotal in raising teaching standards, fostering research innovation, and facilitating interdisciplinary exchanges. Based on these insights, we recommend several practical measures to enhance the quality of pathophysiology education in China. These include establishing comprehensive training programs that integrate teaching innovation and research skills; developing structured mentorship systems with clear pathways for career advancement; creating platforms that support technology-enhanced teaching and international collaboration; and implementing systematic evaluation mechanisms to assess teaching effectiveness. These targeted interventions will require a coordinated effort from department heads, educational institutions, and policymakers to ensure a sustained improvement in the quality of pathophysiology education.