Objective To investigate the expression level of centromere protein(CENP)Ⅰin lung adenocarcinoma cells,to study the effects of CENPⅠon the proliferation,invasion,migration,apoptosis,and epithelial-mesenchymal transition(EMT)of lung adenocarci-noma cells,and to explore the possible mechanisms related to its occurrence.Methods The expression of CENPⅠmRNA and protein in four types of lung adenocarcinoma cells and normal alveolar epithelial cells were detected by quantitative real-time polymerase chain reaction(RT-qPCR)and Western blotting.The expression of CENPⅠin H1650 cells was knocked down by the siRNA technique,The transfection efficiency was detected by RT-qPCR and Western blotting.The effects of knock-down CENPⅠon proliferation,cell cycle,apoptosis,invasion and migration of H1650 cells were detected by the cell counting kit-8 assay,the transwell assay,and flow cytometry.Western blotting was used to detect the expression of E-cadherin,N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,PI3K,AKT,mTOR,p-PI3K,p-AKT,and p-mTOR.Results After the knock-down of CENPⅠ,the proliferative ability of the H1650 cells significantly decreased,the number of apoptotic cells significantly decreased,and the cell invasion and migration abilities significantly decreased(P<0.01).E-cadherin expression was upregulated and N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,p-PI3K,p-AKT,and p-mTOR expres-sion were down-regulated in the CENTI group compared with the control group(P<0.05).The expression of p-PI3K,p-AKT,and p-mTOR in the si-CENPⅠ+IGF-1 group was upregulated compared to that in the si-CENPⅠgroup(P<0.05).Conclusion High expression of CENPⅠin lung adenocarcinoma cells promotes the proliferation,invasion,and migration of lung adenocarcinoma H1650 cells and EMT inhibits apoptosis,which may be related to the activation of the PI3K/AKT/mTOR signaling pathway.

Programmed cell death plays an important role in the growth and development of organ-ism and homeostasis of tissues and organs.Necroptosis,a new mode of programmed cell death,characterized by necrosis in morphology,can cause cell breakdown and release of a significant num-ber of damage-associated molecular patterns,which play an important role in the occurrence and development of diseases.Viral infection is a serious health risk to both humans and domestic ani-mals.Research has confirmed that necroptosis functions as a cell death pathway in viral infections.In this paper,we review the current research advances on necroptosis related to viral infections,e-lucidate the molecular mechanism of mutual regulation between viral infection and necroptosis,and discuss the progress in the application of necroptosis inhibitors,to provide new ideas for the pre-vention and treatment of viral infections.

Background Exposure to volatile organic compounds (VOCs) has been observed in both living and working environments. Volatile organic compounds metabolites (VOCMs) in urine can be used to assess the exposure to VOCs and potentially cause adverse effects on human body. Objective To quantitatively evaluate urinary VOCMs and their associations with renal function damage, and further trace the characteristics of potential environmental exposure to provide scientific evidence for effective prevention measures. Methods The study included a total of 6028 samples from four cross-sectional studies in the National Health and Nutrition Examination Survey (NHANES) conducted between 2011 and 2018, with exposure and health outcomes matched. Generalized linear models were employed to assess the associations of urinary VOCMs (urinary creatinine adjusted) with urinary protein levels and estimated glomerular filtration rate (eGFR), with coviriables including gender, age, body mass index, education, smoking, alcohol consumption, exercise frequency, diabetes, and hypertension. Weighted quantile sum (WQS) approach was utilized to analyze the effects of mixed exposure and to rank the contribution of individual VOCMs. The associations between VOCMs and associated living environments and occupational exposure characteristics were further investigated. Results Among the enrolled study participants (n=6028), a total of 11 urinary VOCMs were measured, with 10 metabolites having a positive rate of over 80% (84.59%-99.99%). There were 604 individuals (10.0%) having urinary protein abnormalities and 2831 individuals (47.0%) with eGFR reduced. Through a single and a multiple generalized linear model, 5 VOCMs exhibited statistically significant associations with urinary protein abnormalities and/or reduced eGFR levels (P<0.05): N-acetyl-S-(N-methylaminocarbonyl)-L-cysteine (AMC), N-acetyl-S-(2-carboxyethyl)-L-cysteine (CEM), N-acetyl-S-(3,4-dihydroxybutyl)-L-cysteine (DHB), 2-hydroxy-2-phenylacetic acid (MAD), and N-acetyl-S-(4-hydroxy-2-butenyl)-L-cysteine (MB3). The WQS index indicated a significantly positive association between VOCMs and urinary protein abnormalities, and DHB contributed the most. The analysis on the potential sources of VOCs exposure showed that those who worked as a private entrepreneur or an employee (vs. government employees), rent houses (vs. owned real estate), had less number of rooms in the residence, fueled cars at self-service gas stations, and inhaled paint fumes in the past 48 h associated with higher VOCMs (P < 0.05) and DHB contributed the most. Conclusion Multiple VOCMs in urine are associated with significantly kidney function injuries. The mixture exposure to VOCMs is significantly associated with higher risks of urinary protein abnormalities. Occupational category, housing ownership, ways to fuel a car, and inhalation of paint odors are closely related with VOCMs levels.

Objective To investigate the expression level of centromere protein(CENP)Ⅰin lung adenocarcinoma cells,to study the effects of CENPⅠon the proliferation,invasion,migration,apoptosis,and epithelial-mesenchymal transition(EMT)of lung adenocarci-noma cells,and to explore the possible mechanisms related to its occurrence.Methods The expression of CENPⅠmRNA and protein in four types of lung adenocarcinoma cells and normal alveolar epithelial cells were detected by quantitative real-time polymerase chain reaction(RT-qPCR)and Western blotting.The expression of CENPⅠin H1650 cells was knocked down by the siRNA technique,The transfection efficiency was detected by RT-qPCR and Western blotting.The effects of knock-down CENPⅠon proliferation,cell cycle,apoptosis,invasion and migration of H1650 cells were detected by the cell counting kit-8 assay,the transwell assay,and flow cytometry.Western blotting was used to detect the expression of E-cadherin,N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,PI3K,AKT,mTOR,p-PI3K,p-AKT,and p-mTOR.Results After the knock-down of CENPⅠ,the proliferative ability of the H1650 cells significantly decreased,the number of apoptotic cells significantly decreased,and the cell invasion and migration abilities significantly decreased(P<0.01).E-cadherin expression was upregulated and N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,p-PI3K,p-AKT,and p-mTOR expres-sion were down-regulated in the CENTI group compared with the control group(P<0.05).The expression of p-PI3K,p-AKT,and p-mTOR in the si-CENPⅠ+IGF-1 group was upregulated compared to that in the si-CENPⅠgroup(P<0.05).Conclusion High expression of CENPⅠin lung adenocarcinoma cells promotes the proliferation,invasion,and migration of lung adenocarcinoma H1650 cells and EMT inhibits apoptosis,which may be related to the activation of the PI3K/AKT/mTOR signaling pathway.

Objective:To analyze the distribution of human immunodeficiency virus 1（HIV-1）genotypes and antiretroviral drug resistance patterns among individuals infected with HIV and patients with acquired immunodeficiency syndrome（AIDS）in Fuyang，with the aim of informing the optimization of antiretroviral therapy strategies.Methods:Blood samples were collected from HIV/AIDS patients who failed antiviral treatment in Fuyang from 2023 to 2024，as well as newly reported HIV-infected individuals who were first diagnosed and did not receive antiviral treatment. The HIV-1 pol gene was amplified and sequenced. Genotypic resistance was assessed using the Stanford University HIV Drug Resistance Database，and analyses were conducted on HIV-1 subtypes and drug resistance-associated mutations.Results:A total of 571 HIV/AIDS patients were included in this study，comprising 320 newly reported HIV-infected individuals and 251 HIV/AIDS patients who failed antiviral treatment. Both groups were predominantly male，middle-aged and elderly individuals over 45 years old，and heterosexual contact was the primary transmission route. The most prevalent HIV-1 subtypes differed between groups：CRF07_BC（36.88%，118/320）dominated among newly reported HIV-infected patients，whereas subtype B（43.03%，108/251）was predominant in HIV/AIDS patients who failed antiviral treatment. The drug resistance rate was significantly lower in newly reported HIV-infected patients（15.63%，50/320）compared to the HIV/AIDS patients who failed antiviral treatment（38.25%，96/251； χ2=37.825， P<0.001）. Non-nucleoside reverse transcriptase inhibitors（NNRTIs）exhibited the highest resistance rates in both cohorts. Compared to newly reported HIV-infected patients，HIV/AIDS patients who failed antiviral treatment showed a significantly higher prevalence of drug resistance mutations（ P<0.001），with greater diversity in mutation patterns. Key resistance-associated mutation site demonstrated statistically significant differences in mutation rates between the two groups（ P<0.05）. The results of the molecular transmission network showed that the proportion of elderly people over 60 years old and patients with CRF07_BC and B subtypes was higher among the networked cases in the two groups of newly reported and antiviral treatment failure. Conclusion:The study revealed a diverse distribution of HIV-1 subtypes among HIV/AIDS patients in Fuyang. NNRTIs exhibited the most prominent resistance challenges，accompanied by diversified resistance mutation profiles. These findings highlight the need for enhanced surveillance of resistance to curb the spread of resistant strains and improve clinical outcomes.

Myasthenia gravis(MG)is an autoimmune disease characterized primarily by skeletal muscle weakness and,in severe cases,respiratory involvement.Western medical treatment predominantly relies on immunosuppressants,but long-term administration often leads to notable side effects.In contrast,traditional Chinese medicine(TCM)offers the advantage of multi-target interventions.However,the pathogenesis of MG has not been fully elucidated,and the establishment of animal models that accurately reflect the clinical characteristics of both Chinese and Western medicine is essential for mechanism research and new drug development.This paper systematically reviews the etiology and pathogenesis,diagnostic criteria,and progress of animal model research for MG from both Chinese and Western medicine perspectives.In Western medicine,the pathogenesis of MG is closely related to genetic susceptibility,environmental factors,and autoantibody-mediated postsynaptic membrane damage.In TCM,MG is classified under the category of"flaccidity syndrome",attributed to congenital deficiencies and acquired malnourishment.Western diagnostic criteria involve a combination of clinical symptoms,fatigue testing,serum antibody assays,and electrophysiological evaluation.In contrast,TCM diagnosis emphasizes the integration of primary and secondary symptoms with tongue and pulse pattern differentiation.Currently available animal models mainly include experimental autoimmune myasthenia gravis(EAMG)and passive transfer myasthenia gravis(PTMG).The Toredo acetylcholine receptor(AChR)induced EAMG model aligns well with Western diagnostic criteria,but poorly matches secondary symptoms in TCM.The synthetic AChR peptide model is widely used,but shows low conformity with TCM syndromes.Models induced by muscle-specific tyrosine kinase(MuSK),low-density lipoprotein receptor-related protein 4(LRP4),and transgenic models demonstrate high innovation but exhibit low clinical conformity.Evaluation of these models requires integration of behavioral,electrophysiological,and immunological indicators.However,a systematic framework for modelling TCM syndromes is still lacking.Future research should integrate TCM-based etiological modelling methods with the Western pathological mechanisms to construct disease-syndrome combination models.Additionally,it is crucial to establish a TCM syndrome evaluation system based on"validation by prescription",as well as to improve the scientific rigor and practicality of animal models by the incorporation of emerging technologies.This review provides a theoretical foundation for optimizing MG animal model design,advancing the research on the combination of Chinese and Western medicine,and supporting efficacy assessment and mechanism exploration of Chinese herbal prescriptions.

With the rapid development of digital technology, digital twin technology shows great potential for application in the medical and nursing fields. This paper reviews the main elements and key aspects of digital twins, their application scenarios and effects in medicine and nursing, and application challenges faced, with a view to providing innovative solution ideas for healthcare professionals and promoting the application and development of digital twins in medicine and nursing.

Myasthenia gravis(MG)is an autoimmune disease characterized primarily by skeletal muscle weakness and,in severe cases,respiratory involvement.Western medical treatment predominantly relies on immunosuppressants,but long-term administration often leads to notable side effects.In contrast,traditional Chinese medicine(TCM)offers the advantage of multi-target interventions.However,the pathogenesis of MG has not been fully elucidated,and the establishment of animal models that accurately reflect the clinical characteristics of both Chinese and Western medicine is essential for mechanism research and new drug development.This paper systematically reviews the etiology and pathogenesis,diagnostic criteria,and progress of animal model research for MG from both Chinese and Western medicine perspectives.In Western medicine,the pathogenesis of MG is closely related to genetic susceptibility,environmental factors,and autoantibody-mediated postsynaptic membrane damage.In TCM,MG is classified under the category of"flaccidity syndrome",attributed to congenital deficiencies and acquired malnourishment.Western diagnostic criteria involve a combination of clinical symptoms,fatigue testing,serum antibody assays,and electrophysiological evaluation.In contrast,TCM diagnosis emphasizes the integration of primary and secondary symptoms with tongue and pulse pattern differentiation.Currently available animal models mainly include experimental autoimmune myasthenia gravis(EAMG)and passive transfer myasthenia gravis(PTMG).The Toredo acetylcholine receptor(AChR)induced EAMG model aligns well with Western diagnostic criteria,but poorly matches secondary symptoms in TCM.The synthetic AChR peptide model is widely used,but shows low conformity with TCM syndromes.Models induced by muscle-specific tyrosine kinase(MuSK),low-density lipoprotein receptor-related protein 4(LRP4),and transgenic models demonstrate high innovation but exhibit low clinical conformity.Evaluation of these models requires integration of behavioral,electrophysiological,and immunological indicators.However,a systematic framework for modelling TCM syndromes is still lacking.Future research should integrate TCM-based etiological modelling methods with the Western pathological mechanisms to construct disease-syndrome combination models.Additionally,it is crucial to establish a TCM syndrome evaluation system based on"validation by prescription",as well as to improve the scientific rigor and practicality of animal models by the incorporation of emerging technologies.This review provides a theoretical foundation for optimizing MG animal model design,advancing the research on the combination of Chinese and Western medicine,and supporting efficacy assessment and mechanism exploration of Chinese herbal prescriptions.

Programmed cell death plays an important role in the growth and development of organ-ism and homeostasis of tissues and organs.Necroptosis,a new mode of programmed cell death,characterized by necrosis in morphology,can cause cell breakdown and release of a significant num-ber of damage-associated molecular patterns,which play an important role in the occurrence and development of diseases.Viral infection is a serious health risk to both humans and domestic ani-mals.Research has confirmed that necroptosis functions as a cell death pathway in viral infections.In this paper,we review the current research advances on necroptosis related to viral infections,e-lucidate the molecular mechanism of mutual regulation between viral infection and necroptosis,and discuss the progress in the application of necroptosis inhibitors,to provide new ideas for the pre-vention and treatment of viral infections.

With the rapid development of digital technology, digital twin technology shows great potential for application in the medical and nursing fields. This paper reviews the main elements and key aspects of digital twins, their application scenarios and effects in medicine and nursing, and application challenges faced, with a view to providing innovative solution ideas for healthcare professionals and promoting the application and development of digital twins in medicine and nursing.