ObjectiveTo investigate the effects of the classical Chinese medicine compound prescription Erjingwan on the inflammatory response and apoptosis of skeletal muscle cells in a mouse model of sarcopenia and decipher the mechanism based on the silent information regulator 1 （SIRT1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway. MethodsForty C57/BL6 male mice were randomized into a control group， a model group， and groups with different doses of Erjingwan （8，16，32 g·kg^-1）. The mouse model of sarcopenia was established by D-gal-induced skeletal muscle senescence. The body weight and grip strength of mice treated with different doses of Erjingwan were examined to evaluate their physiological functions. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathological changes and fibrosis in the skeletal muscle of mice. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum samples of mice， and biochemical tests were conducted to quantify the levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， and glutathione （GSH） in the serum. The protein and mRNA levels of SIRT1， Nrf2， B-cell lymphoma （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsAfter 4 weeks of drug intervention， the model group exhibited significant reductions in body weight and grip strength （P0.01） compared with the control group. Compared with the model group， all doses of Erjingwan increased the body weight in mice at week 8 （P0.01） and grip strength from week 6 （P0.01）. HE staining revealed clear muscle fiber structure in the control group， muscle fiber rupture and atrophy in the model group， and dose-dependent repair of muscle fiber structure in the Erjingwan groups. Masson staining showed minimal collagen fibers and mild fibrosis in the control group， collagen fiber proliferation and severe fibrosis in the model group， and collagen proliferation with dose-dependent inhibition of fibrosis in the Erjingwan groups. ELISA results showed that serum levels of TNF-α and IL-6 were elevated in the model group compared with those in the control group （P0.01）. After intervention， the low-dose Erjingwan group exhibited a decreased TNF-α level （P0.05）， while the medium and high-dose groups showed decreases in both TNF-α and IL-6 levels （P0.01）. Biochemical assays revealed that the model group had decreased SOD and GSH levels （P0.01） and an increased MDA level （P0.01） compared with the control group. The medium and high-dose Erjingwan groups exhibited increases in SOD and GSH levels （P0.01） and decreases in MDA level （P0.01）， compared with the model group. WB and Real-time PCR results showed that compared with the control group， the model group presented down-regulated protein and mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 in the muscle tissue （P0.01） and up-regulated protein and mRNA levels of Bax （P0.01）. Compared with the model group， Erjingwan at different doses up-regulated the protein levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01） and down-regulated the protein and mRNA levels of Bax （P0.01） in the muscle tissue. Low-dose Erjingwan elevated the mRNA levels of Nrf2 and HO-1 （P0.05， P0.01）， and medium and high-dose Erjingwan up-regulated the mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01）. ConclusionErjingwan reduced the content of inflammatory factors in skeletal muscle cells， improved the antioxidant capacity， and attenuated pathological changes and fibrosis in the muscle of the mouse model of sarcopenia by regulating the SIRT1/Nrf2/HO-1 pathway， inflammatory response， and apoptosis network.

ObjectiveTo investigate the effects of the classical Chinese medicine compound prescription Erjingwan on the inflammatory response and apoptosis of skeletal muscle cells in a mouse model of sarcopenia and decipher the mechanism based on the silent information regulator 1 （SIRT1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway. MethodsForty C57/BL6 male mice were randomized into a control group， a model group， and groups with different doses of Erjingwan （8，16，32 g·kg^-1）. The mouse model of sarcopenia was established by D-gal-induced skeletal muscle senescence. The body weight and grip strength of mice treated with different doses of Erjingwan were examined to evaluate their physiological functions. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathological changes and fibrosis in the skeletal muscle of mice. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum samples of mice， and biochemical tests were conducted to quantify the levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， and glutathione （GSH） in the serum. The protein and mRNA levels of SIRT1， Nrf2， B-cell lymphoma （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsAfter 4 weeks of drug intervention， the model group exhibited significant reductions in body weight and grip strength （P0.01） compared with the control group. Compared with the model group， all doses of Erjingwan increased the body weight in mice at week 8 （P0.01） and grip strength from week 6 （P0.01）. HE staining revealed clear muscle fiber structure in the control group， muscle fiber rupture and atrophy in the model group， and dose-dependent repair of muscle fiber structure in the Erjingwan groups. Masson staining showed minimal collagen fibers and mild fibrosis in the control group， collagen fiber proliferation and severe fibrosis in the model group， and collagen proliferation with dose-dependent inhibition of fibrosis in the Erjingwan groups. ELISA results showed that serum levels of TNF-α and IL-6 were elevated in the model group compared with those in the control group （P0.01）. After intervention， the low-dose Erjingwan group exhibited a decreased TNF-α level （P0.05）， while the medium and high-dose groups showed decreases in both TNF-α and IL-6 levels （P0.01）. Biochemical assays revealed that the model group had decreased SOD and GSH levels （P0.01） and an increased MDA level （P0.01） compared with the control group. The medium and high-dose Erjingwan groups exhibited increases in SOD and GSH levels （P0.01） and decreases in MDA level （P0.01）， compared with the model group. WB and Real-time PCR results showed that compared with the control group， the model group presented down-regulated protein and mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 in the muscle tissue （P0.01） and up-regulated protein and mRNA levels of Bax （P0.01）. Compared with the model group， Erjingwan at different doses up-regulated the protein levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01） and down-regulated the protein and mRNA levels of Bax （P0.01） in the muscle tissue. Low-dose Erjingwan elevated the mRNA levels of Nrf2 and HO-1 （P0.05， P0.01）， and medium and high-dose Erjingwan up-regulated the mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01）. ConclusionErjingwan reduced the content of inflammatory factors in skeletal muscle cells， improved the antioxidant capacity， and attenuated pathological changes and fibrosis in the muscle of the mouse model of sarcopenia by regulating the SIRT1/Nrf2/HO-1 pathway， inflammatory response， and apoptosis network.

Lung cancer represents as one of the most prevalent malignant tumors globally,necessitating the urgent identification of additional biomarkers to facilitate precise stratified treatment and elevate its survival rates.Previous studies have focused on the correlation between the histopathological characteristics,driver gene mutations,and progno-sis of non-small cell lung cancer(NSCLC),with the aim of predicting the potential molecular background,treatment efficacy,and possible clinical outcomes of patients from the morphological perspective.This article aims to briefly sum-marize the advancements in emerging histopathological indicators of NSCLC,and discuss their implications for guiding the prognosis of this disease.

Objective This study aims to construct and evaluate a clinical decision support system for individualized frequency repositioning in ICU patients using big data and modern information technology,with the goal of improving ICU nursing quality.Methods From February to August 2023,a dedicated research team was established to construct a data model based on real-world data from 3,988 ICU patients,assessing the impact of different position change frequencies on the incidence of pressure injuries.Based on this model,a decision support system was designed and developed,incorporating modules for personalized patient characteristics input,data analysis and result queries,decision recording,and patient file management.From September to November 2023,ICU nurses at a tertiary hospital in Qingdao city was selected to use the system.A usability survey was conducted using the System Usability Scale(SUS)to evaluate the system's usability.Results The constructed decision support system can display the outcomes for patients under 7 different position change frequencies based on the input of personalized patient characteristics and the calculation results from the data model,providing precise decision support for nurses.A total of 85 nurses participated in the system usability evaluation,with the SUS score of 64.22±13.9.Conclusion The constructed individualized frequency of repositioning decision support system for ICU patients demonstrates good scientific validity and usability,providing clinical nurses with a valuable reference for implementing personalized position change frequencies for patients.

Sneddon syndrome is a rare neurocutaneous disorder that primarily affects small-and medium-sized arteries.Its clinical manifestations include livedo racemosa and recurrent cerebral ischemic events,and it may also involve multiple organs such as the heart,spleen,and kidneys.This disease can lead to early-onset stroke,making it a rare cause of stroke in young adults.This article reported a case of a young female patient who experienced two cerebral infarctions within one month.Genetic testing identified a homozygous mutation in the adenosine deaminase 2 gene,confirming the diagnosis of Sneddon syndrome.This case serves as a reference to improve clinical recognition of this disease.

Sneddon syndrome is a rare neurocutaneous disorder that primarily affects small-and medium-sized arteries.Its clinical manifestations include livedo racemosa and recurrent cerebral ischemic events,and it may also involve multiple organs such as the heart,spleen,and kidneys.This disease can lead to early-onset stroke,making it a rare cause of stroke in young adults.This article reported a case of a young female patient who experienced two cerebral infarctions within one month.Genetic testing identified a homozygous mutation in the adenosine deaminase 2 gene,confirming the diagnosis of Sneddon syndrome.This case serves as a reference to improve clinical recognition of this disease.

Lung cancer represents as one of the most prevalent malignant tumors globally,necessitating the urgent identification of additional biomarkers to facilitate precise stratified treatment and elevate its survival rates.Previous studies have focused on the correlation between the histopathological characteristics,driver gene mutations,and progno-sis of non-small cell lung cancer(NSCLC),with the aim of predicting the potential molecular background,treatment efficacy,and possible clinical outcomes of patients from the morphological perspective.This article aims to briefly sum-marize the advancements in emerging histopathological indicators of NSCLC,and discuss their implications for guiding the prognosis of this disease.

Male reproductive aging is characterized by degenerative changes in the structure and function of the testes. Testicular aging involves alterations in various types of cells, among which lysosomal dysfunction in Sertoli cells is particularly critical. Recent studies have shown that abnormal lysosomal acidification leads to impaired phagosome degradation, which fails to maintain normal nutrient cycling and thereby exacerbates damage to the testicular microenvironment. In addition, endoplasmic reticulum stress, mitochondrial dysfunction, and epigenetic changes are also important factors contributing to reproductive aging. Therefore, molecular intervention strategies targeting lysosomal dysfunction, mitochondrial oxidative stress, and endoplasmic reticulum stress, such as the use of lysosomal activators like ML-SA1 and antioxidants, may offer new therapeutic directions for alleviating male reproductive aging. Future research should further explore the interactions between these mechanisms and potential intervention targets to improve reproductive health and quality of life in middle-aged and older men.

Objective To investigate the correlation between plasma vitamin D levels and a novel inflam-matory marker,the systemic immune-inflammatory index(SII),in patients with type 2 diabetes.Methods This study adopted a cross-sectional design,in which patients diagnosed with type 2 diabetes who were admitted to the First Affiliated Hospital of Guangxi Medical University were enrolled as study participants.Data on demographic characteristics,medical history,physical examination findings,and laboratory test results were systematically collected.Participants were categorized into three groups based on their serum vitamin D levels:deficient,insuffi-cient,and sufficient.The relationship between vitamin D levels and the SII was evaluated using a multivariate linear regression model.Additionally,a restricted cubic spline model was employed to assess the nonlinear dose-response association between vitamin D levels and SII.Results This study enrolled a total of 5,716 patients with type 2 diabetes.A statistically significant difference in the SII was observed across groups with varying vitamin D levels(P<0.05),with the highest SII value found in the vitamin D-deficient group.Multivariate linear regression analysis revealed that,after adjusting for potential confounding factors including gender,age,season of blood collection,body mass index,hypertension,dyslipidemia,and chronic kidney disease,vitamin D levels were negatively associ-ated with SII(β=-2.68,95%CI:-3.56 to-1.81,P<0.001).Compared with the vitamin D-deficient group,the vitamin D-sufficient group exhibited significantly lower SII levels(β=-78.42,95%CI:-137.90 to-18.93,P=0.01).Furthermore,the restricted cubic spline model indicated a nonlinear dose-response relationship between vita-min D levels and SII(P<0.001).Conclusion There is a significant inverse correlation between plasma vitamin D levels and the SII in patients with type 2 diabetes.

Objective To study the plasma metabolomics of mice poisoned by different dosage of the combination of diazepam and ethanol,and to reveal the toxicological mechanisms of combined poisoning of diazepam and ethanol.Methods Female Kunming mice were randomly divided into blank group,single and combined poisoning group(n=6),Based on the LD50 of diazepam co-administered with graded ethanol doses,mice in the single-drug and combined groups received oral gavage at 1/2,1,and 2 × LD50.Retro-orbital blood samples(～500 μL)were collected within 24 hours post-administration and analyzed by UPLC-QE-MS technology.Principal component analysis and orthogonal partial least squares discriminant analysis were used to identify differential metabolites and associated metabolic pathways.Results A total of 387 differential metabolites were identified in the combined poisoning group of diazepam and ethanol implicating the key pathways including tryptophan metabolism,phenylalanine metabolism,arginine and proline metabolism,Glycerophospholipid metabolism,phenylalanine,tyrosine and tryptophan biosynthesis.Conclusion Combined diazepam and ethanol poisoning exerts significant systemic effects by disrupting neurotransmitters conduction,exacerbating oxidative stress response and dysregulating energy metabolism.