Background Existing studies have confirmed that fine particulate matter (PM_2.5)is one of the important factors inducing pulmonary fibrosis. Pulmonary fibrosis is the terminal stage of a major category of lung diseases characterized by the destruction of tissue structure, and eventually leading lung ventilation and ventilation dysfunction. No effective pulmonary fibrosis treatment is available yet. Objective To investigate the protective effect of salidroside on pulmonary fibrosis induced by the exposure of PM_2.5 and its molecular mechanism. Methods Seventy 7-week-old male C57BL/6 mice were randomly divided into four groups: control group (intratracheal instillation of normal saline + saline by gavage, n=25), Sal group (intratracheal instillation of normal saline + Sal 60 mg·kg⁻¹ by gavage, n=10), PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ + saline by gavage, n=10), and Sal + PM_2.5 group (intratracheal instillation of PM_2.5 5 mg·kg⁻¹ +Sal 60 mg·kg⁻¹ by gavage, n=10). The mice were administered by gavage once daily, intratracheal instillation once every 3 d, and every 3 d constituted an experimental cycle. At the end of the 26-30th cycles, 3 mice in the control group and 3 mice in the PM_2.5 group were randomly sacrificed, and the lung tissues were collected for Masson staining to verify whether the pulmonary fibrosis model was successfully established. After 30 cycles, the model was successfully constructed. After 1 week of continuous observation, the mice were sacrificed, and the blood and lung tissues of the mice were collected to make lung tissue sections. Assay kits were correspondingly employed to detect oxidative stress indicators such as serum malondialdehyde (MDA) and superoxide dismutase (SOD). Western blotting was used to detect the expression of fibrosis-related proteins (Collagen-III, α-SMA), mitochondrial dynamics-related proteins (MFN1, Drp1), and mitophagy-related proteins (PINK1, Parkin, and LC3). Results Compared with the control group, the weight gain rate of the PM_2.5 group was slowed down (P<0.05), which was alleviated by the Sal intervention (P<0.05). The lung coefficient increased after the PM_2.5 exposure (P<0.05), which was alleviated by Sal intervention. Compared with the control group, the PM_2.5 group showed severe alveolar structure damage, inflammatory cell infiltration, and blue collagen deposition, and significantly increased the lung injury score, collagen volume fraction (CVF), Szapiel score, and Ashcroft score (P<0.05), as well as serum oxidative stress levels (P<0.05). The protein expression levels of Collagen-III, α-SMA, Drp1, PINK1, Parkin, and LC3 II/I were increased (P<0.05), and the expression of MFN1 was decreased (P<0.05). Compared with the PM_2.5 group, the Sal intervention alleviated lung injury, reduced inflammatory cell infiltration and collagen deposition, showing decreased lung injury score, CVF, Szapiel score, and Ashcroft score (P<0.05), and decreased serum oxidative stress levels (P<0.05); the protein expression levels of Collagen-III, α-SMA, PINK1, Parkin, and LC3 II/I were decreased (P<0.05), the expression level of Drp1 was decreased, and the expression level of MFN1 was increased. Conclusion In the process of pulmonary fibrosis induced by PM_2.5 exposure in mice, Sal may affect mitochondrial autophagy through PINK1/Parkin pathway and play a protective role. The specific mechanism needs to be further verified.

Objective : To pathological changes and inducible nitric oxide synthase(iNOS), phosphorylated insulin receptor substrate 1 serine 307(p-IRS1ser 307), phosphorylated protein kinase B serine 473(p-AKTser 473), glycogen synthase kinase-3β(GSK-3β), and gluconeogenic synthase(GS) proteins were observed in the liver of rats under the condition of chronic intermittent hypoxia-replicated oxygen in control. And to explore the role of iNOS/IRS1/AKT/GSK-3β signaling pathway in chronic intermittent hypoxia-induced insulin resistance. Methods : Forty SD rats were randomly divided into a control group(NC group) and an experimental group(CIH group), with 20 rats in each group. The NC group was placed in a normoxic environment for 12 weeks, while the CIH group was first subjected to intermittent hypoxia for 8 weeks, and then resumed normoxic rearing until the 12th week. Fasting blood glucose(FBG) and fasting insulin(FINS) were measured at baseline, week 8 and week 12, and liver tissues were taken for pathology and measurement of iNOS, p-IRS1ser 307, p-AKTser 473, GSK3β and GS levels, to compare the differences between groups. Results: t baseline, there was no significant difference in liver pathology between the two groups, and the observed indexes were not statistically significant(P>0.05); at 8 weeks, compared with the NC group, liver pathology in the CIH group showed significant disorganization of hepatic blood sinusoids and hepatocyte cords, obvious hepatocyte edema, smaller nuclei, increased lymphocyte infiltration, and a small number of fat vacuoles, significantly higher levels of FBG, FINS, insulin resistance index(HOMA-IR), iNOS mRNA, p-IRS1ser 307 protein, GSK-3β protein levels, and decreased p-AKTser 473 protein and GS protein levels, all of which were statistically significant(allP<0.05). IRS1ser 307 protein, GSK-3β protein levels were increased, p-AKTser 473 protein and GS protein levels were decreased, and the differences were statistically significant(allP<0.05); at 12 weeks, no lymphocyte infiltration was seen in the CIH group compared with that of the NC group and fat vacuoles significantly increased, and there was no improvement in the other pathological damage that had already occurred, and the levels of p-AKTser 473 protein significantly increased. AKTser 473 protein level significantly increased, p-IRS1ser 307 protein and GS protein levels were significantly reduced, all of which were statistically significant(allP<0.05), and the rest of the observational indexes were not statistically significant. Pearson′s correlation analysis showed that HOMA-IR of CIH group was significantly positively correlated with the levels of iNOS mRNA, p-IRS1ser 307 protein, and GSK-3β protein at 8 weeks(r=0.874, 0.817,0.872;allP<0.05), and significantly negatively correlated with the levels of p-AKTser 473 protein and GS protein(r=-0.886,-0.879;allP<0.05). Conclusion Chronic intermittent hypoxia can lead to hepatic pathological damage that cannot be reversed even by reoxygenation interventions and may mediate the development of insulin resistance by upregulating the IRS1/AKT/GSK-3β signaling pathway through the upregulation of iNOS mRNA expression.

Objective The objective of this study was to analyze the longitudinal trend of multidimensional treatment quality of breast cancer based on the latent growth mixture model(LGMM),identify potential change patterns and influencing factors,and pro-vide scientific basis for improving treatment quality and patient prognosis.Methods The quality monitoring data of breast cancer from four consecutive years were obtained in the National"Quality Monitoring System for Specific(single)Disease";Based on the item response theory(IRT),the treatment quality of breast cancer in the three dimensions of preoperative examination,treatment,and out-come was calculated;LGMM was constructed to analyze the independent and joint change trend of breast cancer treatment quality in all dimensions,and the optimal model was determined based on practical significance and statistical indicators.Results In the inde-pendent trend analysis,2 potential categories were identified for preoperative examination,treatment,and outcome dimensions.Among them,9%showed a rapid upward trend in the preoperative examination dimension,and 91%showed a relatively stable trend;The sta-ble growth accounted for 23%and slow decline accounted for 77%in the treatment dimension;13%of the outcome dimensions showed an upward trend,while 87%showed a downward trend.In the joint trend analysis of changes,2 potential categories were identified:the first category accounted for about 8%,and the preoperative examination dimension of this category had a good treatment quality,with mean intercepts and slopes of 3.326 and 3.367,respectively.The treatment quality in the treatment and outcome dimensions had steadily improved;The second category accounted for about 92%,and the treatment quality in this dimension was relatively good.Its mean intercept and slope were 0.548 and 0.018,respectively.There is still room for improvement in the treatment quality of the pre-operative examination and outcome dimensions;BMI and M stage in patient characteristics are important influencing factors on the trend of combined changes in treatment quality.Conclusion The treatment quality of breast cancer during this study period has im-proved to varying degrees in all dimensions of preoperative examination,treatment and outcome;In the joint trend analysis of the three dimensions,the improvement of treatment quality in the preoperative examination dimension can provide feasible references for subse-quent treatment and achieve the goal of reducing complications.

Objective Based on polynomial logistic regression model,this study aimed to analyze the optimal length of hospi-tal stay for patients with non-small cell lung cancer(NSCLC)at different stages to achieve the best treatment quality,providing refer-ence for improving treatment quality and formulating relevant policies.Methods The data of NSCLC cases were collected and 16 di-agnosis and treatment process indicators were selected.Patients were stratified according to the stage of lung cancer.A polynomial lo-gistic regression model was constructed,including patient characteristics to analyze the impact of first hospitalization days on the quali-ty of comprehensive treatment.Results A total of 10,053 patients with NSCLC were collected in this study,with a median compre-hensive treatment quality score of 0.60.According to the staging of lung cancer,patients were divided into the early stage group(stageⅠ-Ⅱ),locally advanced stage group(stage Ⅲ),and advanced stage group(stage Ⅳ).The first hospitalization days and treatment quality of each subgroup showed a non-linear relationship.The polynomial model results showed that after adjusting the characteristics of patients,the length of hospitalization day and the quadratic term of hospital stay had a statistically significant impact on treatment quality in each subgroup:early patients had a first hospital stay of 18 days,and locally advanced and advanced patients had a first hos-pital stay of 22 days,with the highest probability of achieving high treatment quality.Conclusion Patients in different stages have va-rying degrees of illness and treatment plans,resulting in different first hospitalization days corresponding to the highest probability of obtaining high-quality treatment.Hospitals can improve the treatment quality and medical efficiency by implementing standardized di-agnosis and treatment guidelines,strengthening the management of the diagnosis and treatment process,and reasonably controlling the first hospitalization time of patients in different stages.

Objective The aim of this study was to estimate the causal effects of non-small cell lung cancer(NSCLC)treat-ment process on in-hospital mortality based on the double robust estimation(DR)method,and provide a reference basis for reducing in-hospital mortality of NSCLC.Methods According to the quality evaluation system of NSCLC treatment,the utilization rate of treatment process indicators was calculated,and patients were divided into the high-quality or low-quality groups based on the aver-age score of treatment process quality.In-hospital mortality was used as the outcome indicator,Kaplan-Meier method and Cox regres-sion adjusted for propensity score inverse probability of treatment weighting(IPTW)correction were used to analyze the impact of treat-ment process quality on in-hospital mortality in NSCLC.DR was combined to estimate the causal effects of the treatment process on in-hospital mortality.Results The median utilization rate of treatment process indicators was 66.88%,and the mean and standard de-viation of patients′ treatment process quality scores were 0.270±0.124,including 0.358±0.069 in the high-quality group,and 0.158±0.081 in the low-quality group.After the IPTW weighting,the standardized mean difference(SMD)of patients′baseline characteris-tics decreased;The difference in survival curves between the two groups of patients before and after ITPW was statistically significant(P<0.05),and the prognosis of patients in the high-quality group was better than that of patients in the low-quality group(pre-IPTW:HR=0.367,95%CI:0.275-0.491;post-IPTW:HR=0.228,95%CI:0.167-0.312).Compared with the low-quality group,the average causal effect of treatment process on in-hospital mortality was-0.026 in the high-quality group.Conclusion DR can compensate for the shortcomings of logistic or IPTW,avoid the risk of model error,and obtain for the causal effect of treatment process on in-hospital mortality.In medical practice,the utilization rate of treatment process indicators should be increased to improve patient prognosis;The study of causal effects suggests that besides the treatment process,other factors that affect in-hospital mortality cannot be ignored.

The advancement of computers and data explosion have ushered in the third wave of artificial intelligence(AI). AI is an interdisciplinary field that encompasses new ideas, new theories, and new technologies, etc. AI has brought convenience to ophthalmology application and promoted its intelligent, precise, and minimally invasive development. At present, AI has been widely applied in various fields of ophthalmology, especially in oculoplastic surgery. AI has made rapid progress in image detection, facial recognition, etc., and its performance and accuracy have even surpassed humans in some aspects. This article reviews the relevant research and applications of AI in oculoplastic surgery, including ptosis, single eyelid, pouch, eyelid mass, and exophthalmos, and discusses the challenges and opportunities faced by AI in oculoplastic surgery, and provides prospects for its future development, aiming to provide new ideas for the development of AI in oculoplastic surgery.

Objective To investigate the effects of chronic intermittent hypoxia(CIH)and reoxygenation on insulin resistance(IR)and expressions of miR-27a-3p/PPARγ/IRS1/PI3K/AKT in rat skeletal muscle.Methods GEO database was used for screening the differentially expressed miRNAs in CIH,and their target genes were subjected to GO and KEGG enrichment analysis followed by construction of the miRNA-mRNA-pathway regulatory network using Cytoscape.In the animal experiment,48 male SD rats were randomly divided into normoxia group and CIH group(8 weeks of CIH followed by 4 weeks of normoxic recovery).Blood and skeletal muscle samples were collected at baseline,8 weeks,and 12 weeks to evaluate the changes in fasting blood glucose(FBG)and fasting insulin(FINS)levels and muscular pathology.RT-qPCR and Western blotting were used to detect the changes in the expressions of miR-27a-3p,PPARγ,GLUT4,IRS1,p-IRS1,PI3K,p-AKT and AKT in the muscular tissues.Results No muscular miRNA datasets for CIH were available in GEO database,from which only a kidney-related dataset(GSE202480)was obtained,based on which a total of 165 differentially expressed miRNAs were identified.GO/KEGG analysis suggested that these miRNAs were involved in muscular regulation and insulin signaling.The miRNA-mRNA-pathway network highlighted miR-27a-3p as a crucial regulator in the PPAR and PI3K/AKT pathway.In the animal experiment,the rats subjected to CIH for 8 weeks showed significantly increased FBG,FINS,HOMA-IR,and PPARγ levels,loose muscle fiber arrangement,decreased cross-sectional area of the muscle fibers,and lowered expressions of miR-27a-3p,p-IRS1/IRS1,PI3K,and p-AKT/AKT in the skeletal muscles.Conclusion CIH increases IR,causes skeletal muscle pathology,downregulates miR-27a-3p expression,upregulates PPARγ expression,and inhibits IRS1/PI3K/AKT insulin signaling in the skeletal muscles of rats,and these changes can be reversed by reoxygenation.MiR-27a-3p may participate in CIH-induced IR by modulating the PPAR γ/IRS1/PI3K/AKT signaling pathway.

Objective: To explore the association of the interaction between vitamin D deficiency and dyslipidemia with the comorbidity risk of overweight and obesity in children and adolescents, so as to provide the theoretical basis for prevention and control of overweight and obesity in children and adolescents. Methods: The data for the study was obtained from the population aged 6-17 in Hebei Province during the 2022-2023 monitoring of nutrition and health status of Chinese residents. A stratified cluster random sampling method was used to conduct questionnaire surveys, physical measurements, and laboratory tests on 2 118 children and adolescents. Logistic regression was used to analyze the association of vitamin D deficiency and dyslipidemia with overweight and obesity, and multiplication and addition models were used to analyze the interaction of vitamin D deficiency and dyslipidemia with overweight and obesit. Results: The prevalence of vitamin D deficiency in the surveyed children and adolescents was 67.80%, the incidence of dyslipidemia was 24.46%, and the prevalence of overweight and obesity was 41.97%. After adjusting for confounding factors, the results of multivariate Logistic regression analysis showed that there was no multiplicative interaction of vitamin D deficiency and dyslipidemia with overweight and obesit ( OR=0.90, 95%CI=0.57-1.43, P >0.05). However, the risk of overweight and obesity among children and adolescents with vitamin D deficiency and dyslipidemia was 3.99 times higher than that of those with sufficient vitamin D and normal blood lipids ( OR=3.99, 95%CI=2.93-5.45, P <0.01). There was a positive additive interaction between vitamin D deficiency and dyslipidemia, with relative excess risk of interaction, attributable proportion of interaction and synergy index of 14.40, 81.50% and 7.35, respectively. Conclusions For children and adolescents, there is a synergistic effect between vitamin D deficiency and dyslipidemia, and the coexistence of both increases the risk of overweight and obesity. Comprehensive prevention and control measures should be taken to timely supplement vitamin D and maintain normal blood lipid levels, to reduce the occurrence of overweight and obesity in children and adolescents.

Objective To investigate the effects of chronic intermittent hypoxia(CIH)and reoxygenation on insulin resistance(IR)and expressions of miR-27a-3p/PPARγ/IRS1/PI3K/AKT in rat skeletal muscle.Methods GEO database was used for screening the differentially expressed miRNAs in CIH,and their target genes were subjected to GO and KEGG enrichment analysis followed by construction of the miRNA-mRNA-pathway regulatory network using Cytoscape.In the animal experiment,48 male SD rats were randomly divided into normoxia group and CIH group(8 weeks of CIH followed by 4 weeks of normoxic recovery).Blood and skeletal muscle samples were collected at baseline,8 weeks,and 12 weeks to evaluate the changes in fasting blood glucose(FBG)and fasting insulin(FINS)levels and muscular pathology.RT-qPCR and Western blotting were used to detect the changes in the expressions of miR-27a-3p,PPARγ,GLUT4,IRS1,p-IRS1,PI3K,p-AKT and AKT in the muscular tissues.Results No muscular miRNA datasets for CIH were available in GEO database,from which only a kidney-related dataset(GSE202480)was obtained,based on which a total of 165 differentially expressed miRNAs were identified.GO/KEGG analysis suggested that these miRNAs were involved in muscular regulation and insulin signaling.The miRNA-mRNA-pathway network highlighted miR-27a-3p as a crucial regulator in the PPAR and PI3K/AKT pathway.In the animal experiment,the rats subjected to CIH for 8 weeks showed significantly increased FBG,FINS,HOMA-IR,and PPARγ levels,loose muscle fiber arrangement,decreased cross-sectional area of the muscle fibers,and lowered expressions of miR-27a-3p,p-IRS1/IRS1,PI3K,and p-AKT/AKT in the skeletal muscles.Conclusion CIH increases IR,causes skeletal muscle pathology,downregulates miR-27a-3p expression,upregulates PPARγ expression,and inhibits IRS1/PI3K/AKT insulin signaling in the skeletal muscles of rats,and these changes can be reversed by reoxygenation.MiR-27a-3p may participate in CIH-induced IR by modulating the PPAR γ/IRS1/PI3K/AKT signaling pathway.

A 66-year-old female patient presented with blisters on the scalp and neck for 1 month. She had a history of type 2 diabetes for 6 years, and started taking the dipeptidyl peptidase-4 inhibitor linagliptin at a dose of 5 mg once a day 6 months before the onset of eruption. Skin examination showed scattered mung bean- to peanut-sized blisters on the scalp, and some blisters broke with exudation and crusts. There was a pigeon egg-sized bulla and two mung bean-sized blisters on the left neck, with tense blister walls, clear blister fluids, non-erythematous base, and Nikolsky′s sign was negative. Enzyme-linked immunosorbent assay revealed that the serum levels of anti-BP180 NC16A and anti-BP230 antibodies were 5.81 and 139.76 kU/L respectively. Histopathological examination of the blister on the neck showed subepidermal blister formation, and infiltration with neutrophils and a few eosinophils in the blister. The patient was finally diagnosed with localized anti-BP230-type bullous pemphigoid. This case of anti-BP230-type bullous pemphigoid associated with the dipeptidyl peptidase-4 inhibitor linagliptin was firstly reported in China.