Lung cancer constitutes the most prevalent and lethal malignant tumor in China. Approximately 85% of lung cancer diagnoses correspond to the non-small cell histological subtype [non-small cell lung cancer (NSCLC)]. Despite surgery being the mainstay for early-stage disease, postoperative recurrence remains high and adjuvant chemotherapy offers limited benefit. In recent years, targeted therapy has demonstrated substantial advantages in driver mutation-positive NSCLC. To this end, the Lung Cancer Medical Education Committee of the Chinese Medical Education Association developed guidelines based on a systematic review of evidence through November 2025, using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and a modified Delphi method. Focusing on epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and addressing ROS proto-oncogene 1 (ROS1), B-Raf proto-oncogene serine/threonine kinase (BRAF) V600E mutation, and mesenchymal-epithelial transition factor (MET) exon 14 (METex14) skipping, the guideline covers molecular testing, neoadjuvant/adjuvant therapy, perioperative strategies, minimal residual disease monitoring, and postoperative surveillance. It defines testing requirements, specifies stage-directed and subtype-specific treatments, and standardizes minimal residual disease monitoring. These recommendations emphasize precision and feasibility to improve survival and quality of life.

Objective: To understand the health status of primary school freshmen in Guiyang and the health management service needs of parents after examination, so as to provide a reference for establishment of a collaborative health management framework involving schools, families, and healthcare providers. Methods: From September to October 2024, a stratified random cluster sampling method was used in Guiyang City to select 3 210 students and 3 133 parents who participated in the physical examination for primary school freshmen. Demographic indicators, physical examination indicators and laboratory examination indicators of students were collected, and parents needs for post examination health management service were investigated by self designed questionnaire. Multiple linear regression analysis was adopted to investigate the related factors of parents health management service needs after the examination. Results: The detection rates of common illness among primary school freshmen were 60.22% for dental caries, 17.23 % for screening myopia, 6.11% for obesity, 3.86% for iron deficiency anemia, and 1.15% for scoliosis. The co-occurrence rate of common illness among freshmen during the physical examination was 23.89% ( n =767), among which the comorbidity rate of screening myopia and dental caries (8.22%) and obesity and dental caries (4.27%) were higher. About 63.80% parents indicated that the physical examination items were simple, and 2 366 parents (75.52%) indicated a demand for post examination management services; the average score of parents demands for post examination services was (3.12±0.70). In terms of the scores of each dimension, the mean score of nutrition and health (3.58±0.74) was the highest, while the lowest mean score was for traditional Chinese medicine health care (2.77±0.67). The mean scores for the other dimensions were as follows:exercise intervention (3.29± 0.79 ), psychological monitoring (3.17±0.58), and health education and signing (2.81±0.73). The results of multiple linear regression analysis showed that parents educational level (junior high school, high school/vocational school, college/undergraduate and above), living conditions (floating), and children s illness status (1, 2, >3 types) were the related factors of parents health management service needs after the entrance examination for new students ( B =2.16, 3.07, 3.68; -2.19; 3.14, 3.34, 3.11, P <0.05). Conclusions The prevalence of common illness in primary schools in Guiyang is characterized by a heavy burden from single diseases, with a notable occurrence of multiple comorbidities. After the physical examination, parents have obvious demand for follow up health management services. These health management services should integrate the concept of multi disease prevention according to the needs of parents.

The cribriform fascia is formed by the fusion of deep and superficial fascias in the axilla,and it forms the base of the axilla together with the subcutaneous tissue and skin,which is a key part of the system of the membranous anatomy of breast surgery.The loose anatomical structure of the cribriform fascia makes it an important anatomical landmark in the axillary region,which plays an important role in accurate localization of lymph nodes.The sentinel lymph node biopsy through cribriform fascia has less intraoperative blood loss and shorter catheterization time compared with the traditional axillary fold approach.However,the anatomical structure of the cribriform fascia and its significance in the membranous anatomy of breast surgery have not been fully elucidated.This article analyzes the anatomical structure of the cribriform fascia and its adjacent tissues,and emphasizes the anatomical structure that needs to be paid attention to in sentinel lymph node biopsy through the axillary cribriform fascia,so as to provide a reference for clinicians to fully understand the cribriform fascia structure.

Objective To explore the application effect of hospital-community-home remote pulmonary rehabilita-tion management in patients with chronic obstructive pulmonary disease(COPD)and to provide references for clinical nursing practice.Methods The convenience sampling method was adopted to select patients from October 2023 to March 2024.Totally 86 COPD patients admitted to the respiratory department of a tertiary hospital in Nanjing were randomly divided into an experimental group(n=43)and a control group(n=43).The experimental group received the hospital-community-family triadic closed-loop remote pulmonary rehabilitation care,while the control group received only conventional home-based pulmonary rehabilitation care,and the duration of intervention is 3 months.The dif-ferences in adherence to pulmonary rehabilitation training,exercise endurance,degree of dyspnea,quality of life,and lung function were compared between the 2 groups after intervention.Results The experimental group and control group each included 42 cases and 40 cases finally.After intervention,the experimental group showed better out-comes than the control group in adherence to pulmonary rehabilitation training,exercise endurance,degree of dysp-nea,quality of life with statistically significant differences(P＜0.05).There were no statistically significant differences between the 2 groups in lung function(P＞0.05).Conclusion The hospital-community-family remote pulmonary re-habilitation management can improve COPD patients'adherence to pulmonary rehabilitation training,exercise en-durance,reduce patient's dyspnea symptoms and improve quality of life.

This review has introduced the Coronary Artery Tree description and Lesion EvaluaTion(CatLet or Hexu)angiographic scoring system,which,based solely on coronary angiography results,has characterized 6 types of right coronary artery,3 types of left descending artery,and 3 types of diagonal size,together resulting in 54 types of coronary circulation pattern.This novel angiographic scoring system can be utilized to account for coronary anatomy in its diversity,severity and complexity of diseased coronary arteries,and their subtended myocardial territories in jeopardy.The CatLet angiographic scoring system is unique in that the importance of a coronary artery is weighted according to its subtended myocardial segments,by which the variability of coronary artery has been accounted for and measured.Researchers at home and abroad have increasingly paid attention to its clinical utilities,which warrant further validation in the context of large sample size,prospective,and randomized controlled trials.The CatLet angiographic scoring system is accessible at www.catletscore.com.

Objective:To explore the role of Caveolin-1 (CAV-1) in radiation-induced premature senescence of vascular endothelial cells.Methods:A cell model with stable knockdown of CAV-1 was constructed in human microvascular endothelial cells (HMEC-1) by lentiviral transfection using puromycin screening. The cells were divided into NC group and sh-CAV-1 group based on whether they were infected with lentivirus shRNA-CAV-1. The protein expression levels of CAV-1, p53 and p21 were detected by Western blot at 24, 48, and 72 h after 0, 2, and 4 Gy X-ray irradiation. The β-galactosidase staining kit was used to detect β-galactosidase in cells. CCK-8 kit was used to detect cell viability, and vascular endothelial cell function was detected by vascular tube-forming assay.Results:CAV-1 protein expression was significantly decreased at 48 h after 2 and 4 Gy X-ray irradiation ( t=3.50, 3.89, P < 0.05), and β-galactosidase in sh-CAV-1 group was significantly increased at 72 h after 0, 2 and 4 Gy X-ray irradiation ( t=12.91, 11.54, 6.04, P < 0.05) compared with the NC group. Knockdown of CAV-1 resulted in the decrease in the expression level of the cellular senescence-associated protein p53 protein ( t=4.09, 3.13, 3.43, P < 0.05), but increase in the expression level of p21 protein ( t=-3.63, -3.33, -3.06, P < 0.05). Compared with the NC group, knockdown CAV-1 significantly decreased cell viability ( t=2.97-25.89, P<0.05) and reduced vessel-forming capacity ( t=3.39-39.68, P < 0.05). Conclusions:CAV-1 is involved in the process of radiation-induced premature senescence of vascular endothelial cells through positive regulation of p53 and negative regulation of p21.

[This corrects the article DOI: 10.1016/j.apsb.2021.10.012.].

Acute kidney injury (AKI) has high morbidity and mortality, but effective clinical drugs and management are lacking. Previous studies have suggested that macrophages play a crucial role in the inflammatory response to AKI and may serve as potential therapeutic targets. Emerging evidence has highlighted the importance of forkhead box protein O1 (FoxO1) in mediating macrophage activation and polarization in various diseases, but the specific mechanisms by which FoxO1 regulates macrophages during AKI remain unclear. The present study aimed to investigate the role of FoxO1 in macrophages in the pathogenesis of AKI. We observed a significant upregulation of FoxO1 in kidney macrophages following ischemia-reperfusion (I/R) injury. Additionally, our findings demonstrated that the administration of FoxO1 inhibitor AS1842856-encapsulated liposome (AS-Lipo), mainly acting on macrophages, effectively mitigated renal injury induced by I/R injury in mice. By generating myeloid-specific FoxO1-knockout mice, we further observed that the deficiency of FoxO1 in myeloid cells protected against I/R injury-induced AKI. Furthermore, our study provided evidence of FoxO1's pivotal role in macrophage chemotaxis, inflammation, and migration. Moreover, the impact of FoxO1 on the regulation of macrophage migration was mediated through RhoA guanine nucleotide exchange factor 1 (ARHGEF1), indicating that ARHGEF1 may serve as a potential intermediary between FoxO1 and the activity of the RhoA pathway. Consequently, our findings propose that FoxO1 plays a crucial role as a mediator and biomarker in the context of AKI. Targeting macrophage FoxO1 pharmacologically could potentially offer a promising therapeutic approach for AKI.

Sleep deprivation (SD) has emerged as a significant modifiable risk factor for Alzheimer’s disease (AD), with mounting evidence demonstrating its multifaceted role in accelerating AD pathogenesis through diverse molecular, cellular, and systemic mechanisms. SD is refined within the broader spectrum of sleep-wake and circadian disruption, emphasizing that both acute total sleep loss and chronic sleep restriction destabilize the homeostatic and circadian processes governing glymphatic clearance of neurotoxic proteins. During normal sleep, concentrations of interstitial Aβ and tau fall as cerebrospinal fluid oscillations flush extracellular waste; SD abolishes this rhythm, causing overnight rises in soluble Aβ and tau species in rodent hippocampus and human CSF. Orexinergic neurons sustain arousal, and become hyperactive under SD, further delaying sleep onset and amplifying Aβ production. At the molecular level, SD disrupts Aβ homeostasis through multiple converging pathways, including enhanced production via beta-site APP cleaving enzyme 1 (BACE1) upregulation, coupled with impaired clearance mechanisms involving the glymphatic system dysfunction and reduced Aβ-degrading enzymes (neprilysin and insulin-degrading enzyme). Cellular and histological analyses revealed that these proteinopathies are significantly exacerbated by SD-induced neuroinflammatory cascades characterized by microglial overactivation, astrocyte reactivity, and sustained elevation of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) through NF‑κB signaling and NLRP3 inflammasome activation, creating a self-perpetuating cycle of neurotoxicity. The synaptic and neuronal consequences of chronic SD are particularly profound and potentially irreversible, featuring reduced expression of critical synaptic markers (PSD95, synaptophysin), impaired long-term potentiation (LTP), dendritic spine loss, and diminished neurotrophic support, especially brain-derived neurotrophic factor (BDNF) depletion, which collectively contribute to progressive cognitive decline and memory deficits. Mechanistic investigations identify three core pathways through which SD exerts its neurodegenerative effects: circadian rhythm disruption via BMAL1 suppression, orexin system hyperactivity leading to sustained wakefulness and metabolic stress, and oxidative stress accumulation through mitochondrial dysfunction and reactive oxygen species overproduction. The review critically evaluates promising therapeutic interventions including pharmacological approaches (melatonin, dual orexin receptor antagonists), metabolic strategies (ketogenic diets, and Mediterranean diets rich in omega-3 fatty acids), lifestyle modifications (targeted exercise regimens, cognitive behavioral therapy for insomnia), and emerging technologies (non-invasive photobiomodulation, transcranial magnetic stimulation). Current research limitations include insufficient understanding of dose-response relationships between SD duration/intensity and AD pathology progression, lack of long-term longitudinal clinical data in genetically vulnerable populations (particularly APOE ε4 carriers and those with familial AD mutations), the absence of standardized SD protocols across experimental models that accurately mimic human chronic sleep restriction patterns, and limited investigation of sex differences in SD-induced AD risk. The accumulated evidence underscores the importance of addressing sleep disturbances as part of multimodal AD prevention strategies and highlights the urgent need for clinical trials evaluating sleep-focused interventions in at-risk populations. The review proposes future directions focused on translating mechanistic insights into precision medicine approaches, emphasizing the need for biomarkers to identify SD-vulnerable individuals, chronotherapeutic strategies aligned with circadian biology, and multi-omics integration across sleep, proteostasis and immune profiles may delineate precision-medicine strategies for at-risk populations. By systematically examining these critical connections, this analysis positions sleep quality optimization as a viable strategy for AD prevention and early intervention while providing a comprehensive roadmap for future mechanistic and interventional research in this rapidly evolving field.

Objective: To investigate the influencing factors for kinesiophobia among elderly patients with chronic obstructive pulmonary disease (COPD), so as to provide the reference for alleviating kinesiophobia among COPD patients. Methods: From December 2023 to July 2024, COPD patients aged 60 years and above who sought medical treatment at a tertiary grade-a hospital in Guiyang City were selected. Demographic information was collected through questionnaire surveys. Kinesiophobia, exercise self-efficacy, social support, type D personality and coping styles were assessed using the Chinese version of Tampa Scale for Kinesiophobia, the Chinese version of the Self-Efficacy for Exercise Scale, Social Support Rating Scale, Type D Personality Scale and Chinese version of the Medical Coping Modes Questionnaire, respectively. Factors affecting kinesiophobia among elderly patients with COPD were analyzed using a multiple linear regression model. Results: A total of 300 COPD patients were surveyed, including 238 males (79.33%) and 62 females (20.67%). The majority of patients had a disease duration of less than 5 years, with 130 cases (43.33%). The average kinesiophobia score was (48.01±7.74) points. The average exercise self-efficacy score was (3.39±1.01) points. The average social support score was (34.42±6.76) points. There were 280 patients (93.33%) with type D personality. The average scores of the confrontation, avoidance, and resignation dimensions of coping styles were (17.42±5.00), (13.76±1.91), and (11.81±2.95) points, respectively. Multiple linear regression analysis showed that age (70-<80 years, β'=0.124; ≥80 years, β'=0.205), educational level (primary school and below, β'=0.228; junior high school, β'=0.182), household monthly income per capita (<3 000 yuan, β'=0.234; 3 000~<5 000 yuan, β'=0.165), social support (β'=0.294), type D personality (β'= 0.170), and coping styles (confrontation dimension, β'=-0.140; avoidance dimension, β'=0.154; resignation dimension, β'=0.175) statistically associated with kinesiophobia among elderly patients with COPD. Conclusion Kinesiophobia among elderly patients with COPD is associated with age, educational level, household monthly income per capita, social support, type D personality and coping styles.