1.Guidelines for the perioperative diagnosis and treatment of oncogene-driven non-small cell lung cancer (2026)
Weidong WANG ; Yongbin LIN ; Hui TIAN ; Gaofeng LI ; Shun XU ; Yongde LIAO ; Haitao MA ; Junfeng LIU ; Chundong GU ; Xiaolong YAN ; Shumin WANG ; Daqiang SUN ; Jianyang LIU ; Tao XUE ; Shaohua MA ; Zhigang LI ; Shuanghu YUAN ; Gen LIN ; Ling CAI ; Jianping ZHOU ; Wenzhao ZHONG ; Naixin LIANG ; Yi HAN ; Junfeng WANG ; Weidong ZHANG ; Xin WANG ; Lianjuan CHEN ; Lunxu LIU ; Xiuyi ZHI ; Lanjun ZHANG
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery 2026;33(09):1337-1353
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.
2.A Latent Class Trajectory Model Based Analysis of KCCQ Symptom Score Trajectories and Readmission Risk in Heart Failure Patients during the Vulnerable Period
Yuan XU ; Yan JIANG ; Yanan ZHANG ; Hui HU ; Dan XIAO
Journal of Sun Yat-sen University(Medical Sciences) 2026;47(5):899-912
ObjectiveThis study examined KCCQ symptom score trajectories during the vulnerable phase of heart failure and their association with readmission within 6 months. MethodsThis prospective cohort study included 1 109 patients hospitalized for chronic heart failure at a tertiary hospital in Nanchang, China, between August 2020 and July 2025. KCCQ scores were assessed at six time points: day 3 after admission, discharge, and 1, 2, 3, and 6 months after discharge. Group-based trajectory modeling was used to identify patterns of change in KCCQ scores. Multiple logistic regression was used to assess the association between trajectory membership and readmission risk. ResultsDuring follow-up, 229 patients were readmitted, accounting for 20.6% of the cohort. Four KCCQ trajectories were identified: persistently declining scores (n=228, 20.6%), persistently improving scores (n=110, 9.9%), stable intermediate scores (n=545, 49.1%), and stable high scores (n=226, 20.4%). Compared with the stable intermediate group, the persistently declining group had a higher risk of readmission in the fully adjusted model (OR=2.099, 95% CI: 1.027–4.315, P=0.043), whereas the stable high-score group had a lower risk (OR=0.260, 95% CI: 0.127–0.494, P<0.001). The association between the persistently improving trajectory and readmission was not statistically significant (OR=0.614, 95% CI: 0.306–1.154, P=0.147). ConclusionsKCCQ symptom score trajectories during the vulnerable phase of heart failure show marked heterogeneity and are associated with readmission within 6 months. A persistently declining trajectory is associated with higher readmission risk, whereas a stable high-score trajectory is associated with lower risk. Longitudinal monitoring of KCCQ score changes may help inform post-discharge risk stratification and follow-up management in patients with heart failure.
3.A Latent Class Trajectory Model Based Analysis of KCCQ Symptom Score Trajectories and Readmission Risk in Heart Failure Patients during the Vulnerable Period
Yuan XU ; Yan JIANG ; Yanan ZHANG ; Hui HU ; Dan XIAO
Journal of Sun Yat-sen University(Medical Sciences) 2026;47(5):899-912
ObjectiveThis study examined KCCQ symptom score trajectories during the vulnerable phase of heart failure and their association with readmission within 6 months. MethodsThis prospective cohort study included 1 109 patients hospitalized for chronic heart failure at a tertiary hospital in Nanchang, China, between August 2020 and July 2025. KCCQ scores were assessed at six time points: day 3 after admission, discharge, and 1, 2, 3, and 6 months after discharge. Group-based trajectory modeling was used to identify patterns of change in KCCQ scores. Multiple logistic regression was used to assess the association between trajectory membership and readmission risk. ResultsDuring follow-up, 229 patients were readmitted, accounting for 20.6% of the cohort. Four KCCQ trajectories were identified: persistently declining scores (n=228, 20.6%), persistently improving scores (n=110, 9.9%), stable intermediate scores (n=545, 49.1%), and stable high scores (n=226, 20.4%). Compared with the stable intermediate group, the persistently declining group had a higher risk of readmission in the fully adjusted model (OR=2.099, 95% CI: 1.027–4.315, P=0.043), whereas the stable high-score group had a lower risk (OR=0.260, 95% CI: 0.127–0.494, P<0.001). The association between the persistently improving trajectory and readmission was not statistically significant (OR=0.614, 95% CI: 0.306–1.154, P=0.147). ConclusionsKCCQ symptom score trajectories during the vulnerable phase of heart failure show marked heterogeneity and are associated with readmission within 6 months. A persistently declining trajectory is associated with higher readmission risk, whereas a stable high-score trajectory is associated with lower risk. Longitudinal monitoring of KCCQ score changes may help inform post-discharge risk stratification and follow-up management in patients with heart failure.
4.INVESTIGATION OF PATHOGENS CARRIED BY RODENTS AT YUNNAN HEKOU PORT
Xiao-Long ZHANG ; Dong WANG ; Jing ZHAO ; Zhi-Liang ZHAO ; Ling-Rui YUAN ; Run-Yi ZHOU ; Jie TIAN ; Hui-Lin GUO ; Chun-Yan GAO
Acta Parasitologica et Medica Entomologica Sinica 2025;32(1):27-33,51
Objective This research was performed to identify rodent-borne pathogens in Hekou Port,Yunnan Province.Methods Rodents were captured using cages and dissected to collect their lungs,liver,spleen,and other viscera.Eight pathogens,including Yersinia pestis,Leptospira,Bartonella,and Anaplasmataceae,were identified using polymerase chain reaction amplification.Amplified pathogen sequences from positive samples were sequenced,and BLAST homology searches were conducted using GenBank to confirm pathogen identities.A phylogenetic tree of the identified pathogens was constructed using the neighbor joining method.Results The total of 31 rodents,identified as Rattus tanezumi,R.norvegicus,and Mus musculus,were captured.Among these,R.tanezumi was the dominant species,accounting for 64.52%of the total.Two pathogens,Leptospira interrogans and Neoehrlichia mikurensis,were detected,with positivity rates of 9.68%and 29.03%,respectively.No other pathogens were detected.The overall positivity rate for rodent-borne pathogens was 35.48%.Conclusions The single 16S rRNA gene fragment is insufficient for the molecular identification of all Neoehrlichia species.Accurate species identification should be based on a combined analysis of multiple genes.The prevalence of rodent-borne pathogens in Hekou Port indicates the necessity for enhanced surveillance of rodent-borne diseases and implementation of additional prevention and control measures in border ports.
5.Regulation of Immune Function by Exercise-induced Metabolic Remodeling
Hui-Guo WANG ; Gao-Yuan YANG ; Xian-Yan XIE ; Yu WANG ; Zi-Yan LI ; Lin ZHU
Progress in Biochemistry and Biophysics 2025;52(6):1574-1586
Exercise-induced metabolic remodeling is a fundamental adaptive process whereby the body reorganizes systemic and cellular metabolism to meet the dynamic energy demands posed by physical activity. Emerging evidence reveals that such remodeling not only enhances energy homeostasis but also profoundly influences immune function through complex molecular interactions involving glucose, lipid, and protein metabolism. This review presents an in-depth synthesis of recent advances, elucidating how exercise modulates immune regulation via metabolic reprogramming, highlighting key molecular mechanisms, immune-metabolic signaling axes, and the authors’ academic perspective on the integrated “exercise-metabolism-immunity” network. In the domain of glucose metabolism, regular exercise improves insulin sensitivity and reduces hyperglycemia, thereby attenuating glucose toxicity-induced immune dysfunction. It suppresses the formation of advanced glycation end-products (AGEs) and interrupts the AGEs-RAGE-inflammation positive feedback loop in innate and adaptive immune cells. Importantly, exercise-induced lactate, traditionally viewed as a metabolic byproduct, is now recognized as an active immunomodulatory molecule. At high concentrations, lactate can suppress immune function through pH-mediated effects and GPR81 receptor activation. At physiological levels, it supports regulatory T cell survival, promotes macrophage M2 polarization, and modulates gene expression via histone lactylation. Additionally, key metabolic regulators such as AMPK and mTOR coordinate immune cell energy balance and phenotype; exercise activates the AMPK-mTOR axis to favor anti-inflammatory immune cell profiles. Simultaneously, hypoxia-inducible factor-1α (HIF-1α) is transiently activated during exercise, driving glycolytic reprogramming in T cells and macrophages, and shaping the immune landscape. In lipid metabolism, exercise alleviates adipose tissue inflammation by reducing fat mass and reshaping the immune microenvironment. It promotes the polarization of adipose tissue macrophages from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype. Moreover, exercise alters the secretion profile of adipokines—raising adiponectin levels while reducing leptin and resistin—thereby influencing systemic immune balance. At the circulatory level, exercise improves lipid profiles by lowering pro-inflammatory free fatty acids (particularly saturated fatty acids) and triglycerides, while enhancing high-density lipoprotein (HDL) function, which has immunoregulatory properties such as endotoxin neutralization and macrophage cholesterol efflux. Regarding protein metabolism, exercise triggers the expression of heat shock proteins (HSPs) that act as intracellular chaperones and extracellular immune signals. Exercise also promotes the secretion of myokines (e.g., IL-6, IL-15, irisin, FGF21) from skeletal muscle, which modulate immune responses, facilitate T cell and macrophage function, and support immunological memory. Furthermore, exercise reshapes amino acid metabolism, particularly of glutamine, arginine, and branched-chain amino acids (BCAAs), thereby influencing immune cell proliferation, biosynthesis, and signaling. Leucine-mTORC1 signaling plays a key role in T cell fate, while arginine metabolism governs macrophage polarization and T cell activation. In summary, this review underscores the complex, bidirectional relationship between exercise and immune function, orchestrated through metabolic remodeling. Future research should focus on causative links among specific metabolites, signaling pathways, and immune phenotypes, as well as explore the epigenetic consequences of exercise-induced metabolic shifts. This integrated perspective advances understanding of exercise as a non-pharmacological intervention for immune regulation and offers theoretical foundations for individualized exercise prescriptions in health and disease contexts.
6.Nogo-A Protein Mediates Oxidative Stress and Synaptic Damage Induced by High-Altitude Hypoxia in the Rat Hippocampus.
Jin Yu FANG ; Huai Cun LIU ; Yan Fei ZHANG ; Quan Cheng CHENG ; Zi Yuan WANG ; Xuan FANG ; Hui Ru DING ; Wei Guang ZHANG ; Chun Hua CHEN
Biomedical and Environmental Sciences 2025;38(1):79-93
OBJECTIVE:
High-altitude hypoxia exposure often damages hippocampus-dependent learning and memory. Nogo-A is an important axonal growth inhibitory factor. However, its function in high-altitude hypoxia and its mechanism of action remain unclear.
METHODS:
In an in vivo study, a low-pressure oxygen chamber was used to simulate high-altitude hypoxia, and genetic or pharmacological intervention was used to block the Nogo-A/NgR1 signaling pathway. Contextual fear conditioning and Morris water maze behavioral tests were used to assess learning and memory in rats, and synaptic damage in the hippocampus and changes in oxidative stress levels were observed. In vitro, SH-SY5Y cells were used to assess oxidative stress and mitochondrial function with or without Nogo-A knockdown in Oxygen Glucose-Deprivation/Reperfusion (OGD/R) models.
RESULTS:
Exposure to acute high-altitude hypoxia for 3 or 7 days impaired learning and memory in rats, triggered oxidative stress in the hippocampal tissue, and reduced the dendritic spine density of hippocampal neurons. Blocking the Nogo-A/NgR1 pathway ameliorated oxidative stress, synaptic damage, and the learning and memory impairment induced by high-altitude exposure.
CONCLUSION:
Our results demonstrate the detrimental role of Nogo-A protein in mediating learning and memory impairment under high-altitude hypoxia and suggest the potential of the Nogo-A/NgR1 signaling pathway as a crucial therapeutic target for alleviating learning and memory dysfunction induced by high-altitude exposure.
GRAPHICAL ABSTRACT
available in www.besjournal.com.
Animals
;
Oxidative Stress
;
Hippocampus/metabolism*
;
Rats
;
Nogo Proteins/genetics*
;
Male
;
Rats, Sprague-Dawley
;
Hypoxia/metabolism*
;
Altitude
;
Synapses
;
Humans
;
Altitude Sickness/metabolism*
7.Comparative Transcriptomic and Metabolomic Analyses Reveal the Mechanism by Which Foam Macrophages Restrict Survival of Intracellular Mycobacterium Tuberculosis.
Xiao PENG ; Yuan Yuan LIU ; Li Yao CHEN ; Hui YANG ; Yan CHANG ; Ye Ran YANG ; Xuan ZHANG ; An Na JIA ; Yong Bo YU ; Yong Li GUO ; Jie LU
Biomedical and Environmental Sciences 2025;38(7):781-791
OBJECTIVES:
This study aimed to investigate the impact of foam macrophages (FMs) on the intracellular survival of Mycobacterium tuberculosis (MTB) and identify the molecular mechanisms influencing MTB survival.
METHODS:
An in vitro FM model was established using oleic acid induction. Transcriptomic and metabolomic analyses were conducted to identify the key molecular pathways involved in FM-mediated MTB survival.
RESULTS:
Induced FMs effectively restricted MTB survival. Transcriptomic and metabolomic profiling revealed distinct changes in gene and metabolite expression in FMs during MTB infection compared with normal macrophages. Integrated analyses identified significant alterations in the cyclic adenosine monophosphate (cAMP) signaling pathway, indicating that its activation contributes to the FM-mediated restriction of MTB survival.
CONCLUSIONS
FMs inhibit MTB survival. The cAMP signaling pathway is a key contributor. These findings enhance the understanding of the role of FMs in tuberculosis progression, suggest potential targets for host-directed therapies, and offer new directions for developing diagnostic and therapeutic strategies against tuberculosis.
Mycobacterium tuberculosis/physiology*
;
Transcriptome
;
Metabolomics
;
Foam Cells/microbiology*
;
Humans
;
Metabolome
;
Tuberculosis/microbiology*
;
Gene Expression Profiling
8.Association of Body Mass Index with All-Cause Mortality and Cause-Specific Mortality in Rural China: 10-Year Follow-up of a Population-Based Multicenter Prospective Study.
Juan Juan HUANG ; Yuan Zhi DI ; Ling Yu SHEN ; Jian Guo LIANG ; Jiang DU ; Xue Fang CAO ; Wei Tao DUAN ; Ai Wei HE ; Jun LIANG ; Li Mei ZHU ; Zi Sen LIU ; Fang LIU ; Shu Min YANG ; Zu Hui XU ; Cheng CHEN ; Bin ZHANG ; Jiao Xia YAN ; Yan Chun LIANG ; Rong LIU ; Tao ZHU ; Hong Zhi LI ; Fei SHEN ; Bo Xuan FENG ; Yi Jun HE ; Zi Han LI ; Ya Qi ZHAO ; Tong Lei GUO ; Li Qiong BAI ; Wei LU ; Qi JIN ; Lei GAO ; He Nan XIN
Biomedical and Environmental Sciences 2025;38(10):1179-1193
OBJECTIVE:
This study aimed to explore the association between body mass index (BMI) and mortality based on the 10-year population-based multicenter prospective study.
METHODS:
A general population-based multicenter prospective study was conducted at four sites in rural China between 2013 and 2023. Multivariate Cox proportional hazards models and restricted cubic spline analyses were used to assess the association between BMI and mortality. Stratified analyses were performed based on the individual characteristics of the participants.
RESULTS:
Overall, 19,107 participants with a sum of 163,095 person-years were included and 1,910 participants died. The underweight (< 18.5 kg/m 2) presented an increase in all-cause mortality (adjusted hazards ratio [ aHR] = 2.00, 95% confidence interval [ CI]: 1.66-2.41), while overweight (≥ 24.0 to < 28.0 kg/m 2) and obesity (≥ 28.0 kg/m 2) presented a decrease with an aHR of 0.61 (95% CI: 0.52-0.73) and 0.51 (95% CI: 0.37-0.70), respectively. Overweight ( aHR = 0.76, 95% CI: 0.67-0.86) and mild obesity ( aHR = 0.72, 95% CI: 0.59-0.87) had a positive impact on mortality in people older than 60 years. All-cause mortality decreased rapidly until reaching a BMI of 25.7 kg/m 2 ( aHR = 0.95, 95% CI: 0.92-0.98) and increased slightly above that value, indicating a U-shaped association. The beneficial impact of being overweight on mortality was robust in most subgroups and sensitivity analyses.
CONCLUSION
This study provides additional evidence that overweight and mild obesity may be inversely related to the risk of death in individuals older than 60 years. Therefore, it is essential to consider age differences when formulating health and weight management strategies.
Humans
;
Body Mass Index
;
China/epidemiology*
;
Male
;
Female
;
Middle Aged
;
Prospective Studies
;
Rural Population/statistics & numerical data*
;
Aged
;
Follow-Up Studies
;
Adult
;
Mortality
;
Cause of Death
;
Obesity/mortality*
;
Overweight/mortality*
9.Preservation and Utilization of Clinical Bronchoalveolar Lavage Fluid Specimen
Hui ZHANG ; Le LI ; Yun FANG ; Ning YANG ; Xin YUAN ; Yan LIU
Medical Journal of Peking Union Medical College Hospital 2025;16(6):1587-1592
Bronchoalveolar lavage fluid (BALF) is rich in various bioactive substances such as cytokines and enzymes, making it a high-quality clinical specimen and research sample. It holds significant value in fields such as etiological analysis, proteomics, pathology, and disease diagnosis and treatment. This article systematically reviews the key technical points for the preservation of BALF samples and provides an in-depth interpretation of bronchoalveolar lavage fluid from an application perspective. The aim is to offer references for the standardization of sample preservation practices and to promote the widespread use of BALF samples in clinical research.
10.Clinical characteristics and prognostic analysis of elderly patients with acute myeloid leukemia
Gang ZHANG ; Xiaohui GAO ; Shuping MO ; Yan ZHOU ; Mengjie WU ; Haibing WU ; Xiaoyan ZHAO ; Minchao YAN ; Yuan LI ; Hui ZENG
China Modern Doctor 2025;63(22):1-4
Objective To investigate the clinical characteristics and prognostic risk factors in elderly patients with acute myeloid leukemia(AML).Methods A retrospective analysis was conducted on the clinical data of 101 elderly AML patients admitted to Affiliated Hospital of Jiaxing University from January 2022 to December 2024.All patients were treated with azacitidine+venetoclax regimen.The clinical characteristics of patients and the risk factors related to prognosis were explored.Results The median follow-up was 14 months.Among the 101 patients,74 achieved complete remission or complete remission with incomplete hematological recovery.The median overall survival(OS)of patients with aged ≥70 years,white blood cell count>50 × 109/L,TP53 mutation,complex chromosomes,and high-risk European leukemia net(ELN)risk stratification was significantly shortened(P<0.05).Multivariate analysis showed that age(HR=0.125,95%CI:0.023-0.662,P=0.015),white blood cell count(HR=0.145,95%CI:0.032-0.662,P=0.013),and ELN risk stratification(HR=100.397,95%CI:14.395-700.207,P<0.001)were all independent influencing factors for OS in elderly AML patients.Conclusion Age,white blood cell count and ELN risk stratification are all independent influencing factors affecting OS in elderly AML patients.

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