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- Abstract：Immune-mediated inflammatory diseases （IMIDs） are a broad category of chronic inflammatory disorders caused by abnormal activation of immune system， characterized by an imbalance between excessive release of proinflammatory cytokines and insufficient anti-inflammatory regulatory signals. Interleukin-6 （IL-6）， a pleiotropic cytokine， serves as a "molecular bridge" connecting innate immunity and adaptive immunity due to its unique "trinity" signaling mechanism （classical signaling， trans-signaling， and trans-presenting pathway）. The IL-6 signaling pathway drives acute-phase inflammatory responses and participates in the activation of innate immunity and the regulation of adaptive immunity through multiple mechanisms， which is the key pathway that leads to the inflammatory responses and multi-organ damage of IMIDs.Therapeutic agents targeting the IL-6 pathway， which inhibit aberrant signaling by blocking IL-6/IL-6 receptor/gp130 signaling axis， have been widely used in the clinical practice for treating various IMIDs such as rheumatoid arthritis， juvenile idiopathic arthritis/ adult-onset Still's disease， giant cell arteritis， Takayasu’s arteritis and Castleman's disease. Currently approved medications in this class include tocilizumab， satralizumab， sarilumab， and siltuximab. However， IL-6 inhibitors also encounter various safety challenges in clinical applications， including increased infection risk， metabolic abnormalities and cardiovascular risks， hypofibrinogenemia， and DRESS syndrome. This review systematically elaborates on the molecular mechanism of the IL-6 signaling pathway and its pathogenic role in IMIDs， the progress in the development of targeted drugs， and the safety issues in clinical applications， aiming to promote the transformation of IL-6 targeted therapy from bench to clinic， provide a "mechanism-guided individualized" framework for optimizing treatment decisions， and point out the direction for the establishment of a long-term safety management system.Keywords：interleukin-6;immune-mediated inflammatory diseases;cytokines;targeted therapy;medication management995|2869|1<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：Chikungunya fever （CHIKF） is a mosquito-borne infectious disease caused by Chikungunya virus （CHIKV） infection. The acute phase of CHIKF is mainly characterized by fever， severe polyarthralgia， and rash. Most cases are self-limited， however， atypical manifestations and chronic complications also occur in a minor proportion of cases. High-risk cases are at risk of complicating with severe condition. For these years， the emergence and spread of CHIKF place it as an international public health disease. This article summarizes the current knowledge and advances about CHIKF， with a focus on the diagnosis， differential diagnosis， evaluation， treatment， prevention and control. For individuals with a history of traveling to CHIKF prevalence areas within 12 days， presenting with fever， arthralgia， and rash， combined with laboratory tests such as positive IgM antibody， specific IgG antibody， CHIKV isolation， or viral nucleic acid testing in acute stage， could establish the diagnosis. Differential diagnosis with infection caused by similar viruses such as dengue virus and Zika virus should be considered too. Regarding treatment， there is no specific antiviral drug available currently. Supportive method is the dominating treatment， with non-steroidal anti-inflammatory drugs used to alleviate fever and arthralgia. The core strategy in prevention and control of CHIKF is to interrupt the transmission and eliminate mosquitoes. To meet challenges posed by the spread of CHIKF， the future researches should emphasize on developing specific antiviral drugs， safe and effective vaccines， and convenient and accurate diagnostic means.Keywords：Chikungunya fever;diagnosis;differential diagnosis;treatment;prevention and control820|2746|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
Invited Review
- Abstract：With the acceleration of global population aging， sarcopenia， characterized by a progressive loss of skeletal muscle mass， strength， and physical function， has become a major public health issue that seriously threatens the health and quality of life in older adults. The development and progression of sarcopenia involve complex， multi-level， and cross-system cellular and molecular mechanisms. Recent studies have highlighted the central role of programmed cell death （PCD） in maintaining skeletal muscle homeostasis， regulating metabolism， and mediating tissue repair. The classic forms of PCD-apoptosis， autophagy， pyroptosis， and ferroptosis-interact through critical nodes such as reactive oxygen species（ROS） accumulation， mitochondrial dysfunction， and iron homeostasis disruption， ultimately driving muscle fiber loss， functional decline， and chronic inflammation. These processes underpin the pathology of sarcopenia. Exercise， the most effective non-pharmacological intervention to date， has been shown to precisely regulate multiple PCD pathways. It improves muscle mass， strength， and metabolic stability， and delays the progression of sarcopenia. Specifically， appropriate exercise could inhibit excessive apoptosis， activate protective autophagy， alleviate NLRP3 inflammasome-mediated pyroptosis， and suppress ferroptosis by enhancing antioxidant defenses and maintaining iron homeostasis. This review systematically summarizes the roles and mechanisms of apoptosis， autophagy， pyroptosis， and ferroptosis in sarcopenia. It particularly focuses on the molecular targets and physiological effects of exercise-mediated PCD regulation. The aim is to provide theoretical and practical support for developing personalized and precision exercise interventions targeting PCD pathways for the prevention and management of sarcopenia.Keywords：sarcopenia;programmed cell death;exercise intervention;apoptosis;autophagy;pyroptosis;ferroptosis1203|7030|2<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：The relationship between iron and hypertension has emerged as a significant frontier in cardiovascular research in recent years. Ferroptosis， a newly identified iron-dependent form of regulated cell death， has been demonstrated to play a critical role in the onset and progression of numerous cardiovascular diseases and their related conditions. The core mechanisms of ferroptosis involve dysregulated iron metabolism， lipid peroxidation， and impairment of antioxidant systems， all of which contribute importantly to the pathophysiology of hypertension. Among these， imbalance in iron metabolism and lipid peroxidation are the key drivers of hypertension associated vascular injury， vascular remodeling， and target organ damage. This review systematically summarizes the molecular correlation between ferroptosis and hypertension， focusing on the pathological and physiological mechanisms of iron metabolism disorders and lipid peroxidation， and explores their potential roles in hypertensive pathology. Furthermore， it also analyzes the synergistic physiological and pathological effects for ferroptosis in hypertension. By elucidating the regulatory mechanisms ferroptosis， this work proposes novel perspectives and directions for the early diagnosis and treatment of hypertension， offering a theoretical basis for clinical application. Additionally， therapeutic strategies targeting ferroptosis including iron chelators， antioxidants， and ferroptosis inhibitors are discussed.The aim is to provide a comprehensive and reliable theoretical foundation for future research and to offer innovative ideas for the early diagnosis and intervention of hypertension.Keywords：hypertension;ferroptosis;iron metabolism disorders;lipid peroxidation;iron overload429|1204|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
Hot Spot Tracking: Cell Death
- Abstract：Macrophages， key cells in the heart's innate immune system， are highly heterogeneous and plastic， playing dual roles in cardiac physiology and pathology. In recent years， macrophage-derived exosomes have drawnsignificant attention for their regulatory mechanisms and potential therapeutic applications in heart disease， as they serve as crucial mediators of intercellular communication. This paper aims to comprehensively summarize the origin， distribution， and function of cardiac-resident macrophages. It also explores the roles of M1and M2 macrophages in cardiac inflammatory responses and tissue repair， and delves into the regulatory mechanisms and therapeutic application prospects of macrophage exosomes in heart disease. In the acute phase of cardiac injury， M1 macrophages secrete pro-inflammatory cytokines to induce inflammation and clear cellular debris. Nevertheless， their overactivation can result in myocardial cell damage and fibrosis. During the recovery phase，M2 macrophages take the lead， releasing anti-inflammatory cytokines and growth factors to inhibit inflammation and facilitate tissue repair. Macrophage exosomes， which contain proteins， lipids， and nucleic acids， can regulate inflammation， tissue repair， and angiogenesis. In various types of heart disease， including myocardial infarction， ischemia-reperfusion injury， atherosclerosis， myocarditis， and dilated cardiomyopathy， macrophage exosomes exhibit different functions. While M1-derived exosomes often exacerbate cardiac damage through pro-inflammatory actions， M2-derived exosomes protect cardiac tissue via anti-inflammatory and pro-repair effects. These findings offer new insights and targets for developing macrophage-exosome-based heart disease therapies， which is expected to promote the innovative development of diagnosis and treatment for heart diseases， improve patients' prognosis， and alleviate the burden of public health.Keywords：macrophages;exosomes;heart disease;M1/M2 polarization;cellular communication504|387|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：Bone complications such as osteoporosis and delayed bone healing caused by long-term hyperglycemia in patients with diabetes mellitus （DM） have become clinical problems that significantly reduce their quality of life. The core mechanism is closely related to the impaired osteogenic differentiation ability of adipose-derived stem cells （ADSCs）. In bone tissue engineering， ADSCs are considered as seed cells for bone defect repair due to their minimal invasiveness， rapid proliferation and multi-directional differentiation ability. However， the pathological environment of DM significantly inhibits the osteogenic potential of ADSCs， which affects the treatment efficiency of diabetic bone diseases. Therefore， it is of great significance to explore the underlying mechanism of impaired osteogenic ability of ADSCs in hyperglycemic environment for optimizing the treatment strategy of diabetic bone diseases. This article systematically reviewed and summarized the potential mechanisms of decreased migration ability， reduced proliferation activity， accelerated senescence and apoptosis， and impaired osteogenic differentiation of ADSCs in high glucose environment. High glucose environment can inhibit the expression of osteogenesis-related genes by activating oxidative stress， accumulation of advanced glycation end products， and disrupting Wnt/β-catenin， PI3K/Akt/mTOR， Notch and other key signaling pathways. In addition， DNA methylation in epigenetic modification and non-coding RNA network can jointly silence osteogenic genes. Further elucidation of the above mechanisms not only helps to understand the pathogenesis of diabetic bone diseases， but also provides a direction for the development of intervention strategies. This review aims to promote the application of ADSCs in regenerative medicine for DM management and provide a theoretical basis for further development of strategies for autologous ADSCs repair and treatment of bone defects in DM patients.Keywords：adipose-derived stem cells;osteogenic differentiation;diabetic osteoporosis;diabetes mellitus;bone tissue engineering329|722|1<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：Polycystic ovary syndrome （PCOS）， one of the most prevalent endocrine disorders among women of reproductive age， is characterized by ovulatory dysfunction， hyperandrogenemia， and polycystic ovarian morphology. As a leading cause of female infertility， PCOS affects 6%-20% of women globally. The complex and heterogeneous nature of PCOS has hindered the full elucidation of its pathogenesis. Emerging evidence suggests that gut microbiota dysbiosis and abnormal bile acid metabolism may contribute to the development of PCOS. Patients with PCOS exhibit reduced alpha diversity of gut microbiota， marked by decreased butyrate-producing bacteria and the proliferation of harmful genera such as Bacteroides. This shift leads to intestinal barrier dysfunction， chronic inflammation， and exacerbation of insulin resistance and hyperandrogenemia through dysregulation of short-chain fatty acid and sex hormone metabolism. Additionally， PCOS patients display distinct bile acid metabolic abnormalities， including elevated total bile acids， impaired classical synthesis pathways， activated alternative pathways， and abnormal accumulation of primary unconjugated bile acids. A bidirectional regulatory axis exists between gut microbiota and bile acids： microbiota modulate bile acid synthesis and metabolism， while bile acids shape microbial composition and abundance. Dysregulation of this gut microbiota-bile acid axis promotes the pathogenesis of PCOS. Therefore， optimizing gut microbiota composition and modulating bile acid metabolism represent novel therapeutic targets for PCOS. Further mechanistic exploration requires integrated animal models and population-based cohort studies to address individualized variability and safety concerns. This review summarizes the roles of gut microbiota and bile acid metabolism in PCOS pathogenesis， highlights their interactions， and discusses therapeutic potential， aiming to provide insights for both theoretical research and clinical management.Keywords：polycystic ovary syndrome;gut microbiota;bile acid metabolism;hyperandrogenemia;insulin resistance436|1418|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：With the intensification of population aging， the proportion of people with dementia in our country is rising sharply， bringing a heavy economic and caregiving burden to families and society. Alzheimer's disease （AD） is a spectrum of progressive cognitive impairment disorders that onset in old age， characterized by memory decline， reduced attention and executive function， and in the late stages of the disease， it can even progress to dementia， ultimately leading to the loss of self-care abilities and further increasing the pressure on families and society. Patients with Alzheimer's disease （AD） can be in a preclinical stage for decades without obvious clinical cognitive decline， but significant pathological changes have already occurred in the brain， including the aggregation of beta-amyloid （Aβ） to form senile plaques， the hyperphosphorylation and aggregation of tau protein to form neurofibrillary tangles， vascular amyloid deposition， synaptic and neuronal loss， as well as neuroinflammation. This stage represents the best opportunity for early intervention in AD. Accurate diagnosis or prediction of AD risk and implementation of intervention measures can significantly delay or prevent the progression of AD. In recent years， the application of various tracers that track the neuropathological changes of AD in PET/CT has led to significant progress in clinical research on the imaging diagnosis， treatment monitoring， and prognostic prediction of preclinical and early-stage AD. This article will review the application of PET/CT and PET/MR techniques marked with Aβ， tau protein， fluorodeoxyglucose （FDG）， synaptic， and inflammatory tracers in the early diagnosis， differential diagnosis， disease staging， treatment monitoring， and prognostic prediction of AD， and compare the relative utility and limitations of these tracers as biomarkers， providing a basis and reference for clinicians to choose appropriate PET markers in the research of early diagnosis and treatment of preclinical AD and early-stage AD.Keywords：PET/CT;Alzheimer's disease;tracers;PET/MR;early diagnosis and treatment483|1591|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
Review
- Abstract：ObjectiveTo explore the molecular mechanism of the chemo-resistance in NR2F1-mediated dormant ovarian cancer（OC） cells.MethodsThe expression of the NR2F1 molecule in OC patients and its relationship with the overall survival of patients were analyzed using the GEPIA database. Nuclear receptor subfamily 2 group F member 1（NR2F1） overexpressed OC cell and control cell were constructed by lentivirus in vitro transfection. The proliferation of OC cells was analyzed by CCK-8 method. Real-time fluorescent quantitative PCR（qRT-PCR） was used to analyze the mRNA expression of dormancy-related molecular genes in OC cells. Western blot was performed to analyze the protein expression levels of related molecules. The viability of OC cells treated with different chemotherapy drugs was analyzed by trypan blue exclusion method. Annexin V-FITC/PI double-staining assay was used to detect the apoptosis of OC cells treated by different chemotherapy drugs. Transcriptome sequencing technology was used to analyze the differentially expressed genes in NR2F1 overexpressed SKOV3 cell line， and the relevant signaling pathways were screened through KEGG enrichment analysis. qRT-PCR was performed to verified the mRNA expression level of drug resistance-related molecules in OC cells. The GEPIA database was used to further verify the correlation between the expression of NR2F1 and the drug resistance-related genes.ResultsThe NR2F1 expression is low in the tumor tissues and the high expression of NR2F1 correlates with poor overall survival in the OC patients. Compared with the control group， the proliferation ability of the NR2F1 overexpressed OC cell lines was significantly reduced. The expression of dormancy-related molecules， cyclin-dependent kinase inhibitor 1B（p27）， differentiated embryonic cartilage gene-2（DEC2） and transforming growth factor-β2（TGF-β2）， increased significantly in the NR2F1 overexpressed OC cell lines， and anti-apoptotic molecule B-cell lymphoma gene-2（BCL-2） also increased. In contrast， the expression of the proliferation-related molecule KI67 was decreased. In addition， the NR2F1 overexpressed OC cell lines significantly enhanced the resistance to chemotherapy drugs. Transcriptome sequencing and KEGG enrichment analysis showed that the upregulated genes in NR2F1 overexpressed OC cells were enriched in phosphatidylinositol-3-kinase-protein kinase（PI3K-Akt） signaling pathway， focal adhesion pathway， extracellular matrix-receptor interactions and signaling pathways regulating pluripotency of stem cells， and the downregulated genes in NR2F1 overexpressed OC cells were mainly enriched in cell cycle pathway. The results of qRT-PCR verification showed that drug resistance-related molecules kinesin family member 26B（KIF26B）， secreted protein acidic and rich in cysteine（SPARC）， collagen type Ⅵ alpha 1（COL6A1）， collagen type Ⅴ alpha 2 chain（COL5A2）， frizzled homolog 1（FZD1） and inhibin subunit beta A gene（INHBA） were up-regulated in NR2F1 overexpressed OC cells. GEPIA database analysis showed that the expression of NR2F1 in OC tumor tissues was positively correlated with the expression of drug resistance-related genes KIF26B， SPARC， COL6A1， COL5A2， FZD1 and INHBA.ConclusionsThis study shows that upregulation of NR2F1 may induce dormancy in OC cells and enhance their resistance to chemo-drugs. The NR2F1-mediated drug resistance of dormant OC cells might be associated with the PI3K-Akt signaling pathway and signaling pathways regulating pluripotency of stem cells， and closely related to the upregulation of KIF26B， SPARC， COL6A1， COL5A2， FZD1 and INHBA.Keywords：dormancy;nuclear receptor subfamily 2 group F member 1;ovarian cancer;chemotherapeutic agents;drug resistance396|796|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo investigate the dynamic expression profiles and potential regulatory mechanisms of long non-coding RNAs （lncRNAs） in male reproductive system aging.MethodsA naturally aging C57BL/6 mouse model was used and 4 mice were selected each at 3， 15， and 21 months of age. RNA was extracted from seven regions of the male reproductive tract （testis， efferent duct， initial segment of epididymis， caput epididymis， corpus epididymis， cauda epididymis， and vas deferens）， followed by RNA sequencing and bioinformatics analysis.ResultsRegion-specific dynamic expression profiles of lncRNAs were constructed in the testis， epididymis （efferent duct， initial segment， caput， corpus， and cauda）， and vas deferens of male mice. Combined with gene functional enrichment analysis， the functional associations of lncRNAs were elucidated in reproductive system aging. The differentially expressed lncRNAs in the aging testis were primarily involved in hormone biosynthesis and extracellular matrix organization， while those in the initial segment of the epididymis were closely related to cell recognition and epithelial cell migration. A comprehensive lncRNA expression atlas associated with male reproductive aging was established.ConclusionLncRNAs may participate in male reproductive aging through the regulation of the reproductive microenvironment， which provides key molecular targets and a research foundation for understanding age-related fertility decline.Keywords：long non-coding RNAs;male reproductive tract;reproductive aging;testis;epididymis359|1006|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo investigate the effect of secreted frizzled related protein 1（SFRP1） via Wnt/β-catenin signaling pathway on calcification of vascular smooth muscle cell.MethodsPrimary human aortic vascular smooth muscle cells were transfected with SFRP1-specific small interfering RNA （siSFRP1） to knock down SFRP1 expression， transfected with lentiviral vector Lenti-Sfrp1 to overexpress SFRP1， and stimulated with 3 mmol/L sodium dihydrogen phosphate （Pi） to establish a cellular vascular calcification model. In vivo， a mouse model of acute vascular calcification was established using vitamin D3 （VD3） treatment. The SFRP1 inhibitor WAY-316606 was administered intraperitoneally （0.5 mg/kg daily for 7 days）. Aortic calcification was quantified by micro-computed tomography （micro-CT）. Western blot analysis was performed to detect the expression of osteogenic differentiation markers （RUNX2 and BMP2）， vascular smooth muscle cell contractile marker SM22α， and β-catenin protein in the Wnt signaling pathway. The severity of vascular calcification was evaluated through calcium content measurement and Alizarin Red staining. These approaches were employed to investigate the effect of SFRP1 on VSMC calcification.ResultsIn the primary human vascular smooth muscle cell calcification model and the acute vascular calcification model， the expression of SFRP1 protein was significantly down-regulated （0.30
- Abstract：ObjectiveTo explore the protective effect of glucocorticoid-induced transcription factor 1 （GLCCI1） on cognitive dysfunction in diabetic mice and its mechanism.MethodsTwenty-four C57BL/6J mice were randomly divided into 4 groups， namely Control， DM， DM+AAV-Glcci1， and DM+AAV-NC. The Control group was intraperitoneally injected with saline， while the other groups were all injected with streptozotocin （STZ）. Two weeks after successful modeling， the DM+AAV-Glcci1 group was brain stereotactic injected with Glcci1 overexpressing adeno-associated virus， and the DM+AAV-NC group was stereoscopically injected with the control virus. After 12 weeks， the Morris water maze test was used to evaluate the learning and memory abilities of mice in each group. Subsequently， the localized expression of GLCCI1 in the hippocampus were determined by immunofluorescence and immunohistochemistry experiments. The myelin morphology in the hippocampus was observed by LFB staining， the neuronal morphology was observed by Nissl staining， and the myelin-related proteins MBP and CNPase were stained by immunohistochemistry. Molecular docking was used to predict the interaction between GLCCI1 and HSPA5. The expression of endoplasmic reticulum stress-related proteins was detected by Western blot.ResultsThe results of the behavioral experiment showed that compared with the mice in the Control group， DM mice exhibited obvious cognitive dysfunction behaviors （P＜0.000 1）， and the learning and memory abilities of mice improved after overexpression of Glcci1 （P=0.000 7）. The results of immunofluorescence and immunohistochemistry showed that GLCCI1 was expressed in hippocampal neuron cells. Compared with Control mice， the expression level of GLCCI1 in DM mice was significantly downregulated （P＜0.000 1）. The molecular docking results revealed that GLCCI1 interacts with HSPA5. The Western blot results indicated that， compared with the Control group， the expression levels of endoplasmic reticulum stress-related proteins HSPA5 （P＜0.000 1）， ATF4 （P＜0.000 1）， ATF6 （P=0.001 1）， and p-ELF2α/elF2α （P=0.000 1） in the DM group were significantly increased； Compared with the DM group， the expression of the corresponding protein HSPA5 （P＜0.000 1）， ATF4 （P＜0.000 1）， ATF6 （P=0.000 2）， and p-ELF2α/elF2α （P=0.000 1） was significantly down-regulated after overexpression of Glcci1. LFB staining showed that compared with the Control group， the myelin integrity of DM mice decreased significantly （P=0.010 3）， the expressions of myelin-related proteins MBP and CNPase decreased significantly （P=0.000 4， P=0.000 2）， and Nissl staining observed disordered neuronal arrangement. Compared with the mice in the DM group， the myelin integrity in the hippocampal region significantly increased after overexpression of Glcci1 （P=0.000 3）， the expressions of myelin-related proteins MBP and CNPase significantly increased （P=0.001 4， P=0.000 1）， and the ordered arrangement of neurons was observed by Nissl staining.ConclusionThe down-regulation of GLCCI1 expression in hippocampal neurons promotes demyelination of hippocampal neurons and thereby induces diabetic cognitive dysfunction. The specific mechanism may be related to endoplasmic reticulum stress.Keywords：glucocorticoid-induced transcription factor 1;demyelination;endoplasmic reticulum stress;neuron;diabetic cognitive dysfunction255|305|1<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo explore the relationship between self-assessed health and age-adjusted Charlson comorbidity index （AICC） in older adults， and to further analyze the differences in this relationship across gender groups.MethodsBased on the China health and retirement longitudinal study （CHARLS） database， this study selected data on basic characteristics， chronic disease status， depressive symptoms， and self-assessed health of older adults aged ≥60 years. Chi-square tests were used to perform a preliminary analysis of the association between these factors and AICC scores. A multifactorial ordered logistic regression model was constructed to assess the effects of each influencing factor on AICC， while multiple linear regression analysis was used to explore the linear relationship between self-rated health and AICC scores. Additionally. Stratified analysis by gender was performed to evaluate gender differences.ResultsA total of 10 911 participants were included， with a mean age of 67.40±5.94 years； 6 249 （57.3%） were male and 4 662（42.7%） were female. The distribution of AICC scores was categorized into low-risk， moderate-risk， higher-risk， and high-risk groups， accounting for 23.5%， 50.2%， 20.6%， and 5.7%， respectively. Multifactorial logistic regression analysis revealed that self-rated health was negatively associated with AICC in the total population and in the male geriatric group （OR=0.843， 95% CI： 0.776， 0.917， P=0.001）， （OR=0.886， 95% CI： 0.796 ， 0.987， P=0.028）， but did not reach statistical significance in the female geriatric group . Linear regression analysis further indicated a significant negative linear relationship between self-rated health and AICC （b=-0.485， 95% CI： -0.516，-0.455， P＜0.001）.This relationship was consistent in both male （b=-0.356， 95% CI： -0.406，-0.305， P＜0.001） and female （b=-0.373， 95% CI： -0.435，-0.310， P＜0.001） subgroups， with a stronger negative association in females.ConclusionSelf-rated health is significantly negatively associated with AICC， and attention should be given to self-rated health in the female geriatric population. Self-rated health can serve as an important tool for identifying elderly group at high risk of comorbidities providing a valuable basis for precise intervention.Keywords：elder;self-assessed health;age-corrected Charlson co-morbidity index;gender differences;cross-sectional study285|614|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
Preclinic Research
- Abstract：ObjectiveTo investigate the association between Eya3 expression and CD8+ T cell infiltration levels in the tumor microenvironment， as well as their prognosis in esophageal carcinoma （EC） patients following neoadjuvant chemoradiation （neo-CRT）.MethodsThe pathological specimens before treatment and after surgery and clinical data were collected from 50 patients with EC who received neo-CRT combined with surgery. The correlation between the Eya3 expression and postoperative pathological features， CD8+ T cell infiltration levels， disease-free survival（DFS） and overall survival （OS） were analyzed using immunohistochemistry（IHC） and multicolor immunofluorescence staining.ResultsThe rate of pathological complete response （pCR） was higher in patients with low baseline Eya3 expression in the EC before treatment（P=0.001 8）. Both median DFS （37.2 months vs. 15.3 months， HR：2.731，95% CI：1.167-6.394，P=0.021） and median OS （not reached vs. 26.7 months， HR：3.959，95%CI：1.539-10.18，P=0.004 3） are significantly longer for patients with low Eya3 than those with high Eya3. The expression of Eya3 significant negatively correlated with tumor-infiltrating CD8+T lymphocytes （ P＜0.001）， GZMB+CD8+T lymphocytes P=0.002） in surgical pathological specimens . The patients with high CD8+T lymphocytes and GZMB+CD8+T lymphocytes had significantly longer DFS than those with low level.ConclusionPatients with EC who have high expression of Eya3 have a poorer prognosis， and the infiltration levels of CD8+T lymphocytes and GZMB+CD8+T lymphocytes in the tumor microenvironment are lower. This suggests that the expression of Eya3 may affect the tumor immune microenvironment and thereby influence the prognosis of EC patients， and it may become a molecular marker for predicting the prognosis of EC patients..Keywords：esophageal carcinoma;neoadjuvant chemoradiation;Eya3;CD8+ T lymphocytes;antitumor immunity304|508|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo investigate pulmonary function levels and associated influencing factors among rural elderly in Guangzhou， to identify high-risk populations for poor pulmonary function， and to reveal the relationship between the influencing factors of pulmonary function.MethodsWe recruited 1 500 residents aged 60 to 94 years from rural area of Conghua District， Guangzhou City using convenience sampling in 2023. Data on demographics， body measurements， medical history and lifestyle were collected via face-to-face questionnaires and physical examination. Meanwhile， expiratory function parameters including forced expiratory volume in one second （FEV1）， forced vital capacity （FVC）， FEV1/FVC， and the prevalence of airflow obstruction （AFO） were assessed using a portable spirometer. Age and sex distribution of pulmonary function in older adults at 5-year intervals was reported， and risk factors of AFO using multifactorial logistic regression models were analyzed. Furthermore， path analysis was further employed to explore the role of lifestyle in the association between other influencing factors and lung function.ResultsAmong the 1 500 participants， the median age was 71 years （67-75）， and 44.2% were male. Subjects identified as AFOs were generally older， more likely male， less educated， and had lower rates of moderate to vigorous physical activity （＜1 time/week） and lower lean body mass. Mean FEV1/FVC ratio was （82.0±16.4） %. FEV1/FVC was （79.80±17.58） % in men and （83.66±15.22） % in women. Older age， lower education， male sex and leanness were negatively associated with all pulmonary function outcomes （all P values＜0.05）. Path analysis identified that age， gender， marital status， occupation and income may influence pulmonary function indirectly through lifestyle.ConclusionRural elderly in Guangzhou exhibited lower pulmonary function levels， and male sex， non-married status， advanced age， lower education， smoking habits， insufficient engagement in moderate to vigorous physical activity， and lean body type were all associated with worse pulmonary function.Keywords：pulmonary ventilation;influencing factors;aged people;rural areas;cross-sectional study315|886|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo investigate the relationship between the non-fasting triglyceride and glucose （TyG） index and hyperglycemia in pregnancy during the third trimester in high altitudes.MethodsThis study selected clinical and laboratory data of 774 Tibetan singleton pregnant women who delivered at Chaya People's Hospital of Qamdo city in Xizang autonomous region， from January 2023 to April 2025. The non-fasting TyG index was calculated from non-fasting triglyceride （TG） and random plasma glucose （PG）. Based on the tertiles of the non-fasting TyG index values， the individuals were split into three groups （corresponding to non-fasting TyG index of 8.89 and 9.21， respectively）. The baseline clinical characteristics， lipid levels and the occurrence of developing hyperglycemia in pregnancy were compared among the three groups. Statistical analyses were performed using ANOVA， Kruskal-Wallis H test， Chi-square test， or Fisher exact test and the relationship between the non-fasting TyG index and hyperglycemia in pregnancy were examined using multivariate logistic regression models and curve fitting.ResultsA total of 774 Tibetan singleton pregnant women were included， with a average age of 27.3 ± 6.1 years， a pre-delivery body mass index （Pre-BMI） of （25.2±2.3）kg/m2 ， a proportion of 26.7% （207/774） primigravid women， the mean non-fasting TyG index was 9.1 ± 0.4。Thirty pregnant women were diagnosed with hyperglycemia in pregnancy， with a detection rate of 3.9% （30/774）. Statistically significant differences in serum total cholesterol （TC）， TG， low-density lipoprotein cholesterol （LDL-C） and high-density lipoprotein cholesterol （HDL-C） levels were identified when comparing different non-fasting TyG groups （all P values <0.05）. Subsequent trend test analysis indicated that the levels of TC， TG， LDL-C， and PG gradually increased with elevated the non-fasting TyG index （ Ftrend TC=95.61， P<0.001； Ftrend TG=1 051.91， P<0.001； Ftrend LDL-C = 97.20， P < 0.001； Ftrend TG=195.20； P<0.001）. After adjustment for maternal age， pre-delivery BMI， altitude， TC， LDL-C， and HDL-C， multivariate Logistic regression models revealed independent positive associations between non-fasting TyG index and hyperglycemia in pregnancy （Model 1： OR=2.72， 95% CI： 1.13-6.53， P=0.026； Model 2： OR=2.56， 95% CI： 1.01-6.50， P=0.048； Model 3： OR=2.72， 95% CI： 1.06-6.97， P=0.037； Model 4： OR=4.02， 95% CI： 1.42-11.40， P=0.009） and the incident of hyperglycemia in pregnancy showed an increasing tendency as increasing with the non-fasting TyG index， however， this association did not statistical significance （P trend >0.05）. Curve fitting by restricted cubic splines （RCS） were used to assess linearity between non-fasting TyG and hyperglycemia in pregnancy， and there was a linear dose-response relationship between non-fasting TyG and hyperglycemia in pregnancy （P for non-linear = 0.515）.ConclusionNon-fasting TyG index in the third trimester is a risk factor for hyperglycemia in pregnancy among the Tibetan singleton pregnant women at high altitudes and there was a possible linear dose-response relationship between the non-fasting TyG index and hyperglycemia in pregnancy.Keywords：altitude;Tibetan;pregnancy trimester， third;non-fasting triglyceride-glucose index;hyperglycemia in pregnancy315|460|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveHepatic tuberculosis （HTB）， an exceptionally rare and clinically heterogeneous form of extrapulmonary tuberculosis， is frequently misdiagnosed as hepatocellular carcinoma， lymphoma， or pyogenic liver abscess， this diagnostic challenge contributing to persistently high rates of missed and incorrect diagnoses. This study aims to systematically analyze clinical profiles of HTB patients to provide evidence-based guidance for early identification， accurate diagnosis， and timely intervention.MethodsWe conducted a retrospective analysis of all HTB cases confirmed at Sun Yat-sen Memorial Hospital between January 2012 and December 2023. Comprehensive data were collected and evaluated， including demographic characteristics， clinical presentations， laboratory findings， imaging features， and histopathological results.ResultsTen patients （9 males， 1 female； mean age 44.6±15.5 years） were enrolled totally， with prevalent symptom of abdominal pain or distension （8/10）. Among the patients tested， purified protein derivative （PPD） was positive in 2 of 6 cases， serum tuberculosis antibody was positive in 1 of 5， and T-cell spot of tuberculosis （T-SPOT） was positive in 3 of 5. Chest imaging （n=9） revealed active miliary tuberculosis in 1 case and inactive post-tuberculous sequelae in 5 cases， while the remainder showed no abnormalities. Contrast-enhanced CT （n=6） demonstrated hypodense patchy or nodular lesions with absent or mild heterogeneous enhancement. MRI （n=3） showed well-circumscribed oval/round hypointense lesions on T1-weighted imaging （T1WI） and mildly hyperintense ones on T2-weighted imaging （T2WI） and diffusion weighted imaging （DWI）. Percutaneous or surgical liver biopsy was performed in 8/10 cases， revealing chronic granulomatous inflammation in all subjects and acid-fast bacilli in 2 specimens.ConclusionHTB lacks pathognomonic clinical or radiological features， and conventional laboratory tests exhibit low sensitivity. A high index of suspicion is warranted for patients presenting with hepatic nodular lesions accompanied by fever， abdominal pain， or emaciation. Early pathogen detection and histopathological confirmation via liver biopsy are critical to minimize diagnostic delays and ensure prompt initiation of anti-tuberculous therapy.Keywords：hepatic tuberculosis;clinical features;histopathological diagnosis;early identification;retrospective analysis326|1193|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo explore the outcomes and surgical experiences of 267 cases of extracardiac conduit total cavopulmonary connection （TCPC） in patients with functional single ventricles.MethodsClinical data were collected from 267 patients who underwent extracardiac conduit TCPC at Guangdong Provincial People's Hospital from October 2004 to August 2021. Among them， 185 were male （69.3%） and 82 were female （30.7%）. The age was 5.71 （4.08-10.90） year， and the weight was 17.5 （14.5-26.2） kg. A median sternotomy approach was used， and the surgery was completed under cardiopulmonary bypass. The preoperative， intraoperative and postoperative follow-up data of the patients were collected， and the survival prognosis and its influencing factors were analyzed.ResultsThe operative time was 330.0 （267.5-405.0） min， the cardiopulmonary bypass time was 124.0 （96.0-163.0） min， and the aortic cross-clamp time was 48.0 （0.0-81.0） min. The duration of mechanical ventilation after surgery was 8.7 （5.0-19.1） h， and the hospital stay was 34.0 （28.0-49.0） d. The follow-up period was 8.0 （4.6-11.0） year， with 8 early deaths （3.0%）， 20 late deaths （7.5%）. The independent risk factors of fatality in patients after extracardiac conduit TCPC included male， heterotaxy syndrome， preoperative pulmonary artery pressure， intraoperative blood loss， the duration of mechanical ventilation， and the 48 h average vasoactive-inotropic score.ConclusionsThe extracardiac conduit TCPC is quite effective in treating patients with functional single ventricle. The early postoperative fatality is low， while the late fatality is relatively high. Therefore， it is necessary to pay close attention to the long-term survival situation of this group of patients. The analysis of risk factors emphasizes the importance of perioperative refined assessment and individualized treatment. It may help further improve the therapeutic outcomes of such surgeries， including selecting appropriate patients， performing careful operations， ensuring meticulous hemostasis， and shortening the duration of postoperative mechanical ventilation.Keywords：single ventricle;total cavopulmonary connection;extracardiac conduit;fatality;influence factors263|597|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo develop a classification model based on complete blood count （CBC） parameters combined with clinical factors to predict severe respiratory infections caused by Human adenovirus （HAdV） in pediatric patients.MethodsFrom September 2023 to September 2024， the CBC parameters and related clinical data from pediatric patients diagnosed with HAdV infection were collected. Principal component analysis and random forest models were used to identify potential predictors of severe cases.ResultsA total of 668 pediatric patients were included， with 564 cases assigned to the training cohort and 104 cases to the validation cohort. Severe cases were defined as pneumonia and/or fever lasting ≥5 days （pneumonia or prolonged fever， PorPF）. Principal component analysis and feature importance analysis （Mean Decrease Gini value） identified the monocytosis ratio （PMono）， red blood cell count （RBC）， and platelet count （PLT） as the most critical CBC parameters. Logistic regression analysis revealed that oxygen therapy （OR = 4.367， 95% CI： 1.568–12.161） and increased work of breathing （OR = 3.904， 95% CI： 2.146–7.101） were relative risk factors for PorPF. Meanwhile， higher PMono （OR = 0.696， 95% CI： 0.640–0.757）， RBC （OR = 0.201， 95% CI： 0.124–0.325）， and PLT （OR = 0.990， 95% CI： 0.987–0.994） were protective factors. When PMono was used as a predictive marker for PorPF， the area under the receiver operating characteristic curve （AUC） was 0.648 and 0.705， respectively. A random forest model incorporating four risk factors ［PMono， RBC， PLT， and hematocrit （HCT）］ was constructed to classify PorPF and general cases， achieving AUCs of 0.688 and 0.768， respectively.ConclusionsPMono， RBC， and PLT may serve as characteristic CBC indicators for predicting pneumonia or prolonged fever in children with HAdV infection. A risk factor model built using PMono， RBC， PLT， and HCT offers a relatively simple and accurate approach to predicting severe cases in pediatric HAdV infections.Keywords：Human adenovirus;complete blood count;pediatrics;pneumonia;fever249|575|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
- Abstract：ObjectiveTo analyze the clinical characteristics and imaging features of effectively treated pediatric Mycoplasma pneumoniae pneumonia （MPP） with pulmonary consolidation， follow up the volume changes of pulmonary consolidation on lung CT scans of the affected children， and investigate the resolution patterns of pulmonary consolidation， and predict the time required for complete resolution.MethodsWe enrolled children with MPP and pulmonary consolidation hospitalized in the Department of General Pediatrics at Children's Hospital of Chongqing Medical University between January 2018 and May 2024. Data collected included demographics， clinical symptoms， laboratory indicators， treatment status， imaging data during hospitalization， as well as follow-up lung CT data and reexamination intervals after discharge. Consolidation volumes were measured before and after the treatment to calculate the resolution rate and resolution velocity. Descriptive statistical analysis was performed on clinical characteristics， imaging features and consolidation resolution.ResultsAmong 238 children with MPP and lung consolidation， females slightly outnumbered males （the male to female ratio is 109 vs.129）， with a mean age of approximately 5 years. At admission， the median cough and fever durations were 7 （5-9） days and 6 （ 4-7） days， respectively. No significant increase was found in white blood cells count or lactate dehydrogenase（LDH）， and hypersensitive high-sensitivity C-reactive protein （CRP） slightly increased. Azithromycin was the first line of treatment in most cases， though second-line drugs increased in the recent two years due to the rising resistance. Bronchoalveolar lavage was performed in 66.8% （159/238） of children， and 33.2% （79/238） did not receive lavage. Consolidation was predominantly unilateral （206 unilateral vs. 32 bilateral） and right-sided （117 right-sided vs. 89 left-sided）. The ratio of consolidation volume to total lung volume was 4.48 （2.61-7.35） %， the consolidation resolution rate at follow-up was 96.08 （ 88.02-98.95） %， the reexamination interval was 17 （ 15-21） days， the resolution velocity was 2.15 （1.23-4.01） cm3/d， and the time to complete resolution was 18.96 （16.14-23.33） days .ConclusionsPulmonary consolidation in pediatric MPP achieves substantial resolution on CT within 2-3 weeks after effective clinical treatment. Initial consolidation volume and resolution velocity can predict the time required for complete resolution， thereby clinically guiding optimal CT follow-up scheduling.Keywords：children;Mycoplasma pneumoniae pneumonia;lung CT;pulmonary consolidation volume;consolidation resolution velocity354|1329|0<HTML><L-PDF> <Meta-XML>Updated：2025-09-20
Clinical Research
