With the accelerating trend of population aging, the number of elderly patients with lung cancer continues to rise, and the disease burden is becoming increasingly heavy. The clinical management of these patients faces severe challenges due to their decreased physiological reserve, complex comorbidities, and significant individual heterogeneity. Consequently, under traditional diagnosis and treatment models, doctors often struggle to identify the individualized risks of elderly patients in a timely and comprehensive manner, which can easily lead to decision biases such as undertreatment or overtreatment. In view of this, this study advocates for the establishment of an umbrella decision-making model specifically tailored for elderly lung cancer patients. Grounded in a multidisciplinary team (MDT) platform, this model deeply integrates oncological indicators with the comprehensive geriatric assessment (CGA) system. By holistically considering multidimensional variables including tumor burden, organ function, frailty index, cognitive status, and social support, the model establishes an operational mechanism characterized by "single entry, precise stratification, and targeted selection". Accordingly, patients can be scientifically triaged into distinct intervention tiers, such as active surveillance, minimally invasive surgery, drug therapy, radiotherapy, and best supportive care, thereby achieving real-time alignment between treatment intensity and patient fitness. This article elaborates on the construction logic and key operational procedures of this novel decision-making framework, aiming to guide clinical practice beyond the limitations of a tumor-centric perspective toward a holistic, dynamic, whole-course management strategy. This transition seeks to ensure optimal quality of life and clinical net benefit for elderly patients alongside survival prolongation.

Objective To explore the clinical characteristics of autoimmune encephalitis (AE) and the related factors of social frailty. Methods A total of 412 patients with AE admitted to the hospital between January 2020 and August 2025 were collected as research subjects. According to the occurrence status of social frailty, the above patients were classified into social frailty group (n=166) and control group (n=246). The clinical data of patients were analyzed, Multivariate logistic regression analysis was used to analyze the related factors of social frailty in patients with AE.. Results Among the 412 patients, 166 cases (40.29%) had social frailty and 246 cases (59.71%) did not have social frailty. The proportions of age≥40 years old, language disorder, epileptic seizure, acute onset and abnormal cranial magnetic resonance imaging (MRI) in the social frailty group were higher than those in the control group (Multivariate logistic regression analysis was used to analyze the related factors of social frailty in patients with AE.P<0.05). Age≥40 years old, language disorder, acute onset, Abnormal cranial magnetic resonance imaging is a related factor for the occurrence of social frailty in patients with AE (P<0.05). The area under the curve of the logistic regression model for prediction was 0.851, suggesting that the model had good predictive value. Conclusion Age, language disorder, epileptic seizure, acute onset and cranial MRI abnormality are important risk factors of social frailty in patients with AE. The prediction model based on these factors exhibits good clinical application value.

Treatment resistance, recurrence, and metastasis of breast cancer remain critical issues affecting long-term patient survival. Chronic psychological stress may act as a host biological driver of breast cancer treatment resistance rather than a mere comorbidity. Through the sustained activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, also referred to as the "brain-tumor axis", stress signaling reshapes inflammatory, immune, and metabolic networks within the tumor microenvironment and thereby influences chemotherapy, endocrine therapy, anti-HER2 therapy, immunotherapy, and radiotherapy. Current evidence indicates that the key pathways with translational potential are mainly the β-adrenergic axis and the glucocorticoid receptor (GR) pathway. The former is more involved in amplifying inflammatory responses, promoting immunosuppression and metastasis, whereas the latter is closely associated with anti-apoptosis, maintenance of tumor stemness, and reprogramming of estrogen receptor function. This review focuses on the discrepancies in evidence regarding these pathways between population-based studies and preclinical models, and discusses clinically operable non-pharmacologic interventions such as cognitive behavioral stress management, nurse navigation and treatment adherence support, and exercise interventions during the neoadjuvant phase. Although high-level evidence for direct survival benefit remains limited, these interventions have shown favorable effects on cortisol levels, depressive symptoms, quality of life, adherence, relative dose intensity, and some biology-related intermediate endpoints, making them valuable complementary approaches in comprehensive breast cancer management.

OBJECTIVE To investigate the mechanism of Yangfei tongluo formula in delaying airway remodeling in post-infectious bronchiolitis obliterans （PIBO） model rats.METHODS Forty-eight 2-week-old SPF male SD rats were randomly divided into control group （Control group）， PIBO model group （Model group）， Prednisone Acetate tablets+Azithromycin tablets group [positive control group， Prednisone Acetate tablets 0.006 3 g/（kg·d）+Azithromycin tablets 0.031 5 g/（kg·d）]， and high-， medium-， and low-dose Yangfei tongluo formula groups [42.42， 21.21， 10.60 g/（kg·d）]. The PIBO rat model was established by intratracheal instillation of diacetyl. After modeling， rats in each group were administered corresponding drug solution or distilled water by gavage once daily for 21 consecutive days. Hematoxylin-eosin staining was used to evaluate the pathological changes of lung tissue， and Masson staining was used to assess the degree of pulmonary fibrosis. Western blot and real-time quantitative PCR were performed to detect the protein and mRNA expression levels of epithelial-mesenchymal transition （EMT）-related markers [E-cadherin， N-cadherin， α -smooth muscle actin （ α -SMA）， Vimentin] and transcription factors [snail homolog 1（Drosophila）-like 1 protein （Snail1）， zinc finger E-box-binding homeobox protein 1 （ZEB1）， Twist-related protein 1 （Twist1）] in lung tissue. ELISA was used to detect the levels of transforming growth factor-β 1 （TGF-β 1 ） and vascular endothelial growth factor （VEGF） in blood and bronchoalveolar lavage fluid.RESULTS Compared with the Control group， the lung tissues of rats in the Model group showed extensive destruction of alveolar structure and massive inflammatory cell infiltration in the interstitium. The protein and mRNA expression levels of E-cadherin were significantly decreased， while the protein and mRNA expression levels of N-cadherin， Vimentin， α -SMA， Snail1， ZEB1， and Twist1， as well as the collagen-positive area and the levels of TGF-β 1 and VEGF， were significantly increased （ P ＜0.05）. Compared with the Model group， the pathological injury of lung tissue in each administration group was significantly improved， and the above indicators （except collagen-positive area） were significantly reversed （ P ＜0.05）.CONCLUSIONS Yangfei tongluo formula may delay airway remodeling in PIBO by regulating the TGF-β 1 /VEGF-mediated signaling network and inhibiting the activation of EMT-related transcription factors， thereby blocking the EMT process.

Mucins are a class of large, highly glycosylated proteins that play a critical role in maintaining ocular surface homeostasis, tear film stability and the ocular surface barrier. This article provides a systematic review of recent advances in clinical and basic research on mucins, summarizing their role in maintaining ocular surface health and their involvement in the onset and progression of ocular surface diseases. It also reviews current methods for detecting mucins and therapeutic strategies targeting mucins. Particular emphasis is placed on examining changes in the mucin expression profile in different subtypes of dry eye, ocular surface diseases and following ocular surface surgery, with the aim of providing guidance for the diagnosis, assessment and treatment of mucin-related ocular surface diseases.

BACKGROUND:Ca2+expression in astrocytes has been found to be closely related to cognitive function,and the Ca2+signaling pathway regulated by inositol 1,4,5-trisphosphate receptors(IP3R2)and ryanodine receptor(RYR)2 receptors has become a hot spot in the study of cognitive disorder-related diseases. OBJECTIVE:To investigate the expression of Ca2+signals mediated by IP3R2 and RYR2 in hippocampal astrocytes in animal models of delayed encephalopathy after acute carbon monoxide poisoning,and to explore the possible pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning. METHODS:C57BL mice with qualified cognitive function were selected by Morris water maze experiment and randomly divided into control group and experimental group.An animal model of delayed encephalopathy after acute carbon monoxide poisoning was established by static carbon monoxide inhalation in the experimental group,and the same amount of air was inhaled in the control group.Behavioral and neuronal changes,astrocyte specific marker glial fibrillary acidic protein,IP3R2,RYR2 receptor and Ca2+concentration in astrocytes of the two groups were detected using Morris water maze,hematoxylin-eosin staining,western blot,immunofluorescence double labeling and Ca2+fluorescence probe at 21 days after modeling. RESULTS AND CONCLUSION:In the Morris water maze,the escape latency of the experimental group was significantly longer than that of the control group(P<0.05).Hematoxylin-eosin staining results showed that in the experimental group,the number of hippocampal pyramidal cells decreased,the cell structure was disordered,and the nucleus was broken and dissolved.Immunofluorescence results showed that IP3R2 and RYR2 were co-expressed with glial fibrillary acidic protein in the hippocampus,and the expressions of IP3R2,RYR2 and glial fibrillary acidic protein were up-regulated in the hippocampus of the experimental group(P<0.05).Western blot analysis showed that the expressions of IP3R2,RYR2,and glial fibrillary acidic protein in the hippocampus of the experimental group were increased(P<0.05).Ca2+concentration in hippocampal astrocytes increased significantly in the experimental group(P<0.05).To conclude,astrocytes may affect Ca2+signals by mediating IP3R2 and RYR2 receptors,then impair the cognitive function of mice with carbon monoxide poisoning,and eventually lead to delayed encephalopathy after acute carbon monoxide poisoning.

ObjectiveThis study leverages structural data from antigen-antibody complexes of the influenza A virus neuraminidase (NA) protein to investigate the spatial recognition relationship between the antigenic epitopes and antibody paratopes. MethodsStructural data on NA protein antigen-antibody complexes were comprehensively collected from the SAbDab database, and processed to obtain the amino acid sequences and spatial distribution information on antigenic epitopes and corresponding antibody paratopes. Statistical analysis was conducted on the antibody sequences, frequency of use of genes, amino acid preferences, and the lengths of complementarity determining regions (CDR). Epitope hotspots for antibody binding were analyzed, and the spatial structural similarity of antibody paratopes was calculated and subjected to clustering, which allowed for a comprehensively exploration of the spatial recognition relationship between antigenic epitopes and antibodies. The specificity of antibodies targeting different antigenic epitope clusters was further validated through bio-layer interferometry (BLI) experiments. ResultsThe collected data revealed that the antigen-antibody complex structure data of influenza A virus NA protein in SAbDab database were mainly from H3N2, H7N9 and H1N1 subtypes. The hotspot regions of antigen epitopes were primarily located around the catalytic active site. The antibodies used for structural analysis were primarily derived from human and murine sources. Among murine antibodies, the most frequently used V-J gene combination was IGHV1-12*01/IGHJ2*01, while for human antibodies, the most common combination was IGHV1-69*01/IGHJ6*01. There were significant differences in the lengths and usage preferences of heavy chain CDR amino acids between antibodies that bind within the catalytic active site and those that bind to regions outside the catalytic active site. The results revealed that structurally similar antibodies could recognize the same epitopes, indicating a specific spatial recognition between antibody and antigen epitopes. Structural overlap in the binding regions was observed for antibodies with similar paratope structures, and the competitive binding of these antibodies to the epitope was confirmed through BLI experiments. ConclusionThe antigen epitopes of NA protein mainly ditributed around the catalytic active site and its surrounding loops. Spatial complementarity and electrostatic interactions play crucial roles in the recognition and binding of antibodies to antigenic epitopes in the catalytic region. There existed a spatial recognition relationship between antigens and antibodies that was independent of the uniqueness of antibody sequences, which means that antibodies with different sequences could potentially form similar local spatial structures and recognize the same epitopes.

Objective: To identify an optimal back-flush solution for leukocyte-depleted filters that maximizes peripheral blood mononuclear cell (PBMC) recovery with high viability, long-term storage stability, and sterility of the harvested residues, thereby providing a clinically translatable strategy. Methods: Three sterile bag-packaged solutions—Saline, Solvent, and Hanks' balanced salt solution (HBSS)—were used to back-flush randomly assigned leukocyte-depleted filters. Nucleated cell recovery rate and viability of the harvested residues were compared. The optimal solution identified was applied to an expanded sample set. PBMC viability and yield were evaluated after 1h vs 48h storage of the residues. PBMCs isolated from the residues were cryopreserved in liquid nitrogen for 1 month, followed by post-thaw comparisons of viability and T-cell expansion capacity. Results: The Solvent group achieved the highest and most consistent nucleated cell recovery rate. Post-flush recovery rate from filters after 400 mL whole blood processing was (21.3±1.6)% for the Solvent group, significantly higher than Saline group (19.2±6.3)% and HBSS group (11.2±5.0)%, with residues from all groups maintaining viability >90%. No biologically significant difference in residue viability was observed between 48h vs 1h storage groups (93.3±2.3)% vs (95.7±1.8)%). PBMC recovery rates from residues showed no statistical difference between 48h vs 1h storage groups [(48.2%±9.5%)vs (40.41%±8.35%), P>0.05], with (17.7±2.6)×10 cells. After 1-month cryopreservation and 10-day expansion, PBMCs isolated from 48-hour-stored residues retained (91.2±3.2)% viability and achieved a (61.9±15.9)-fold expansion. Conclusion: The bag-packaged Solvent, as a back-flush solution, enables sterile acquisition of leukocyte-depleted filter residues through closed-system tubing connections. These residues maintained PBMC viability and recovery rates after 48h storage at 2℃-8℃, with post-cryopreservation (1-month liquid nitrogen) viability and expansion capacity remaining stable. This protocol complies with blood bank regulatory criteria, addresses the concerns about the infectious window period in cell therapy raw materials, and provides a clinically translatable strategy for PBMC-based applications.

Laparoscopic subtotal cholecystectomy (LSC) has been a safe and viable alternative to conversion to laparotomy in cases of severe cholecystitis. The objective of this study is to determine the utility of intraoperative choledochoscopy in LSC for the exploration of the gallbladder, cyst duct, and subsequent stone clearance of the cystic duct in cases of severe cholecystitis. A total of 72 patients diagnosed with severe cholecystitis received choledochoscopy-assisted laparoscopic subtotal cholecystectomy (CALSC). A choledochoscopy was performed to explore the gallbladder cavity and/or cystic duct, and to extract stones using a range of techniques. The clinical records, including the operative records and outcomes, were subjected to analysis. No LSC was converted to open surgery, and no bile duct or vascular injuries were sustained. All stones within the cystic duct were removed by a combination of techniques, including high-frequency needle knife electrotomy, basket, and electrohydraulic lithotripsy. A follow-up examination revealed the absence of residual bile duct stones, with the exception of one common bile duct stone, which was extracted via endoscopic retrograde cholangiopancreatography. In certain special cases, CALSC may prove to be an efficacious treatment for the management of severe cholecystitis. This technique allows for optimal comprehension of the situation within the gallbladder cavity and cystic duct, facilitating the removal of stones from the cystic duct and reducing the residue of the non-functional gallbladder remnant.

Objective:To explore the protective mechanism of dexmedetomidine (Dex) in a model of broncho-pulmonary dysplasia (BPD) in mice exposed to hyperoxia.Methods:Neonatal rats were randomly assigned to four groups:air control group,hyperoxia injury group,Dex control group,and hyperoxia+Dex group,with six animals in each group.The air control and Dex control groups were exposed to ambient air,while the hyperoxia injury and hyperoxia+Dex groups were exposed to 90% O 2.The Dex control and hyperoxia+Dex groups received daily intraperitoneal injections of Dex at a dosage of 500 μg/kg.Lung tissue samples were collected after 7 days.Histomorphological changes in lung tissue were evaluated using hematoxylin and eosin (HE) staining,and mitochondrial ultrastructural changes in type I epithelial cells of neonatal rat lung tissue were observed via transmission electron microscopy.The activity of Complex Ⅰ in neonatal rat lung tissue was assessed.The expression levels of PINK1 and Parkin in neonatal rat lung tissue were measured using quantitative PCR (qPCR).Western blot analysis was conducted to determine the protein expression levels of PINK1 and Parkin in lung tissues. Results:Under transmission electron microscopy,mitochondrial structures were intact in the lung tissues of both the air control group and the Dex control group.However,significant mitochondrial damage was observed in the hyperoxia injury group,while the hyperoxia+Dex group exhibited some relief from mitochondrial damage compared to the hyperoxia injury group.The activity of the oxidized respiratory chain Complex Ⅰ in the hyperoxia injury group was significantly lower than that in the air control group (4.824±0.804 vs.15.276±0.804, P<0.05) and the hyperoxia+Dex group(4.824±0.804 vs.9.648±0.804, P<0.05).After qPCR analysis,the expression levels of PINK1 and Parkin in the hyperoxia injury group were higher than those in the air control group(1.80±0.06 vs.1.00±0.07,2.10±0.14 vs.1.00±0.09, P<0.05),but lower than those in the hyperoxia+Dex group(1.80±0.06 vs.3.61±0.19,2.10±0.10 vs.4.24±0.43, P<0.05).Western blot analysis revealed that the expression levels of PINK1 and Parkin in the hyperoxia injury group were higher than those in the air control group(2.16±0.11 vs.1.00±0.01,3.82±0.13 vs.1.00±0.01, P<0.05),but lower than those in the hyperoxia+Dex group(2.16±0.11 vs.3.35±0.14,3.82±0.13 vs.5.48±0.15, P<0.05).There were no significant differences in mitochondrial structure integrity,Complex Ⅰ enzyme activity,or the expression levels of PINK1 and Parkin,as assessed by qPCR and Western blot analysis,between the air control and Dex control groups( P>0.05). Conclusion:Dex effectively mitigates mitochondrial ultrastructural damage in BPD model mice,enhances the activity of Complex Ⅰ in the oxidative respiratory chain,reduces mitochondrial damage,and increases the activation of the PINK1-Parkin-mediated mitophagy pathway,thereby promoting lung protection.