With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

Intra-abdominal Hernia with Bowel Obstruction Triggering Multi-organ Failure: The Role of Preoperative Enteritis This report details the clinical course of a 41-year-old male who developed fulminant multiple organ dysfunction syndrome following emergency surgery for a strangulated intra-abdominal hernia. Preoperative manifestations, including diarrhea and marked leukocytosis, pointed towards an underlying infectious enteritis. We posited that surgical release of the obstructed, ischemic bowel segment precipitated a massive systemic influx of endotoxins and inflammatory mediators, triggering septic shock and rapid sequential organ failure. This case underscored the critical need to suspect concomitant gastrointestinal infection in patients presenting with mechanical bowel obstruction accompanied by infectious signs. Aggressive perioperative sepsis management encompassing early empiric antimicrobial therapy, vigilant hemodynamic monitoring, and preparedness for advanced organ support is essential to mitigate this severe complication.

Background/Aims: Dysregulated cholesterol metabolism is a hallmark of hepatocellular carcinoma (HCC) that drives tumor initiation and progression. However, clinical targeting of cholesterol metabolism has yielded limited benefits due to stringent feedback in tumor cells. Identifying a central mediator capable of restoring cholesterol homeostasis within the cell’s intrinsically fine-tuned regulatory framework is urgently needed. Methods: We integrated a proteomic dataset from patients with cholesterol-dysregulated HCC into a global cholesterol metabolic regulatory network to identify potential therapeutic targets for disrupted cholesterol homeostasis. The prognostic significance of the candidate targets was further validated in an independent cohort through immunohistochemistry. Functional and mechanistic studies were conducted in vitro using HCC cell lines and in vivo using mouse models. The pharmacological efficacy of the candidate agent was evaluated in both subcutaneous and orthotopic HCC mouse models. Results: ER lipid raft-associated 1 (ERLIN1), a pivotal regulator of cholesterol metabolism reprogramming, was identified as an independent favorable prognostic indicator in HCC. ERLIN1 constrains HCC progression both in vitro and in vivo by stabilizing the INSIG1–SCAP–SREBP2 axis and maintaining the metabolic balance of intracellular cholesterol. Under hypoxia, impaired factor-inhibiting hypoxia-1-dependent hydroxylation of ASB11 at asparagine residues 90 and 92 enhances ASB11-mediated ERLIN1 degradation. Pharmacological targeting of this axis using zoledronic acid (ZoA) attenuated HCC progression by weakening the ASB11–ERLIN1 interaction and restoring cholesterol homeostasis. Conclusions ERLIN1 represents a druggable metabolic vulnerability in cholesterol-dysregulated HCC. Targeting the ASB11–ERLIN1 axis with the clinically approved ZoA reestablishes cholesterol homeostasis and offers a promising therapeutic strategy to overcome the current limitations of cholesterol-targeted HCC therapies.

ObjectiveTo elucidate the effects of autonomic neuromodulators [calcium chloride (CaCl₂)-acetylcholine (ACh)] on atrial electrical remodeling and histopathological changes in rats, thereby providing evidence for further investigation into the pathological mechanisms by which autonomic imbalance induces atrial fibrillation (AF). MethodsTen 8-week-old male Sprague-Dawley (SD) rats were randomly divided into experimental and control groups, with 5 rats in each group. The experimental group received daily tail vein injections of a CaCl₂-ACh mixed solution for 28 days, while the control group received an equal volume of saline. Surface electrocardiograms were recorded before and after daily administration. On day 28 of administration, under isoflurane inhalation anesthesia, echocardiography was performed, and then the rats were euthanized by exsanguination under isoflurane anesthesia for tissue collection. Body weight and heart weight of rats were measured, and electrophysiological parameters including AF inducibility, conduction velocity, and conduction dispersion in isolated rat hearts were monitored using the MappingLab multichannel electrophysiological mapping system. HE staining was performed to evaluate atrial tissue architecture and inflammatory cell infiltration. The expression levels of matrix metalloproteinase 9 (MMP-9) and interleukin-1 beta (IL-1β) were analyzed by Western blotting. Masson staining was used to quantitatively analyze the proportional distribution of collagen fibers and myocardial fibers, and to calculate the area of collagen deposition, thereby evaluating the degree of myocardial fibrosis. Wheat germ agglutinin (WGA) staining was used to evaluate morphological changes of cardiomyocytes. Dihydroethidium (DHE) staining was used to detect the level of oxidative stress in atrial myocytes. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining was used to detect atrial cell apoptosis. ResultsCompared with the control group, the experimental group showed obvious arrhythmias on electrocardiograms. Echocardiography after 28 days of administration revealed significant structural remodeling in the experimental group, with a marked increase in left atrial anteroposterior diameter (P < 0.05), and also showed cardiac dysfunction, with significant decreases in left ventricular ejection fraction and left ventricular fractional shortening (P < 0.01). Compared with the control group, the experimental group showed a significantly increased heart weight-to-body weight ratio (P < 0.05), a markedly higher AF inducibility (P < 0.001), a significantly slowed atrial conduction velocity (P < 0.05), an uneven isochronal map with irregular directions, and a significantly increased conduction dispersion (P < 0.01). HE staining showed that atrial myocytes in the experimental group were disorganized, with slight inflammatory cell infiltration. Western blotting showed that the expression levels of MMP-9 and IL-1β in the atrial tissue of the experimental group were significantly upregulated (P < 0.05). Masson staining showed a significant increase in collagen deposition and a significant increase in fibrosis area in the atrial tissue of the experimental group (P < 0.001). WGA staining showed that cardiomyocytes in the experimental group were significantly hypertrophied compared with the control group (P < 0.05). DHE staining and TUNEL staining revealed that the level of oxidative stress in atrial myocytes (P < 0.001) and the apoptotic rate (P < 0.01) were both significantly increased. Conclusion Daily tail vein injections of the autonomic neuromodulator CaCl₂-ACh mixed solution for 28 days can successfully induce AF in rats, accompanied by significant atrial structural remodeling, electrical remodeling, and oxidative stress.

ObjectiveTo compare female C57BL/6J and BALB/c mice models of ulcerative colitis (UC) induced by dextran sulfate sodium salt (DSS), providing a reference for selecting female animal models in studies of innovative drugs for UC treatment. MethodsA total of 48 female mice aged 6–8 weeks, including 24 C57BL/6J and 24 BALB/c mice, were divided into four groups: control group, UC-3d group (2.5% DSS drinking for 3 days), UC-7d group (2.5% DSS drinking for 7 days), and UC-withdrawal group (2.5% DSS drinking for 7 days followed by 3 days of pure water replacement), with 6 mice in each group. Body weight, fecal occult blood, and stool characteristics were recorded daily, and disease activity index (DAI) scores were calculated. At the end of DSS induction, mice were gavaged with fluorescein isothiocyanate (FITC)-labeled dextran solution before tissue collection. Four hours later, under deep anesthesia induced by inhalation of 4% isoflurane, blood samples were collected from the retro-orbital venous plexus, and euthanasia was performed by cervical dislocation. The colon was then separated immediately, and its length from the anus to the ileocecal junction was measured. Colon tissues were fixed, embedded, and sectioned, and they were evaluated using hematoxylin-eosin (HE) staining and alcian blue-periodic acid-Schiff (AB-PAS) staining to comprehensively assess the degree of colonic inflammation. The spleen was also collected and weighed, and the spleen coefficient was calculated. Serum FITC fluorescence intensity and D-lactic acid concentration were measured to evaluate intestinal permeability and barrier injury. The grooming duration, the number of buried marbles, the time spent in the center of the open field, and the total distance traveled were measured to evaluate anxiety/depression-like behaviors in mice. ResultsFecal occult blood appeared in both C57BL/6J and BALB/c mice after 3 days of ad libitum access to DSS. Compared with the control group, there was no significant change in the weight loss rate of female BALB/c mice in the UC-7d and UC-withdrawal groups (P > 0.05), but the DAI score increased (P < 0.01). Conversely, both the weight loss rate and DAI score increased for female C57BL/6J mice in the UC-7d and UC-withdrawal groups (P < 0.01). In female C57BL/6J mice, both the UC-7d and UC-withdrawal groups had higher spleen coefficients than the control group (P < 0.05). Additionally, in these groups, colon length was significantly reduced (P < 0.01), FITC fluorescence intensity in serum was markedly increased (P < 0.01), obvious inflammatory reaction areas appeared in the colon, and the goblet cells and acidic mucus layer were damaged. In contrast, in female BALB/c mice, no significant differences were observed in colon length, serum FITC fluorescence intensity, or D-lactic acid concentration between the UC-7d and UC-withdrawal groups compared with the control group (P > 0.05). Only a few inflammatory cells and damaged goblet cells were observed in the colonic mucosal layer, and no other obvious pathological changes were detected. In addition, female C57BL/6J mice in the UC-7d group showed a significantly reduced total distance in the open field and fewer buried marbles (P < 0.05), indicating depression-like behavior, as well as prolonged grooming duration (P < 0.05), indicating anxiety-like behavior. ConclusionFemale BALB/c mice are not sensitive to 2.5% DSS and do not show typical colonic pathological changes of UC. In contrast, ad libitum access to 2.5% DSS for 7 days successfully induces typical UC pathological symptoms and colonic pathological changes in female C57BL/6J mice. These changes persist for 3 days after DSS withdrawal, and the mice also exhibit symptoms of anxiety/depression. The results suggest that this model can be used for research on the pathogenesis and therapeutic drugs of UC.

Although global brain science research has progressed rapidly in recent decades, several fundamental questions in neuroscience remain unresolved. In particular, the physical mechanism underlying neural signal transmission remains controversial, and the carriers responsible for neural information storage and retrieval have not yet been fully clarified. These unresolved issues motivate us to re-examine the processes of neural information generation, transmission, integration, storage, and retrieval from multiple perspectives. A key observation is that neural electromagnetic activities are closely associated with time. Their duration, temporal structure, and dynamic evolution play crucial roles in neural information processing. In this work, we analyze neural electromagnetic activities from the perspective of temporal scales (referred to here as the “time course”). By reviewing and integrating findings from previous studies, we examine the characteristic time requirements and dynamic features of neural processes occurring at different stages of information processing. These stages include neural signal generation, signal transmission along axons, synaptic integration, synaptic plasticity, and memory formation and retrieval. Based on this temporal analysis, we outline a framework describing neural electromagnetic activities across a wide range of time scales, spanning from microseconds to minutes, hours, or even longer periods associated with long-term memory, which suggests that neural information processing involves multiple physical processes operating at different time levels. Rapid electromagnetic events may occur on microsecond scales, whereas electrophysiological phenomena such as action potentials typically last on the order of milliseconds. Longer time scales are associated with synaptic plasticity and memory-related processes. From this perspective, we propose that the physical carrier of neural information may be transient electromagnetic pulses with durations on the microsecond scale. In this framework, action potentials can be interpreted as the macroscopic electrophysiological manifestation of underlying electromagnetic processes triggered by ionic currents across neuronal membranes. Rather than being the fundamental neural signal itself, the action potential may represent a measurable membrane-level response associated with the successful activation of these electromagnetic events. Moreover, we discuss a possible mechanism for long-term memory storage. Considering the apparent temporal contradiction between the millisecond-scale excitation of neurons and the long-term persistence of memories, we believe that long-term memory information may be stored within neural network topologies formed by electrical synapse coupling. Such structures, referred to as electrically coupled memory networks (ECMNs), may enable neurons within the same network to respond rapidly and synchronously to stimuli, thereby facilitating efficient memory retrieval. Overall, this study emphasizes the importance of considering the temporal organization of neural electromagnetic activities when interpreting neural signaling mechanisms. It may provide new insights into the physical nature of neural information carriers and the mechanisms of memory storage and retrieval. Furthermore, highlighting the potential role of electromagnetic interactions in neural activity may contribute to the development of new theoretical frameworks and experimental approaches in neuroscience. Such perspectives may also offer valuable references for future research on neural coding, brain function mechanisms, and neuromodulation technologies.

ObjectiveCerebral ischemic injury triggers a complex pathological cascade characterized by excessive reactive oxygen species (ROS) accumulation, persistent oxidative stress, and sustained neuroinflammation in the injured brain microenvironment. These events collectively drive mitochondrial dysfunction, microglial overactivation, pro-inflammatory cytokine release, and progressive neuronal apoptosis, ultimately leading to severe and irreversible neurological deficits. However, conventional therapeutic strategies face critical limitations, including poor blood-brain barrier penetration, insufficient local drug concentration, uncontrolled drug release, and off-target systemic side effects. To address this pathological process, we rationally designed and fabricated an injectable ROS-responsive hydrogel loaded with polydopamine nanoparticles (PDA NPs) for spatiotemporally controlled antioxidation, anti-inflammation, and neuroprotection in the ischemic injury microenvironment. The present study aimed to systematically characterize the physicochemical properties, ROS-responsive drug release behavior, biocompatibility, and neuroprotective efficacy of this composite hydrogel system in vitro. MethodsPDA NPs were fabricated via oxidative self-polymerization. The ROS-responsive hydrogel was cross-linked using N1-(4-boronobenzyl)-N3-(4-boronophenyl)-N1,N1,N3,N3-tetramethylpropane-1, 3-diaminium (TSPBA) and polyvinyl alcohol (PVA). Morphology, particle size, Zeta potential, and structure of PDA NPs were characterized by dynamic light scattering (DLS), Zeta potential analysis, scanning electron microscopy (SEM), and transmission electron microscopy (TEM). Microstructure, rheological properties, shear-thinning behavior, and ROS-triggered release profiles of the hydrogel were examined by SEM and rheometry. Biocompatibility was evaluated using HT22 mouse hippocampal neurons with CCK-8 and live/dead staining. An oxygen-glucose deprivation/reoxygenation (OGD/R) model was established to simulate ischemic injury in vitro. ROS levels and neuronal apoptosis were detected by DHE staining and TUNEL assay. Microglial polarization and pro-inflammatory cytokine expression were analyzed using immunofluorescence and RT-qPCR in BV-2 microglia. Transwell co-culture was used to verify the indirect neuroprotection mediated by modulated microglia. ResultsCharacterization results confirmed that the as-prepared PDA NPs were monodispersed spherical nanoparticles with uniform diameter and negative surface potential, demonstrating favorable dispersibility and robust ROS-scavenging activity. The TSPBA-PVA hydrogel exhibited a highly porous interconnected network, suitable mechanical strength, and obvious shear-thinning behavior, supporting its application as an injectable implant. More importantly, the hydrogel displayed typical ROS-responsive degradation and on-demand PDA NP release in a ROS-concentration-dependent manner. In vitro cellular experiments demonstrated that the PDA NP-loaded hydrogel possessed excellent biocompatibility with HT22 cells. In the OGD/R model, the hydrogel significantly reduced intracellular ROS accumulation and markedly suppressed neuronal apoptosis. Furthermore, the composite hydrogel effectively redirected BV-2 microglia from the pro-inflammatory M1 toward the anti-inflammatory M2 phenotypes, downregulated the expression of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6, and reduced inflammatory damage. Transwell co-culture assays further validated that M2-polarized microglia mediated by the hydrogel significantly enhanced the survival of OGD/R-injured HT22 neurons and attenuated apoptosis. ConclusionIn this study, we successfully developed a novel injectable ROS-responsive hydrogel loaded with PDA NPs for synergistic antioxidative and anti-inflammatory neuroprotection. This intelligent hydrogel system enables ROS-triggered on-demand release of PDA NPs, efficiently scavenges excessive ROS, inhibits oxidative stress injury, modulates microglial polarization, and suppresses neuroinflammation, thereby exerting robust neuroprotective effects in vitro. This biomaterial platform provides a promising strategy for the targeted and controlled delivery of bioactive nanomaterials in the central nervous system diseases and establishes a solid experimental foundation for the development of in situ injectable therapies for ischemic brain injury.

Objective To explore the predictive role of pathological risk score of gastric cancer (PRS_GC) in the prognosis of gastric cancer patients, and to further investigate the correlation between PRS_GC and tumor biological behavior. Methods Clinicopathological data were retrospectively collected from 1 120 patients with gastric cancer who underwent surgical resection at Zhongshan Hospital, Fudan University, between April 2006 and November 2019. PRS_GC was calculated using the previously established DeepRisk model, and patients were divided into high and low PRS_GC groups (560 patients per group) based on the median PRS_GC value. The proportions and spatial distances of immune cell subsets in gastric cancer tissues were assessed between the two groups. Data from stomach adenocarcinoma samples in The Cancer Genome Atlas was integrated to analyze PRS_GC-associated genetic mutations and signaling pathways. Results The survival rate of the high PRS_GC group was lower than that of the low PRS_GC group, and the recurrence rate was higher than that of the low PRS_GC group (P<0.000 1). Compared with the low-PRS_GC group, the high-PRS_GC group exhibited increased infiltration of regulatory T cells (Tregs) and neutrophils within the tumor region (P＜0.05), while the infiltration levels of natural killer T cells and cytotoxic T cells were markedly decreased (P＜0.05). Spatial analysis revealed that a shortened spatial distance between CD4⁺ T cells and Tregs was closely associated with poor prognosis in the high-PRS_GC group (P＝0.03). Furthermore, in the high-PRS_GC group, the number of TIM3⁺ cells showed a positive correlation with the infiltration levels of Tregs (r＝0.69, P＝0.01), CD8⁺ T cells (r＝0.61, P＝0.04), and CD4⁺ T cells (r＝0.67, P＝0.02). Gene set enrichment analysis indicated that a high PRS_GC was associated with the activation of pathways related to actin cytoskeleton regulation, the cGMP-PKG pathway, the Hippo pathway, and tumor proteoglycans. Conclusion A high PRS_GC is associated with an immunosuppressive tumor microenvironment, as well as tumor invasion and metastasis. It effectively predicts the prognosis of patients with gastric cancer and, by doing so, provides a potential theoretical basis for developing individualized strategies that combine targeted therapy with immunotherapy.

Objective To explore the impact of tumor-associated myeloid cell infiltration signatures on postoperative overall survival (OS) in patients with gastric cancer. Methods A retrospective analysis was performed on patients who underwent radical gastrectomy at Zhongshan Hospital, Fudan University from January 2005 to December 2019. Patients were randomly divided into a training set (n＝167) and an internal validation set (n＝168) at a 1:1 ratio. Meanwhile, 147 patients with gastric cancer treated at Zhongshan Hospital (Xiamen), Fudan University during the same period were enrolled as the external validation set (n＝147). Immunohistochemistry was used in all patients to evaluate the distribution characteristics of 18 immune markers in three regions of gastric cancer tissues, namely primary tumor (PT), invasive margin (IM), and normal tissue (NT). These markers include 11 myeloid cell markers (CD11b, CD33, CD11c, CD14, CD15, CD16, CD68, CD86, CD163, CD206, and CD66b) and 7 immune checkpoints (CD73, IDO, LAG3, PD-1, SIGLEC9, SIRPA, and TIM3). LASSO regression and Cox proportional hazards model were applied to screen immune markers associated with postoperative OS in gastric cancer patients, and a predictive model for 1-, 3-, and 5-year postoperative OS was established. Data from the internal and external validation set were used for internal and external verification of the predictive model. Receiver operating characteristic (ROC) curves were plotted and the area under the curve (AUC) was calculated to assess the discriminative ability of the model. Results In the training set, LASSO regression and Cox proportional hazards model identified 4 immune marker signatures (CD14_PT, CD15_PT, CD206_PT, and SIGLEC9_PT) to construct the predictive model. ROC curve analysis showed that the AUCs of the model for predicting 1-, 3-, and 5-year postoperative OS were 0.74, 0.75, and 0.84, respectively. When the model was applied to the internal and external validation sets, the AUCs for 1-, 3-, and 5-year postoperative OS were 0.74, 0.72, 0.72 (internal validation set) and 0.72, 0.71, 0.74 (external validation set), respectively. Cox multivariate regression analysis showed that the risk score was an independent risk factor for postoperative OS in patients with gastric cancer. Conclusion The model constructed based on LASSO-Cox regression exhibits good predictive performance and can effectively predict postoperative OS in gastric cancer patients, which may serve as a basis for intensive treatment of high-risk patients after surgery.

It is considered that "latent wind in stomach collaterals" is the core pathogenesis underlying the inflammation-caner transformation of helicobacter pylori-associated gastritis （HpAG）. The concept of "latent wind in stomach collaterals" integrates stomach wind theory， latent pathogen theory， and collateral disease theory， referring to wind pathogen deeply hidden in the stomach collaterals， characterized by both external and internal wind pathogen as well as latent pathogen that remain concealed and may be triggered under certain conditions. Accordingly， the Correa cascade is reclassified into four stages including the prodromal stage， progressive stage， transitional stage and carcinogenic stage. In the prodromal stage， the fundamental pathogenesis is described as "wind toxin invading externally with collateral deficiency and stirring of wind". In the progressive stage， wind is accompanied by qi constraint， fire pathogen， and dryness pathogen， manifesting as "wind pathogen complicated by constraint" "wind-fire agitation" and "wind-dryness interaction". In the transitional stage， "wind transforming into phlegm-drool and stomach collaterals being obstructed by stasis" is identified as a critical window for disease reversal. In the carcinogenesis stage， "wind-qi hyperactivity leading to pathological transformation， and collateral damage resulting in abdominal masses" drives tumor progression and metastasis. This paper proposes the treatment principle of "wind-dispelling throughout the entire process and stage-based treatment"， according to the pathological evolution of "collateral deficiency-collateral stagnation-collateral accumulation". In the prodromal stage， it is suggested to dispel wind and resolve toxin， fortify spleen and tonify collaterals； in the progressive and transitional stage， the method of dispelling wind pathogen， clearing phlegm and eliminating stasis should be used； in the carcinogenesis stage， it is suggested to expel wind and remove pathogens from collaterals， disperse concretions and eliminate tumors.