BACKGROUND:This study aimed to evaluate the predictive value of C1q (complement activation regulatory factor) for the occurrence of postoperative delirium (POD) following surgery for acute aortic dissection. METHODS:We prospectively included patients undergoing surgery for aortic dissection. Serum levels of C1q were measured preoperatively and on the first postoperative day. POD was assessed daily postoperatively using the confusion assessment method (CAM) or the confusion assessment method for the intensive care unit (CAM-ICU) for patients in the intensive care unit (ICU). Statistical analyses included the Pearson correlation coefficient and multivariate logistic regression to evaluate the association between C1q levels and POD. RESULTS:A total of 67 patients were enrolled in the study. Serum C1q levels were significantly higher in the Delirium group compared to the non-Delirium group both preoperatively and postoperatively. Univariate logistic analysis revealed that preoperative serum C1q levels were predictive of POD (OR = 1.379, 95% CI = 1.176-1.683, p < 0.001). The area under the curve (AUC) for preoperative serum C1q was 0.788 (95% CI = 0.671-0.880). CONCLUSIONS:C1q is a potential biomarker for predicting POD in patients undergoing aortic dissection surgery. These findings suggest that C1q may be valuable for early diagnose and intervention strategies for POD.
ABSTRACT Background Myasthenia gravis (MG), an autoimmune neuromuscular disorder, may rarely coexist with malignancies such as lung cancer. Case Presentation This case report presents the first documented use of ofatumumab, a fully human anti‐CD20 monoclonal antibody, in a 75‐year‐old female with acetylcholine receptor (AChR)‐antibody‐positive generalized MG (gMG) following lung adenocarcinoma resection. Initially diagnosed with ocular MG (MGFA Class I), the patient progressed to refractory gMG (MGFA Class IIIa) post‐thymectomy and tumor resection, unresponsive to corticosteroids, tacrolimus, and intravenous immunoglobulin. Due to persistent symptoms and steroid‐induced complications, subcutaneous ofatumumab (20 mg on Days 1, 7, and 14) was administered off‐label. Rapid clinical improvement was observed, with Myasthenia Gravis Composite (MGC) and MG Activities of Daily Living (MG‐ADL) scores declining from 20 to 10 and 17 to 10, respectively, within weeks. Minimal manifestation status (MMS) was sustained for 2 years with intermittent ofatumumab re‐administration (triggered by CD19/CD20 + B‐cell reconstitution > 1%), alongside no tumor recurrence or adverse events. Conclusion This case highlights ofatumumab's potential efficacy and safety in managing refractory gMG post‐cancer resection, possibly via robust B‐cell depletion and reduced immunogenicity. These findings advocate for targeted B‐cell therapies as a viable strategy in complex, refractory MG cases, particularly where conventional immunosuppressants pose oncological concerns.
ABSTRACT Background Neurological disorders are a major global health challenge in the current era, and they need new therapeutic treatments. Aims This review evaluates the neurobiological activity of Paeonol (PNL) focusing on its antioxidant, anti‐inflammatory, and cognitive enhancing effects in various neurodegenerative disorders. Methods A literature search (up to March 2025) was conducted via PubMed, ScienceDirect, Scopus, and other databases using MeSH terms related to PNL's pharmacology and neuroprotection. Inclusion criteria encompassed preclinical studies (in vitro and in vivo) and clinical trials, while exclusion criteria eliminated non‐English papers and non‐neurodegenerative research. Results PNL, a bioactive phenolic compound from Paeonia suffruticosa , has shown antioxidative, anti‐inflammatory, and neuroprotective effects. PNL reduces oxidative stress by boosting the activity of superoxide dismutase (SOD) and glutathione (GSH) while decreasing reactive oxygen species (ROS) and lipid peroxidation. It also reduces neuroinflammation by inhibiting key pathways such as nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), toll‐like receptor 4 (TLR4), and mitogen‐activated protein kinase (MAPK), and it affects apoptosis‐related proteins like B‐cell lymphoma 2 (Bcl‐2) and Bcl‐2‐associated X protein (Bax). In Alzheimer's disease (AD) models, PNL reduces amyloid‐β plaques and some pro‐inflammatory cytokines like interleukin‐1 beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α), improving cognitive function. For ischemic stroke, it reduces infarction volume and microglial activation by targeting TLR2/4 and NF‐κB. PNL has anticonvulsant effects in epilepsy and protects dopaminergic neurons in Parkinson's disease (PD). It also demonstrates anxiolytic and antidepressant properties by modulating Brain‐Derived Neurotrophic Factor (BDNF), Nerve Growth Factor (NGF), and oxidative stress markers. PNL is quickly absorbed with moderate bioavailability and low blood–brain barrier permeability. It effectively treats unstable angina but is less effective for osteoarthritis pain. Though safe at therapeutic doses, high concentrations can be cytotoxic. Conclusion Further clinical research is needed to confirm its neurotherapeutic potential.
ABSTRACT Background Obesity is characterized by chronic low‐grade systemic inflammation, in which adipose tissue macrophages (ATMs) play a pivotal role in driving immune and metabolic dysfunction. Objective This review summarizes current evidence on the roles of ATMs in obese adipose tissue and examines how macrophage polarization and metabolic reprogramming are linked to fatty acid metabolism, insulin resistance (IR), and gut microbiota dysbiosis. Recent Findings Previous studies have often addressed macrophage dysfunction, fatty acid metabolism, IR, and gut microbiota alterations as separate processes. In contrast, this review integrates these obesity‐related events within a unified immunometabolic framework centered on ATMs. Obesity induces marked phenotypic shifts and metabolic reprogramming in ATMs, thereby promoting chronic inflammation and IR. Disturbed fatty acid metabolism and gut microbiota dysbiosis further impair metabolic homeostasis and intestinal barrier integrity, reinforcing a vicious cycle of macrophage‐driven immunometabolic dysfunction. Conclusions This review highlights the central role of ATM‐mediated immune‐metabolic crosstalk in obesity and emphasizes the therapeutic potential of targeting macrophage dysfunction and gut microbiota alterations to attenuate obesity‐related metabolic complications.
ABSTRACT Background and Objective Central Line‐Associated Bloodstream Infections (CLABSIs) considered a significant challenge in healthcare settings, necessitating vigilant monitoring and intervention strategies especially among patients undergoing Hematopoietic Stem Cell Transplantation (HSCT). This study aims to conduct comprehensive analysis of CLABSI cases among HSCT patients; trends in incidence, device associations, causative organisms, and multidrug‐resistant patterns. Methodology A retrospective analysis was conducted on HSCT patients who developed CLABSI at the King Hussein Cancer Center between January 2019 and December 2023. Data collected included demographic data (age and sex), Diagnosis, type of vascular access device (VAD), Organism, bacterial resistance pattern, and last follow‐up status and date were collected for patients. Overall survival analysis was performed using the Kaplan–Meier method, with results reported at 30, 60, and 100 days post‐infection. Results Over the 5‐year period, 169 HSCT patients had CLABSI were included, the majority were male (65.7%), with 73% adults and 27% pediatric patients, and a mean age of 33.6 years. The most common diagnoses were lymphoma (25.4%) and leukemias (24.9%). Gram‐negative bacteria were the predominant cause of infection, accounting for 85% of cases, followed by Gram‐positive bacteria (13.0%) and fungi (2.4%). Escherichia coli was the most frequent causative organism (46%), followed by Klebsiella pneumoniae (8%) and Pseudomonas aeruginosa (5%). Multidrug‐resistant pathogens, particularly Extended‐Spectrum Beta‐Lactamase (ESBL) producing strains and Carbapenem‐resistant Enterobacteriaceae (CRE), were prevalent. Hickman devices were associated with the highest number of CLABSI cases (63.9%). The overall survival rates were 83.4% at 30 days, 80.5% at 60 days, and 78.1% at 100 days post‐CLABSI. Conclusion This study provides a comprehensive overview of CLABSI epidemiology among HSCT patients in Jordan, highlighting the high prevalence of Gram‐negative and multidrug‐resistant organisms. These findings underscore the critical need for continuous surveillance, targeted infection control measures, and effective antimicrobial stewardship to improve patient safety and outcomes in this high‐risk population.
ABSTRACT This study aimed to investigate the associations of the C‐reactive protein‐triglyceride glucose index (CTI) and the triglyceride‐glucose (TyG) index with prehypertension and hypertension in a Chinese population aged 45 years and older. Based on blood pressure diagnostic criteria, 8389 eligible participants were categorized into three groups. In the multivariate logistic regression analysis, after adjusting for potential confounders (Model 2), individuals in the highest quartiles (Q4) of both indices exhibited a significantly increased risk of hypertension compared to those in the lowest quartiles (Q1). Specifically, the adjusted odds ratios (ORs) for Q4 were 1.592 (95% CI: 1.354–1.872) for the TyG index and 1.588 (95% CI: 1.356–1.860) for CTI. A similar independent association was observed for prehypertension. Notably, the CTI demonstrated an enhanced responsiveness in identifying hypertension at lower exposure levels, maintaining a significant association in the second quartile (Q2 OR: 1.201, 95% CI: 1.034–1.395). Furthermore, RCS analysis revealed a more pronounced non‐linear dose‐response relationship for CTI (P‐non‐linear < 0.001) than for TyG (P‐non‐linear = 0.045). Both CTI and the TyG index are independent indicators of prehypertension and hypertension in middle‐aged and elderly Chinese adults. Although their standalone discriminatory power is modest (AUC ≈ 0.59), CTI may serve as a supplementary and cost‐effective monitor for the early risk stratification of hypertension, given its responsiveness to non‐linear risk transitions.
OBJECTIVE:Mometasone furoate (MF) is a widely used intranasal corticosteroid for the management of allergic and non-allergic rhinitis. Recent evidence suggests that its therapeutic efficacy may involve mechanisms beyond traditional anti-inflammatory actions, including modulation of death in nasal mucosa cells. This study aimed to investigate the therapeutic effects of MF on chronic rhinitis, elucidates the underlying molecular mechanisms, and explores its clinical implications in rhinitis management. METHODS:Enzyme-linked immunosorbent assay was used to detect cytokine release. Reverse transcription quantitative PCR was applied for detecting mRNA expression. Immunofluorescence was used detect LC3 expression. Protein express was detected using Western blot. Lactate dehydrogenase leakage assay was used to detect cytotoxicity. Terminal deoxynucleotidyl transferase dUTP nick-end labeling assay was used to detect death of nasal mucosa cells (NMCs). Luciferase and chromatin immunoprecipitation assays were used to verify the interaction between signal transducer and activator of transcription 3 (STAT3) and absent in melanoma 2 (AIM2). RESULTS:MF significantly suppressed inflammatory response induced by PM2.5. MF suppressed PM2.5-induced cytotoxicity and pyroptosis of NMCs. Moreover, MF promotes the activation of autophagy. Mechanically, MF inhibited PM2.5-induced activation of Janus kinase 2/STAT3 signaling. STAT3 transcriptionally upregulated AIM2. The activation of AIM2 inflammasome attenuated the effects of MF and promoted the inflammation and pyroptosis of NMCs as well as suppressed the activation of autophagy. CONCLUSION:In summary, MF protects against chronic rhinitis via suppressing AIM2-dependent pyroptosis of NMCs. Therefore, MF can be a therapeutic strategy for chronic rhinitis.
Spinal cord injury (SCI) leads to severe neurological dysfunction. Current therapeutic strategies remain limited, with poor recovery rates. Oxidative stress and ferroptosis are key mechanisms underlying secondary SCI. Paeoniflorin has anti‐inflammatory, antioxidant, and neuroprotective properties; however, its role in regulating apoptosis and ferroptosis after SCI remains unclear. An in vitro SCI model was established by treating PC12 cells with 300 μM H₂O₂ for 24 h, followed by intervention with various concentrations of paeoniflorin. Cell viability was assessed using the 3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyl tetrazolium bromide (MTT) assay, apoptosis was analyzed by flow cytometry, lipid reactive oxygen species (ROS) levels were detected by immunofluorescence, and cysteine (Cys), glutathione (GSH), and glutathione peroxidase 4 (GPX4) levels were measured using enzyme‐linked immunosorbent assay (ELISA) kits. Western blotting and reverse transcription quantitative polymerase chain reaction (RT‐qPCR) were performed to evaluate the expression of sirtuin 3 (SIRT3), B‐cell lymphoma‐2 (Bcl‐2), and BCL2‐Associated X (Bax). In addition, the SIRT3‐specific inhibitor, 3‐TYP, was used to validate the role of SIRT3 in paeoniflorin‐mediated protection. Paeoniflorin increased cell viability; reduced apoptosis; suppressed ROS accumulation; and restored Cys, GSH, and GPX4 levels in a dose‐dependent manner. Paeoniflorin significantly upregulated SIRT3 mRNA and protein expression. Co‐treatment with 3‐TYP attenuated the protective effects of paeoniflorin, indicating that the role of paeoniflorin is mediated through activation of the SIRT3 pathway. Paeoniflorin exerts significant neuroprotective effects against SCI‐induced injury by activating the SIRT3 signaling pathway and regulating apoptosis, oxidative stress, and ferroptosis, offering a novel potential therapeutic target for SCI treatment.
ABSTRACT Background Chandipura virus (CHPV), a neurotropic, negative‐sense RNA virus belonging to the genus Vesiculovirus (family Rhabdoviridae), has emerged as a significant cause of acute encephalitis syndrome (AES) in India, predominantly affecting children. Since the major outbreaks in 2003–2004 and the recent resurgence in 2024, CHPV has re‐emerged as a high‐fatality, climate‐sensitive arboviral threat transmitted primarily by phlebotomine sandflies. The absence of specific antivirals or licensed vaccines underscores the need for comprehensive understanding and preparedness. Methods This narrative review synthesizes available literature on CHPV epidemiology, outbreak history, molecular virology, transmission ecology, neuropathogenesis, host immune responses, diagnostic modalities, therapeutic candidates, and preventive strategies. Data from published outbreak reports, genomic analyses, experimental studies, and public health updates were critically examined to provide an integrated One Health perspective. Results CHPV outbreaks have been characterized by rapid disease progression, high case‐fatality rates (often 30%–70%), and marked pediatric predominance. Molecular studies reveal a conserved vesiculovirus genomic organization (3′‐N‐P‐M‐G‐L‐5′), with emerging phylogenomic evidence indicating geographic clustering but limited global genomic representation. Neurotropism is mediated by rapid viral replication in the central nervous system, triggering microglial activation, oxidative stress, cytokine dysregulation, complement interactions, and Fas‐mediated neuronal apoptosis. Diagnosis relies primarily on RT‐PCR during the early viremic phase and IgM ELISA in later stages, though rapid field‐deployable diagnostics remain unavailable. Experimental antiviral strategies, including ribavirin, favipiravir, lycorine, RNA interference, and immunomodulatory approaches, demonstrate preclinical promise but lack human clinical validation. Vector control and environmental management remain the cornerstone of prevention. Conclusion Chandipura virus represents a re‐emerging neuroinvasive arbovirus with significant public health implications in India. Strengthening AES surveillance, integrating genomic monitoring, developing rapid diagnostics, advancing antiviral and vaccine research, and implementing climate‐informed vector control strategies are critical priorities. A coordinated One Health framework is essential to mitigate future outbreaks and reduce pediatric mortality.
BACKGROUND:Although the contributions of neutrophils and neutrophil extracellular trap (NET) in chronic respiratory diseases associated with environmental dust inhalation has advanced, changes in neutrophil populations and their response following acute dust inhalation are relatively limited. Our understanding of neutrophil response during acute lung injury relies on blood and lung samples, which limit investigations on neutrophil dynamics such as neutrophil production, release, trafficking, and NET formation in response to acute exposures. METHODS:To address this limitation, we designed a spectral flow cytometry panel to identify neutrophil progenitors, banded, and mature neutrophils across different sites; bone marrow, blood, lung, and bronchoalveolar lavage fluid (BALF) following acute organic dust extract (ODE) exposure. RESULTS:We demonstrate that acute ODE exposure increases band and mature neutrophils in the lung and BALF while decreasing band neutrophils in the bone marrow and blood. Interestingly, the proportion of pro-neutrophils (ProNeu1 and ProNeu2) was altered following ODE in the blood but not bone marrow. We also analyzed the expression of surface markers associated with neutrophil recruitment and activation, as well as their size and granularity after ODE exposure. Regardless of their maturation status, neutrophils in BALF and lung exhibited significant changes in CD11b, CXCR2, and CXCR4 levels post-ODE, while CD62L levels were specifically elevated in the blood. Finally, we identified lytic and vital NET forming neutrophils via Hoechst 33342 intensity in the lung and BALF, demonstrating increases in NET-forming neutrophil counts following ODE. CONCLUSION:Our spectral flow cytometry method provides valuable insight into neutrophil response, activation, and NET-forming capacity in response to acute ODE exposure.
ABSTRACT Background Sepsis‐induced liver injury (SILI) is a fatal complication of organ failure that currently lacks reliable biomarkers for early diagnosis and risk prediction. This study aimed to explore the link between the systemic immune‐inflammatory index (SII) and SILI in adult patients with sepsis in the intensive care unit (ICU) at Nanjing Drum Tower Hospital. Methods This single‐center retrospective study analyzed the baseline characteristics of patients with sepsis admitted to the ICU between 2020 and 2024. Multifactorial logistic regression was used to identify independent risk factors for SILI. Curve fitting and Subgroup analyzes were performed to provide evidence for the stratified management of patients with different clinical characteristics. Receiver operating characteristic (ROC) curve analysis was performed to determine the predictive capacity of the SII. Results A total of 231 patients were included, of whom 53 (22.9%) developed SILI during ICU hospitalization. Patients with SILI exhibited a significantly higher in‐hospital mortality rate than non‐SILI cases (52.8% vs. 25.3%, p < 0.001). Elevated SII at ICU admission was strongly associated with SILI development (p < 0.001). Multivariable logistic regression identified the SII as an independent risk factor for SILI. ROC curve analysis demonstrated that SII had superior predictive performance for SILI occurrence, with an area under the curve of 0.85 (95% CI: 0.784–0.907). Conclusion This retrospective study revealed a substantial association between high SII and SILI in adult ICU patients with sepsis, suggesting that SII is a promising indicator for post‐sepsis SILI risk prediction.
BACKGROUND:Multiple sclerosis (MS) is a neuroimmunological disorder marked by demyelination and neuronal damage, significantly impacting young individuals' health and quality of life. Recent studies suggest a pivotal role of the gut microbiota and immune system in MS development, though the precise mechanisms remain unclear. METHODS:This study utilizes Mendelian randomization (MR) to explore the causal relationships between gut microbiota, immune traits, and MS. We conducted MR analysis using genetic data from 18,340 participants for gut microbiota, 3757 individuals for immune traits, and 47,429 MS cases alongside 68,374 controls. RESULTS:Our results suggested six microbial taxa with nominally significant associations to MS, with two taxa (Roseburia and Ruminococcus2) exhibiting putative mediating trends through specific immune cell phenotypes (CD28 on CD28+ CD4+ T cells and CD45 on HLA-DR+ CD8+ T cells). Mediation analysis demonstrated that 8.97% and 12.18% of the nominal effects of these taxa on MS were potentially mediated through the aforementioned immune traits, respectively. These results only represent exploratory trends and need to be interpreted with caution. CONCLUSION:These nominally significant exploratory findings provide hypothesis-generating clues that immune cell activation, particularly in CD4+ and CD8+ T cells, might be involved in the microbiota-MS relationship. These findings require validation in independent populations and experimental studies.
ABSTRACT Introduction Inflammation is increasingly recognized as a key contributor to the development and progression of major depressive disorder (MDD). This case–control study aims to assess the expression of inflammatory pathway components (TRIF, MyD88, NF‐κB) and serum levels of TNF‐α and IL‐6 in remitted and untreated MDD patients compared to healthy controls. Methods This study included 150 participants: 50 newly diagnosed and untreated MDD patients, 50 MDD patients who achieved complete clinical remission following at least 8 weeks of continuous TCA treatment (TCA remitters), and 50 matched healthy controls. MDD diagnosis was based on DSM‐V criteria and Beck Depression Inventory (BDI). Peripheral blood samples were collected to isolate serum and PBMCs. mRNA expression of NF‐κB, TRIF, and MyD88 was quantified by qRT‐PCR, while serum levels of TNF‐α and IL‐6 were measured using ELISA. Data were analyzed using one‐way ANOVA with Tukey's post hoc test, considering p < 0.05 as statistically significant. Results No significant differences were found in age or gender among the three groups, confirming demographic comparability. BDI scores were markedly higher in both untreated and remitted MDD patients compared to controls, with untreated patients showing the most severe symptoms. Gene expression analysis revealed a significant upregulation of MYD88 (~5‐fold) and NF‐κB (~2.5‐fold) in untreated MDD patients compared to controls (p < 0.001); treated patients also showed higher expression, though to a lesser extent. TRIF expression was higher in treated patients, but not significantly. Serum levels of TNF‐α and IL‐6 were significantly higher in untreated MDD patients versus controls (p < 0.001); IL‐6 and TNF‐α levels were also higher in treated patients but significantly lower than in the untreated group. Conclusion The results support the hypothesis of a link between immune dysregulation and MDD. However, further human studies are necessary to validate the findings of the present study.
ABSTRACT Purpose Influenza‐induced respiratory failure is a severe complication of influenza that can rapidly progress to multi‐organ failure or even death due to severe impairment of pulmonary ventilation or gas exchange function. Early prediction and intervention can decrease the mortality in patients with respiratory failure. Methods A comprehensive analysis was conducted on 182 influenza‐positive patients who were admitted in Affiliated Hospital of Chengde Medical University between December 2018 and May 2019. 78 patients with influenza were used for external validation at Hebei Chest Hospital. We assessed the relationship between respiratory failure and demographic characteristics, preexisting diseases, and laboratory test results in the training group. First, the variables of the nomogram of respiratory failure with influenza were selected using Least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression analysis. A nomogram was developed to predict respiratory failure due to influenza. The accuracy of the proposed model was validated by utilizing the area under the receiver operating characteristic (ROC) and calibration curve. The clinical utility of the proposed model was evaluated using decision curve analysis (DCA) and clinical impact curve (CIC). Results A total of 182 influenza‐positive patients were included, with the incidence of respiratory failure reaching 29.1% ( n = 53). Risk factors contributing to respiratory failure encompassed age, tumor, influenza type, and red cell distribution width coefficient of variation (RDW.CV). Utilizing ROC and calibration curve assessment, the constructed nomogram exhibited accurate prediction of respiratory failure risk, and the AUC value in the training group was 0.79. Of the 78 patients diagnosed with influenza, 35 (accounting for 44.9%) developed respiratory failure. Using the ROC curve, the established nomogram accurately predicted the risk of respiratory failure, and the area under the curve was 0.73 in the validation cohort. Decision curve analysis and clinical impact curve verified that this model demonstrated excellent clinical utility in predicting respiratory failure among influenza patients. Conclusion A nomogram based on the expression levels of RDW.CV, influenza type, tumor, and age was an efficient model for the early identification of respiratory failure in patients with influenza. These results will be useful for guiding the prevention and treatment of respiratory failure caused by influenza.
ABSTRACT Objective To systematically review the structural features of secreted frizzled‑related protein 5 (SFRP5) and its dual regulation of canonical/non‑canonical Wnt signaling, analyze its association with metabolic disorders, and specifically explore the role and mechanisms of the SFRP5–lipid metabolism axis in neural and optic nerve development. Methods A systematic literature search was performed to review the molecular structure of SFRP5, its regulation of Wnt pathways, and its relationship with metabolic dysregulation. The mechanisms by which SFRP5 modulates the microglia/astrocyte‑mediated neuroimmune microenvironment, myelination, synaptic plasticity, and neuronal mitochondrial energy homeostasis were analyzed, and current therapeutic strategies targeting the SFRP5 network were summarized. Results SFRP5 participates in normal central nervous system development by shaping the neuroimmune microenvironment, promoting myelination, regulating synaptic plasticity, and maintaining mitochondrial energy balance. Under obese and diabetic conditions, downregulation of SFRP5 leads to overactivation of Wnt5a/JNK signaling, resulting in lipid metabolic disturbances and neuroinflammation. These changes share common pathological features with neurodevelopmental disorders such as autism spectrum disorder, intellectual disability, optic nerve hypoplasia, and retinal vascular dysplasia. The SFRP5–lipid metabolism axis plays a critical role in neural and optic nerve development, and its dysregulation underlies the neuropathology associated with metabolic diseases. Therapeutic interventions explored to date—including recombinant protein, gene therapy, small‑molecule activators, and acupuncture—have shown promising potential. Conclusion The SFRP5–lipid metabolism axis represents a key link connecting metabolic disorders with neurodevelopmental abnormalities. Future research should focus on spatiotemporal specificity at single‑cell resolution, elucidation of gene–environment interactions, and the development of efficient central nervous system delivery systems, thereby providing new avenues for the prevention and treatment of neural and optic nerve developmental abnormalities.
ABSTRACT Background Guillain–Barré syndrome (GBS) is an immune‐mediated neuropathy that may be influenced by infectious, demographic, and healthcare‐related factors. Although increasing attention has been paid to neurological complications during the COVID‐19 pandemic, the global burden, inequalities, and future trends of GBS remain insufficiently characterized. Methods This population‐based observational epidemiological study used data from the Global Burden of Disease Study 2021 to assess the burden of GBS across 204 countries and territories from 1990 to 2021. The main outcomes included prevalence, years lived with disability (YLDs), age‐standardized prevalence rate (ASPR), age‐standardized YLD rate (ASYR), and estimated annual percentage change (EAPC). Analyses were stratified by sex, age group, country, region, and socio‐demographic index (SDI). Inequality analysis, decomposition analysis, Joinpoint regression, and Bayesian age‐period‐cohort modeling were further used to assess socioeconomic disparities, driving factors, temporal changes, and future trends. Results From 1990 to 2021, the global burden of GBS increased substantially. In 2021, the global number of prevalent cases reached 471,850, and the ASPR was 5.91 per 100,000 population. The corresponding number of YLDs was 139,639, with an ASYR of 1.75 per 100,000 population. The burden was lowest among children younger than 5 years and increased progressively with age. Males generally had a higher burden than females, particularly among older adults. Low‐SDI regions experienced disproportionately higher ASPR and ASYR, indicating substantial global inequalities. The increases observed after 2019 temporally coincided with the COVID‐19 pandemic; however, this association should be interpreted cautiously. Decomposition analysis suggested that epidemiological changes, population growth, and population aging collectively contributed to the increasing burden of GBS. Conclusion The global burden of GBS increased markedly from 1990 to 2021, with substantial regional, sex‐, age‐, and SDI‐related heterogeneity. The post‐2019 increase temporally coincided with the COVID‐19 pandemic, but causal inference should be avoided due to the observational nature of this study. Strengthening neurological surveillance, improving early diagnosis and treatment capacity, and reducing healthcare disparities in low‐SDI regions may help mitigate the future burden of GBS.
ABSTRACT Background Non‐alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder driven by inflammation, in which the NLRP3 inflammasome plays a central role. Current targeted inhibitors face challenges in patient stratification and long‐term safety. Methods A narrative literature review was conducted using PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and Google Scholar from database inception to February 2026. Search terms included combinations of “non‐alcoholic fatty liver disease”, “NAFLD”, “NASH”, “NLRP3 inflammasome”, “traditional Chinese medicine”, “TCM”, “herbal medicine”, “syndrome differentiation”, and “precision medicine”. Peer‐reviewed original articles, systematic reviews, and clinical studies addressing NLRP3 in NAFLD or TCM‐based interventions targeting this pathway were prioritized. Results TCM syndrome patterns (e.g., damp‐heat, phlegm‐damp) correlate with distinct NLRP3 activation states and inflammatory phenotypes. Herbal compounds such as berberine and curcumin, as well as classical TCM formulae, exert multi‐target effects by suppressing NLRP3 inflammasome assembly, enhancing antioxidant defenses, and modulating the gut‐liver axis. Based on this evidence, we propose an integrative “TCM Syndrome–NLRP3 Molecular Endotype–Precision Targeted Therapy” model that links specific TCM syndromes to canonical, non‐canonical, or sustained NLRP3 activation, thereby providing hypothesis‐driven strategies for personalized intervention. Discussion This integrative framework bridges TCM holistic principles with modern inflammasome biology. It provides a theoretical basis for personalized, biomarker‐driven NAFLD therapies, highlighting the synergy between traditional medicine and precision hepatology.
ABSTRACT Background Anti‐dipeptidyl‐peptidase‐like protein 6 encephalitis (DPPXE) is an exceptionally rare form of autoimmune encephalitis characterized by a highly heterogeneous clinical phenotype. Methods In this study, we report a Chinese patient presenting with severe abdominal pain as a prominent symptom; furthermore, we conducted a systematic review and analysis of 125 cases of DPPXE (including the present case). Results This rare case presented with severe abdominal pain as a prominent symptom. We comprehensively summarized the clinical presentations, patterns of recurrence, and therapeutic responses of DPPXE. Notably, by comparing the clinical characteristics of DPPXE cases reported in China with those from other regions, we found some differences in disease presentation, suggesting potential racial or geographic variability. Conclusion Our findings may provide up‐to‐date and comprehensive insights into the pathophysiology and clinical course of this rare disorder from multiple perspectives.
