External stimuli elicit behavioral responses through neural circuits, and growing evidence demonstrates that this regulatory process is closely associated with the immune system. The complex interplay between stress and immunity, as highlighted by recent interdisciplinary studies, is central to this relationship, highlighting the bidirectional communication between the nervous system and multiple peripheral organ systems. To better elucidate how the brain responds to external stressors, we propose the concept of the "brain-organ axis." Analogous to coordinated teamwork, this framework emphasizes the synergistic interactions between the brain and peripheral organs. Under psychological stress, activation of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system modulates the peripheral immunity in an organ-specific manner. Neurotransmitters, neuropeptides, and glucocorticoids collectively demonstrate that stress exerts differential effects on immune cell populations and local tissue microenvironments, particularly in the skin, gut, liver, heart, spleen, and lungs. These alterations promote the release of proinflammatory mediators, modify the immune surveillance states, and increase the susceptibility to infection. Conversely, peripheral inflammation affects central nervous system function via vagal afferent pathways and circulating cytokines, thereby forming a closed neuroimmune regulatory loop. This review integrates the recent findings on the brain-organ axis in the context of stress and psychological disorders from a radiating network perspective. Based on the neuroimmune interaction mechanisms, it explores how stress-induced emotional states achieve organ-specific regulation of local immune environments through a targeted modulation of neurotransmitters and immune cells, ultimately driving peripheral inflammation. By delineating stress-induced tissue-specific immune responses, this work clarifies the mechanisms through which psychological states influence somatic disease and provides a comprehensive overview of the role of psychological factors in systemic immunity.

Subcortical vascular cognitive impairment (SVCI) is a heterogeneous cognitive impairment caused by small vessel disease. Diagnosis of SVCI remains challenging when neuropsychological assessment is impractical. This study proposes a diffusion tensor imaging (DTI)-based DenseNet to identify SVCI from subcortical ischemic vascular disease (SIVD) and to profile multidomain cognitive risks. We collected neuropsychological scales and DTI from 134 SVCI and 171 SIVD patients in our internal dataset for model development. An external target-domain dataset of 90 SVCI and 103 SIVD patients was used for unsupervised domain adaptation (UDA). Within this dataset, 45 SVCI and 53 SIVD patients were used for unlabeled UDA fitting; the remaining 45 SVCI and 50 SIVD patients were held out as a target-domain test set. Model-generated salient maps identified white matter (WM) regions associated with SVCI. Mutual information (MI) maps between DTI and 6 neuropsychological scales were computed to identify structural correlates of cognitive domains for cognitive profiling. We computed structural similarity index measure (SSIM) between individual-level salient maps derived from DenseNet and the MI maps for unsupervised clustering to stratify domain-specific cognitive impairment risk in SVCI. The DenseNet achieves high accuracy (0.902 internal, 0.926 target-domain) with AUCs of 0.951 and 0.942, respectively. SVCI probabilities reflect cognitive severity, and salient maps are associated with neuropsychological performance. Regarding cognitive profiling, each cognitive domain is divided into low, moderate, and high subgroups, with significantly different SSIM. Our DTI-based study demonstrates accurate SVCI identification and individualized multi-domain cognitive profiling. This offers a complementary framework to support diagnosis and personalized intervention.

AIMS:To investigate alterations in basal forebrain (BF) subregional functional connectivity (FC), cerebral glucose metabolism, and their spatial correspondence with atlas-based neurotransmitter distributions in Alzheimer's disease (AD). METHODS:Forty-two Aβ-PET-positive AD patients and forty-one matched healthy controls (HC) underwent simultaneous PET/MRI. We analyzed resting-state FC of BF subregions (Ch1-3, Ch4) and measured cerebral glucose metabolism using 18F-FDG PET standardized uptake value ratio (SUVR). Spatial correlations with neurotransmitter maps were assessed using the JuSpace toolbox. RESULTS:Compared with HC, AD patients showed decreased FC between the left Ch4 and hippocampus/posterior cingulate gyrus, and increased FC between the right Ch4 and precentral/postcentral gyrus. Additionally, AD patients showed increased FC between the left Ch1-3 and superior temporal gyrus/insula, decreased FC between the right Ch1-3 and the orbitofrontal gyrus, and increased FC between the right Ch1-3 and the left temporal lobe (voxel-level p < 0.001, cluster-level p < 0.05, GRF correction). These FC changes were spatially correlated with serotonergic (5HT1a, 5HT4, SERT) and dopaminergic (D1, D2, DAT) receptor distributions (p < 0.05, FDR corrected). Widespread cerebral hypometabolism in temporoparietal and frontal regions was spatially correlated with serotonin, dopamine, GABA, glutamate, and kappa-opioid systems (p < 0.05, FDR corrected). CONCLUSION:The FC of BF and cerebral metabolic changes in AD show distinct spatial correspondence with specific neurotransmitter systems, highlighting the crucial involvement of serotonin and dopamine in AD pathophysiology.

Scope: Imiquimod (IMQ)-induced psoriasis-like mouse models are widely used for psoriasis research, but existing methods fail to sustain disease manifestation over time. This study explores the effect of different IMQ dosing frequencies on maintaining psoriasis symptoms in mice. Methods and Results: We compared a general IMQ model (General Model) with models that used spaced dosing (D-D Model) or 5-6 doses per week (3D-D Model) over a 28-day duration. Each experimental group consisted of eight mice (n=8) to ensure statistical significance. Both the D-D and 3D-D models maintained classic pathological features of psoriasis, including immune cell accumulation in skin and sustained levels of psoriasis-related inflammatory factors in the blood, compared to the control and General Model groups. Transcriptomic analysis revealed that D-D Model and 3D-D models mice exhibited more severe psoriasis-like lesions and significantly increased expression of IL-17 and IL-23 signaling genes (IL-17A, IL-17F, S100A9) compared to the General Model. Furthermore, adjusted dosing frequencies influenced the metabolic profile, with higher regulation of TRP channels and 2-oxocarboxylic acid metabolism in the skin of D-D mice. Subsequent, Identification and validation of a conserved psoriasis biomarker signature via machine learning and cross-species analysis. Conclusion: Adjusting the dosing frequency of conventional imiquimod-induced psoriasis-like mouse models to alternate-day administration (D-D) or three days on followed by one day off (3D-D) maintained long-term psoriasis symptoms. enhancing IL-17/ IL-23 signaling pathways. This modification resulted in a model exhibiting biological characteristics more closely resembling those in humans, thereby providing a more clinically relevant model for chronic psoriasis. Despite these advantages, the current model has not yet fully recapitulated the complex seasonal and cyclical nature of clinical psoriasis.

BackgroundTriggering receptor expressed on myeloid cells 2 (TREM2) is a genetic risk factor for Alzheimer's disease (AD). While TREM2 facilitates central nervous system lipid clearance, its influence on peripheral lipid metabolism remains unclear.ObjectiveTo investigate the association between plasma sTREM2 and peripheral lipid profiles in AD and to explore the mechanistic role of TREM2 in peripheral lipid regulation.MethodsWe conducted a cross-sectional study of 59 AD patients and 54 healthy controls and measured plasma biomarkers including sTREM2 as well as performed targeted lipidomics profiling. Mechanistic exploration was performed via plasma and hippocampal lipidomics in Trem2 knockout and APP/PS1 mice.ResultsPlasma sTREM2 levels were elevated in AD and were negatively correlated with the plasma p-tau217/Aβ42 ratio and p-tau217. Multivariate analysis revealed a distinct lipidomics signature in AD, in which 30 lipid species were significantly altered. We prioritized significantly altered biomarkers to inform a composite biomarker panel combining sTREM2 with a set of sphingomyelins, phosphatidylinositols, diacylglycerols, fatty acids, and cholesteryl esters, which showed strong discrimination between AD and controls (AUC = 0.93). In a mouse model of APP/PS1, we found that Trem2 knockout partially normalized plasma sphingomyelins and hexosylceramide levels. Finally, cross-tissue comparisons further suggested that TREM2 exerted distinct effects on peripheral sphingolipid metabolism that were less evident in hippocampal tissue.ConclusionsOur findings associate TREM2 with lipid dysregulation in AD and support development of a plasma sTREM2-lipid panel for patient classification.

Background:Keloids are pathological fibroproliferative skin disorders resulting from abnormal wound healing, characterized by excessive extracellular matrix (ECM) deposition and chronic local inflammation. While dermal fibroblasts are the primary effector cells in this process, the role of keloid keratinocytes (KKs) and their metabolic alterations in sustaining the pro-inflammatory and fibrotic microenvironment remains poorly understood. Methods:We performed single-cell RNA sequencing (scRNA-seq) on 46,690 cells from keloid and normal skin tissues. Cellular metabolic activities were assessed using scMetabolism and scFEA, and transcriptional regulatory networks were analyzed via pySCENIC. In vitro experiments utilizing glycolysis inhibitors (2-DG and Fasentin) were conducted to validate the relationship between metabolic reprogramming and epithelial-mesenchymal transition (EMT). Results:scRNA-seq analysis identified a distinct subpopulation of basal keratinocytes (Basal1/2) exhibiting an arrested differentiation trajectory and elevated glycolytic activity. This metabolic shift is functionally coupled with an EMT-prone state and is regulated by transcription factors including REL and ESRRA. Pseudotime analysis revealed that these KKs transition into a terminal state characterized by high expression of the chemokine CCL2 and the stress-response gene ATF3. Cell-cell communication analysis indicated that these glycolytically active KKs maintain intensive crosstalk with a specific pro-inflammatory fibroblast subset (Fibroblasts3) via the ligand-receptor pair SEMA3C-EPHA2 and IGFBP3-ADGRG1 signaling pathways. In vitro experiments confirmed that pharmacological inhibition of glycolysis with 2-DG or Fasentin significantly attenuated the EMT-related features in KKs. Conclusion:Collectively, glycolysis-driven EMT in KKs actively contributes to the pro-inflammatory and fibrotic signaling in keloids, suggesting that targeting this metabolic reprogramming could be a potential strategy for therapeutic intervention.

The pathogenesis of type 2 diabetes (T2D) is complex. Oxidative stress has been demonstrated to be closely related to the pathogenesis of T2D. Oenothera biennis (OeB) is a type of plant exhibiting antioxidant activity. However, the effect and mechanism of OeB in treating T2D are unclear. Thus, OeB was investigated for its effect and potential mechanism in treating T2D. The chemical compounds of OeB stem extract were identified via ultra-performance liquid chromatography-mass spectrometry in series (UPLC-MS/MS). The targets of OeB were predicted via network pharmacology and molecular docking. The T2D model mice were induced via high-fat diet feeding and intraperitoneal injections of streptozotocin (STZ). The high glucose (HG) model cells were induced via the addition of 25 mmol/L glucose in MIN6 cells. The effects of OeB on T2D mice and cells were investigated by using an enzyme-linked immunosorbent assay (ELISA) and western blotting. Changes in the microbiota of colon content were measured by using 16 S rRNA sequencing. Pancreatic metabolomics was detected by using UHPLC-Q-TOF. A total of 20 active compounds, 130 common T2D targets, and 9 hub targets were predicted. In-vivo experiments revealed that the OeB stem extract significantly reduced the levels of fasting plasma glucose (FPG), Homeostasis model assessment-Insulin resistance (HOMA-IR), and malondialdehyde (MDA), improved glucose tolerance, elevated the levels of insulin (INS), superoxide dismutase (SOD), and glutathione (GSH), and increased the number and area of pancreatic islets in T2D mice (p < 0.05). Metabolomics indicated that OeB may regulate the metabolism of choline and aspartate. OeB could reduce the abundances of Alistipes, Lachnospiraceae_UCG-006, Lachnospiraceae_UCG-001, and Eubacterium_nodatum_group, as well as increase the abundance of Lactobacillus, Sporosarcina, and Candidatus_Stoquefichus. Spearman correlation analysis indicated that Lachnospiraceae_UCG-001, Eubacterium_nodatum_group, and Candidatus_Stoquefichus might be closely related to Choline and Aspartate metabolism. In-vitro experiments revealed that OeB stem extract significantly decreased the levels of proINS and MDA, but increased the levels of INS, SOD, and GSH in MIN6 cells (p < 0.05). Moreover, OeB stem extract significantly increased the levels of p-Akt and p-GSK-3β (p < 0.05). In conclusion, OeB stem extract might ameliorate the pathology of T2D mice by modulating the composition of microbiota in colon content and participating in the metabolism of choline, alanine, aspartate, and glutamate.

BACKGROUND:Methotrexate (MTX) is the anchor drug for rheumatoid arthritis (RA) treatment, but its clinical application is limited by dose-dependent adverse events, such as hepatotoxicity and gastrointestinal intolerance, and incomplete efficacy in some patients. Cannabidiol (CBD) is a nonpsychotropic cannabinoid that has powerful therapeutic efficacy in alleviating pain and inflammation, as well as favourable safety and tolerability profiles. However, whether CBD can synergize with MTX to enhance therapeutic outcomes and mitigate toxicity remains unclear. This study aimed to investigate the synergistic efficacy, safety profile, and underlying molecular mechanism of the CBD-MTX combination in the treatment of RA. METHODS:Mice were randomly divided into 8 groups (n = 5 per group): a normal control group (NC), a model control group (MC), 3 MTX monotherapy groups (low/medium/high dose), and 3 CBD + MTX combination groups (low/medium/high dose). Arthritis severity was assessed by clinical scoring and micro-CT. Systemic safety was evaluated via histopathological examination of the liver, kidney, and testis. Flow cytometry, ELISA and Western blotting were used to validate the mechanisms involved. Network pharmacology and molecular docking were used to predict potential targets. RESULTS:Compared with MTX monotherapy, the CBD-MTX combination had dose-dependent synergistic effects, significantly attenuating joint swelling, inflammation, and bone erosion. The medium-dose combination approached the efficacy of high-dose MTX (dose-sparing effect). CBD mitigated MTX-induced testicular toxicity and spermatogenic failure. Mechanistically, the combination suppressed M1 macrophage polarization and proinflammatory cytokine (TNF-α, IL-6, and IL-1β) secretion by inhibiting STAT3 and NF-κB signalling (downregulation of p-STAT3 and p-NF-κB p65). CONCLUSION:The CBD-MTX combination exerts superior antiarthritic effects by inhibiting STAT3/NF-κB-mediated M1 macrophage polarization and protecting against MTX-induced reproductive toxicity. This study provides a preclinical rationale for this novel combination strategy in RA management.

BackgroundRituximab-induced serum sickness (RISS) is an uncommon delayed hypersensitivity reaction with incompletely characterized clinical features and management. We aimed to synthesize published case reports/series to delineate clinical patterns, therapeutic strategies, and outcomes.MethodsPubMed, EMBASE, Web of Science, WanFang Data, and China National Knowledge Infrastructure (CNKI) were searched for rituximab-induced serum sickness reports published up to Nov 31, 2025, using keywords and free-text terms (e.g., “Rituximab,” “Serum Sickness,” “Serum Sickness-Like Reaction,” “Hypersensitivity,” “Adverse Drug Reaction,” “RISS,” and “anti-CD20”) with Boolean operators. Eligible case reports/series were screened and data were extracted with a standardized form. Study quality was evaluated using the JBI Critical Appraisal Checklist for Case Reports.Results30 eligible articles identified 39 patients. The median age was 33 years (range 6, 86), with a female predominance (71.8%). The median symptom onset time was 7 days (range 1, 18) after last rituximab exposure. The most common indications were multiple sclerosis (23.1%), nephrotic syndrome (20.5%), and immune thrombocytopenia (20.5%). Clinically, arthralgia/arthritis (92.3%), fever (82.1%), and rash (66.7%) predominated. Anti-rituximab antibodies were positive in 90.9% of tested cases. Inflammatory markers were frequently elevated, with 93.3% of patients showing elevated erythrocyte sedimentation rate (ESR) and 91.3% showing elevated C-reactive protein (CRP). Complement consumption were frequent, with decreased C3 and C4 levels observed in 76.5% and 78.6% of tested patients, respectively. Corticosteroids were commonly used as the treatment for RISS, while switching to another anti-CD20 agent was primarily a strategy for managing the underlying disease. Overall, 82.1% achieved complete recovery and 15.4% improved, with a median recovery time of 3.0 days. Rechallenge was reported in 10 patients, with recurrence in 60.0%.ConclusionRISS is a delayed reaction occurring after a free interval of several days, but it may clinically present shortly after a subsequent infusion in repeated dosing regimens. Its main features include the classic triad of fever, rash, and arthralgia or arthritis, commonly accompanied by elevated inflammatory markers and hypocomplementemia. Most patients improve rapidly after drug withdrawal, supportive care, and short-course corticosteroid therapy; however, rechallenge carries a substantial risk of recurrence and should be approached cautiously.

ObjectivesThe pleiotropic effects of lipid-lowering therapies on mental health remain incompletely understood. This study aimed to investigate the causal impact of genetically proxied inhibition of three major lipid-lowering drug targets, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), Niemann-Pick C1-like protein 1 (NPC1L1), and proprotein convertase subtilisin/kexin type 9 (PCSK9), on a spectrum of psychiatric disorders using a drug-target Mendelian randomization approach.MethodsWe used genetic variants located within or near the HMGCR, NPC1L1, and PCSK9 gene regions that are associated with low-density lipoprotein cholesterol levels as proxies for pharmacological inhibition. Summary-level data were obtained from large-scale genome-wide association studies for seven psychiatric outcomes: anorexia nervosa, anxiety, bipolar disorder, major depressive disorder, neuroticism, obsessive compulsive disorder, and schizophrenia. The inverse-variance weighted method was employed as the primary Mendelian randomization approach, supplemented by multiple sensitivity analyses to assess robustness.ResultsGenetically proxied inhibition of HMGCR was associated with an increased risk of major depressive disorder (odds ratio = 1.16; 95% confidence interval: 1.07-1.25; p = 4.5e-04). In contrast, NPC1L1 inhibition was associated with a decreased risk of major depressive disorder (odds ratio = 0.88; 95% confidence interval: 0.84-0.92; p = 8.1e-08). PCSK9 inhibition was significantly associated with an increased risk of major depressive disorder (odds ratio = 1.16; 95% confidence interval: 1.06-1.26; p = 8.2e-04) and bipolar disorder (odds ratio = 1.28; 95% confidence interval: 1.19-1.38; p = 9.4e-12). No significant associations were observed between these targets and the remaining psychiatric outcomes.ConclusionsThis study provides genetic evidence that lipid-lowering drug targets exert distinct effects on psychiatric disorders. These findings highlight the importance of further clinical and mechanistic studies, particularly given the widespread use of lipid-lowering therapies in aging populations who are vulnerable to mental health conditions.

Background:Nasal Streptococcus pyogenes (SP) infection triggers psoriasis relapse, with the systemic-to-cutaneous immune relay poorly understood. This study aims to elucidate role of dendritic cell (DC) metabolic reprogramming and trafficking in driving SP-induced psoriasis relapse. Methods:A murine psoriasis model was established using imiquimod (IMQ) and intranasal SP challenge, with disease severity evaluated via PASI scoring and histology, epidermal proliferation (Ki67) and T cell (CD3) via immunofluorescence, immunohistochemistry, and IL-23, IL-17A, and IL-1β levels via enzyme-linked immunosorbent assay (ELISA) in skin. Immune cell infiltration (DCs, γδ T cells) was analyzed by flow cytometry, RNA-seq identified affected genes and pathways, and real-time polymerase chain reaction (qPCR) /Western blot (WB) detected transcription and protein levels of target genes in SP lipoteichoic acid (LTA)-activated BMDCs in vitro. Oxygen consumption rate (OCR), extracellular acidification rate (ECAR), wound healing, Transwell migration, and co-culture assays assessed metabolic reprogramming and migration function of BMDCs in response to LTA in vitro. CD11c-Luc reporter mice were monitored via bioluminescence imaging (BLI) to dynamically track DC migration in vivo, and confocal immunofluorescence co-localization was used to visualize DC-γδT cell interactions in skin. Results:Nasal SP infection exacerbated psoriasis-like lesions by increasing PASI scores (10.3 ± 0.2 in Re-SP vs 8.2 ± 0.4 in Re, P < 0.01), epidermal thickness, pro-inflammatory cytokines (IL-17A levels increased by approximately 2.1-fold in Re-SP compared to Re), and promoting DC maturation, γδT cell infiltration, and IL-17A production via TLR2/NF-κB/nitric oxide synthase 2(NOS2) signaling. RNA-seq and in vitro assays demonstrated SP induces DC aerobic glycolysis (as evidenced by significantly increased ECAR and suppressed OCR) and hyper-mobility through TLR2 activation, upregulating TLR2, NF-κB markers (p-IKBα, p-p65), NOS2, and myosin-related proteins (p-myosin phosphatase target subunit 1, MYPT1 and p-myosin light chain, MLC), with inhibited TLR2 reducing these effects. In vivo, SP triggered rapid DC activation and trafficking to skin, forming immunological synapse with γδT cells to induce IL-17A. Conclusion:These findings suggest that nasal SP infection may exacerbate psoriasis relapse through TLR2-dependent DC metabolic reprogramming and trafficking, which in turn promote γδ T cell IL-17A production. However, as these findings are derived from preclinical mouse models and in vitro experiments, validation in human psoriasis cohorts and chronic disease models is required before clinical translation can be considered.

Background. The post-stroke inflammatory response denotes the inflammatory damage inflicted upon brain tissue following stroke. Plasma fibrinogen (FIB) can permeate the compromised blood-brain barrier (BBB) after ischemic stroke, leading to the activation of the NLRP3 inflammasome. Tong-Qiao-Huo-Xue-Decoction (TQHXD), a traditional formula used to promote blood circulation and resolve blood stasis, has shown potential in this context. Nevertheless, the precise therapeutic mechanisms of TQHXD in mitigating cerebral ischemia-reperfusion injury remain to be fully elucidated. Objective. To examine the reparative effects and underlying mechanisms of TQHXD-CSF on inflammatory damage in BV-2 cells subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) injury. Methods. To establish an in vitro model of OGD/R injury and an inflammatory BV-2 cells model induced by FIB. The protective effects of TQHXD-CSF on OGD/R-injured cells were verified using CCK-8 and LDH assays. Immunofluorescence, SEM, Western blotting, and CHIP-PCR were employed to confirm that TQHXD reduces the inflammatory response by downregulating FIB levels. Pull-down and co-immunoprecipitation (CO-IP) assays were conducted to detect the interaction between FIB and NLRP3. Results. TQHXD-CSF can significantly inhibit the abnormal increase in LDH levels induced by OGD/R, enhance cell viability, and mitigate cell pyroptosis. Additionally, TQHXD-CSF reversed the marked upregulation of FIB, NLRP3, and GSDMD fluorescence intensity and protein expression caused by the FIB inflammation model, demonstrating an effect comparable to that of lumbrokinase, a fibrinolytic agent for FIB. Furthermore, it notably reduced the acetylation of H3 and H4 in the NLRP3 promoter. Importantly, the pull-down and CO-IP results indicated a robust binding affinity between FIB and NLRP3. Conclusion. TQHXD-CSF can inhibit inflammation by downregulating the FIB-NLRP3 pathway and exert a protective effect on BV-2 cells under OGD/R and FIB inflammatory injury.

Purpose:This study aims to evaluate the triglyceride-glucose (TyG) index as a biomarker for identifying prediabetes mellitus (PDM) in children and adolescents with obesity and to compare its predictive ability with traditional indicators. Methods:A cross-sectional study was conducted with 213 children and adolescents with obesity, aged 8 to 18 years. Key inclusion criteria included obesity, defined as a BMI above the 95th percentile. Diagnostic criteria were based on fasting plasma glucose (FPG) and the oral glucose tolerance test (OGTT). Correlation analysis, least absolute shrinkage and selection operator (LASSO) logistic regression, logistic regression, and ROC curve analysis were performed to assess predictive performance. Results:The TyG index showed significant positive correlations with triglyceride (TG; r = 0.751), hemoglobin A1c (HbA1c; r = 0.422), 2hPG (r = 0.387), and FPG (r = 0.385) (all p < 0.001). LASSO regression identified TyG, HbA1c, and homeostasis model assessment of insulin resistance (HOMA-IR) as key predictors. Multivariate logistic regression demonstrated that the TyG index was an independent risk factor for PDM (OR = 13.287; 95% confidence interval [CI]: 5.357-32.956; p < 0.001). ROC analysis revealed an AUC of 0.776 (95% CI: 0.715-0.837) for the TyG index, with an optimal cutoff of 8.895, yielding a sensitivity of 55.1% and specificity of 85.2%, outperforming TG, FPG, and HOMA-IR. Conclusion:The TyG index is a reliable and practical marker for identifying prediabetes in children and adolescents with obesity. Its predictive performance exceeds that of several conventional indicators, providing clinical value for early screening and intervention.

The amount and patterns of physical activity to benefit cognitive health remains unclear. In UK Biobank cohort, individuals with a full week of accelerometer‐based moderate‐to‐vigorous PA (MVPA) and light PA (LPA) data were analysis. The last date for dementia was April 2024. Associations between the incidence of all‐cause dementia, Alzheimer's disease (AD), and Vascular dementia (VaD), and the level and patterns of PA were assessed using Cox proportional hazards regression models. These including: 1) MVPA gradients were compared with less than 150 min/week; 2) Compared active intensive (≥50% of MVPA in 1–2 days), active regular (not meeting active intensive), and inactive (<300 min/week); 3) performed stratified analyses by age, sex and APOE ε 4 carrier status; 4) Investigated the effect of LPA among inactive MVPA. 91512 individuals (mean [SD] age, 56.03[7.8] years; 55.9% female) were included. Compared with <150 min, 150–299 min of moderate to vigorous physical activity (MVPA) in weekend or regular pattern did not have significantly lower dementia incidence, but over 300 min/week had. When stratified at 300 min/week of MVPA, hazard ratios for dementia were 0.73 (95% CI: 0.60–0.89) for weekend pattern and 0.79 (95% CI: 0.64–0.98) for regular pattern. For inactive MVPA, >840 min/week of light physical activity (LPA) was associated with lower dementia incidence. More than 300 min/week of MVPA, whether concentrated within 1 to 2 days or distributed evenly, was associated with decreased risk of dementia. LPA partially compensated inactive MVPA.

BACKGROUND:The amount and patterns of physical activity to benefit cognitive health remains unclear. METHOD:In UK Biobank cohort, individuals with a full week of accelerometer-based moderate-to-vigorous PA (MVPA) and light PA (LPA) data were analysis. The last date for dementia was April 2024. Associations between the incidence of all-cause dementia, Alzheimer's disease (AD), and Vascular dementia (VaD), and the level and patterns of PA were assessed using Cox proportional hazards regression models. These including: 1) MVPA gradients were compared with less than 150 min/week; 2) Compared active intensive (≥50% of MVPA in 1-2 days), active regular (not meeting active intensive), and inactive (<300 min/week); 3) performed stratified analyses by age, sex and APOE ε4 carrier status; 4) Investigated the effect of LPA among inactive MVPA. RESULT:91512 individuals (mean [SD] age, 56.03[7.8] years; 55.9% female) were included. Compared with <150 min, 150-299 min of moderate to vigorous physical activity (MVPA) in weekend or regular pattern did not have significantly lower dementia incidence, but over 300 min/week had. When stratified at 300 min/week of MVPA, hazard ratios for dementia were 0.73 (95% CI: 0.60-0.89) for weekend pattern and 0.79 (95% CI: 0.64-0.98) for regular pattern. For inactive MVPA, >840 min/week of light physical activity (LPA) was associated with lower dementia incidence. CONCLUSION:More than 300 min/week of MVPA, whether concentrated within 1 to 2 days or distributed evenly, was associated with decreased risk of dementia. LPA partially compensated inactive MVPA.

Objective:The purpose of this study was to observe the relationship between sarcopenic obesity and prediabetes in adolescents. Methods: A cross-sectional retrospective study was conducted on United States adolescents aged 12-19 years. Data were extracted from the National Health and Nutrition Examination Survey (NHANES) 2011-2012, 2013-2014, and 2015-2016 cycles. Sarcopenic obesity was defined as waist circumference at or above the 90th percentile for age and sex and appendicular skeletal muscle mass divided by weight below the lower quintile for age and sex. Results:The prevalence of prediabetes was 22.2 % in the normal group, 15.0 % in the sarcopenia alone group, 22.3 % in the obesity alone group, and 36.9 % in the sarcopenic obesity group. In univariate logistic regression, adolescents with sarcopenic obesity had a higher odds of prediabetes compared to the normal group (odds ratio = 2.048, 95 % CI: 1.125-3.728, P = 0.020). After adjusting for confounders, the odds remained significantly elevated (adjusted odds ratio = 2.060, 95 % CI: 1.178-3.604, P = 0.012). Conclusion:The present study demonstrates that sarcopenic obesity was closely associated with an increased odds of prediabetes in United States adolescents.

Inspection is the first of the four diagnoses.Skin inspection is not only an important part of the four diagnoses of Chinese medicine,but also the characteristic and essence of Chinese dermatology.The development of artificial intelligence(AI)technology provides an opportunity for the intelligent research of skin inspection in traditional Chinese medicine(TCM).This study aims to review the application status of artificial intelligence in TCM skin inspection,and summarize the research progress of various artificial intelligence technologies in skin lesion differentiation,syndrome differentiation and location differentiation,and propose future directions for AI empowerment in TCM dermatology.Based on the basic theory of Chinese medicine and skin clinical thinking of Chinese medicine,this article puts forward the prospect of AI empowerment from the aspects of macro and micro combination,point and surface combination,mind-body combination and time-space combination.This study discusses the existing problems and challenges in the intersection of AI and TCM dermatology.The intersection of AI and TCM dermatological inspection is at the developmental stage.AI has broad application prospects within TCM dermatology,but it also faces numerous challenges.While AI offers opportunities to modernize TCM dermatology,challenges such as aligning AI with TCM's holistic principles and ensuring clinical relevance remain.Further research integrates AI with TCM skin inspection methods,the intricate connotations and applications of TCM dermatological Inspection will be fully realized,thereby providing reference for the development of artificial intelligence to help TCM dermatology diagnosis and treatment technology.

Bacteria-infected atopic dermatitis (AD) is an infectious inflammatory skin disease that profoundly disrupts patients' daily lives. As a viable alternative to antibiotic therapy, reactive oxygen species (ROS) treatment has emerged, effectively eradicating bacteria without the risk of antibiotic resistance. Nevertheless, the excess production of ROS can subsequently trigger inflammation in surrounding healthy tissues. To tackle this challenge, a ROS-balancing hydrogel dressing is devised. This dressing integrates a nanocomposite comprising zinc-doped ferricyanide-derived metal-organic framework (ZnMOF) loaded with curcumin (Cur), embedded in a hydrogel matrix of gelatin (Gel) crosslinked with silk fibroin (SF). Upon light activation, the Cur/ZnMOF/SF@Gel hydrogel dressing generates a significant quantity of ROS, enabling rapid bacterial elimination at the infection site. Concurrently, the enzymatic antioxidant activity of ZnMOF and the polyphenolic compounds in Cur within the hydrogel work in synergy to neutralize excess ROS by chelating iron ions, thereby inhibiting the Fenton and Haber-Weiss reactions. This mechanism restores ROS balance and mitigates oxidative stress in the skin tissues. Additionally, the synthesized hydrogel dressing demonstrates remarkable self-healing properties, robust adhesive capabilities, and outstanding mechanical performance. This intelligent, multifunctional hydrogel offers a promising substitute for traditional antibiotic-loaded surgical dressings in the rapid and effective management of bacteria-infected AD.

BackgroundMyocardial ischemia-reperfusion (I/R) injury which leads to continuously worsening ventricular remodeling and cardiac dysfunction in the chronic stage, is a significant contributor to the global prevalence of heart failure. Traditional Chinese herbal formulas have been shown to prevent myocardial I/R injury.MethodThis study aims to investigate whether Danqi soft caspule (DQ), a classical traditional Chinese medicine (TCM) preparation, exerted the protective effects against myocardial I/R injury and explore the potential underlying mechanisms. A rat model of myocardial I/R and a cell model of H2O2 induced oxidative stress injury were established to assess the effects of DQ on cardiac injury, cardiomyocyte apoptosis, as well as mitochondrial structure and function.ResultDQ pre-treatment reduced both the proportion of infarct area and ischemic risk area and decreased cardiomyocyte apoptosis in myocardial I/R injury rats. In H2O2 induced cells, DQ was found to reduce cell apoptosis and lower oxidative stress levels. Furthermore, DQ inhibited mitochondrial fission, prevented alterations in mitochondrial membrane potential, and suppressed Cytochrome C release from the mitochondria, thereby preventing apoptosis. DQ has protective effects against I/R induced oxidative stress injury by reducing cardiomyocyte apoptosis through inhibition mitochondrial fission. Moreover, DQ could restore mitochondrial structure and function by suppressing the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and dynamin-related protein 1 (Drp-1).ConclusionDQ inhibited I/R injury and cardiomyocyte apoptosis by reducing mitochondrial fission associated with suppressing the phosphorylation of CaMKII and Drp-1.

This scoping review synthesizes existing research comparing traditional Chinese medicine (TCM) and contemporary treatments (CTs) for managing psoriasis vulgaris (PsV). A thorough literature search was conducted across multiple databases through February 2024, identifying relevant systematic reviews, randomized controlled trials (RCTs), quasi-experimental, and observational studies that contrast TCM approaches with CTs for PsV. From an initial pool, 195 articles were analyzed, indicating a growing interest in this comparative area, with most studies involving sample sizes between 30 and 100 participants. Key interventions included both internal and topical applications of Chinese herbal medicines, notably Rehmanniae Radix, Arnebiae Radix, and Smilacis Glabrae Rhizoma. Outcomes focused on PASI scores, quality of life metrics, and adverse effects. Results suggest that TCM offers efficacy in improving PASI scores and quality of life; however, evidence concerning toxicity profiles, recurrence rates, and comorbidity outcomes remains sparse. Notable research gaps include a lack of comprehensive data on newer treatment modalities, particularly biologics. Future studies should aim to delineate subjects and interventions in greater detail to support clinical applicability.