Ask about this productRelated genes to: ICAM1 antibody
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
Related products to: ICAM1 antibody
Related articles to: ICAM1 antibody
- Metabolic syndrome (MetS) definitions may perform differently in indigenous populations with distinct genetic and lifestyle exposures. The Negrito community remains under-represented in cardiometabolic research despite emerging risk. Building on earlier observations of atypical biomarker patterns in this population, potentially linked to CDH13-related vascular mechanisms, this study aimed to determine MetS prevalence using the International Diabetes Federation (IDF) and Harmonized Joint Interim Statement (JIS) definitions, evaluate agreement between these definitions and their concordance with cardiovascular risk scores (CRS), and examine relationships between inflammatory and vascular biomarkers in the context of MetS. A cross-sectional study was conducted among Negrito adults. MetS was categorized using the IDF and JIS definitions. CRS included the Framingham risk score (FRS), Castelli risk index (CRI)-I, CRI-II and the atherogenic index of plasma (AIP). High-sensitivity C-reactive protein, lipoprotein(a), soluble intercellular adhesion molecule-1 (sICAM-1), and T-cadherin were quantified. Agreement statistics, correlations, logistic and linear regression models were applied. Among 153 adults, MetS prevalence was 11.8% (IDF) and 16.3% (JIS) with near-perfect agreement (κ = 0.81), although McNemar testing indicated slight asymmetry between definitions. Concordance between MetS and CRS was generally weak, with AIP showing the highest agreement (IDF κ = 0.17; JIS κ = 0.30), followed by CRI-II (IDF κ = 0.05; JIS κ = 0.20). CRI-I showed slight agreement with both definitions (IDF κ = 0.07; JIS κ = 0.15), while FRS showed no meaningful alignment (IDF κ = -0.07; JIS κ = -0.01). sICAM-1 showed weak but consistent positive correlations with all CRS (r = 0.20-0.26, P = .017-.002). T-cadherin did not correlate with CRS but was inversely associated with sICAM-1 (r = -0.28, P = .001). In multivariable logistic models, CRI-I (OR = 3.20), CRI-II (OR = 2.32) and AIP (OR = 2.15) remained independently associated with MetS. In linear models, sICAM-1 showed consistent associations with each CRS (FRS R2 = 0.03; CRI-I R2 = 0.06; CRI-II R2 = 0.06; AIP R2 = 0.03). IDF and JIS definitions classified MetS similarly but showed limited concordance with CRS. AIP and CRI demonstrated stronger cross-sectional associations with MetS than FRS. Biomarker analyses indicated that sICAM-1 correlated with CRS. The inverse relationship between T-cadherin and sICAM-1 raises the possibility of compensatory vascular-protective mechanisms. Collectively, these findings suggest a distinct lipid-inflammatory cardiometabolic phenotype in the Negrito population, where endothelial activation markers may capture early vascular stress beyond traditional risk scores. - Source: PubMed
Mokhsin AtiqahFaisal Andrian AlifOthman Noor Mohd FirdausOthman Nor'AshikinMohd Ismail AletzaChen Xin WeeHoh Boon-PengAbdul Rahman Thuhairah - Extracellular vesicles (EVs) contribute to stroke rehabilitation by mediating intercellular signaling during inflammation and tissue repair. Here we report EV-associated surface proteins as potential biomarkers for predicting recovery of activities of daily living (ADL) during the subacute phase of ischemic stroke (IS). IS patients and healthy controls (HCs) were recruited for this study, with serum samples analyzed across three study stages. In the discovery subset (10 IS, 6 HCs), serum proteomics was used to identify differentially expressed proteins (DEPros) and perform Gene Ontology (GO) enrichment analysis. In the exploration subset (7 IS, 12 HCs), a proximity-dependent barcoding assay (PBA) was employed to profile surface proteins on individual EVs and screen for biomarker candidates. In a validation cohort, patients were grouped by ADL improvement (little-effect recovery, LE, = 30; obvious-effect recovery group, OE, = 22) based on Longshi Scale and Barthel Index assessments at admission and at 3 months follow-up. Targeted biomarker validation was performed with enzyme-linked immunosorbent assay (ELISA) and receiver operating characteristic (ROC) analysis. A total of 113 DEPros were identified, with GO term enrichment in EV-related pathways. PBA profiling revealed matrix metalloproteinase 9 (MMP9), carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), melanoma cell adhesion molecule (MCAM), and gelsolin (GSN) as candidate biomarkers. In the validation cohort, MMP9 and CEACAM1 were significantly elevated in the LE group. ROC analysis showed area under the curve (AUC) of 0.726 for MMP9 and 0.700 for CEACAM1 in distinguishing LE from OE. Elevated serum levels of EV-associated biomarkers MMP9 and CEACAM1 were associated with poor ADL recovery, supporting their potential as prognostic biomarkers for stroke rehabilitation outcomes. - Source: PubMed
Publication date: 2026/04/13
Luo JiaoCai YouCai YanlingZhang ChunxiaLiu AnkangHuo YongyangFan XuehuiYe RuixueGao HongHuang MeilingZhang XiaohuaZhou MingchaoWang Yulong - To assess the prognostic value of apoptotic (CD95), endothelial (CD54), and systemic inflammatory biomarkers (SII, SIRI, AISI) for predicting the effectiveness of modified selective diode transscleral cyclophotocoagulation (TSCPC) in patients with neovascular glaucoma using regression and neural network-based models. - Source: PubMed
Guzun Olga VolodymyrivnaZadorozhnyy Oleg SerhiyovichBogdanici Camelia MargaretaVychuzhanin Volodymyr ViktorovychVelichko Liudmyla MykolayivnaKorol Andrii RostyslavovichCușnir Valeriu NiconDumbrăveanu Lilia Gheorghe - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Traumatic brain injury (TBI) triggers secondary neurovascular damage characterized by oxidative stress, blood-brain barrier (BBB) disruption, and neuroinflammation, leading to long-term cognitive deficits. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cellular antioxidant defense, but its role in maintaining neurovascular integrity after TBI remains unclear. Here, using fluid percussion injury in wild-type, , and mice, and stretch injury in human brain microvascular endothelial cells (hBMVECs), we demonstrate that TBI suppresses Nrf2 signaling, reducing antioxidant gene expression, and increasing oxidative and nitrosative stress. Nrf2 impairment enhances BBB permeability, ICAM-1-mediated leukocyte transmigration and promotes neutrophil extracellular trap (NET) formation. ICAM-1 deletion rescues these effects, confirming the mechanistic link between Nrf2, ICAM-1, and immune-mediated vascular damage. Preservation of Nrf2 signaling maintains antioxidant defenses, limits immune cell infiltration, and restricts NET-mediated injury. Importantly, Nrf2 deficiency impairs functional recovery, whereas its presence correlates with improved neurological outcomes. Targeting the Nrf2-ICAM-1 axis may reduce immune-mediated neurovascular injury, limit NET formation, and improve functional recovery after traumatic brain injury. - Source: PubMed
Publication date: 2026/05/06
Muneer P M AbdulBhowmick SauravPoovanthodi Yemin AAlikunju Saleena