FAIM3 antibody
- Known as:
- FAIM3 (anti-)
- Catalog number:
- orb101548
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- FAIM3 antibody
Related genes to: FAIM3 antibody
- Gene:
- FCMR NIH gene
- Name:
- Fc fragment of IgM receptor
- Previous symbol:
- FAIM3
- Synonyms:
- TOSO
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-04-04
- Date modifiied:
- 2015-04-24
Related products to: FAIM3 antibody
Related articles to: FAIM3 antibody
- Musculoskeletal injuries, a major impediment to medical military readiness, are often associated with muscle fatigue caused by prolonged, repeated activities, including running and walking with load carriage. Here, we investigated the biomechanics of women running without a load and walking with load carriage to identify kinetic and kinematic parameters affected by exertion-related changes under both conditions. We collected motion-capture data and computed tomography images from 20 young, healthy women running without a load for 5 km at a subject-specific pace and walking with a 22.7-kg load for 5 km at a speed of 1.5 m/s. We developed individualized musculoskeletal models for each condition and characterized changes in kinetic and kinematic parameters for each subject between the start (0 km) and end of each 5-km session. We found that peak trunk flexion angle increased for both conditions (effect size ≥ 0.80), with the same trend for 18 of the 20 subjects. Peak hip extension, ankle dorsiflexion, and subtalar inversion internal moments had the same directional changes in both conditions, although not always meeting the significance threshold adjusted for multiple comparisons or yielding an effect size ≥ 0.80. In conclusion, this exploratory study identified exertional effects in women running without a load or walking with load carriage that resulted in biomechanical gait changes in the same direction, which could be used to develop countermeasures to reduce the risk of musculoskeletal injury. - Source: PubMed
Publication date: 2026/06/05
Rubio Jose ECanales FabricioSubramaniyan ManivannanArif Md ArifuzzamanPadhye AnkurMeardon StaceyWillson JohnReifman Jaques - Systemic lupus erythematosus (SLE) and idiopathic pulmonary fibrosis (IPF) share immune-inflammatory features, yet their convergent peripheral-blood transcriptomic signatures remain incompletely defined. We sought to identify shared blood gene programs linking SLE and IPF, prioritize robust cross-disease markers, and evaluate parsimonious diagnostic models with experimental and external assessments. - Source: PubMed
Publication date: 2026/02/20
Pang LijunLi YunfeiChen JunjieShang ShuangshuangLi MingHuang Chuanbing - To understand the heterogeneity of single-B cell responses to Metabolic Dysfunction-Associated Steatohepatitis (MASH), we performed Single-cell RNA sequencing (scRNA-seq) on single-B cells isolated from control and MCD-fed mice livers. Subsequent analyses included clustering, identification of differentially expressed genes (DEGs) and enrichment analysis. The expressions of high specific DEGs were validated using quantitative real-time PCR (qRT-PCR), immunofluorescence staining and function study. Four single-B cell clusters (3, 14, 16 and 20) were identified. The total number and proportion of B cells significantly decreased in MASH mice livers. In cluster 3, the decreasing mature B cells were supposed with anti-inflammatory role associated with B cell activation and differentiation of other immune cells in MASH. The DEGs (, , and ) of cluster 3 were consistently downregulated in B cells cocultued with lipotoxic hepatocytes. And the portal area of livers contained fewer B cells in MASH patients and mice compared with controls. B cells attenuated lipotoxicity-driven inflammation by enhancing anti-inflammatory factor (IL-10, IL-35) secretion and inhibiting T cell inflammatory factor (IFN-γ, TNF-α, IL-17) production and proliferation. The other 3 clusters (14, 16 and 20) contained small numbers of single-B cell. plasmacytes (PCs) of cluster 14 were identified with the effect related to endoplasmic reticulum stress and N-Glycan biosynthesis. B cells of cluster 16 were implicated in regulating immune response in MASH. B cells of cluster 20 participated in apoptosis, NF-κB, TNF and JAK-STAT signaling pathway in MASH. Thus, a subgroup of mature B cells, diminished in MASH, may exerted anti-inflammatory or immunosuppressive effects. - Source: PubMed
Publication date: 2026/02/25
Lu Jia-ChunXiong Min-LiCai Zhi-QiMao TingTang LongLi Hui-YiXu Ming-YiLuo Sheng-Zheng - Medication-related osteonecrosis of the jaw (MRONJ) is a serious adverse effect of antiresorptive and antiangiogenic therapies, yet its molecular mechanisms remain poorly defined. The present study employed an analysis of microarray data (GSE7116) from peripheral blood mononuclear cells of patients with multiple myeloma, myeloma patients with MRONJ, and healthy controls. Differentially expressed genes were identified using the limma package, followed by functional enrichment analysis, weighted gene co-expression network analysis, and LASSO regression and CytoHubba network ranking. The predictive performance was validated by means of nested cross-validation, Firth logistic regression, and safe stratified 0.632+ bootstrap ridge regression. The profiling revealed distinct gene expression patterns between the groups: the upregulation of ribosomal and translational pathways, as well as the suppression of neutrophil degranulation and antimicrobial defense mechanisms, and identified key candidate genes, including , , , , , , and . These genes demonstrated substantial discriminatory capability, with an area under the curve ranging from 0.95 to 0.99, and were found to be functionally linked to immune system dysfunction, cytokine signaling, NF-κB activation, and a maladaptive stress response. These findings link MRONJ to systemic immune-inflammatory imbalance and translational stress disruption, offering novel insights and potential biomarkers for diagnosis and risk evaluation. - Source: PubMed
Publication date: 2025/12/05
Laputková GalinaTalian IvanSabo Ján - Fluid resuscitation immediately following a hemorrhagic injury improves clinical outcome. However, future military conflicts are expected to result in mass-casualty incidents with limited availability of fluid-resuscitation resources. Here, we developed and assessed the performance of a reinforcement learning AI method that optimized clinical outcome and fluid allocation under constrained resources. We generated a large cohort of synthetic trauma casualties using a validated cardio-respiratory computational model, simulating vital-sign time-series data for realistic battlefield scenarios involving hemorrhage, tourniquet application, and fluid resuscitation. For each casualty, we simulated three intervention options—infusion or no infusion of one fluid unit every 30 min over 90 min—and assessed whether the interventions restored the vital signs to “healthy” levels. Using these data, we trained the reinforcement learning model to predict the optimal sequence of interventions that maximized the number of casualties restored while minimizing fluid utilization. Using independent simulated data, we found that the AI model was twice as efficient and restored more than twice as many casualties as the current standard of care across varying numbers of casualties and resource limitations. These results highlight the model’s potential to enable personalized interventions, enhance treatment efficiency, and support automated medical decision-making in resource-constrained environments. - Source: PubMed
Publication date: 2025/12/24
Subramaniyan ManivannanJin XinNagaraja SrideviWallqvist AndersReifman Jaques