C-reactive Protein (1-point-calibration) ELISA Kit

Background: Platelets are critical mediators of vascular homeostasis and thrombosis, and also contribute to the development of inflammation. NLRP3 inflammasome is a cytosolic multi-protein complex that consists of NLRP3, ASC and caspase-1, and regulates IL-1 beta-mediated inflammation. Method and Results: Using two mouse models of thrombosis (i.e., occlusion of the middle cerebral artery and inferior vena cava), we found that thrombus formation was significantly enhanced in ASC-deficient (ASC(-/-)) mice, compared to that in wild-type (WT) and IL-1 beta(-/-) mice. ASC deficiency had no effects on blood coagulation parameters (i.e., prothrombin time [PT] and activated partial thromboplastin time [APTT]). Platelets from WT mice express ASC, but neither NLRP3 nor caspase-1. ASC deficiency significantly enhanced the expression of P-selectin and GPIIb/IIIa in response to a GPVI agonist (collagen-related peptide [CRP]), but not to thrombin, in platelets. CRP induced ASC speck formation in WT platelets. ASC deficiency also enhanced cytosolic Ca2+ elevation and phosphorylation of ERK1/2 and Akt in platelets. Conclusion: Our results demonstrate that ASC negatively regulates GPVI signaling in platelets and enhances thrombus formation, independent of NLRP3 inflammasome and IL-1 beta, and provide novel insights into the link between inflammation and thrombosis. (C) 2020 Elsevier Inc. All rights reserved.

The aim of this study was to investigate the relationship between long-term spinal mobility improvements and early disease activity changes or achievement of clinical response criteria in patients with ankylosing spondylitis (AS) treated with tumor necrosis factor (TNF-alpha) blockers. This retrospective study included 112 patients with AS treated with TNF-alpha blockers for up to 33 months. The pairedt-test was used to compare outcome measures between visits. The correlation between disease activity changes and metrological improvements was analyzed using cumulative probability plots, Spearman correlation coefficient, and canonical correlation. The difference in metrological outcomes between responders and non-responders to clinical response criteria was also examined. Metrological and disease activity outcomes improved most markedly in month 3. All disease activity outcomes and ESR from baseline to month 3 (3-month) were significantly correlated with the Bath Ankylosing Spondylitis Metrology Index (BASMI(10)) improvements from baseline to month 33 (33-month). The 3-month changes in ankylosing spondylitis disease activity score (ASDAS-CRP) and patient's global assessment showed a significant correlation with the 33-month changes in chest expansion. Only responders according to ASDAS major improvement at month 3 demonstrated significant 33-month improvements in both BASMI(10)and chest expansion, compared to non-responders. Responders according to Assessment of Spondylo Arthritis international Society 40 at month 3 showed significant 33-month improvements in BASMI(10), but not chest expansion, compared to non-responders. The degree of early changes in disease activity outcomes influenced the extent of long-term metrological improvements in AS treated with TNF-alpha blockers. Additionally, the achievement of ASDAS- major improvement at month 3 predicted significant metrological improvements throughout long-term TNF-alpha-blocker therapy.