Laugesenbech9536

l FLIm-Raman dataset using a descriptive modeling approach led to the identification of LDL accumulation as the primary source of lifetime contrast in atherosclerotic lesions in the violet spectral range. Earlier FLIm validation studies relying on histopathological findings had associated this contrast to increased collagen content, also present in advanced lesions, thus demonstrating the benefits of alternative validation methods.Background To date, the benefit of successful revascularization of chronic total occlusions (CTOs) on prognosis remains uncertain, and there is a paucity of data on the impact of successful revascularization for CTO patients on long-term cardiovascular survival. This study aimed to investigate the long-term cardiovascular survival for patients with successful and unsuccessful CTO revascularization in a large cohort of patients. Methods There were 1,655 consecutive patients with at least one CTO included and were grouped into successful revascularization (n = 591) and unsuccessful revascularization (n = 1,064). Propensity score matching (PSM) was carried out to balance the clinical and the angiographic characteristics. Cardiac mortality was defined as the primary endpoint. Major adverse cardiac event (MACE) was assessed as a "secondary endpoint." Results After 3.6 years of follow-up, there was no significant difference between the successful and the unsuccessful revascularization groups in the rate of cardiac mortality [adjusted hazard ratio (HR) 0.96, 95% confidence interval (CI) 0.59-1.58, p = 0.865]. After the PSM analysis (371 pairs) between the two groups, the cardiac mortality rate values (HR 0.51, 95% CI 0.23-1.15, p = 0.104) were equivalent, whereas the adjusted risk of MACE (HR 0.43, 95% CI 0.32-0.58, p = 0.001) and target-vessel revascularization (HR 0.41, 95% CI 0.29-0.58, p less then 0.001) were significantly higher in patients with unsuccessful revascularization. Conclusion For the treatment of CTO patients, successful revascularization was not associated with a lesser risk for cardiac mortality as compared with unsuccessful revascularization. However, successful revascularization reduced MACE and target-vessel revascularization.Background Atrial fibrillation (AF) is the most common arrhythmia associated with high risk of venous thromboembolism. Inflammatory mechanisms may be involved in the pathophysiology of AF and in the AF-related thrombogenesis, and patients with AF might benefit from the use of anticoagulants with anti-inflammatory properties. However, the evidence is still scarce, and it points out the need of trials seeking to investigate the levels of inflammatory mediators in patients with AF under different anticoagulant therapies. Therefore, this study was designed to define whether patients with AF treated either with an activated coagulation factor X (FXa) inhibitor (rivaroxaban) or with a vitamin K inhibitor (warfarin) present changes in peripheral levels of inflammatory mediators, mainly cytokines and chemokines. Methods A total of 127 subjects were included in this study, divided into three groups patients with non-valvular atrial fibrillation (NVAF) using warfarin (N = 42), patients with NVAF using rivaroxaban (N = 29), and controls (N = 56). Plasma levels of inflammatory mediators were quantified by immunoassays. Results Patients with AF (both warfarin and rivaroxaban groups) presented increased levels of inflammatory cytokines in comparison with controls. The use of rivaroxaban was associated with decreased levels of inflammatory cytokines in comparison with warfarin. On the other hand, patients with AF using rivaroxaban presented increased levels of the chemokines (MCP-1 in comparison with warfarin users; MIG and IP-10 in comparison with controls). Conclusions AF is associated with an inflammatory profile that was less pronounced in patients on rivaroxaban in comparison with warfarin users. Further studies are necessary to assess the clinical implications of our results and whether patients with AF would benefit from rivaroxaban anti-inflammatory effects.Ankylosis spondylitis (AS) is a disease mainly characterized by sacroiliac joint and spinal attachment point inflammation. Long non-coding RNA (lncRNA) plays a key role in the progression of many diseases. However, few studies have been conducted on the function of lncRNA maternally expressed gene 3 (MEG3) in AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the relative levels of MEG3, microRNA let-7i, sclerostin (SOST), and inflammatory cytokines. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay were used to confirm the interaction between MEG3 and let-7i or let-7i and SOST. In addition, western blot (WB) analysis was performed to detect the protein levels of osteogenesis markers and SOST. The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS.Placental leucine aminopeptidase/insulin-regulated aminopeptidase (P-LAP/IRAP) regulates vasopressin and oxytocin levels in the brain and peripheral tissues by controlled degradation of these peptides. In this study, we determined the relationship between P-LAP/IRAP and vasopressin levels in subregions of the murine brain. P-LAP/IRAP expression was observed in almost all brain regions. read more The expression patterns of P-LAP/IRAP and vasopressin indicated that cells expressing one of these protein/peptide were distinct from those expressing the other, although there was significant overlap between the expression regions. In addition, we found reciprocal diurnal rhythm patterns in P-LAP/IRAP and arginine vasopressin (AVP) expression in the hippocampus and pituitary gland. Further, synchronously cultured PC12 cells on treatment with nerve growth factor (NGF) showed circadian expression patterns of P-LAP/IRAP and enzymatic activity during 24 h of incubation. Considering that vasopressin is one of the most efficient peptide substrates of P-LAP/IRAP, these results suggest a possible feedback loop between P-LAP/IRAP and vasopressin expression, that regulates the function of these substrate peptides of the enzyme via translocation of P-LAP/IRAP from intracellular vesicles to the plasma membrane in brain cells.