Suspected Fatal Arrhythmic Events in Japanese Patients With Coronary Artery Disease - From the CREDO-Kyoto PCI/CABG Registries Cohorts-2 and -3.

Background: Fatal arrhythmic events (FAEs), such as sudden cardiac death (SCD) and fatal ventricular arrhythmias, are a devastating complication in patients with coronary artery disease (CAD). Therefore, in this study we aimed to assess the incidence of FAEs in more recent Japanese patients with CAD and to examine whether risk stratification of FAEs can still be feasible using the left ventricular ejection fraction (LVEF).

Methods And Results: In the CREDO Kyoto PCI/CABG registry cohorts-2 and -3, there were 25,843 patients with LVEF data who received a first coronary revascularization (LVEF ≤35% group: N=1,671, 35%45%: N=21,503).

Plasma and serum concentrations of VEGF-A121, but not of VEGF-A165, increase post-bevacizumab administration.

Background: VEGF-A concentrations were measured in the blood of bevacizumab-treated cancer patients in previous studies, but a consensus has not formed that would develop VEGF-A into a clinical biomarker. Recently, methods to strictly distinguish between the VEGF-A isoforms have been developed but have not yet been applied to cancer patients undergoing bevacizumab treatment.

Methods: An ELISA that strictly distinguishes between VEGF-A121 and VEGF-A165-the major isoforms of VEGF-A-and a commercially available ELISA for VEGF-A are used to determine the concentration of VEGF-A121, VEGF-A165, and VEGF-A in the blood of 12 patients with advanced colorectal cancer receiving bevacizumab therapy.

Oral Inflammation and Microbiome Dysbiosis Exacerbate Chronic Graft-versus-host Disease.

The oral microbiota, second in abundance to the gut, is implicated in chronic systemic diseases, but its specific role in GVHD pathogenesis has been unclear. Our study finds that mucositis-induced oral dysbiosis in patients post-hematopoietic cell transplantation associated with increased chronic GVHD (cGVHD) even in patients receiving post-transplant cyclophosphamide. In murine HCT models, oral dysbiosis caused by bilateral molar ligatures exacerbated cGVHD and increased bacterial load in the oral cavity and gut with Enterococcaceae significantly increasing in both organs.

Lipid mediator palmitoylethanolamide (PEA) inhibits pathogenic T cell differentiation in vitro and in vivo.

Lipid mediator, palmitoylethanolamide (PEA) has recently attracted attention as a potential therapeutic option for various inflammatory autoimmune diseases. It has been reported that PEA exerts an inhibitory effect on inflammation triggered by PRRs, particularly Toll-like receptors expressed on myeloid antigen-presenting cells. However, the precise role of PEA in T cell development and function has not yet been elucidated.