Background: Atrial septal defects (ASDs) are a common cause of congenital heart disease worldwide.
Objectives: The purpose of the study was to assess change over time in surgical outcomes for ASD repair and identify patient-level risk factors for adverse postoperative outcomes.
Methods: We analyzed cases of isolated ASD in patients <18 years from 2010 to 2020 from 71 sites participating in the International Quality Improvement Collaborative for Congenital Heart Disease.
We present the genomes of nine cultured microbes isolated from two freshwater sites in Wellesley, MA. The dataset is useful for exploring genomic diversity among freshwater taxa, including , , , and .
View Article and Find Full Text PDFThe oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLDs). PTLD can also arise in the absence of EBV, but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions, respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines.
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