Hypertrophic Cardiomyopathy (HCM) is often caused by heterozygous mutations in β-myosin heavy chain (MYH7, β-MyHC). In addition to hyper- or hypocontractile effects of HCM-mutations, heterogeneity in contractile function (contractile imbalance) among individual cardiomyocytes was observed in end-stage HCM-myocardium. Contractile imbalance might be induced by burst-like transcription, leading to unequal fractions of mutant versus wildtype mRNA and protein in individual cardiomyocytes (allelic imbalance).
View Article and Find Full Text PDFPurpose: Electrocardiography (ECG) and respiratory-gated preclinical cardiac CEST-MRI acquisitions are difficult because of variable saturation recovery with T, RF interference in the ECG signal, and offset-to-offset variation in Z-magnetization and cardiac phase introduced by changes in cardiac frequency and trigger delays.
Methods: The proposed method consists of segmented saturation modules with radial FLASH readouts and golden angle progression. The segmented saturation blocks drive the system to steady-state, and because center k-space is sampled repeatedly, steady-state saturation dominates contrast during gridding and reconstruction.
The aim of this study was to provide a follow-up to the 2015 national survey of women in dental education to re-examine factors and perceived barriers to pursuing administrative and leadership roles. At the beginning of 2023, a survey was administered to full-time women faculty in predoctoral dental programs in the United States. The survey instrument employed a structured format along with open-ended questions to capture qualitative data.
View Article and Find Full Text PDFTumor Necrosis Factor-α (TNF-α) is a proinflammatory cytokine and a master regulator of immune cell function in vertebrates. While previous studies have implicated TNF signaling in invertebrate immunity, the roles of TNF in mosquito innate immunity and vector competence have yet to be explored. Herein, we confirm the identification of a conserved TNF-α pathway in consisting of the TNF-α ligand, Eiger, and its cognate receptors Wengen and Grindelwald.
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