Perceptions of Magnetic Resonance Imaging During Pregnancy: A Newfoundland and Labrador Perspective.

Objectives: This study aimed to identify enablers and barriers to participation in MRI for clinical indications and scientific research, and to determine the perceptions of MRI performed during pregnancy.

Methods: We conducted a survey of 156 pregnant people in Newfoundland and Labrador including sociodemographic information, obstetrical history, MRI history, and willingness to participate in an MRI. Categorical variables were analyzed using a Fisher exact test and open-ended questions were analyzed using thematic analysis.

Genetic Analysis of Obesity-Induced Diabetic Nephropathy in BTBR Mice.

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the U.S. and has a significant impact on human suffering.

Identifying placental metabolic biomarkers of preterm birth using nuclear magnetic resonance of intact tissue samples.

Introduction: Our understanding of the etiology of preterm birth (PTB) is incomplete; however, recent evidence has found a strong association between placental dysfunction and PTB. Altered placental metabolism may precede placental dysfunction and therefore the study of placental metabolic profiles could identify early biomarkers of PTB. In this study, we evaluated the placental metabolome in PTB in intact tissue samples using nuclear magnetic resonance (NMR) and spectral editing.

Novel regulators of islet function identified from genetic variation in mouse islet Ca oscillations.

Insufficient insulin secretion to meet metabolic demand results in diabetes. The intracellular flux of Ca into β-cells triggers insulin release. Since genetics strongly influences variation in islet secretory responses, we surveyed islet Ca dynamics in eight genetically diverse mouse strains.

An Enhancer Within Abcb11 Regulates G6pc2 in C57BL/6 Mouse Pancreatic Islets.

G6PC2 is predominantly expressed in pancreatic islet β-cells where it encodes a glucose-6-phosphatase catalytic subunit that modulates the sensitivity of insulin secretion to glucose by opposing the action of glucokinase, thereby regulating fasting blood glucose (FBG). Prior studies have shown that the G6pc2 promoter alone is unable to confer sustained islet-specific gene expression in mice, suggesting the existence of distal enhancers that regulate G6pc2 expression. Using information from both mice and humans and knowledge that single nucleotide polymorphisms (SNPs) both within and near G6PC2 are associated with variations in FBG in humans, we identified several putative enhancers 3' of G6pc2.