Gene and protein expression and metabolic flux analysis reveals metabolic scaling in liver ex vivo and in vivo.

Metabolic scaling, the inverse correlation of metabolic rates to body mass, has been appreciated for more than 80 years. Studies of metabolic scaling have largely been restricted to mathematical modeling of caloric intake and oxygen consumption, and mostly rely on computational modeling. The possibility that other metabolic processes scale with body size has not been comprehensively studied.

Vascular pathobiology of pulmonary hypertension.

Pulmonary hypertension (PH), increased blood pressure in the pulmonary arteries, is a morbid and lethal disease. PH is classified into several groups based on etiology, but pathological remodeling of the pulmonary vasculature is a common feature. Endothelial cell dysfunction and excess smooth muscle cell proliferation and migration are central to the vascular pathogenesis.

Flow-induced endothelial mitochondrial remodeling mitigates mitochondrial reactive oxygen species production and promotes mitochondrial DNA integrity in a p53-dependent manner.

Tumor suppressor p53 plays a pivotal role in orchestrating mitochondrial remodeling by regulating their content, fusion/fission processes, and intracellular signaling molecules that are associated with mitophagy and apoptosis pathways. In order to determine a molecular mechanism underlying flow-mediated mitochondrial remodeling in endothelial cells, we examined, herein, the role of p53 on mitochondrial adaptations to physiological flow and its relevance to vascular function using endothelial cell-specific p53 deficient mice. We observed no changes in aerobic capacity, basal blood pressure, or endothelial mitochondrial phenotypes in the endothelial p53 mull animals.

Eccentric hypertrophy in an animal model of mid- and long-term premature ventricular contraction-induced cardiomyopathy.

Background: Tachycardia and heart rate irregularity are proposed triggers of premature ventricular contraction-induced cardiomyopathy (PVC-cardiomyopathy). Bigeminal premature atrial and ventricular contractions (PACs and PVCs) increase heart rate and result in rhythm irregularities but differ in their effects on ventricular synchrony. Comparing chronic bigeminal PACs with PVCs would provide insights into mechanisms of PVC-cardiomyopathy.

Neuroprotection against stroke and encephalopathy after cardiac surgery.

Cerebral ischemia in the perioperative period is a major risk factor for stroke, encephalopathy, and cognitive decline after cardiothoracic surgery. After coronary artery bypass grafting, both stroke and encephalopathy can result in poor patient outcomes and increased mortality. Neuroprotection aims to lessen the severity and occurrence of further injury mediated by stroke and encephalopathy and to aid the recovery of conditions already present.

Coronary artery bypass graft markers: history, usage, and effects.

Coronary artery bypass grafting (CABG) is one of the most common procedures in the United States as many Americans suffer from coronary heart disease and undergo CABG each year. While CABG has been performed for decades, questions remain regarding the benefits graft marker placement provides for patient therapy and outcomes. Markers at the proximal graft anastomosis aim to improve the efficiency and reduce the risks of subsequent, post-coronary artery bypass grafting coronary angiography by decreasing fluoroscopy time and contrast volume used.

Consequences of chronic frequent premature atrial contractions: Association with cardiac arrhythmias and cardiac structural changes.

Introduction: Frequent premature ventricular contractions (PVCs) can cause cardiomyopathy (CM). Postextrasystolic potentiation (PESP) and irregularity have been in implicated as triggers of PVC-CM. Because both phenomena can also be found in premature atrial contractions (PACs), it is speculated that frequent PACs have similar consequences.