Interplay of CT Coronary Plaque Characteristics and Ischemia to Predict Adverse Outcomes.

In 134 patients with stable coronary artery disease, high-risk plaque features at CT and physiologic stenosis were found to act in a synergistic fashion to predict adverse outcomes.

Impact of 2016 SCCT/STR guidelines for coronary artery calcium scoring of noncardiac chest CT scans on lung cancer screening CT reporting.

The 2016 SCCT/STR guideline for coronary artery calcification (CAC) scoring on non-cardiac chest CT (NCCT) scans explicitly calls for the reporting of CAC. Whether the publication of the 2016 SCCT/STR guideline has had any impact on CAC reporting in lung cancer screening (LCS) scans has not been investigated. Consecutive patients with a LCS scan were identified from the University of Minnesota LCS registry and evaluated for CAC reporting in 3 separate cohorts: 6 months before, 6 months after, and 1 year after the publication of the 2016 SCCT/STR guideline.

Transgenic overexpression of the SUR2A-55 splice variant in mouse heart reduces infract size and promotes protective mitochondrial function.

ATP-sensitive potassium channels found in both the sarcolemma (sarcK) and mitochondria (mitoK) of cardiomyocytes are important mediators of cardioprotection during ischemic heart disease. Sulfonylurea receptor isoforms (SUR2), encoded by , an ATP-binding cassette family member, form regulatory subunits of the sarcK channel and are also thought to regulate mitoK channel activity. A short-form splice variant of SUR2 (SUR2A-55) was previously shown to target mitochondria and display diaxoxide and ATP insensitive K activity when co-expressed with the inward rectifier channels Kir6.

Transient complex I inhibition at the onset of reperfusion by extracellular acidification decreases cardiac injury.

A reversible inhibition of mitochondrial respiration by complex I inhibition at the onset of reperfusion decreases injury in buffer-perfused hearts. Administration of acidic reperfusate for a brief period at reperfusion decreases cardiac injury. We asked if acidification treatment decreased cardiac injury during reperfusion by inhibiting complex I.