A Historical Perspective on Presentations of Hypertensive Acute Heart Failure.

Background: The initial systolic blood pressure (SBP) in patients presenting to the hospital with acute heart failure (AHF) informs prognosis, diagnosis, and guides initial treatment. However, over time AHF presentations with elevated SBP appear to have declined. The present study examined whether the frequency of AHF presentations with systolic hypertension (SBP >160 mmHg) declined over a nearly two-decade time interval.

Polyclonal Secondary Mutations Drive Acquired Resistance to FGFR Inhibition in Patients with FGFR2 Fusion-Positive Cholangiocarcinoma.

Genetic alterations in the fibroblast growth factor receptor (FGFR) pathway are promising therapeutic targets in many cancers, including intrahepatic cholangiocarcinoma (ICC). The FGFR inhibitor BGJ398 displayed encouraging efficacy in patients with FGFR2 fusion-positive ICC in a phase II trial, but the durability of response was limited in some patients. Here, we report the molecular basis for acquired resistance to BGJ398 in three patients via integrative genomic characterization of cell-free circulating tumor DNA (cfDNA), primary tumors, and metastases.

Cost reductions associated with a quality improvement initiative for patients with ST-elevation myocardial infarction.

Background: Efforts to reduce door-to-balloon (DTB) times for patients presenting with an ST-elevation myocardial infarction (STEMI) are widespread. Reductions in DTB times have been shown to reduce short-term mortality and decrease inpatient length of stay (LOS) in these high-risk patients. However, there is a limited literature examining the effect that these quality improvement (QI) initiatives have on patient care costs.

BCR-ABL suppresses autophagy through ATF5-mediated regulation of mTOR transcription.

The oncoprotein BCR-ABL transforms myeloid progenitor cells and is responsible for the development of chronic myeloid leukemia (CML). In transformed cells, BCR-ABL suppresses apoptosis as well as autophagy, a catabolic process in which cellular components are degraded by the lysosomal machinery. The mechanism by which BCR-ABL suppresses autophagy is not known.