Reducing Door-to-Balloon Time Using EMS-Initiated App-Based Communication.

Background: Reducing door-to-balloon (D2B) time for ST-segment elevation myocardial infarction (STEMI) has been shown to improve outcomes. Delays still occur due to various factors such as time to laboratory activation and diagnostic clarification in equivocal cases. We propose that early communication through a mobile application (app) between emergency medical services (EMS) and in-hospital providers can reduce EMS-to-balloon time and provide coordinated care to impact D2B time.

Hypoxia-induced epigenetic regulation of breast cancer progression and the tumour microenvironment.

The events that control breast cancer progression and metastasis are complex and intertwined. Hypoxia plays a key role both in oncogenic transformation and in fueling the metastatic potential of breast cancer cells. Here we review the impact of hypoxia on epigenetic regulation of breast cancer, by interfering with multiple aspects of the tumour microenvironment.

A novel Na1.5-dependent feedback mechanism driving glycolytic acidification in breast cancer metastasis.

Solid tumours have abnormally high intracellular [Na]. The activity of various Na channels may underlie this Na accumulation. Voltage-gated Na channels (VGSCs) have been shown to be functionally active in cancer cell lines, where they promote invasion.

Right to Left Cardiac Power Output- New Prognosticator in STEMI Patients With Cardiogenic Shock (R-Shock).

ST elevation myocardial infarction (STEMI) is a leading cause of cardiogenic shock (CS) and carries substantial mortality. Cardiac power output (CPO) is the strongest predictor of clinical outcome in CS, and worse outcomes result from concomitant right and left ventricular failure. Right ventricular performance is calculated using right sided CPO.

Subcellular dynamics and functional activity of the cleaved intracellular domain of the Na channel β1 subunit.

The voltage-gated Na channel β1 subunit, encoded by SCN1B, regulates cell surface expression and gating of α subunits and participates in cell adhesion. β1 is cleaved by α/β and γ-secretases, releasing an extracellular domain and intracellular domain (ICD), respectively. Abnormal SCN1B expression/function is linked to pathologies including epilepsy, cardiac arrhythmia, and cancer.

Inhibition of the Na/K-ATPase by cardiac glycosides suppresses expression of the IDO1 immune checkpoint in cancer cells by reducing STAT1 activation.

Despite extensive basic and clinical research on immune checkpoint regulatory pathways, little is known about the effects of the ionic tumor microenvironment on immune checkpoint expression and function. Here we describe a mechanistic link between Na/K-ATPase (NKA) inhibition and activity of the immune checkpoint protein indoleamine-pyrrole 2',3'-dioxygenase 1 (IDO1). We found that IDO1 was necessary and sufficient for production of kynurenine, a downstream tryptophan metabolite, in cancer cells.

Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.

Ion channels are key regulators of cancer cell pathophysiology. They contribute to a variety of processes such as maintenance of cellular osmolarity and membrane potential, motility (via interactions with the cytoskeleton), invasion, signal transduction, transcriptional activity and cell cycle progression, leading to tumour progression and metastasis. Ion channels thus represent promising targets for cancer therapy.