Clinical and Analytical Performance of a Novel Point-of-Care High-Sensitivity Cardiac Troponin I Assay.

Background: Point-of-care (POC) high-sensitivity cardiac troponin assays may further accelerate the diagnosis of myocardial infarction (MI).

Objectives: This study sought to assess the clinical and analytical performance of the novel high-sensitivity cardiac troponin I (hs-cTnI)-SPINCHIP POC test.

Methods: Adult patients presenting with acute chest discomfort to the emergency department were enrolled in an international, diagnostic, multicenter study.

mTOR signaling is required for phagocyte free radical production, GLUT1 expression, and control of infection.

Mammalian target of rapamycin (mTOR) is a key regulator of metabolism in the mammalian cell. Here, we show the essential role for mTOR signaling in the immune response to bacterial infection. Inhibition of mTOR during infection with revealed that mTOR signaling is required for bactericidal free radical production by phagocytes.

High pressure behaviour of the organic semiconductor salt (TTF-BTD)I.

This study focuses on the effect of structure compression and cooling on the stereoelectronic properties of the planar π-conjugated TTF-BTD (TTF = tetrathiafulvalene; BTD = 2,1,3-benzothiadiazole) molecule, a prototypical example in which an electron-donor moiety is compactly annulated to an electron-acceptor moiety. Its partially oxidised iodine salt (TTF-BTD)I is a crystalline semiconductor featuring segregated columns of TTF units stacked alternating short and long π-π interactions. We studied TTF-BTD at temperatures ranging from 300 K to 90 K and at pressures up to 7.

Computational Exploration of Potential CFTR Binding Sites for Type I Corrector Drugs.

Cystic fibrosis (CF) is a recessive genetic disease that is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The recent development of a class of drugs called "correctors", which repair the structure and function of mutant CFTR, has greatly enhanced the life expectancy of CF patients. These correctors target the most common disease causing CFTR mutant F508del and are exemplified by the FDA-approved VX-809.