Improving risk stratification in patients with chest pain: the Erlanger HEARTS3 score.

Background: The HEART score uses elements from patient History, Electrocardiogram, Age, Risk Factors, and Troponin to obtain a risk score on a 0- to 10-point scale for predicting acute coronary syndromes (ACS). This investigation seeks to improve on the HEART score by proposing the HEARTS(3) score, which uses likelihood ratio analysis to give appropriate weight to the individual elements of the HEART score as well as incorporating 3 additional "S" variables: Sex, Serial 2-hour electrocardiogram, and Serial 2-hour delta troponin during the initial emergency department valuation.

Methods: This is a retrospective analysis of a prospectively acquired database consisting of 2148 consecutive patients with non-ST-segment elevation chest pain.

1,1-Dichloroethylene-induced mitochondrial damage precedes apoptotic cell death of bronchiolar epithelial cells in murine lung.

1,1-Dichloroethylene (DCE) causes pulmonary injury that is characterized by necrosis of bronchiolar Clara cells. Mitochondria have been identified as an early target in the toxic response. Because mitochondria have been implicated in both necrotic and apoptotic cell death, we have undertaken studies to test the hypothesis that DCE induces apoptosis, in addition to necrosis, in murine lung.

Evidence that 1,1-dichloroethylene induces apoptotic cell death in murine liver.

1,1-Dichloroethylene (DCE) causes dysfunction of hepatic mitochondria. As mitochondria have been implicated in apoptosis through opening of the permeability transition pore (PTP), we have undertaken studies to test the hypothesis that DCE induces apoptosis, in addition to necrosis, in murine liver. Our primary objective was to identify the biochemical events associated with DCE-induced apoptosis.

Mitochondrial dysfunction is an early manifestation of 1,1-dichloroethylene-induced hepatotoxicity in mice.

Hepatotoxicity induced by 1,1-dichloroethylene (DCE) is mediated by cytochrome P450-dependent metabolism to reactive intermediates, including the epoxide. We have tested the hypothesis that mitochondria are a primary target of toxicity by investigating dose- and time-dependent effects of DCE on mitochondrial respiration. Hepatotoxicity, as assessed by serum alanine aminotransferase (ALT) activity, was evaluated.