Relationship between treatment delay and final infarct size in STEMI patients treated with abciximab and primary PCI

Background Studies on the impact of time to treatment on myocardial infarct size have yielded   conflicting results. In this study of ST-Elevation Myocardial Infarction (STEMI) treated   with primary percutaneous coronary intervention (PCI), we set out to investigate the   relationship between the time from First Medical Contact (FMC) to the demonstration   of an open infarct related artery (IRA) and final scar size. Between February 2006 and September 2007, 89 STEMI patients treated with primary PCI   were studied with contrast enhanced magnetic resonance imaging (ceMRI) 4 to 8 weeks   after the infarction. Spearman correlation was computed for health care delay time   (defined as time from FMC to PCI) and myocardial injury. Multiple linear regression   was used to determine covariates independently associated with infarct size. Results An occluded artery (Thrombolysis In Myocardial Infarction, TIMI flow 0-1 at initial   angiogram) was seen in 56 patients (63%). The median FMC-to-patent artery was 89 minutes.   There was a weak correlation between time from FMC-to-patent IRA and infarct size,   r = 0.27, p = 0.01. In multiple regression analyses, LAD as the IRA, smoking and an occluded vessel   at the first angiogram, but not delay time, correlated with infarct size. Conclusions In patients with STEMI treated with primary PCI we found a weak correlation between   health care delay time and infarct size. Other factors like anterior infarction, a   patent artery pre-PCI and effects of reperfusion injury may have had greater influence   on infarct size than time-to-treatment per se

Unexpected Role for Helicobacter pylori DNA Polymerase I As a Source of Genetic Variability

Helicobacter pylori, a human pathogen infecting about half of the world population, is characterised by its large intraspecies variability. Its genome plasticity has been invoked as the basis for its high adaptation capacity. Consistent with its small genome, H. pylori possesses only two bona fide DNA polymerases, Pol I and the replicative Pol III, lacking homologues of translesion synthesis DNA polymerases. Bacterial DNA polymerases I are implicated both in normal DNA replication and in DNA repair. We report that H. pylori DNA Pol I 5′- 3′ exonuclease domain is essential for viability, probably through its involvement in DNA replication. We show here that, despite the fact that it also plays crucial roles in DNA repair, Pol I contributes to genomic instability. Indeed, strains defective in the DNA polymerase activity of the protein, although sensitive to genotoxic agents, display reduced mutation frequencies. Conversely, overexpression of Pol I leads to a hypermutator phenotype. Although the purified protein displays an intrinsic fidelity during replication of undamaged DNA, it lacks a proofreading activity, allowing it to efficiently elongate mismatched primers and perform mutagenic translesion synthesis. In agreement with this finding, we show that the spontaneous mutator phenotype of a strain deficient in the removal of oxidised pyrimidines from the genome is in part dependent on the presence of an active DNA Pol I. This study provides evidence for an unexpected role of DNA polymerase I in generating genomic plasticity

ICAR: endoscopic skull‐base surgery

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