Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Einzelreferate und Buchbesprechungen

Journal of Molecular Medicine -     

Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Evaluating how electronic charting affects resident productivity

Electronic medical records (EMRs) are becoming standard to improve the communication of information and longevity of patient records. Using an EMR in the emergency department (ED) could potentially slow residents evaluating patients. We evaluated how introducing an EMR affected resident productivity in an academic ED. We retrospectively studied first year emergency medicine residents from a large, academic, tertiary care center before-and-after the institution of an EMR on July 1st, 2010. No residents from the 2009–2010 class used the EMR, while all of the 2010–2011 residents used the EMR. We performed univariate and multivariate analyses using productivity, measured in patients per hour (pt/hr), as the primary outcome. A mixed-model multivariate regression, stratified by acuity zone, was created incorporating EMR and other possible confounders: admissions, signouts, daily ED volume, and days after July 1st for each shift. The study was granted IRB waiver of informed. We reviewed 2,405 shifts: 1,259 shifts before and 1,146 shifts after EMR implementation. When using the EMR, the univariate analysis estimated a 0.084 pt/hr increase in the high acuity zone (p = 0.1317) and 0.029 pt/hr decrease (p = 0.7085) in the low acuity zone. The multivariate regression estimated a 0.038 pt/hr increase (p = 0.3413) in the high acuity zone and a 0.009 pt/hr increase (p = 0.9049) in the low acuity zone with the EMR. Despite the expectation that electronic charting is detrimental to resident productivity, our analyses do not suggest a significant relationship between resident productivity and using the EMR.     

Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury

Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there is one common pathway in which CypD and RIPK1 act in or whether separate RN pathways exist. Here, we demonstrate that necroptosis in ischemia–reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroptosis, are protected from IRI. Protection of RIPK3-knockout mice was significantly stronger than of CypD-deficient mice. Mechanistically, in vivo analysis of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis. We, therefore, generated CypD-RIPK3 double-deficient mice that are viable and fertile without an overt phenotype and that survived prolonged IRI, which was lethal to each single knockout. Combined application of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with mutant mice. The data demonstrate the pathophysiological coexistence and corelevance of two separate pathways of RN in IRI and suggest that combination therapy targeting distinct RN pathways can be beneficial in the treatment of ischemic injury.