Comparison of a silver-coated needleless connector and a standard needleless connector for the prevention of central line-associated bloodstream infections.

Objective: To assess the impact of a novel, silver-coated needleless connectors (NCs) on central-line-associated bloodstream infection (CLABSI) rates compared with a mechanically identical NCs without a silver coating.

Design: Prospective longitudinal observation study SETTING Two 500-bed university hospitals

Patients: All hospitalized adults from November 2009 to June 2011 with non-hemodialysis central lines

Interventions: Hospital A started with silver-coated NCs and switched to standard NCs in September 2010; hospital B started with standard NCs and switched to silver-coated NCs. The primary outcome was the difference revealed by Poisson multivariate regression in CLABSI rate using standard Centers for Disease Control and Prevention surveillance definitions.

Ectonucleotide triphosphate diphosphohydrolase-1 (CD39) mediates resistance to occlusive arterial thrombus formation after vascular injury in mice.

Modulation of purinergic signaling, which is critical for vascular homeostasis and the response to vascular injury, is regulated by hydrolysis of proinflammatory ATP and/or ADP by ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD-1; CD39) to AMP, which then is hydrolyzed by ecto-5'-nucleotidase (CD73) to adenosine. We report here that compared with littermate controls (wild type), transgenic mice expressing human ENTPDase-1 were resistant to the formation of an occlusive thrombus after FeCl(3)-induced carotid artery injury. Treatment of mice with the nonhydrolyzable ADP analog, adenosine-5'-0-(2-thiodiphosphate) trilithium salt, Ado-5'-PP[S], negated the protection from thrombosis, consistent with a role for ADP in platelet recruitment and thrombus formation.

Transgenic swine: expression of human CD39 protects against myocardial injury.

Unlabelled: CD39 (ectonucleoside triphosphate diphosphohydrolase-1; ENTPD-1) rapidly hydrolyzes ATP and ADP to AMP; AMP is hydrolyzed by ecto-5'-nucleotidase (CD73) to adenosine, an anti-thrombotic and cardiovascular protective mediator. While expression of human CD39 in a murine model of myocardial ischemia/reperfusion (I/R) injury confers cardiac protection, the translational therapeutic potential of these findings requires further testing in a large animal model. To determine if transgenic expression of CD39 reduces infarct size in a swine model of myocardial ischemia/reperfusion injury, transgenic pigs expressing human CD39 (hCD39) were generated via somatic cell nuclear transfer and characterized.