Emulsions photographiques positives directes aux halogénures d'argent

publication date: 1976-05-18; filing date: 1973-07-09Direct-positive silver halide emulsions comprising fogged silver halide grains and having adsorbed to the surface of said grains an electron-acceptor have improved stability and speed when subsequent to fogging of said grains and addition of the said electron acceptor the pH of the emulsion is lowered, preferably below pH 6.Mass production of silver halide recording material for full colourholographi

Dabigatran inhibits staphyloccus aureus coagulase

The ability of Staphylococcus aureus to clot plasma through conformational activation of prothrombin by staphylocoagulase is used to distinguish S. aureus from coagulase-negative staphylococci. We show that while the direct thrombin inhibitor dabigatran inhibits staphylocoagulase activity, the clinical use of dabigatran etexilate is not expected to interfere with direct tube coagulase testing.status: publishe

Binding to Von Willebrand Factor enable Staphylocccus aureus to overcome shear stress and cause infective endocarditis

status: publishe

Shear-resistant Binding to Von Willebrand Factor Allows Staphylococcus Lugdunensis to Adhere to the Cardiac Valves and Initiate Endocarditis

 Staphylococcus lugdunensis (S. lugdunensis) is an emerging cause of endocarditis. To cause endovascular infections S. lugdunensis requires mechanisms to overcome shear stress. We investigated whether platelets and von Willebrand factor (VWF) mediate bacterial adhesion to the vessel wall and the cardiac valves under flow.status: publishe

Staphylococcus aureus endocarditis: distinct mechanisms of bacterial adhesion to damaged and inflamed heart valves

Aims The pathogenesis of endocarditis is not well understood resulting in unsuccessful attempts at prevention. Clinical observations suggest that Staphylococcus aureus infects either damaged or inflamed heart valves. Using a newly developed endocarditis mouse model, we therefore studied the initial adhesion of S. aureus in both risk states. Methods and results Using 3D confocal microscopy, we examined the adhesion of fluorescent S. aureus to murine aortic valves. To mimic different risk states we either damaged the valves with a surgically placed catheter or simulated valve inflammation by local endothelium activation. We used von Willebrand factor (VWF) gene-deficient mice, induced platelet and fibrinogen depletion and used several S. aureus mutant strains to investigate the contribution of both host and bacterial factors in early bacterial adhesion. Both cardiac valve damage and inflammation predisposed to endocarditis, but by distinct mechanisms. Following valve damage, S. aureus adhered directly to VWF and fibrin, deposited on the damaged valve. This was mediated by Sortase A-dependent adhesins such as VWF-binding protein and Clumping factor A. Platelets did not contribute. In contrast, upon cardiac valve inflammation, widespread endothelial activation led to endothelial cell-bound VWF release. This recruited large amounts of platelets, capturing S. aureus to the valve surface. Here, neither fibrinogen, nor Sortase A were essential. Conclusion Cardiac valve damage and inflammation predispose to S. aureus endocarditis via distinct mechanisms. These findings may have important implications for the development of new preventive strategies, as some interventions might be effective in one risk state, but not in the other.status: publishe