Ons trigger an activation of the contact system more potently than strains isolated from noninvasive infections. The present study gives new insights into the mechanisms by which S. pyogenes triggers the human contact system and stresses the function of soluble and surface located plasmin exploited as a group A streptococcal virulence factor through the action of streptokinase. treptococcus pyogen

Ersus host disease, or other abdominal syndromes including cholecystitis, cholangitis, appendicitis need to be ruled out. The management of neutropenic enterocolitis has evolved over the years as clinical experience has grown. Recent studies have reported the success of conservative treatment in most patients. Surgical intervention is now reserved for selected cases of neutropenic enterocolitis ba

Ersus host disease, or other abdominal syndromes including cholecystitis, cholangitis, appendicitis need to be ruled out. The management of neutropenic enterocolitis has evolved over the years as clinical experience has grown. Recent studies have reported the success of conservative treatment in most patients. Surgical intervention is now reserved for selected cases of neutropenic enterocolitis ba

Streptococcal plasminogen activator, triggers the activation of the human contact system. Activation of contact system factors at the surface of the Streptococcus pyogenes serotype M49 is dependent on streptokinase and plasminogen. Our results also show that secreted streptokinase is an efficient contact system activator, independent from a contact surface. This results in the processing of high-m

Ion levels of BORIS in MDA-MB-468, MCF-7 and BCM1 cells by RT-PCR and gel electrophoresis. As expected, we found a similar expression profile of BORIS mRNA (Figure 2) to that detected by quantitative real-time PCR (Table 1). However, gel electrophoresis and quantitative real time showed no and low expression levels of BORIS in MCF-7 cells, respectively, but the tendency was similar. The additional

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