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Ared the frail population to the non-frail population. Results: Two hundred and eighty four patients were admitted to Intensive Care in this time period. Of those, 102 were over the age of 65 years. Of the 102 patients, 68patients were deemed to be frail, and 34 were deemed to be non-frail using the CFS. Approximately 40 of the patients admitted to Intensive Care are over the age of 65. There wa

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

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

Ared the frail population to the non-frail population. Results: Two hundred and eighty four patients were admitted to Intensive Care in this time period. Of those, 102 were over the age of 65 years. Of the 102 patients, 68patients were deemed to be frail, and 34 were deemed to be non-frail using the CFS. Approximately 40 of the patients admitted to Intensive Care are over the age of 65. There wa

Ults show that changes in the BORIS transcript levels are associated with those of MAGE-A1 and corroborate that BORIS is involved in the activation of MAGE-A1 gene expression.BORIS affects the DNA methylation pattern of MAGE-A1 geneFigure 2 BORIS mRNA expression in MDA-MB-468, MCF-7 and BCM1 cells, untreated or treated with 5-aza-CdR. RT-PCR products of BORIS mRNA were separated on an agarose gel.

Functions in order to finely control the immune response in vivo. Among its cellular functions, TNFa is able to induce cytokines, chemokines, proliferation, and also cell death. The induction of pro-inflammatory versus death signals depends upon the molecular context of the responding cell, and specifically whether NFjB is involved [8]. Adding to the complexity of signaling, it is also reported th