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Biomedical subjects

H Rus

Publications and source records attributed to H Rus.

22 records · Page 2Linked to original sources
PubMed1983

Comparative behaviour of the components of the factor VIII complex in acute myocardial infarction.

The three components of the factor VIII complex: VIII coagulant (VIII:C), VIII related antigen (VIII R:Ag) and the VIII related von Willebrand factor (VIII R:WF) were studied in patients with acute myocardial infarction (AMI). Using a carefully standardized technique for the determination of VIII R:WF, a significantly higher R:WF level was found in 32 patients compared to 19 control subjects, confirming our previous results. However VIII R:AG was increased to an even greater extent, resulting in a VIII R:Ag/VIII R:WF ratio of 1.58 +/- 0.084 in patients, compared to 1.21 +/- 0.045 in controls. A similar increase of the VIII R:AG/VIII:C ratio was noted in the 13 patients in whom VIII:C was investigated. In 7 patients with severe AMI who could be investigated twice the plasma levels of both VIII R:Ag and VIII R:WF were found to be lower a week after the acute event than during the first 48 hours. However the VIII R:Ag/VIII R:WF ratio was not significantly reduced after 7 days. Acute phase reaction and endothelial injury resulting in release of multimers which are less polymerised are probably involved in the above changes.

Adult↗
PubMedDate not supplied

Complement activation and atherosclerosis.

Atherosclerosis is an inflammatory disease mediated through the action of monocyte/macrophages, complement and T-lymphocytes. C5a and monocyte chemotactic factor released during complement activation in the arterial wall may participate in the initial monocyte recruitment. Assembly of C5b-9 on cells of the arterial wall may also induce cell lysis. On the other hand, sublytic assembly of C5b-9 on smooth muscle cells (SMC) and endothelial cells (EC) induces cell activation and proliferation. Analysis of mitogen activated protein kinases (MAPK) pathways induced by C5b-9 in aortic SMC revealed that extracellular signal regulated kinase (ERK) 1, c-jun NH2-terminal kinase (JNK) 1, and p38 MAPK are all activated by C5b-9. ERK1 activity was inhibited by wortmannin suggesting that ERK1 pathway is activated through phosphatidyl inositol -3 (PI 3-) kinase. Sublytic C5b-9 assembly on the plasma membrane was also able to activate Janus kinase (JAK) 1, signal transducer and activator (STAT) 3 and STAT4 in EC. JAK1 but not STAT3 activation induced by C5b-9 is dependent on Gi protein activation. New evidence accumulated during the last decade support the role of complement activation in both initiation and progression of the atherosclerotic lesions. Complement system activation is a major component of the chronic inflammatory process associated with atherosclerosis.

Animals↗