False chordae tendineae in right ventricle of adult human hearts - morphological aspects.

Introduction: False chordae tendineae are fibrous-muscular bundles which do not interconnect with right atrioventricular valves. The structures have occasionally been described in the right ventricle. There are reports suggesting their influence on electromechanical processes taking place in the heart, in thromboembolic events as well as in the course of cardiac invasive procedures.

DQA1*03011 allele: protective or an adverse effect on the development of sarcoidosis; preliminary study.

Background: Sarcoidosis (SA) is a multisystem granulomatous disorder of unknown etiology. It seems likely that in genetically different predisposed hosts, the same antigen(s) may cause the development of sarcoid Th1 response. The interaction of the T-cell receptor with the human leukocyte antigen-DQA1*03011 peptide-complex can affect T lymphocytes activation in a dose-response manner.

Comparative analysis of mycobacterial heat shock proteins-induced apoptosis of peripheral blood mononuclear cells in sarcoidosis and tuberculosis.

Sarcoidosis (SA) is a granulomatous disorder of an unknown etiology. Mycobacterium tuberculosis heat shock proteins (Mtb-hsp), considered as causative agents, play an important role in apoptosis. A role for apoptosis has been proposed in pathogenesis of SA and tuberculosis (TB) granuloma formation but results remain controversial.

[Apoptosis mononuclear cells in sarcoidosis].

Sarcoidosis (SA) is a systemic granulomatous disorder of unknown etiology. The diagnosis is firmly established when clinicoradiological findings are supported by histological evidence of noncaseating epithelioid cell granulomas found on tissue biopsy Diagnosis of SA requires exclusion of other causes of granuloma formation, first of all Mycobacterium tuberculosis. Sarcoidosis is a disease known to be associated with various immunological alterations, including depression of cutaneous delayed-type hypersensitivity and an activation of monocytes/macrophages and a heightened helper T cell type 1 immune response at sites of disease but the mechanism leading to the persistent accumulation of inflammatory cells is not understood.