ANTIPHOSPHOLIPID SYNDROME AND MONOCYTES: NEW ASPECTS.

After discovery of antiphospholipid syndrome (APS) our understanding of molecular mechanisms of living matter has become more sophisticated and on this way monocytes has become crucial player, particularly in pathogenesis of APS. Thrombotic and non-thrombotic complications of APS could be explained by monocytes' activation too. But mechanisms underlying their activation are poorly investigated.

Differential regulation of proinflammatory mediators following LPS- and ATP-induced activation of monocytes from patients with antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by recurrent thrombosis and pregnancy morbidity in association with the presence of antiphospholipid antibodies. Growing evidence supports the involvement of monocytes in APS pathogenesis. Inflammatory activation of monocytes promotes thrombus formation and other APS complications.

[The stability of cell composition of fetus blood in norm and under hypoferric anemia].

The article deals with indicators of cell composition of umbilical blood (fetus blood) in case of normal pregnancy (n = 38) and hypoferric anemia of light degree (n = 14)10 the hematologic analyzer of medium class was applied. The parameters of erythrocytes of fetus blood in case of hypoferric anemia of light degree were sufficiently stable and had no differences with normal values both in mean values and variability. The variety of adaptive index of fetus blood (Garkavi index) was significantly higher in case of hypoferric anemia as compared with normal values.