Pathological remodeling of the myocardium in chronic heart failure includes the development of pathological cardiac hypertrophy, reactivation of the fetal genetic program, and disorders in cardiac energy metabolism. Coactivator-1α of receptor γ activated by peroxisome proliferator (PGC-1α), a transcription coactivator of nuclear receptors and metabolism master regulator, plays an important role in cardiac metabolism regulation. Studies on the animals models of chronic heart failure have demonstrated the development of pathological cardiac hypertrophy, metabolic disorders, and reactivation of the fetal genetic program; these processes are mutually related. An important role in regulation of these processes belongs to PGC-1α; its low expression indicates low activity and down-regulation of this coactivator. Pathological cardiac hypertrophy, decrease of PGC-1α activity, and reactivation of the fetal genetic program in chronic heart failure are demonstrated.

The somatodendritic structure of projection neurons was morphometrically examined in the nucleus accumbens of human brain. In contrast to reticular neurons, spiny neurons of the nucleus accumbens and dorsal striatum have different somatodendritic structure. In both parts of the striatum, reticular neurons were NADPH-diaphorase-positive.

Morphometric analysis of 35 biopsy specimens from patients with stable (n=10) and unstable (n=25) atherosclerotic lesions was carried out. The structure of the plaques and their connective tissue caps was studied by various methods of histological sections staining. A new morphometric approach to quantitative evaluation of atherosclerotic lesions instability is suggested. It consists in calculation of the morphological "rigidity" coeffi cient, due to which the plaque is characterized more accurately. The proportion of areas of the "rigid" (connective tissue and calcium salt deposition areas) to "soft" (atheronecrotic nuclei, microvessels, clots and hemorrhages) structures of the plaque is evaluated. Plaque instability (liability of a to rupture) is associated with changes in the extracellular matrix components in the cap: accumulation of collagen and reduction of elastic fi ber content reducing vessel elasticity and making its locally more rigid. . Address for correspondence: ShishkinaValya@mail.ru. V. S. ShishkinaAcute clinical manifestations of cardiovascular diseases are associated with the development of unstable atherosclerotic lesions liable to ruptures in the main arterial walls. The mechanisms of atherosclerotic plaque instability development are different and not amply studied. The risk of plaque rupture is explained primarily by its structure: thickness of the fi brous cap and content of extracellular matrix proteins (collagen, elastin, and glycosaminoglycans), size and consistence of atheromatous nuclei, and infl ammatory phenomena [4,7]. Rupture of an unstable plaque can lead to acute circulatory disorders (acute coronary syndrome and brain stroke) and death [6]. High positive correlation between atherosclerosis and increase of pulse wave velocity (PWV) has been demonstrated [13]. The PWV is determined by morphological characteristics of the vessel and other parameters [1-3]; it characterizes the elastic stress of the vascular wall and increases with increasing artery rigidity [5]. The content and proportion of collagen (responsible for the vessel strength) and elastic fi bers (responsible for elasticity and stretching/compression of the vessel) largely determine biomechanics of the vascular wall [11,13]. Arterial wall with increased content of collagen fi bers and reduced content of elastic fi bers becomes more rigid [5]. Pathological changes in the composition of vascular matrix components are fraught with higher risk of cardiovascular complications of hypertensive nature [8,9].Here we use morphological criteria for evaluation of vascular wall rigidity based on the morphometric analysis of carotid artery sections from patients with atherosclerosis. We hypothesized that vascular rigidity can serve as an indicator of plaque instability.The relationship between vascular wall rigidity and plaque instability was investigated. To this end, detailed morphological analysis of biopsy specimens of carotid arteries and extracellular matrix components was carried out and the plaque rigidity coeffi cient was

Contents:Oxytocin, progesterone and testosterone production of porcine granulosa cell culture in absenceor inpresence of 0.01 -1 0 pglml LH-RH or its antagonist (D Phe2* D Phe6) LH-RH were analysed. It was found that both LH-RH and its analoque stimulated granulosa oxytocin and progesterone (but not testosterone) secretion in a dose-dependent manner. Present results demonstrate ( I ) a direct stimulatory influence of LH-RH and its antagonist on porcine ovarian peptide and steroid hormone production, as well as (2) the relative independence of the LH-RH -related peptides actions at the hypophysial and at the ovarian level. Inhalt: Hinweise auf den direkten EinfluB des ,,Gonadotropin-Releasing Hormone" auf das Ovar beim Schwein: Effekte von LH-RH und seines Antagonisten auf Oxytocin-, Progesteron-und Testosteronproduktion durch Granulosazellen unter in vitro Bedingungen Oxytocin, Progesteron und Testosteronproduktion porciner Granulosazellkulturen wurde in Abwesenheit oder Anwesenheit von 0,01-IOpglmI LH-RH bzw. des Antagonisten (d-Phe2a d Phe@L.H-RH analysiert. Es wurde festgestellt, dapsowohlLH-RH als auch einAnalogprdparat die Oxytocin und Progesteronsekretion in dosisabhangiger Form stimulieren, Testosteron abernicht beein,tluJtwird. Die Ergebnisse ZeigeneinenstimulierendenEffekt von LH-RHund auch des Antagonisten auf die Synthese ovarieller Peptide und Steroidhormone. Gleichzeitig stellt sich eine relative Unabhiingigkeit von LH-RH gebundeFen Peptiden auf hypophysarem und ovariellen Level dar.

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