Cerebral hemodynamic changes during the trigeminocardiac reflex: description of a new animal model protocol.

The trigeminocardiac reflex (TCR) is a well-known brainstem reflex, first described in skull base and neurosurgery by the senior author in 1999, leading to reflex apnea, bradycardia, and changes of mean arterial pressure. There seem to be differences between peripheral and central stimulation of the TCR, and there is a lack of clear data about the cerebral hemodynamic changes during the TCR. However, the research of this reflex principally focused on clinical cases for peripheral and central stimulation during the last years, and on rabbits for peripheral stimulation several decades ago, so there was a need for an animal model that allows us to use the current state-of-the-art imaging methods.

Mitochondrial glutathione.

Many functions of mitochondrial GSH are significantly different from those of cytosolic GSH. This review considers the peculiarity of functions of mitochondrial GSH and enzymes of its metabolism, especially glutathione peroxidase 4, glutaredoxin 2, and kappa-glutathione transferase.

Biochemical aspects of inflammation.

This review considers biochemical aspects of inflammation. The international literature until December 2006 has been analyzed, with the principal attention paid to the most dynamic problems: enzymology of inflammation, its regulation by hormones and signal transducers, and negative feedbacks, which underlie intensive current studies on pathogenesis, diagnostics, and therapy of inflammation. Such achievements as discoveries of defensins, toll-like receptors, interconnections of inflammation and iron metabolism, the roles of oxidative stress and antioxidant defense, lipoxins, inflammatory components of "non-inflammatory" diseases, and action mechanisms of effective drugs are discussed.

Molecular mechanisms of hormonal activity. II. Kinase systems. Systems with intracellular receptors. Transactivation of STS.

Hormone receptors and other components, functional mechanisms, and biological role of analyzed signal transduction systems (STS) are described. The recently revealed module principle of the structure and STS transactivation providing diversity and plasticity of regulation are highlighted. STS activities are significantly changed in many diseases.

Molecular mechanisms of hormonal activity. I. Receptors. Neuromediators. Systems with second messengers.

Hormone signal transfer along all of the cell compartments including nucleus is powered by signal transduction systems. Characteristics and importance of hormone receptors, principal components, functional mechanisms, and biological role of different systems with second messengers are described. Considerable examples of the importance of these systems for medicine are adduced.

Influence of changes in glutathione concentration on body temperature and tolerance to cerebral ischemia.

Two compounds that deplete glutathione (buthionine sulfoximine and diethyl maleate) with different mechanisms of action decrease body temperature and increase tolerance to complete global cerebral ischemia, both correlating closely with the glutathione concentration decrease. Glutathione apparently participates in the regulations of these functional parameters. GSH diethyl ester does not influence the latter, though it increases moderately the GSH concentration.

Role of adenosine receptors in neuroprotective effect during global cerebral ischemia.

Selective A(1)adenosine receptor agonists produced a considerable neuroprotective effect during global cerebral ischemia. The neuroprotective effect decreased in the order: A(1)agonists-NECA-adenosine-A(2A)agonist CGS 21680, while selective A(3)adenosine receptor agonist was ineffective. Inhibitory analysis showed that A(1)adenosine receptors mediate the neuroprotective effect of CPA, are involved in the effects of NECA and adenosine (but not CGS 21680), and participate in natural resistance to cerebral ischemia.

Catecholamine control of enzymes involved in isocitrate oxidation of rat liver mitochondria.

Treatment of rats or liver homogenates with catecholamines (isoproterenol or noradrenaline) increased activities of both NAD+ -dependent isocitrate dehydrogenase and NAD(P)+-transhydrogenase (in the direction of hydrogen transfer NADPH----NAD+) with no change in NADP+ -dependent isocitrate dehydrogenase. These effects were realized via beta-adrenoceptors. Cyclic AMP mimicked the catecholamine action on incubation with liver homogenate.

[Study of mechanisms of regulation of disulphide reductase in mouse liver].

An increase in activity of disulphide reductase system (DRS) in supernatant of liver tissue was caused by 3',5'-AMP, ATP, GTP, UTP, Mg2+, Ca2+, EDTA, protamine, noradrenaline and F-. The effect was connected with arsenite resistant fraction of DRS. After rapid homogenization the effect of noradrenaline disappeared and the effects of ATP, GTP, UTP and Ca2+ were distinctly decreased.