[Perfusion-Metabolic Myocardial Scintigraphy in Prognosis of Left Ventricular Remodeling After Complex Surgical Treatment of Ischemic Cardiomyopathy].

PURPOSE: To study capabilities of perfusion-metabolic myocardial scintigraphy for prediction of the left ventricular (LV) reverse remodeling after comprehensive surgical treatment of ischemic cardiomyopathy (ICMP). METHODS: The study included ICMP patients aged 56±7 years (n=32) who underwent surgical correction of LV dysfunction (myocardial revascularization, LV reconstruction, and mitral valve restoration). Inclusion criteria were significant coronary artery disease; myocardial infarction; New York Heart Association (NYHA) class III-IV heart failure; LV ejection fraction (EF) ≤45%; LV end-systolic index (ESI) >60 mL/m2; and LV akinesia or dyskinesia according to echocardiography. Before surgery all patients were subjected to scintigraphy with 99mTc-MIBI (to assess perfusion) and with 123I-BMIPP (to assess myocardial metabolism). Scintigraphy results were expressed as median and lower; upper quartile (Me [lQ; hQ]). The clinical status and ventricular volume indicators were evaluated before surgery, in the early post-operative period (up to 4 weeks), and in the late post-operative period (12 months). RESULTS: At 12 months after intervention patients were divided into two groups: group 1 comprised patients (n=18) with beneficial outcome of the operation that stopped LV remodeling (ESI decreased, remained unchanged, or increased by.

[What do the doctors of different specialties know about sleep disorders and their treatment].

OBJECTIVE: To assessdoctor's knowledge on the relevance of the problem of sleep disorders, methods of their diagnosis and treatment. MATERIAL AND METHODS: The survey was conducted among90physicians of different the rapeuticspecialties of Kazan medical institutions. RESULTS: The doctors believe that main causes of sleep disorders are stressors (20%), depression (13%), neurosis (13%), chronic diseases (13%), asthenia (10%), pain (10%). An analysis of treatment prescribed to patients with sleep disorders revealed large differences. CONCLUSION: Physicians are not well informed about the problems of sleep disorders, have a small idea of the methods of sleepresearch and drugs for their treatment as well as of a sequence of operations that should be used to resolve this problem.

Galantamine prevents long-lasting suppression of excitatory synaptic transmission in CA1 pyramidal neurons of soman-challenged guinea pigs.

Galantamine, a drug currently approved for the treatment of Alzheimer's disease, has recently emerged as an effective pretreatment against the acute toxicity and delayed cognitive deficits induced by organophosphorus (OP) nerve agents, including soman. Since cognitive deficits can result from impaired glutamatergic transmission in the hippocampus, the present study was designed to test the hypothesis that hippocampal glutamatergic transmission declines following an acute exposure to soman and that this effect can be prevented by galantamine. To test this hypothesis, spontaneous excitatory postsynaptic currents (EPSCs) were recorded from CA1 pyramidal neurons in hippocampal slices obtained at 1h, 24h, or 6-9 days after guinea pigs were injected with: (i) 1×LD50 soman (26.3µg/kg, s.c.); (ii) galantamine (8mg/kg, i.m.) followed 30min later by 1×LD50 soman, (iii) galantamine (8mg/kg, i.m.), or (iv) saline (0.5ml/kg, i.m.). In soman-injected guinea pigs that were not pretreated with galantamine, the frequency of EPSCs was significantly lower than that recorded from saline-injected animals. There was no correlation between the severity of soman-induced acute toxicity and the magnitude of soman-induced reduction of EPSC frequency. Pretreatment with galantamine prevented the reduction of EPSC frequency observed at 6-9 days after the soman challenge. Prevention of soman-induced long-lasting reduction of hippocampal glutamatergic synaptic transmission may be an important determinant of the ability of galantamine to counter cognitive deficits that develop long after an acute exposure to the nerve agent.

In vitro effects of pulmonary surfactant on macrophage morphology and function.

The effects of pulmonary surfactant on the morphology and functioning of young macrophages were studied on the model of monocyte/macrophage differentiation in vitro and on macrophages of the bronchial alveolar lavage fluid. Surfactant is not a differentiation inductor, but it stimulated the maturation and phagocytic activity of young macrophages. The stimulatory effect of surfactant on phagocytic activity of macrophages persisted even after its removal from the culture medium.

Differences between some properties of acetylated and nonacetylated forms of HMG1 protein.

There are data suggesting that HMG1 protein may be involved in DNA replication. Recently we have found that only the acetylated form of the protein generates tetramers, stimulates the activity of DNA polymerase alpha (EC 2.7.7.7) (with activated DNA as a template) and forms a specific complex with it. This paper compares some properties of the acetylated and nonacetylated forms of HMG1 protein and shows that it is only the acetylated form which serves as a histone assembly factor, increases the melting temperature of poly d[(A-T)] and stimulates the activity of DNA polymerase alpha when histone H1-depleted chromatin is used as a template.

Acetylated HMG1 protein interacts specifically with homologous DNA polymerase alpha in vitro.

The acetylated, deacetylated and nonacetylated forms of HMG1 proteins from Guerin ascites tumour cells and calf thymus were separated and their in vitro interactions with homologous and heterologous DNA polymerases were studied. It has been found that only the acetylated form of HMG1 proteins forms a specific complex with homologous DNA polymerase alpha and stimulates its activity in vitro. The acetylation therefore is necessary for their possible function in DNA replication. This finding represents an evidence for a relationship between the acetylation of HMG1 proteins and their biological role.

Differences between HMG1 proteins isolated from normal and tumour cells.

The properties of the non-histone chromosomal high-mobility-group 1 (HMG1) proteins from rat liver and Guerin ascites tumour cells (GAT cells) were compared and showed the following differences: (1) five spots were missing in the peptide map of HMG1 from GAT cells in comparison with that of HMG1 from rat liver; (2) HMG1 from GAT cells was about 5-times more poly(ADP)-ribosylated; (3) HMG1 from GAT cells which was found acetylated in vivo and incorporated [14C]acetate in vitro, whereas no incorporation of the label was detected in HMG1 from rat liver; (4) HMG1 from GAT cells exhibited pronounced ability to form oligomers at physiological ionic strength, while HMG1 from rat liver was predominantly in monomeric form. This property of HMG1 from GAT cells was lost upon deacetylation.

Involvement of protein HMG1 in DNA replication.

Antibodies against HMG1 inhibit the incorporation of [3H]thymidine in Ehrlich ascites cell nuclei. By the use of specific inhibitors it is shown that HMG1 is needed for the action of the replicative DNA polymerase and not for the reparative one. This is supported by the fact that the addition of exogenous HMG1 to the nuclei enhances the replication process.