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S Spasic

Publications and source records attributed to S Spasic.

7 recordsLinked to original sources
PubMed2005

Fractal analysis of rat brain activity after injury.

With application of the Higuchi algorithm, fractal dimension (FD) values of the electrocortical activity of the rat parietal cerebral and paravermal cerebellar cortex were calculated, before and after unilateral discrete injury of the left parietal cortex. Immediately following the first acute injury, in a group of six rats, a reversible increase in mean FD was found at the left (ipsilateral side to the injury) cerebral cortex, from 1.38 to 1.59, and at the left cerebellar cortex from 1.51 to 1.73. In addition, an indication of plastic changes after repeated (third) injury was found as an irreversible increase in mean FD: 1.54 on the left and 1.48 on the right side of parietal cortex.

Animals↗
PubMed2004

Estimation of neuronal population activity changes in rat cerebellum using one electrode.

Activity of neuronal populations is usually measured with multielectrode systems. In this paper a procedure is described for estimating population activity changes in rat cerebellar cortex, using one microelectrode. Signals consisted of simple, complex spikes and interspike recorded background activity (RBA). After their separation, simple spikes were averaged, forming a simple spike template (SST). The remaining RBA was simulated (SBA), by superimposing SST waveforms with random time delays and intensities. A series of SBA was formed, differing in the superposition frequency (f(sup)) of individual SST. Mean amplitude spectra (Amp(SBA)) were calculated and Amp(SBA)=f(f(sup)) treated as a calibration line for estimating activity level of the surrounding neuronal population. Since the uniform probability distribution of SST intensities proved inadequate, we derived a new one, based on the power function for spike intensity vs. electrode distance attenuation. A family of new lines emerged, depending on the model parameters. Since all were linear in the log-log plots, with slopes not varying significantly, we proposed a method for estimating population activity changes in different experimental conditions, using two measured values of Amp(RBA). Relative nature of the results makes this method suitable for comparative studies.

Animals↗
PubMed2004

Oxidative stress in diabetic pregnancy: SOD, CAT and GSH-Px activity and lipid peroxidation products.

Diabetic pregnancy is often complicated by a number of pathological conditions among which is increased oxidative stress. This study was conducted to investigate the parameters of oxidative stress in 90 patients divided into the three groups: pregnant women with Type 1 diabetes mellitus, healthy pregnant women and non-pregnant women. In pregnancy groups all parameters were followed in 1st, 2nd and 3rd trimester. Diabetic control was monitored by fasting blood glucose and glycosylated hemoglobin (HbA(1c)) and these values, as well as measured biochemical parameters (urea, creatinine, total cholesterol and uric acid), were appropriate throughout the study. The concentration of TBARS, as a measure of lipid peroxidation, and activity of antioxidant enzymes superoxide dismutase (Cu, Zn-SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were investigated in hemolysate of erythrocytes. TBARS concentration increased significantly in pregnant women when compared with control group (non-pregnant women), as well as in pregnant diabetics compared with healthy pregnant women. The SOD activity was gradually increased in the group of normal pregnant women vs. non-pregnant group, but decreased significantly in the group of diabetic pregnant women. Catalase activity was significantly increased only in 3rd trimester diabetic pregnant women. Increased lipid peroxidation and reduced antioxidant status, despite good diabetic control, show that pregnant women are exposed to oxidative stress to a greater degree than controls.

Blood Glucose↗
PubMed1997

The involvement of immune reactions in cardiac damage during acute myocardial infarction: role of cell-mediated immune response.

This study was undertaken with the aim of investigating humoral and cell-mediated immune response in acute myocardial infarction (AMI) as possible mechanisms involved in the infarction enlargement. Twenty three patients with first AMI and 15 healthy volunteers were examined. Of the AMI patients, 14 had extensive infarction (group A), while 9 patients had small infarction (group B). Immunologic analyses were performed at admission, and repeated after 3, 7, 14 and 21 days of the acute event. Following parameters were tested: number of CD3+, CD4+, CD8+ and CD20+ cells; serum IgG, IgA, IgM, C3, C4, immune complex and anticardiac antibody levels; polymorphonuclear cell (PMN) function (chemotaxis, phagocytosis, metabolic activity); leukocyte migration in vitro in the presence of water-soluble homologous heart extract. It was demonstrated that the number of B cells, serum IgG, C3, immune complex and anticardiac antibody levels were elevated from 7th-14th days after AMI. Concerning these parameters, however, no significant differences were obtained between group A and group B of AMI patients. Chemotaxis and metabolic activity of peripheral blood PMN, but not phagocytosis, were enhanced during AMI, again changes of PMN did not correlate with the extension of infarction. In contrast, leukocyte migration inhibition in vitro revealed that only patients with extensive AMI have developed positive reaction during the first 14 days after the onset of the disease, while leukocyte inhibition reaction appeared in patients with nonextensive AMI not earlier than the 21st day after the infarction. These findings demonstrate generation of immune reactivity during AMI and indicate that humoral immune response seems more likely to be an epiphenomenon related to tissue necrosis, while cell-mediated immune reactions could influence the extensiveness of cardiac damage.

Acute Disease↗