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Biomedical subjects

A Jurkiewicz

Publications and source records attributed to A Jurkiewicz.

At least 37 records · Page 2Linked to original sources
PubMed1998

Quantitative analysis of the high-affinity binding sites for [3H]ouabain in the rat vas deferens and their immunological identification as the alpha 2 isoform of Na+/K(+)-ATPase.

Binding assays were performed with [3H]ouabain to investigate the presence of, and to characterize, a Na+/K(+)-ATPase isoform with high affinity for cardiac glycosides in the rat vas deferens. Nonlinear regression analysis of equilibrium experiments carried out with crude preparations in a Mg-Pi medium indicated the presence of high-affinity sites characterized with good precision (individual coefficients of variation = 11-35%) by their density (Bmax = 0.42 to 0.72 pmol/mg protein) and dissociation constant (Kd = 0.069 to 0.136 microM) values. The values of the dissociation rate constant (kappa-1) and the association rate constant (kappa+1) for these sites were 0.151 to 0.267 min-1 and 2.87 to 3.60 microM-1.min-1, respectively. A higher number of low-affinity sites (Kd around 15 microM), supposed to correspond to the alpha 1 isoform, was also identified, but their Kd and Bmax values were not quantified precisely in this crude preparation. Western blot assays indicated hybridization with specific anti-alpha 1 and anti-alpha 2 isoform antibodies but not with anti-alpha 3 isoform antibody. Taken together, the present results indicate the existence of a low proportion of the alpha 2 isoform of Na+/K(+)-ATPase in the rat vas deferens that can be quantified precisely by [3H]ouabain binding even in a crude membrane preparation that is suitable for studies under conditions of plasticity.

Animals↗
PubMed1998

Ca2+ release-activated channels in rat stomach smooth muscle cells.

In rat stomach fundus, contractions induced by Ca2+ (1.8 mM) were strikingly potentiated by thapsigargin. This potentiation was partially inhibited by the blockers of Ca2+ release activated channels (CRACs), miconazole and SK&F96365 ([1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole, HCL]) and slightly blocked by the antagonist of calcium voltage-operated channels (VOCs), isradipine. In dissociated cells in a 0Ca solution, thapsigargin potentiated the increase in intracellular calcium after reintroduction of Ca2+. This potentiation was partially reduced by the CRAC blockers, but not by the VOC blockers. This data suggests that calcium influx increased due to the depletion of intracellular calcium by thapsigargin and that this influx occurs predominantly through CRACs.

Animals↗
PubMed1998

Synergism between toxin-gamma from Brazilian scorpion Tityus serrulatus and veratridine in chromaffin cells.

Toxin-gamma (Tgamma) from the Brazilian scorpion Tityus serrulatus venom caused a concentration- and time-dependent increase in the release of norepinephrine and epinephrine from bovine adrenal medullary chromaffin cells. Tgamma was approximately 200-fold more potent than veratridine judged from EC50 values, although the maximal secretory efficacy of veratridine was 10-fold greater than that of Tgamma (1.2 vs. 12 microg/ml of catecholamine release). The combination of both toxins produced a synergistic effect that was particularly drastic at 5 mM extracellular Ca2+ concentration ([Ca2+]o), when 30 microM veratridine plus 0.45 microM Tgamma were used. Tgamma (0.45 microM) doubled the basal uptake of 45Ca2+, whereas veratridine (100 microM) tripled it. Again, a drastic synergism in enhancing Ca2+ entry was seen when Tgamma and veratridine were combined; this was particularly pronounced at 5 mM [Ca2+]o. Veratridine induced oscillations of cytosolic Ca2+ concentration ([Ca2+]i) in single fura 2-loaded cells without elevation of basal levels. In contrast, Tgamma elevated basal [Ca2+]i levels, causing only small oscillations. When added together, Tgamma and veratridine elevated the basal levels of [Ca2+]i without causing large oscillations. Tgamma shifted the current-voltage (I-V) curve for Na+ channel current to the left. The combination of Tgamma with veratridine increased the shift of the I-V curve to the left, resulting in a greater recruitment of Na+ channels at more hyperpolarizing potentials. This led to enhanced and more rapid accumulation of Na+ in the cell, causing cell depolarization, the opening of voltage-dependent Ca2+ channels, and Ca2+ entry and secretion.

Adrenal Medulla↗
PubMed1997

omega-Conotoxins block neurotransmission in the rat vas deferens by binding to different presynaptic sites on the N-type Ca2+ channel.

Electrically-induced twitch responses of the prostatic segment of vas deferens (0.1 Hz, 65 V, 1 ms) are mainly due to the transient presynaptic release of ATP, which acts postsynaptically on non-adrenergic receptors to contract smooth muscle cells. These responses were fully blocked by nanomolar concentrations of the omega-conotoxins GVIA, MVIIA, and MVIIC, most likely by inhibiting Ca2+ entry through presynaptic N-type Ca2+ channels controlling the release of ATP. Repeated washout of the toxins allowed the recovery of contractions, except for omega-conotoxin GVIA, whose inhibitory effects remained unchanged for at least 60 min. In addition, micromolar concentrations of omega-conotoxin MVIIC were unable to protect against the irreversible inhibition of twitch contractions induced by nanomolar concentrations of omega-conotoxin GVIA. At low extracellular Ca2+ concentrations (1.5 mM), 20 nM of omega-conotoxin GVIA or MVIIA inhibited completely the twitch contractions in about 10 min. In 5 mM Ca2+ the blockade of twitch contractions after 10 min was 70% for both toxins. In 1.5 mM Ca2+ omega-conotoxin MVIIC (1 microM) inhibited completely the twitch contraction after 10 min. In 5 mM Ca2+ blockade developed very slowly and was very poor after 30 min, omega-conotoxin MVIIC depressed the response by only 20%. These results are compatible with the idea that the three omega-conotoxins block the purinergic neurotransmission of the vas deferens by acting on presynaptic N-type voltage-dependent Ca2+ channels. However, omega-conotoxin MVIIC seems to bind to sites different from those recognised by omega-conotoxin GVIA and MVIIA, which are markedly differentiated by their Ca2+ requirements for binding to their receptors.

Animals↗
PubMed1997

[Database for assessment of treatment results in patients with multiple trauma].

Data base for assessment of results of treatment of politrauma patients is presented. It was created on the basis of Abbreviated Injury Scale, Injury Severity Score and Revised Trauma Score. Examination was supplemented with TRISS method inclusive of graphic assessment PRE-CHART and statistic Z and M. The software was created on the basis of Excel 7.0 and Windows 95.

Computer Graphics↗
PubMed1996

Functional properties of agmatine in rat vas deferens.

Experiments were performed with rat vas deferens to verify whether agmatine, an endogenous ligand for adrenoceptors and imidazoline receptors, can influence sympathetic neurotransmission, with respect to contractions induced by transmural nerve stimulation, contractions induced by exogenous noradrenaline, and overflow of endogenous noradrenaline. It was shown that agmatine (a) caused a dose-dependent potentiation of electrically induced twitches, up to about 70% in relation to controls, (b) shifted to the right the inhibitory concentration-response curves for clonidine on electrically induced twitches, indicating competitive antagonism at presynaptic alpha-adrenoceptors, with a pA2 value of 4.12 +/- 0.10, (c) shifted to the right the concentration-response curves for noradrenaline-induced contractions, indicating competitive antagonism at postsynaptic alpha-adrenoceptors as well, with a pA2 value of 4.03 +/- 0.10, and (d) caused a dose-dependent increase of KCI-induced overflow of noradrenaline, up to about 90% in relation to controls. It is concluded that agmatine has multiple effects on sympathetic neurotransmission in rat vas deferens.

Agmatine↗
PubMed1996

[Surgical treatment for femoral shaft fracture in children and adolescents with multiple trauma].

Results of surgical treatment for 13 femoral shaft fractures in 12 children and adolescents with multitrauma have been presented. In 12 cases plate has been used, in one case Kuntcher nail was employed. Age of the patient at the trauma was 3 years 4 months on an average. There was no infection in postoperative period. The fracture healed after 8 weeks on an average. Anatomical reduction has been achieved in all cases. Some physical activity limitation (not related to the treatment) has been found in two patients. Surgical treatment for femoral shaft fracture in children and adolescents with multitrauma rendered good results.

Adolescent↗
PubMed1995

The femur capitulum as a biomarker of contamination due to indicating lead content in the air by participation of the other metals.

The occurrence of nine elements in the coxarthrosis human femoral capitula is described. The atomic absorption spectrophotometry (AAS) method was used to determine Cd, Pb, Cr, Cu, Mn, Fe, Zn, Ni and Co concentrations in the three kinds of tissues: spongious and cortical bone and joint surface cartilage. Based on the Pb bone concentrations, an ecotoxicological Pb contamination risk for the industrial region can be predicted.

Air Pollutants↗
PubMed1994

Decreased density of binding sites for the Ca2+ channel antagonist [3H]isradipine after denervation of rat vas deferens.

Radioligand binding assays were performed with the selective antagonist of dihydropyridine-sensitive Ca2+ channels [3H]PN200-110 (isradipine) in rat vas deferens, before and 7 days after denervation, and data were compared with those obtained for K(+)-induced contractions, which are Ca(2+)-dependent. The density (Bmax) of dihydropyridine binding sites was decreased to almost one-third of its normal value after denervation. The respective affinity (KD) was not significantly changed. In addition, it was observed that the K(+)-induced tonic contraction, which corresponded to 55 +/- 2% of the respective phasic contraction, was decreased to 41 +/- 3% after denervation. It is assumed that the decreased density of Ca2+ channels causes a decrease in K(+)-induced influx of Ca2+ and consequently of the corresponding tonic contraction. These results indicate that autonomic innervation can regulate the density of dihydropyridine-sensitive Ca2+ channels in the rat vas deferens.

Animals↗
PubMed1994

Evidence for participation of nitric oxide in excitatory neurotransmission in rat vas deferens.

A depression of the fast, non-adrenergic, and also of the slow, adrenergic, components of muscle contraction in response to intramural nerve stimulation was induced by the blocker of nitric oxide synthase NG-nitro-L-arginine methyl ester (L-NAME), in rat vas deferens. Effects of exogenous noradrenaline or ATP were not reduced by L-NAME. However, L-arginine also caused an inhibition of electrically induced effects in most of the preparations, contrary to the expectations for a precursor of nitric oxide synthesis. In spite of these difficulties L-arginine antagonized the action of L-NAME. These results indicate that nitric oxide is involved in excitatory nerve-muscle transmission in vas deferens.

Adenosine Triphosphate↗