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Dorota Szpak

Publications and source records attributed to Dorota Szpak.

7 recordsLinked to original sources

Mechanism and effect of thrombospondin-4 polymorphisms on neutrophil function.

High-throughput genomic technology identified an association between a single nucleotide polymorphism (SNP), a proline (P387) rather than the predominant alanine (A387) at position 387 in thrombospondin-4 (TSP-4) and premature myocardial infarction. The inflammatory hypothesis of atherosclerosis invokes a prominent role of leukocytes and cytokines in pathogenesis. As the expression of TSP-4 by vascular cells permits its exposure to circulating leukocytes, the interactions of human neutrophils (polymorphonuclear leukocytes [PMNs]) with both TSP-4 variants were investigated. Phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs adhered and migrated well and equally on the TSP-4 variants. Integrin alpha(M)beta2 was identified as the TSP-4 receptor mediating these responses, and the 3 epidermal growth factor (EGF)-like domains of TSP-4 harboring the SNPs interacted with the alpha(M)I-domain. Despite the similarity in these responses, the P387 variant induced more robust tyrosine phosphorylation of the stress-related mitogen-activated protein kinases (MAPKs): p38MAPK and c-Jun NH2-terminal kinase (JNK), as well as signal transducer and activator of transcription-1 (STAT1) and heat shock protein 27 (HSP27) than the A387 variant. Additionally, cells adherent to P387 TSP-4 variant released 4-fold more H2O2 and secreted 2-fold more interleukin 8 (IL-8) as compared with the A387. H2O2 release and p38MAPK activation were totally inhibited by blockade of alpha(M)beta2. Thus, alpha(M)beta2 plays a central role in proinflammatory activities of TSP-4 (P387) and may contribute to the prothrombotic phenotype associated with this variant.

Cell Adhesion↗

[Clinical course of acute poisoning with olanzapine].

Olanzapine is a new atypical antipsychotic drug acting on different receptors. A variety of pharmacologic effects are responsible for toxicity and the variety of clinical symptoms seen in overdose: tachycardia, agitation or aggression, dysarthria, extrapyramidal dystonic effects, sedation or coma, small pupils, blurred vision, respiratory depression, hypotension. A retrospective analysis of clinical course of eight acute olanzapine intoxication treated at the Department of Clinical Toxicology Jagiellonian University Medical College is presented. CNS symptoms manifested in fluctuations between somnolence/coma and agitation/aggression and miosis were observed in most of the patients. Increased CPK activity was stated in the most of patients. All of the patients recovered, poisoning severity according PSS was moderate and severe.

Acute Disease↗

Comparison of fluorescence polarization immunoassay and high performance liquid chromatography for determination of carbamazepine concentration in blood of poisoned patients.

Carbamazepine is an antiepileptic drug widely used by neurological and psychiatric patients. Because of it's low therapeutic index and increasing number of acute carbamazepine intoxications there is a need of routine serum carbamazepine assay in toxicological laboratories. Determinations of serum carbamazepine concentrations are 5.3% of all toxicological analysis carried on in Department of Analytical Toxicology and Therapeutic Drug Monitoring, Collegium Medicum, Jagiellonian University in Kraków. The goal of the study was comparison of two analysis methods: FPIA and HPLC-DAD for the diagnostics of patients intoxicated with carbamazepine. Material for analysis were 21 samples of blood collected from poisoned patients treated in Department of Clinical Toxicology in Kraków. Measurements of serum carbamazepine concentration by FPIA method and carbamazepine and it's main active metabolite carbamazepine-10,11-epoxide concentrations by HPLC-DAD method were made. Statistical analysis showed that serum carbamazepine concentrations measured by FPIA method were higher than serum carbamazepine concentrations measured by HPLC-DAD method (t21 = 2.21, p = 0.0384). The mean difference of serum carbamazepine concentrations measured by the two methods was 2.67 mg/l (SD = 5.69 mg/l) and didn't depend on the carbamazepine concentration measured by FPIA method (r = -0.137, p = 0.5431). There was no statistical difference between serum carbamazepine concentration measured by FPIA method and the sum of serum carbamazepine and carbamazepine-10,11-epoxide concentrations measured by HPLC-DAD method (t21 = 1.42, p = 0.1690).

Acute Disease↗

[Cardiotoxic plants].

In statistics from Poison Information Center in Kraków plant poisonings comprise 2% of the total registered poisonings. In toxicology cardiac glycosides poisonings existing in common foxglove plant, lilies of the valley, oleander are essential. Species of cardiotoxic plants which may cause a danger in Poland are presented in the research. The toxic mechanisms of cardiac glycosides are specified.

Cardiac Glycosides↗

[Severe mixed poisoning with diltiazem, potassium and magnesium: a case report].

We report the case of 52-year-old woman, who ingested 3.6 g of diltiazem, 16 g of potassium chloride and 6.5 g of magnesium, in a suicide attempt 4 hours before admission. She developed cardiorespiratory failure, with severe hypotonia and acute renal failure, in ECG third degree atrioventricular block was stated. The highest potassium concentration was 8.0 mmol/l, magnesium 2.15 mmol/l. As a result of multiple pharmacologic intervention, including intravenous fluids, calcium, glucagon, dopamine, dobutamine, norepinephrine, transvenous pacing and peritoneal dialysis (haemodynamic instability makes haemodialysis noneffective) the haemodynamic stabilization of cardiovascular system and normalization of potassium and magnesium concentration were achieved. The diltiazem concentration was measured using liquid chromatography, the result was 0.89 microgram/ml. She was discharged in a good clinical condition on day 26th.

Antihypertensive Agents↗

[Acute poisoning with nifedipine and acebutol: two cases].

In this paper the case of intoxication in two women (19-year-old and 23-year-old), who in suicide attempts ingested at the same time different doses of nifedipine and acebutol. In 23-year-old woman 4 hours post ingestion cardiorespiratory arrest was stated. Resuscitation procedures were ineffective, she died. Acebutol concentration in postmortem blood was 24.1 mg/l and nifedipine-1.8 mg/l. The second one (19-year-old) was treated successfully, only mild cardiac disturbances were observed. Acebutol concentration in blood was 1.8 mg/l, nifedipine was not stated.

Acebutolol↗

[Cardiotoxicity of amantadine in acute poisoning: a case report].

We report the case of an adolescent, 15-year-old woman, who ingested 4.0 g of amantadine in a suicide attempt 2 hours before admission. She developed central nervous system symptoms including confusion and psychomotor agitation. The main cardiovascular symptoms were due to disturbances in atrioventricular conduction and propagation of stimuli in sinus node. All cardiovascular symptoms disappearanced after 12 hours of admission, CNS symptoms were observed 48 hours. No other systems were involved. She was discharged in a good state on day 5th.

Adolescent↗