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Biomedical subjects

A Skoczyńska

Publications and source records attributed to A Skoczyńska.

At least 19 recordsLinked to original sources

Characterisation of Neisseria meningitidis C:2b:P1.2,5 isolates in Poland.

This study aimed to characterise Neisseria meningitidis C:2b:P1.2,5 isolates from Poland, which have now become predominant among serogroup C isolates in this country. Overall, 44 isolates (25 invasive and 19 from contact carriers) were typed by whole-cell ELISA and pulsed-field gel electrophoresis. Additionally, the invasive isolates were analysed by multilocus sequence typing, which revealed that they all belonged to the ST-8 complex/cluster A4. The emergence of this clone in other countries has resulted in mass immunisation campaigns and has been associated with a higher level of decreased susceptibility to penicillin; however the present study detected only one isolate that was penicillin-non-susceptible.

Female↗

Lead-cadmium interaction effect on the responsiveness of rat mesenteric vessels to norepinephrine and angiotensin II.

The comparison of the reactivity to norepinephrine (NE) and angiotensin II (A II) of isolated mesenteric blood vessels obtained from rats simultaneously poisoned with lead and cadmium to those responses of rats treated singly with lead or cadmium was performed. Male Buffalo rats aged 6-8 weeks were administered intragastrically with lead (35 mg Pb/kg body wt.) and/or cadmium (5 mg Cd/body wt.), once a week for a period of 7 weeks. Control rats were given equimolar amounts of sodium acetate and/or sodium chloride. Changes in mesenteric vascular resistance due to NE and A II injections were measured ex vivo as an increase in perfusion pressure in vessels prepared by McGregor's method. The dose-response curve for NE (0.01-5.0 microg) determined for vessels of rats poisoned simultaneously with lead and cadmium was shifted to the left in comparison to controls (not poisoned rats), similarly to these determined for rats poisoned with lead or cadmium. ED(50) NE pointed out in the control group (0.83+/-0.5 microg) was significantly greater than in metal treated groups (0.44+/-0.09; 0.45+/-0.26 and 0.5+/-0.11 microg in lead, cadmium, lead and cadmium-treated rats, respectively). This study indicated a tachyphylaxis in responses of isolated mesenteric vessels to A II injected in increasing doses, and the weaker, in comparison to controls, response of vessels of rats poisoned with lead and/or cadmium to A II at a dose of 0.4 microg. The decreasing response to A II could result from changes in calcium ions transport through L-type channels in vascular smooth muscle cells, because verapamil (2.0 microM) inhibited the A II-induced vasoconstriction more weakly in rats poisoned with metals than in controls. Inhibitor of prostaglandins synthesis, ketoprofen (200 microg/ml per min.) attenuated the pressor effect of NE in blood vessels obtained from all rats, but this effect was less potent in arteries of cadmium poisoned rats. Ketoprofen also inhibited the vasoconstrictory action of A II in all groups, but this effect was lower in vessels of rats poisoned simultaneously with lead and cadmium. We suggest that the release of vasoactive prostaglandins as a consequence of endothelial angiotensin receptor stimulation changes more under the influence of metals administered to rats simultaneously than under the influence or lead or cadmium administered singly. Treatment with a nitric oxide synthase inhibitor (L-NOARG; 22 microg/ml per min.) potentiated a NE-induced pressor response in all groups. However, the increase in perfusion pressure was greater in rats poisoned with cadmium in comparison to controls. L-NOARG potentiated the A II induced vasoconstriction only in cadmium poisoned rats, also indicating a greater influence of nitric oxide in cadmium treated rat vasculature. Two-way ANOVA showed the existence of lead-cadmium interactions effects on the reactivity of rat isolated mesenteric vessels to NE, A II and papaverine.

Analysis of Variance↗

[Activity of cefepime compared with other antibiotics against major hospital bacterial pathogens].

The aim of the study was to evaluate susceptibility of 976 bacterial isolates from nosocomial infections to cefepime and 9 other antibiotics used in the treatment of hospitalised patients. Bacterial strains were mainly derived from wound and soft tissue infections, sputum, abscesses and blood. The most prevalent etiologic agents were: Pseudomonas aeruginosa (18.7%), Escherichia coli (13.8%), Staphyloccocus aureus (9.7%, Acinetobacter baumannii (9.12%), Klebsiella pneumoniae (7.38%), Enterobacter cloacae (5.6%). The most susceptible to cefepime were strains of K. pneumoniae (98.62%), E. coli (98.52%) and E. cloacae (98.19%) including those producing extended spectrum beta-lactamases. The degree of susceptibility to cefepime was equal to that of imipenem. A. baumannii was the least susceptible species (67.42%). This study indicate that cefepime may play an important role in therapy of nosocomial infections in particular caused by Enterobacteriace.

Anti-Bacterial Agents↗

[Is there any risk interaction between electromagnetic field generated by mobile phones and artificial pacemakers].

Electromagnetic noise is rapidly increasing in the environment. Electromagnetic fields (EMF) originating from a variety of different sources have been shown to interfere with the function of implanted cardiac pacemaker. The authors present the effect of EMF generated by wireless telephones on different types of artificial pacemakers. In addition, instructions on safe use of mobile phones addressed to people with implanted artificial pacemaker are provided.

Arrhythmias, Cardiac↗

[Urinary trehalase activity as an indicator of renal dysfunction in lead smelters].

Epidemiological and experimental studies have demonstrated that lead and cadmium are responsible for renal dysfunction. Urinary trehalase is known as a good marker of proximal tubular renal brush border destruction in the population environmentally exposed to cadmium. The aim of this study was to determine the impact of occupational exposure to lead on the renal function and urinary trehalase activity. The study was carried out in 68 workers, aged 46 +/- 6 years, employed in a copper foundry. Blood lead, cadmium, copper and manganese concentrations were measured by atomic absorption spectrophotometry. Urinary trehalase activity was determined by the method of Nakano and Itoh. Trehalase activity was increased in copper smelters as compared to controls. There also was a positive linear correlation between blood lead level and urinary trehalase activity (r = 0.44; p < 0.05). Negative correlations between blood lead and copper concentrations (r = -0.30; p < 0.05) and between serum copper and trehalase level (r = 0.68; p < 0.001) were found. The results show that urinary trehalase activity could be a good indicator of the renal brush border dysfunction in copper smelters. This marker could be useful in the early diagnosis of nephrotoxic effect of lead.

Cadmium↗

[High density lipoprotein cholesterol level in rats poisoned with cadmium].

The effect of cadmium on lipid metabolism in persons occupationally and environmentally exposed to this metal may lead to the occurrence of cardiovascular diseases. The disturbances of the reverse transport of cholesterol could be responsible for the vascular changes. The aim of this study was to evaluate the impact of cadmium on the cholesterol level in the main fraction and subfractions of high density lipoprotein (HDL). The cholesterol level was measured in serum of rats treated with cadmium in a weekly dose of 5 mg/kg b.w. for seven weeks and in controls. After a seven-week exposure, the decreased HDL2, and the increased HDL3 cholesterol levels were observed in cadmium-poisoned animals as compared to controls. The results of the study suggest that a cadmium-impaired mechanism of the cholesterol transport in blood may induce vascular changes.

Animals↗

Characteristics of the major etiologic agents of bacterial meningitis isolated in Poland in 1997-1998.

Bacterial meningitis remains a major cause of morbidity and mortality worldwide, especially in children. In this paper, we present the results of the first two years (1997-98) of activity of the National Reference Centre for Bacterial Meningitis (NRCBM) on the etiologic agents of bacterial meningitis in Poland. Of the 220 isolates sent to the NRCBM, the most frequently identified was Neisseria meningitidis (n = 90, 40.9%), followed by Haemophilus influenzae (n = 58, 26.4%), and Streptoccus pneumoniae (n = 46, 20.9%). Of the meningococcal isolates, 88.9% belonged to serogroup B and 10.0% to serogroup C, and the most prevalent serotype was 22 (43.3%). Most meningococci were highly sensitive to penicillin; however, 10% of them had decreased susceptibility to penicillin. More than 90% of H. influenzae belonged to serotype b, and all were susceptible to third generation cephalosporins and chloramphenicol. A broad distribution of serotypes was found among pneumococcal isolates, of which the most common were serotypes 3 and 8. Penicillin nonsusceptible isolates constituted 13% of all pneumococcal isolates. Three of the resistant pnemococci belonged to serotype 23F. Data presented in this paper demonstrate the current epidemiological situation of bacterial meningitis in Poland.

Adolescent↗

[Serum selectin E level in lead-exposed workers].

Lead is recognised as a potential atherogenic factor. One of the earliest events in the development of atherosclerosis is monicyte attachment to the endothelial surface. This is followed by recruitment of monocytes into the subendothelial space and ingestion of modified LDL by these cells. In turn, modified LDL stimulates endothelial cells to induce expression of proinflammatory adhesion molecules, such as selectins, which further promote monocyte migration. It was observed that atherosclerotic vascular damage is associated with increased level of circulating selectin E. The aim of this study was to determine the impact of the occupational exposure to lead on the serum selectin E level. The study involved 80 patients, including 37 workers of a copper foundry and 43 people not exposed to lead. The subjects were matched in pairs according to sex, age and cholesterol concentration in blood. There were 25 hipercholesterolemic pairs and 9 pairs with normal serum total cholesterol. People exposed to lead had higher (about 7 ng/ml) serum selectin E concentration than those not exposed. There was positive linear correlation between selectin E and triglycerides in the whole group (p < 0.01), and the strongest correlation was observed in the group of subjects not exposed to lead (aged 40-60, r = 0.74). In the context of the described hypertriglyceridemic action induced by lead, these results suggest that lead could potentially act as an atherogenic factor in the early, inflammatory stage of atherosclerosis.

Adult↗

[Function of dopamine in mesenteric blood vessels of rats poisoned with lead and cadmium].

The aim of this study was to evaluate the impact of combined exposure to lead and cadmium, used in hypertensive doses, on the reactivity of isolated mesenteric rat vessels to dopamine. Experiments were performed on 64 male Buffalo rats (195-245 g body weight) administered intragastrically with lead acetate (35 mg Pb/kg b.w.) and/or cadmium chloride (5 mg Cd/kg b.w.) once a week for seven weeks. The isolated mesenteric bed was prepared according to McGregor's method. Dopamine (800 micrograms) was injected before and during the infusion, one after the other, of angiotensin converting enzyme (0.0004 j/ml/min), ketoprofen (0.2 mg/ml/min), and losartan (0.05 mg/ml/min) or infusion of nitric oxide synthase blocker, N-omega-nitro-L-argine (22 micrograms/ml/min), verapamil (0.001 mg/ml/min), and then propranolol (0.3 mg/ml/min). The results show an unchanged, in comparison to controls, vascular effect of dopamine in lead and cadmium poisoned rats. However, these metals modified the reactivity of mesenteric vessels to endogenous angiotensin and prostaglandins mediated pressor action of dopamine.

Animals↗

[Effect of arsenic and its compounds on the circulatory system].

Arsenic is a metal which occurs widely in both occupational and physical environments. Therefore, its easy accessibility and high toxicity raise the question on whether arsenic, particularly in relatively small doses, can cause damage of relevant molecular, biochemical and clinical significance to the cardiovascular system. The present review is focused on the confirmed and potential mechanisms of arsenic effect on the function and structure of vascular endothelium (nitric oxide, peroxynitrite), its role in stimulating the oxidative species formation (hydroxyperoxide, superoxide and lipid peroxide formation), as well as in decreasing the antioxidative response (enzymes: superoxide dysmutase, catalase, glutation peroxidase), its cytotoxic effects, including immunotoxic properties, arsenic action in the signal transduction pathways network (kinases and DNA transcription factors), impact on cell proliferation, differentiation and apoptosis, not to mention its interference with DNA synthesis and repair processes. Apart from mechanisms of arsenic action, the article provides the up-to-date information on various cardiovascular diseases of the established or presumed arsenic origin.

Animals↗

Outbreak of mupirocin-resistant staphylococci in a hospital in Warsaw, Poland, due to plasmid transmission and clonal spread of several strains.

An outbreak of mupirocin-resistant (MuR) staphylococci was investigated in two wards of a large hospital in Warsaw, Poland. Fifty-three MuR isolates of Staphylococcus aureus, S. epidermidis, S. haemolyticus, S. xylosus, and S. capitis were identified over a 17-month survey which was carried out after introduction of the drug for the treatment of skin infections. The isolates were collected from patients with infections, environmental samples, and carriers; they constituted 19.5% of all staphylococcal isolates identified in the two wards during that time. Almost all the MuR isolates were also resistant to methicillin (methicillin-resistant S. aureus and methicillin-resistant coagulase-negative staphylococci). Seven of the outbreak isolates expressed a low-level-resistance phenotype (MuL), whereas the remaining majority of isolates were found to be highly resistant to mupirocin (MuH). The mupA gene, responsible for the MuH phenotype, has been assigned to three different polymorphic loci among the strains in the collection analyzed. The predominant polymorph, polymorph I (characterized by a mupA-containing EcoRI DNA fragment of about 16 kb), was located on a specific plasmid which was widely distributed among the entire staphylococcal population. All MuR S. aureus isolates were found to represent a single epidemic strain, which was clonally disseminated in both wards. The S. epidermidis population was much more diverse; however, at least four clusters of closely related isolates were identified, which suggested that some strains of this species were also clonally spread in the hospital environment. Six isolates of S. epidermidis were demonstrated to express the MuL and MuH resistance mechanisms simultaneously, and this is the first identification of such dual MuR phenotype-bearing strains. The outbreak was attributed to a high level and inappropriate use of mupirocin, and as a result the dermatological formulation of the drug has been removed from the hospital formulary.

Anti-Bacterial Agents↗

[Susceptibility of Pseudomonas aeruginosa isolated from hospital infections to antibiotics].

A total of 674 clinical isolates of Pseudomonas aeruginosa were collected from 30 different hospitals located in 26 cities of Poland. These were 12 big regional hospitals, 7 large teaching hospitals, 4 specialised hospitals curing patients from the whole country, 6 small local hospitals and one regional paediatric hospital. The majority of strains were collected from patients hospitalised at ICUs (25.7%), surgical (21.7%), and internal medicine wards (9.9%). The isolates were recovered from different types of infections, mostly from respiratory tract infections (33.7%), wound infections (22.3%), and urinary tract infections (22.0%). All the isolates were subjected to antimicrobial susceptibility testing by MIC values evaluation. MICs of 13 different antibiotics (beta-lactams, aminoglycosides, chinolones) were determined by the agar dilution method. The general level of resistance of P.aeruginosa observed in the study was high, especially when compared to results of surveys obtained in other countries. Out of the antimicrobials used the highest activity in vitro was observed with meropenem, imipenem, piperacillin--tazobactam and ceftazidime. The high in vitro activity of ceftazidime was striking considering the long time of the use of this antibiotic in Polish hospitals. The highest levels of resistance were observed to some of the aminoglycosides. Populations of strains isolated in different wards or hospitals of different size were characterised by different susceptibility patterns.

Anti-Bacterial Agents↗

[Lipoprotein lipase (LPL) in the pathogenesis of atherosclerosis].

The role of lipoprotein lipase (LPL) in the development of atheromatosis is subject of the increased interest for about 20 years, since then Zilversmit observed that LPL activity is found in greater amounts in atherosclerotic than normal arteries. The general action of this enzyme is hydrolysis of triglycerides in triglyceride rich lipoproteins and thus regulation of metabolism of circulating as well antiatherogenic as proatherogenic lipoproteins. The effect of LPL on the biology of arterial wall seems to be atherogenic. The mechanisms of this effect of LPL is 1) augmentation of the adhesion and aggregation of LDL; 2) influence on the oxygen modification of LDL and increased uptake of oxy-LDL by macrophages; 3) dysfunction of endothelial barrier and retention of atherogenic lipoproteins in the arterial wall and 4) the activity of LPL macrophage origin. Possible atherogenic actions of LPL based on in vitro experimental studies are reviewed.

Adipose Tissue↗

Effect of angiotensin II on the reactivity of isolated mesenteric vessels to norepinephrine in rats poisoned with cadmium.

This study was designed to investigate the effect of cadmium on vascular response to norepinephrine (NE) administered before and during infusion of angiotensin II. The experiments were performed on isolated mesenteric vessels obtained from rats administered cadmium chloride intragastrically in doses of 20 mg Cd/kg body wt. once a week for 7 weeks. Changes in mesenteric vascular resistance due to NE were measured in the constant flow system as an increase in perfusion pressure. There was significant difference in the 50% effective doses (ED50) for NE between the two groups of rats when the dose-response curves were normalized to their respective maximal responses: ED50 NE for cadmium-exposed rats was lower and the dose-response curve was shifted to the left. Another change indicating an increased vasoconstrictor action of NE due to cadmium is more effective potentiation of exogenous NE responses produced by angiotensin II infused in dose of 5 mg/ml. In contrast to the controls in cadmium poisoned rats, propranolol in a dose of 300 ng/ml did not change significantly the vasoconstrictor response to NE and diminished the difference between angiotensin effect in vessels. Nifedipine (100 ng/ml), infused together with angiotensin II, inhibited pressor response to norepinephrine in preparation from both control and cadmium treated rats, to 60.5% and 69.3%, respectively. These results suggest an increase in the postsynaptic alpha adrenergic response and show a stronger potentiation of exogenous NE responses produced by angiotensin II, probably due to its influence on the calcium homeostasis in vessels of cadmium poisoned rats.

Analysis of Variance↗

[Lipid peroxidation as a toxic mode of action for lead and cadmium].

Recent studies have shown that lead and cadmium deplete glutathione and protein-bound sulfhydryl groups, resulting in the production of reactive oxygen species. As a consequence enhanced lipid peroxidation, DNA damage and altered calcium and sulfhydryl homeostasis occur. Lipid peroxidation is often discussed as a cause of metal-induced toxicity, although many other authors suggest a pivotal role of interaction with sensitive SH groups in determining cadmium and lead toxicity.

Animals↗

[Blood lipid parameters in smelters chronically exposed to heavy metals].

A group of 120 male workers, employed in copperworks (mean age = 41.5 years; mean exposure duration = 17,9 years) at workposts with the highest level of exposure to lead, were covered by the study. Blood levels of the following heavy metals were measured in all workers: Pb, Cd, Mn, Cu, Zn, Ca, Mg as well as concentrations of FEP and GSH, SOD activity in erythrocytes, parameters of lipid metabolism: total cholesterol, HDL2- HDL3-cholesterol, triglycerides, lipid peroxides (LPO), and lecithin-cholesterol acyltransferase (LCAT) activity. Mean blood lead level accounted for 251,86 micrograms/l, and mean level of FEP was slightly above normal. That may indicate moderate lead deposits in smelters. Concentrations of other metals remained within normal limits. No significant disturbances in lipid metabolism were observed. Along with expected positive correlation between lead blood level and FEP, a significant negative correlation between lead and cholesterol levels as well as between FEP and serum cholesterol was found. Moreover, a significant negative correlation between FEP and serum LPO, as well as a significant positive correlation between concentration and HDL2-cholesterol level and between FEP concentration and SOD activity in erythrocytes were noted. We believe that unexpected outcome of our investigations could result from the adaptation of healthy smelters to the environmental conditions. It is assumed that further exposure could weak antioxidant mechanisms and lead, in consequence, to the manifestation of symptoms induced by harmful effect of free radicals.

Adult↗

[Renin-angiotensin-aldosterone system in chronic poisoning of rats with lead and cadmium].

The aim of the study was to investigate the impact of the chronic, single and combined exposure to lead and cadmium on renin-angiotensin-aldosterone system in rats. Experiments were performed on male Buffalo rats which were intragastrically administered of lead acetate in doses of 35 mg Pb/kg body weight once a week or in doses of 70 mg Pb/kg body wt. twice a week and/or cadmium chloride in doses of 20 mg Cd/kg body wt. once a week for a period of seven weeks. One day after the feeding was over, the following parameters were measured: plasma renin activity, activity of angiotensin converting enzyme, serum concentration of angiotensin II and aldosterone. Metal content (lead, cadmium and zinc) in blood, kidneys and brain was determined by means of atomic absorption spectrophotometry. No clinical signs of lead or cadmium toxicity effects were observed. Rats poisoned with different doses of lead displayed no changes in renin-angiotensin system. In comparison to controls, in rats poisoned with cadmium, decrease in the plasma renin activity, serum angiotensin II and aldosterone concentrations were observed, but it was associated with unchanged activity of angiotensin converting enzyme. The decrease in plasma renin activity depended on cadmium levels in blood. In comparison to rats given cadmium, in rats treated with cadmium and lead together the inhibitor of the renin-angiotensin-aldosterone systems was weaker, although cadmium was used in the same dose.

Aldosterone↗