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Quinolone-resistant Salmonella Infantis (n = 64) isolated from human stool samples, food and poultry during the years 2006-2011 were analysed for their resistance phenotypes, macrorestriction patterns and molecular mechanisms of decreased susceptibility to fluoroquinolones. Minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were determined by the agar dilution procedure, and the susceptibility to additional antimicrobial agents was determined by the disc diffusion method. To assess the influence of enhanced efflux activity, MICs were determined in the presence and absence of the inhibitor PAßN. The results of pulsed-field gel electrophoresis (PFGE) typing revealed that quinolone-resistant S. Infantis in Serbia had similar or indistinguishable PFGE profiles, suggesting a clonal spread. All S. Infantis showed combined resistance to NAL and tetracycline, whereas multiple drug resistance to three or more antibiotic classes was rare (2 isolates of human origin). The MICs ranged between 512 and 1024 µg/mL for NAL and 0.125-2 µg/mL for CIP. A single-point mutation in the gene gyrA leading to a Ser83→Tyr exchange was detected in all isolates, and a second exchange (Ser80→Arg) in the gene parC was only present in eight S. Infantis isolates exhibiting slightly higher MICs of CIP (2 µg/mL). The inhibitor PAßN decreased the MIC values of CIP by two dilution steps and of NAL by at minimum 3-6 dilution steps, indicating that enhanced efflux plays an important role in quinolone resistance in these isolates. The plasmid-mediated genes qnr, aac(6')-lb-cr and qepA were not detected by PCR assays.

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Molecular typing and resistotyping coupled with gyrA single nucleotide polymorphism (SNP) of 60 Salmonella Enteritidis (SE) isolates originated from poultry, food, and humans in Serbia is described. Molecular fingerprinting was performed by randomly amplified polymorphic DNA (RAPD) using four primers, and the diversity index (D) was 0.688. In combination with resistotyping and gyrA SNP, D increased to 0.828. A total of 23 genetic groups were obtained. When four RAPD primers were combined, epidemic isolates from a fast-food restaurant outbreak were clustered in a distinctive genetic group. Among 60 SE strains, three had multiple resistances to three or more antibiotics. Nine strains were resistant to nalidixic acid (NAL; a non-fluorinated quinolone). The mutations in quinolone resistance-determining region (QRDR) found in NAL-resistant strains were attributed to Asp(87) → Asn in six strains, Asp(87) → Gly in one strain, and Ser(83) → Phe in one strain. One NAL-resistant strain had no mutations in QRDR, suggesting another mechanism of resistance.

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The human parvovirus B 19 was discovered in 1975 by Cossart in England. Later (1984) evidence was provided that this virus is the etiological agent of erythema infectiosum and hydrops foetalis, and in 1985 it was provided that it is also the etiological agent of some types of arthritis or arthropaties and vasculitis. The diagnosis of the disease caused by this agent is most frequently based on evidence of specific immunoglobulins. The epidemiological and clinical impact of parvoviral infections in the Czech Republic was not known so far. Examination of sera from 562 subjects aged 0-60 years assembled in 1992 in three Czech regions revealed in children, age 0 - 4 years 9.8%, during preschool and school age 27 - 35.7% and in age groups above 15 years a 53.3 - 57.7% seroprevalence of IgG parvovirus B 19, roughly equally distributed among both sexes. The more frequent prevalence of specific immunoglobulins was proved in small groups of female workers in nurseries (66.7%), nursery schools (91.7%) and in blood transfusion stations (77.8%). The seropositivity of the general female population of matched age groups, with the exception of women aged 20 - 24 years, was 53.86%.

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Metabolically stable adenosine (ADO) agonists were infused into cannulas chronically implanted in the lateral cerebral ventricle intracerebroventricularly (icv) while responses in skin microcirculation of pentobarbital-anesthetized hamsters were observed with intravital microscopy. Cyclohexyladenosine (CHA; A1-receptor selective; 0.0001-1 pmol) and N-ethylcarboxoamidoadenosine (NECA; A2-receptor selective; 0.01-0.05 pmol) were delivered in 10 microliters of bicarbonate-buffered Ringer vehicle. Mean systemic arterial blood pressure, heart rate, skin arteriolar diameter, and red blood cell velocity were continuously monitored. Blood flow was calculated from measurements of arteriolar diameter (20-40 microns) and red blood cell velocity. CHA icv caused dose-related decreases in blood pressure and heart rate, as well as increases in cutaneous perfusion. Comparable amounts of CHA administered intravenously evoked no response. Pretreatment with an A1-selective antagonist xanthine amine congener (XAC, 5 pmol icv or 1 mg/kg iv) had no effect on the depressor response but antagonized the bradycardia. In contrast, a nonselective antagonist 8-phenyltheophylline (8pTHEO, 5 pmol icv or 0.3 mg/kg iv) had no effect on the bradycardia but attenuated the depressor response. By either route, both antagonists prevented the cutaneous microcirculatory responses evoked by icv CHA. NECA icv produced hypotension but no change in the skin, and the depressor response was not altered by icv XAC. These observations provide direct evidence that chemical stimulation of central nervous system (CNS) ADO receptors is linked to a cutaneous vascular response that can be dissociated from other cardiorespiratory depressant actions of CNS ADO.

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To determine whether the vasoconstriction evoked by A1-adenosine receptor stimulation in the skin circulation caused the release of other substances or whether A1 stimulation modulated the vasoconstriction evoked by other compounds, a potent A1-selective, synthetic agonist, cyclohexyladenosine (CHA), was topically applied simultaneously with several different vasoconstrictor agonists or antagonists. CHA was chosen instead of adenosine because the parent compound is metabolized quickly and also does not discriminate between A1 or A2 receptors. Blood flow was calculated from measurements of arteriolar diameter (40-60 microns) and red blood cell velocity using intravital videomicroscopy. Responses were recorded only in a steady state. The dose-related vasoconstriction evoked by CHA (ED50, 2.07 +/- 0.80 nM; half-minimal response, 93 +/- 1%) was not attenuated by antagonists to norepinephrine (phentolamine [11 microM] or prazosin [10 microM]), serotonin (methysergide [11 microM]), angiotensin II (saralasin [0.11 microM]), thromboxane (SK&F 88046 [13 microM]), or leukotrienes (SK&F 102922 [2.1 microM]). The vasoconstriction evoked by 2 nM CHA was attenuated by a subthreshold concentration (1 nM) of norepinephrine, whereas the vasoconstriction evoked by 0.1-1 microM norepinephrine was attenuated by a threshold concentration (1 nM) of CHA. Higher concentrations (10-100 nM) of CHA had no additional inhibitory effect. In contrast, CHA had no effect on the vasoconstrictions evoked by angiotensin II (10 nM or 1 microM) or serotonin (100 or 500 nM). Therefore, it is unlikely that A1-receptor stimulation causes the release of norepinephrine, serotonin, angiotensin, thromboxane, or leukotrienes in the skin microcirculation. Because norepinephrine attenuated the vasoconstriction evoked by CHA while CHA attenuated that evoked by norepinephrine, there appears to be a negative interaction between alpha-adrenergic and A1-adenosinergic receptors.

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The A1 and A2 adenosine receptor agonists (5'-(N-ethylcarboxamido)-adenosine, 2-chloroadenosine, adenosine (ADO) and N6-cyclohexyladenosine) were topically applied to 30- to 60-microns arterioles in the s.c. microcirculation of hamsters at different skin temperatures. Vasoconstrictor responses evoked by nanomolar concentrations of ADO and N6-cyclohexyladenosine were enhanced when local skin temperature (Ts) was increased, but unchanged when Ts was decreased. All these responses were antagonized by 8-phenyltheophylline, which suggests that temperature-sensitive vasoconstrictions were mediated by A1 receptors. In contrast, norepinephrine (10(-7) M) caused vasoconstrictions that were not enhanced at high Ts and were markedly reduced at low Ts, while angiotensin II (10(-8) M) caused vasoconstrictions that were temperature-insensitive. Vasodilator responses evoked by micromolar concentrations of ADO, 2-chloroadenosine and 5'-(N-ethylcarboxamido)-adenosine were temperature-insensitive. All these responses were antagonized by 8-phenyltheophylline, except those mediated by 10(-6) to 10(-4) M ADO, which can be explained by simple override of the receptor blockade. Thus, A1, but not A2, receptors show temperature-dependent actions in vivo, which suggests that temperature sensitivity could be an additional criterion for classification of ADO receptors.

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To characterize adenosine-mediated vascular responses, synthetic A1 and A2 receptor agonists (N-ethyl carboxamido adenosine [NECA], 2-chloro adenosine [2CA], or cyclohexyl adenosine [CHA]), the parent compound (adenosine [ADO]), an uptake inhibitor (dipyridamole [DIPYRID]) or a nonselective, competitive antagonist (8-phenyl theophylline [8pTHEO]) were topically applied to 20-60 microns arterioles in the subcutaneous microcirculation of the hamster. Blood flow was calculated from arteriolar diameter and red blood cell velocity using intravital microscopy. At greater than 10(-8) M, the potency order for vasodilation (maximum, 170-190% of control) was NECA greater than 2CA greater than ADO; these responses were attenuated by 10(-5) M 8pTHEO. From 10(-8) to 10(-6) M, 2CA evoked vasodilation whereas ADO, which has an identical affinity at A1 and A2 receptors, evoked lesser responses. ADO-induced vasodilation was potentiated by 10(-5) M DIPYRID; this response was similar to that evoked by 2CA alone or 2CA + DIPYRID. In contrast to ADO, 2CA is a poor substrate for cellular uptake, which suggests that uptake reduces the A2 effect of exogenous ADO. From 10(-10) to 10(-8) M, CHA and ADO were equipotent antagonized by 8pTHEO. Norepinephrine was a more potent vasoconstrictor and 8pTHEO did not alter these responses. Since ADO is a metabolic substrate and a nonselective receptor agonist, while CHA is A1-selective and a poor substrate for cellular uptake, neither A2 activation nor cellular uptake altered expression of the A1 effect of exogenous ADO. Furthermore, DIPYRID had no effect on the A1 response.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cancer mortality in endemic and non-endemic villages from a region with endemic nephropathy (EN) of Vratza district, Bulgaria has been compared for the period 1965--1974. The total and for all cancer sites mortality rates in all studied villages were comparable to European and world standards except a very high mortality from tumors of urinary organs in the endemic villages. Age-adjusted to world population rates/10(5) population in hyperendemic villages have been estimated as 16.8 for males and 14.9 for females in case of kidney tumors and as 7.1 in males and 10.2 for females in case of urinary bladder tumors. On village group basis a very close correlation between mortality rates from urinary system tumors and EN incidence rates has been disclosed although endemic and non-endemic villages are neighbouring and are very similar in ecological and cultural terms.

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