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ABSTRACT: Two distinct diarrheagenic Escherichia coli pathotypes, enteroaggregative E. coli (EAEC) and Shiga toxin-producing E. coli, were observed in association with O113 strains isolated from human and nonhuman sources in Brazil, respectively. The O113 strains from human diarrhea belonged to a diversity of serotypes, and nine (53%) of them harbored virulence traits of typical EAEC.
Journal of Clinical Microbiology 07/2007; 45(6):2028-30. · 4.15 Impact Factor
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ABSTRACT: 1. Lungs can take up from the vasculature, circulating forms of atrial natriuretic peptide (Turrin and Gillis, 1986, 1987) and also to synthesize ANP. 2. The lung peptide directly delivered by lungs into the lung vasculature could play a role in the local water/electrolytic balance. 3. Using Spontaneously Hypertensive Rats (SHR), isogenic normotensive controls, the Wistar-Kyoto strain (WKY), and the regular Wistar strain as second control (W), and using a highly sensitive RIA, we measured the immunoreactive IR-ANP content of extracted plasma, lung homogenate and lung perfusate, since there are references of altered ANP levels in this kind of hypertension. 4. The IR-ANP measured in the lung vasculature effluent collected throughout 32 min of Krebs perfusion, was significantly different in all of the three analyzed strains (SHR > WKY > W). 5. The results support the idea of a local function for the peptide hormone directly delivered into the lung vasculature of SHR, which could represent a local adaptation to haemodynamics SHR characteristics besides a genetic characteristic distinguishing WKY from W strains.
Comparative Biochemistry and Physiology Part C Comparative Pharmacology and Toxicology 02/1993; 104(2):233-8.
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ABSTRACT: We investigated the effect of hyperprolactinemia induced by long-term domperidone treatment (10.0 mg/kg, single daily dose, ip) on striatal dopamine (DA) receptor sensitivity in male Wistar rats weighing 250-300 g (N = 8). Domperidone treatment for 7 days continued to produce an increase in serum concentration of prolactin (PRL) from 17.3 +/- 2.2 to 33.1 +/- 7.3 and from 16.8 +/- 2.3 to 21.9 +/- 2.1, 2 and 72 h after domperidone withdrawal, respectively. Hyperprolactinemia induced by long-term domperidone treatment did not change binding sites (Bmax) and dissociation constant (Kd) of [3H]-spiroperidol binding when compared to controls. These results show that hyperprolactinemia induced by long-term domperidone treatment does not effect the sensitivity of striatal DA receptors presumably because the effect of neuroleptic drugs is due to their interaction with the receptors and not to the concomitant hyperprolactinemia.
Brazilian Journal of Medical and Biological Research 02/1991; 24(6):591-4. · 1.13 Impact Factor
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ABSTRACT: Stimulation of the region antero-ventral to the third cerebral ventricle (AV3V) by a cholinergic drug, carbachol, and lesions of the AV3V have been demonstrated in previous studies to either augment or decrease sodium excretion, respectively. Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Consequently, to evaluate a possible role of brain ANP in evoking the changes in renal sodium excretion that follow stimulations or lesions of the AV3V, we determined the effect of injection of carbachol into the AV3V of rats on the concentration of plasma ANP and its content in several neural tissues, the pituitary gland, lungs, and atria. Conversely, the effect of lesions in the AV3V on plasma ANP and the content of the polypeptide in the various organs was determined. Injection of carbachol into the AV3V produced the expected natriuresis, which was accompanied within 20 min by a dramatic rise in the plasma ANP concentration and a rise in ANP content in the medial basal hypothalamus, the neurohypophysis, and particularly the anterior hypophysis but without alterations in the content of ANP in the lungs or the right or left atrium. Conversely, there was a dramatic decline in plasma ANP at both 24 and 120 hr after the AV3V lesions had been placed. This was accompanied by a slight decline in the content of the peptide in the lungs. There was no change in its content in the right atrium at 24 hr after lesions, but there was a significant increase at 120 hr. There was a small decline in the content in the left atrium at 24 hr, followed by a rebound to slightly elevated levels at 120 hr. These small changes contrasted sharply with the dramatic decline in content of the peptide in the medial basal hypothalamus, median eminence, neurohypophysis, choroid plexus, anterior hypophysis, and olfactory bulb. These declines persisted or became greater at 120 hr; except in the olfactory bulb in which the decline was no longer significant. The dramatic increase in plasma ANP after carbachol stimulation of the AV3V that was accompanied by marked elevations in content of the peptide in basal hypothalamus and neuro- and adenohypophysis suggests that the natriuresis resulting from this stimulation is brought about at least in part by release of ANP from the brain. Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. In view of the much larger quantities of the peptide stored in the atria, it is still possible that changes in atrial release may contribute to the alterations in plasma ANP observed after stimulation or ablation of the AV3V region; however, these results suggest that the dramatic changes in plasma ANP that followed these manipulations may be due to altered release of the peptide from brain structures as well as the atria and lungs.
Proceedings of the National Academy of Sciences 01/1990; 86(23):9621-5. · 9.68 Impact Factor
