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- ItemAcesso aberto (Open Access)Changes in sodium appetite evoked by lesions of the commissural nucleus of the tractus solitarius(Associação Brasileira de Divulgação Científica, 2009-06-01) Ogihara, Cristiana Akemi [UNIFESP]; Schoorlemmer, Gerhardus Hermanus Maria [UNIFESP]; Colombari, Eduardo [UNIFESP]; Sato, Monica Akemi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Faculdade de Medicina do ABC Departamento de FisiologiaAblation of the area postrema/caudal nucleus of the tractus solitarius (NTS) complex increases sodium intake, but the effect of selective lesions of the caudal NTS is not known. We measured depletion-induced sodium intake in rats with electrolytic lesions of the commissural NTS that spared the area postrema. One day after the lesion, rats were depleted of sodium with furosemide (10 mg/kg body weight, sc) and then had access to water and a sodium-deficient diet for 24 h when 1.8% NaCl was offered. Water and saline intakes were measured for 2 h. Saline intake was higher in lesioned than in sham-lesioned rats (mean ± SEM: 20 ± 2 vs 11 ± 3 mL/2 h, P < 0.05, N = 6-7). Saline intake remained elevated in lesioned rats when the tests were repeated 6 and 14 days after the lesion, and water intake in these two tests was increased as well. Water intake seemed to be secondary to saline intake both in lesioned and in sham-lesioned rats. A second group of rats was offered 10% sucrose for 2 h/day before and 2, 7, and 15 days after lesion. Sucrose intake in lesioned rats was higher than in sham-lesioned rats only 7 days after lesioning. A possible explanation for the increased saline intake in rats with commissural NTS lesions could be a reduced gastrointestinal feedback inhibition. The commissural NTS is probably part of a pathway for inhibitory control of sodium intake that also involves the area postrema and the parabrachial nucleus.
- ItemAcesso aberto (Open Access)Efeito de fármacos ototóxicos na audição de recém-nascidos de alto risco(Sociedade Brasileira de Fonoaudiologia, 2010-01-01) Camara, Marília Fontenele e Silva; Azevedo, Marisa Frasson de [UNIFESP]; Lima, José Wellington de Oliveira; Sartorato, Edi Lúcia; Universidade de Fortaleza; Universidade Federal de São Paulo (UNIFESP); Universidade Estadual do Ceará; Universidade Estadual de Campinas (UNICAMP)PURPOSE: To calculate the incidence of sensorineural hearing loss (SNHL), to verify if there is a causal association between the use of ototoxic drugs and SNHL, and to establish the frequency of genetic mutations related to SNHL in high risk newborns. METHODS: The study was a retrospective and prospective cohort research with 250 children. Data was gathered from subjects' charts and with their caregivers. Moreover, subjects were submitted to auditory evaluation with distortion product otoacoustic emissions, timpanometry, visual reinforcement audiometry, auditory brainstem response and transient otoacoustic emissions. The study of the genetic mutation 35delG, and the mitochondrial mutations A1555G and A7445G was essential to evaluate the possibility that SNHL had a non-syndromic genetic origin. The association between the medicine use and the occurrence of hearing loss had been analyzed. RESULTS: The incidence of SNHL in high risk newborns was 11.6%, and causal associations between SNHL and the drugs administered were: amikacin and cefotaxime (OR=5.35), cefotaxime and furosemide (OR=7.02), ceftazidime and vancomycin (OR=9.12). The frequencies of the mutation 35deIG and mitochondrial mutations A1555G and A7445G were, respectively, 0.8% and 0%. CONCLUSION: The incidence of SNHL in high risk newborns was high, showing an important causal relation with the use of ototoxic drugs and a small relation with genetic mutations.
- ItemSomente MetadadadosIonized hypocalcemia is an early event and is associated with organ dysfunction in children admitted to the intensive care unit(Elsevier B.V., 2013-10-01) Barbosa Dias, Cacilda Rosa [UNIFESP]; Leite, Heitor Pons [UNIFESP]; Nogueira, Paulo Cesar Koch [UNIFESP]; Carvalho, Werther Brunow de [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)Purpose: the purpose was to determine the frequency and risk factors of ionized hypocalcemia and to evaluate this disturbance as a predictor of mortality in a pediatric intensive care unit (ICU).Materials and Methods: in a prospective cohort study, 337 children admitted consecutively to an ICU were monitored regarding serum ionized calcium concentrations during the first 10 days of admission. the following variables were analyzed as independent of hypocalcemia: age; malnutrition; sepsis; Pediatric Index of Mortality 2; first 3 days organ dysfunction score (Pediatric Logistic Organ Dysfunction); and use of steroids, furosemide, and anticonvulsants. Hypocalcemia was defined as a serum ionized calcium concentration less than 1.15 mmol/L.Results: the rate of hypocalcemia was 77.15%. in a multivariate model, higher Pediatric Logistic Organ Dysfunction scores during the first 3 days of ICU stay were independently associated with hypocalcemia (odds ratio, 2.24; 95% confidence interval, 1.23-4.07; P = .008). Medications associated with hypocalcemia were furosemide (dose >= 2 mg/[kg d]) and methylprednisolone (dose >= 2 mg/[kg d]). No significant association was found between hypocalcemia and 10-day mortality.Conclusions: Ionized hypocalcemia is common during the ICU stay, particularly in the first 3 days of admission. This disturbance was not found to be a predictor of mortality, but it is independently associated with more severe organ dysfunction. (C) 2013 Elsevier Inc. All rights reserved.