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1.
AJNR Am J Neuroradiol ; 42(5): 955-960, 2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33632737

RESUMO

BACKGROUND AND PURPOSE: The signal intensity of the thyroid in neonates is high on T1WI. It is affected by gestational and postnatal ages. However, the extent of the influence of these ages is unknown. This study investigated the relationship of signal intensities of the infant thyroid with postnatal and gestational ages and anterior pituitary using 3D gradient-echo T1WI. MATERIALS AND METHODS: This retrospective study included 183 T1-weighted images from 181 infants. Using a multiple linear regression analysis, we evaluated the effects of postnatal and gestational ages on the thyroid-muscle signal intensity ratio. The relationship between the thyroid and anterior pituitary signal intensities on T1WI and the age of the infants was evaluated. RESULTS: Multiple linear regression analysis showed that the thyroid signal intensity was affected negatively by postnatal age at examination and positively by gestational age at birth (P < .01 and P = .04, respectively). According to the standardized partial regression coefficients, the influence of postnatal age at examination was stronger than that of gestational age at birth (-0.72 and 0.13, respectively). The thyroid and anterior pituitary signal intensities reached constant values at 12 weeks' postnatal age, and the mean thyroid-anterior pituitary signal intensity ratios were almost 1 throughout the entire period. CONCLUSIONS: The signal intensity of the infant thyroid on T1WI was more strongly influenced by the postnatal age at examination than the gestational age at birth, and it was almost equal to that of the anterior pituitary.


Assuntos
Idade Gestacional , Imageamento por Ressonância Magnética/métodos , Glândula Tireoide/diagnóstico por imagem , Humanos , Processamento de Imagem Assistida por Computador , Lactente , Recém-Nascido , Masculino , Hipófise/diagnóstico por imagem , Estudos Retrospectivos
3.
Eur J Endocrinol ; 143(4): 535-41, 2000 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-11022201

RESUMO

BACKGROUND: Human growth hormone (hGH) transgenic (TG) rats have been produced in our laboratory. These TG rats are characterized by low circulating hGH levels, virtually no endogenous rGH secretion, and massive obesity. OBJECTIVE: To elucidate how energy balance and leptin sensitivity contributed to the establishment of this obesity. DESIGN AND METHODS: Food intake, locomotor activity and leptin concentrations in serum and cerebrospinal fluid were measured in TG rats and their non-transgenic littermates (control). The effect of intraperitoneal and intracerebroventricular injection of leptin on food intake and body weight gain was also examined. RESULTS: An increase in food intake and a decrease in locomotor activity were observed from 4 and 7 weeks of age, respectively, in the transgenic rats compared with control. Serum leptin concentrations of the transgenic rats were more than twice as high as those of control rats and were associated with an increased white adipose tissue mass and ob gene expression. Intraperitoneal injection of leptin significantly decreased food intake and body weight gain in control rats, but not in transgenic rats. Leptin concentration in the cerebrospinal fluid of transgenic rats was not different from that of control rats, and intracerebroventricular injection of leptin was similarly effective in reducing food intake and body weight gain as it was in control rats. CONCLUSIONS: These results suggest that the transgenic rats, whose GH secretion is suppressed, develop obesity due to early onset of an increase in food intake and a decrease in locomotor activity with leptin resistance resulting from deteriorating leptin transport from peripheral blood to cerebrospinal fluid.


Assuntos
Hormônio do Crescimento Humano/sangue , Leptina/farmacologia , Obesidade/fisiopatologia , Tecido Adiposo/fisiologia , Animais , Animais Geneticamente Modificados , Northern Blotting , Peso Corporal/efeitos dos fármacos , Ingestão de Alimentos/efeitos dos fármacos , Regulação da Expressão Gênica/fisiologia , Hormônio do Crescimento Humano/deficiência , Hormônio do Crescimento Humano/genética , Humanos , Leptina/sangue , Leptina/líquido cefalorraquidiano , Masculino , Atividade Motora/efeitos dos fármacos , Ratos
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