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Biomedical subjects

R Noto

Publications and source records attributed to R Noto.

At least 19 recordsLinked to original sources
PubMed1990

[Evaluation of genetic predisposition and acquired risk factors in development of essential hypertension and its acute complications].

The authors studied a population of 4.023 subjects from several rural and urban communities selected on the basis of age, work tasks and social class. Genetic predisposition to essential hypertension was evaluated by determining intraerythrocyte sodium levels in all subjects with essential hypertension and their families. The authors also verified the behaviour of some biohumoral factors (PRA, aldosterone, ANP, intraerythrocyte, Na) as possible markers of essential hypertension and the role of some acquired risk factors in the development of the disease and its cerebrocardiovascular complications. The hypertense subjects were divided into groups and treated with diet alone or diet associated with drugs depending on the prevalence of pathogenetic factors. The results were evaluated after 1, 3, 6 and 12 months.

Erythrocytes↗
PubMed1990

In vivo SPECT imaging of CNS D-2 dopamine receptors: initial studies with iodine-123-IBZM in humans.

Iodobenzamide (IBZM) is a D-2 dopamine receptor antagonist. In this paper the results of Phase I clinical studies of iodine-123-(123I)IBZM in humans are reported. Preliminary imaging studies, both planar and single-photon emission tomography (SPECT), of no-carrier added [123I]IBZM in humans show specific localization in the basal ganglia of the brain. At 2 hr after an i.v. injection, the brain uptake was 3.72% of the dose, and at 20 hr later the uptake diminished to 0.7%. Radiation dosimetry calculation indicated that the radiation dose to the brain was minimum, 0.039 rad/mCi, while the large intestine wall received the highest dose, 0.28 mrad/mCi. The radiation dosimetry and pharmacology data suggest that this agent is safe for human use.

Adult↗
PubMed1989

[Plasma lipids, insulin, C-peptide, and glucagon levels in cirrhosis: personal observations].

The authors report preliminary data on the behavior of some lipid fractions in cirrhosis of the liver and correlate them with the changes in the insulin, glucagon and C-peptide levels. Elevated FFA (Free Fatty Acids) and normal cholesterol, triglyceride and total lipid values indicate a prevalent insulin induced effect and a reduction of liver metabolism of these fractions. This hypothesis is supported by the fact that L-carnitine, which reestablishes the carnitine-dependent intracellular transport system, reduces the levels of all the lipid fractions studied. The normal C-peptide values in these patients with liver cirrhosis show that hyperinsulinemia is caused by impaired metabolism of this hormone and not by hyperincretion. This hyperinsulinemia seems to react positively to the improvement of the intracellular transport systems. A fall in the hyperglucagonemia follows the decreased hyperinsulinemia leading to a hormone balance with lower values and a consequent reduction of the hormonal stimuli on the lipid metabolism. The possibility of administering drugs, which can act on the metabolic pathways responsible for the high FFA plasma levels, which seem to play a role in the physiopathology of encephalopathies and hepatic coma is clinically interesting.

Adult↗
PubMed1988

Hypercalcemia in childhood renal tumors.

Hypercalcemia is an uncommon complication of childhood renal tumors. It is exclusively seen in infants 6 months of age or younger with malignant rhabdoid tumor of the kidney (MRTK) or congenital mesoblastic nephroma (CMN). Secretion of parathormone or prostaglandin E2 by the tumor cells is responsible for the hypercalcemia in most of these patients. Bone metastasis has been notably absent in these patients, and the hypercalcemia completely resolves with the removal of the tumor. Hypercalcemia in itself probably does not have any prognostic significance; however, it may serve as a tumor marker in some patients. Early recognition and effective management of this complication may prevent the acute life-threatening as well as the longstanding complications of this serious metabolic disorder.

Female↗
PubMed1988

Prolactin and thyroid status in prepubertal children with mild to moderate obesity.

Prolactin (PRL) response to thyrotropin releasing hormone (TRH) in 21 prepubertal children with mild to moderate obesity was compared with that in 21 normal prepubertal children (controls). Basal PRL levels were normal but the mean peak PRL response and mean increment in PRL levels following TRH administration were significantly lower in prepubertal obese children (p less than 0.001). The mean PRL responses to TRH were significantly impaired at all time intervals in prepubertal obese boys and girls compared to the control subjects. Linear regression and correlation coefficient analysis did not reveal any significant relation between the percent overweight and PRL response. Basal T4, T3 levels and T3 and TSH response to TRH were similar in both groups. The findings suggest that neuroendocrine regulation of prolactin is impaired in prepubertal children even with mild to moderate obesity. This could be secondary to altered neurotransmitter status at the hypothalamic level. Further studies are needed to determine whether the defect is innate or acquired, primary or secondary.

Child↗