Search PubMed⌕ Search

Biomedical subjects

Y Liel

Publications and source records attributed to Y Liel.

61 records · Page 4Linked to original sources
PubMed1981

Prolactin response to metoclopramide and chlorpromazine in primary testicular failure and isolated gonadotrophin deficiency.

The aim of the present study was to measure the PRL response to metoclopramide (MET) and chlorpromazine (CPZ) in seventeen patients with primary testicular failure and eight patients with isolated gonadotrophin deficiency (IGD). The responses were compared with those to TRH. Basal gonadotrophins and peak responses to LHRH were increased in testicular failure and reduced in IGD. Basal PRL levels were normal in both groups of patients. However, when compared with controls, the PRL response to both MET and CPZ as well as to TRH was exaggerated in primary testicular failure, whereas the responses wee decreased in IGD. In both patient groups, as well as in the controls, the PRL response to MET exceeded that to TRH and CPZ. It is suggested that alterations in the steroid milieu are responsible for the exaggerated PRL response to MET, CPZ and TRH in primary testicular failure and the reduced response observed in IGD.

Adolescent↗
PubMed1981

The TSH response to TRH is exaggerated in primary testicular failure and normal in the male castrate.

Basal TSH levels and the TSH response to TRH have been evaluated in 26 males aged 20-48 years with primary testicular failure, and 6 males aged 58-69 years who had been orchidectomised for prostatic carcinoma. The patients with testicular failure were sequentially challenged at 30 min intervals with iv LRH (100 microgram), TRH (200 microgram) and the dopaminergic antagonist, metoclopramide (10 mg). The castrates received a bolus of LRH and TRH given together. The responses in the 2 patient groups were compared to a group of 28 healthy male controls aged 20-40 years, who received the sequential protocol and 8 elderly controls aged 65-79 years, who were given the LRH, TRH bolus. Mean +/- SD basal TSH levels were 3.0 +/- 1.2 muU/ml in primary testicular failure and significantly greater than both control and castrate groups. The peak TSH response to TRH was 18.4 +/- 7.4 muU/ml in testicular failure and significantly greater than in the young controls, where it was 11.5 +/- 5.0 muU/ml. The peak levels in the castrates and in the elderly controls were similar to the young male controls. Total T4 and T3, as well as FTI, primary testicular failure had a reduction in their T3 resin uptake. The normal TSH profile in the castrates indicates that a testicular factor produces the exaggerated responses in primary testicular failure.

Adult↗
PubMed1980

Acid-induced gastric inhibitory polypeptide secretion in man.

This study has assessed the effect of oral or intraduodenal HCl, administered alone or in combination with glucose, on gastric inhibitory polypeptide (GIP) and insulin secretion. Eight young males were given the following three oral tests: 30 g glucose, 150 cc 0.1 N HCl and the glucose-acid combination. Another group of eight controls received intraduodenal infusions of 20 g glucose, 75 cc 0.1 N HCl and their combination. All tests were performed in a random fashion at weekly intervals. When given alone, HCl did not influence glucose or insulin levels. However, HCl did produce an increase in GIP. The GIP response to acid was less than that to glucose and was delayed. The peak insulin and GIP responses with the glucose and glucose/acid combinations were similar with both the oral and intraduodenal routes. There was, however, a potentiation of both the GIP and insulin responses when intraduodenal acid was given with glucose. This effect on GIP and insulin was not evident with the oral glucose/acid load. It is concluded that HCl by itself is capable of stimulating GIP secretion. Since there was only a potentiation of insulin and GIP secretion when large doses of HCl were given together with glucose via the intraduodenal route, the physiological relevance of acid-induced GIP secretion remains to be resolved.

Administration, Oral↗
PubMedDate not supplied

Fine needle aspiration of the hot thyroid nodule.

The use of fine needle aspiration (FNA) cytology in the evaluation of solitary hot thyroid nodules was examined in 24 patients. Satisfactory FNA specimens were obtained from 22 patients. None of the cytologic samples was considered malignant or suspicious for malignancy. The cytologic findings were indeterminate in one instance--a smear with follicular features. The smears from the other 21 patients were judged to be benign. If FNA had been used as the initial diagnostic step, the need for a thyroid scan would thus perhaps have been avoided in 21 of the 24 patients. These results support the idea that FNA is the most effective procedure in the evaluation of the solitary thyroid nodule, whether functional or not.

Adult↗
PubMedDate not supplied

Peroxidase activity as a marker for estrogenicity: studies in uterus and mammary tumors.

We examined the possibility that peroxidase activity might be a marker for estrogen activity in established estrogen-dependent tissues: dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors and human breast cancer. In DMBA-induced tumors undergoing regression after ovariectomy or tamoxifen treatment, tumor size decreased by 50%, estradiol receptors (ER) and progesterone receptors (PgR) decreased by 25 and 20%, respectively, but peroxidase activity paradoxically increased six- to sevenfold. In DMBA tumors stimulated by estradiol treatment or by the cessation of tamoxifen administration in intact rats, tumor size increased threefold. ER and PgR increased two- and threefold, respectively, while peroxidase activity decreased 50%. These data indicate an inverse relation between tumor growth, ER and PgR on the one hand, and peroxidase activity on the other. In the human breast cancers there was a significant negative relation between the presence of ER and peroxidase activity. By using a calibrated Sephadex G-100 column it was shown that uterine peroxidase differs in molecular weight from the peroxidase of rat mammary tumors and that of human breast cancer.

Animals↗