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Biomedical subjects

J J Legros

Publications and source records attributed to J J Legros.

At least 19 recordsLinked to original sources
PubMed1992

Oxytocin blocks the environmentally conditioned compensatory response present after tolerance to ethanol-induced hypothermia in mice.

The present study tested the hypothesis that the attenuation by oxytocin of tolerance to ethanol-induced hypothermia relies upon an impairment of the putative conditioning processes underlying environment-specific tolerance. According to the conditioning model of tolerance, such tolerance occurs because an opposite compensatory response conditioned to ethanol-paired cues attenuates ethanol's effects. Tolerance to ethanol-induced hypothermia was established to a particular environment over 4 days by injecting mice (daily) with oxytocin 2 h before ethanol, outside the colony room. As controls, other mice were injected similarly but following testing in the animal room. We found that oxytocin suppressed the conditioned compensatory response, revealed by injecting saline to every group in the tolerance-associated environment. These results suggest that oxytocin acted, at least partly, via an inhibition of the associative learning processes that facilitate tolerance development.

Animals↗
PubMed1992

Apomorphine stimulation of vasopressin- and oxytocin-neurophysins. Evidence for increased oxytocinergic and decreased vasopressinergic function in schizophrenics.

Apomorphine challenge tests (0.5 mg SC) were performed in 14 normal male volunteers and in 9 male schizophrenic inpatients, drug-free for at least 2 wk. In the normal volunteers, apomorphine induced an increase of serum growth hormone (GH) (maximum at 40 min), of vasopressin-neurophysin (hNpI) (maximum at 20 min), and oxytocin-neurophysin (hNpII) (maximum at 20 min). The release of neurophysins was independent of digestive side effects. In the schizophrenics, the GH level and release pattern were similar to those in the controls. The basal level of hNpI was reduced (t0: 0.42 +/- 0.1 ng/ml in the schizophrenics and 0.66 +/- 0.05 ng/ml in the controls, p < 0.02). In contrast, the basal level of hNpII was increased (3.34 +/- 0.04 ng/ml in the schizophrenics to 0.92 +/- 0.21 ng/ml in the controls, p = 0.001). The response to apomorphine was blunted, with no significant release of hNpI or of hNpII. Although the hNpII data are consistent with an increased dopaminergic tone, the psychopathological meaning of the increased basal oxytocinergic and decreased vasopressinergic functions remains to be defined.

Adult↗
PubMed1979

[Neurophysins].

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Diabetes Insipidus↗
PubMed1979

[Hereditary motor neuron disease: the proximal, adult, sex-linked form (or Kennedy disease). Clinical and neuroendocrinologic observations].

Clinical, electrophysiological, histological and neuroendocrinological findings in a peculiar form of progressive spinal and bulbar muscular atrophy affecting 4 members in two different families are reported. The clinical hallmarks, which characterize this entity among the group of degenerative motor neuron diseases are: sex-linked recessive inheritance; onset in the third decade; slow progression; involvement of facial and bulbar muscles in addition to wasting of the proximal and, in some cases, the distal musculature; asymmetry of clinical signs; consistent and abundant fasciculations predominantly in the peri-oral muscles; intention tremor and a well-developed gynaecomastia, which is the first clinical sign. Electrophysiological and histological findings confirm the neurogenic origin of the muscular atrophy; in addition, muscle biopsy shows "myopathic-like" changes in one case and serum muscle enzyme levels are elevated in all neurologically affected patients. It is believed that the clinical entity corresponds to the rare type III proximal hereditary motor neuropathy (or "Kennedy's disease"), of which 25 published cases are reviewed. Neuroendocrinological data in two patients demonstrate an androgenic insufficiency of hypothalamo-hypophyseal origin and high levels of circulating oestrogens, which probably have induced gynaecomastia. Dynamic neuroendocrinological tests suggest that lesions of certain hypothalamic nuclei may exist, which should be looked for in the forthcoming anatomical studies.

Adult↗
PubMed1979

[Systematic evaluation of 8 arginine vasopressin and neurophysins plasma levels in 10 patients with oat cells carcinoma of the lung (author's transl)].

Plasma AVP level, neurophysins and osmolality have been measured in 10 patients with oat cell carcinoma of the lung but without any biological signs of syndrome of inappropriate secretion of ADH (SIADH), before and 15 mn after an intravenous injection of Ethanol. No statistically significant difference was noted in the AVP, neurophysins and osmolality values between 10 patients with asymptomatic oat cell carcinoma and control population (10 normal volunteers, 12 patients with non neoplasic lung pathology and 10 patients with different lung carcinoma). We concluded that AVP and neurophysins cannot be considered as a good tumoral marker in the detection of oat cell carcinoma of the lung.

Arginine Vasopressin↗
PubMed1978

[Neurohormones].

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Angiotensins↗
PubMed1978

Serum Neurophysins in familial central diabetes insipidus.

Antibovine neurophysin antibodies (anti-bNpI and/or anti-bNpII) are present in certain patients with familial central diabetes insipidus; these are exogenous origin, as they are not present in patients who have not received treatment with crude posterior pituitary extracts over the years preceding the analysis. Immunoreactive neurophysins were detectable in the blood of five patients with familial central diabetes insipidus, and in two of them, the levels increased after a short period of water restriction. There is marked polymorphism of these neurophysins from one serum to another: neurophysin I was consistently absent, while neurophysin II, accessory neurophysins, and other immunoreactive substances not present in normal sera were sometimes present in variable amounts. Immunoreactive AVP was undetectable in the urine of all patients, while immunoreactive OT was found in three of them; the latter substance could, however, be arginine vasotocin. Data are presented suggesting that the association between the biosynthesis of neurophysin I and AVP on the one hand, and neurophysin II and OT on the other hand is maintained in patients with isolated AVP deficiency on the basis of a congenital defect.

Adolescent↗
PubMed1978

Urinary excretion of neurophysins in patients with kidney disease.

The mean rate of excretion of neurophysins in the urine of 16 patients with kidney disease but without tubular dysfunction was 0.48 +/- 0.14 (S.E.M.) ng/min, whereas the rate in 16 patients with tubular dysfunction was 3.64 +/- 1.56 ng/min (significantly different; 2P less than 0.01). In the whole group of 32 patients there was a relationship (r = 0.57) between the rate of excretion of neurophysins in the urine and the clearance of lysozyme. The increased rate of urinary excretion of neurophysins observed in some patients with kidney disease therefore appears to be related to a disorder of renal tubular function. It is shown that the raised levels of neurophysins observed in the serum of some patients with kidney disease are not attributable to a decrease in the urinary clearance of neurophysins.

Creatinine↗