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Biomedical subjects

J J Legros

Publications and source records attributed to J J Legros.

At least 163 records · Page 9Linked to original sources
PubMed1981

[Hypodypsia and selective dysfunction of osmoreceptors in the hypernatremia syndrome].

We studied a patient with the rare syndrome of chronic hypernatremia associated with a frontal expansive process. The pituitary function was evaluated during dynamic tests bearing on radioimmunoassay of serum neurophysins levels. A test of water restrictionloading was performed during which urine appeared diluted (190-200 mOsm/kg) while the degree of serum osmolality was high (310-317 mOsm/kg). An hemodynamic stimulation resulted in a significant increase in serum neurophysins (from 3.5 +/- 0.3 to 5.5 +/- 0.2 ng/ml). After one intravenous injection of 2 mg nicotine, vomiting was observed, followed by a sharp rising of serum neurophysins levels (from 3.2 +/- 0.5 to 10.6 +/- 0.2 ng/ml). During hypertonic saline infusion, serum osmolality increased from 270 to 310 mOsm/kg, while neurophysins showed no significant change. Such results evidence a selective impairment of the hypothalamic-neurohypophyseal response to osmotic stimuli, with intact mechanisms of non-osmotic stimulation. In this patient, natremia was brought back to normal values by adequate water supply.

Adolescent↗
PubMed1981

[Modulation of the hypothalamo-neurohypophyseal system following environmental changes in rats].

The innate light-dark avoidance (step-through apparatus) was observed daily on 5 successive days in dehydrated and normal rats, the dehydration starting 24 hr before the first observation. We noted that latency scores from dehydrated groups and from the hydrated group tested together with a dehydrated group increased progressively. These significantly increased latencies did not appear when normally hydrated rats were tested alone. These changes in the temporal development of latencies seemed to be due to the fact that dehydrated rats were able to produce "fear odors" which increased the emotional reactivity of normal rats as well as theirs. The hypothalamo-neurohypophyseal function, characterized by the peripheral total neurophysins levels, also seemed to be modulated by these psychosocial and physical stresses. The neurophysins values from the hydrated group tested together with a dehydrated group were not statistically different from those of the latter group whereas they were higher than those of the hydrated group tested alone (Mann-Whithney; U = 28; n1 = n2 = 10; approach the significance). Further investigations are needed before establishing a definite relationship between the changes in latency scores on the one hand and the changes in neurophysins levels on the other hand. Nevertheless, one may well suppose that peripheral neurophysins levels play their own role in the adaptation of the organism to the environmental variations rather than only reflect the activity of the hypothalamo-neurohypophyseal axis.

Animals↗
PubMed1981

[Sexual dysfunction and disordered carbohydrate metabolism (author's transl)].

Sexual impotence with inability to produce erection is a frequent accompaniment of diabetes. Only exceptionally however is impotence complained of as a symptom. Though in no direct sense a danger to the patient's life, impotence is sometimes a source of major distress and, in a few exceptional cases, may lead to suicide. It is therefore important to distinguish the different mechanisms underlying impotence, and in particular to differentiate psychogenic mechanisms, far more relevant than formerly thought in diabetic patients, from organic mechanisms, in particular neuropathic and vascular, uncommonly, endocrine. Besides cases of unequivocal diabetes, there is an abnormally high proportion of patients suffering from "psychogenic" impotence affecting erection who have impaired glucose tolerance. In such patients the disordered metabolism could reflect at neuroendocrine level the existence of neuro-psychological dysfunction, either a cause or a consequence of the impotence. A second possibility is that the metabolic disorder directly impairs neurological function, resulting in neuropathic impotence. Clearer understanding of the complex mechanisms relating disturbance of carbohydrate metabolism to sexual impotence requires multidisciplinary approaches. Such arrangements are necessary for the planning and conduct of schemes of treatment involving to varying extents the special approaches of psychology, sexology, endocrinology, urology and vascular surgery. The success of such treatment will depend largely upon the quality of the diagnostic and therapeutic approach which requires individualised planning.

Blood Glucose↗
PubMed1980

Plasma AVP, neurophysin, renin activity, and aldosterone during submaximal exercise performed until exhaustion in trained and untrained men.

The effect of intense muscular work (80% of maximal oxygen uptake) on responses of plasma hormones involved in electrolyte and water balance were measured in 14 male subjects. They were divided into three groups according to their maximal oxygen uptake and the duration of exercise performed until exhaustion: well trained subjects (group I), trained subjects (group II), and untrained subjects (group III). Pulmonary gas exchange, heart rate, rectal and skin temperature, and weight loss were measured as well as hematocrit and plasma and urine sodium and potassium concentrations. Rectal temperature increased significantly in all subjects after exhaustion. The variation of hematocrit was smallest and the weight loss greatest in the well-trained subjects. Plasma aldosterone, renin activity (PRA), vasopressin (AVP), and neurophysin (Np) displayed highly significant increases after exercise in all three groups: PRA was increased 4.5 times (p < 0.01), aldosterone 13 times (p < 0.05), Np 2.6 times (p pe 0.05), and AVP 4.8 times (p < 0.05). Nevertheless, there was no correlation between the changes in PRA and those in plasma aldosterone, nor between aldosterone and plasma sodium or potassium. At the urinary level, the only striking observation was that free water clearance tends to become positive after exercise. Our results provide evidence that this kind of exercise produces a highly significant increase in plasma levels of the hormones involved in electrolyte and water balance. They also indicate that it is among the well-trained subjects that sweat loss is highest though the hematocrit increase is the smallest; this suggests that water is shifted more efficiently from the extravascular compartment.

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↗