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P Vallet

Publications and source records attributed to P Vallet.

24 records · Page 2Linked to original sources
PubMed1980

Neural lobe of pituitary modulates corticotropin release in the rat.

The hypothesis was tested that the neural lobe of the pituitary may modulate the release of anterior pituitary hormones. The neural lobe of anesthetized lactating rats was electrically stimulated at 30 Hz (5 sec on and 5 sec off) for 3 min while taking blood samples for RIA of ACTH. Plasma ACTH increased within 3 min by 22 +/- 9% (average +/- SEM; P less than 0.025) in intact rats and by 38 +/- 17% (P less than 0.025) in rats where the nerve supply to the median eminence and neural lobe was interrupted. Electrical stimulation of the anterior pituitary was ineffective. No significant changes in plasma ACTH were observed in rats with coagulated hypophysial portal vessels or in Brattleboro rats with congenital diabetes insipidus. Apparently, neither peripheral plasma vasopressin (estimated at 150 microU/ml maximum) nor intermediate lobe ACTH could account for the observed rise in ACTH. Results suggest a vasopressin dependent modulation of ACTH release by the neural lobe, mediated either by axon collaterals to the median eminence or by a vascular interconnection between posterior and anterior pituitaries.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Nuclear magnetic relaxation dispersion studies of water-soluble gadolinium(III)-texaphyrin complexes.

Water proton 1/T1 nuclear magnetic relaxation dispersion (NMRD) profiles were measured for a water-soluble gadolinium(III) texaphyrin (Gd-tex) complex as a function of temperature and in the presence and absence of 5% human serum albumin (HSA). Upon dissolving the complex in water (0.259 mM), the water relaxivity values decreased with time but remained higher than those of free GD3+(aq) at all fields. Concurrent measurements of free Gd3+ using metallochromic dyes indicated that demetallation of the texaphyrin did not occur over a period of several days at 37 degrees C. The high relaxivity values and shape of the NMRD profile of this complex may be ascribed to a combination of large water coordination number (q estimated at 3.5) and long tau R. Upon mixing an aqueous solution of the complex with 5% HSA, the low-field water relaxivity slightly decreased whereas the high-field relaxivity increased relative to the free complex in water, and the relaxivities became nearly independent of temperature. These observations indicate that water exchange between the inner coordination sphere of Gd-tex and bulk water becomes limiting in the presence of HSA.

Contrast Media↗
PubMedDate not supplied

[Alzheimer's disease and Down's syndrome. Some recent etiopathogenic data].

The present status of research clearly demonstrates the occurrence of lesions characteristic of Alzheimer's disease in patients suffering from a Down's syndrome or trisomy 21. The senile plaques appear very early in trisomy 21 (from the age of 20) and are constant after 40 or 45 years. In these two illnesses, the beta-amyloid protein or A4 protein (4.2 kD) leads to deposits in preferential regions of the central nervous system within two compartments: 1) intracellular, contributing to the formation of neurofibrillary tangles and 2) extracellular, making up the amyloid center of senile plaques as well as around the wall of some blood vessels, then corresponding to the amyloid congophilic angiopathies. Unexpectedly, larger proteins including the A4 sequence have been shown to be normally present in several tissues of normal as well as sick individuals and represent possible precursors of the A4 protein. Alzheimer's disease may happen either sporadically or following a familial incidence associated with an autosomic dominant mode of transmission. Moreover, the risk of incidence of trisomy 21 seems to be enhanced for collaterals of Alzheimer's disease patients. Since 1987, the use of molecular biology tools has revealed particularly fruitful. A linkage analysis has been undertaken that showed an association of the putative gene for the familial form of Alzheimer's disease (FAD) with the gene coding for amyloid precursor proteins (APP).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗