Imbalanced triacyglycerol metabolism in fat cells from estrogen-treated rats.
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Biomedical subjects
Publications and source records attributed to L Mercier.
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This article reports the effect of a single injection of 17 beta-oestradiol on RNA synthesis, in the male rat pituitary. An increase in RNA polymerase I activity, with a maximum effect between 10 and 15 hours, is described. No modification in RNA polymerase II activity was detected. These results were extended and confirmed, using in vitro double labelling of RNA, following in vivo oestrogen treatment. Polyacrylamide gel electrophoresis of nuclear and cytoplasmic RNA showed an increased incorporation of adenine into 28S and 18S rRNA, in the pituitaries of oestrogen-treated animals. The 5S rRNA was not modified by the hormonal treatment. These effects on RNA polymerase I activity and on 28S and 18S rRNA synthesis were closely correlated with the long-term nuclear retention of receptor-oestradiol complexes, in vivo. Taken together, these observations argue in favor of the nucleolus as a preferential target for receptor-bound oestradiol, in the cell nucleus of the male rat pituitary.
Variations in spinal motoneuronal excitability were assessed during wakefulness and non-REM sleep in hyperkinetic and normal children by determining the recovery cycle of the H-reflex following a conditioning stimulus. Reflex facilitation which generally occurs 100-300 msec after a conditioning stimulus was markedly reduced during sleep in both groups and during wakefulness as well in hyperkinetic subjects. Among possible mechanisms which might underlie the observed reductions in facilitation, emphasis is placed on decreased central excitability resulting from depressed fusimotor activity.
Glucocorticoid responses in two independently derived lines of rat hepatoma tissue culture cells (HTC and FU5-5) were examined. FU5-5 cells exhibited induction of the enzyme tyrosine aminotransferase (TAT) at concentrations of dexamethasone that were approximately 7-fold lower than that required for HTC cells. FU5-5 cells also displayed substantial TAT induction with steroids that were partial agonists, or antagonists, in HTC cells. The increased sensitivity of FU5-5 cells was not, however, due to an increased affinity of FU5-5 cell receptors for dexamethasone, as determined from cell-free and whole cell binding experiments. The differential steroid sensitivity for TAT induction was observed with three other, structurally different glucocorticoids, thus apparently ruling out steroid metabolism in one of the cell lines as a cause. Also, induction of TAT in FU5-5 cells occurred at approximately 9-fold lower steroid concentrations than were required for the induction of glutamine synthetase (GS) in the same cells. Thus, the dose-response curves for TAT induction in HTC cells and for GS induction in FU5-5 cells are closely correlated with the saturation curve for whole cell steroid binding to receptor sites, while the dose-response curve for TAT induction in FU5-5 cells is shifted to lower steroid concentrations. This represents the first report of dissociation of two supposedly primary, glucocorticoid-induced functions and indicates that identical receptor-mediated processes cannot be utilized by FU5-5 cells for the induction of TAT and GS. The involvement of second messengers or different nuclear processes are possible explanations for the unusual behavior of FU5-5 cells during glucocorticoid induction of TAT.
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Variations in amplitude of the spinal monosynaptic H-reflex were examined during relaxed wakefulness in three unmedicated groups of subjects, hyperactive children (n=5), an age-matched group of control children (n=5), and a group of young adults (n=10), using techniques involving equal intensity percutaneous stimuli delivered in pairs or trains at varying rates. The paired-stimuli procedure generates a recovery function, the outstanding features of which are early depression, a peak of facilitation occurring between 100-300 msec, and complete recovery by 2-5 sec. Trains of stimuli delivered at rates greater than or equal to 1/sec effect a reduction in reflex amplitude which is termed homosynaptic depression. Both procedures revealed differences between hyperkinetic children and comparison groups. The paired-stimulus technique revealed a generalized reduction in excitability for hyperkinetic children for intervals extending up to 800 msec. In particular, hyperkinetic children were characterized by a significantly increased variability at the longer stimulus intervals. Hyperkinetic children also showed a more rapid reduction in reflex amplitude to initial stimuli in stimulus trains delivered at rates greater than or equal to 1/sec. Trains of stimuli at rates effecting facilitation in terms of the paired stimulus technique, i.e., 3,4 and 5/sec, revealed sustained amplitude enhancement for control subjects only. The recovery function data are consonant with spinal motoneuronal hypoexcitability in hyperkinetic children. Possible neruophysiological and neurochemical mechanisms underlying the reduced capability of hyperkinetic children to respond to rapidly delivered, repetitive stimuli are discussed.
This method can assay simultaneously, using 300 microliters of plasma, of the three principle local anesthetic agents used by peridural injection for post-operative anesthesia and analgesia: xylocaïne, etidocaïne, bupivacaïne. The assay method consists of three steps: (a) the addition of an internal calibrating agent (mepivacaïne). (b) defecation using trichlorocetic acid. (c) alcalinization of the supernatent (pH 11), extraction with dichloromethane and concentration at room temperature of the organic phase. (d) chromotography using an SE 30 or OV 17 impregnated column. The method is sensitive between 0.37 mumoles per l-1 (0.1 microgram . ml-1) and the coefficient for the mean deviation is 10.9% for concentration between 0.37 mumoles 1-1 and 75 mumole1-1 (0.1 microgram . ml-1 and 20 micrograms . ml-1). The correspondence of the figures recorded in this large concentration range without any change in the technique means that the kinetics of the plasma concentrations before and after peridural injection can be followed. The results obtained by gas liquid chromatography for the assay of lidocaïne were compared in 115 different plasma samples with concentrations obtained by an immuno enzymatic method ("EMIT") fitted to a centrifuge analyser. The correlation coefficient between the two methods was: (r = 0.95 with y = 0.09 x +0.25 microgram . ml-1 implying the absence of any interference and the specificity of the two methods. The columns also separate in 20 minutes the two main metabolites of lidocaïne: monoethylglycinexylidide (M.E.G.X.) and glycinexylidide (G.X.). These results demonstrate that continuous peridural injection of lidocaïne produces a high plasma concentration without any clinical toxic phenomena.
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Comparisons were made in 13 normal young adults of alpha motoneuronal excitability during non-rapid-eye-movement (NREM) sleep (stages 2--4) and wakefulness based on a study of the recovery cycle of the H-reflex after a conditioning stimulus. During sleep, excitability was generally decreased and a peak of secondary facilitation, which characteristically occurs 100--300 msec after the conditioning stimulus during wakefulness, was reduced or absent. A variety of mechanisms, including long-loop reflexes and afferent discharges from reflex muscle contraction and cutaneous fibers, has been proposed to account for this phase of facilitation in the waking recovery curve. However, since studies to date indicate the absence of tonic presynaptic or postsynpatic inhibitory influences acting on the monosynatpic reflex pathway during NREM sleep, but report tonic reduction in fusimotor activity at this time, it is suggested that a primary factor underlying the absence of facilitation during sleep is a reduction in central excitability deriving from depressed fusimotor activity.
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