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G Pelletier

Publications and source records attributed to G Pelletier.

At least 451 records · Page 25Linked to original sources
PubMed1987

In situ hybridization to rat brain and pituitary gland of growth hormone cDNA.

Using in situ hybridization, we have investigated the presence of mRNA coding for growth hormone (GH) in the rat brain. Using 32P-labeled GH cDNA as a probe, the pituitary gland showed hybridization in unfixed sections. Using 3H-labeled GH cDNA hybridized to fixed sections, only cells in the anterior pituitary were labeled in good agreement with the localization of somatotropes. In the brain, wide zones were labeled with 32P-GH cDNA: the caudate putamen, the striatum, the ventral thalamus, the formatio reticularis and the basal cortex. With the 3H GH-cDNA probe, more discrete regions of the brain showed hybridization: the basal cortex, the outside part of the hippocampus and the caudate putamen.

Animals↗
PubMed1987

Prognostic factors in patients with hepatocellular carcinoma. Attempts for the selection of patients with prolonged survival.

A prognostic study based on 127 untreated patients with hepatocellular carcinoma was undertaken to evaluate their survival time and to find clinical and biologic criteria which allow the selection of patients with a survival time longer than 60 days who could enter a therapeutic trial. Twenty-eight clinical and biologic variables were assessed using univariate and multivariate semiparametric regression (Cox's) models. Ten variables were isolated by univariate analysis. Multivariate analysis found a negative relationship between a survival time longer than 60 days and five of these variables; these variables were in decreasing order: encephalopathy, alcohol consumption, aspartate amino transferase (AST), blood urea nitrogen, and total bilirubin. Prevalence, positive, and negative predictive values of encephalopathy were 20%, 27.5%, and 97% respectively. When three other criteria: ASAT greater than four times the upper limit of the normal (N), blood urea nitrogen greater than N, and total bilirubin greater than 2N were added, their prevalence, positive, and negative predictive values were 72%, 89.7%, and 57.1% respectively. These results suggest that in countries where incidence of hepatocellular carcinoma is low and recruitment of patients difficult, absence of encephalopathy must be the only criterion for selection of patients with hepatocellular carcinoma in therapeutic trials; whereas, in countries with a high incidence of hepatocellular carcinoma the other criteria may be added.

Age Factors↗
PubMed1987

Atrial natriuretic factor (ANF) stimulates the release of alpha-MSH from frog neurointermediate lobes in vitro. Interaction with dopamine, GABA and neuropeptide Y.

The action of atrial natriuretic factor (ANF) on alpha-MSH release from frog neurointermediate lobe was studied in vitro using a perifusion technique. Synthetic ANF Arg101-Tyr 126, at concentrations ranging from 10(-7) to 10(-5)M, caused a dose-related stimulation of alpha-MSH release. In addition, dopamine, GABA and NPY, three neuroendocrine factors which inhibit alpha-MSH secretion totally suppressed the action of ANF on alpha-MSH production. The neural lobe of the amphibian pituitary contains numerous ANF immunoreactive fibers, and this regulatory peptide may diffuse from nerves terminating in the pars nervosa to the pars intermedia. Thus, our results suggest that ANF of hypothalamo-neurohypophysial origin may be involved in the multineuronal regulation of amphibian melanotrophs.

Animals↗
PubMed1987

Melanotropin release inhibiting activity of neuropeptide Y: structure-activity relationships.

We have recently shown that the release of alpha-MSH by the intermediate lobe of the frog pituitary is inhibited by neuropeptide Y (NPY). Using the perifusion technique, we have compared in the present study, the alpha-MSH release inhibiting activities of NPY, various NPY short chain analogues and two other members of the pancreatic polypeptide family, peptide YY (PYY) and avian pancreatic polypeptide (APP). The order of biological potency was NPY greater than NPY[2-36] greater than NPY[16-36] greater than NPY[25-36] greater than NPY[1-15]. Among the two pancreatic polypeptides tested, PYY appeared to be almost as potent as NPY while APP was 6 times less active than NPY. Neither NPY[1-15] nor NPY[16-36] could antagonize the inhibitory effect of NPY on alpha-MSH release. The structure-activity relationship study suggests that the bioactive determinant of NPY is located in the C-terminal part of the molecule.

Animals↗
PubMed1987

Co-distribution of neuropeptide Y and its C-terminal flanking peptide in the brain and pituitary of the frog Rana ridibunda.

By means of the peroxidase-anti-peroxidase technique, the distribution of neuropeptide tyrosine (NPY) and its C-terminal flanking peptide (C-PON) has been studied on serial sections of the brain and pituitary of the frog Rana ridibunda. Throughout the brain, NPY and C-PON-immunoreactive perikarya exhibited a remarkable co-distribution. These two peptides were found to be co-located within the same cell bodies in various brain regions including the dorsal and ventral pallium, the dorsal and ventral infundibular nuclei and the preoptic nucleus. The distribution of NPY- and C-PON-containing fibers in the brain and pituitary was similar. Sequential double immunohistochemical staining using the indirect immunofluorescence method, showed that NPY and C-PON were actually located within the same nerve processes throughout the frog brain and in the intermediate lobe of the pituitary. These studies indicate that the deduced C-PON sequence is present within the frog precursor to NPY and is formed in vivo in the frog brain. Like NPY, C-PON is transported distally in nerve terminals and is likely released with NPY in various regions of the brain and in the intermediate lobe of the pituitary.

Animals↗
PubMed1987

Mapping of neuropeptide Y-like immunoreactivity in the feline hypothalamus and hypophysis.

The distribution of neuropeptide Y (NPY) in the cat hypothalamus and hypophysis was studied with the indirect immunofluorescence technique of Coons and co-workers (Coons, Leduc, and Connolly: J. Exp. Med. 102:49-60, 1955), which provided a detailed map of NPY-like immunoreactive neurons. The immunolabelling was detected in cell bodies, fibers, and terminallike structures widely distributed throughout the whole hypothalamus. A large population of medium-sized NPY-like immunoreactive cell bodies was localized in the area of arcuate nucleus. The number of immunoreactive cell bodies visualized was dramatically increased after intracerebroventricular injections of colchicine. Numerous immunolabelled cell bodies were also visible in the median eminence and scattered in the lateral hypothalamic area. Dense plexuses of NPY-immunoreactive fibers were observed in the arcuate nucleus, internal layer of median eminence, periventricular zone, and paraventricular nucleus. Other regions of hypothalamus displaying numerous NPY-like immunoreactive fibers included dorsal and ventrolateral hypothalamic areas. In contrast, certain hypothalamic areas were almost devoid of NPY-like immunoreactive fibers-namely, the mammillary bodies and suprachiasmatic nucleus. Finally, in neurohypophysis, bright immunofluorescent fibers were observed along the pituitary stalk and penetrating the neural lobe. These results suggest the widespread distribution of the NPY-containing neuronal systems in the cat hypothalamus and hypophysis.

Animals↗
PubMed1987

Characterization and autoradiographic localization of LHRH receptors in the rat brain.

Luteinizing-hormone-releasing hormone (LHRH) is distributed in several extrahypothalamic areas, suggesting that it might act as a neurotransmitter or neuromodulator in the central nervous system. This study was undertaken to characterize and localize LHRH receptors in the rat brain by using slide-mounted frozen sections. The radioligand used was an iodinated stable LHRH agonist, [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide. It was clearly established that LHRH receptors with characteristics similar to those of pituitary LHRH receptors were present in the brain. They were found in high concentrations in the dorsal hippocampus, amygdala, septum, and subiculum and in very low amounts in the hypothalamus. Generally, a good correlation could be observed between receptor distribution and immunohistologically localized LHRH. These results strongly suggest that LHRH has multiple sites of action in the rat brain and reinforce the hypothesis that the peptide could act as a neurotransmitter/neuromodulator in the central nervous system.

Animals↗
PubMed1987

Thyroxine accelerates the differentiation of granular convoluted tubule cells and the appearance of epidermal growth factor in the submandibular gland of the neonatal mouse. A fine-structural immunocytochemical study.

The effects of the administration of thyroxine (T4) on the postnatal cytodifferentiation of granular convoluted tubule (GCT) cells of the submandibular gland (SMG) of Lewiss-Webster mice were studied by light and electron microscopy. From birth, mice of both sexes were injected daily with T4 (sc 0.4 micrograms/g BW) and were sacrificed 24 h after the last injection at 7, 9, 11, 14 and 21 days of age. Control mice received vehicle only. In control mice, granulated striated duct (SD) cells were first detected at 9 days and 7 days of age by light- and electron microscopy, respectively. Furthermore, a few scattered granulated SD cells were observed by light microscopy as early as day 7 in T4-treated mice of both sexes. At 21 days of age, in mice given T4, GCT cells were larger and more numerous and the Golgi apparatus, rough endoplasmic reticulum, and secretion granules were more abundant. In control mice, immunocytochemical staining for epidermal growth factor-(EGF) was first detectable at day 21 at the light- and electron-microscopic levels. However, positively stained cells were first observed in T4-treated mice by light- and electron-microscopic immunocytochemistry at 14 and 11 days of age, respectively. Moreover, in the 21-day-old T4-treated mice, the number of immunoreactive GCT cells, as well as the intensity of the staining per cell, was markedly increased as compared to controls. EGF immunostaining was restricted to GCT cells, and by immuno-electron-microscopy was only seen in apical secretory granules in granulated SD cells and GCT cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1987

Morphological correlates of serotonin-neuropeptide Y interactions in the rat suprachiasmatic nucleus: combined radioautographic and immunocytochemical data.

The morphological substrate of putative serotonin (5-HT)/neuropeptide Y (NPY) interactions in the suprachiasmatic nucleus (SCN) was investigated by combined radioautography and immunocytochemistry after intraventricular administration of (3H)5-HT in the rat. In the ventral portion of the SCN, the distribution of (3H)5-HT uptake sites overlapped closely the NPY-immunoreactive terminals. Previous investigations have shown that the dense 5-HT and NPY innervations of the SCN originate in different structures, i.e., the midbrain raphe nuclei and the ventral lateral geniculate nucleus, respectively. Accordingly, in the present study, destruction of 5-HT afferents by 5,7-dihydroxytryptamine was not found to induce any modification in NPY staining and, in ultrastructural immuno-radioautographic preparations, two distinct pools of axonal varicosities could be identified. Both 5-HT and NPY terminals established morphologically defined synaptic junctions, sometimes on the same neuronal target. Some cases of direct axo-axonic appositions between the two types of terminals were also encountered. These data constitute additional criteria for characterizing the cytological basis of the multiple transmitter interactions presumably involved in the function of the SCN as a central regulator of circadian biological rhythms.

Animals↗
PubMed1987

Radioautographic study of glycoprotein synthesis and fate in the hypothalamo-neurohypophyseal system of vasopressin-deficient Brattleboro rats.

L-3H-fucose was injected into the lateral cerebral ventricle of vasopressin-deficient Brattleboro and control Long-Evans rats which were subsequently killed at several time intervals after the injection. The hypothalamus and the neurohypophysis were processed for light- and electronmicroscopic radioautography. Other complementary experiments using immunocytochemical and enzyme-histochemical techniques were also undertaken. L-3H-fucose was incorporated into newly synthesized glycoproteins in the Golgi apparatus of supraoptic and paraventricular neurons, and later on labelled glycoproteins migrated to lysosomes and the plasma membrane surrounding the perikaryon. The Golgi apparatus of the vasopressin-deficient neurons remained heavily labelled as long as 3 days after injection, in sharp contrast with the normal neurons in which there was a remarkable decrease of label in the Golgi region between 4 and 24 h after the isotope administration. Labelled glycoproteins also migrated to the neurohypophysis and were mainly found in the axonal plasma membrane, vesicles and axoplasm. The renewal of glycoproteins in the neurohypophysis of Brattleboro rats was faster than in the normal rats and this was attributed to the lack of formation of products which are normally packaged in secretory granules in the perikaryon and released at the axon terminal in the neurohypophysis. Colchicine caused a disturbance in the topography of the organelles of the perikaryon and the most striking features were the displacement of Golgi stacks to the periphery of the perikaryon and an accumulation of mitochondria in this neuronal region. No secretory granules were observed in the vasopressin-deficient neurons of untreated or colchicine-treated Brattleboro rats. By contrast, secretory granules (most of them labelled with 3H-fucose) were concentrated in the perikaryon of colchicine-treated Long-Evans rats. In these rats, colchicine caused a severe block in the migration of 3H-fucose-labelled glycoproteins to the neurohypophysis, but this did not occur in the Brattleboro rats. The results of the experiments were interpreted in the light of the genetic defect known to occur in Brattleboro rats which causes the inability to produce vasopressin and also remarkable morphological and physiological changes in the affected neurons.

Acid Anhydride Hydrolases↗
PubMed1987

Interobserver agreement in the physical diagnosis of alcoholic liver disease.

Agreement among six physicians for 18 clinical signs in 50 alcoholic patients was prospectively studied. Twenty patients had alcoholic cirrhosis, 14 noncirrhotic alcoholic liver disease, and 16 alcoholics had no clinical or biochemical abnormalities. Agreement was assessed by kappa index for categorical variables and by intraclass correlation coefficient for the others. A good agreement was observed for ascites (r = 0.75) and splenomegaly (r = 0.75). It was fair for jaundice (r = 0.65), Dupuytren's contracture (r = 0.65), and vascular spiders (r = 0.64). However, it was poor for white nails (r = 0.27) and hepatic consistency (r = 0.11). Agreement was better among senior physician's than junior physicians. In order to assess which signs contributed to differentiate the three groups of patients, a stepwise discriminant analysis was realized; it identified three variables: vascular spiders (P less than 0.001), splenomegaly (P less than 0.001), and abdominal wall collateral veins (P less than 0.01). These results suggest that studies based on physical findings must be cautiously considered.

Adult↗
PubMed1987

Upper gastrointestinal endoscopy. An unrecognized cause of hyperamylasemia.

The prevalence of hyperamylasemia 2 hr and 24 hr after upper gastrointestinal endoscopy without attempts to cannulate the ampulla of Vater was prospectively studied in 50 consecutive patients. In the 2-hr sample, hyperamylasemia was observed in nine patients (18%) (serum amylase range 59-191 units/liter with a mean value of 102 units/liter; reference range: 12-46 units/liter). Five of the nine patients still had an increased serum amylase (range 54-118 units/liter, mean 78.4) 24 hr after endoscopy. When hyperamylasemia occurred, it always appeared in and was higher in the 2-hr sample. The increased serum amylase activity was due to a rise of S-type isoamylase. The cause of hyperamylasemia after gastrointestinal endoscopy is speculative but is probably due to an hypersalivation.

Adult↗
PubMed1987

Atrial natriuretic factor-like immunoreactivity in the central nervous system of the frog.

The distribution of atrial natriuretic factor-like immunoreactivity in the central nervous system of the frog Rana ridibunda was investigated by indirect immunofluorescence and the immunogold technique, using an antiserum generated in rabbits against synthetic atrial natriuretic factor (Arg 101-Tyr 126). A stereotaxic atlas of neurons containing atrial natriuretic factor-like material was prepared to show the widespread distribution of atrial natriuretic factor-positive cell bodies and fibres in the brain. Appreciable numbers of immunoreactive perikarya were observed in the dorsal and medial pallium, the medial septal nucleus, the anteroventral and ventrolateral areas of the thalamus, the lateral forebrain bundle, the posterocentral and posterolateral thalamic nuclei, the preoptic nucleus, the dorsal infundibular nucleus and the anteroventral tegmental nucleus of the mesencephalon. A heavy accumulation of atrial natriuretic factor-like immunoreactive cell bodies and very dense fibre bundles were noted in the interpeduncular nucleus of the mesencephalon. Fibres were generally seen where cell bodies were observed, particularly in all regions of the pallium and septum nuclei, in the ventral thalamus, the infundibular nucleus and the tegmental area. Moderate numbers of fibres were also noted in several regions where cell bodies were absent, mainly in the amygdala and the infundibular nucleus, the median eminence and most mesencephalic regions. At the electron microscopic level, the immunoreactivity was restricted to dense core vesicles and absent in clear vesicles. These results provide the first evidence for the presence of atrial natriuretic factor in the brain of a non-mammalian chordate. The localization of atrial natriuretic factor-positive material in the frog central nervous system suggests that this peptide may act as a neuromodulator or a neurotransmitter in amphibians.

Animals↗
PubMed1987

Coexistence of melanin-concentrating hormone (MCH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the preoptic nucleus of the frog brain.

Coexistence of MCH- and alpha-MSH-like peptides in specific neurons of the frog hypothalamus has been investigated on serial frozen sections using the indirect immunofluorescence method. In the anterior region of the preoptic nucleus, perikarya containing MCH- and alpha-MSH-immunoreactive materials were co-distributed and the two peptides were generally co-sequestered within the same neurons. In contrast, alpha-MSH immunoreactive neurons of the ventral infundibular nucleus did not contain any MCH-like peptide. These data suggest that MCH and alpha-MSH are transported by the same nerve fibers originating from preoptic perikarya and are likely released together by axon terminals. Since MCH and alpha-MSH exert antagonistic hormonal activities on dermal melanophores, our results suggest that the two regulatory peptides may also interact in the central nervous system.

Animals↗
PubMed1987

Synergism and diurnal variations of human growth hormone-releasing factor (1-29)NH2 and thyrotropin-releasing factor on growth hormone release in dairy calves.

Sixteen male Holstein calves averaging 168 kg body weight (BW) were used to determine the effects of human growth hormone-releasing factor (1-29)NH2 (hGRF (1-29)NH2; .22 micrograms/kg BW), thyrotropin-releasing factor (TRF; .165 micrograms/kg BW) or hGRF (1-29)NH2 plus TRF (.22 and .165 micrograms/kg BW, respectively) on growth hormone (GH) release in animals exposed to 16 hr of light (L): 8 hr of dark (D) (lights on at 0100 hr) and hGRF plus TRF (.22 and .165 micrograms/kg BW, respectively) in animals exposed to 8L:16D (lights on at 0900 hr). For each treatment, times of iv injection were 0400, 1000, 1600 and 2200 hr. In animals exposed to 16L:8D, average GH peaks reached after hGRF (1-29)NH2 or TRF injections were 49.7 and 32.0 ng/ml while the area under the GH response curve (AUC) were 1247 and 1019 ng/ml.min, respectively. There was no significant effect of times of injection on GH release following the separate injection of hGRF(1-29)NH2 or TRF. In animals exposed to 16L:8D, GH peaks and AUC after hGRF plus TRF injections were 226.4, 189.2 and 116.8 ng/ml, and 4340, 3660 and 2415 ng/ml.min at 0400, 1000 and 1600 hr (lights on), respectively but only 42.3 ng/ml and 1692 ng/ml.min at 2200 hr (lights off). In animals exposed to 8L:16D, GH levels and AUC after hGRF plus TRF injections reached 177.5 and 180.5 ng/ml, and 2759 and 3704 ng/ml.min at 1000 and 1600 hr (lights on) but only 84.0 and 72.7 ng/ml, and 1544 and 1501 ng/ml.min at 0400 and 2200 hr (lights off), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Influence of age and sex on basal secretion of growth hormone (GH) and on GH-induced release by porcine GH-releasing factor pGRF(1-29NH2) in growing pigs.

The aim of this study was to determine the effect of age and sex on basal secretory patterns of growth hormone (GH) and growth hormone-releasing factor (GRF) induced GH release. Eighteen pigs (9 castrated males and 9 females) were stimulated with pGRF(1-29)NH2 at 7,11,15,19 and 23 weeks of age. Blood samples were taken from each animal via jugular vein cannulae every 20 min, from 6 hr before to 5 hr after iv GRF administration at a dose of 4 micrograms/kg. GH baseline levels, amplitude of the GH peaks, area under the GH peaks and the overall mean of GH serum levels decreased (P less than .001) with age in both sexes. Age also had a marked effect on GRF-induced GH release: the amplitude of GH peaks and area under the GH peaks decreased (P less than .001) with age. The GH response to pGRF(1-29)NH2 varied considerably, depending on the timing of the episodic endogenous secretion of GH. An immediate response (less than 30 min) was observed when GRF was injected at the end of a trough period or at the beginning of a peak, but there was no immediate response when GRF was injected at the end of a peak or at the beginning of a trough period. Our results show that both endogenous GH secretion and pGRF(1-29)NH2-induced GH release declines with age, suggesting a decreased sensitivity of the somatotroph cells to GRF with age; and that the high variability of the GH response to pGRF(1-29)NH2 stimulation depends greatly on the timing of the episodic endogenous GH release, thus implying a possible episodic endogenous somatostatin secretion by the hypothalamus.

Age Factors↗
PubMed1987

Hyperprolactinemia associated with clinically silent adenomas: endocrinologic and pathologic studies; a report of two cases.

Pituitary adenomas containing adrenocorticotropic hormone (ACTH) in one case, and ACTH, beta-lipotropin, and beta-endorphin in the other, were demonstrated in two patients who had amenorrhea-galactorrhea and hyperprolactinemia with no manifestation of Cushing's disease. Neither adenoma contained prolactin (PRL). Initial bromocriptine therapy resulted in cessation of amenorrhea-galactorrhea and normalization of PRL levels. However, there was radiologic evidence of tumor enlargement in both patients. After pituitary adenomectomy, the two patients resumed regular menses and normal PRL dynamics. These patients illustrate the need for bromocriptine therapy for possible enlargement of their pituitary adenomas. The diagnosis of silent corticotroph adenoma should be kept in mind.

Adenoma↗