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Biomedical subjects

G Pelletier

Publications and source records attributed to G Pelletier.

At least 433 records · Page 24Linked to original sources
PubMed1988

Light chain deposition disease presenting with hepatomegaly: an association with amyloid-like fibrils.

We report an unusual case of lambda light chain deposits without overt plasma cell dyscrasia. The clinical presentation was hepatomegaly without biochemical sign of renal involvement. Portal hypertension, spontaneous rupture of the spleen and fracture of the 12th thoracic vertebra occurred during the course of the disease. Ultrastructural studies showed that lambda light chain deposits were associated with amyloid-like deposits. This case suggests that light chain deposition disease and amyloidosis could be two expressions of the same disease.

Amyloidosis↗
PubMed1988

Distribution of atrial natriuretic factor-like immunoreactivity in the brain of the frog Rana ridibunda.

The localization of atrial natriuretic factor (ANF)-like immunoreactivity in the central nervous system of the frog Rana ridibunda was examined by the indirect immunofluorescence technique, using an antiserum against synthetic ANF (Arg101-Tyr126). Immunoreactive cell bodies were principally found in the dorsal and medial pallium, the medial septal nucleus, the ventrolateral and anteroventral areas of the thalamus, the lateral forebrain bundle, the posterolateral thalamic nuclei, the preoptic nucleus, the dorsal infundibular nucleus, and the anteroventral tegmentum nucleus of the mesencephalon. Numerous cell bodies and a very dense fiber bundle were visualized in the interpeduncular nucleus. All the areas mentioned above contained a high density of immunoreactive fibers. In addition, the amygdala, the infundibular nucleus, the median eminence, and most of the areas of the mesencephalon contained a moderate number of ANF-positive nerve processes. In the frog pituitary, fibers and nerve terminals were found in the peripheral zone of the neural lobe. The intermediate and anterior lobes of the frog pituitary were totally devoid of ANF immunoreactivity. These results indicate that ANF-like material is widely distributed in the frog brain and that ANF may be involved in various brain functions including neuroendocrine regulations.

Animals↗
PubMed1988

High-resolution radioautographic localization of beta-adrenergic receptors in the pars intermedia of the rabbit pituitary.

In order to study the cellular and subcellular distribution of beta-adrenergic receptors in the pars intermedia of the rabbit pituitary, we have developed a technique for the high-resolution radioautographic localization of beta-adrenergic receptors, using [125]-cyanopindolol as the ligand. The most suitable fixative was the McLean fixative to which 0.1% glutaraldehyde was added. In semithin sections, specific labeling was localized over all the secretory cells. At the ultrastructural structural level, plasma membrane, nuclear envelope, and mitochondria appeared to be significantly labeled. These observations are consistent with previous results indicating the presence of beta-adrenergic receptors at the level of the plasma membrane. On the other hand, the exact role of intracellular receptors remains to be clarified. Moreover, this technique which allows the localization of beta-adrenergic receptors at the ultrastructural level should be very useful to study the distribution of these receptors in other tissues, especially the central nervous system.

Animals↗
PubMed1988

Evidence for a direct action of neuropeptide Y in the rat pituitary gland.

Neuropeptide Y (NPY) has recently been localized in the rat hypothalamus. In order to evaluate the putative effects of NPY on pituitary function, its action was examined on anterior pituitary cells in culture. Also, an immunocytochemical method was used with the aim of localizing endogenous NPY-like material at the cellular and subcellular levels of the pituitary gland. In vitro studies using dispersed anterior pituitary cells indicated that NPY (10(-6) to 10(-9)M) increased the secretion of luteinizing hormone, growth hormone and prolactin, whereas beta-lipotropin hormone and thyrotropin secretions were not affected. The presence of endogenous NPY was demonstrated in gonadotrophs, somatotrophs, corticotrophs and some lactotrophs, but not in thyrotrophs. In immunoreactive cells, NPY-like material was detected in the cytoplasmic matrix, in the secretory granules and in the nucleus distributed primarily in the euchromatin, in the vicinity of the heterochromatin. NPY-like immunoreactivity was also observed at the plasma membrane but only scarcely. These biochemical and immunocytochemical results indicate that NPY may play a direct regulatory role in adenohypophyseal secretion.

Animals↗
PubMed1988

Autoradiographic localization of beta-adrenoreceptors in rat uterus.

The inhibitory effects of catecholamines on uterine smooth muscle are known to be mediated through beta-adrenergic receptors. To investigate further the distribution of these receptors in the rat uterus, we utilized in vitro autoradiography using [125I]-cyanopindolol [CYP], a specific beta-receptor ligand that has equal activity for both beta 1- and beta 2-receptor subtypes. The specificity of the labeling and the characterization of receptor subtypes in different cell types were achieved by displacement of radioligand with increasing concentrations of zinterol, a beta-adrenergic agonist with preferential affinity for the beta 2-adrenoreceptor subtype, and practolol, a beta-adrenergic antagonist that binds preferentially to the beta 1-subtype. Quantitative estimation of ligand binding was performed by densitometry. It was shown that the vast majority of beta-adrenoreceptors were of the beta 2-subtype and were found in high concentration not only in the myometrium but also in the endometrial and serosal epithelia. Specific labeling was also observed in glandular elements. These results suggest that beta-adrenoreceptors might be involved in different functions in the uterus.

Animals↗
PubMed1988

Role of calcium in thyrotrophin-releasing hormone-stimulated release of melanocyte-stimulating hormone from frog neurointermediate lobe.

The effect of modifications of extracellular calcium concentrations on alpha-MSH release has been studied using perifused frog neurointermediate lobes. Increasing concentrations of calcium (from 2 to 10 mmol/l) gave rise to a dose-related stimulation of alpha-MSH secretion, whereas reduction of Ca2+ from 2 to 1.5 mmol/l partially inhibited alpha-MSH release. The direct effect of extracellular Ca2+ on alpha-MSH secretion was confirmed by the dose-dependent stimulation of alpha-MSH release induced by the calcium ionophore A23187. Perifusion with a calcium-free medium or blockade of Ca2+ channels by 4 mmol Co2+/l both resulted in an inhibition of spontaneous and TRH-induced alpha-MSH release. Conversely, administration of verapamil or methoxyverapamil (10 mumol/l each) did not alter basal secretion and had no effect on the response of the glands to TRH. Nifedipine (10 mumol/l), which was able to block KCl (20 mmol/l)-evoked alpha-MSH release, induced a slight inhibition of basal alpha-MSH secretion, indicating that extracellular Ca2+ levels may regulate alpha-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels. In contrast TRH-induced alpha-MSH release was not affected by nifedipine or dantrolene (10 mumol/l), and BAY-K-8644 (1 mumol/l) did not significantly modify the response of neurointermediate lobes to TRH. Taken together, these results suggest that TRH-induced alpha-MSH secretion is associated with calcium influx across the plasma membrane and that calcium entry caused by TRH may occur through nifedipine/verapamil-insensitive Ca2+ channels.

Animals↗
PubMed1988

Effects of sex steroids on regulation of the levels of C1 peptide of rat prostatic steroid-binding protein mRNA evaluated by in-situ hybridization.

Prostatic steroid-binding protein (PBP) is the most abundant protein synthesized in the rat ventral prostate. The protein is under strict androgenic control and is made of two subunits containing the polypeptides C1, C2 and C3. Using an 35S-labelled cDNA probe, we have used quantitative in-situ hybridization to assess the regulation of polypeptide C1 mRNA levels by sex steroids in the adult male rat. Densitometric quantification of autoradiographic hybridization signals revealed that a significant decrease in C1 mRNA levels could be detected 5 h after castration. Levels of C1 mRNA decreased by 50% 2.5 days after castration, while undetectable levels were reached within 7 days. Administration of the potent androgen 5 alpha-dihydrotestosterone to castrated rats caused a progressive increase in C1 mRNA levels which became significant 5 h after the first injection, while prolonged treatment, for 3 and 7 days, caused 50 and 100% reversals respectively of the effect of castration on C1 mRNA levels. Similar results were obtained by dot-blot hybridization using the same 32P-labelled cDNA probe, thus confirming the specificity and quantification achieved by in-situ hybridization. Administration of oestradiol-17 beta to orchiectomized adult rats for 14 days had no effect on steady-state C1 mRNA levels. Progesterone, on the other hand, at the dose used (2 mg twice daily) caused a marked increase in C1 mRNA levels, measured by in-situ hybridization, which was completely reversed by concomitant administration of the pure antiandrogen flutamide. The present data clearly demonstrate that the expression of PBP C1 peptide mRNA is under strict androgenic control and is a very sensitive and specific parameter of androgenic activity. They also indicate that quantitative in-situ hybridization is a powerful, sensitive and most efficient tool to study the regulation of gene expression while, in addition, providing precise information about the site of mRNA localization as well as information about the histology of the tissue, particularly the heterogeneous nature of the acinar response to androgenic stimulation and deprivation.

Androgen-Binding Protein↗
PubMed1988

Involvement of the cytoskeleton in the steroidogenic response of frog adrenal glands to angiotensin II, acetylcholine and serotonin.

In order to determine the role of the cytoskeleton in adrenal steroidogenesis, we have studied the effect of cytochalasin B (a microfilament-disrupting agent) and vinblastine (an antimicrotubular drug) on corticosteroid secretion by frog interrenal tissue in vitro. Perifusion of interrenal fragments with cytochalasin B (50 mumol/l) induced a marked inhibition of basal corticosteroid output. In addition, stimulation of corticosteroidogenesis by all corticotrophic factors was also inhibited by cytochalasin B. Using an immunohistochemical technique and specific anti-tubulin antiserum, we verified that vinblastine (10 mumol/l) was responsible for the disappearance of the microtubular network in adrenocortical cells. Administration of vinblastine (10 mumol/l) did not affect the spontaneous secretion of corticosterone and aldosterone and had no effect on the steroidogenic response of interrenal glands to angiotensin II and acetylcholine. In contrast, vinblastine was responsible for a marked decrease in serotonin-induced stimulation of corticosteroid production. On the other hand, data from high-performance liquid chromatography showed that infusion of cytochalasin B or vinblastine was not associated with the production of any new steroid which could interfere in the radioimmunoassays. Taken together, these data suggest that microfilaments are involved in a late and common step of corticosteroidogenesis while microtubules are only required for the coupling of the secretory response to certain corticotrophic factors such as ACTH and serotonin.

Acetylcholine↗
PubMed1988

Effect of human growth hormone-releasing factor (1-29)NH2 on growth hormone release and milk production in dairy cows.

Twelve cows (209 d in lactation, 642 kg BW) were used in an experiment conducted over four 10-d periods (one preinjection, one injection, and two postinjection). Gelatine (n = 6) or 10 mg of growth hormone-releasing factor in gelatine (n = 6) was injected subcutaneously at 1000 h every day on d 11 to 20. Data were averaged for the last 5 d of each period. During the injection period, milk, fat, and protein yields increased by 3 kg.d-1 (14.3%), .14 kg.d-1 (16.7%), and .12 kg.d-1 (15.4%), respectively. Moreover, milk, fat, and protein yields for the treated cows remained higher than for the control cows until the last postinjection period. Growth hormone response was evaluated from blood samples withdrawn from 2 h prior to 8 h postinjection on d 11, 15, and 20 and on d 40. After growth hormone-releasing factor injection, peaks and area under the curve were 24.5, 30.8, and 47.0 ng.ml-1 and 2475, 3979, and 3741 ng.ml-1.min-1 on d 11, 15, and 20, respectively. On d 40, there was no difference in growth hormone concentrations in blood between control and treated cows. These results demonstrate that 10 d of daily injection of a growth hormone-releasing factor increases milk production by 14.3% (3 kg.d-1) and still induces growth hormone release at the end of the injection period without any sign of refractoriness.

Animals↗
PubMed1988

[Imaging of nodular regenerative hyperplasia of the liver. Study of 9 cases].

Radiologic patterns of the liver in nodular regenerative hyperplasia are poorly known. The authors describe the features of the liver observed during ultrasonography, angiography, computed tomography and magnetic resonance imaging in 9 patients with nodular regenerative hyperplasia. Generally the liver appeared normal, occasionally with signs of portal hypertension. However, a pseudotumoral pattern was observed in 2 patients: they had well limited hypoechoic lesions on ultrasonography, and in one patient angiography showed hypervascularity.

Adult↗
PubMed1988

Serum growth hormone release in response to a growth hormone-releasing factor analog during and after anesthesia in pigs.

The objective of this study was to evaluate the time course for full recovery of the growth hormone governing system and somatocrinin response after anesthesia. Sixteen Yorkshire gilts aged 32 weeks were divided into three groups: saline (n = 6), anesthesia + saline (n = 5) and anesthesia + somatocrinin (n = 5). Under anesthesia, the area under the growth hormone curve was increased (P less than 0.05) from 1172 +/- 184 to 2807 +/- 1002 ng.min.mL-1, and a more consistent growth hormone response to somatocrinin was observed; all animals responded immediately, while only three out of five did so four hours before anesthesia. Sixteen and 40 hours after anesthesia, basal and stimulated growth hormone levels were comparable to those of unanesthetized controls, suggesting a prompt recovery from the effects of anesthesia. These data indicate that anesthetized pigs release higher quantities of growth hormone and have a more consistent growth hormone response to somatocrinin. A full recovery of basal and somatocrinin-induced growth hormone release was observed as soon as 16 hours after anesthesia.

Anesthesia↗
PubMed1988

Three cases of nodular regenerative hyperplasia of the liver following renal transplantation.

We report three cases of nodular regenerative hyperplasia of the liver: the clinical onset of hepatic disease occurred between 24 and 30 months after renal transplantation. Nodular regenerative hyperplasia was associated with peliosis hepatitis in two cases, and with veno-occlusive disease in one case. Two patients developed portal hypertension, but are doing well. The third patient developed jaundice and died of septic shock. We discuss the aetiological role of renal transplantation, cytomegalovirus infection, and azathioprine in the development of nodular regenerative hyperplasia of the liver.

Adult↗
PubMed1988

Characterization of anti-idiotypic antibodies and their use as probes for determination of shared idiotopes expressed on murine and human IgE anti-rye I antibodies.

This study describes the production and characterization of rabbit anti-idiotypic antibodies (anti-ID Abs) against three idiotypes of three mAbs with different specificities. The anti-ID Abs were rendered idiotype specific by appropriate adsorption. Binding of labelled mAb to homologous anti-ID Ab bound to a polystyrene matrix was completely inhibited when the same mAb was added. In contrast, addition of other mAbs sharing the same isotype and the same light chain but with different specificity did not affect the binding reaction. Each anti-ID Ab inhibited completely and selectively the reaction between the allergen and the homologous mAb idiotype. Labelled rye I binding to a given polystyrene-bound mAb idiotype was completely blocked if the relevant anti-ID Ab was used as an inhibitor. Murine polyclonal anti-rye I antisera inhibited the reaction between all three mAbs and the antigens, as well as the reaction between all three mAb idiotypes and their homologous anti-ID Abs. On another hand, goat polyclonal anti-rye I antisera only inhibited the reaction between the mAbs and the antigens. These results suggest that the anti-ID Abs produced are directed against idiotopes located within the paratopes and such idiotopes are shared by murine monoclonal and polyclonal Abs. Human rye I-specific IgE and murine anti-rye I mAbs could share common idiotopes, since human IgE binding to the antigen was inhibited by the anti-ID Abs. These observations imply structural similarity in the V gene coding for the variable region of the antibody of two different species.

Allergens↗
PubMed1987

Hypothalamic alpha-melanocyte-stimulating hormone (alpha-MSH) is not under dopaminergic control.

A possible dopaminergic regulation of hypothalamic proopiomelanocortin (POMC)-containing neurons has been investigated in rats by means of in vivo and in vitro approaches. Acute or 3-weeks chronic in vivo treatments with the dopaminergic agonists apomorphine (1 mg/kg: s.c.) and 2-Br-alpha-ergocriptine (2.5 mg/kg; s.c.) or the dopaminergic antagonist haloperidol (0.15-3 mg/kg; i.p.) had no significant effect on the concentration of alpha-melanocyte-stimulating hormone (alpha-MSH) in two hypothalamic regions: arcuate nucleus (AN) and dorsolateral area (DLH). In the same way, chronic administration of the dopaminergic agonists or antagonist did not induce any change in hypothalamic contents of beta-endorphin, another peptide derived from POMC. Reverse-phase high-performance liquid chromatographic analysis revealed that acetic acid extracts of AN and DLH both contained two major forms of alpha-MSH-like peptides: deacetylated alpha-MSH and authentic alpha-MSH. The ratio between these two forms was not altered after acute haloperidol treatment (3 mg/kg, i.p.). The possible effect of dopamine on the release of hypothalamic alpha-MSH was studied in vitro using perifused rat hypothalamic slices. Infusion of dopamine (10(-7)-10(-5)M) or its antagonist haloperidol (10(-5)M) had no effect on spontaneous alpha-MSH release from hypothalamic tissue. In addition, none of these drugs had any effect on potassium (50 mM)-induced alpha-MSH release. It is concluded that dopaminergic neurons are not involved in the regulation of synthesis, post-translational processing (acetylation) or release of hypothalamic alpha-MSH.

Animals↗
PubMed1987

Melanin-concentrating hormone (MCH) is colocalized with alpha-melanocyte-stimulating hormone (alpha-MSH) in the rat but not in the human hypothalamus.

Melanin-concentrating hormone (MCH)-containing neurons have recently been localized in the dorsolateral region of the rat hypothalamus, an area where the second alpha-MSH system is found which contains only alpha-MSH and none of the pro-opiomelanocortin (POMC)-related peptides. In order to study the morphological relationships between the MCH and alpha-MSH neuronal systems, we have studied the immunocytochemical localization of both MCH and alpha-MSH in the rat hypothalamus. The same study was also performed in the human hypothalamus where there is only one alpha-MSH system which contains alpha-MSH as well as the other POMC-related peptides (first alpha-MSH system). In the rat dorsolateral hypothalamus, we could demonstrate that most neuronal cell bodies stained for MCH also contained immunoreactive alpha-MSH. In the human hypothalamus, neuronal cell bodies stained for MCH were observed only in the periventricular area whereas cell bodies containing alpha-MSH were exclusively located in the infundibular (arcuate) nucleus. In the rat, immunoelectron microscopy showed labelling for MCH in the dense core vesicles of positive neurons and double-staining techniques clearly demonstrated that both immunoreactive MCH and alpha-MSH could be consistently detected in the same dense core vesicles. These ultrastructural studies then suggest that these two peptides should be released simultaneously from neurons located in the rat dorsolateral hypothalamus.

Animals↗