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S Dufour

Publications and source records attributed to S Dufour.

At least 73 records · Page 4Linked to original sources
PubMed1994

[Prediction of somatization disorders in pre-pubertal girls].

Several studies of female adult populations suggest that somatization problems appear during adolescence and that they are related to behavioural problems during childhood. This study uses Cloninger's personality model to verify the link between personality traits and the beginning of somatization problems in elementary school girls. This model is based on the interaction of three dimensions: novelty seeking, harm avoidance and social reward dependence. Subjects were part of a longitudinal study of the social adjustment of children from Montreal and Val d'Or families. Evaluations of the girls' behaviour in kindergarten were used to establish personality types according to Cloninger's model. The somatization problems were assessed at age ten following interviews with mothers and girls, and ratings by mothers and teachers. The results showed that somatization problems at age ten were more likely when novelty seeking and harm avoidance were high in kindergarten. The kindergarten girls with 'passive-aggressive' or 'explosive-schizoid' personality profiles were more at risk of higher levels of somatization problems at age ten. However, Cloninger's hypothesized link between high levels of somatization problems and the 'histrionic' personality profile was not confirmed.

Adolescent↗
PubMed1993

Compartmentation of inorganic phosphate in perfused rat liver. Can cytosol be distinguished from mitochondria by 31P NMR?

Compartmentation of inorganic phosphate was studied in intact perfused rat liver at 4 degrees C by 31P NMR. It was shown that decreases in cytosolic pH or cytosolic Pi concentration induced the appearance of an additional Pi resonance at low field which was assigned to Pi from an alkaline compartment. Valinomycin (K+ ionophore) induced a further splitting of the lines whereas nigericin (K+/H+ antiport) or potassium cyanide (inhibitor of cytochrome oxidase) had opposite effects. As valinomycin acts mainly on the cytosolic/mitochondrial K+ gradient and KCN on the mitochondrial respiratory chain, it was deduced that the alkaline compartment as revealed by the second Pi resonance was probably mitochondria. Single Pi lines observed on perchloric extracts of livers exhibiting two resonances during cold perfusion confirmed that the split peaks in the intact liver indeed arose from the same molecular species.

Animals↗
PubMed1992

E-cadherin expression during the acidic FGF-induced dispersion of a rat bladder carcinoma cell line.

Cell dissociation and acquisition of cell motility are major events in morphogenesis, wound repair, and cancer invasion and metastasis. We have used the NBT-II bladder carcinoma cell line as a model system to study the mechanisms of these events. Upon exposure to acidic fibroblast growth factor (aFGF), NBT-II cells undergo morphological changes that resemble those described in epithelial-mesenchymal transitions, i.e., dissociation of some or all polygonal epithelial cells and their transformation into motile, fibroblastic-like cells. The disruption of intercellular contacts, which accompanies cell dissociation and acquisition of motility, is correlated with a redistribution of E-cadherin, a Ca(2+)-dependent cell adhesion molecule, over the entire cell surface and within the cytoplasm. However, these modifications are not accompanied by a reduction of the intercellular adhesiveness or a loss of E-cadherin expression. Moreover, the formation of intercellular contacts between fibroblastic-like NBT-II cells results in the relocation of epithelial cadherin (E-cadherin) immunoreactivity on lateral membranes, but is not sufficient to abrogate cell motility. Finally, the overexpression of E-cadherin by NBT-II cells stably transfected with a plasmid containing the mouse E-cadherin cDNA does not impair the scattering effect of aFGF, indicating that high levels of E-cadherin expression do not prevent cells from disrupting their intercellular connections. Altogether, these results suggest that the scattering activity of aFGF is not mediated by direct modulations of E-cadherin expression.

Animals↗
PubMed1992

[Adhesion and mobility of embryonic and tumoral cells].

Regulation of a number of adhesion molecules during neural crest cell migration was studied. The neural crest, a transient embryonic neural epithelium structure, undergoes mesenchymal transformation (epithelial-mesenchymal transition). The cells then migrate, giving rise to a variety of elements including the peripheral nervous system and melanocytes. During migration, neural crest cells do not express functional cell Adhesion Molecules but interact specifically with cell-binding domains in fibronectin molecules. A rat bladder carcinoma cell line was used as an in vitro model to study conversion of epithelial cells to a migratory fibroblast-like state. Conversion can be induced by culture on collagen or exposure to acidic Fibroblast Growth Factor (aFGF). Furthermore, constitutive fibroblast-like transformation can be induced by transfection with cDNA encoding aFGF. Growth factor-producing clones exhibit increased invasive and metastatic properties as compared with non-FGF-producing control cells. This model may provide increased understanding of the role of the different adhesion molecules in processes involving cell remodeling, such as tumor spread and development of metastases.

Cadherins↗
PubMed1991

Generation of full-length cDNA recombinant vectors for the transient expression of human fibronectin in mammalian cell lines.

In order to study the roles of the different alternatively spliced variants of human fibronectin (FN) as well as of its binding sites and structural domains in the processes of extracellular matrix assembly, cell adhesion, and cell migration, we constructed expression vectors coding for different human full-length FN polypeptides and deleted versions of these constructs. We expressed them transiently in mammalian cells by calcium phosphate transfection and microinjection techniques. While the deleted recombinants were expressed by both transfection and microinjection, the full-length recombinants could be only expressed by microinjection. Calcium phosphate transfection leads to the accumulation of recombinant FN in cytoplasmic vesicles of both matrix-forming and nonforming cells. On the contrary, microinjection leads to the accumulation of recombinant FN in cytoplasmic vesicles in cells that do not form a matrix, but to the rapid incorporation into the extracellular matrix of matrix-forming cells in addition to a cytoplasmic localization. Identical results were obtained when the FN signal and propeptides were replaced by those of E-cadherin.

Animals↗
PubMed1991

Accumulation of fetal fibronectin mRNAs during the development of rat cardiac hypertrophy induced by pressure overload.

Cardiac pressure overload induces a shift towards the fetal form of major proteins expressed by the myocytes, and an accumulation of extracellular matrix proteins. One of them, fibronectin (FN), accumulates soon after the imposition of pressure overload. Because FN exists both as cellular FN (c-FN) locally synthesized by nonmuscle cells and as "plasma-FN" (p-FN) synthesized by the hepatocytes, the first issue of this study was to determine whether FN accumulation within the myocardium in response to pressure overload is paralleled by a local increase in mRNA. The expression of c-FN isoforms being developmentally regulated in a tissue-specific manner, the types of FN exons expressed by cardiac cells were analyzed. Pressure overload was induced in 25-d-old rats by stenosis of the thoracic aorta. Using in situ hybridization, we show that the mRNAs encoding the fetal forms of c-FN are accumulated in the interstitial tissue of fetal rat hearts but are absent in adult. 1-3 d after aortic stenosis, the fetal forms of c-FN mRNAs were found in the wall of coronary arteries and in focal areas of the myocardium. Thus nonmuscle cells and smooth muscle cells, like myocytes, do respond to pressure overload by reexpressing fetal gene transcripts.

Animals↗
PubMed1991

Neural crest cell locomotion induced by antibodies to beta 1 integrins. A tool for studying the roles of substratum molecular avidity and density in migration.

Migration of neural crest cells depends on direct, transient interactions between fibronectin molecules and their corresponding Arg-Gly-Asp integrin receptors. We have previously suggested that the moderate-activity interaction between integrin receptors and fibronectin may be critical for the transient association of the cells with their substratum. In order to test this hypothesis, we have examined the in vitro locomotory behavior of neural crest cells on substrata of differing apparent avidities for integrin receptors. As substrata, we used a variety of monoclonal and polyclonal antibodies to the integrin beta 1 subunit that were characterized for their respective relative apparent avidities for the receptor. Neural crest cells were able to migrate on these antibodies and exhibited an organization of substratum-adhesion sites and of cytoskeletal elements virtually identical to that observed on fibronectin, indicating that they can at least partially mimic the migration-promoting activity of fibronectin. However, the number of migrating cells as well as their morphology and their speed of locomotion varied significantly with both the concentration of the antibody substratum and its relative avidity for the receptor. Thus, on high-avidity monoclonal antibodies and on polyclonal divalent antibodies at high concentrations only a limited number of cells escaped from the neural tube, and the rate of their migration was reduced compared to that on fibronectin (23 +/- 5 microns h-1 versus 65 +/- 10 microns h-1). In addition, cells were unusually flattened and cohesive. Time-lapse videomicroscopy revealed that, on high-avidity substrata, neural crest cells were able to extend cell processes that adhered to the substratum, but showed a dramatically reduced capability of breaking pre-existing substratum contacts. In contrast, the same antibodies at low concentrations produced neural crest cell migration at rates very similar to those on fibronectin at the same concentrations. Low-avidity monoclonal antibodies and polyclonal monovalent antibodies at all concentrations tested permitted extensive migration of neural crest cells, which exhibited the same morphology and locomotory behavior as on fibronectin. These results indicate that both the avidity of receptors for the substratum and the number of receptors bound to the substratum are critical in regulating the locomotory behavior of neural crest cells in vitro, and therefore might help to regulate the directionality of migration and final localization pattern of neural crest cells in vivo.

Actins↗
PubMed1990

Generation and amplification of the cytosolic calcium signal during secretory responses to gonadotropin-releasing hormone.

Gonadotropin-releasing hormone (GnRH) stimulates characteristic biphasic increases in cytosolic calcium concentration ([Ca2+]i) and in luteinizing hormone (LH) release in cultured gonadotrophs, with an early peak followed by a prolonged plateau in both responses. Analysis of [Ca2+]i by dual-wavelength fluorimetric assay and of LH release at 5-sec intervals in perifused pituitary cells revealed increases in both responses within a few seconds of exposure to GnRH. The maximum elevation of [Ca2+]i occurred within 20 sec, and the peak gonadotropin release in 35 sec; the total duration of the spike phase for both [Ca2+]i and LH release was 2.5 min. Under extracellular Ca2(+)-deficient conditions, the GnRH-induced peak in [Ca2+]i was reduced by about 20% and the plateau phase was abolished. Concomitantly, the magnitude of the acute phase of LH release was reduced by 40% and that of the second phase by about 90%. Recovery of the plateau phase of LH release occurred within 25 sec after addition of 1.25 mM Ca2+ to Ca2(+)-deficient medium. In a dose-dependent manner, the non-selective Ca2+ channel blockers Co2+ and Cd2+ reduced the Ca2+ current measured by whole-cell recording in pituitary gonadotrophs and abolished the extracellular Ca2(+)-dependent component of LH release. The selective calcium channel blocker, nifedipine, decreased the magnitude of the Ca2+ current and reduced the plateau phase of LH release by 50%; conversely, the dihydropyridine agonist methyl, 1,4,dihydro-2,6-dimethyl 3-nitro-4-(2-trifluorome) (Bay K 8644) consistently enhanced the amplitudes of both Ca2+ current and GnRH-induced LH release. These data reveal a close temporal correlation between changes in [Ca2+]i and LH release during GnRH action, with Ca2+ mobilization during the spike phase and Ca2+ influx through dihydropyridine-sensitive and insensitive sets of receptor-operated calcium channels during the spike and plateau phases. In addition, analysis of the magnitudes of the [Ca2+]i and LH responses to a wide range of GnRH concentrations in the presence and absence of extracellular Ca2+ is consistent with amplification of the [Ca2+]i signal in agonist-stimulated gonadotrops.

Animals↗
PubMed1988

The migratory behavior of avian embryonic cells does not require phosphorylation of the fibronectin-receptor complex.

When locomotory embryonic cells become stationary, they acquire new substratum-adhesion properties. In particular, the distribution of fibronectin receptors shifts from diffuse and highly mobile on the cell membrane to immobilized in close association with fibronectin molecules and cytoskeletal elements in focal contacts. Receptor phosphorylation has been proposed as a possible regulator of the interaction between the receptor and its intracellular and extracellular ligands. In the present study, we have compared the phosphorylation state of the fibronectin receptor in motile neural crest and somitic cells, in stationary somitic cells, and in Rous-sarcoma virus transformed-chick embryo fibroblasts, using immunoprecipitation following metabolic labeling. While no receptor phosphorylation was detected in motile embryonic cells, the beta subunit of the receptor was phosphorylated in stationary cells. This subunit was also highly phosphorylated in Rous-sarcoma virus-transformed chicken cells. These results suggest that phosphorylation of the fibronectin receptor cannot account for its distribution in the cell membrane and for the nature of the interactions between this receptor and its ligands in embryonic cells.

Animals↗
PubMed1988

Attachment, spreading and locomotion of avian neural crest cells are mediated by multiple adhesion sites on fibronectin molecules.

Cellular adhesion to fibronectin (FN) can be mediated by several sequences located in different portions of the molecule. In human FN, these are: (i) the bipartite RGDS domain containing the RGDS cell-binding sequence functioning in synergy for full cellular adhesion with a second site (termed here the synergistic adhesion site) and (ii) the recently characterized CS1 and REDV adhesion sites within the alternatively-spliced type III homology-connecting segment. Using specific adhesive ligands and inhibitory probes, we have examined the role of each of these domains in the adhesion, spreading, and motility of avian neural crest cells in vitro. Both the RGDS domain and the CS1 adhesion site were found to promote attachment of neural crest cells, but only the RGDS domain supported their spreading. However, the RGDS sequence could mediate both attachment and spreading efficiently only when it was associated with the synergistic adhesion site. In migratory assays, it was found that both the RGDS domain and the CS1 site are required in association, each with functional specificity, to permit effective locomotion of neural crest cells. The REDV adhesion site was apparently not recognized by avian neural crest cells, presumably because this sequence is absent from chicken FN. Finally, it was found that recognition of both the RGDS domain and CS1 binding site by neural crest cells involved receptors belonging to the integrin family. From these results, we conclude that neural crest cells can interact with several binding sites of FN molecules, and use them for distinct functions. Our results also suggest the possibility of an instructive role for FN in the control of adhesive and migratory events during embryonic development.

Animals↗
PubMed1988

Stimulation of gonadotropin release and of ovarian development, by the administration of a gonadoliberin agonist and of dopamine antagonists, in female silver eel pretreated with estradiol.

In freshwater or seawater female silver eel, the release of gonadotropin (GTH) accumulated in the pituitary under estradiol (E2) influence could be stimulated by a conjugated treatment with a mammalian gonadoliberin agonist (GnRH-A = des-Gly10, (D-Ala6)-LH-RH ethylamide) and a blocker of dopamine receptor (pimozide). Furthermore, despite the GTH release, no reduction or even a significant increase in pituitary GTH levels were noted, indicating a stimulation of GTH synthesis. In consequence of the endogenous GTH release, a stimulation of ovarian development was induced, as demonstrated by the gonadosomatic index and histological study. Similar results were obtained with a combined treatment with GnRH-A and an inhibitor of catecholamine synthesis (L-alpha-methyl-3,4-dihydroxyphenylalanine). In contrast, no effect was produced by GnRH-A, pimozide, or L-alpha-methyl-DOPA, given alone. The results suggest that a double neuroendocrine mechanism (a lack of GnRH production and a dopaminergic inhibition of GnRH action) is involved in the prepubertal blockage of eel gonadotropic function before the reproductive migration.

Anguilla↗
PubMed1988

Acute monoblastic leukemia with osteosclerosis and extensive myelofibrosis.

A 4-month-old infant was admitted with a monoblastic infiltration of the skin associated with osteosclerosis. Both lesions spontaneously disappeared within a few months, but 2 years later, a monoblastic leukemia occurred that was associated with marked skin erythema and myelofibrosis. Skin and bone marrow specimens showed a monoblastic infiltration with numerous intermingled mast cells of normal appearance. Whether myelofibrosis was a feature of a systemic mastocytosis or of the leukemic process is discussed in this case.

Humans↗
PubMed1988

Cell-adhesion and substrate-adhesion molecules: their instructive roles in neural crest cell migration.

The individualization of crest cells from the neural folds and neural tube involves distinct mechanisms affecting both the tissue shape and the cell environment. Though these mechanisms are not fully understood at the molecular level, the analysis of the distribution of several molecules reported to promote intercellular contacts indicates a correlation between cell detachment from the neurepithelium and the decrease of cell adhesion molecule expression. During the following phase of migration, the mode of adhesion of crest cells switches preferentially to the cell-to-substratum type. Various experiments showed that among the major extracellular matrix components, fibronectins were decisive in promoting cell attachment, spreading and motility. Additional studies on receptors for fibronectins gave new insights on the differences between a motile and a stationary cell. These results will be discussed with particular reference to the migration at the cephalic level where most perturbation experiments were performed. The molecular biology of fibronectins provided a finer understanding of the interactions between a cell and these molecules. The tools derived from this technique will open new areas of investigation hopefully leading to a better understanding of (i) the regulation of the cell-fibronectins interaction and (ii) the specificity of the pathways of migration followed by migrating cells, like the descendants of the neural crest.

Animals↗
PubMed1988

[Radioimmunoassay, in Ascidiella aspersa, of a gonadoliberin (GnRH)- like factor with an apparent molecular weight higher than that of the mammalian decapeptide].

A radiommunoassay (RIA) for mammalian gonadoliberin (mGnRH) showed the presence of a GnRH-like factor in the neural complex of a Protochordate, Ascidiella aspersa (about 0,6 pg eq mGnRH/complex). The slope of the displacement curves was slightly lower than with mGnRH indicating antigene differences. No cross reactive material was found in mantle and siphonal area. The KD on Sephadex G25 was 0.45 versus 0.90 with mGnRH. That suggests that the molecular weight of the Ascidian GnRH-like factor is higher than that of known Vertebrate GnRH's, possibly due to a different processing of the precursor.

Animals↗
PubMed1987

Adhesion molecules during somitogenesis in the avian embryo.

In avian embryos, somites constitute the morphological unit of the metameric pattern. Somites are epithelia formed from a mesenchyme, the segmental plate, and are subsequently reorganized into dermatome, myotome, and sclerotome. In this study, we used somitogenesis as a basis to examine tissue remodeling during early vertebrate morphogenesis. Particular emphasis was put on the distribution and possible complementary roles of adhesion-promoting molecules, neural cell adhesion molecule (N-CAM), N-cadherin, fibronectin, and laminin. Both segmental plate and somitic cells exhibited in vitro calcium-dependent and calcium-independent systems of cell aggregation that could be inhibited respectively by anti-N-cadherin and anti-N-CAM antibodies. In vivo, the spatio-temporal expression of N-cadherin was closely associated with both the formation and local disruption of the somites. In contrast, changes in the prevalence of N-CAM did not strictly accompany the remodeling of the somitic epithelium into dermamyotome and sclerotome. It was also observed that fibronectin and laminin were reorganized secondarily in the extracellular spaces after CAM-mediated contacts were modulated. In an in vitro culture system of somites, N-cadherin was lost on individual cells released from somite explants and was reexpressed when these cells reached confluence and established intercellular contacts. In an assay of tissue dissociation in vitro, antibodies to N-cadherin or medium devoid of calcium strongly and reversibly dissociated explants of segmental plates and somites. Antibodies to N-CAM exhibited a smaller disrupting effect only on segmental plate explants. In contrast, antibodies to fibronectin and laminin did not perturb the cohesion of cells within the explants. These results emphasize the possible role of cell surface modulation of CAMs during the formation and remodeling of some transient embryonic epithelia. It is suggested that N-cadherin plays a major role in the control of tissue remodeling, a process in which N-CAM is also involved but to a lesser extent. The substratum adhesion molecules, fibronectin and laminin, do not appear to play a primary role in the regulation of these processes but may participate in cell positioning and in the stabilization of the epithelial structures.

Animals↗
PubMed1987

Estradiol has inverse effects on pituitary glycoprotein hormone alpha-subunit messenger ribonucleic acid in the immature European eel and the gonadectomized rat.

In teleosts, the pituitary contains a single glycoprotein gonadotropic hormone (GTH) composed of two dissimilar alpha- and beta-subunits. The European eel, Anguilla anguilla L, is sexually immature at the silver stage due to a deficiency in GTH synthesis and secretion. In previous studies we (S.D., YA.F.) have demonstrated a strong stimulatory action of estradiol (E2) on eel pituitary GTH content. In contrast, we (R.C., M.J.) have shown that in the rat E2 negatively regulates gonadotropin subunit synthesis via changes in specific mRNA levels. The purpose of our present work was to check for such effects of E2 on the synthesis of GTH alpha- and beta-subunits in the European eel. Eel pituitary mRNA was translated in a cell-free system in the presence of [35S]Met + Cys. We demonstrate that one of the translated polypeptides, characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography, cross-reacts with an antiserum to denatured bovine alpha-subunit. Its apparent mol wt (18.5K), which is slightly higher than that of the corresponding rat alpha-precursor, suggests that it represents the precursor of the alpha-subunit of eel glycoprotein hormones. The specificity of immunoprecipitation was confirmed by competition with ovine alpha (but not with ovine LH beta or bovine TSH beta). Quantitative evaluation of the putative eel alpha-subunit precursor showed that it represents 0.2% of the total protein translated by RNA from the normal silver eel. Chronic treatment of eels for 3 weeks with 17 beta-E2 increased by 8.0- to 8.5-fold the proportion of the putative alpha-subunit precursor among translation products. Due to the lack of cross-reactivity with the presumed GTH beta precursor, no radioactive material could be specifically detected in translation medium of eel pituitary mRNA using antisera to either denatured bovine LH beta or ovine FSH beta. Our data suggest that E2, depending on vertebrate group and probably on sexual status, may exert either positive or negative control on gonadotropin synthesis by opposite effects on the levels of specific mRNA.

Anguilla↗