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Journal articles on the topic 'Sert'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Radlinski, Mark J., Calvin X. Geng, William A. Bigelow, Ross C. Buerlein, Alexander J. Podboy, and Andrew Copland. "ARE WE “SERT-AN” ABOUT SERT?" Gastrointestinal Endoscopy 95, no. 6 (June 2022): AB183—AB184. http://dx.doi.org/10.1016/j.gie.2022.04.472.

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2

Alayón González, José Javier. "Villanueva-Sert." Bitácora arquitectura, no. 22 (June 8, 2011): 56. http://dx.doi.org/10.22201/fa.14058901p.2011.22.25568.

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<p>Siendo Carlos Villanueva y José Luis Sert dos personajes contemporáneos, sus obras no suelen relacionarse, ambos tenían la voluntad de conjugar las artes en una sola expresión, encontrar la emoción plástica del espacio.</p> <p>Los itinerarios propuestos, recorren parte de la geografía moderna que ambos transitaron: París, Caracas, Puerto Ordaz, Ciudad Bolívar, y Saint Paul-de-Vence. Tres obras de cada arquitecto, de programas similares, de tres tipologías y momentos distintos, darán cuenta de la evolución de sus respectivas teorías, y con ello la evolución del concepto en distintos estadios de la modernidad. Sin abandonar los grandes caminos abiertos por Le Corbusier, buscaron adaptarse a unas topografías locales desde la impronta meridional y tropical de su cultura latina. En la aproximación a sus obras, sumaremos las reflexiones del artista Léger para definir un marco teórico dentro del amplio espectro histórico –en palabras del suizo- por “alcanzar una perfección absoluta en la ocupación del espacio.”</p>

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3

Mesko, Shane, and Daniel R. Gomez. "In Reply to Sert." International Journal of Radiation Oncology*Biology*Physics 109, no. 3 (March 2021): 832–33. http://dx.doi.org/10.1016/j.ijrobp.2020.09.062.

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4

Hessel, Stéphane. "À quoi sert l'ONU ?" Le journal de l'école de Paris du management 68, no. 6 (2007): 16. http://dx.doi.org/10.3917/jepam.068.0016.

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5

Bercovier, Hervé. "À quoi sert Israël ?" Outre-Terre 9, no. 4 (2004): 281. http://dx.doi.org/10.3917/oute.009.0281.

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6

Robin, Gabriel. "A quoi sert l'OTAN ?" Politique étrangère 60, no. 1 (1995): 171–80. http://dx.doi.org/10.3406/polit.1995.4393.

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7

Maurin, Éric. "À quoi sert l'école ?" Regards croisés sur l'économie 12, no. 2 (2012): 11. http://dx.doi.org/10.3917/rce.012.0011.

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8

Granger, Gilles Gaston. "A quoi sert l'Epistémologie ?" Droit et société 20, no. 1 (1992): 39–44. http://dx.doi.org/10.3406/dreso.1992.1134.

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9

Loiseau, Nathalie. "À quoi sert l’éna ?" Le Débat 194, no. 2 (2017): 3. http://dx.doi.org/10.3917/deba.194.0003.

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10

Andersson, Nils. "À quoi sert l’OTAN ?" La Pensée N° 385, no. 1 (January 1, 2016): 71–83. http://dx.doi.org/10.3917/lp.385.0071.

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11

Boucheron, Patrick, and Martine Fournier. "À quoi sert l'histoire ?" Sciences Humaines N° 279, no. 3 (March 1, 2016): 16. http://dx.doi.org/10.3917/sh.279.0016.

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12

Molénat, Xavier. "A quoi sert l'éthnométhodologie ?" Sciences Humaines N°194, no. 6 (June 1, 2008): 30. http://dx.doi.org/10.3917/sh.194.0030.

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13

Eustache, Francis. "À quoi sert d'oublier ?" Sciences Humaines N° 264, no. 11 (November 2, 2014): 25. http://dx.doi.org/10.3917/sh.264.0025.

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14

Labica, Georges. "À quoi sert l'identité ?" L Homme et la société 135, no. 1 (2000): 71–85. http://dx.doi.org/10.3406/homso.2000.3025.

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15

Orhon, Göze. "Sert Kadınlar, Rasyonel Düşler." Moment Journal 4, no. 2 (December 15, 2017): 535–44. http://dx.doi.org/10.17572/mj2017.2.535544.

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16

Sarradon-Eck, Aline. "À quoi sert Amades ?" Bulletin Amades, no. 72 (December 1, 2007): 1–2. http://dx.doi.org/10.4000/amades.57.

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17

Ogien, Albert. "À quoi sert l'ethnométhodologie ?" Critique 737, no. 10 (2008): 804. http://dx.doi.org/10.3917/criti.737.0804.

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18

Boucheron, Patrick, and Martine Fournier. "À quoi sert l'histoire ?" Sciences Humaines N° Hors-série, HS25 (July 1, 2020): 74–76. http://dx.doi.org/10.3917/sh.hs25.0074.

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19

Ren, Wenying, Stephanie W. Watts, and Barry L. Fanburg. "Serotonin transporter interacts with the PDGFβ receptor in PDGF-BB-induced signaling and mitogenesis in pulmonary artery smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 3 (March 2011): L486—L497. http://dx.doi.org/10.1152/ajplung.00237.2010.

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The serotonin transporter (SERT) and the platelet-derived growth factor receptor (PDGFR) have been implicated in both clinical and experimental pulmonary hypertension (PH) and the facilitation of pulmonary artery smooth muscle cell (PASMC) growth. To gain a better understanding of the possible relationship of these two cell surface molecules we have explored interactions between SERT and PDGFR. We have previously demonstrated that SERT transactivates PDGFRβ in serotonin-stimulated PASMC proliferation. We now provide evidence for a role for SERT in PDGF-BB signaling and PASMC proliferation by using pharmacological inhibitors, genetic ablation, and construct overexpression of SERT. The results show that four tested SERT blockers dose dependently inhibit PDGF-stimulated human and bovine PASMC proliferation with comparable efficacy to that of PDGFR inhibitors, whereas 5-HT1B or 5-HT2A receptor inhibitors had no effect. Combinations of the SERT and PDGFR inhibitors led to synergistic/additive inhibition. Similarly, PDGF-induced PASMC proliferation was attenuated by small interfering RNA downregulation of SERT. Inhibition of SERT in PASMCs attenuated PDGF-induced phosphorylation of PDGFRβ, Akt, and p38 but not Erk. Overexpression of SERT in HEK293 cells led to enhanced Akt phosphorylation by PDGF, which was blunted by a SERT PDZ motif mutant, indicating the mechanistic need for the PDZ motif of SERT in PDGF signaling. Furthermore, coimmunoprecipitation experiments showed that SERT and PDGFRβ become physically associated upon PDGF stimulation. In total, the data show for the first time an important interactive relationship between SERT and the PDGFRβ in the production of PASMC proliferation triggered by PDGF that may be important in PH.

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20

Gill, Ravinder K., Anoop Kumar, Pooja Malhotra, Daniel Maher, Varsha Singh, Pradeep K. Dudeja, Waddah Alrefai, and Seema Saksena. "Regulation of intestinal serotonin transporter expression via epigenetic mechanisms: role of HDAC2." American Journal of Physiology-Cell Physiology 304, no. 4 (February 15, 2013): C334—C341. http://dx.doi.org/10.1152/ajpcell.00361.2012.

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The serotonin (5-HT) transporter (SERT) facilitates clearance of extracellular 5-HT by its uptake and internalization. Decreased expression of SERT and consequent high 5-HT levels have been implicated in various diarrheal disorders. Thus, appropriate regulation of SERT is critical for maintenance of 5-HT homeostasis in health and disease. Previous studies demonstrated that SERT is regulated via posttranslational and transcriptional mechanisms. However, the role of epigenetic mechanisms in SERT regulation is not known. Current studies investigated the effects of histone deacetylase (HDAC) inhibition on SERT expression and delineated the mechanisms. Treatment of Caco-2 cells with the pan-HDAC inhibitors butyrate (5 mM) and trichostatin (TSA, 1 μM) decreased SERT mRNA and protein levels. Butyrate- or TSA-induced decrease in SERT was associated with decreased activity of human SERT (hSERT) promoter 1 (upstream of exon 1a), but not hSERT promoter 2 (upstream of exon 2). Butyrate + TSA did not show an additive effect on SERT expression, indicating that mechanisms involving histone hyperacetylation may be involved. Chromatin immunoprecipitation assays demonstrated enrichment of the hSERT promoter 1 (flanking nt −250/+2) with tetra-acetylated histone H3 or H4, which was increased (∼3-fold) by butyrate. Interestingly, specific inhibition of HDAC2 (but not HDAC1) utilizing small interfering RNA decreased SERT mRNA and protein levels. The decrease in SERT expression by HDAC inhibition was recapitulated in an in vivo model . SERT mRNA levels were decreased in the ileum and colon of mice fed pectin (increased availability of butyrate) compared with controls fed a fiber-free diet (∼50–60%). Our results identify a novel role of HDAC2 as a regulator of SERT gene expression in intestinal epithelial cells.

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21

Liu, Min-Tsai, Stephen Rayport, Yan Jiang, Dennis L. Murphy, and Michael D. Gershon. "Expression and function of 5-HT3 receptors in the enteric neurons of mice lacking the serotonin transporter." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 6 (December 1, 2002): G1398—G1411. http://dx.doi.org/10.1152/ajpgi.00203.2002.

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The actions of enteric 5-HT are terminated by 5-HT transporter (SERT)-mediated uptake, and gastrointestinal motility is abnormal in SERT −/− mice. We tested the hypothesis that adaptive changes in enteric 5-HT3receptors help SERT −/− mice survive despite inefficient 5-HT inactivation. Expression of mRNA encoding enteric 5-HT3Asubunits was similar in SERT +/+ and −/− mice, but that of 5-HT3B subunits was fourfold less in SERT −/− mice. 5-HT3B mRNA was found, by in situ hybridization, in epithelial cells and enteric neurons. 5-HT evoked a fast inward current in myenteric neurons that was pharmacologically identified as 5-HT3 mediated. The EC50 of the 5-HT response was lower in SERT +/+ (18 μM) than in SERT −/− (36 μM) mice and desensitized rapidly in a greater proportion of SERT −/− neurons; however, peak amplitudes, steady-state current, and decay time constants were not different. Adaptive changes thus occur in the subunit composition of enteric 5-HT3 receptors of SERT −/− mice that are reflected in 5-HT3 receptor affinity and desensitization.

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22

Pettie, Michaela, Alana Oakly, David N. Harper, and Bart A. Ellenbroek. "A genetic deletion of the serotonin transporter differentially influences the behavioural effects of MDMA." Journal of Psychopharmacology 33, no. 3 (January 22, 2019): 355–63. http://dx.doi.org/10.1177/0269881118822156.

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Background: While (±)-3,4-methylenedioxymethamphetamine (MDMA) primarily induces serotonin release, it also affects dopamine and noradrenaline transmission. It is, however, unclear what role each of these neurotransmitters play in the behavioural profile of MDMA. Methods: In this study we used the drug discrimination (DD) and the acoustic startle (ASR) paradigms to examine the behaviour of rats with and without a genetic deletion of the serotonin transporter SERT (SERT−/− and SERT+/+ rats). In DD, rats were trained to respond on different levers following an injection of 1.5 mg/kg MDMA, or saline. After acquisition, they were given a challenge dose of 0.5 mg/kg amphetamine (AMPH). In the ASR paradigm, SERT+/+ and SERT−/− rats were given 0, 5 or 10 mg/kg MDMA. Results: In DD, significantly fewer SERT−/− rats acquired MDMA discrimination. When the acquirers were challenged with AMPH, SERT+/+ showed partial, while SERT−/− rats showed full generalisation to MDMA. In the ASR paradigm, MDMA significantly reduced prepulse inhibition and startle habituation in SERT+/+ rats, while having no effect in SERT−/− rats. Conclusion: Together these data suggest that in wildtype rats the interoceptive cues of MDMA are primarily mediated by serotonin and to a lesser extent by dopamine and noradrenaline, while the effects in the startle paradigm are almost exclusively mediated via serotonin. Together, these data contribute to our understanding of the complex pharmacodynamics of MDMA.

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23

Gill, Ravinder K., Nitika Pant, Seema Saksena, Amika Singla, Talat M. Nazir, Lisa Vohwinkel, Jerrold R. Turner, Jay Goldstein, Waddah A. Alrefai, and Pradeep K. Dudeja. "Function, expression, and characterization of the serotonin transporter in the native human intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 1 (January 2008): G254—G262. http://dx.doi.org/10.1152/ajpgi.00354.2007.

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The enteric serotonin transporter (SERT) plays a critical role in modulating serotonin availability and thus has been implicated in the pathogenesis of various intestinal disorders. To date, SERT expression and function in the human intestine have not been investigated. Current studies were designed to characterize the function, expression, distribution, and membrane localization of SERT in the native human intestine. Real-time PCR studies showed relatively higher SERT mRNA expression in the human small intestine compared with colon (ileum >> duodenum >> jejunum). Northern blot analysis revealed three mRNA hybridizing species encoding SERT (3.0, 4.9, and 6.8 kb) in the human ileum. Consistent with SERT mRNA expression, SERT immunostaining was mainly detected in the epithelial cells of human duodenal and ileal resected tissues. Notably, SERT expression was localized predominantly to the apical and intracellular compartments and was distributed throughout the crypt-villus axis. Immunoblotting studies detected a prominent protein band (∼70 kDa) in the ileal apical plasma membrane vesicles (AMVs) isolated from mucosa obtained from organ-donor intestine. Functional studies showed that uptake of [3H]serotonin (150 nM) in human ileal AMVs was 1) significantly increased in the presence of both Na+ and Cl−; 2) inhibited (∼50%) by the neuronal SERT inhibitor, fluoxetine (10 μM) and by unlabeled 5-HT; and 3) exhibited saturation kinetics indicating the presence of a carrier-mediated process. Our studies demonstrated differential expression of SERT across various regions of the human intestine and provide evidence for the existence of a functional SERT capable of removing intraluminal serotonin in human ileal epithelial cells.

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24

Gill, Ravinder K., Arivarasu Natarajan Anbazhagan, Ali Esmaili, Anoop Kumar, Saad Nazir, Jaleh Malakooti, Waddah A. Alrefai, and Seema Saksena. "Epidermal growth factor upregulates serotonin transporter in human intestinal epithelial cells via transcriptional mechanisms." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 4 (April 2011): G627—G636. http://dx.doi.org/10.1152/ajpgi.00563.2010.

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Serotonin transporter (SERT) regulates extracellular availability of serotonin and is a potential pharmacological target for gastrointestinal disorders. A decrease in SERT has been implicated in intestinal inflammatory and diarrheal disorders. However, little is known regarding regulation of SERT in the intestine. Epidermal growth factor (EGF) is known to influence intestinal electrolyte and nutrient transport processes and has protective effects on intestinal mucosa. Whether EGF regulates SERT in the human intestine is not known. The present studies examined the regulation of SERT by EGF, utilizing Caco-2 cells grown on Transwell inserts as an in vitro model. Treatment with EGF from the basolateral side (10 ng/ml, 24 h) significantly stimulated SERT activity (∼2-fold, P < 0.01) and mRNA levels compared with control. EGF increased the activities of the two alternate promoter constructs for human SERT gene: SERT promoter 1 (hSERTp1, upstream of exon 1a) and SERT promoter 2 (hSERTp2, upstream of exon 2). Inhibition of EGF receptor (EGFR) tyrosine kinase activity by PD168393 (1 nM) blocked the stimulatory effects of EGF on SERT promoters. Progressive deletions of the SERT promoter indicated that the putative EGF-responsive elements are present in the −672/−472 region of the hSERTp1 and regions spanning −1195/−738 and −152/+123 of hSERTp2. EGF markedly increased the binding of Caco-2 nuclear proteins to the potential AP-1 cis-elements present in EGF-responsive regions of hSERTp1 and p2. Overexpression of c-jun but not c-fos specifically transactivated hSERTp2, with no effects on hSERTp1. Our findings define novel mechanisms of transcriptional regulation of SERT by EGF via EGFR at the promoter level that may contribute to the beneficial effects of EGF in gut disorders.

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25

Singhal, Megha, Christopher Manzella, Vinay Soni, Waddah A. Alrefai, Seema Saksena, Gail A. Hecht, Pradeep K. Dudeja, and Ravinder K. Gill. "Role of SHP2 protein tyrosine phosphatase in SERT inhibition by enteropathogenic E. coli (EPEC)." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 5 (May 1, 2017): G443—G449. http://dx.doi.org/10.1152/ajpgi.00011.2017.

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Enteropathogenic Escherichia coli (EPEC), one of the diarrheagenic E. coli pathotypes, is among the most important food-borne pathogens infecting children worldwide. Inhibition of serotonin transporter (SERT), which regulates extracellular availability of serotonin (5-HT), has been implicated previously in EPEC-associated diarrhea. EPEC was shown to inhibit SERT via activation of protein tyrosine phosphatase (PTPase), albeit the specific PTPase involved is not known. Current studies aimed to identify EPEC-activated PTPase and its role in SERT inhibition. Infection of Caco-2 monolayers with EPEC strain E2348/69 for 30 min increased the activity of Src-homology-2 domain containing PTPase (SHP2) but not SHP1 or PTPase 1B. Similarly, Western blot studies showed increased tyrosine phosphorylation of (p-tyrosine) SHP2, indicative of its activation. Concomitantly, EPEC infection decreased SERT p-tyrosine levels. This was associated with increased interaction of SHP2 with SERT, as evidenced by coimmunoprecipitation studies. To examine whether SHP2 directly influences SERT phosphorylation status or function, SHP2 cDNA plasmid constructs (wild type, constitutively active, or dominant negative) were overexpressed in Caco-2 cells by Amaxa electroporation. In the cells overexpressing constitutively active SHP2, SERT polypeptide showed complete loss of p-tyrosine. In addition, there was a decrease in SERT function, as measured by Na+Cl−-sensitive [3H]5-HT uptake, and an increase in association of SERT with SHP2 in Caco-2 cells expressing constitutively active SHP2 compared with dominant-negative SHP2. Our data demonstrate that intestinal SERT is a target of SHP2 and reveal a novel mechanism by which a common food-borne pathogen uses cellular SHP2 to inhibit SERT. NEW & NOTEWORTHY The data presented in the current study reveal that intestinal serotonin transporter (SERT) is a target of the tyrosine phosphatase SHP2 and show a novel mechanism by which a common diarrheagenic pathogen, EPEC, activates cellular SHP2 to inhibit SERT function. These studies highlight host-pathogen interactions, which may be of therapeutic relevance in the management of diarrhea associated with enteric infections.

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26

Tsai, Chi-Jung, Chuang-Hsin Chiu, Yu-Yeh Kuo, Wen-Sheng Huang, Tsung-Hsun Yu, Leo Garcia Flores, Skye Hsin-Hsien Yeh, and Kuo-Hsing Ma. "3,4-Methylenedioxymethamphetamine (MDMA) Model: In Vivo 4-[18F]-ADAM PET Imaging." International Journal of Molecular Sciences 23, no. 13 (June 24, 2022): 7035. http://dx.doi.org/10.3390/ijms23137035.

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Numerous studies have confirmed that 3,4-Methylenedioxymethamphetamine (MDMA) produces long-lasting changes to the density of the serotonin reuptake transporter (SERT). Amitriptyline (AMI) has been shown to exert neuroprotective properties in neuropathologic injury. Here, we used a SERT-specific radionuclide, 4-[18F]-ADAM, to assess the longitudinal alterations in SERT binding and evaluate the synergistic neuroprotective effect of AMI in a rat MDMA model. In response to MDMA treatment regimens, SERT binding was significantly reduced in rat brains. Region-specific recovery rate (normalized to baseline) in the MDMA group at day 14 was 71.29% ± 3.21%, and progressively increased to 90.90% ± 7.63% at day 35. AMI dramatically increased SERT binding in all brain regions, enhancing average ~18% recovery rate at day 14 when compared with the MDMA group. The immunochemical staining revealed that AMI markedly increased the serotonergic fiber density in the cingulate and thalamus after MDMA-induction, and confirmed the PET findings. Using in vivo longitudinal PET imaging, we demonstrated that SERT recovery was positively correlated with the duration of MDMA abstinence, implying that lower SERT densities in MDMA-induced rats reflected neurotoxic effects and were (varied) region-specific and reversible. AMI globally accelerated the recovery rate of SERT binding and increased SERT fiber density with possible neuroprotective effects.

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27

Miller, David, and Alain Boyer. "À quoi sert la logique ?" Hermès 15, no. 1 (1995): 291. http://dx.doi.org/10.4267/2042/15173.

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28

Joschke, Christian. "À quoi sert l’iconographie politique ?" Perspective, no. 1 (June 30, 2012): 187–92. http://dx.doi.org/10.4000/perspective.646.

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29

Aynié, Jean-Philippe, and Anne-Laurence Mennessier. "À quoi sert un CR ?" Des régions et des spécialités, no. 59 (July 1, 2010): 4–5. http://dx.doi.org/10.35562/arabesques.1977.

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30

Saint-Girons, Baldine. "À quoi sert la sublimation ?" Figures de la psychanalyse 7, no. 2 (2002): 57. http://dx.doi.org/10.3917/fp.007.0057.

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31

Colin, Patrick. "A quoi sert la psychopathologie ?" Cahiers de Gestalt-thérapie 19, no. 2 (2006): 25. http://dx.doi.org/10.3917/cges.019.0025.

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32

Martin, Gilles. "À quoi sert la famille ?" Idées économiques et sociales N° 162, no. 4 (2010): 1. http://dx.doi.org/10.3917/idee.162.0001.

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33

Roshandel, Jalil. "À quoi sert l'armée iranienne ?" Outre-Terre 28, no. 2 (2011): 107. http://dx.doi.org/10.3917/oute.028.0107.

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34

Lo Prete, Marco Valerio. "À quoi sert la BCE ?" Outre-Terre 31, no. 1 (2012): 131. http://dx.doi.org/10.3917/oute.031.0131.

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35

Bouche-Florin, Luc-Émile. "À quoi sert le paysage ?" Outre-Terre 33-34, no. 3 (2012): 43. http://dx.doi.org/10.3917/oute.033.0043.

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36

Théry, Hervé. "À quoi sert la Guyane ?" Outre-Terre N° 43, no. 2 (2015): 211. http://dx.doi.org/10.3917/oute1.043.0211.

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37

Donzelot, Jacques. "À quoi sert la sociologie ?" Esprit Août/septembre, no. 8 (2009): 40. http://dx.doi.org/10.3917/espri.0908.0040.

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38

Nusinovici, Valentin. "À quoi sert un psychanalyste ?" La revue lacanienne 1, no. 1 (2008): 62. http://dx.doi.org/10.3917/lrl.081.0062.

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39

Ruffat, Michèle. "A quoi sert le néocorporatisme ?" Vingtième Siècle, revue d'histoire 13, no. 1 (1987): 95–104. http://dx.doi.org/10.3406/xxs.1987.1829.

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40

Jacquesy, Rose Agnès, and Armand Lattes. "À quoi sert l’industrie chimique ?" Annales des Mines - Réalités industrielles Mai 2015, no. 2 (2015): 8. http://dx.doi.org/10.3917/rindu1.152.0008.

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41

Coutau-Bégarie, Hervé. "À quoi sert une marine ?" Stratégique N° 109, no. 2 (2015): 11. http://dx.doi.org/10.3917/strat.109.0011.

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42

Huerre, Patrice. "L'adolescence : à qui ça sert ?" Le Télémaque 38, no. 2 (2010): 7. http://dx.doi.org/10.3917/tele.038.0007.

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43

Ruffat, Michele. "A quoi sert le neocorporatisme?" Vingtième Siècle. Revue d'histoire, no. 13 (January 1987): 95. http://dx.doi.org/10.2307/3769904.

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44

Cometti, Jean-Pierre. "À quoi sert Marcel Duchamp ?" Cahiers philosophiques 131, no. 4 (2012): 9. http://dx.doi.org/10.3917/caph.131.0009.

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45

Tubiana, Michel. "À quoi sert le droit ?" Migrations Société N° 109, no. 1 (2007): 175. http://dx.doi.org/10.3917/migra.109.0175.

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46

Mucchielli, Laurent. "À quoi sert la vidéosurveillance ?" VST - Vie sociale et traitements N° 154, no. 2 (May 4, 2022): 23–29. http://dx.doi.org/10.3917/vst.154.0023.

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47

Monnier, Gérard. "José Maria Sert (1874-1945)." Sociétés & Représentations 34, no. 2 (2012): 193. http://dx.doi.org/10.3917/sr.034.0193.

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48

Parienty, Arnaud. "A quoi sert la finance ?" Alternatives Économiques N° 305, no. 9 (October 7, 2011): 66. http://dx.doi.org/10.3917/ae.305.0066.

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49

Parienty, Arnaud. "A quoi sert le marché ?" Alternatives Économiques 286, no. 12 (December 1, 2009): 72. http://dx.doi.org/10.3917/ae.286.0072.

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50

Chiche, Sarah. "À quoi sert la PNL ?" Sciences Humaines N° 274, no. 9 (September 1, 2015): 28. http://dx.doi.org/10.3917/sh.274.0028.

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