Relevant bibliographies by topics / Potentiateurs

Academic literature on the topic 'Potentiateurs'

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Published: 20 April 2024

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Journal articles on the topic "Potentiateurs"

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S, Hanumitha, Mahalakshmi V, and Abirami S. "Biosynthesis of Zinc Oxide Nanoparticles Using Bacillus Species Potentiates Anticancer and Antimicrobial Activity." International Journal of Trend in Scientific Research and Development Volume-2, Issue-5 (August 31, 2018): 1796–802. http://dx.doi.org/10.31142/ijtsrd17137.

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&NA;. "Ecadotril potentiates captopril." Inpharma Weekly &NA;, no. 1005 (September 1995): 10. http://dx.doi.org/10.2165/00128413-199510050-00021.

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Zahl, K., J. B. Eisenkraft, I. H. Sampson, and R. Miller. "LIDOCAINE POTENTIATES VECURONIUM." Anesthesiology 71, Supplement (September 1989): A789. http://dx.doi.org/10.1097/00000542-198909001-00789.

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Nagai, Shigeki, Ralph E. Davis, Pierre Jean Mattei, Kyle Patrick Eagen, and Roger D. Kornberg. "Chromatin potentiates transcription." Proceedings of the National Academy of Sciences 114, no. 7 (January 30, 2017): 1536–41. http://dx.doi.org/10.1073/pnas.1620312114.

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Chromatin isolated from the chromosomal locus of the PHO5 gene of yeast in a transcriptionally repressed state was transcribed with 12 pure proteins (80 polypeptides): RNA polymerase II, six general transcription factors, TFIIS, the Pho4 gene activator protein, and the SAGA, SWI/SNF, and Mediator complexes. Contrary to expectation, a nucleosome occluding the TATA box and transcription start sites did not impede transcription but rather, enhanced it: the level of chromatin transcription was at least sevenfold greater than that of naked DNA, and chromatin gave patterns of transcription start sites closely similar to those occurring in vivo, whereas naked DNA gave many aberrant transcripts. Both histone acetylation and trimethylation of H3K4 (H3K4me3) were important for chromatin transcription. The nucleosome, long known to serve as a general gene repressor, thus also performs an important positive role in transcription.
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Fondevila, C., S. Meschengieser, and M. A. Lazzari. "Amiodarone potentiates acenocoumarin." Thrombosis Research 53, no. 2 (January 1989): 203–8. http://dx.doi.org/10.1016/0049-3848(89)90381-2.

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Visan, Ioana. "Mn potentiates cGAS." Nature Immunology 19, no. 6 (May 18, 2018): 511. http://dx.doi.org/10.1038/s41590-018-0126-y.

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Suzuki, Hajime, Akihiro Asakawa, Namiko Kawamura, Takakazu Yagi, and Akio Inui. "Hesperidin Potentiates Ghrelin Signaling." Recent Patents on Food, Nutrition & Agriculture 6, no. 1 (December 10, 2014): 60–63. http://dx.doi.org/10.2174/2212798406666140825120623.

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&NA;. "Paracetamol potentiates warfarin anticoagulation." Reactions Weekly &NA;, no. 692 (March 1998): 4. http://dx.doi.org/10.2165/00128415-199806920-00006.

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&NA;. "Paracetamol potentiates warfarin anticoagulation." Inpharma Weekly &NA;, no. 1128 (March 1998): 20. http://dx.doi.org/10.2165/00128413-199811280-00039.

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&NA;. "Dipyridamole potentiates nucleoside antivirals." Inpharma Weekly &NA;, no. 957 (October 1994): 19. http://dx.doi.org/10.2165/00128413-199409570-00050.

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Dissertations / Theses on the topic "Potentiateurs"

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Mareux, Elodie. "Pharmacothérapie ciblée des déficits en ABCB11." Electronic Thesis or Diss., université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL083.

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ABCB11/BSEP (Bile Salt Export Pump) est exprimé à la membrane canaliculaire des hépatocytes. Sa fonction de transport d’acides biliaires dans la bile est essentielle à la sécrétion biliaire. Près de 400 variations du gène ABCB11 ont été identifiées et sont associées à des maladies hépatobiliaires rares, la plus sévère étant la cholestase intrahépatique progressive familiale de type 2 (PFIC2). L’efficacité des traitements médicaux est limitée. Par conséquent, une transplantation hépatique est indiquée avant l’âge adulte pour près de deux tiers des patients. Dans ce contexte, l’identification de thérapies alternatives est un enjeu capital.Cette thèse s’intéresse à la recherche de stratégies thérapeutiques personnalisées permettant de corriger les conséquences pathologiques de certaines variations d’ABCB11 identifiées chez des patients. Dans le cadre d’une stratégie de traitement par des molécules potentiatrices, nous avons étudié les variations A257V, G562D et T463I d’ABCB11 par modélisation moléculaire 3D. L’étude de l’expression et de la fonction de ces variants dans différents modèles cellulaires a confirmé que ces variations étaient responsables d’un défaut de fonction du transporteur Abcb11. L’ivacaftor (VX 770, Kalydeco®), approuvé cliniquement pour le traitement de la mucoviscidose, corrigeait le défaut d’activité de ces trois variants.Des effets similaires ont été observés avec les molécules GLPG1837, SBC040 et SBC219, connues comme potentiateurs de CFTR (Cystic Fibrosis Transmembrane conductance Regulator). Dans une optique de thérapie combinatoire, nous avons également mis en évidence la capacité de ces potentiateurs à corriger le défaut de fonction des variants R1090C et R1090W, produits potentiels de la translecture du variant non-sens R1090X. Nous avons également évalué les molécules correctrices elexacaftor (VX-445) et tezacaftor (VX-661). Ces correcteurs, en monothérapie ou en combinaison, permettaient de restaurer l’adressage du variant R1128C, s’accompagnant d’une augmentation significative du transport de taurocholate. De façon intéressante, l’addition de molécules potentiatrices réduisait ces effets.L’ensemble de ces travaux constitue une preuve de concept que les défauts de certains variants d’ABCB11 peuvent être corrigés par ces molécules potentiatrices à haut potentiel thérapeutique. Ce type de traitements pourrait être envisagé pour les patients atteints de déficit en ABCB11 et permettrait ainsi d’augmenter la pharmacopée disponible pour traiter ce genre de pathologies et ainsi repousser voir palier à la transplantation hépatique pour les cas les plus sévères
ABCB11/BSEP (Bile Salt Export Pump) is expressed at the canalicular membrane of hepatocytes. It ensures bile acids secretion into bile which is essential for biliary secretion. Nearly 400 variations of the ABCB11 gene have been identified and are associated with rare hepatobiliary diseases, the most severe being progressive familial intrahepatic cholestasis type 2 (PFIC2). The effectiveness of medical treatments is limited. Consequently, liver transplantation is required before adulthood for almost 2/3 of PFIC2 patients. In this context, the identification of alternative therapies is a major challenge.This thesis focuses on personalized therapeutic strategies to correct the pathological consequences of some ABCB11 variations identified in patients. The A257V, G562D and T463I variations of ABCB11 were studied by 3D molecular modelling. These variations were responsible for a defect in Abcb11 transport function. Ivacaftor (VX-770, Kalydeco®), a clinically approved cystic fibrosis treatment, corrects the activity defect of the three variants.Similar effects were observed with GLPG1837, SBC040 and SBC219, known as potentiators of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator).From a combinatory therapy perspective, we also demonstrated the ability of these potentiators to correct the transport defect of the R1090C and R1090W variants, potential readthrough products of the R1090X nonsense variant. We also evaluated the ability of Elexacaftor (VX-445) and Tezacaftor (VX 661) correctors of CFTR. These correctors, alone or in combination, restored trafficking of the R1128C missense variant, leading to a significant increase in the transport function. Interestingly, the addition of potentiators abolishes this effect.Altogether, this thesis constitutes a proof of concept that molecules with high therapeutic potential can correct the molecular defects of ABCB11 variants. These treatments could increase the pharmacopoeia available for patients with ABCB11 deficiency and thus delay or even suppress the need for liver transplantation
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Hanoteau, Aurélie. "Chemotherapy potentiates immune responses against murine tumors." Doctoral thesis, Universite Libre de Bruxelles, 2016. https://dipot.ulb.ac.be/dspace/bitstream/2013/231745/5/Thesis.pdf.

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There is increasing evidence that the effect of chemotherapy on tumor rejection is not cell autonomous but relies on the immune system. Indeed, several reports have shown that human and murine tumors respond to chemotherapeutic agents more efficiently when the host immune system is intact. In particular, we have shown that cyclophosphamide treatment of DBA/2 mice bearing P815 mastocytoma induces rejection and long term protection in a CD4- and CD8-dependent manner. We used this tumor model, as it is poorly immunogenic, expresses tumor-associated P1A and tumor-specific P1E antigens, encoded by germline and mutated genes, respectively, and allows the identification of some tumor-specific CD8+ T cells.We have previously reported that tumor regression correlates with selective infiltration of CD8+ T cells specific for P1E/H-2Kd antigen in tumor bed upon cyclophosphamide treatment. Unexpectedly, the proportion of CD8+ T cells specific for the tumor-associated antigen P1A in the context of H-2Ld decreases concomitantly, indicating that cyclophosphamide alters the repertoire of CD8+ T cells recognizing tumor antigens. Using P1A KO mice, we found that preferential activation of CD8+ T cells to P1E is not solely due to thymic negative selection. The major role of “mutated” antigens in tumor resistance has been recently highlighted in humans and raises an interesting question about the immune mechanisms of tumor rejection. Additionally to its effect on the specific immune response, cyclophosphamide promotes tumor infiltration by effector memory (P1E/H-2Kd)+ CD8+ T cells which are characterized by higher expression of KLRG1 and Eomes. Our data point to a role of IL-15 and type 1 IFNs for their development, as increased levels of IL-15 and IRF7 were measured in tumor after cyclophosphamide. IFNAR1 blockade interferes with the tumor rejection in 50% of mice and decreases the (P1E/H-2Kd)+ CD8+ T cell infiltration induced by cyclophosphamide, suggesting a role of this cytokine in the expansion and/or recruitment of (P1E/H-2Kd)+ CD8+ T cells in vivo.Altogether, our results suggest that type 1 IFNs and IL-15 induced after cyclophosphamide promote the reprogramming of CD8+ T cells specific for the “mutated” P1E/H-2Kd antigen into effector memory lymphocytes.
Option Biologie moléculaire du Doctorat en Sciences
info:eu-repo/semantics/nonPublished
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Khalil, Dayekh. "Novel Combination Therapy: Monensin Potentiates Erlotinib-Induced Cytotoxicity." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24405.

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Receptor Tyrosine Kinase (RTK) inhibitors, such as erlotinib/tarceva, have been introduced in the past decade as a promising therapeutic option in Head and Neck Squamous Cell Carcinoma (HNSCC), however, they lack significant efficacy as single agents. As a result, RTK inhibitors require a combination based therapeutic approach with other treatment modalities. To uncover such a combination of agents, we performed a high throughput Prestwick library screen that included 1200 compounds approved by the FDA on HNSCC cell lines and found that monensin, a coccidial antibiotic, synergistically enhanced the cytotoxicity of erlotinib. RT-PCR revealed that monensin induced the expression of Activation of Transcription Factor (ATF) 3 and its downstream target C/EBP homologous protein (CHOP) which are key regulators of apoptosis. Furthermore, RNA-Seq analysis suggests that monensin augments erlotinib cytotoxicity by disturbing lipid and sterol biosynthesis. Therefore, identifying the mechanism of action exerted by monensin may open alternative avenues of cancer treatment.
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Lortie, Karine. "The growth-arrest-specific protein gas7 potentiates neuronal differentiation." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26701.

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The growth-arrest-specific gas7 protein is involved in neuronal development. Its role in neuronal differentiation and its potential neuroprotective activity were investigated in PC 12 and NT2 cells. gas7 overexpression in PC12 cells promoted neurite outgrowth and potentiated nerve growth factor-induced expression of the neuronal markers betaIII-tubulin, synaptotagmin, alpha7 subunit of the acethylcholine receptor, and dihydropyrimidinase related protein-3. This effect was exerted independently of cellular proliferation, as gas7 did not affect cell cycle progression. Endogenous gas7 expression was induced during neuronal differentiation of NT2 cells with retinoic acid, suggesting a role for gas7 in neuronal development. Finally, gas7 overexpression in PC 12 cells did not protect against toxicity triggered by oxygen-glucose deprivation, the calcium ionophore A23187 or sodium nitroprusside. The ability of gas7 to potentiate neuritogenesis and neuronal differentiation makes it a potential therapeutic target to promote re-establishment of neuronal connections in the injured or diseased brain, such as following stroke.
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Ho, Wing-tak, and 何永德. "Glycyrrhizic acid potentiates dsRNA-induced nitric oxide generation inalveolar macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31971799.

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Ho, Wing-tak. "Glycyrrhizic acid potentiates dsRNA-induced nitric oxide generation in alveolar macrophages." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31971799.

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Nakamura, Takanori. "Disruption of multidrug and toxin extrusion MATE1 potentiates cisplatin-induced nephrotoxicity." Kyoto University, 2011. http://hdl.handle.net/2433/142112.

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Liang, Xiaoting, and 梁小婷. "Activation of NRG1-ERBB4 signaling potentiates mesenchymal stem cell-mediated myocardial repairs." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/208584.

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Mesenchymal stem cell (MSC) transplantation has achieved only modest success in the treatment of ischemic heart disease due to poor cell viability in the diseased microenvironment. Genetic manipulation on the MSCs holds promising prospects in enhancing cell tolerance against adverse environmental conditions. Recent studies demonstrate that the activation of the NRG1 (neuregulin 1) - ERBB4 (v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 4) pathway can enhance pro-survival signaling, stimulate mature cardiomyocyte cell cycle re-entry and cell division. In this study, I aimed to determine whether activating NRG1-ERBB4 in MSCs can enhance their cardioprotective effects following myocardial infarction. In chapter 3, I determined that MSC endogenously expresses NRG1, but not ERBB4. Considering the absence of ERBB4 in the MSCs might lead to mute response to its ligand NRG1, I exogenously manipulated ERBB4 into MSCs. In chapter 4, MSCs, with or without ERBB4 overexpression were transplanted into mice following myocardial infarction. The transplantation of MSCs with ERBB4 expression considerably improved left ventricular ejection fraction and reduced infarctsize, compared to unmodified MSCs and direct NRG1 injection. ERBB4 overexpression induced greater MSC survival following infarction. The transduction of ERBB4 in MSCs increased cell mobility and apoptotic resistance via a PI3K/Akt pathway under hypoxic conditions in the presence of NRG1. The transplantation of MSCs with ERBB4 expression induced cardiomyocyte division and protected them against apoptosis during early phase of infarction. In chapter 5, a novel autocrine loop regarding to NRG1-ERBB4-NRG1 signaling was identified. MSCs with ERBB4 overexpression in turn increased NRG1 synthesis and secretion. Conditioned medium of ERBB4-expressing MSCs containing elevated NRG1, promoted cardiomyocyte growth, division and anti-senescence, whereas neutralization of NRG1 blunted these effects. Injecting ERBB4-expressing MSCs restored NRG1 in the infarcted myocardium to a level comparable with that of the normal myocardium. These findings collectively suggest overexpressing ERBB4 in MSCs enhances the effectiveness of MSCtherapy following myocardial in farction through potentiating MSC survival and revitalizing endogenous repair and regeneration. The combination of ERBB4 and MSC is more efficient than naïve MSC or solely recombinant NRG1 injection, emerging as potential target for developing novel strategy in treating myocardial diseases.
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Medicine
Doctoral
Doctor of Philosophy
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Taylor, Marlon D., and Marlon D. Taylor. "Sulforaphane Potentiates Non-Melanoma Skin Cancer in UVB-Treated Nrf2 Knockout Mice." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/622859.

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Sulforaphane is a natural product found in cruciferous vegetables which is known to have many chemopreventive properties including the induction of apoptosis and the inhibition of inflammation, cellular proliferation, and reactive oxygen species (ROS) formation. The reduction of ROS activity by sulforaphane is likely linked to the activation of NF-E2 related factor-2 (Nrf2), a transcription factor involved in cytoprotection against ROS and electrophilic stress. The skin is particularly vulnerable to oxidative stress caused by ultraviolet (UV) light, which is an established complete carcinogen. Sulforaphane has been shown to reduce both chemical and UVB-induced skin carcinogenesis in mouse models. Suppression of DMBA/TPA-induced skin tumorigenesis by sulforaphane has been shown to be dependent upon Nrf2 activity. Additional studies have shown that genetic activation of Nrf2 can protect keratinocytes against UVB-induced ROS. Nrf2 has also been implicated in regulating inflammatory responses after UVB exposure in the skin. However, the role of Nrf2 in the antitumorigenic activity of sulforaphane in the context of UVB-induced skin tumors is not well understood. We therefore performed murine experiments in order to clarify whether sulforaphane requires Nrf2 in order to block UVB-induced non-melanoma skin cancer. Consistent with the literature, we observed that wildtype (WT) mice topically treated with sulforaphane were less susceptible to UVB-induced tumor incidence and tumor burden compared to the vehicle control WT group. However, Nrf2 KO mice treated with sulforaphane presented with significantly greater UVB-induced tumor incidence and burden compared to the WT sulforaphane group, suggesting that sulforaphane may potentiate tumorigenesis in the context of UVB exposure if Nrf2 is absent. We therefore performed acute in vivo and in vitro experiments using topical sulforaphane (as per the tumor experiment) to investigate why Nrf2 KO mice developed more tumors than WT mice during UVB and sulforaphane treatment. Topical treatment of SKH-1 mice with sulforaphane did result in slight reduction of UV-induced epidermal hyperplasia in wildtype mice which was not present in Nrf2 KO mice (trends were not significant). Surprisingly, while wildtype mice developed significantly more epidermal inflammation in our acute treatment model than did the Nrf2 KO strain (as measured by skin fold thickness), inflammation was not significantly influenced by topical sulforaphane treatment in either strain of mice. However, cell culture studies using primary mouse keratinocytes indicate that sulforaphane’s ability to block UVB-induced ROS is lost in Nrf2 KO cells. Taken together, our ROS data may strengthen the hypothesis that sulforaphane increases the oxidative stress of cells during UVB treatment in the absence of Nrf2.
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Scarpa, Richard C. "Neurotensin potentiates the proliferative effects of growth factors in human embryonic lung fibroblasts /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2004.

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Thesis (Ph.D.)--Tufts University, 2004.
Adviser: David E. Cochrane. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 137-165). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Books on the topic "Potentiateurs"

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Dare, Amos O. Ouabain potentiates kainate neurotoxicity: A new rat model of human temporal lobe epilepsy. [New Haven, Conn: s.n.], 1996.

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Main, Jeffrey Scott *. Heart failure potentiates the modulatory influence of the endothelium on alpha-adrenergic-mediated responses in canine coronary arteries. 1989.

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Bulterys, Marc, Julia Brotherton, and Ding-Shinn Chen. Prevention of Infection-Related Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0066.

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This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).
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Tritten, Tyler. On the Primacy of Matter: Neoplatonism Right-Side Up. Edinburgh University Press, 2018. http://dx.doi.org/10.3366/edinburgh/9781474428194.003.0004.

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This chapter provides a close reading of Schelling’s early commentary on Plato’s Timaeus and then contrasts this reading with Neoplatonism’s, particularly Proclus’, understanding of this same text. While Neoplatonism views being according to a hierarchy of degradation or descent, with matter at the bottom, Schelling affirms that being potentiates itself into higher and greater degrees of order such that matter is not the last but the first. He is able to do this, however, only by rejecting the Platonic notion of participation. For Schelling, the participating acquires an independence from the participated so that an effect can be greater than its cause and, moreover, the effect exerts a retroactive after effect on the cause. The identity of a cause or antecedent is only constituted in and through its consequents. If matter is said to process from the One, then matter, in turn, is the consequent condition of the identity of the One as one rather than as many.
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Bechara, Antoine. Impulse Control Disorders in Neurological Settings. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0126.

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This chapter will argue that impulse control disorders, including addiction, are the product of an imbalance between two separate but interacting neural systems: (1) an impulsive amygdala-striatum–dependent neural system that promotes automatic and habitual behaviors and (2) a reflective prefrontal cortex–dependent neural system for decision making, forecasting the future consequences of a behavior, and inhibitory control. The reflective system controls the impulsive system via several mechanisms. However, this control is not absolute; hyperactivity within the impulsive system can override the reflective system. While most prior research has focused on the impulsive system (especially the ventral striatum and its mesolimbic dopamine projection) in promoting the motivation and drive to seek drugs, or on the reflective system (prefrontal cortex) and its mechanisms for decision making and impulse control, more recent evidence suggests that a largely overlooked structure, namely the insula, plays a key role in maintaining poor impulse control, including addiction. This review highlights the potential functional role the insula plays in addiction. We propose that the insula translates bottom-up, interoceptive signals into what subjectively may be experienced as an urge or craving, which in turn potentiates the activity of the impulsive system and/or weakens or hijacks the goal-driven cognitive resources that are needed for the normal operation of the reflective system.
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Book chapters on the topic "Potentiateurs"

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Sedikides, Constantine, Tim Wildschut, and Elena Stephan. "Nostalgia Shapes and Potentiates the Future." In The Social Psychology of Living Well, 181–99. New York, NY : Routledge, 2018. | Series: The Sydney Symposium of Social Psychology series: Routledge, 2018. http://dx.doi.org/10.4324/9781351189712-11.

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Franconi, Flavia, Mauro Miceli, Federico Bennardini, Antonella Mattana, Jesus Covarrubias, and Giuseppe Seghieri. "Taurine Potentiates the Antiaggregatory Action of Aspirin and Indomethacin." In Advances in Experimental Medicine and Biology, 181–86. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3436-5_20.

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Sano, Hitoshi, Hitoshi Okada, Yoshihito Sakata, Hiroshi Okamoto, Hideaki Kawaguchi, Hisakazu Yasuda, and Akira Kitabatake. "Angiotensin II Potentiates Collagen Synthesis in the Hypertrophied Heart." In New Aspects in the Treatment of Failing Heart, 199–201. Tokyo: Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-68219-6_41.

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A. Rodrigues, Fabrício, Renata Sousa Resende, Leandro José Dallagnol, and Lawrence E. Datnoff. "Silicon Potentiates Host Defense Mechanisms Against Infection by Plant Pathogens." In Silicon and Plant Diseases, 109–38. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22930-0_5.

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Steyger, Peter S. "Inflammation Potentiates Cochlear Uptake of Ototoxins and Drug-Induced Hearing Loss." In Inflammatory Mechanisms in Mediating Hearing Loss, 133–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_7.

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Liao, Junyi, Ning Hu, Nian Zhou, Chen Zhao, Xi Liang, Hong Chen, Wei Xu, Cheng Chen, Qiang Cheng, and Wei Huang. "Sox9 Potentiates BMP2-Induced Chondrogenic Differentiation and Inhibits BMP2-Induced Osteogenic Differentiation." In Regenerative Medicine and Plastic Surgery, 263–80. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19962-3_19.

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Toufektsian, Marie-Claire, Stéphane Tanguy, Sandrine Morel, Nada Benajiba, François Boucher, and Joël Leiris. "Hypoxic Reperfusion after Brief Ischemia Potentiates Ischemic Preconditioning in Isolated Rat Hearts." In Myocardial Ischemia and Preconditioning, 219–33. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0355-2_16.

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Zucker, Tom-Philipp, Detlef Bönisch, Stephanie Muck, Artur-Aron Weber, Ellen Bretschneider, Erika Glusa, and Karsten Schrör. "Thromboxane A2 Potentiates Thrombin-Induced Proliferation of Coronary Artery Smooth Muscle Cells." In Advances in Experimental Medicine and Biology, 387–90. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1810-9_84.

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Osna, Natalia A., Moses New Aaron, Ragubendra Singh Dagur, Siva Koganti, Mojisola Ogunnaike, Paul Thomes, Murali Ganesan, and Larisa Y. Poluektova. "Alcohol Potentiates HIV-Induced Hepatotoxicity Via Induction of Lysosomal Damage in Hepatocytes." In Alcohol and Alcohol-related Diseases, 1195–207. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-32483-3_63.

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Iturriaga, R. "Intracellular Acidosis Potentiates Carotid Chemoreceptor Responses to Hypoxia in the Absence of CO2-HCO3 −." In Frontiers in Arterial Chemoreception, 211–16. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5891-0_30.

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Conference papers on the topic "Potentiateurs"

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Schaible, N., R. Guo, E. Phalen, K. Chmiel, X. Ai, Y. Bai, A. A. Zeki, and R. Krishnan. "Pitavastatin Potentiates Beta2-Agonist Induced Bronchodilation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5496.

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Sherrill, Taylor P., George Stathopoulos, Fiona E. Yull, Barbara Fingleton, and Timothy S. Blackwell. "Host-Derived Interleukin-5 Potentiates Lung Metastasis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2522.

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Hanthazi, Aliénor, Samantha Gomart, Caroline Gaudreau Ménard, Pascale Jespers, Jean-Yves Springael, Robert Naeije, Laurence Dewachter, and Kathleen Mc Entee. "Chemerin potentiates pulmonary artery reactivity to endothelin-1." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2440.

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Kurai, Jun, Rebecca L. Toonkel, Alain Borczuk, and Charles A. Powell. "Oxidative Stress Potentiates Carcinogenesis In Chronic Lung Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4953.

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Bårzu, T., P. Molho, R. Cariou, G. Tobelem, and J. Caen. "HEPARIN BINDING TO ENDOTHELIAL CELLS POTENTIATES THROMBINSTIMULATED PGI2 PRoDUCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642840.

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We studied the consequences of hepari n (H) binding to endothel iaI cells (EC) on their basal and thrombin-stimulated PGI2 production. Primary cultures of human umbilical vein EC were incubated with different H concentrations, in serum free medium for 5 hrs. The amount of 6-keto-pGF1α was measured in the medium after 5 hrs with an enzyme-linked inmunoassay. At all concentrations used (0.75 to 75 μg/ml) H did not alter the 5-hour basal production of PGI2 (control, 10.1 α 1.4 ng/106 cells; H 15 μg/m1 ; 10.8 ± 2.7 ng/106 cells). Basal or thrombin (0.1 U/m])-rtimulated (10 min) pGI2 production was then determined using EC bearing only bound heparin. The low, unstimulated PGI2 release (0.412 ± 0.04 ng/106 cells) was not significantly changed in the presence of bound H, but the thrombin-stimulated release was potentiated.The KD for H binding to EC is 2.5 μg/ml. Thus at 3 μg/ml, half maximal saturation of binding sites and maximal potentiation of thrombin action were achieved. This concentration of bound H shifted the dose-response curve of thrombin induced PGI2 production to the left. Similar effect was obtained with half maximal saturating concentration of low molecular weight H (CY 222). Neither arachinodate nor LC4-induced PGI2 release were modified by H binding to EC, suggesting that potentiation is specific to thrombin. Since bound H was shown to not modify the high affinity thrombin binding to EC, the potentiating effect of bound H could related rather to interference with the specific mechanism of thrombin-stimulation of PGI2 production.
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Özhan, Hanife, Ebru SaraÇ, Eylül Sena Ceylan, and Mustafa Kemal Ruhİ. "Potassium Chloride Potentiates Chlorin e6-Mediated Antimicrobial Photodynamic Inactivation." In 2023 Medical Technologies Congress (TIPTEKNO). IEEE, 2023. http://dx.doi.org/10.1109/tiptekno59875.2023.10359206.

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Pandey, Manoj K., Jagat J. Mukherjee, Dhimant H. Desai, Shantu G. Amin, and Subodh Kumar. "Abstract 2734: Ethanol potentiates tobacco smoke carcinogens-induced MAPK activation." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2734.

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Ding, Ying, and Thu A. Nguyen. "Abstract 3712: Gap junction enhancer potentiates cytotoxic effect of cisplatin." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3712.

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Mi, Jun, Yongbin Wang, Guifang Gan, and Jiangmin Zhao. "Abstract 1580: Cancer-associated fibroblasts potentiates tumor relapse after radiotherapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1580.

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Stancil, I. T., J. E. Michalski, J. S. Kurche, and D. A. Schwartz. "MUC5B Promoter Variant Potentiates the Unjammed State in Airway Epithelia." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4450.

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Reports on the topic "Potentiateurs"

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Fisher, Joshua L. Selenium Potentiates Chemotherapeutic Selectivity: Improving Efficacy and Reducing Toxicity. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470578.

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Green, Lora M. Low Dose Gamma Irradiation Potentiates Secondary Exposure to Gamma Rays or Protons in Thyroid Tissue Analogs. Office of Scientific and Technical Information (OSTI), May 2006. http://dx.doi.org/10.2172/882942.

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Zlotkin, Eliahu, Shizuo G. Kamita, Nor Chejanovsky, and S. Maeda. Targeting of an Expressed Insect Selective Neurotoxin by its Recombinant Baculovirus: Pharmacokinetic and Pharmacodynamic Aspects. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7571354.bard.

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Objectives: 1) Clarification of the mode of potentiation of an expressed insect selective neurotoxin (AaIT) by its recombinant baculovirus. 2) In vitro formation and/or modification of neuroactive polypeptides for the design of new improved recombinant baculoviruses. Results: 1) A combined utilization of bioassays, LM-cytochemistry, the highly resolutive EM immunogold and electrical recording from the CNS of baculovirus and AaIT - expressing – recombinant baculovirus infected larvae it has been shown that the recombinant virus potentiates the effect of the toxin. Potentiation is achieved through its continuous expression in the infected tracheal epithelia thus providing a: a) Local supply of freshly produced toxin in the vicinity of its traget sites; b) Translocation of the expressed toxin to the insect CNS. The latter exposes the recombinant toxin to new, critical, target sites which are inaccessible through the natural route of scorpion envenomation. 2) Subjecting a recombinant AaIT toxin to a newly designed system of random mutagenesis results in large numbers of new AaIT genes with amino acid substitutions. The new or modified toxin genes were inserted into a linear BmNPV expressed in silkworm cell culture and assayed on blowfly and silkworm larvae. Thus a system for mass formation and screening of neuroactive agents was developed. Contribution to agriculture: 1) Demonstration of the insecticidal mechanism, capacity and utility of the combination of neuroactive polypeptides and recombinant pathogens. 2) Development of a simple in vitro system for the formation and selection of new neuroactive polypeptides.
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Yaron, Zvi, Martin P. Schreibman, Abigail Elizur, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon Piceus) and the Striped Bass (Morone Saxatilis). United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568102.bard.

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The black carp (bc)GtH IIb cDNA was amplified and isolated, cloned and sequenced. Comparison of the bcGtH IIb deduced a.a. sequence with that of GtH IIb from other teleosts revealed high homology to cyprinid species and a lower homology to salmonid or perciform fish. The gene coding for the GtH IIb was isolated and sequenced. Three bc recombinant phages which hybridized to the goldfish GtH Ib cDNA probe were isolated and are currently being characterized. The region coding for the mature GtH IIb was expressed in a bacterial expression vector resulting in the production of a recombinant protein. In vitro folding resulted in a protein only 1.3% of which displaced the native common carp GtH II in a RIA. Therefore, the common carp GtH RIA was utilized for the physiological studies at the current phase of the project. Two non-functional sites were identified along the brain-pituitary gonadal axis in the immature black carp. The pituitary is refractory to GnRH stimulation due to a block proximal to the activation of PKA and PKC probably at the level of GnRH receptors. The gonads, although capable of producing steroids, are refractory to gonadotropic stimulation but do respond to cAMP antagonists, indicating a block at the GtH receptor level. Attempts to advance puberty in 2 and 3 y old black carp showed that testosterone (T) stimulates GtH synthesis in the pituitary and increases its sensitivity to GnRh. A 2 month treatment combining T+GnRH increased the circulating GFtH level in 3 y old fish. Addition of domperidone to such a treatment facilitated both the accumulation of GtH in the pituitary and its response to GnRH. The cDNA of striped bass GtH a, Ib and IIb subunits were amplified, isolated, cloned and sequenced, and their deduced a.a. sequences were compared with those of other teleosts. A ribonuclease protection assay was developed for a sensitive and simultaneous determination of all GtH subunits, and of b-actin mRNAs of the striped bass. GnRH stimulated dramatically the expression of the a and GtH IIb subunits but the level of GtH Ib mRNA increased only moderately. These findings suggest that GtH-II, considered in salmonids to be involved only in final stages of gametogenesis, can be induced by GnRH to a higher extent than GtH-I in juvenile striped bass. The native GtH II of the striped bass was isolated and purified, and an ELISA for its determination was developed. The production of all recombinant striped bass GtH subunits is in progress using the insect cell (Sf9) culture and the BAC-TO-BAC baculovirus expression system. A recombinant GtH IIb subunit has been produced already, and its similarity to the native subunit was confirmed. The yield of the recombinant glycoprotein can reach 3.5 mg/ml after 3 days culture. All male striped bass reach puberty after 3 y. However, precocious puberty was discovered in 1 and 2 y old males. Females become vitellogenic during their 4th year. In immature 2 y old females, T treatment elevates the pituitary GtH II content while GnRH only potentiates the effect. However, in males GnRH and not T affects GtH accumulation in the pituitary. Neither GnRH, nor T treatment resulted in gonadal growth in 2 y old striped bass, indicating that either the accumulated GtH II was not released, or if released, the gonads were refractory to GtH stimulation, similar to the situation in the immature black carp. In 3 y old female striped bass, 150 day GnRHa treatment resulted in an increase in GSI, while T treatment, with or without GnRHa, resulted in a decrease in oocyte diameter, similar to the effect seen in the black carp. Further attempts to advance puberty in both fish species should take into account the positive effect of T on pituitary GtH and its negative effect of ovarian growth.
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