Relevant bibliographies by topics / Membranes, physiopathology

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Membranes, physiopathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Membranes, physiopathology.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Membranes, physiopathology"

1

Coraboeuf, E., and D. Escande. "Ionic Currents in the Human Myocardium." Physiology 5, no. 1 (February 1, 1990): 28–31. http://dx.doi.org/10.1152/physiologyonline.1990.5.1.28.

Full text
Abstract:
Recent measurements by patch-clamp techniques of membrane currents from enzymatically isolated human cardiac cells have shown the existence in human atrial membranes of seven different types of ionic channels. Such studies open new perspectives for human cardiac pharmacology and physiopathology.
APA, Harvard, Vancouver, ISO, and other styles
2

Arsenijevic, Tatjana, Jason Perret, Jean-Luc Van Laethem, and Christine Delporte. "Aquaporins Involvement in Pancreas Physiology and in Pancreatic Diseases." International Journal of Molecular Sciences 20, no. 20 (October 11, 2019): 5052. http://dx.doi.org/10.3390/ijms20205052.

Full text
Abstract:
Aquaporins are a family of transmembrane proteins permeable to water. In mammals, they are subdivided into classical aquaporins that are permeable to water; aquaglyceroporins that are permeable to water, glycerol and urea; peroxiporins that facilitate the diffusion of H2O2 through cell membranes; and so called unorthodox aquaporins. Aquaporins ensure important physiological functions in both exocrine and endocrine pancreas. Indeed, they are involved in pancreatic fluid secretion and insulin secretion. Modification of aquaporin expression and/or subcellular localization may be involved in the pathogenesis of pancreatic insufficiencies, diabetes and pancreatic cancer. Aquaporins may represent useful drug targets for the treatment of pathophysiological conditions affecting pancreatic function, and/or diagnostic/predictive biomarker for pancreatic cancer. This review summarizes the current knowledge related to the involvement of aquaporins in the pancreas physiology and physiopathology.
APA, Harvard, Vancouver, ISO, and other styles
3

Simó, Rafael, Marta Villarroel, Lídia Corraliza, Cristina Hernández, and Marta Garcia-Ramírez. "The Retinal Pigment Epithelium: Something More than a Constituent of the Blood-Retinal Barrier—Implications for the Pathogenesis of Diabetic Retinopathy." Journal of Biomedicine and Biotechnology 2010 (2010): 1–15. http://dx.doi.org/10.1155/2010/190724.

Full text
Abstract:
The retinal pigment epithelium (RPE) is an specialized epithelium lying in the interface between the neural retina and the choriocapillaris where it forms the outer blood-retinal barrier (BRB). The main functions of the RPE are the following: (1) transport of nutrients, ions, and water, (2) absorption of light and protection against photooxidation, (3) reisomerization of all-trans-retinal into 11-cis-retinal, which is crucial for the visual cycle, (4) phagocytosis of shed photoreceptor membranes, and (5) secretion of essential factors for the structural integrity of the retina. An overview of these functions will be given. Most of the research on the physiopathology of diabetic retinopathy has been focused on the impairment of the neuroretina and the breakdown of the inner BRB. By contrast, the effects of diabetes on the RPE and in particular on its secretory activity have received less attention. In this regard, new therapeutic strategies addressed to modulating RPE impairment are warranted.
APA, Harvard, Vancouver, ISO, and other styles
4

LACABARATZ-PORRET, Christine, Elisabeth CORVAZIER, Tünde KOVÀCS, Régis BOBE, Raymonde BREDOUX, Sophie LAUNAY, Béla PAPP, and Jocelyne ENOUF. "Platelet sarco/endoplasmic reticulum Ca2+ATPase isoform 3b and Rap 1b: interrelation and regulation in physiopathology." Biochemical Journal 332, no. 1 (May 15, 1998): 173–81. http://dx.doi.org/10.1042/bj3320173.

Full text
Abstract:
Platelet Ca2+ signalling involves intracellular Ca2+ pools, whose content is controlled by sarco/endoplasmic reticulum Ca2+ATPases (SERCAs). Among these, a key role is played by the inositol trisphosphate-sensitive Ca2+ pool, associated with the SERCA 3b isoform. We have investigated the control of this Ca2+ pool through the cAMP-dependent phosphorylation of the GTP-binding protein, Rap (Ras-proximate) 1b. We first looked for this Ca2+ pool target of regulation by studying the expression of the different SERCA and Rap 1 proteins in human platelets and various cell lines, by Western blotting and reverse transcription-PCR. Since co-expression of Rap 1b and SERCA 3b was obtained, we looked for their protein–protein interaction as a function of the cAMP-dependent phosphorylation of Rap 1b. Co-immunoprecipitations of SERCA 3b and Rap 1b proteins were found in the absence of phosphorylation, induced by the catalytic subunit of the cAMP-dependent protein kinase (csPKA). In contrast, upon pre-treatment of platelet membranes with csPKA, the SERCA 3b dissociated from the Rap 1b protein, in agreement with a role of its phosphorylated state in their interaction. Finally, we looked for adaptation of this complex in a platelet pathological model of hypertension. We investigated the expression of both proteins, as well as the cAMP-dependent phosphorylation of Rap 1b and SERCA 3b activity in platelets from control normotensive Wistar-Kyoto rats and from spontaneously hypertensive rats (SHRs). A decrease in SERCA 3b activity was associated with a decrease in Rap 1b endogenous phosphorylation in SHR platelets, consistent with a functional role in the regulation of the SERCA 3b-associated Ca2+ pool.
APA, Harvard, Vancouver, ISO, and other styles
5

Adrien, Vladimir, Hugo Fumat, Cédric Tessier, Philippe Nuss, and David Tareste. "T202. THE EFFECT OF ANTIPSYCHOTIC DRUGS ON MEMBRANE FUSION: AN IN VITRO STUDY." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S308—S309. http://dx.doi.org/10.1093/schbul/sbaa029.762.

Full text
Abstract:
Abstract Background Common clinical use of antipsychotics (AP) drugs shows that their therapeutic mode of action still needs further clarification although it is admitted that the Dopamine receptor D2 (D2R) antagonism plays a significant role. For instance, clozapine (CLOZ) - which is known to be the most effective AP in treating schizophrenic symptoms - has strikingly the lowest D2R antagonism. Non direct receptor-related effects might thus be involved in the activity of AP at the synapse level. AP, as well as neurotransmitters, are mostly lipophilic and insert within membranes. This characteristic is of interest as a significant proportion of schizophrenic patients has specific and abnormal membrane lipid composition. This possible proxy of the disease biotype can participate in the disease’s physiopathology but also be critical for the effect of AP drugs. We hypothesize that AP insertion into lipid membranes also contribute to their therapeutic effect. AP-induced modifications of synaptic membranes biophysics are likely to influence neurotransmission. In this study, we focus on the effect of AP on membrane fusion, a crucial step for the exocytosis of neurotransmitters. Methods Liposomes modelling synaptic vesicles were reconstituted in saline buffer. Two standard ternary and quaternary lipid mixtures have been studied: phosphatidylcholine:phosphatidylethanolamine:phosphatidylserine (PC:PE:PS) [65:25:10] and the synaptic-like PC:PE:PS:sphingomyelin:cholesterol (PC:PE:PS:SM:CHOL) [25:25:10:10:30]. Some liposomes were protein-free and others were functionalized with Soluble N-ethylmaleimide-sensitive-factor Attachment protein Receptor (SNARE) proteins, which trigger in vivo the fusion of synaptic vesicles with the pre-synaptic plasma membrane. The liposome size was checked by Dynamic Light Scattering. Insertion of AP within the membrane was checked by second derivative spectroscopy. Fusion was measured by Fluorescence Resonance Energy Transfer in the absence or presence of CLOZ or chlorpromazine (CPZ) at various lipid:AP ratios (10:1 to 100000:1). Protein-free liposomes were fused with Polyethylene glycol (PEG) and SNARE liposomes through the action of cognate SNARE proteins residing in their membrane. Results Liposomes of the same lipid composition were of the same size, with no effect of the addition of AP drugs at various concentrations. Molar partition coefficient of AP drugs within the membrane of protein-free liposomes was approximately 70–85%. CPZ or CLOZ inhibited the fusion of PC:PE:PS liposomes by about 20–40%. When liposomes were synaptic-like (PC:PE:PS:SM:CHOL), the inhibition of fusion by AP drugs reached 50%. CLOZ also inhibited SNARE-mediated fusion of PC:PE:PS liposomes by about 30%. This effect on SNARE-mediated fusion was not observed with CPZ. Discussion Altogether, these results, despite preliminary, could help to understand partially a non direct receptor-related effect of antipsychotics. Indeed, these drugs also seem to modify membrane dynamics at the synapse level. This seems to be particularly the case of CLOZ on SNARE-mediated fusion and could explain its specific therapeutic efficiency.
APA, Harvard, Vancouver, ISO, and other styles
6

Fernandes, Tânia, Rosa Resende, Diana F. Silva, Ana P. Marques, Armanda E. Santos, Sandra M. Cardoso, M. Rosário Domingues, Paula I. Moreira, and Cláudia F. Pereira. "Structural and Functional Alterations in Mitochondria-Associated Membranes (MAMs) and in Mitochondria Activate Stress Response Mechanisms in an In Vitro Model of Alzheimer’s Disease." Biomedicines 9, no. 8 (July 24, 2021): 881. http://dx.doi.org/10.3390/biomedicines9080881.

Full text
Abstract:
Alzheimer’s disease (AD) is characterized by the accumulation of extracellular plaques composed by amyloid-β (Aβ) and intracellular neurofibrillary tangles of hyperphosphorylated tau. AD-related neurodegenerative mechanisms involve early changes of mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) and impairment of cellular events modulated by these subcellular domains. In this study, we characterized the structural and functional alterations at MAM, mitochondria, and ER/microsomes in a mouse neuroblastoma cell line (N2A) overexpressing the human amyloid precursor protein (APP) with the familial Swedish mutation (APPswe). Proteins levels were determined by Western blot, ER-mitochondria contacts were quantified by transmission electron microscopy, and Ca2+ homeostasis and mitochondria function were analyzed using fluorescent probes and Seahorse assays. In this in vitro AD model, we found APP accumulated in MAM and mitochondria, and altered levels of proteins implicated in ER-mitochondria tethering, Ca2+ signaling, mitochondrial dynamics, biogenesis and protein import, as well as in the stress response. Moreover, we observed a decreased number of close ER-mitochondria contacts, activation of the ER unfolded protein response, reduced Ca2+ transfer from ER to mitochondria, and impaired mitochondrial function. Together, these results demonstrate that several subcellular alterations occur in AD-like neuronal cells, which supports that the defective ER-mitochondria crosstalk is an important player in AD physiopathology.
APA, Harvard, Vancouver, ISO, and other styles
7

Joël, Ngoumen Ngassa Dany, Ngondi Judith Laure, and Oben Julius Enyong. "Effect of Autranellacongolensis on Lipid Profile of Rats’ Brain with Experimentally Induced Alzheimer’s Disease." Journal of Food Research 9, no. 4 (July 15, 2020): 60. http://dx.doi.org/10.5539/jfr.v9n4p60.

Full text
Abstract:
Lipids are essentials components of the brain. Changes in brain lipid composition affect the physical and functional properties of the neuronal cell membrane and have been implicated in the physiopathology of Alzheimer disease (AD). We evaluated in this study the effect of hydroethanolicbark extract of A. Congolensis on lipid profile of rats’ brain with experimentally induced AD. The experimental model consisted of female rats, which received orally for 8 consecutive weeks a single dose of 50 mg/Kg b.w./day of aluminum trichloride (AlCl3) (except control group) followed by distilled water (disease control group) or doses of the extract (150 or 300 mg/Kg b.w./day) or vitamin E (100 mg/Kg b.w./day) or galanthamine (2 mg/Kg b.w. /day). Brain cholesterol, phospholipids and plasmalogenlevels and fluidity were evaluated. Brain membranes ATPase activities, Ca2+, Mg2+and glucose levels were also assayed. Significant modifications of brain lipid composition and fluidity were observed in disease control group compared with control. In addition, Na+, K+-ATPase and Mg2+-ATPase activities significantly decreased, the level of intracellular Ca2+ increased, Mg2+ content decreased and brain glucose level was significantly higher. Standard drugs (vitamin E,galanthamine) showed a negative effect on brain lipid profile. The extract of 150 mg showed significant improvements of brain lipid profile and fluidity. It also indicated improved brain ATPase activities, ions and glucose brain homeostasis. The extract (150 mg/Kg b.w. dose) by maintaining the brain lipid composition may protect neuronal cell membraneand probably preventing the progression of AD.
APA, Harvard, Vancouver, ISO, and other styles
8

Moulis, Manon, Elisa Grousset, Julien Faccini, Kevin Richetin, Gary Thomas, and Cecile Vindis. "The Multifunctional Sorting Protein PACS-2 Controls Mitophagosome Formation in Human Vascular Smooth Muscle Cells through Mitochondria-ER Contact Sites." Cells 8, no. 6 (June 25, 2019): 638. http://dx.doi.org/10.3390/cells8060638.

Full text
Abstract:
Mitochondria-associated ER membranes (MAMs) are crucial for lipid transport and synthesis, calcium exchange, and mitochondrial functions, and they also act as signaling platforms. These contact sites also play a critical role in the decision between autophagy and apoptosis with far reaching implications for cell fate. Vascular smooth muscle cell (VSMC) apoptosis accelerates atherogenesis and the progression of advanced lesions, leading to atherosclerotic plaque vulnerability and medial degeneration. Though the successful autophagy of damaged mitochondria promotes VSMC survival against pro-apoptotic atherogenic stressors, it is unknown whether MAMs are involved in VSMC mitophagy processes. Here, we investigated the role of the multifunctional MAM protein phosphofurin acidic cluster sorting protein 2 (PACS-2) in regulating VSMC survival following a challenge by atherogenic lipids. Using high-resolution confocal microscopy and proximity ligation assays, we found an increase in MAM contacts as in PACS-2-associated MAMs upon stimulation with atherogenic lipids. Correspondingly, the disruption of MAM contacts by PACS-2 knockdown impaired mitophagosome formation and mitophagy, thus potentiating VSMC apoptosis. In conclusion, our data shed new light on the significance of the MAM modulatory protein PACS-2 in vascular cell physiopathology and suggest MAMs may be a new target to modulate VSMC fate and favor atherosclerotic plaque stability.
APA, Harvard, Vancouver, ISO, and other styles
9

Baud, O., R. H. Fontaine, P. Olivier, L. Maury, F. El Moussawi, I. Bauvin, M. Arsac, S. Hovhannisyan, C. Farnoux, and Y. Aujard. "Rupture très prématurée des membranes: physiopathologie des conséquences neurologiques." Archives de Pédiatrie 14 (January 2007): S49—S53. http://dx.doi.org/10.1016/s0929-693x(07)80011-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Blanchon, L., M. Accoceberry, C. Belville, A. Delabaere, C. Prat, D. Lemery, V. Sapin, and D. Gallot. "Rupture des membranes : physiopathologie, diagnostic, conséquences et prise en charge." Journal de Gynécologie Obstétrique et Biologie de la Reproduction 42, no. 2 (April 2013): 105–16. http://dx.doi.org/10.1016/j.jgyn.2012.12.012.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Membranes, physiopathology"

1

Lavergne, Marilyne. "Rôle des protéines NLRP dans la physiopathologie des membranes foetales humaines." Thesis, Université Clermont Auvergne‎ (2017-2020), 2019. http://www.theses.fr/2019CLFAS025.

Full text
Abstract:
L’inflammation joue un rôle central dans la rupture des membranes fœtales (MF), que celle-ci ait lieu à terme ou prématurément, mais l’ensemble des mécanismes reste encore à élucider. Dans ce contexte, les études sur les inflammasomes, un des acteurs clés de l’inflammation, se sont récemment intensifiées. Ces plateformes intracellulaires, formées suite à un signal pro-inflammatoire, sont impliquées dans la mise en place et la propagation d’une réaction inflammatoire. Leur fonction au sein des MF commence à être décrite mais de nombreuses zones d’ombre persistent. L’objectif de ce travail a donc été de compléter la caractérisation des processus inflammatoires dépendant des inflammasomes dans les MF, en se focalisant sur les inflammasomes de type NLRP.Les inflammasomes NLRP sont constitués d’un récepteur NLRP, de l’adaptateur ASC et de la pro-caspase-1. Après avoir vérifié la présence de ces acteurs dans les MF à terme, un intérêt particulier a été porté à l’inflammasome de type NLRP7. En effet, sa fonction a déjà été étudiée dans la sphère placentaire mais jamais dans les MF. La stimulation de cellules épithéliales amniocytaires primaires avec un ligand spécifique de l’inflammasome NLRP7 a permis de montrer (i) l’augmentation du niveau protéique des trois acteurs de cet inflammasome (NLRP7, ASC et pro-caspase-1), (ii) la formation de l’inflammasome par co-localisation entre NLRP7 et ASC, (iii) l’activation de cet inflammasome montré par le clivage de deux effecteurs terminaux, la pro-caspase-1 et la gasdermine D. Ces résultats indiquent pour la première fois que les MF sont capables de mettre en jeu la signalisation de l’inflammasome NLRP7 en réponse à un signal pro-inflammatoire.En parallèle, deux activateurs naturels de l’inflammasome NLRP7 ont été identifiés pour la première fois dans les MF humaines à terme : il s’agit de Mycoplasma salivarium et Mycoplasma fermentans. Leur présence suggère le fait que l’inflammasome NLRP7 puisse jouer un rôle majeur dans les processus inflammatoires au sein des MF. L’ensemble de ce travail suggère donc fortement l’implication de l’inflammasome NLRP7 dans la physiopathologie de la rupture des membranes fœtales humaines, qui pourrait être une cible thérapeutique potentielle pour prévenir les ruptures prématurées des membranes fœtales
Inflammation plays a pivotal role in term or preterm fetal membranes (FM) rupture, but the detailed mechanisms remain unclear. In this context, studies on inflammasomes, one of the key inflammation actors, recently intensified. These intracellular platforms, formed following a pro-inflammatory signal, are involved in the establishment and propagation of an inflammatory reaction. Their functions in FM begin to be described but grey areas remain. Thus, the aim of this work was to complete the characterization of inflammasomes-dependent inflammatory processes, focusing on NLRP inflammasomes.NLRP inflammasomes are composed of a NLRP receptor, the adapter ASC and the pro-caspase-1. After verifying the presence of these actors in term human FM, we focused our interest on NLRP7 inflammasome. Indeed, its function has been studied in the placental area but never in FM. The stimulation of primary amnion epithelial cells with an NLRP7 inflammasome specific ligand demonstrated (i) an increased protein level of the three actors of this inflammasome (NLRP7, ASC and pro-caspase-1), (ii) the formation of this inflammasome by NLRP7 and ASC colocalization and (iii) the activation of this inflammasome, by cleavages of two end-effectors, pro-caspase-1 and gasdermin D. These results indicate for the first time that FM are able to activate NLRP7 inflammasome signalization in response to a pro-inflammatory signal. Moreover, two natural activators of NLRP7 inflammasome have been newly identified in term human FM: Mycoplasma salivarium and Mycoplasma fermentans. Their presence suggests that NLRP7 inflammasome could play an essential role in inflammatory processes in FM. All this work strongly suggests the involvement of NLRP7 inflammasome in pathophysiology of human FM rupture, which could be a potential therapeutic target to prevent premature rupture of FM
APA, Harvard, Vancouver, ISO, and other styles
2

Raynal, François. "Les poches de rétraction tympaniques." Caen, 1991. http://www.theses.fr/1991CAEN3109.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bidaux, Gabriel Prevarskaya Natalia. "Caractérisation du canal calcique TRPM8 dans la physiopathologie de la prostate humaine." Villeneuve d'Ascq : Université des sciences et technologies de Lille, 2008. https://iris.univ-lille1.fr/dspace/handle/1908/1143.

Full text
Abstract:
Reproduction de : Thèse de doctorat : Biologie-Santé : Lille 1 : 2006.
N° d'ordre (Lille 1) : 3912. Articles en anglais, reproduits et intégrés au texte. Résumé en français et en anglais. Titre provenant de la page de titre du document numérisé. Bibliogr. p. 310-326. Liste des publications.
APA, Harvard, Vancouver, ISO, and other styles
4

Audard, Vincent. "Rôle de la protéine c-mip dans la physiopathologie du syndrome néphrotique idiopathique." Thesis, Paris Est, 2010. http://www.theses.fr/2010PEST0033.

Full text
Abstract:
Le syndrome néphrotique idiopathique (SNI) est une néphropathie glomérulaire définie par une protéinurie massive associée à une hypoalbuminémie, sans lésions inflammatoires rénales, ni dépôts de complexes immuns circulants. Les travaux réalisés au cours de ma thèse concernent l’étude du rôle potentiel du gène c-mip dans la physiopathologie du SNI.Dans un premier temps, nous avons étudié la physiopathologie moléculaire de l’association maladie de Hodgkin et SNI. Nous avons démontré que cette association était liée à une forte induction de c-mip à la fois dans les cellules de Reed Sternberg (dont la présence signe le lymphome hodgkinien) et les podocytes qui sont des cellules spécialisées du glomérule rénal (Audard, et al. 2010). Nous avons montré que l’induction de c-mip résultait d’un défaut quantitatif et/ou qualitatif du gène Fyn, à la fois chez les patients et dans un modèle de souris déficiente en Fyn. Nous avons trouvé que c-mip était fortement induit dans les podocytes au cours du SNI ainsi que dans la glomérulopathie extramemenbraneuse (GEM). La surexpression de c-mip par transgénèse chez la souris déclenche une protéinurie néphrotique dont le mécanisme implique une rupture, médiée par c-mip, de la voie de signalisation de la néphrine (Science Signaling, 2010 co-auteur). L’étude de la néphrite de Heyman, le modèle expérimental de la GEM humaine, a permis de montrer que l’induction de c-mip coincidait avec l’apparition de la protéinurie et était associée à l’inhibition de l’activité RhoA, à une perte de la synaptopodine, à une diminution du VEGF tandis que l’expression de la DAPK (death-associated protein kinase) est fortement augmentée (Audard et al, manuscrit soumis 1). Nous avons recherché si l’hypogammaglobulinémie au cours du SNI était associée à des anomalies fonctionnelles des lymphocytes B (LB). Nous avons trouvé que c-mip interagit avec la sous unité régulatrice de la PI3 kinase et empêche la dissociation de la sous unité catalytique, p110, nécessaire à l’activation de la PI3 kinase. Enfin, l’expression de l’IL 21, une cytokine–clé secrétée par les lymphocytes T et intervenant dans la commutation isotypique, était fortement réduite dans le SNI (Audard et al, manuscrit en préparation 2). Ces résultats donnent un éclairage nouveau sur la physiopathologie moléculaire du SNI et suggèrent un rôle crucial de c-mip dans les anomalies lymphocytaires et podocytaires observées chez les patients
Idiopathic nephrotic syndrome comprises several podocyte diseases of unknown origin, affecting the glomerular podocyte, which plays a key role in controlling the permeability of the kidney filter to proteins. It is characterized by massive proteinuria and hypoalbuminemia, with no inflammatory lesions or cell infiltration. This works focused on the potential role of c-mip in the pathogenesis of INS. We showed that occurrence of minimal change nephrotic syndrome in the course of Hodgkin lymphoma (cHL-MCNS) is closely related to the induction of c-mip in both Hodgkin-Reed Sternberg cells and podocytes (Audard, et al. 2010), which is caused by a qualitative and/or quantitative defect in Fyn in both HRS and podocytes cells. We found that c-mip is upregulated in podocytes of patients with membranous nephropathy (MN). Transgenic mice overproducing c-mip in the podocytes developed heavy proteinuria without morphological alterations, inflammatory lesions or cell infiltrations. We showed that c-mip turned off podocyte proximal signaling by preventing the interaction between Fyn and nephrin, resulting in the inhibition of nephrin signaling pathway (Science signaling, 2010 coauthor). Moreover, the induction of c-mip in passive type Heymann nephritis (the experimental model of MN) was concomitant to proteinuria occurrence and is associated with reduction of RhoA activity, downregulation of synaptopodin and VEGF expression whereas DAPK expression is significantly increased (Audard et al manuscript submitted 1).We demonstrated that hypogammaglobulinemia, a common feature in INS patients, may result from a defect in B lymphocytes. We found that c-mip interacts with p85 regulatory subunit and prevent its dissociation from p110 catalytic subunit, resulting in inactivation of PI3 kinase. Finally, the expression of IL21, a key cytokine involved in class switching recombination, is repressed in active phases of INS, which may contribute for immunoglobulin disorders commonly observed in these patients (Audard et al manuscript in progress 2).Altogether, these results suggest that c-mip is a major player of lymphocyte and podocytes dysfunction observed in patients with INS
APA, Harvard, Vancouver, ISO, and other styles
5

Gibrat, Isabelle. "Cryoglobulinémie et virus c : physiopathologie et implications thérapeutiques : à propos d'un cas." Montpellier 1, 1996. http://www.theses.fr/1996MON11159.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Mollet, Géraldine. "Physiopathologie de la nephronophtise juvenile : identification de la nephrocystine-4 et caractérisation des partenaires protéiques des nephrocystines." Paris 7, 2003. http://www.theses.fr/2003PA077076.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bidaux, Gabriel. "Caractérisation du canal calcique TRPM8 dans la physiopathologie de la prostate humaine." Lille 1, 2006. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/2006/50376-2006-Bidaux.pdf.

Full text
Abstract:
Seconde cause de mortalité par cancer chez l'individu de sexe masculin, le cancer de la prostate présente une incidence croissante liée à l'augmentation de l'espérance de vie dans les pays développés. Les variations pathologiques d'homéostasie calcique sont connues pour participer à l'évolution du cancer de la prostate. Cette thèse porte sur l'étude du canal ionique TRPM8 dont l'expression est spécifique de la prostate et augmente dans les cellules cancéreuses. Nos résultats montrent que l'expression de TRPM8 est finement régulée par le récepteur aux androgènes dans les cellules épithéliales apicales de la prostate et que son apparition coïncide avec la différenciation terminale de ces cellules. Nous démontrons que le canal est fonctionnel dans le plasmalemme des cellules épithéliales apicales, mais aussi dans la membrane du réticulum endoplasmique. Finalement, en corrélant ces travaux avec d'autres réalisés sur des cellules cancéreuses de la prostate, nous avons proposé un modèle d'évolution de l'activité du canal TRPM8 au cours de la différenciation et de l'oncogenèse des cellules de la prostate. Nous avons, d'autre part, mis en évidence l'existence d'isoformes de TRPM8 dont certaines sont des canaux ioniques fonctionnels alors que d'autres sont des petites protéines tronquées agissant comme sous-unités régulatrices du canal TRPM8. Pour finir, nous avons caractérisé une voie d'activation du canal TRPM8 par la phospholipase A2 indépendante du calcium et nous avons réalisé une étude pharmacologique démontrant l'activation de TRPM8 par une classe de molécules dérivées de l'iciline.
APA, Harvard, Vancouver, ISO, and other styles
8

Laiguillon, Marie-Charlotte. "Implication de deux acteurs métaboliques dans la physiopathologie de l'arthrose : la visfatine/Nampt et le glucose." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066325.

Full text
Abstract:
L’arthrose, maladie articulaire la plus fréquente, se décline en plusieurs phénotypes selon les facteurs de risque : vieillissement, traumatisme et obésité. Dans l’arthrose liée à l’obésité il existe une origine mécanique mais aussi systémique faisant intervenir les adipokines. De plus, chez les sujets obèses, la présence d’un syndrome métabolique, et singulièrement un diabète de type 2 augmente fortement le risque d’arthrose. L’objectif de ce travail a été d’étudier les rôles d’une adipokine, la visfatine/Nampt (nicotinamide phosphoribosyltransférase), et de l’hyperglucidie dans l’arthrose. Ainsi, la visfatine est produite et libérée sous forme dimérique par l’ensemble des tissus articulaires, et son activité enzymatique Nampt est présente dans le tissu synovial. Elle induit un profil pro-inflammatoire des chondrocytes et des ostéoblastes murins caractérisé par la production de cytokines (IL-6, IL -8, MCP-1) qui implique en partie l’activité Nampt, démontré par utilisation de l’inhibiteur pharmacologique APO866. Sur chondrocytes murins, l’hyperglucidie potentialise l’effet de l’IL-1β sur l’activation pro-inflammatoire (IL-6, PGE2), sans stress osmotique. Cette potentialisation pro-inflammatoire passe par l’activation de la voie alternative des polyols, ainsi que par un stress oxydant, démontré par utilisation de l’inhibiteur de l’aldose réductase (epalrestat) et de deux antioxydants (Mitotempo et L-NAME). Chez l’Homme, le cartilage issu de patients arthrosiques diabétiques est plus sensible à l’IL-1β (libération d’IL-6 et de PGE2) et exprime plus l’AGE carboxyméthyllysine, que celui issu de patients non diabétiques de même âge et poids
Osteoarthritis,the most frequent joint disease, can be declined in different phenotypes, depending on its risk factors: aging, trauma and obesity. In obesity-linked osteoarthritis, there is a mechanical stress but also a systemic stress involving adipokines. Moreover, in obese patients, a metabolic syndrome, and particularly a type 2 diabetes, increases the risk of developing osteoarthritis. The aims of the thesis were to study the roles of the adipokine visfatin/Nampt (nicotinamide phosphoribosyltransferase) et high glucose in osteoarthritis. Then, we demonstrate that visfatin is produced and released in an enzymatic dimeric form by all the articular tissues and that its enzymatic activity Nampt is present in synovium. Visfatin/Nampt induces a pro-inflammatory phenotype of murine chondrocytes and osteoblasts characterized by the production of cytokines (IL-6, IL-8, MCP-1), involving in part the enzymatic activity Nampt, demonstrated by using the pharmacological inhibitor APO866. On murine chondrocytes, high glucose potentiates the effect of IL-1β on pro-inflammatory activation (IL-6, PGE2), without inducing an osmotic stress. This potentiation involves the alternative polyol pathway and oxidative stress, demonstrated by using an inhibitor of aldose reductase (epalrestat) and two antioxidants (Mitotempo and L-NAME). In human, the cartilage from osteoarthritic diabetic patients is more sensitive to IL-1β (release of IL-6 and PGE2) and expresses more the AGE carboxymethyllysine than the one from non diabetic patients, of same age and weight
APA, Harvard, Vancouver, ISO, and other styles
9

Eymard, Florent. "Caractérisation des tissus adipeux intra-articulaires du genou et de la hanche arthrosiques et implication du tissu de Hoffa, principal tissu adipeux du genou, dans la physiopathologie de l'arthrose." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066162.

Full text
Abstract:
Les tissus adipeux (TA) intra-articulaires (TAIA) sont présents dans la majorité des articulations, au contact de la membrane synoviale. Le genou est l'articulation la plus riche en TA, comprenant le TA de Hoffa (TAH) et les TA suprapatellaires (TASP). A l'inverse, la hanche ne comprend qu'un petit TA, le TA acétabulaire (TAA). Le TAH de sujets arthrosiques est une source plus importante de cytokines inflammatoires que les TA sous-cutanés (TASC). Nous émettons l'hypothèse que les cytokines sécrétées par les TAH modifient le phénotype de la membrane synoviale arthrosique et que l'ensemble des TAIA partage des caractéristiques histologiques et biologiques communes les distinguant des TASC. Nous avons d'abord montré que la stimulation par les milieux conditionnés de TAH autologues induisait une expression et une libération plus importantes d'IL-6, d'IL-8, de PGE2, de MMP-1, de MMP-3 et de MMP-9 par les synoviocytes fibroblastiques (SF) comparativement aux TASC. La PGE2, sécrétée en plus grande quantité par les TAIA que les TASC (75 fois plus), joue un rôle central dans l'activation des SF. A l'instar des TAH, les autres TAIA de genou et de hanche sécrétent également plus de médiateurs inflammatoires que les TASC. Ils sont le siège de plus de remaniements fibreux, de vaisseaux et d'infiltrats leucocytaires que les TASC. Au sein des TAIA, les adipocytes sont plus petits et l'expression génique des médiateurs du métabolisme lipidique (ATGL, LPL, FABP4 et CD36) diminuée. Les TAIA de genou et de hanche arthrosiques partagent donc un phénotype commun et ont la capacité d'interagir avec la membrane synoviale, pouvant ainsi contribuer à la maladie arthrosique
Intra-articular adipose tissues (IAAT) are located in most joints, lined by synovial membrane. IAAT within the knee are the most numerous and voluminous. They are principally constituted by the infrapatellar fat pad (IFP) and suprapatellar fat pad (SPFP). Inversely, the hip is only constituted by a small single AT, called acetabular fat pad (AFP). Moreover, several studies brought out that IFP from OA patients were a greater source of inflammatory cytokines as compared to subcutaneous AT (SCAT). So, we hypothesized that cytokines released by IFP could modify the phenotype of synovial membrane and also that all IAAT share similar histological, biological and cellular characteristics distinguishing them from SCAT. First, we showed that synoviocyte stimulation by autologous IFP-conditioned media induced a higher gene expression and release of IL-6, IL-8, PGE2, MMP-1, MMP-3 and MMP-9 as compared to SCAT. We also confirmed that IFP released higher rate of inflammatory cytokines than SCAT, particularly PGE2, whom secretion rate was 75 fold higher and which had a central impact in synoviocyte activation. Next, we demonstrated that other IAAT from knee and hip also released higher levels of IL-6, IL-8, and PGE2 as compared to SCAT. IAAT were composed by greater fibrosis remodeling and higher vessel area and leucocyte infiltration as compared to autologous SCAT. In IAAT, adipocytes were smaller and gene expression for most factors involved in lipid metabolism (ATGL, LPL, FABP4 et CD36) were decreased. The specificity of inflammatory secretion and metabolic phenotype were also observed in preadipocytes isolated from knee IAAT and SCAT. To conclude, IAAT from OA knee and hip share a common phenotype and have the ability to interact with synovial membrane, contributing to the onset and/or the progression of OA disease
APA, Harvard, Vancouver, ISO, and other styles
10

Esteve, Clothilde. "Génétique et physiopathologie de la maladie de Charcot-Marie-Tooth de type 4H." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5082.

Full text
Abstract:
CMT4H est une forme de CMT démyélinisant, à transmission autosomique récessive, pour laquelle notre équipe a identifié le gène responsable. Il s'agit du gène FGD4, codant pour FRABIN, protéine de 766 AA possédant 5 domaines fonctionnels: le domaine FAB de liaison à l'actine, un domaine DH responsable de l'échange GDP/GTP, et trois domaines de liaison avec des polyphosphoinositides. C'est une RhoGEF, connue pour activer les RhoGTPases Cdc42 et Rac1.Mon projet de thèse vise à mieux comprendre les bases moléculaires et les mécanismes physiopatologiques qui sous-tendent CMT4H grace à l'étudie de modèles cellulaires et murins. Dans un premier temps, j'ai identifié deux nouvelles mutations dans le gène FGD4. J'ai pu démontrer l'impact fonctionnel des mutations p.Met298fs*8 et p.Ala172Glyfs*27 et une absence totale la protéine dans les fibroblastes de ces patients, donnant lieu à une augmentation de l'activation de Cdc42.L'étude d'un modèle murin d'ablation conditionnelle de FGD4 dans les cellules de Schwann, m'a permis de démontrer la présence d' anomalies myéliniques dans le nerf périphérique de ces souris, ainsi qu'une diminution de l'activation de Cdc42.J'ai également montré, que dans les fibroblastes, FRABIN était localisée au niveau des endomembranes et que l'endocytose semblait déficient dans des cellules de patients. Finalement, l'identification de SNX3,comme partenaire protéique de FRABIN constitue un argument supplémentaire fort en faveur du rôle de FRABIN dans le trafic membranaire.La poursuite de l'étude de nos modèles et de modèles iPS ,permettra de poursuivre l'exploration de ces mécanismes et de mieux comprendre la physiopathologie de la forme CMT4H
Charcot-Marie-Tooth neuropathy type 4H (CMT4H) is an inherited, autosomal recessive, peripheral neuropathy characterized by demyelination of sensory-motor nerves and due to mutations in FGD4. FGD4 encodes FRABIN, a GDP/GTP nucleotide exchange factor (GEF), specific for the GTPase Cdc42, composed of five functional domains: an N-terminal F-actin binding (FAB) domain, one Dbl homology (DH) domain, two pleckstrin homology (PH) domains, and one cysteine-rich FYVE domain.The main goal of my project is to understand the mechanisms leading to the pathology in CMT4H. To this purpose, I studied both cellular and mouse models.First, molecular screening of FGD4 allowed us to identify two additional mutations in FGD4. We also demonstrated a complete absence of the 105 kDa FRABIN isoform in patients homozygous for splicing and frameshift mutations, which unexpectedly was related to abnormally high levels of Cdc42 activation.The study of a mouse model with conditional ablation of fgd4 in Schwann cells, that we have generated, demonstrates the presence of abnormal myelin outfoldings in sciatic nerves from KO mice, which might be linked to decreased levels of Cd42 in mouse sciatic nerves. Finally, altered recycling of transferrin receptors in patients, with complete absence of FRABIN described above, as well as the identification of SNX3, a protein involved in endosomal trafficking, as a partner for FRABIN are new elements that I provide in favour of a role for FRABIN in membrane and cellular trafficking.Still, there are many points to understand, notably the relation between the RhoGTPase and the endosomal pathways, and the study of our models will help answer these questions
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Membranes, physiopathology"

1

Working Party on Platelet Membrane: Biochemistry and Physicology (1987 Villard de Lans, France). Biochemistry and physiopathology of platelet membrane: Proceedings of the Working Party on Platelet Membrane, Biochemistry, and Physiopathology, held in Villard-de-Lans (France) 29-31 January 1987 = Biochimie et physiopathologie de la membrane plaquettaire. Paris: Editions INSERM, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Jelinek, Raz. Lipids and cellular membranes in amyloid diseases. Weinheim: Wiley-VCH, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bkaily, Ghassan, ed. Membrane Physiopathology. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

T, Galeotti, ed. Cell membranes and cancer: Proceedings of the Second International Workshop on Membranes in Tumour Growth, Rome, Italy, June 17-20, 1985. Amsterdam: Elsevier Science, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ron, Wallace. Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

C, Berman Mervyn, Gevers Wieland, Opie Lionel H, and International Union of Biochemistry, eds. Membranes and muscle: Proceedings of an international symposium, Cape Town, Republic of South Africa, March 18-21, 1985. Oxford, U.K: Published for the ICSU Press by IRL Press, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gérard, Marguerie, Zwaal R. F. A, European Thrombosis Research Organisation, and Institut national de la santé et de la recherche médicale (France), eds. Biochemistry and physiopathology of platelet membrane =: Biochimie et physiopathologie de la membrane plaquettaire : proceedings of the Working Party on Platelet Membrane : Biochemistry and Physiopathology, held in Villard-de-Lans (France), 29-31 Januagy 1987. London: Libbey, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ėĭdus, L. Kh. Membrannyĭ mekhanizm biologicheskogo deĭstvii͡a︡ malykh doz: Novyĭ vzgli͡a︡d na problemu. Moskva: In-t teoreticheskoĭ i ėksperimentalʹnoĭ biofiziki Rossiĭskoĭ akademii nauk, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Brian, Henderson. The Synovial lining in health and disease. London: Chapman and Hall, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Membranes, physiopathology"

1

Boivin, Dominique, Denis Gingras, and Richard Béliveau. "Carboxyl Methylation of Proteins in Kidney Membranes: Implications in the Repair of Damaged Proteins and in Signal Transduction." In Membrane Physiopathology, 227–48. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Jasmin, Gaétan, and Libuse Proschek. "Hamster Cardiomyopathy: New Insights in the Pathogenesis of this Hereditary Disease." In Membrane Physiopathology, 1–11. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Sperelakis, Nicholas, Zhiling Xiong, and John Lorenz. "Regulation of Ca2+ Channels in Vascular Smooth Muscle Cells by Cyclic Nucleotides and by G-Protein Gating." In Membrane Physiopathology, 155–72. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bkaily, Ghassan, Pedro d’Orléans-Juste, Radha Naik, Demetri Economos, Shimin Wang, Elias Abdulnour, and Jean-Luc Ardilouze. "Role of the R-Type Ca2+ Channel in Cardiovascular Physiopathology." In Membrane Physiopathology, 173–83. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Plante, Gérard E., and Mouna Chakir. "Passive Endothelial Transport: Studies in Experimental Arterial Hypertension, Diabetes Mellitus and Chronic Renal Failure." In Membrane Physiopathology, 185–206. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

D’Orléans-Juste, Pedro, and Sabine Télémaque. "Pharmacology of the Human Precursors of Endothelin: Role of Functional Receptors and Endothelin-Converting Enzyme." In Membrane Physiopathology, 207–26. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sahai, Animesh, and Pallab K. Ganguly. "Transport Systems in Kidney Basolateral Membrane: Pathophysiologic Implications." In Membrane Physiopathology, 249–70. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Bikhazi, Anwar B., George E. Haddad, Habib M. Alloush, Fadia H. Uthman, Najla A. Fakruddin, and Muna El-Kasti. "Effect of Insulin and Glucagon on Hepatocellular Alanine Uptake in Normal and Streptozocin-Induced Diabetic Rats." In Membrane Physiopathology, 271–89. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Liu, Kanzhi, and Grant N. Pierce. "The Modulation of Membrane Ion Movements by Cholesterol." In Membrane Physiopathology, 291–317. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Ménard, Daniel, and Jean-François Beaulieu. "Human Intestinal Brush Border Membrane Hydrolases." In Membrane Physiopathology, 319–41. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Membranes, physiopathology' for particular source types:
Journal articles Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography