Relevant bibliographies by topics / Antiporno

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

Academic literature on the topic 'Antiporno'

Author: Grafiati
Published: 25 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Antiporno"

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Tonnessen, T. I., K. Sandvig, and S. Olsnes. "Role of Na(+)-H+ and Cl(-)-HCO3- antiports in the regulation of cytosolic pH near neutrality." American Journal of Physiology-Cell Physiology 258, no. 6 (June 1, 1990): C1117—C1126. http://dx.doi.org/10.1152/ajpcell.1990.258.6.c1117.

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In Vero cells, Na(+)-H+ antiport as well as Na(+)-coupled and Na(+)-independent Cl(-)-HCO3- antiport are involved in regulation of cytosolic pH (pHi) after large (unphysiological) deviations from neutrality. In this paper we have studied to which extent each of the three antiports is involved in regulation of pHi after small deviations from neutrality expected to occur under physiological conditions. At physiological extracellular pH (pHo), inhibition of Na(+)-H+ exchange by amiloride did not alter pHi. At neutral and alkaline pHo, pHi was found to be lower in the presence of HCO3- than in its absence, whereas at acidic pHo, pHi was higher in the presence of HCO3- than in its nominal absence. Above pHi 6.5, the activity of the Na(+)-coupled Cl(-)-HCO3- antiport was higher than the Na(+)-H+ antiport. After a small reduction of pHi, the recovery of steady-state pHi was entirely dependent on Na(+)-coupled Cl(-)-HCO3- antiport, whereas after more pronounced acidification, also Na(+)-H+ exchange contributed to the acid extrusion. The Na(+)-independent Cl(-)-HCO3- antiport, which acts as an acidifying mechanism, was strongly activated at pHi greater than 7.1. The results indicate that at physiological pHo the steady-state pHi is largely determined by the activity of the two Cl(-)-HCO3- antiports, and they suggest that Na(+)-H+ exchange does not influence the resting pHi under these conditions.
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Cheng, J., K. Baldwin, A. A. Guffanti, and T. A. Krulwich. "Na+/H+ antiport activity conferred by Bacillus subtilis tetA(L), a 5' truncation product of tetA(L), and related plasmid genes upon Escherichia coli." Antimicrobial Agents and Chemotherapy 40, no. 4 (April 1996): 852–57. http://dx.doi.org/10.1128/aac.40.4.852.

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An Escherichia coli transformant expressing the Bacillus subtilis tetA(L) gene from a weak promoter was challenged by growth on medium with low, increasing tetracycline concentrations. Changes in the substrate preference ratios of the TetA(L)-mediated resistances and antiports were examined in view of recent findings suggesting that TetA(L) catalyzes efflux of Na+ in exchange for protons in addition to having the ability to catalyze metal-tetracycline/H+ antiport. After growth of the transformant on 1 microgram or more of tetracycline per ml for 12 to 15 h, the tetA(L) gene in the plasmid was found to be disrupted by an IS10 element 50 bp from the 5' end of the coding sequence. This disrupted recombinant plasmid, pKB1, conferred greater tetracycline resistance and higher levels of membrane metal-tetracycline/proton antiport than the original plasmid, pJTA1, but conferred lower NA+ resistance and Na+/H+ antiport levels than the original plasmid. The results indicate that the 5' end of the gene is necessary for optimal Na+/H+ antiport but that some such activity as well as robust tetracycline/H+ antiport persists in its absence. Two plasmid genes, tet(K) and qacA, were compared with tetA(L) vis-à-vis their abilities to enhance the Na+/H+ antiporter activity of everted vesicles from E. coli transformants. tet(K), which is more closely related to tetA(L), catalyzed 22Na+ uptake by energized vesicles, whereas the less closely related qacA gene did not.
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Houle, Karen. "Antiporn Cons and Pros." International Studies in Philosophy 30, no. 1 (1998): 79–90. http://dx.doi.org/10.5840/intstudphil1998301110.

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Eaton, A. W. "A Sensible Antiporn Feminism." Ethics 117, no. 4 (July 2007): 674–715. http://dx.doi.org/10.1086/519226.

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CAVALIERE, MATTEO, and VINCENZO DEUFEMIA. "FURTHER RESULTS ON TIME-FREE P SYSTEMS." International Journal of Foundations of Computer Science 17, no. 01 (February 2006): 69–89. http://dx.doi.org/10.1142/s012905410600370x.

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Membrane systems (currently called P systems) are parallel computing devices inspired by the structure and the functioning of living cells. A standard feature of P systems is that each rule is executed in exactly one time unit. Actually, in living cells different chemical reactions might take different times to be executed; moreover, it might be hard to know precisely such time of execution. For this reason, in [7] two models of P systems (time-free and clock-free P systems) have been defined and investigated, where the time of execution of the rules is arbitrary and the output produced by the system is always the same, independently of this time. Preliminary results concerning time-free and clock-free P system have been obtained in [6, 7, 8]. In this paper we continue these investigations by considering different combinations of possible ingredients. In particular, we present the universality of time-free P systems using bi-stable catalysts. Then, we prove that this result implies that is not possible to decide whether an arbitrary bi-stable catalytic P system is time-free. We present several results about time-free evolution-communication P systems, where the computation is a mixed application of evolution and symport/antiport rules. In this case we obtain the universality even by using non-cooperative evolution rules and antiports of weight one. Finally, we formulate several open problems.
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Ng, L. L., P. Delva, and J. E. Davies. "Intracellular pH regulation of SV-40 virus transformed human MRC-5 fibroblasts and cell membrane cholesterol." American Journal of Physiology-Cell Physiology 264, no. 4 (April 1, 1993): C789—C793. http://dx.doi.org/10.1152/ajpcell.1993.264.4.c789.

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Alterations in membrane cholesterol could affect the activity of various membrane transporters, including the Na(+)-H+ antiport. The effect of cellular cholesterol depletion (with phosphatidylcholine liposomes) and enrichment (with cholesterol and phosphatidylcholine liposomes) on cellular pH regulation was studied in SV-40 virus transformed human MRC-5 fibroblasts. Cellular cholesterol depletion led to activation of the Na(+)-H+ antiport by an increased maximal velocity (Vmax) of the transporter, with no changes in the apparent dissociation constant (Kd) or Hill coefficient for intracellular H+. Cholesterol enrichment had no effect on the activation of the Na(+)-H+ antiport by intracellular acidosis. However, activation of the Na(+)-H+ antiport by an osmotic stimulus was enhanced in cholesterol-depleted cells and reduced in cholesterol-enriched cells. Liposomes that had no effect on cellular cholesterol did not alter the activation of Na(+)-H+ antiport activity by intracellular acidosis or an osmotic stimulus. Thus in situ modification of cellular cholesterol altered Na(+)-H+ antiport activity differently depending on the type of activating stimulus.
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Cutaia, M. V., N. Parks, J. Centracchio, S. Rounds, K. P. Yip, and A. M. Sun. "Effect of hypoxic exposure on Na+/H+antiport activity, isoform expression, and localization in endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 3 (September 1, 1998): L442—L451. http://dx.doi.org/10.1152/ajplung.1998.275.3.l442.

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Little is known about the effects of prolonged hypoxic exposure on membrane ion transport activity. The Na+/H+antiport is an ion transport site that regulates intracellular pH in mammalian cells. We determined the effect of prolonged hypoxic exposure on human pulmonary arterial endothelial cell antiport activity, gene expression, and localization. Monolayers were incubated under hypoxic or normoxic conditions for 72 h. Antiport activity was determined as the rate of recovery from intracellular acidosis. Antiport isoform identification and gene expression were determined with RT-PCR and Northern and Western blots. Antiport localization and F-actin cytoskeleton organization were defined with immunofluorescent staining. Prolonged hypoxic exposure decreased antiport activity, with no change in cell viability compared with normoxic control cells. One antiport isoform [Na+/H+exchanger isoform (NHE) 1] that was localized to the basolateral cell surface was present in human pulmonary arterial endothelial cells. Hypoxic exposure had no effect on NHE1 mRNA transcript expression, but NHE1 protein expression was upregulated. Immunofluorescent staining demonstrated a significant alteration of the F-actin cytoskeleton after hypoxic exposure but no change in NHE1 localization. These results demonstrate that the decrease in NHE1 activity after prolonged hypoxic exposure is not related to altered gene expression. The change in NHE1 activity may have important consequences for vascular function.
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Southworth, Thomas W., Arthur A. Guffanti, Anne Moir, and Terry A. Krulwich. "GerN, an Endospore Germination Protein ofBacillus cereus, Is an Na+/H+-K+ Antiporter." Journal of Bacteriology 183, no. 20 (October 15, 2001): 5896–903. http://dx.doi.org/10.1128/jb.183.20.5896-5903.2001.

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ABSTRACT GerN, a Bacillus cereus spore germination protein, exhibits homology to a widely distributed group of putative cation transporters or channel proteins. GerN complemented the Na+-sensitive phenotype of an Escherichia coli mutant that is deficient in Na+/H+ antiport activity (strain KNabc). GerN also reduced the concentration of K+ required to support growth of an E. coli mutant deficient in K+ uptake (strain TK2420). In a fluorescence-based assay of evertedE. coli KNabc membrane vesicles, GerN exhibited robust Na+/H+ antiport activity, with a Km for Na+ estimated at 1.5 mM at pH 8.0 and 25 mM at pH 7.0. Li+, but not K+, served as a substrate. GerN-mediated Na+/H+ antiport was further demonstrated in everted vesicles as energy-dependent accumulation of 22Na+. GerN also used K+ as a coupling ion without completely replacing H+, as indicated by partial inhibition by K+ of H+ uptake into right-side-out vesicles loaded with Na+. K+translocation as part of the antiport was supported by the stimulatory effect of intravesicular K+ on22Na+ uptake by everted vesicles and the dependence of GerN-mediated86Rb+ efflux on the presence of Na+ in trans. The inhibitory patterns of protonophore and thiocyanate were most consistent with an electrogenic Na+/H+-K+antiport. GerN-mediated Na+/H+-K+antiport was much more rapid than GerN-mediated Na+/H+ antiport.
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Jin, Jie, Arthur A. Guffanti, Catherine Beck, and Terry A. Krulwich. "Twelve-Transmembrane-Segment (TMS) Version (ΔTMS VII-VIII) of the 14-TMS Tet(L) Antibiotic Resistance Protein Retains Monovalent Cation Transport Modes but Lacks Tetracycline Efflux Capacity." Journal of Bacteriology 183, no. 8 (April 15, 2001): 2667–71. http://dx.doi.org/10.1128/jb.183.8.2667-2671.2001.

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ABSTRACT A “Tet(L)-12” version of Tet(L), a tetracycline efflux protein with 14 transmembrane segments (TMS), was constructed by deletion of two central TMS. Tet(L)-12 catalyzed Na+/H+antiport and antiport with K+ as a coupling ion as well as or better than wild-type Tet(L) but exhibited no tetracycline-Me2+/H+ antiport inEscherichia coli vesicles.
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Incerpi, S., S. Spagnuolo, F. Terenzi, and S. Leoni. "EGF modulation of Na+/H+ antiport in rat hepatocytes: different sensitivity in adult and fetal cells." American Journal of Physiology-Cell Physiology 270, no. 3 (March 1, 1996): C841—C847. http://dx.doi.org/10.1152/ajpcell.1996.270.3.c841.

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The modulation by epidermal growth factor (EGF) of the Na+/H+ antiport in fetal and adult rat hepatocytes was studied in nominally HCO3- free solution. EGF (10 nM) activated the antiport in adult rat hepatocytes by 0.22 +/- 0.03 (mean +/- SD;n=10) pH units over basal value, measured with the fluorescent pH-sensitive intracellular probe, 2',7'-bis(carboxyethyl)-5(6)- carboxyfluorescein (BCECF). The effect of EGF was inhibited by amiloride analogue 5-(N-ethyl-N-isopropyl) amiloride (EIPA), by ouabain, inhibitor of the Na+ pump, and by erbstatin analogue, an inhibitor of the tyrosine kinase activity of the EGF receptor. The effect of EGF on Na+/H+ antiport in adult rat hepatocytes appeared to be mediated by both protein kinase C (PKC) and G protein system. No effect of EGF and phorbol 12-myristate 13-acetate, an activator of PKC, on the Na+/H+ antiport was observed in fetal hepatocytes of 20 and 22 days. A different sensitivity of the antiport to high concentrations of amiloride and EIPA suggests that altered amount of the Na+/H+ antiport units or different isoforms could be expressed in fetal compared with adult cells.
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Dissertations / Theses on the topic "Antiporno"

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Hjelm, Zara Luna. "Mirror, Mirror : Embodying the sexed posthuman body of becoming in Sion Sono’s Antiporno (アンチポルノ, 2016) and Mika Ninagawa’s Helter Skelter (ヘルタースケルター, 2012)." Thesis, Linköpings universitet, Tema Genus, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-177284.

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This thesis examines the embodiment of the sexed body and the struggle of fitting into the narrow frames of what a woman is supposed to behave and look like in Japanese cinema. Using the medium of film, I, therefore, seek to produce knowledge regarding the internalized gaze of the oppressor, and self-objectification, caused by the capitalist heteropatriarchy. Thus, I am drawing from cyborg feminism, and the second wave of sexual difference theory’s concept of becoming, expanded upon by the Italian-Australian philosopher Rosi Braidotti. I further use the French sociologist Pierre Bourdieu’s notion of masculine domination and the American philosopher Gayle Rubin’s charmed circle, in creating a theoretical framework, and using the methods of cultural and feminist film analysis to contextualize the films and locate the subjectification of the women. The movies that I will be analyzing are the Japanese director and poet Sion Sono’s Antiporno (アンチポルノ, 2016) and the Japanese director and photographer Mika Ninagawa’s Helter Skelter (ヘルタースケルター, 2012), which both center around two women and their struggle in becoming-cyborg, in relation to power, trauma, sexuality, technology, and beauty ideals in ‘modernized’ Japan. In that sense, I will study the phenomenon of operating outside the lines of social norms of femininity and desire.
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Matranga, Andrea [Verfasser]. "Antiinflammatorische Effekte des Na+/H+-Antiport-Inhibitors Cariporide / Andrea Matranga." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1026883458/34.

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Duan, Shili. "Cloning and characterization of an Arabidopsis thaliana vacuolar Na§+/H§+ antiport-AtNHX3." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62905.pdf.

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Pataro, Carla. "Efeitos biológicos do amiloride em herpetomonas samuelpessoai: evidência da presença do antiporte Na+/H+." Universidade Federal de Minas Gerais, 1994. http://hdl.handle.net/1843/BUOS-9BHKRY.

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Os tripanosomatídeos são protozoários flagelados pertencentes à ordem Kinetoplastida (HONIBERG et al., 1964). São caracterizados por possuírem uma única mitocôndria que percorre toda extensão da célula, na qual se localiza o cinetoplasto, composto por uma rede de fibras circulares de DNA, unidas entre si (HOARE & WALLACE, 1966; CAMARGO, 1979). Encontram-se comumente parasitando animais invertebrados, vertebrados e plantas (VICKERMAN, 1976). Dentre os membros da família Trypanosomatidae, os gêneros Trypanosoma e Leishmania são constituídos de protozoários digenéticos de vertebrados e insetos (CAMARGO, 1979) e são os que mais despertam interesse em medicina humana e veterinária (CANÇADO, 1968). Os graves problemas implicados nas doenças causadas por algumas espécies destes gêneros, tem atraído o interesse de um grande número de pesquisadores para o estudo da biologia dos membros da família Trypanosomatidae. Entre estes incluem-se não só os que se dedicam aos problemas de ordem prática relativos ao controle das tripanosomíases, mas também os voltados para os problemas biológicos de interesse mais geral, que vão desde os estudos filogenéticos até os relacionados com a ultraestrutura e biologia molecular
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VIMONT, SOPHIE. "Role des antiports na +/h + dans la physiologie et la virulence de vibrio cholerae o1." Paris 7, 2000. http://www.theses.fr/2000PA077231.

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Vibrio cholerae, l'agent du cholera est une bacterie halotolerante capable de survivre dans les environnements sales. Chez escherichia coli, l'expulsion du sodium est liee a un flux de h + via un antiport na +/h + qui permet de maintenir un gradient de na + sur une large gamme de concentration de na + extracellulaire. L'extrusion du na + jouerait egalement un role dans la regulation du ph intracytoplasmique. Le but de ce travail etait d'etudier le role des antiports na + /h + dans la survie et la virulence de v. Cholerae. En effet, de tels mecanismes doivent permettre a la bacterie de maintenir son homeostasie intracellulaire (na + et ph) en fonction des variations de son environnement. Nous avons etudie 3 antiports de v. Cholerae : nhaa, nhab et nhad. Nous avons montre que ces trois proteines ont une fonction antiport na +(li +)/h + en restaurant la croissance d'un mutant nhaab, chaa de e. Coli en milieu sale (0,2m nacl, ph 7,5, et 0,01m licl, ph 7,5). Les genes nhaa, nhab et nhad ont ete inactives et l'etude de la croissance des mutants a ete realisee en presence de na + et de li +. Un mutant nhaa ne pousse plus en licl 120 mm a ph 8,5. Il en est de meme pour les mutants nhaab, nhaad et nhaabd. En revanche, a la difference des mutants nhaa ou nhaab de e. Coli, les mutants nhaa, nhab, nhad, nhaab, nhaad, nhabd et nhaabd de v. Cholerae continuent de croitre a differentes concentrations de nacl. L'inactivation des antiports n'entraine pas de difference de virulence chez le souriceau. L'absence de phenotype de ces mutants suggere qu'il existerait d'autres antiports na +/h +. L'analyse recente de la sequence complete du genome de la bacterie a permis de mettre en evidence la presence de 3 autres antiports putatifs : yqki, nhap, nhac-1. Notre travail constitue la premiere etude des antiports de v. Cholerae. Une etude plus complete du cycle du na + permettrait de mieux comprendre les facteurs qui contribuent a sa survie dans l'environnement et au cours du processus infectieux chez l'hote.
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Saleh, Basel. "Contribution à l'étude des déterminants physiologiques, génétiques et moléculaires de la tolérance des agrumes à la salinité." Montpellier, ENSA, 2005. http://www.theses.fr/2005ENSA0003.

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Une étude de l'impact de la polyploïdie sur des indicateurs physiologiques précoces de la tolérance au sel chez les agrumes a été réalisée. De même, une étude de la diversité du gène cNHXI potentiellement impliqué dans la compartimentation vacuolaire du sodium a été initiée. L'évaluation in vitro de l'aptitude des porte-greffe à compartimenter les ions sodium et chlorures a apporté des résultats contradictoires par rapport aux comportements physiologiques observés sur jeunes plants et sur des plants âgés de 3 ans franc de pied ou greffés. Les porte-greffe sensibles (Poncirus et Citranges) favorisent le transport des chlorures vers les feuilles et limitent celui du sodium tandis que les porte-greffe du genre Citrus réputés tolérants présentent un comportement inverse. De même, la tétraploïdie favorise la tolérance en condition de stress salin. La croissance des autotétraploïdes dans ces conditions est meilleure que celle des parents diploïdes, et les symptômes foliaires (brûlures et défoliations) sont moins marqués. Enfin l'hybride somatique allotétrapoïde FLHORAGI présente lui une limitation du transport des ions sodium et chlorures vers les feuilles. La diversité du gène cNHXl hétérologue de l'antiport Na+nr, a permis de monter que ce gène n'est présent qu'en une seule copie chez les agrumes. Il apparaît que pour l'ensemble des espèces du genre Citrus les séquences génomiques sont très proches, alors que le Poncirus, considéré comme un excluant du sodium, présente une délétion de 54 paires de bases en 5' et une insertion de 70 bases en 3'. L'ensemble de ces résultats souligne l'intérêt des porte-greffe tétraploïdes vis-à-vis de la tolérance au stress salin et la nécessité de les étudier au niveau physiologique et moléculaire
The impact of ploidy on early physiological indicators of salt tolerance in citrus has been studied. We also examined the genetic diversity of the cNHXl gene that is involved in the accumulation of sodium in vacuolar compartment. Ln vitro tests on the ability of a rootstock to translocate chloride and sodium ions was not in agreement with the results we obtained on 1 year and 3 years old plants grafted or not. Sensitive rootstocks (Poncirus and Citrange) promoted the transport of chloride ions to leaves and limited the ones of sodium. On the other hand, tolerant rootstocks from the genus Citrus presented an opposite pattern. As weIl, our results shown that tetraploid had a better growth when compared to parental diploid plants. Moreover, symptoms of chlorosis and bum were observed. The somatic allotetraploid, hybrid FLHORAG 1 presented a limitation in sodium and chloride transport in the leaves. Genetic diversity of the Na+/H+ exchanger gene shown that this gene was present only in one single copy in the citrus genome. Moreover, it seems that for all species of the genus Citrus, the genomic sequences were very similar. However, for Poncirus that is believed to exclude sodium, has a deletion of 54 pair bases in the 5' region and an insertion of 70 pair bases in the 3' region. These results underline the interest of tetraploid rootstocks for their tolerance to salt stress. It is then necessary to study such rootstocks at the physiological and molecular level
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Delvaulx, Michel. "Antiport Na+/H+ des cellules acineuses pancréatiques : régulation par les peptides neuro-digestifs et rôle dans la prolifération cellulaire." Toulouse 3, 1990. http://www.theses.fr/1990TOU30009.

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L'antiport na/h est un mecanisme de transport membranaire, echangeant un ion na pour un proton. L'activation de cet echange par la cck et la gastrine conduit a une augmentation du ph intracellulaire. L'effet de la cck est medie par le recepteur cck et semble impliquer la stimulation de la kinase c. L'activation de l'antiport par la gastrine ne passe pas par le recepteur cck a. L'antiport na/h est egalement present au niveau de la lignee cellulaire ar4-2j, derivee d'un cancer pancreatique de rat et presente les memes caracteristiques pharmacologiques: dependance vis-a-vis des concentrations externes en na, inhibition par l'amiloride. L'activation de l'echange na/h et la stimulation de la proliferation cellulaire par le serum de veau ftal sont correlees. L'amiloride et ses analogues inhibent echange na/h et proliferation cellulaire aux memes concentrations, temoignant du role de l'antiport dans le controle de la proliferation de cette lignee cellulaire. D'autres agents sont capables de stimuler l'echange na/h sans etre des facteurs de croissances, indiquant que d'autres processus metaboliques sont controles par l'activation de l'antiport na/h, notamment des phenomenes d'hypertrophie cellulaire
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Kalayil, Sissy Verfasser], Werner [Akademischer Betreuer] [Kühlbrandt, and Volker [Akademischer Betreuer] Dötsch. "Insights into the mechanism of substrate/product antiport by CaiT / Sissy Kalayil. Betreuer: Werner Kühlbrandt. Gutachter: Volker Dötsch ; Werner Kühlbrandt." Frankfurt am Main : Univ.-Bibliothek Frankfurt am Main, 2016. http://d-nb.info/1083227432/34.

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Bartsch, Anna Margarida [Verfasser], Reinhard [Akademischer Betreuer] Krämer, and Ulf-Ingo [Akademischer Betreuer] Flügge. "Identification and functional characterization of cation/proton antiport systems in Corynebacterium glutamicum / Anna Margarida Bartsch. Gutachter: Reinhard Krämer ; Ulf-Ingo Flügge." Köln : Universitäts- und Stadtbibliothek Köln, 2014. http://d-nb.info/1065374518/34.

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Flinois, Thomas. "Modification d'électrodes par des films redox-actifs, des lipides et des transporteurs ioniques membranaires : vers l'élaboration d'une pile biomimétique." Thesis, Rennes 1, 2019. http://www.theses.fr/2019REN1S093.

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En s'inspirant des processus transmembranaires de transport d'ions à l'œuvre dans les cellules vivantes, la conception d'une pile biomimétique peut être envisagée. Le principe de cette pile est d'utiliser les gradients de concentration en ions ou en protons induits par la protéine NhaA, un antiport transmembranaire Na+/2H+, pour générer de l'énergie électrique. Cette thèse contribue à l'élaboration de cette pile à travers des modifications d'électrodes permettant de détecter l'activité de transporteurs ioniques à l'interface électrode / membrane biomimétique. Une revue bibliographique des aspects fondamentaux des membranes cellulaires et du principe de la pile est présentée. Des électrodes modifiées par électrodéposition de dérivés d'acides salicyliques ont permis l'obtention de films redox-actifs sensibles aux variations de pH ou à la concentration en ions monovalents et monoatomiques. La stabilité du dépôt lipidique sur électrode a été significativement augmentée par l'électro-greffage de la 4-decylaniline. Ce dépôt lipidique stable dans le temps permet d'obtenir des membranes biomimétiques et l'insertion de transporteurs ioniques. L'activité des transporteurs ioniques insérés dans les membranes biomimétiques est suivi à travers les variations de potentiel dépendant du pH ou de la concentration en ions sodium ou potassium à l'interface électrode/membrane
Based on the transmembrane ion transport processes of living cells, the design of a biomimetic fuel cell can be considered. Its principle relies on ion or proton concentration gradients induced by the protein NhaA, a transmembrane Na+/2H+ antiport, to generate electrical energy. This thesis contributes to the development of this device through electrode modifications to detect the activity of ionic transporters at the electrode/biomimetic membrane interface.A bibliographic review of the fundamental aspects of cell membranes and of the biomimetic fuel cell principle is presented. Electrodes modified by electrodeposition of salicylic acid derivatives have yielded redox-active films sensitive to pH changes or monovalent and monoatomic ions concentration. The stability of the lipid deposit onto the electrodes was significantly increased by the electrografting of 4-decylaniline. This anchored and stable lipid deposit makes it possible to obtain biomimetic membranes allowing the insertion of ionic transporters. The activity of the ion carriers inserted into the biomimetic membranes has been monitored through the redox-active films' potential that is dependent on pH or on sodium or potassium ions concentrations at the electrode/membrane interface
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Books on the topic "Antiporno"

1

Mountes, Matthaios. Ta antipoina: Poiēsē. 2nd ed. Athēna: Kastaniōtēs, 1993.

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Villiers, Gérard de. Antipoina gia ten ptese 800. Athens: Papyrus, 1997.

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Le porte della storia: L'età moderna attraverso antiporte e frontespizi figurati. Roma: Viella, 2012.

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Grammatikas, Vasileios E. Ta enopla antipoina kai hē thesē tous stē synchronē diethnē pragmatikotēta. Athēna: Ekdoseis Ant. N. Sakkoula, 2002.

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Stampolidēs, Nikolaos Chr. "Antipoina": Symvolē stē meletē tōn ēthōn kai tōn ethimōn tēs geōmetrikēs-archaikēs periodou. Rethymno: [s.n.], 1996.

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Barkla, Bronwyn Jane. Characterization and identification of the vacuolar Nap+s/Hp+s antiport of Beta vulgaris. Ottawa: National Library of Canada, 1990.

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Media, and Gender Policy Conference (1997 Antipolo Philippines). Engendering communication policy in Asia: Papers presented at the Media and Gender Policy Conference in Antipolo, The Philippines, 1997. New Delhi: The Asian Network of Women in Communication, 1997.

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Alejandro, Reynaldo G. Tahanan: A house reborn. [Malabon City]: Duende Pub., 2003.

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Seminar, on the State-of-the-Art of Filipiniana Collections in the Philippines (2000 Antipolo Philippines). The proceedings on the state of the art of Filipiniana collections in the Philippines in commemoration of the 40th anniversary of the Lopez Memorial Museum, Eugenio López Center, Sumulong Highway, Antipolo, 29 November 2000. [Pasig City]: Eugenio López Foundation, 2000.

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Yasunobu, Suketa, and Excerpta Medica (Firm), eds. Control and diseases of sodium dependent transport proteins and ion channels: Proceedings of the First International Conference held in Shizuoka, Japan, 24-28th August 1999. Amsterdam: Elsevier, 2000.

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Book chapters on the topic "Antiporno"

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Gooch, Jan W. "Antiport." In Encyclopedic Dictionary of Polymers, 875. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13154.

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Eaton, A. W. "A Sensible Antiporn Feminism." In Aesthetics, 470–74. 4 [edition]. | New York : Routledge, 2017.: Routledge, 2017. http://dx.doi.org/10.4324/9781315303673-94.

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Lynch, Gordon S., David G. Harrison, Hanjoong Jo, Charles Searles, Philippe Connes, Christopher E. Kline, C. Castagna, et al. "Sodium/Proton Antiport." In Encyclopedia of Exercise Medicine in Health and Disease, 797. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4526.

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Ibarra, Oscar H., and Sara Woodworth. "On Bounded Symport/Antiport P Systems." In DNA Computing, 129–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11753681_10.

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Ibarra, Oscar H., and Sara Woodworth. "On Nonuniversal Symport/Antiport P Systems." In Algorithmic Bioprocesses, 229–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-88869-7_14.

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Brierley, Gerald P., and Dennis W. Jung. "Monovalent Cation Antiport Reactions in Isolated Mitochondria." In Advances in Experimental Medicine and Biology, 47–57. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0007-7_5.

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Nagda, Hitesh, Andrei Păun, and Alfonso Rodríguez-Patón. "P Systems with Symport/Antiport and Time." In Membrane Computing, 463–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11963516_29.

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Verlan, Sergey. "Tissue P Systems with Minimal Symport/Antiport." In Developments in Language Theory, 418–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-30550-7_35.

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Zörb, C., J. Wiese, and S. Schubert. "Molecular insights into maize Na+/H+ antiport." In Plant Nutrition, 58–59. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/0-306-47624-x_27.

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Ibarra, Oscar H., Sara Woodworth, Hsu-Chun Yen, and Zhe Dang. "On Symport/Antiport P Systems and Semilinear Sets." In Membrane Computing, 253–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11603047_18.

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Conference papers on the topic "Antiporno"

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Yun Jiang, Shuo Wang, and Jinbang Xu. "Symport/antiport P systems with look-ahead mode." In 2010 IEEE Fifth International Conference on Bio-Inspired Computing: Theories and Applications (BIC-TA). IEEE, 2010. http://dx.doi.org/10.1109/bicta.2010.5645200.

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Ibarra, O. H., and S. Woodworth. "On symport/antiport P systems with one or two symbols." In Seventh International Symposium on Symbolic and Numeric Algorithms for Scientific Computing (SYNASC'05). IEEE, 2005. http://dx.doi.org/10.1109/synasc.2005.52.

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Akkerman, JW N. "INTRACELLULAR PH CHANGES AND PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644774.

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Abstract:
It is long known that platelet aggregation and secretion are accompanied by acidification of the extracellular medium. Much of the proton extrusion results from hydrolysis of ATP generated in the glycolytic pathway and liberation of secretion granules, which are slightly acidic. Recent eyidence points at a third source for extracellular protons.Following early observations (1) that epinephrine-induced platelet functions depended on extracellular Na+ (Na+ o ), it became evident that platelets possess a Na+ /H+ antiport, which regulates the cytosolic pH (pH.) via stochiometric exchange of intracellular protons with extracellular Na+ (2). Platelet functions triggered by epinephrine, AdP or low doses of thrombin are impaired by (i) the absence of Na+ o, and (ii) the presence of EIPA, an amiloride analogue which blocks the antiport. Ionophores which enhance proton efflux enhance the platelet responses. Thus, the antiport affects platelet functions via changes in pHi, but this has been difficult to establish experimentally. Early studies by Simons based on 6-carboxyfluorescein indeed reported a rise in pHi. during platelet activation, but more precise analysis awaited the development of more sensitive pHi-indicators. Recently (3),1studies employing BCECF, have confirmed that resting platelets maintain a pH. of about 7.1 via an EIPA-sensitive mechanism.Platelet activation induces a rise of 0.1-0.2 pH units, which lasts for several minutes unless the antiport is inhibited. When Na+/H+ exchange is gradually inhibited by lowering Na+ o , EIPA-sensitive proton efflux, mobilization of Ca2+ ions and aggregation are inhibited in parallel following stimulation with a low dose of thrombin. Artificial alkalinization reverses these effects. Alkalinization alone is not a trigger for platelet functions. Furthermore, high doses of thrombin (> 0.2 U/ml) initiate Ca2+ -mobilization and aggregation independent of changes in pHi Possibly, Na+ /H+ exchange enhances Ca mobilization by inositol-P3, generated by weak stimulation of the thrombin receptor, wfiich accords with the pH profile of IP3-induced Ca2+ liberation from isolated dense tubular membranes. However, concurrent measurement of Quin-2 and BCECF-fluoresence indicate that Ca2+ mobilization slightly precedes the rise in pHi which would make Ca+ mobilization a trigger for Na+ /H+ exchange is stead of one of its effects. Recent data favour a role for protein kinase C in activation of the antiport. A rise in pHi. is seen during incubation with OAG, an activator of protein kinase C. Thrombin (low dose)-induced Na /H exchange is inhibited by TFP, an inhibitor of this enzyme. These findings are bes^explained by assuming that low doses of thrombin initiate phospholipase C-mediated formation of inositol-P3, which triggers Ca2+ mobilization. Concurrently, diacylglycerol is formed, which activates protein kinase C. The result is a rise in pHi, which enhances the mobilization of Ca2+ by inositol-P3.This scheme differs from the sequence seen during activation by ADP or epinephrine (1), where Na+ /H2+ exchange is an early step after receptor occupancy and precedes phospholipid A2-mediated PG-endoperoxides/TxA2 formation. These metabolites activate phospholipase C resulting in diacylglycerol and inositol-P3-formation at a rather late stage in signal processing. Recent evidence (4) indicates that in epinephrine-stimulated platelets Na+ /H+ exchange requires fibrinogen binding, which opens the intriguing possibility that occupancy of GPIIb-IIIa starts a process that affects signal processing pathways in platelets.Sweatt, J.D., Limbird, L.E, et al. J.B.C. 1983, 1985, 1986Siffert, W., Akkerman, J.W.N., et al. FEBS Lett 1984, 1987; Nature 1987.Zavoico, G.B., Feinstein, M.B st al. J.B.C. 1986Banga, H.D., Rittenhouse, S.E. PNAS 1986
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Sang, Xiao, and Xiyu Liu. "Tissue-Like P System with Mutational Symport/Antiport Rules and Trigger Mechanism." In 2019 10th International Conference on Information Technology in Medicine and Education (ITME). IEEE, 2019. http://dx.doi.org/10.1109/itme.2019.00175.

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Ciobanu, Gabriel, and Eneia Nicolae Todoran. "Continuation Semantics of a Language Inspired by Membrane Computing with Symport/Antiport Interactions." In 2016 18th International Symposium on Symbolic and Numeric Algorithms for Scientific Computing (SYNASC). IEEE, 2016. http://dx.doi.org/10.1109/synasc.2016.060.

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Siffert, W., P. Scheid, and JW N. Akkerman. "PROTEIN KINASE C CONTROLS CA2+ MOBILIZATION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644509.

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Platelet stimulation has been shown to result in a rise of cytosolic pH (pHi) as a result of an activation of a Na+/H+ antiport. We have investigated the role of pH in Ca2+ mobilization in human platelets. pHi and free Ca2+, {Ca2+)i, were measured in platelets loaded with the fluorescent indicators BCECF and quin2, respectively. Stimulation of platelets by either thrombin or OAG, an activator of protein kinase C (Pk-C), increased pHi. Pretreatment of platelets with inhibitors of Pk-C, trifluoperazine (TFP) or sphingosine (SPH), blocked the stimulus-induced rise in pHi, suggesting a role of Pk-C in the activation of Na+/H+ exchange. Blocking Na+/H+ exchange by an amiloride analogue or by TFP similarly suppressed the thrombin-induced increase in {Ca2*}i. This effect could be prevented by increasing pHi with the Na+/H+ ionophore monensin or with NH4Cl. The thrombin-induced (0.05 U/ml) rise in {Ca2+}i was more than 3-fold enhanced when the pH was raised from 6.8 to 7.4.Our results demonstrate that pHi controls Ca2+ mobilization in human platelets and suggest that Pk-C contributes to this control by activating the Na+/H+ exchanger.Supported by the Deutsche Forschungsgemeinschaft. No Sche 46/5-2.
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