Relevant bibliographies by topics / Ouabain

Academic literature on the topic 'Ouabain'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Ouabain"

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Fu, Yong, Dalian Ding, Lei Wei, Haiyan Jiang, and Richard Salvi. "Ouabain-Induced Apoptosis in Cochlear Hair Cells and Spiral Ganglion NeuronsIn Vitro." BioMed Research International 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/628064.

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Ouabain is a common tool to explore the pathophysiological changes in adult mammalian cochleain vivo. In prior studies, locally administering ouabain via round window membrane demonstrated that the ototoxic effects of ouabainin vivovaried among mammalian species. Little is known about the ototoxic effectsin vitro. Thus, we prepared cochlear organotypic cultures from postnatal day-3 rats and treated these cultures with ouabain at 50, 500, and 1000 μM for different time to elucidate the ototoxic effects of ouabainin vitroand to provide insights that could explain the comparative ototoxic effects of ouabainin vivo. Degeneration of cochlear hair cells and spiral ganglion neurons was evaluated by hair-cell staining and neurofilament labeling, respectively. Annexin V staining was used to detect apoptotic cells. A quantitative RT-PCR apoptosis-focused gene array determined changes in apoptosis-related genes. The results showed that ouabain-induced damagein vitrowas dose and time dependent. 500 μM ouabain and 1000 μM ouabain were destructively traumatic to both spiral ganglion neurons and cochlear hair cells in an apoptotic signal-dependent pathway. The major apoptotic pathways in ouabain-induced spiral ganglion neuron apoptosis culminated in the stimulation of the p53 pathway and triggering of apoptosis by a network of proapoptotic signaling pathways.
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Lewis, Lynley K., Timothy G. Yandle, Philip J. Hilton, Berit P. Jensen, Evan J. Begg, and M. Gary Nicholls. "Endogenous Ouabain Is Not Ouabain." Hypertension 64, no. 4 (October 2014): 680–83. http://dx.doi.org/10.1161/hypertensionaha.114.03919.

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Teixeira, Mariana Pires, Natalia Ferreira Haddad, Eliza Freitas Passos, Marcelle Novaes Andrade, Maria Luisa Arantes Campos, Joyle Moreira Carvalho da Silva, Camila Saggioro de Figueiredo, et al. "Ouabain Effects on Human Anaplastic Thyroid Carcinoma 8505C Cells." Cancers 14, no. 24 (December 14, 2022): 6168. http://dx.doi.org/10.3390/cancers14246168.

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Anaplastic thyroid carcinoma (ATC) is a rare, but aggressive, carcinoma derived from follicular cells. While conventional treatments may improve patients’ survival, the lethality remains high. Therefore, there is an urgent need for more effective ATC treatments. Cardiotonic steroids, such as ouabain, have been shown to have therapeutic potential in cancer treatment. Thus, we aimed to evaluate ouabain’s effects in human anaplastic thyroid cells. For this, 8505C cells were cultured in the presence or absence of ouabain. Viability, cell death, cell cycle, colony formation and migratory ability were evaluated in ouabain-treated and control 8505C cells. The expression of differentiation and epithelial-to-mesenchymal transition (EMT) markers, as well as IL-6, TGFb1 and their respective receptors were also quantified in these same cells. Our results showed that ouabain in vitro decreased the number of viable 8505C cells, possibly due to an inhibition of proliferation. A reduction in migration was also observed in ouabain-treated 8505C cells. In contrast, decreased mRNA levels of PAX8 and TTF1 differentiation markers and increased levels of the N-cadherin EMT marker, as well as IL-6 and TGFb1, were found in ouabain-treated 8505C cells. In short, ouabain may have anti-proliferative and anti-migratory effect on 8505C cells, but maintains an aggressive and undifferentiated profile.
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Curras, M. C., and J. A. Boulant. "Effects of ouabain on neuronal thermosensitivity in hypothalamic tissue slices." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 1 (July 1, 1989): R21—R28. http://dx.doi.org/10.1152/ajpregu.1989.257.1.r21.

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To determine the role of the electrogenic Na+-K+ pump in neuronal thermosensitivity, single-unit activity was recorded in rat hypothalamic tissue slices before, during, and after perfusions containing 10(-5) or 10(-6) M ouabain, a specific pump inhibitor. Most neurons were recorded in the preoptic-anterior hypothalamus. Some neurons were also tested with high magnesium-low calcium perfusions to determine ouabain's effects on neuronal activity during synaptic blockade. When the neurons were characterized according to thermosensitivity, 24% were warm sensitive, 8% were cold sensitive, and 68% were temperature insensitive. Ouabain increased the firing rate of 60% of all neurons. Ouabain did not reduce the thermosensitivity of cold-sensitive and warm-sensitive neurons; however, temperature-insensitive neurons became more warm sensitive during ouabain perfusion. This increase in warm sensitivity did not occur with ouabain plus high Mg2+-low Ca2+ perfusion, suggesting that Ca2+ is important in this response. These results indicate that the Na-K pump is not responsible for the thermosensitivity of hypothalamic cold-sensitive or warm-sensitive neurons; however, this pump may be actively employed by many neurons that remain insensitive to temperature changes.
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Blanco, Gustavo, and Darren P. Wallace. "Novel role of ouabain as a cystogenic factor in autosomal dominant polycystic kidney disease." American Journal of Physiology-Renal Physiology 305, no. 6 (September 15, 2013): F797—F812. http://dx.doi.org/10.1152/ajprenal.00248.2013.

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The classic role of the Na-K-ATPase is that of a primary active transporter that utilizes cell energy to establish and maintain transmembrane Na+ and K+ gradients to preserve cell osmotic stability, support cell excitability, and drive secondary active transport. Recent studies have revealed that Na-K-ATPase located within cholesterol-containing lipid rafts serves as a receptor for cardiotonic steroids, including ouabain. Traditionally, ouabain was viewed as a toxin produced only in plants, and it was used in relatively high concentrations to experimentally block the pumping action of the Na-K-ATPase. However, the new and unexpected role of the Na-K-ATPase as a signal transducer revealed a novel facet for ouabain in the regulation of a myriad of cell functions, including cell proliferation, hypertrophy, apoptosis, mobility, and metabolism. The seminal discovery that ouabain is endogenously produced in mammals and circulates in plasma has fueled the interest in this endogenous molecule as a potentially important hormone in normal physiology and disease. In this article, we review the role of the Na-K-ATPase as an ion transporter in the kidney, the experimental evidence for ouabain as a circulating hormone, the function of the Na-K-ATPase as a signal transducer that mediates ouabain's effects, and novel results for ouabain-induced Na-K-ATPase signaling in cystogenesis of autosomal dominant polycystic kidney disease.
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Gomez-Sanchez, Elise P., Mark F. Foecking, Deborah Sellers, Mary S. Blankenship, and Celso E. Gomez-Sanchez. "Is the Circulating Ouabain-like Compound Ouabain?" American Journal of Hypertension 7, no. 7_Pt_1 (July 1994): 637–46. http://dx.doi.org/10.1093/ajh/7.7.637.

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Gomez-Sanchez, Elise P., Mark F. Foecking, Sellers Deborah, Mary S. Blankenship, and Celso E. Gomez-Sanchez. "Is the Circulating Ouabain-like Compound Ouabain?" American Journal of Hypertension 7, no. 7_Pt_1 (July 1994): 647–50. http://dx.doi.org/10.1093/ajh/7.7.647.

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Murrell, Julie R., Jeffrey D. Randall, James Rosoff, Ji-liang Zhao, Roderick V. Jensen, Steven R. Gullans, and Garner T. Haupert. "Endogenous Ouabain." Circulation 112, no. 9 (August 30, 2005): 1301–8. http://dx.doi.org/10.1161/circulationaha.105.554071.

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Hamlyn, John M., and Mordecai P. Blaustein. "Endogenous Ouabain." Hypertension 68, no. 3 (September 2016): 526–32. http://dx.doi.org/10.1161/hypertensionaha.116.06599.

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Blaustein, Mordecai P., and John M. Hamlyn. "Ouabain, endogenous ouabain and ouabain-like factors: The Na+ pump/ouabain receptor, its linkage to NCX, and its myriad functions." Cell Calcium 86 (March 2020): 102159. http://dx.doi.org/10.1016/j.ceca.2020.102159.

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Dissertations / Theses on the topic "Ouabain"

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Cellnik, Torsten [Verfasser]. "Defunktionalisierung von Ouabain / Torsten Cellnik." Wuppertal : Universitätsbibliothek Wuppertal, 2019. http://d-nb.info/118842209X/34.

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Magnusson, Emma. "Ouabain Toxicity -Selectivity Towards Renal Cancer Cells." Thesis, KTH, Skolan för kemi, bioteknologi och hälsa (CBH), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-278574.

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Ouabain and other cardiotonic steroids are known to inhibit Na + ,K + -ATPase (NKA), theion pump responsible for the ionic gradient across the plasma membrane. These steroidsdisplay a selective toxicity towards several tumour cells in comparison to primary humancells, however, the mechanism behind this is not yet understood. Here, we examined theouabain toxicity in renal epithelial cells, proximal tubular cells (PTCs) of different origin. Weinvestigated the relative cytotoxicity in cancer cells (A-498) and papilloma virus-transformedPTCs (HK-2) as well as to primary human PTCs (hPTC) to validate key components in theeffect. In exposure to ouabain, we examined the cell viability and density by MTT and CrystalViolet assays, and cell migration by a scratch assay. The cytotoxic effect was also studied invarious pH, glucose and potassium ion concentrations. In addition, apoptosis was examinedby the TUNEL assay, and if ouabain kills cancer cells through activation of thevolume-regulated anion channel VRAC channel via NKA. We found that there is a decrease in viable cells when cells are exposed to ouabain ≥ 10nM, however, the effect was not seen to be selective towards cancer cells, nor due toapoptosis and the activation of VRAC. The cytotoxic effect was greater in more acidicextracellular pH ~6.8, but independent of glucose concentration in the medium. Interestingly,the effect was also reversed at an increased extracellular concentration of potassium, andouabain did selectively inhibit the cancer cells to migrate. Thus, there could be potential forouabain to act as an anti-cancer agent for renal cancer and to inhibit tumour metastasization.
Ouabain och andra kardiotoniska steroider är kända för att inhibera Na + ,K + -ATPas (NKA),membranpumpen som är ansvarig för den aktiva jontransporten av natrium och kalium ochjongradienten över plasmamembranet. De har påvisat en selektiv toxicitet mot vissatumörceller i jämförelse med primära humana celler, men det är dock inte förstått hurmekanismen bakom denna företeelse fungerar. I denna studien undersökte vi ouabainstoxicitet i njurcancerceller (A-498) och papillomavirustransformerade proximala tubuliceller(hPTC) för att identifiera effektens nyckelkomponenter. Vid exponering av ouabain undersökte vi cellviabiliteten och -densiteten genom MTT- ochkristallviolett-analyser, samt cellmigrering genom scratch-analys. Den cytotoxiska effektenstuderades också under olika pH-förhållanden samt glukos- och kaliumkoncentrationer.Dessutom undersöktes det om apoptos orsakar celldöd genom TUNEL-analys, och omouabain dödar njurcancerceller genom aktivering av den volymreglerade anjonkanalen(VRAC) via NKA. Vi fann minskning av cellernas livskraft vid exponering av ≥ 10 nM ouabain, men effektentycktes dock inte se ut att vara selektiv gentemot cancerceller, inte heller på grund av apoptosoch aktivering av VRAC. Den cytotoxiska effekten var större vid lägre pH, men oberoendeav mediets glukoskoncentrationen. Intressant nog motverkades också effekten vid förhöjdkoncentration av kaliumjoner, och ouabain hämmade selektivt cancercellerna att migrera.Således finns det en viss potential för ouabain att kunna fungera som ett anticancermedel motnjurcancer och att hämma metastasutveckling.
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Harwood, Steven Michael. "Development and application of an immunoassay for ouabain and a study of the nature of endogenous ouabain-like compound." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325540.

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Carneiro, Luciana Teles. "Efeito modulador da ouabaína no sistema imunológico." Universidade Federal da Paraí­ba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/6866.

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Initially known as a cardiotonic steroid capable to inhibit the Na+/K+ATPase, ouabain was identified as an endogenous substance present in human plasma, produced by the adrenal, pituitary and hypothalamus and can interfere with various aspects of immune response. In this study, which aimed to study the modulating effect of ouabain on the immune system in vivo and in vitro using mouse models, we demonstrated that treatment for three consecutive days using 0,56 mg/kg ouabain was able to reduce cell migration induced by mitogen Concanavalian A (Con A) to the peritoneum, and this fact reflects a decrease in the number of polymorphonuclear leukocytes, mainly neutrophils. In this same model, ouabain was also able to increase the number of mononuclear leukocytes in the peritoneal cavity. Evaluating the effect of treatment on lymphocytes in peripheral organs, we found that, in lymphocytes from mesenteric lymph nodes, this substance induces a decrease of 20% of T CD3+ lymphocytes, concomitant with an increase in same percentage of B lymphocytes, without, however, modulating the proportion of CD4+ and CD8+ among themselves, as well as the number of regulatory T cells (CD4+/CD25+). In the thymus, the same treatment, does not affect the proportion of lymphocyte subpopulations studied. The analysis qualitative and quantitatively of peripheral blood leukocytes, biometrics and cellularity of spleen, thymus and lymph nodes showed no change in response to ouabain treatment. Comparative studies using treatment for one or two days, with the same dose of 0,56 mg/kg did not trigger modulation, in vivo, in populations of T lymphocytes, B lymphocytes and subpopulations of CD4+ and CD8+ cells in mesenteric lymph nodes. In addition, ouabain was able to inhibit mitochondrial activity of lymphocytes stimulated with Con A, using MTT assay.These findings indicate an immunomodulatory role of ouabain.
Inicialmente, conhecida como um esteróide cardiotônico e por sua propriedade de inibir a Na+/K+ATPase, a ouabaína foi identificada como uma substância endógena presente no plasma humano, produzida pela adrenal, hipófise e hipotálamo e capaz de interferir em vários aspectos da resposta imune. Neste trabalho, que teve como objetivo estudar o efeito modulador da ouabaína no sistema imunológico in vivo e in vitro por meio de modelos murinos, demonstrou-se que o tratamento por três dias consecutivos com ouabaína utilizando a dose de 0,56 mg/kg foi capaz de reduzir a migração celular induzida pelo mitógeno Concanavaliana A (Con A) para o peritôneo, sendo este fato reflexo da redução do número de leucócitos polimorfonucleares, principalmente, neutrófilos. Neste mesmo modelo, a ouabaína também foi capaz de aumentar o número de leucócitos mononucleares no lavado peritoneal. Avaliando-se o efeito desse tratamento no perfil linfocitário de órgãos periféricos, encontrou-se que, em linfócitos de linfonodos mesentéricos, esta substância induz a uma diminuição de 20% de linfócitos T CD3+, concomitante a um aumento de mesmo percentual de linfócitos B, sem, no entanto, modular a proporção de linfócitos TCD4+ e CD8+ entre si, bem como o número de células T regulatórias (CD4+CD25+). No timo, o mesmo tratamento com a ouabaína não interfere na proporção das subpopulações linfocitárias estudadas. As análises qualitativas e quantitativas de leucócitos do sangue periférico, da biometria e celularidade do baço, timo e linfonodos mesentéricos não apresentaram alteração em resposta ao tratamento com a ouabaína. Estudos comparativos utilizando tratamentos de um ou dois dias, com a mesma dose de 0,56 mg/Kg não desencadearam modulação, in vivo, nas populações de linfócitos T, linfócitos B e das subpopulações de linfócitos TCD4+ e CD8+ nos linfonodos mesentéricos. Adicionalmente, a ouabaína foi capaz de inibir a atividade mitocondrial de linfócitos estimulados com Con A, por meio do ensaio de MTT. Estes resultados indicam um papel imunomodulador da ouabaína.
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Tennant, Brian Prichard. "Biosynthesis and physiological characteristics of endogenous ouabain-like substance." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272367.

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Semra, Yemane Kurban. "Endogenous ouabain-like immunoreactive substance (OLIS) : characterisation and physiological studies." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313282.

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Vasconcelos, Danielle Ingrid Bezerra de. "Análise do efeito imunomodulador da ouabaína na inflamação e nocicepção." Universidade Federal da Paraí­ba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/3640.

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Ouabain, known as a cardiotonic glycoside capable of inhibiting the Na+/K+ ATPase, was widely used for heart failure treatment. Identified as an endogenous substance, ouabain is capable of interfering with various physiological functions, including immune system modulation. Besides that, little is known about the involvement of this substance in nociceptive and inflammatory processes. The present study investigated the role of ouabain in acute peripheral inflammation induced by intraplantar administrartion of different phlogistic agents (carrageenan, compound 48/80, histamine, bradykinin, and PGE2) and in nociceptive processes (abdominal writhing induced by acetic acid and hot plate). Ouabain produced a significant reduction in the mouse paw edema induced by carrageenan and compound 48/80. This antiinflammatory effect of ouabain is associated to the inhibition of PGE2, bradykinin, and mast-cell degranulation, but not to histamine. Ouabain also presented a central and peripheral anti-nociceptive activity. This analgesic potential might be related to the inhibition of inflammatory mediators and to activation of opioid receptors, since it was reversed by naloxone, an opioid antagonist. Additionally, the analgesic effect of ouabain was not related to sedative effect or to motor function. Taken together, the present work demonstrated for the first time, in vivo, the antiinflammatory and analgesic potential of ouabain
A Ouabaína é um glicosídeo cardiotônico, inibidor da Na+/K+-ATPase, utilizada na clínica para o tratamento de insuficiência cardíaca. Atualmente, sabe-se que essa substância é endógena, e capaz de interferir em várias funções fisiológicas, inclusive em diversos aspectos do sistema imunológico. Apesar disso, pouco se sabe sobre seu envolvimento em processos inflamatórios e nociceptivos. Neste trabalho, foi avaliada a atividade da Ouabaína na inflamação aguda desencadeada pela administração de diversos agentes flogísticos (carragenina, composto 48/80, histamina, PGE2 e bradicinina) e em modelos nociceptivos (contorções abdominais induzidas por ácido acético e placa quente). A Ouabaína produziu uma redução no edema de pata produzido por carragenina e pelo composto 48/80. Esse potencial anti-inflamatório está relacionado ao bloqueio da degranulação de mastócitos, bem como pela inibição da via da PGE2 e da bradicinina, porém é independente da via da histamina. A Ouabaína também apresentou uma atividade anti-nociceptiva central e periférica. Esse efeito está vinculado à inibição da via dos mediadores inflamatórios e a mecanismos opióides, visto que foi revertido pela administração da naloxona, um inibidor dos receptores opióides. Adicionalmente, foi descrito que a inibição da dor pela Ouabaína não possui envolvimento com sedação ou diminuição da capacidade motora. O conjunto desses dados demonstra pela primeira vez, in vivo, a atividade anti-inflamatória e anti-nociceptiva da Ouabaína.
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Gillingwater, Scott David. "Purification and characterisation of ouabain-like compound(s) from biological material." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418070.

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Harris, Tanoya L. "Ouabain Regulates Caveolin-1 Vesicle Trafficking by a Src-Dependent Mechanism." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1333732028.

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Veerasingham, Shereeni J. "Salt-induced hypertension, central regulation by ouabain-like compounds and angiotensin II." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ58297.pdf.

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Books on the topic "Ouabain"

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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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Morton, Sarah Wentworth. Ouabi; Or The Virtues Of Nature: An Indian Tale In Four Cantos. Kessinger Publishing, LLC, 2007.

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Morton, Sarah Wentworth. Ouabi; Or The Virtues Of Nature: An Indian Tale In Four Cantos. Kessinger Publishing, LLC, 2007.

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Book chapters on the topic "Ouabain"

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Ezzaher, Abdellatif, Renaud Mougenot, Alain Gerbi, Nour el Houda Bouanani, Antoine Baggioni, Bertrand Crozatier, and Jean-Michel Maixent. "Non Effectiveness of Ouabain and Decrease in Na+/K+ -ATPase Affinity for Ouabain in Failing Rabbit Heart." In The Sodium Pump, 828–31. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_151.

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Hamlyn, J. M. "Discovery of Endogenous Ouabain — A New Mammalian Hormone." In The Sodium Pump, 722–31. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-72511-1_132.

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Navaratnam, S., and J. C. Khatter. "Protective Effect of Nifedipine upon Ouabain-Induced Arrhythmias." In Developments in Cardiovascular Medicine, 59–73. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2057-9_5.

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Lingrel, Jerry B., James Van Huysse, William O’Brien, Elizabeth Jewell-Motz, and Patrick Schultheis. "Amino Acid Residues Involved in Ouabain Sensitivity and Cation Binding." In Molecular and Cellular Mechanisms of H+ Transport, 173–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79301-1_20.

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Lee, Yee-Ki, Kwong-Man Ng, Wing-Hon Lai, Yau-Chi Chan, Yee-Man Lau, Hung-Fat Tse, and Chung-Wah Siu. "Differentiation of Embryonic Stem Cells into Cardiomyocytes: Role of Ouabain." In Stem Cells and Cancer Stem Cells, Volume 6, 71–78. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2993-3_7.

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Rhee, Hee Min. "Parallelism Between Transport Inhibition and L1210 Cell Growth by Ouabain." In Oxygen Transport to Tissue X, 727–34. New York, NY: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9510-6_89.

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Stokke, E. S., J. Østensen, and F. Kiil. "Effect of Ouabain and Acetazolamide on Proximal Tubular Transport in Dogs." In Diuretics: Basic, Pharmacological, and Clinical Aspects, 82–84. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2067-8_17.

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Grupp, G., Ingrid L. Grupp, T. Hickerson, S. W. Lee, and A. Schwartz. "Biphasic contractile response to ouabain: Species specific? Calcium dependent? Altered sensitivity?" In Cardiac Glycosides 1785–1985, 99–108. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_15.

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Petzinger, E., K. Fischer, and H. Fasold. "Role of the bile acid transport system in hepatocellular ouabain uptake." In Cardiac Glycosides 1785–1985, 297–304. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_40.

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de Lurdes Gonçalves, Maria. "Ouabain binding to erythrocytes from neonates, blood cord and pregnant women." In Cardiac Glycosides 1785–1985, 343–46. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_46.

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Conference papers on the topic "Ouabain"

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Krivoi, Igor. "ENDOGENOUS OUABAIN AND SKELETAL MUSCLE." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m446.sudak.ns2019-15/245-246.

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Bikmurzina, Anastasia, Arina Fedorova, Igor Krivoi, and Alexander Markov. "CHANGES IN THE BLOOD-BRAIN BARRIER OF RATS WITH CHRONIC INJECTIONS OF OUABAIN." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m951.sudak.ns2020-16/100.

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Wu, Jun, Mariele Mondala, Meng-Yin Hsieh, Eugene Roberts, and Richard Ermel. "Abstract 4403: Antitumor properties of ouabain in lipid double emulsion integrated with tumor cell membrane fractions." 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.am2015-4403.

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Rhee, Chung-Ku, Sung Huyn Bae, So-Young Chang, Phil-Sang Chung, and Jae-Yun Jung. "Effect of low level laser therapy (LLLT) on ouabain induced auditory neuropathy in gerbils (Conference Presentation)." In Optical Imaging, Therapeutics, and Advanced Technology in Head and Neck Surgery and Otolaryngology, edited by Brian J. F. Wong and Justus F. Ilgner. SPIE, 2016. http://dx.doi.org/10.1117/12.2212553.

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Wu, Jun, Meng-Yin Hsieh, Yan Wang, Eugene Roberts, Derek Vallejo, Abraham Lee, and Richard Ermel. "Abstract 5412: Antitumor properties of ouabain in lipid double emulsion in orthotopic canine osteosarcoma xenografted mouse model." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5412.

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Hwang, Mihwa, Dong Wha Jun, Hyun Jung Kim, Soo Kyung Hwang, Chang-Hun Lee, and Sunshin Kim. "Abstract 3335: Ouabain, a cardiac glycoside, inhibits the Fanconi Anemia-BRCA pathway activated by DNA crosslinking agents." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3335.

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Furihata, Kenichi, Diane J. Nugent, Amy L. Bissonette, Elizabeth Vokac, and Thomas J. Kunicki. "PRODUCTION OF HUMAN MONOCLONAL ANTIBODIESSPECIFIC FOR PLATELET MEMBRANE GLYCOPROTEIN IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643705.

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Abstract:
Human monoclonal antibodies specific for platelet membrane glycoproteins (GPs) arepotentially important reagentsfor studies of the immunogenicity of membrane glycoproteins. A human monoclonalautoantibody, 5E5, reactive with plateletGPIIIa has been developed (Nugent, et al.,Blood, 1987, in press). In this report, we describe the production of additional human monoclonal antibodies specific for GPIIIa. Peripheral blood lymphocytes fromone patient with post-transfusion purpur(PTP) and one woman who had delivered an infant with neonatal alloimmune thrombocytopenic purpura (NATP) were used as a source of antigen-specific lymphocytes. A B-lympho-cyte-enriched population was transformed with Epstein Barr virus, strain B95-8, and cultured in microtiter plates. After two weeks, culture supernatants were screened by an antigen-capture ELISA wherein murine monoclonal antibody specificfor the GPIIb-IIIa complex was used to holdcorresponding antigen from a lysate ofnormal platelets. B-lymphoblastoid cell lines producing IgG and/or IgM antibodies were expanded and either cloned by limiting dilution technqiue or hybridized with a HAT-sensitive, ouabain-resistant heterohybrid fusion line, F6, using polyethylene glycol. Hybridomas were selected in medium containing HAT andouabain. After twoweeks, hybridomas producing anti-GPIIb and/or anti-GPIIIa antibody were cloned by limiting dilution. Culture supernatants from cloned B-lymphoblastoid cell lines and cloned hybridomas were rescreened by ELISA wherein affinity-purified GPIIIa or other platelet GP weredirectly conjugatedto microtiter plates. One IgM antibody produced by acloned B-lymphoblastoid cellline (CH16) andtwo IgG antibodies produced bycloned hybridomas(Del5.19 and Del5.23) were shownto react with GPIIIa but not other GP. Further characterization of these human monoclonal antibodies, produced continuouslyin culture now for four months, is in progress.
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