Relevant bibliographies by topics / CysLTs

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  4. Book chapters
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Academic literature on the topic 'CysLTs'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "CysLTs"

1

Baptista-dos-Reis, Renata, Valdirene S. Muniz, and Josiane S. Neves. "Multifaceted Roles of Cysteinyl Leukotrienes in Eliciting Eosinophil Granule Protein Secretion." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/848762.

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Cysteinyl leukotrienes (cysLTs) are cell membrane-impermeant lipid mediators that play major roles in the pathogenesis of eosinophilic inflammation and are recognized to act via at least 2 receptors, namely, cysLT1receptor (cysLT1R) and cysLT2receptor (cysLT2R). Eosinophils, which are granulocytes classically associated with host defense against parasitic helminthes and allergic conditions, are distinguished from leukocytes by their dominant population of cytoplasmic crystalloid (also termed secretory, specific, or secondary) granules that contain robust stores of diverse preformed proteins. Human eosinophils are the main source of cysLTs and are recognized to express both cysLTs receptors (cysLTRs) on their surface, at the plasma membrane. More recently, we identified the expression of cysLTRs in eosinophil granule membranes and demonstrated that cysLTs, acting via their granule membrane-expressed receptors, elicit secretion from cell-free human eosinophil granules. Herein, we review the multifaceted roles of cysLTs in eliciting eosinophil granule protein secretion. We discuss the intracrine and autocrine/paracrine secretory responses evoked by cysLTs in eosinophils and in cell-free extracellular eosinophil crystalloid granules. We also discuss the importance of this finding in eosinophil immunobiology and speculate on its potential role(s) in eosinophilic diseases.
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2

Bandeira-Melo, Christianne, Lesley J. Woods, Mojabeng Phoofolo, and Peter F. Weller. "Intracrine Cysteinyl Leukotriene Receptor–mediated Signaling of Eosinophil Vesicular Transport–mediated Interleukin-4 Secretion." Journal of Experimental Medicine 196, no. 6 (September 16, 2002): 841–50. http://dx.doi.org/10.1084/jem.20020516.

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We investigated whether cysteinyl leukotrienes (cysLT) are intracrine signal transducers that regulate human eosinophil degranulation mechanisms. Interleukin (IL)-16, eotaxin, and RANTES stimulate vesicular transport–mediated release of preformed, granule-derived IL-4 and RANTES from eosinophils and the synthesis at intracellular lipid bodies of LTC4, the dominant 5-lipoxygenase–derived eicosanoid in eosinophils. 5-Lipoxygenase inhibitors blocked IL-16–, eotaxin-, and RANTES-induced IL-4 release; but neither exogenous LTC4, LTD4, nor LTE4 elicited IL-4 release. Only after membrane permeabilization enabled cysLTs to enter eosinophils did LTC4 and LTD4 stimulate IL-4, but not RANTES, release. LTC4-elicited IL-4 release was pertussis toxin inhibitable, but inhibitors of the two known G protein–coupled cysLT receptors (cysLTRs) (CysLT1 and CysLT2) did not block LTC4-elicited IL-4 release. LTC4 was 10-fold more potent than LTD4 and at low concentrations (0.3–3 nM) elicited, and at higher concentrations (>3 nM) inhibited, IL-4 release from permeabilized eosinophils. Likewise with intact eosinophils, LTC4 export inhibitors, which increased intracellular LTC4, inhibited eotaxin-elicited IL-4 release. Thus, LTC4 acts, via an intracellular cysLTR distinct from CysLT1 or CysLT2, as a signal transducer to selectively regulate IL-4 release. These results demonstrate that LTC4, well recognized as a paracrine mediator, may also dynamically govern inflammatory and immune responses as an intracrine mediator of eosinophil cytokine secretion.
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Ballerini, P., P. Di Iorio, R. Ciccarelli, F. Caciagli, A. Polp, A. Beraudi, S. Buccella, et al. "P2Y1 and Cysteinyl Leukotriene Receptors Mediate Purine and Cysteinyl Leukotriene Co-Release in Primary Cultures of Rat Microglia." International Journal of Immunopathology and Pharmacology 18, no. 2 (April 2005): 255–68. http://dx.doi.org/10.1177/039463200501800208.

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Inflammation is widely recognized as contributing to the pathology of acute and chronic neurodegenerative conditions. Microglial cells are pathologic sensors in the brain and activated microglia have been viewed as detrimental. Leukotriene, including cysteinyl leukotrienes (CysLTs) are suggested to be involved in brain inflammation and neurological diseases and ATP, by its receptors is a candidate for microglia activation. A23187 (10μM) stimulated microglia to co-release CysLTs and [3H]adenine based purines ([3H]ABPs), mainly ATP. The biosynthetic production of CysLTs was abolished by 10μM MK-886, an inhibitor of 5-lipoxygenase-activating protein activity. RT-PCR analysis showed that microglia expressed both CysLT1 / CysLT2 receptors, P2Y1 ATP-receptors and several members of the ATP binding cassette (ABC) transporters including MRP1, MRP4 and Pgp. The increase in [Ca2+]i elicited by LTD4 (0.1 μM) and 2MeSATP (100μM), agonists for CysLT- and P2Y1-receptors, was abolished by the respective antagonists, BAYu9773 (0.5 μM) and suramin (50 μM). The stimulation of both receptor subtypes, induced a concomitant increase in the release of both [3H]ABPs and CysLTs that was blocked by the antagonists and significantly reduced by a cocktail of ABC transporter inhibitors, BAPTA/AM (intracellular Ca2+ chelator) and staurosporine (0.1 μM, PKC blocker). P2Y antagonist was unable to antagonise the effects of LTD4 and BAYu9773 did not reduce the effects of 2MeSATP. These data suggest that: i) the efflux of purines and cysteinyl-leukotrienes is specifically and independently controlled by the two receptor types, ii) calcium, PKC and the ABC transporter system can reasonably be considered common mechanisms underlying the release of ABPs and CysLTs from microglia. The blockade of P2Y1 or CysLT1/CysLT2 receptors by specific antagonists that abolished the raise in [Ca2+]i and drastically reduced the concomitant efflux of both compounds, as well as the effects of BAPTA and staurosporine support this hypothesis. In conclusion, the data of the present study suggest a cross talk between the purine and leukotriene systems in a possible autocrine/paracrine control of the microglia-mediated initiation and progression of an inflammatory response.
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4

Voisin, Tiphaine, Caroline Perner, Marie-Angele Messou, Stephanie Shiers, Saltanat Ualiyeva, Yoshihide Kanaoka, Theodore J. Price, et al. "The CysLT2R receptor mediates leukotriene C4-driven acute and chronic itch." Proceedings of the National Academy of Sciences 118, no. 13 (March 22, 2021): e2022087118. http://dx.doi.org/10.1073/pnas.2022087118.

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Acute and chronic itch are burdensome manifestations of skin pathologies including allergic skin diseases and atopic dermatitis, but the underlying molecular mechanisms are not well understood. Cysteinyl leukotrienes (CysLTs), comprising LTC4, LTD4, and LTE4, are produced by immune cells during type 2 inflammation. Here, we uncover a role for LTC4 and its signaling through the CysLT receptor 2 (CysLT2R) in itch. Cysltr2 transcript is highly expressed in dorsal root ganglia (DRG) neurons linked to itch in mice. We also detected CYSLTR2 in a broad population of human DRG neurons. Injection of leukotriene C4 (LTC4) or its nonhydrolyzable form NMLTC4, but neither LTD4 nor LTE4, induced dose-dependent itch but not pain behaviors in mice. LTC4-mediated itch differed in bout duration and kinetics from pruritogens histamine, compound 48/80, and chloroquine. NMLTC4-induced itch was abrogated in mice deficient for Cysltr2 or when deficiency was restricted to radioresistant cells. Itch was unaffected in mice deficient for Cysltr1, Trpv1, or mast cells (WSh mice). CysLT2R played a role in itch in the MC903 mouse model of chronic itch and dermatitis, but not in models of dry skin or compound 48/80- or Alternaria-induced itch. In MC903-treated mice, CysLT levels increased in skin over time, and Cysltr2−/− mice showed decreased itch in the chronic phase of inflammation. Collectively, our study reveals that LTC4 acts through CysLT2R as its physiological receptor to induce itch, and CysLT2R contributes to itch in a model of dermatitis. Therefore, targeting CysLT signaling may be a promising approach to treat inflammatory itch.
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Steinke, John W., Spencer C. Payne, and Larry Borish. "Interleukin-4 in the Generation of the AERD Phenotype: Implications for Molecular Mechanisms Driving Therapeutic Benefit of Aspirin Desensitization." Journal of Allergy 2012 (January 3, 2012): 1–9. http://dx.doi.org/10.1155/2012/182090.

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Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC4S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion. Increased levels of IL-4 have been found in the sinus mucosa and nasal polyps of AERD subjects. Previous studies demonstrated that IL-4 is primarily responsible for the upregulation of LTC4S by mast cells and the upregulation of CysLT1 and 2 receptors on many immune cell types. Prostaglandin E2 (PGE2) acts to prevent CysLT secretion by inhibiting mast cell and eosinophil activation. PGE2 concentrations are reduced in AERD reflecting diminished expression of cyclooxygenase (COX)-2. IL-4 can inhibit basal and stimulated expression of COX-2 and microsomal PGE synthase 1 leading to decreased capacity for PGE2 secretion. Thus, IL-4 plays an important pathogenic role in generating the phenotype of AERD. This review will examine the evidence supporting this hypothesis and describe a model of how aspirin desensitization provides therapeutic benefit for AERD patients.
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Colazzo, Francesca, Paolo Gelosa, Elena Tremoli, Luigi Sironi, and Laura Castiglioni. "Role of the Cysteinyl Leukotrienes in the Pathogenesis and Progression of Cardiovascular Diseases." Mediators of Inflammation 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/2432958.

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Cysteinyl leukotrienes (CysLTs) are potent lipid inflammatory mediators synthesized from arachidonic acid, through the 5-lipoxygenase (5-LO) pathway. Owing to their properties, CysLTs play a crucial role in the pathogenesis of inflammation; therefore, CysLT modifiers as synthesis inhibitors or receptor antagonists, central in asthma management, may become a potential target for the treatment of other inflammatory diseases such as the cardiovascular disorders. 5-LO pathway activation and increased expression of its mediators and receptors are found in cardiovascular diseases. Moreover, the cardioprotective effects observed by using CysLT modifiers are promising and contribute to elucidate the link between CysLTs and cardiovascular disease. The aim of this review is to summarize the state of present research about the role of the CysLTs in the pathogenesis and progression of atherosclerosis and myocardial infarction.
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Theron, A. J., H. C. Steel, G. R. Tintinger, C. M. Gravett, R. Anderson, and C. Feldman. "Cysteinyl Leukotriene Receptor-1 Antagonists as Modulators of Innate Immune Cell Function." Journal of Immunology Research 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/608930.

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Cysteinyl leukotrienes (cysLTs) are produced predominantly by cells of the innate immune system, especially basophils, eosinophils, mast cells, and monocytes/macrophages. Notwithstanding potent bronchoconstrictor activity, cysLTs are also proinflammatory consequent to their autocrine and paracrine interactions with G-protein-coupled receptors expressed not only on the aforementioned cell types, but also on Th2 lymphocytes, as well as structural cells, and to a lesser extent neutrophils and CD8+cells. Recognition of the involvement of cysLTs in the immunopathogenesis of various types of acute and chronic inflammatory disorders, especially bronchial asthma, prompted the development of selective cysLT receptor-1 (cysLTR1) antagonists, specifically montelukast, pranlukast, and zafirlukast. More recently these agents have also been reported to possess secondary anti-inflammatory activities, distinct from cysLTR1 antagonism, which appear to be particularly effective in targeting neutrophils and monocytes/macrophages. Underlying mechanisms include interference with cyclic nucleotide phosphodiesterases, 5′-lipoxygenase, and the proinflammatory transcription factor, nuclear factor kappa B. These and other secondary anti-inflammatory mechanisms of the commonly used cysLTR1 antagonists are the major focus of the current review, which also includes a comparison of the anti-inflammatory effects of montelukast, pranlukast, and zafirlukast on human neutrophilsin vitro, as well as an overview of both the current clinical applications of these agents and potential future applications based on preclinical and early clinical studies.
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Bankova, Lora G., Juying Lai, Eri Yoshimoto, Joshua A. Boyce, K. Frank Austen, Yoshihide Kanaoka, and Nora A. Barrett. "Leukotriene E4 elicits respiratory epithelial cell mucin release through the G-protein–coupled receptor, GPR99." Proceedings of the National Academy of Sciences 113, no. 22 (May 16, 2016): 6242–47. http://dx.doi.org/10.1073/pnas.1605957113.

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Cysteinyl leukotrienes (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammatory lipid mediators with pathobiologic function in asthma. LTE4, the stable cysLT, is a weak agonist for the type 1 and type 2 cysLT receptors (CysLTRs), which constrict airway smooth muscle, but elicits airflow obstruction and pulmonary inflammation in patients with asthma. We recently identified GPR99 as a high-affinity receptor for LTE4 that mediates cutaneous vascular permeability. Here we demonstrate that a single intranasal exposure to extract from the respiratory pathogen Alternaria alternata elicits profound epithelial cell (EpC) mucin release and submucosal swelling in the nasal mucosa of mice that depends on cysLTs, as it is absent in mice deficient in the terminal enzyme for cysLT biosynthesis, LTC4 synthase (LTC4S). These mucosal changes are associated with mast cell (MC) activation and absent in MC-deficient mice, suggesting a role for MCs in control of EpC function. Of the three CysLTRs, only GPR99-deficient mice are fully protected from EpC mucin release and swelling elicited by Alternaria or by intranasal LTE4. GPR99 expression is detected on lung and nasal EpCs, which release mucin to doses of LTE4 one log lower than that required to elicit submucosal swelling. Finally, mice deficient in MCs, LTC4S, or GPR99 have reduced baseline numbers of goblet cells, indicating an additional function in regulating EpC homeostasis. These results demonstrate a novel role for GPR99 among CysLTRs in control of respiratory EpC function and suggest that inhibition of LTE4 and of GPR99 may have therapeutic benefits in asthma.
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Różańska, Małgorzata, Paweł Bielecki, Joanna Reszeć, Krzysztof Kowal, and Marek Rogowski. "Cysteinyl leukotriene 1 receptor expression in nasal polyps." Otolaryngologia Polska 72, no. 5 (October 1, 2018): 1–5. http://dx.doi.org/10.5604/01.3001.0012.5422.

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Cysteinyl leukotrienes (CysLTs) have been implicated in the pathogenesis of chronic rhinosinusitis (CRS). This study was undertaken to better understand the role of CysLTs in the development of CRS through 1). assessment of the pattern of expression of CysLT1 receptor in nasal polyps from patients with CRS and 2). correlation of expression of CysLT1 receptor with clinical features. Expression of CysLT1 receptor was evaluated immunohistochemically in nasal polyps from 20 patients with CRS and nasal mucosa from 10 control subject undergoing plastic surgery of the nose. Patients with CRS showed significantly higher expression of CysLT1 receptor as compared with the control group (p<0.05). The expression of CysLT1 receptor in sub-epithelial inflammatory infiltrates tended to be higher in patients with CRS and allergy as compared with patients with CRS but without allergy (p=0.07). In particular, the expression of CysLT1 receptor in sub-epithelial inflammatory infiltrates was significantly greater in 3 patients with CRS and drug allergy as compared with patients with CRS but without drug allergy (p=0.03). Increased expression of CysLT1 receptor in inflamed mucosa of nasal polyps in patients with allergy might suggest particular role of CysLTs in the pathogenesis of nasal polyps in this group of patients.
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Sasaki, Fumiyuki, and Takehiko Yokomizo. "The leukotriene receptors as therapeutic targets of inflammatory diseases." International Immunology 31, no. 9 (May 28, 2019): 607–15. http://dx.doi.org/10.1093/intimm/dxz044.

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Abstract Leukotrienes (LTs) are inflammatory mediators derived from arachidonic acid. LTs include the di-hydroxy acid LT (LTB4) and the cysteinyl LTs (CysLTs; LTC4, LTD4 and LTE4), all of which are involved in both acute and chronic inflammation. We and other groups identified a high-affinity LTB4 receptor, BLT1; the LTC4 and LTD4 receptors, CysLT1 and CysLT2; and the LTE4 receptor, GPR99. Pharmacological studies have shown that BLT1 signaling stimulates degranulation, chemotaxis and phagocytosis of neutrophils, whereas CysLT1 and CysLT2 signaling induces airway inflammation by increasing vascular permeability and the contraction of bronchial smooth muscle. Recently, we and other groups suggested that the LTB4–BLT1 axis and the cysteinyl LTs–CysLT1/2 axis are involved in chronic inflammatory diseases including asthma, atopic dermatitis, psoriasis, atherosclerosis, arthritis, obesity, cancer and age-related macular degeneration using animal models for disease and gene knockout mice. This review describes the classical and novel functions of LTs and their receptors in several inflammatory diseases and discusses the potential clinical applications of antagonists for LT receptors and inhibitors of LT biosynthesis.
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Dissertations / Theses on the topic "CysLTs"

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Poulin, Sébastien. "Modulation de l'expression du facteur angiogénique VEGF (vascular endothelial growth factor) par les cysteinyl-leucotriènes." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4007.

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Les cysteinyl-leucotriènes (cysLTs) ont des rôles majeurs dans la pathophysiologie de l'asthme et sont impliqués dans le remodelage des voies respiratoires, un processus caractérisé par plusieurs changements structuraux incluant entre autre [i.e. autres] la fibrogenèse et l'hyperplasie des cellules musculaires lisses. Dans cette étude, nous avons investigué le rôle potentiel des cysLTs dans la modulation du « vascular endothelial growth factor » (VEGF), un facteur de croissance connu pour être important dans une autre facette du remodelage, c'est-à-dire l'angiogenèse. Nous avons montré que le LTD[indice inférieur 4] induit l'expression du VEGF chez les monocytes humains et les cellules musculaires lisses bronchiques humaines avec une inhibition complète par un antagoniste spécifique du récepteur CysLT1. De plus, des cellules de reins embryonnaires humaines (HEK-293) transfectées d'une façon stable avec CysLT1 ont été utilisées pour étudier la régulation transcriptionnelle du promoteur du VEGF. La stimulation de ces cellules avec des cysLTs mène à l'activation du promoteur du VEGF d'une façon dépendante de la concentration et résistante à la Bordetella pertussis toxin (PTX). Aussi, il en résulte une augmentation de l'expression de l'ARNm et de la protéine du VEGF d'une façon dépendante du temps de stimulation. L'utilisation de mutants tronqués en 5' de la construction du promoteur du VEGF de type sauvage démontre que la région en amont de -90 Pb n'est pas requise pour sa régulation transcriptionnelle par les cysLTs. De plus, un prétraitement avec des inhibiteurs pharmacologiques des MAPKs suggère l'implication de JNK et ERK, mais pas de p38 dans l'activation du promoteur du VEGF par LTD[indice inférieur 4]. Également, l'inhibition partielle de l'activation du promoteur du VEGF via la surexpression des formes dominantes négatives des protéines JunD, FosB et Ras suggère un rôle actif pour le complexe AP-1. Cependant, puisqu'un mutant du promoteur avec des substitutions dans le site de liaison d'AP-1 maintient toujours sa transactivation par LTD[indice inférieur 4], le complexe AP-1 semble agir d'une façon indirecte. En fait, l'inhibition complète de l'activation du promoteur du VEGF et de l'augmentation subséquente de son ARNm par un prétraitement avec la mithramycine, un inhibiteur de la transcription Sp1-dépendante, suggère que AP-1 pourrait agir indirectement sur Sp1 pour la modulation du VEGF par les cysLTs. Par surcroît, des expériences utilisant un promoteur du VEGF (-123 +50 pb) avec tous ses sites Sp1 mutés (4) ont montré que ces régions étaient nécessaires à la transactivation du VEGF par LTD[indice inférieur 4]. Bref, nos résultats indiquent pour la première fois que les cysLTs peuvent activer transcriptionnellement la production du VEGF via le récepteur CysLT1, avec l'implication de JNK, ERK, AP-1 et Sp1. Ces résultats proposent que les cysLTs pourraient être importants dans le processus d'angiogenèse associé au remodelage des voies respiratoires et indiquent un possible bénéfice jusqu'à maintenant insoupçonné dans l'utilisation des antagonistes des récepteurs CysLT1 dans la prévention ou le traitement du remodelage dans l'asthme.
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Fleck, Juliana. "MONTELUCASTE DIMINUI AS CRISES CONVULSIVAS EM ANIMAIS ABRASADOS E POTENCIALIZA O EFEITO ANTICONVULSIVANTE DO FENOBARBITAL." Universidade Federal de Santa Maria, 2015. http://repositorio.ufsm.br/handle/1/3855.

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Epilepsy is a chronic neurological disease characterized by recurrent, unprovoked seizures. Evidence suggests that inflammation plays a role in the pathophysiology of seizures. Although cysteinyl leukotrienes (CysLTs) have been implicated in seizures, no study has investigated whether blocking of CysLT1 receptors potentiates the anticonvulsant action of classic antiepileptic drugs, as well as the expression of CysLT receptors is altered by inflammation. In this study we showed that the inverse agonist of CysLT1 receptor, montelukast, synergistically increases the anticonvulsant action of phenobarbital against seizures induced in a model of acute injection of pentylenetetrazole (PTZ). Furthermore, it is shown that LTD4 (leukotriene D4) prevents the effect of montelukast. Isobolographic analysis revealed an ED50 mix value for a fixed-ratio combination (1:1 proportion) of montelukast plus phenobarbital of 0.06 ± 0.02 μmol, whereas the calculated ED50 add value was 0.49 ± 0.03 μmol. The interaction index was 0.12, indicating a synergistic interaction. Montelukast significantly decreased the antiseizure DE50 for phenobarbital (0.74 and 0.04 μmol in the absence and presence of montelukast, respectively) and, consequently, phenobarbital-induced sedation at equieffective doses. We also investigated whether the CysLT1 inverse agonist montelukast and a classical anticonvulsant, phenobarbital, decrease seizures in PTZ-kindled mice and CysLT receptor expression. Montelukast (10 mg/kg, s.c.) and phenobarbital (20 mg/kg, s.c.) increased the latency to generalized seizures in kindled mice. Montelukast increased CysLT1 immunoreactivity only in non-kindled PTZ-challenged mice. Interestingly, PTZ challenge decreased CysLT2 immunoreactivity only in kindled mice. CysLT1 antagonists seem to emerge as promising adjunct therapeutic agents in the treatment of refractory seizures. Notwithstanding, additional studies are necessary to evaluate the clinical implications of this work.
A epilepsia é uma doença que se manifesta por crises epilépticas recorrentes, não provocadas. Evidências sugerem que a inflamação desempenha um papel na patofisiologia destas crises. Embora os leucotrienos cisteínicos (CysLTs) tenham sido implicados no desenvolvimento de crises convulsivas, nenhum estudo investigou se o bloqueio dos receptores CysLT1 potencializa a ação anticonvulsivante de antiepilépticos clássicos, assim como se a expressão dos receptores de CysLT é alterada por inflamação. Neste estudo mostramos que o agonista inverso de CysLT1, montelucaste, sinergicamente aumenta a ação anticonvulsivante do fenobarbital contra crises convulsivas induzidas em um modelo de injeção aguda de pentilenotetrazol (PTZ). Além disso, é mostrado que o LTD4 (leucotrieno D4) previne o efeito do montelucaste. A análise isobolográfica revelou que o valor de DE50 mix, calculado experimentalmente para uma combinação de proporção 1: 1 de montelucaste e fenobarbital foi de 0,06 ± 0,02 umol, ao passo que o valor de DE50 add, calculado foi de 0,49 ± 0,03 umol. O índice de interação encontrado foi de 0,12, indicando uma interação sinérgica. A associação dos fármacos diminuiu significativamente o DE50 para o efeito anticonvulsivante do fenobarbital de 0,74 para 0,04 umol (na ausência e na presença de montelucaste, respectivamente) e, consequentemente, a sedação induzida por fenobarbital em doses equieficazes. Posteriormente foi avaliado se o montelucaste e o fenobarbital diminuem as crises convulsivas em animais previamente abrasados, assim como se o tratamento farmacológico ou o abrasamento alteram a expressão de receptores CysLTs. O montelucaste (10 mg/kg; s.c.) e o fenobarbital (20 mg/kg, s.c.) aumentaram a latência para crises convulsivas generalizadas em camundongos abrasados. O montelucaste aumentou a imunorreatividade do receptor CysLT1 em camundongos não abrasados e que foram desafiados por PTZ que não foram abrasados. Entretanto, o desafio de PTZ diminuiu a imunorreatividade do receptor CysLT2 apenas em camundongos abrasados. Antagonistas do receptor CysLT1 parecem emergir como agentes terapêuticos adjuntos promissores no tratamento de crises refratárias. Não obstante, estudos adicionais são necessários para avaliar as implicações clínicas deste trabalho.
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3

Thompson, Charles. "Signalisation des récepteurs CYSLT1 et CYSLT2 et activation transcriptionnelle induite par les cystéinylleucotriènes dans l'asthme." Thèse, Université de Sherbrooke, 2006. http://savoirs.usherbrooke.ca/handle/11143/4229.

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Depuis quelques années, une population croissante d’enfants et d’adultes est touchée par l’asthme. L’étendue des recherches sur le sujet reflète sans doute la complexité de cette maladie. En effet, la pathogenèse de l’asthme est sous le contrôle de plusieurs médiateurs, générés par une multitude de cellules (inflammatoires et structurelles) qui s’organisent et interagissent entre elles. L’aspect multifactoriel et hétérogène de cette pathologie en fait une cible difficile à atteindre. Parmi ses principales caractéristiques, on retrouve le broncospasme, l’hypersécrétion de mucus, l’hyper-réactivité bronchique, l’inflammation et le remodelage pulmonaire. À la fin des années 1990, les antagonistes classiques des leucotriènes font leur apparition sur le marché et sont prescrits pour le traitement de l’asthme. Il s’agit d’antagonistes spécifiques du récepteur CysLT 1, le premier de deux récepteurs de hautes affinités pour les cystéinyl-leucotriènes (cysLT). Les cysLT sont des médiateurs lipidiques impliqués dans plusieurs processus inflammatoires. En plus d’être augmentés dans l’asthme, ils ont la capacité de mimer les principaux symptômes asthmatiques. Malgré l’utilisation clinique des antagonistes classiques des leucotriènes, plusieurs mécanismes moléculaires et cellulaires des cysLT demeurent inconnus. Dans la présente thèse, nous avons initialement abordé le rôle des cysLT dans le processus inflammatoire impliqué dans les cas plus sévères d’asthme. Nous avons par conséquent étudié la capacité des cysLT à induire la production d’une chimiokine. L’asthme sévère étant caractérisé par un influx neutrophilique, nous nous sommes principalement concentré sur l’expression de l’IL-8, le chimioattractant par excellence de ce type cellulaire. Nous avons observé une très forte induction de l’IL-8 en réponse aux cysLT et ce, par l’intermédiaire du récepteur CysLTl et CysLT2. Un des objectifs principaux de ce travail était l’étude de la signalisation induite par les récepteurs CysLTl et CysLT2. Les deux récepteurs répondant aux mêmes agonistes, nous avons par conséquent généré deux modèles cellulaires, afin d’étudier chacun spécifiquement. Le premier modèle exprime de façon stable le CysLTl, alors que le second exprime le CysLT2. Nous avons donc mis en lumière les mécanismes de régulation transcriptionelle impliqués dans l’expression de l’L-8 par les cysLT. Les voies de signalisation NF-kB et AP-1 sont fortement impliquées dans la transduction de signal de chaque récepteur CysLT. Nous avons donc approfondi l’étude de ces voies de signalisation en réponse au cysLT. Des études récentes proposent un rôle pour les cysLT dans le remodelage pulmonaire. Les changements structuraux des voies aériennes impliquent la participation de plusieurs molécules fibrogéniques et angiogéniques. Parmi ces facteurs, plusieurs sont synthétisés sous forme de précurseur qui nécessite une activation/maturation par clivage endoprotéolytique. Cette tâche peut être accomplie par la furine, une convertase de proprotéine. Ainsi, nous avons étudié l’effet des cysLT sur l’expression de la furine et les mécanismes de régulation concernés. Nous démontrons en fait que le LTD4, via le récepteur CysLTl, induit l’expression de la furine, autant au niveau de l’ARNm que la protéine. De plus, l’augmentation de la furine coïncide avec une hausse de l’activation de la métalloprotéinase MT1-MMP et du TGF|3, deux facteurs impliqués dans le remodelage pulmonaire. Enfin, cette thèse propose de nouveaux mécanismes par lesquels les cysLT et leurs récepteurs participent à la pathogénèse asthmatique. Ainsi, nous démontrons que les cysLT jouent un rôle dans l’inflammation pulmonaire en stimulant la production de chimiokines. Nous avons également approfondi les connaissances sur les voies de signalisation menant à la production d’L-8 en réponse au cysLT. Finalement, nous suggérons l’implication des cysLT dans le remodelage pulmonaire via l’induction de la convertase de proprotéine furine. [Symboles non conformes]
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4

Audette, Karine. "Internalisation différentielle des récepteurs Cysteinyl leucotriène 1 et 2 (CysLT1 et CysLT2) bla voie dépendante des vésicules de clathrine est nécessaire à l'endocytose du CysLT1. /." [S.l. : s.n.], 2007.

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Audette, Karine. "Internalisation différentielle des récepteurs Cysteinyl leucotriène 1 et 2 (CysLT1 et CysLT2) la voie dépendante des vésicules de clathrine est nécessaire à l'endocytose du CysLT1." Mémoire, Université de Sherbrooke, 2007. http://savoirs.usherbrooke.ca/handle/11143/3869.

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Les récepteurs cystéinyl-leucotriène 1 et 2 font partie de la grande famille des récepteurs couplés aux protéines G. Ces deux récepteurs partagent une homologie de séquence de 38%, cette homologie étant particulièrement faible dans la région C-terminale. Tout d'abord, nous avons étudié la localisation et l'internalisation des deux récepteurs chez des lignées cellulaires HEK293 exprimant de façon stable l'un ou l'autre des deux récepteurs. Le récepteur CysLT1, localisé principalement au niveau de la membrane plasmique, s'internalise fortement (60%) au cours de la première heure de stimulation au LTD[indice inférieur 4] (Leucotriène D4) et s'accumule dans la région péri-nucléaire. L'internalisation reste soutenue même après 4 heures de stimulation et est bloquée par le Montélukast, un antagoniste spécifique du récepteur CysLT1. Par contre, le récepteur CysLT2 est situé majoritairement à l'intérieur de la cellule et très faiblement à la surface cellulaire à l'état non-stimulé. Une faible internalisation, soit près de 5%, est observée à des temps de stimulation inférieurs à 1 heure. Toutefois, une augmentation de l'expression à la surface des cellules est observée lorsque les cellules sont stimulées pendant plus de 2 heures au LTC[indice inférieur 4] (Leucotriène C4). Ce phénomène d'externalisation étant intriguant, nous avons étudié la fonctionnalité des récepteurs à la surface via des essais de production d'inositol phosphates après 2 et 4 heures de prétraitement au LTC[indice inférieur 4]. Nous avons obtenu des hausses de 4 fois de la production des inositol phosphates après 2 et 4 heures de prétraitement au LTC[indice inférieur 4] comparativement à un ratio de 2 fois lorsque prétraité à l'EtOH. L'autre partie du projet consistait à mieux définir l'internalisation du récepteur CysLT1 ainsi que les molécules impliquées. Premièrement, nous avons observé que les acides aminés 304 à 321 de la queue C-terminale du CysLT1 étaient cruciaux pour l'internalisation du récepteur. La cotransfection de mutants et dominants négatifs d'arrestines 2 et 3 a suggéré l'indépendance des arrestines pour l'internalisation du récepteur CysLT1. Nous avons aussi montré que les GRK (kinases de RCPG) 2, 5 et 6, la PKA ainsi que la caséine kinase 2 ne semblent pas nécessaires pour l'internalisation du récepteur CysLT1 contrairement aux PKC et à la caséine kinase 1 qui sont importantes dans ce processus. Ensuite, nous avons démontré que la cotransfection d'un dominant négatif de la dynamine 1A (K44A) empêche l'internalisation du récepteur CysLT1. Étant donné que le potentiel de signalisation du récepteur peut dépendre de la voie d'internalisation empruntée, nous avons étudié les voies d'internalisation possibles. Des prétraitements avec le sucrose hyperosmotique et la concanavaline A ont inhibé l'internalisation du CysLT1 respectivement de 90% et 70%, indiquant la participation des vésicules de clathrine. La baisse d'internalisation induite par certains agents désorganisant le cholestérol membranaire a amené certaines évidences de la participation des radeaux lipidiques. De plus, nous avons démontré l'importance d'un réseau d'actine intact dans le processus d'internalisation du récepteur CysLT1 via des agents qui induisent la dépolymérisation de l'actine. Nous avons obtenu des baisses significatives de l'internalisation de 57% et 43% suite à des prétraitements avec respectivement la cytochalasine D et la latrunculine B. Finalement, la réexpression rapide à la surface des récepteurs CysLT1 suite au retrait de l'agoniste suggère un recyclage rapide des récepteurs via les endosomes précoces. Les résultats de ce mémoire exposent des divergences au niveau de la localisation et de l'internalisation des récepteurs CysLT1 et CysLT2. Nos résultats suggèrent également que l'internalisation du récepteur CysLT1 est dépendante de l'activité de la dynamine et du réseau d'actine et qu'elle s'effectue via les vésicules de clathrine et possiblement via les radeaux lipidiques.
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Morisawa, Nobuko. "Magnetic Resonance Imaging Manifestations of Decidualized Endometriotic Cysts: Comparative Study With Ovarian Cancers Associated With Endometriotic Cysts." Kyoto University, 2015. http://hdl.handle.net/2433/199169.

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Duta, Dana-Nicoleta. "Interaction of CysLT1 receptor with importin [alpha] proteins." Mémoire, Sherbrooke : Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/3367.

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Wills, Jennifer Rose. "Diagnosis and mechanisms of bovine ovarian cysts." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12674/.

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Ovarian cysts are a cause of reproductive failure and economic loss in postpartum dairy cows. Using a unique combination of research to approach this problem, this thesis aimed to better understand mechanisms of ovarian cyst formation. The use of progesterone as a tool in cyst diagnosis was initially examined. Results demonstrated that 13/30 (43%) cows had progesterone profiles that disagreed with veterinarian diagnosis. Furthermore treatment in 21/30 (70%) cows was ineffective within 4 weeks of administration, and no pregnancy was established earlier than 8 weeks post treatment in all cows. When veterinarian and hormonal diagnosis agreed pregnancy was achieved, on average, two weeks earlier than when they disagreed. Effects of cow management, specifically the NEB experienced during late gestation and early lactation were investigated to determine whether these increased requirements resulted in the development of ovarian cysts. Results demonstrated that from early lactation all 85 cows were in a state of NEB. Ovarian cysts were confirmed in 31/79 cows, and these cows had significantly higher or lower peripheral concentrations of some metabolites, vs. no-cyst cows. Long term down-regulation with a GnRH agonist, followed by a period of observation to monitor the recovery of reproductive function, was conducted for evaluation as a potential model for ovarian cyst formation. Results indicated that 6/12 cows exhibited an LH surge within 104 hours of luteal regression while 6 animals did not (P<0.001). FSH concentrations in 6/12 cows showed divergence comparable with LH surges. 8/12 had at least 1 follicle >8mm and 5/12 had at least 1 follicle >20 mm. Follicle appearance was heterogeneous, with 63% of follicles showing some degree of luteinisation. Positive immunostaining for steroidogenic enzymes was detected in 12.5% of follicles. In conclusion, these results have important clinical significance in improving the diagnosis and management of ovarian cysts in dairy cows.
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張友明 and Yau-ming Cheung. "Morphometric studies of odontogenic cysts and tumours." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31212190.

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Gilmour, Robert Angus. "Giardia spp cysts and the aquatic environment." Thesis, University of Strathclyde, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293498.

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Books on the topic "CysLTs"

1

A, Zeeb Barbara, Smol J. P, and Wilkinson Anna N, eds. Atlas of chrysophycean cysts. Dordrecht: Kluwer Academic Publishers, 1995.

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Orr, Tamra. Ovarian tumors and cysts. New York: Rosen Pub. Group, 2009.

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Duff, Katharine E., Barbara A. Zeeb, and John P. Smol. Atlas of Chrysophycean Cysts. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-017-0809-8.

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Wilkinson, Anna N., Barbara A. Zeeb, and John P. Smol. Atlas of Chrysophycean Cysts. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0811-1.

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James, Grant. Dermoid cyst of the ovary. [S.l: s.n., 1987.

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Renick, Barry Michael. A survey of jaw cysts. Toronto: B.M. Renick, 1987.

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Shiffman, Melvin A., and Mervin Low, eds. Biofilm, Pilonidal Cysts and Sinuses. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-03077-3.

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Shear, Mervyn. Cysts of the oral regions. 3rd ed. Oxford: Wright, 1992.

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Sciubba, James J. Tumors and cysts of the jaws. Washington, D.C: Armed Forces Institute of Pathology, 2001.

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Powell, A. J., ed. A Stratigraphic Index of Dinoflagellate Cysts. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2386-0.

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Book chapters on the topic "CysLTs"

1

Barua, Ranadhir. "Cysts (Skene’s Duct Cyst)." In Tumours of the Female Lower Genital Tract, 394–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74828-8_26.

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Arnold, M., and J. W. Lotz. "Hydatid Cysts (Echinococcus Cyst)." In ABC of Pediatric Surgical Imaging, 64–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-89385-1_32.

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Malik, Neelima. "Cysts of the “Oro-Maxillofacial Region”." In Oral and Maxillofacial Surgery for the Clinician, 549–75. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_27.

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AbstractCysts of the Oro-Maxillofacial region have common occurrence in comparison to any other parts of the body. These can be true cysts or pseudocysts and can be found in the jaw bones or in the soft tissues. Cysts are of various types, and over the years, various classifications are put forward, which are helpful to identify each cyst, based on its origin and its clinical and histopathological presentation. Based on the classification, one can also decide the treatment plan accordingly. The classifications are given by various researchers and also by WHO. In this chapter, various odontogenic and nonodontogenic cysts and their treatment aspect are discussed in detail.
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Barua, Ranadhir. "Cysts and Cyst-like Conditions." In Tumours of the Female Lower Genital Tract, 270–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74828-8_21.

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Larheim, Tore A. "Jaw Cysts and Cyst-Like Conditions." In Maxillofacial Imaging, 23–56. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53319-3_2.

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Mazabraud, André. "Idiopathic cyst, juxta-articular and related cysts, epidermoid cyst, hydatid cyst." In Pathology of bone tumours, 317–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-95839-7_29.

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Teller, Peter, Hermann König, Ulrich Weber, and Peter Hertel. "Baker’s Cysts, Ganglion Cysts." In MRI Atlas of Orthopedics and Traumatology of the Knee, 175–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55620-3_11.

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Ishikawa, Kinya. "Cysts." In Adnexal Tumors of the Skin, 64–69. Tokyo: Springer Japan, 1987. http://dx.doi.org/10.1007/978-4-431-68054-3_4.

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Rossi, Armando, and Giorgio Rossi. "Cysts." In CT of the Peritoneum, 279–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56488-8_11.

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Braun-Falco, Otto, Gerd Plewig, Helmut H. Wolff, and Richard K. Winkelmann. "Cysts." In Dermatology, 977–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-00181-3_53.

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Conference papers on the topic "CysLTs"

1

Lagemaat, M. W., L. G. E. Cox, M. L. Reilingh, C. C. van Donkelaar, B. van Rietbergen, L. Blankevoort, C. N. van Dijk, and K. Ito. "Fluid Pressure May Lead to Subchondral Bone Cyst Development via Mechanoregulated Bone Remodeling." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19582.

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Ankle trauma associated with an osteochondral defect (OD) of the talus often leads to subchondral bone cysts (Fig. 1, left). These cysts are associated with persistent ankle pain, thereby limiting the patients’ mobility [1]. Histology suggests that bone cyst development may occur in different stages, since some cysts are found to contain fluid, while others contain soft tissues. In addition, talar cysts may grow or shrink in time, and develop a sclerotic rim. The exact mechanism behind the development of talar cysts is unclear, but it has been proposed that fluid intrusion from the joint space through the OD plays a key role [1,2]. Pressurization of this fluid may have an osteolytic effect on the surrounding bone, thereby enlarging the cyst cavity.
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Elangovan, Shreehari, and Gregory M. Odegard. "Finite Element Modeling of Intraneural Ganglion Cysts of the Common Peroneal Nerve." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11637.

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Intraneural Ganglion Cysts [IGC] are a set of medical conditions that result in denervation of the muscles innervated by the cystic nerve leading to pain and loss of function. Current treatment approaches only temporarily alleviate pain and denervation which, however, does not prevent cyst recurrence. Hence, a mechanistic understanding of the pathogenesis of IGC can help clinicians understand them better and therefore device more effective treatment options. In this study, a preliminary analysis methodology is established to investigate the pathogenesis of IGC.
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Chahal, Amandeep, and Pushpa Dahiya. "Evaluation of ovarian reserve in women undergoing ovarian cystectomy by laparoscopy and laparotomy." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685295.

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Ovarian cysts are one of the commonest problems encountered in the gynecological field. Majority of these cysts are functional i.e., disappear spontaneously, while few need cystectomy. Ovarian cystectomy is done by laparotomy and laparoscopic technique. The method to achieve haemostasis in the ovarian bed after cyst removal varies with the type of technique. Electrocoagulation is used to achieve haemostasis in laparoscopic cystectomy while the bleeding vessels are sutured for haemostasis in cystectomy by laparotomy. Both the modalities of management varies in terms of compromise of ovarian reserve. The study was carried out to evaluate the surgical impact of benign ovarian masses on ovarian reserve as measured by serum levels of antimullerian harmone. In this prospective study on 30 women of reproductive age group with benign ovarian masses, 15 women were enrolled for laparoscopic ovarian cystectomy and another 15 women were enrolled for cystectomy by laparotomy and ovarian reserve was measured by levels of serum AMH preoperatively, postoperative one week and postoperative 3 months using standard ELISA assay kit. The preoperative, postoperative one week and postoperative 3 months levels of mean AMH were 4.74 ± 1.86 ng/ml, 2.92 ± 1.45 ng/ml and 2.64 ± 0.96 ng/ml respectively, in women undergoing laparoscopic cystectomy and 3.98 ± 1.35 ng/ml, 2.48 ± 0.64 ng/ml and 2.11 ± 0.63 ng/ml respectively in women undergoing ovarian cystectomy by laparotomy. So there was decline of mean AMH levels in postoperative one week and postoperative 3 months samples in both of the groups of enrolled women. However, this decline varied with the type of cyst removed and is insignificantly greater in laparoscopy group, wherein electrocoagulation may cause extensive and sustained damage to ovarian tissue.
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Moyer, Matthew T., Setareh Sharzehi, Charles E. Dye, Wafik El-Deiry, Thomas J. McGarrity, Abraham Mathew, Niraj Gusani, Raquel E. Davila, and Brooke Ancrile. "Abstract B95: Is ethanol required for cyst ablation in patients with premalignant type pancreatic cysts?" In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b95.

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Lu, Victor, Avital Perry, Christopher Graffeo, Krishnan Ravindran, and Jamie Van Gompel. "Recurrence of Rathke’s Cleft Cysts Based on Gross Total Resection of Cyst Wall: A Meta-analysis." In 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702442.

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Deshpande, Deepak A., Capre Mitchell, Junyan Gu, Colin Funk, and Raymond B. Penn. "Regulation Of Cysteinyl Leukotriene (CysL) Type 1 Receptor (CysLT1R) By Protein Kinase C (PKC)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6360.

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Iankov, Georgi, Mihail Plochev, Anatoli Semkov, Eluar Goranov, Vladimir Stanoev, and Danail Petrov. "Primary extrapulmonary intrathoracic hydatid cysts." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2530.

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Ramachandran, Rajesh, Larry Siu, Vadim Kurbatov, Evan Grossman, Frank Gress, and Laura Martello. "Abstract B33: Classification of pancreatic cysts in a minority population through cytokine profiling of cyst fluid fine-needle aspirate." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b33.

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Farzana Shahar Banu, A., M. Kayalvizhi, Banumathi Arumugam, and Ulaganathan Gurunathan. "Texture based classification of dental cysts." In 2014 International Conference on Control, Instrumentation, Communication and Computational Technologies (ICCICCT). IEEE, 2014. http://dx.doi.org/10.1109/iccicct.2014.6993152.

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Mestan, Hüseyin, Kenan Can Ceylan, and Şeyda Örs Kaya. "Surgery outcomes of the bronchogenic cysts." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1094.

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Reports on the topic "CysLTs"

1

Davies, E. H., and T. P. Poulton. Upper Jurassic Dinoflagellate Cysts From Strata of northeastern British Columbia. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1986. http://dx.doi.org/10.4095/120664.

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Ioannides, N. S. Dinoflagellate cysts from upper cretaceous-lower tertiary sections, Bylot and Devon Islands, Arctic Archipelago. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1986. http://dx.doi.org/10.4095/123641.

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Kurita, H., and T. Uchida. Dinoflagellate cysts from the JAPEX/JNOC/GSC Mallik 2L-38 gas hydrate research well. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1999. http://dx.doi.org/10.4095/210750.

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Fensome, R. A., and G. L. Williams. Dinoflagellate cyst PalyAtlas. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2019. http://dx.doi.org/10.4095/313575.

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Nelson, Brenda L. Solitary Bone Cyst. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada520056.

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Bissonnette, Kaitlyn, Travis Faske, and Albert Tenuta. Soybean Cyst Nematode. United States: Crop Protection Netework, April 2021. http://dx.doi.org/10.31274/cpn-20210423-0.

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Chen, Jun, Jun Xiong, and Si-Yuan Zhu. Effect of fire needle for ganglion cysts: a protocol of systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0032.

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Lawson, Vincent, Gregory L. Tylka, Christopher C. Marett, and Gregory D. Gebhart. Soybean Cyst Nematode Resistant Soybean Trial. Ames: Iowa State University, Digital Repository, 2007. http://dx.doi.org/10.31274/farmprogressreports-180814-938.

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Fan, Ying. Total Cyst Excision of Type I Choledochal Cyst 2 Years After Roux-enY Hepatocholangiojejunostomy: Report of a Case. Science Repository OÜ, April 2019. http://dx.doi.org/10.31487/j.scr.2018.10.001.

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Tylka, Gregory L., Gregory D. Gebhart, Christopher C. Marett, Mark P. Mullaney, and Stith N. Wiggs. Evaluation of Soybean Varieties Resistant to Soybean Cyst Nematode. Ames: Iowa State University, Digital Repository, 2011. http://dx.doi.org/10.31274/farmprogressreports-180814-1142.

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