Relevant bibliographies by topics / Prostaglandine D₂

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  2. Dissertations / Theses
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Academic literature on the topic 'Prostaglandine D₂'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Prostaglandine D₂"

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Laverdière, G., J. J. Dufour, G. L. Roy, D. Lavoie, and J. Proulx. "Comparaison de l'effet de deux analogues de la prostaglandine F2α sur la synchronisation de l'œstrus chez la vache de boucherie." Canadian Journal of Animal Science 74, no. 1 (March 1, 1994): 29–36. http://dx.doi.org/10.4141/cjas94-005.

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The objective of this study was to compare the efficiency of cloprostenol and fenprostalene in synchronizing estrus. Before treatment, estrus was detected during 4.5 d for multiparous cows in exp. 1 (n = 105) and 7.5 d for primiparous and nulliparous females in exp. 2 (n = 86). Females that were not in estrus (exp. 1: n = 74 and exp. 2: n = 58) received at random, either 500 μg of cloprostenol (i.m.) or 1 mg of fenprostalene (s.c). Cattle synchronized with cloprostenol or fenprostalene that presented estrus within 5 d showed similar fertility rates (exp. 1: 86.1% vs. 88.0% and exp. 2: 89.3% vs. 72.2% for cloprostenol and fenprostalene, respectively) and PGF2α-estrus intervals (exp. 1: 68 h vs. 73 h and exp. 2: 57 h vs. 57 h). However, the incidence of synchronization (exp. 1: 97.3% vs. 67.6%, P < 0.001; and exp. 2: 93.3% vs. 64.3%, P < 0.01) and pregnancy rates (exp. 1: 83.8% vs. 59.5%, P < 0.05; and exp. 2: 83.3% vs. 46.4%, P < 0.01) were statistically higher for cloprostenol than for fenprostalene. In exp. 2, primiparous cows and heifers obtained similar reproductive performances. The fertility rate of cattle treated with cloprostenol in exp. 2 was higher than that of untreated cattle (89.3% vs. 50.0%, P < 0.001, n = 56). In exp. 1, the variance of interval to estrus was similar for both analogues, but in exp. 2, it was less variable after the administration of cloprostenol (P < 0.05). Intervals between cloprostenol injection and estrus (0–10 and 0–15 d) were shorter (P < 0.05) and less variable (P < 0.001) than fenprostalene–estrus intervals. These results indicate that cloprostenol has a better potential for estrus synchronization than fenprostalene. Key words: Cloprostenol, fenprostalene, estrus synchronization, prostaglandin F2α, beef cattle
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SHIMURA, Takanori, Masaru MIYAZAKI, Masatoshi KURIHARA, Osamu TAKAHASHI, Shigemi KAWATA, Ikuo UDAGAWA, Hisao KOSHIKAWA, et al. "Effects of prostaglandine-E1 and glucagon-insulin on hepatic regeneration following partial hepatectomy in D-galactosamine induced rat liver." Japanese Journal of Gastroenterological Surgery 20, no. 8 (1987): 1877–82. http://dx.doi.org/10.5833/jjgs.20.1877.

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Adachi, Hisanobu, Takehiro Suzuki, Michiaki Abe, Naoki Asano, Hiroya Mizutamari, Masayuki Tanemoto, Toshiyuki Nishio, et al. "Molecular characterization of human and rat organic anion transporter OATP-D." American Journal of Physiology-Renal Physiology 285, no. 6 (December 2003): F1188—F1197. http://dx.doi.org/10.1152/ajprenal.00402.2002.

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We have isolated and characterized a novel human and rat organic anion transporter subtype, OATP-D. The isolated cDNA from human brain encodes a polypeptide of 710 amino acids ( Mr 76,534) with 12 predicted transmembrane domains. The rat clone encodes 710 amino acids ( Mr 76,821) with 97.6% amino acid sequence homology with human OATP-D. Human and rat OATP-D have moderate amino acid sequence homology with LST-1/rlst-1, the rat oatp family, the prostaglandin transporter, and moat1/MOAT1/KIAA0880/OATP-B. Phylogenetic tree analysis revealed that OATP-D is branched in a different position from all known organic anion transporters. OATP-D transports prostaglandin E1 ( Km 48.5 nM), prostaglandin E2 ( Km 55.5 nM), and prostaglandin F2α, suggesting that, functionally, OATP-D encodes a protein that has similar characteristics to those of the prostaglandin transporter. Rat OATP-D also transports prostaglandins. The expression pattern of OATP-D mRNA was abundant mainly in the heart, testis, brain, and some cancer cells. Immunohistochemical analysis further revealed that rat OATP-D is widely expressed in the vascular, renal, and reproductive system at the protein level. These results suggest that OATP-D plays an important role in translocating prostaglandins in specialized tissues and cells.
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Watzková, Jarmila, Ludmila Křížová, Aleš Pavlík, Věra Schulzová, Jana Hajšlová, and Jaromír Lojza. "The Effect of Soybean-Derived Phytoestrogens on Concentrations of Plasma Isoflavones, 15-keto-13,14-dihydroprostaglandin F2α and Progesterone in Dairy Cows." Acta Veterinaria Brno 79, no. 4 (2010): 525–32. http://dx.doi.org/10.2754/avb201079040525.

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The objective of the study was to determine the effect of soybean-derived phytoestrogens and their metabolites on the activity of sex hormones during the oestrous cycle in multiparous lactating dairy cows. The experiment was carried out on 4 multiparous lactating Holstein cows in the form of replicated Latin square in double reversal design. The experiment in the total length of 168 days was divided into 4 periods of 42 days, each consisting of a 21-day preliminary period and a 21-day collecting period. Cows were divided into 2 groups of 2 cows. The control group (C) was fed a diet based on extruded rapeseed cake while the experimental group (S) was fed a diet containing extruded full-fat soya. The intake of total isoflavones was 3297 mg/d in S and 58.0 mg/d in C (P < 0.001). The concentrations of individual isoflavones, it is daidzein, genistein and equol in plasma were significantly higher in the experimental group S (49.3, 78.7 and 218.8 ng/ml, respectively) than in the control group C (13.5, 42.9 and 18.3 ng/ml, respectively, P < 0.001). Plasma concentration of progesterone throughout the oestrous cycle was not influenced by the diet used (P > 0.05). Plasma concentration of prostaglandine PGFM throughout the oestrous cycle in the experimental group (S) tended to be higher (P = 0.095) than in the control group (C). No differences in the length of the oestrous cycle between the cows fed different diets were observed.
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Kutyrev, Olennikov, Kaschenko, and Mazur. "DYNAMICS OF SECRETION OF PROSTAGLANDINS E2 AND D2 WITH DIBOTHRIOCHEPHALLUS DENDRITICUS (CESTODA) PLEROCERCOIDS IN RESPONSE TO EXPOSURE OF BLOOD SERUM OF BAIKAL CISCO, THE HOST." THEORY AND PRACTICE OF PARASITIC DISEASE CONTROL, no. 21 (May 29, 2020): 180–86. http://dx.doi.org/10.31016/978-5-9902341-5-4.2020.21.180-186.

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Parasites regulate host immune response via secretion of soluble mediators which interact in a certain way with cells and molecules of the immune system. The aim of the study was to determine changes of prostaglandins E2 и D2 content in Dibothriochephallus dendriticus plerocercoids and also in the incubation media during incubation of tapeworms with addition of blood serum from the intermediate host – Baikal cisco. D. dendriticus plerocercoids were retrieved from the host body cavity, ashed in the physiological solution and placed in incubation media. Microcolumn high-performance liquid chromatography was used to detect prostaglandins. Concentration of prostaglandins in the plerocercoid organism increased insignificantly after incubation in the Hanks’ solution with addition of blood serum, when compared with incubation in the Hanks’ solution only. Concentration of prostaglandin E2 increased significantly in the incubation media after incubation of plerocercoids in the Hanks’ solution with addition of blood serum. Prostaglandin D2 was also identified in high concentrations after 12 h and 24 h of incubation, whereas prostaglandin D2 was not quite detected during incubation in Hanks’ solution only.
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Zehbe, Rolf, Bernhard Watzer, Rainer Grupp, Sven Halstenberg, Heinrich Riesemeier, C. James Kirkpatrick, Helmut Schubert, and Christoph Brochhausen. "Tomographic and Topographic Investigation of Poly-D,L-Lactide-Co-Glycolide Microspheres Loaded with Prostaglandine E2 for Extended Drug Release Applications." Advanced Materials Research 89-91 (January 2010): 687–91. http://dx.doi.org/10.4028/www.scientific.net/amr.89-91.687.

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Polymeric, biodegradable microspheres represent a good reliable system to investigate the release of bioactive substances in both in vitro and in vivo applications. Common biomaterials for the synthesis of these microspheres are aliphatic polyesters of the poly(α-hydroxy)acids, especially poly-L-lactides (PLA) and polyglycolides (PGA) or their copolymers poly-D,L-lactide-co-glycolides (PLGA). In our own previous studies we have developed PLGA microspheres with integrated PGE2 as model substance for a wide range of biomedical applications, especially in angiogenesis, fracture healing and cartilage repair. The synthesis is based on a binary solvent in water emulsion approach, where two different solvents are used to dissolve the active agent and the polymer, while being miscible in each other (CHCl3, ethyl acetate). Both, the degradation of the material and the release profiles were investigated using SEM and mass spectrometry coupled with gas- or high performance liquid chromatography. SEM and AFM measurements indicated a porous structure of the microspheres but could not resolve the true three dimensional structure of the microspheres. Therefore, synchrotron radiation-based µCT (SR-µCT) investigations were performed to link the release profile to the structural design of the microspheres. As a result, we were able to cross validate the experimental data from SEM and AFM with SR-µCT, demonstrating both micro-porosity and nano-porosity. The polymer itself appears to consist of 200 nm – 300 nm sized particles.
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Chen, Xiaojie, and Jon D. Levine. "NOS Inhibitor Antagonism of PGE2-Induced Mechanical Sensitization of Cutaneous C-Fiber Nociceptors in the Rat." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 963–66. http://dx.doi.org/10.1152/jn.1999.81.3.963.

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NOS inhibitor antagonism of PGE2-induced mechanical sensitization of cutaneous C-fiber nociceptors in the rat. Prostaglandins, metabolites of arachidonic acid, released during tissue injury and inflammation sensitize primary afferent nociceptors. While it has been suggested that this effect on nociceptors is mediated mainly via the cAMP second messenger system, recent evidence suggests that nitric oxide (NO) is also involved in peripheral pain mechanisms. To test the hypothesis that NO contributes to the sensitization of nociceptors to mechanical stimuli induced by hyperalgesic prostaglandins, we compared von Frey hair mechanical threshold as well as the response evoked by 10-s sustained threshold mechanical stimulation before and after injection of prostaglandin E2(PGE2) alone, and NOS inhibitor N G-methyl-l-arginine (l-NMA) or its inactive stereoisomer N G-methyl-d-arginine (d-NMA) plus PGE2, adjacent to the receptive field of C-fiber nociceptors. The reduction of mechanical threshold and increase in number of action potentials to sustained mechanical stimulation induced by intradermal application of PGE2 was blocked by l-NMA, but not d-NMA. It is suggested that NO contributes to nociceptor sensitization induced by hyperalgesic prostaglandins.
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Sawyer, Sara J., Suzanne M. Norvell, Suzanne M. Ponik, and Fredrick M. Pavalko. "Regulation of PGE2and PGI2release from human umbilical vein endothelial cells by actin cytoskeleton." American Journal of Physiology-Cell Physiology 281, no. 3 (September 1, 2001): C1038—C1045. http://dx.doi.org/10.1152/ajpcell.2001.281.3.c1038.

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Disruption of microfilaments in human umbilical vein endothelial cells (HUVEC) with cytochalasin D (cytD) or latrunculin A (latA) resulted in a 3.3- to 5.7-fold increase in total synthesis of prostaglandin E2(PGE2) and a 3.4- to 6.5-fold increase in prostacyclin (PGI2) compared with control cells. Disruption of the microtubule network with nocodazole or colchicine increased synthesis of PGE21.7- to 1.9-fold and PGI21.9- to 2.0-fold compared with control cells. Interestingly, however, increased release of PGE2and PGI2from HUVEC into the media occurred only when microfilaments were disrupted. CytD treatment resulted in 6.7-fold more PGE2and 3.8-fold more PGI2released from HUVEC compared with control cells; latA treatment resulted in 17.7-fold more PGE2and 11.2-fold more PGI2released compared with control cells. Both increased synthesis and release of prostaglandins in response to all drug treatments were completely inhibited by NS-398, a specific inhibitor of cyclooxygenase-2 (COX-2). Disruption of either microfilaments using cytD or latA or of microtubules using nocodazole or colchicine resulted in a significant increase in COX-2 protein levels, suggesting that the increased synthesis of prostaglandins in response to drug treatments may result from increased activity of COX-2. These results, together with studies demonstrating a vasoprotective role for prostaglandins, suggest that the cytoskeleton plays an important role in maintenance of endothelial barrier function by regulating prostaglandin synthesis and release from HUVEC.
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Nango, Hiroshi, Yasuhiro Kosuge, Nana Yoshimura, Hiroko Miyagishi, Takanori Kanazawa, Kaname Hashizaki, Toyofumi Suzuki, and Kumiko Ishige. "The Molecular Mechanisms Underlying Prostaglandin D2-Induced Neuritogenesis in Motor Neuron-Like NSC-34 Cells." Cells 9, no. 4 (April 10, 2020): 934. http://dx.doi.org/10.3390/cells9040934.

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Prostaglandins are a group of physiologically active lipid compounds derived from arachidonic acid. Our previous study has found that prostaglandin E2 promotes neurite outgrowth in NSC-34 cells, which are a model for motor neuron development. However, the effects of other prostaglandins on neuronal differentiation are poorly understood. The present study investigated the effect of prostaglandin D2 (PGD2) on neuritogenesis in NSC-34 cells. Exposure to PGD2 resulted in increased percentages of neurite-bearing cells and neurite length. Although D-prostanoid receptor (DP) 1 and DP2 were dominantly expressed in the cells, BW245C (a DP1 agonist) and 15(R)-15-methyl PGD2 (a DP2 agonist) had no effect on neurite outgrowth. Enzyme-linked immunosorbent assay demonstrated that PGD2 was converted to 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) under cell-free conditions. Exogenously applied 15d-PGJ2 mimicked the effect of PGD2 on neurite outgrowth. GW9662, a peroxisome proliferator-activated receptor–gamma (PPARγ) antagonist, suppressed PGD2-induced neurite outgrowth. Moreover, PGD2 and 15d-PGJ2 increased the protein expression of Islet-1 (the earliest marker of developing motor neurons), and these increases were suppressed by co-treatment with GW9662. These results suggest that PGD2 induces neuritogenesis in NSC-34 cells and that PGD2-induced neurite outgrowth was mediated by the activation of PPARγ through the metabolite 15d-PGJ2.
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BUHR, M. M., R. M. McKAY, and D. L. GRINWICH. "LUTEOLYTIC ACTION OF PROSTAGLANDINS IN SWINE AND THE EFFECTS OF CLOPROSTENOL ON LUTEINIZING HORMONE RECEPTORS AND MEMBRANE STRUCTURE OF PORCINE CORPORA LUTEA." Canadian Journal of Animal Science 66, no. 2 (June 1, 1986): 415–22. http://dx.doi.org/10.4141/cjas86-043.

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The luteolytic action of prostaglandin F2α (PGF2α), 15-keto-PGF2α, 15-methyl-PGF2α, and cloprostenol was evaluated in cycling gilts and sows after intramuscular injection on day 13 of the estrous cycle. Only cloprostenol significantly shortened the mean cycle length (18.5 vs. 20.3 d, P < 0.05). Cloprostenol also caused a more rapid decline in serum progesterone concentrations than did the other prostaglandins. Serum concentrations of the prostaglandin metabolite 13,14-dihydro-15-keto-PGF2α (PGFM), showed rapid transitory peaks after PGF2α or 15-keto-PGF2α and a lower, later rise after cloprostenol. A second experiment examined luteal luteinizing hormone (LH) receptors and luteal membrane ultrastructure during the estrous cycle and pregnancy and the effect of cloprostenol on these parameters during the estrous cycle. The number of unoccupied luteal LH receptors, as measured by specific 125I-hCG binding, dropped significantly from mid to late pregnancy and from mid to late cycle. Cloprostenol lowered serum progesterone concentrations but did not affect hCG binding. X-ray diffraction showed no correlation of gel or liquid-crystalline phase lipids in luteal microsomes with the stage of the estrous cycle or pregnancy or cloprostenol treatment. Key words: Swine, luteolysis, estrous cycle, prostaglandins, luteal LH receptors
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Dissertations / Theses on the topic "Prostaglandine D₂"

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Partheil, Anna [Verfasser], and Heike [Gutachter] Rittner. "Monozyten und Prostaglandine in der Schmerzentstehung / Anna Partheil. Gutachter: Heike Rittner." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1111815275/34.

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Yue, Li. "Induction de l'apoptose des ostéoclastes humains par la Prostaglandine D[indice inférieur 2] : récepteurs et mécanismes de transduction impliqués." Thèse, Université de Sherbrooke, 2013. http://hdl.handle.net/11143/6259.

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Résumé: La prostaglandine D? (PGD?) est un médiateur lipidique qui active directement deux récepteurs spécifiques, DP et CRTH2, régulant ainsi des processus inflammatoires, immunitaires et apoptotiques. Les ostéoclastes (OC) sont de larges cellules multinucléées participant au métabolisme et remodelage de l’os, ainsi qu’à la réparation de fracture osseuse. Nos travaux ont mis en évidence l’expression des récepteurs DP et CRTH2 chez des OCs humains. Cependant, les effets de la PGD? sur l’apoptose des OCs sont inconnus. L’objectif de la présente étude a été de déterminer si la PGD? induit l’apoptose et les mécanismes qui en découlent dans les OC humains. Les OCs humains différenciés ont été traités avec la PGD?, les agonistes et antagonistes de ses récepteurs. Le traitement des OCs avec la PGD?, en présence de naproxène, qui permet d’inhiber la production endogène de prostaglandines, augmente de façon dépendante de la dose et en fonction du temps le pourcentage d'OCs apoptotiques. Ceci a également été observé lors du traitement des OCs avec l’agoniste spécifique DK-PGD? du récepteur CRTH2, mais pas avec le traitement du composé BW 245C, antagoniste du récepteur DP. En absence de naproxène, l’antagoniste CAY10471 du récepteur CRTH2 réduit le taux d’apoptose des OCs tandis que le composé BW A868C, antagoniste du récepteur DP, n'a aucun effet. L'apoptose des OCs par la PGD? via CRTH2 est associée à l’activation de la caspase-9, et non pas la caspase-8, ce qui entraîne le clivage de la caspase-3. Afin de déterminer plus précisément les mécanismes menant à ces résultats, les OCs ont été traités avec les inhibiteurs de MEK-1/2, PI3K et IKK2/NF-?B. Le traitement des OCs avec la PGD? et l’agoniste de CRTH2 diminue la phosphorylation des protéines ERK1/2 et Akt, tandis que la phosphorylation de ?-arrestine-1 est augmentée. Par ailleurs, les niveaux de phosphorylation d'ERK1/2 et Akt ont été augmentés alors que le taux de protéines ?-arrestine-1 phosphorylees a été diminué par l’antagoniste de CRTH2. En outre, le traitement des OCs avec l’inhibiteur de MEK-1/2 augmente l’apoptose des OCs induite par PGD? et l’agoniste de CRTH2. Cependant, l’antagoniste de CRTH2 diminue l'activité de la caspase-3 induite par l’inhibiteur de MEK1/2. Le traitement des OCs avec l’inhibiteur de la PI3K diminue la phosphorylation d’ERK l/2, tandis que la phosphorylation d'ERK1/2 augmentée par l’antagoniste de CRTH2 a été atténuée par l’inhibiteur de PI3K. Les agonistes et antagonistes du récepteurs DP n'ont pas d’effet sur la phosphorylation d'ERK1/2, Akt, ?-arrestine-1 ni sur l’activité de la caspase-3 chez les OCs. Le traitement des OCs avec PGD? et les ligands de ses récepteurs ne modifie pas la phosphorylation de Re1A/p65. De plus, l’activité de la caspase-3 n'est pas altérée dans les OCs traités avec l’inhibiteur d’IKK2. En conclusion, PGD?, en se liant à CRTH2, induit l’apoptose des OCs via la voie apoptotique intrinsèque qui est associée à la régulation des voies de signalisation des protéines ?-arrestine-1, ERK1/2, et Akt, mais pas celle du IKK2/NF-?B. // Abstract: Prostaglandin D2 (PGD2) is a lipid mediator that directly activates two specific receptors, DP and CRTH2, thereby regulating inflammation, immune response and apoptosis. Osteoclasts (OCs) are large multinucleated cells that participate in bone metabolism, remodeling, and fracture repair. Our previous data show the expression of DP and CRTH2 in human OCs. However, it is unknown whether PGD2 affects OC apoptosis. The objective of the thesis was to determine whether PGD2 induces human OC apoptosis and the underlying mechanisms implicated in this effect. The differentiated human OCs were treated with PGD2, and its receptors agonists/antagonists. Treatment with PGD2 in the presence of naproxen to inhibit endogenous prostaglandins production increased OC apoptosis in a dose- and time-dependent manner, as did the specific CRTH2 agonist compound DK-PGD2 but not the DP agonist compound 13W 245C. In the absence of naproxen, the CRTH2 antagonist compound CAY 10471 reduced OC apoptosis whereas the DP antagonist BW A868C had no such effect. PGD2/CRTH2-induced OC apoptosis was associated with the activation of caspase-9 (an intrinsic apoptosis pathway-initiator caspase), but not caspase-8 (an extrinsic apoptosis pathway-initiator caspase), leading to caspase-3 cleavage. To further determine the mechanisms underlying these findings, human OCs were treated with the inhibitors of MEK-1/2, P13K and IKK2/NF-KB. Treatments with PGD2 and a CRTH2 agonist decreased ERKI/2 and Akt phosphorylation, whereas both treatments increased 13-arrestin- I phosphorylation. Both ERK1/2 and Akt phosphorylation were augmented, whereas the phosphorylated 13-arrestin-1 was reduced by a CRTH2 antagonist. Furthermore, treatment of OCs with a MEK-1/2 inhibitor increased OC apoptosis induced by PGD2 and by a CRTH2 agonist. However, a CRTH2 antagonist diminished the MEK- I /2 inhibitor-induced increase in caspase-3 activity. In addition, treatment of OCs with a PI3K inhibitor decreased ERK I /2 phosphorylation, whereas increased ERK1/2 phosphorylation by CRTH2 antagonist was attenuated by a P13K inhibitor. Both DP receptor agonist and antagonist did not affect either Akt, ERK1/2, 13-arrestin-1 phosphorylation or a specific MEK-1/2 inhibitor-induced increase in caspase-3 activity in OCs. Treatment of OCs with PGD2 and its receptor ligands did not alter ReIA/p65 phosphorylation (ser536). Moreover, the caspase-3 activity was not altered in OCs treated with an IKK2/NF-KB inhibitor. In summary, PGD2 induces human OC apoptosis through a CRTH2-dependent intrinsic apoptosis pathway, which is associated with regulation of the 13-affestin-1, ERK1/2, and Akt, but not with 1KK2/NF-KB, signaling pathways. [symboles non conformes]
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Farhat, Andalib. "Implication de la voie Prostaglandine D synthase/PGD2/SOX9 dans l'ovaire normal et pathologique et régulation par la signalisation estrogénique." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20206.

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L'ovaire représente à la fois un organe cible et le principal organe producteur d'estrogènes et de progestérone qui maintiennent le développement des caractères sexuels féminins et une fonction de reproduction normale. Cette production hormonale est contrôlée par les gonadotropines FSH et LH produites dans l'hypophyse, responsables dans l'ovaire de la croissance folliculaire et de l'ovulation, respectivement. Mon travail de thèse a identifié la signalisation prostaglandine D2 (PGD2), comme un nouvel élément-clé dans la signalisation des gonadotropines, contribuant à l'activation de l'expression des récepteurs FshR et LhR et des enzymes de la stéroïdogenèse SCC et StAR. La PGD2, produite dans plusieurs tissus par deux enzymes de synthèse, les prostaglandines synthases H et L-PGDS, est impliquée dans de nombreuses fonctions physiologiques et pathologiques. Comme dans l'ovaire pathologique, nous avons montré que la PGD2 avait aussi un rôle anti-prolifératif dans la cellule de granulosa de l'ovaire normal. Le cancer de l'ovaire représente la 4ème cause de mortalité par cancer chez la femme. Les mécanismes moléculaires impliqués dans le développement de ces tumeurs sont encore peu connus, bien que l'implication des estrogènes et de la Prostaglandine E2 (PGE2) dans la progression des tumeurs ovariennes épithéliales soit bien établie. D'autre part, les ovaires des souris invalidées pour les gènes codant les récepteurs aux estrogènes ou l'aromatase, possèdent des structures tubulaires contenant des cellules de Leydig et des cellules de Sertoli re-différenciées exprimant le facteur de détermination sexuelle mâle SOX9, alors qu'il n'est pas exprimé dans l'ovaire sain. Mon travail a montré que les estrogènes inhibent la transcription des gènes Sox9 et L-Pgds dans les lignées ovariennes tumorales BG1 et COV434 et que cette régulation est la résultante d'une inhibition, via le récepteur ERa et d'une activation via le récepteur ERß. Ces résultats sont en accord avec les études sur les effets prolifératifs d'ERa et le rôle anti-prolifératif d'ERß et suggèrent donc un rôle anti-prolifératif de la PGD2 dans l'ovaire tumoral et une régulation négative directe ou indirecte de l'expression de Sox9 et des Pgds par les estrogènes
The prostaglandin D2 (PGD2) pathway is involved in numerous biological processes and while it has been identified as a partner of the embryonic sex determining male cascade, the roles it plays in ovarian function remain largely unknown. PGD2 is secreted by two prostaglandin D synthases (Pgds); the male-specific lipocalin (L)-Pgds and the hematopoietic (H)-Pgds. Here, we report the localization of H-Pgds mRNA in the granulosa cells from the primary to pre-ovulatory follicles. We used adult female mice treated with HQL-79, a specific inhibitor of H-Pgds enzymatic activity, to provide evidence of an interaction between H-Pgds-produced PGD2 signaling and FSH signaling. This leads to the activation of steroidogenic Scc and StAR gene expression through increased FshR and LhR receptor expression leading to progesterone secretion. We also identify a role whereby H-Pgds-produced PGD2 is involved in the regulation of follicular growth through inhibition of granulosa cell proliferation in the growing follicles. Indeed, we report an altered H-Pgds expression in human ovarian tumors alongside a partial or complete absence of H-Pgds protein in granulosa cell tumors, suggesting a potential association between decreased levels of H-Pgds expression and a tumoral phenotype. Together, these results show PGD2 signaling to be essential for FSH action within granulosa cells, thus identifying an important and unappreciated role for PGD2 signaling in controlling the balance of proliferation, differentiation and steroidogenic activity of these cells
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Durand, Marianne. "Effets des récepteurs de la prostaglandine D[indice inférieur 2] chez les ostéoclastes humains et étude de la capacité d'ostéoclastogénèse chez les individus." Mémoire, Université de Sherbrooke, 2007. http://savoirs.usherbrooke.ca/handle/11143/3919.

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Les ostéoclastes sont des cellules multinucléées capables de résorber l'os. Cette fonction unique, quoiqu'essentielle, peut devenir dangereuse lorsqu'il y a perte de contrôle et de régulation. En effet, l'ostéoclaste pourrait être le grand responsable de certaines maladies osseuses telles que l'ostéoporose, la maladie de Paget et la polyarthrite rhumatoïde. II existe de nombreuses études sur les molécules impliquées dans le métabolisme de l'os, mais seulement quelques-unes d'entre d'entre elles ont attiré notre attention : les prostaglandines. Celles-ci ont de nombreux effets physiologiques et pathologiques, c'est pourquoi nous avons décidé d'étudier leurs effets sur l'os. Nous avons récemment démontré que les ostéoblastes humains synthétisent la PGD[indice inférieur 2] et qu'ils expriment les deux récepteurs de la PGD[indice inférieur 2], DP et CRTH2. L'activation de DP dans les ostéoblastes engendre la réduction de production d'OPG, alors que l'activation de CRTH2 induit la chimiotaxie des ostéoblastes ainsi que la diminution d'expression de RANKL. Comme les ostéoblastes et les ostéoclastes sont intimement liés, nous avons décidé d'étudier les rôles des récepteurs de la PGD[indice inférieur 2] chez les ostéoclastes humains différenciés. Nos objectifs étaient de déterminer la présence et la distribution des récepteurs de la PGD[indice inférieur 2] dans les ostéoclastes humains et de caractériser leurs rôles dans les activités et la différenciation de ces cellules. Par immunohistochimie, nous avons démontré que les ostéoclastes humains adultes, en conditions physiologiques et pathologiques, et les ostéoclastes foetaux pressentent les deux récepteurs de la PGD[indice inférieur 2]. La stimulation avec la PGD[indice inférieur 2] a induit une réorganisation du cytosquelette caractérisé par une diminution des cellules formant un anneau d'actine et une augmentation des cellules présentant des lamellipodes. L'utilisation d'agonistes des récepteurs de la PGD[indice inférieur 2], BW 245C et DK-PGD[indice inférieur 2], a permis de démontrer que ces effets étaient médiés respectivement par DP et CRTH2. À la suite de ces observations, les ostéoclastes différenciés ont été traités avec les agonistes et les antagonistes des récepteurs de la PGD[indice inférieur 2] afin d'étudier leurs effets sur l'activité de résorption. Ainsi, seul le récepteur DP a eu un effet inhibiteur sur la résorption osseuse alors que le récepteur CRTH2 était impliqué seulement lorsqu'il était bloqué, engendrant une augmentation de l'aire totale de résorption. Un modèle d'ostéoclastogenese in vitro à partir des précurseurs monocytaires du sang périphérique cultive pendant 21 jours en présence de RANKL et M-CSF a montre que l'activation de DP ou CRTH2 diminuait le nombre d'ostéoclastes génères, alors que l'inhibition de chacun des récepteurs augmentait le nombre de ces cellules. Ces résultats suggèrent que la prostaglandine D2 pourrait avoir un effet bénéfique dans certaines maladies osseuses en diminuant la différentiation et l'activité de résorption des ostéoclastes. Lors des essais de différenciation, nous avons remarqué que l'osteoclastogénèse était très variable entre les individus. Ainsi, nous avons décidé d'étudier les caractéristiques démographiques d'une cohorte de 51 individus afin de déterminer les facteurs impliqués dans la capacité ostéoclastogénique. Les analyses statistiques ont démontré que la taille, le poids et le nombre de précurseurs ostéoclastiques étaient associés au nombre d'ostéoclastes différenciés in vitro. De plus, nous avons noté qu'il existait une corrélation statistiquement significative entre le nombre de cellules précurseurs et l'âge. Ces résultats suggèrent donc que la capacité d'ostéoclastogénèse pourrait être une caractéristique spécifique à chaque individu et qu'une activité de différenciation accrue pourrait rendre un individu susceptible à certaines pathologies telles que l'ostéoporose, la polyarthrite rhumatoïde et l'arthrose où l'ostéoclaste est l'élément central de ces maladies osseuses.
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Abdallah, Dina. "Fonctions de la phospholipase D et des récepteurs de la prostaglandine PGE2 durant la maturation des ostéoblastes, le processus de la minéralisation physiologique et la calcification cardiovasculaire." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10152/document.

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Le métabolisme lipidique affecte la maturation et la différenciation des cellules osseuses. L'objectif de ma thèse est d'approfondir deux aspects du métabolisme lipidique mal connus, soit les actions de la phospholipase D (PLD) et celles des récepteurs de prostaglandine PGE2 pendant la différenciation des cellules. Une lignée humaine, les Saos-2 et les ostéoblastes primaires issus de calvaria de souriceaux ont servi de modèles cellulaires de la minéralisation physiologique. La culture d'aorte ex vivo sous des conditions d'hyperphosphatémie a été utilisée pour reproduire la calcification de l'aorte qui est un modèle ex vivo de calcification cardiovasculaire (CCV). Nous avons montré que l'expression et l'activité de la PLD augmentent dans les Saos-2 et les ostéoblastes primaires au bout du 5ème jour de la différenciation tandis qu'elles s'accroissent au bout du 6ème jour de traitement de l'aorte dans un milieu d'hyperphosphatémie. Les inhibiteurs de PLD diminuent l'activité de phosphatase alcaline (TNAP) dans les ostéoblastes et dans l'aorte calcifiée tandis que la surexpression de la PLD1 dans les Saos-2 l'augmente. Dans une deuxième partie de ce travail, nous avons suivi la variation d'expression des récepteurs de PGE2 au cours de la maturation des Saos-2. L'expression du gène EP3 augmente au stade tardif de la minéralisation tandis que celle d'EP4 diminue. Pour conclure, ces résultats indiquent que l'activité de la PLD en affectant l'activité de la TNAP pourrait moduler finement la minéralisation physiologique et la CCV et que la minéralisation s'accompagne d'un changement d'expression des récepteurs de PGE2, dans les Saos-2
Lipid metabolism affects the maturation and the differentiation of bone cells. The aim of my PhD thesis is to explore two unknown sides of lipid metabolism which are the actions of phospholipase D (PLD) and those of prostaglandin PGE2 receptors during cell differentiation. Human lineage, Saos-2 cells and primary osteoblasts from calvaria of mice were used as cellular models of physiological mineralization. The ex vivo aorta culture under hyperphosphatemia conditions has been used to reproduce the calcification of the aorta, which is an ex vivo model of cardiovascular calcification (CVC). We showed that the expression and the activity of PLD increased in Saos-2 and primary osteoblasts after the fifth day of differentiation while in the aorta under hyperphosphatemia condition, PLD activity increased at the end of the sixth day. PLD inhibitors decreased the activity of alkaline phosphatase (TNAP) in osteoblasts and in calcified aorta while the overexpression of PLD1 in the Saos-2 increased it. In the second part of this work, we monitored the variation of the expression of PGE2 receptors during the maturation of Saos-2 cells. The EP3 gene expression increased in the late stage of the mineralization while that of EP4 decreased. In conclusion, these results indicated that the PLD activity by affecting the activity of TNAP could modulate the physiological mineralization and CVC. We showed that the mineralization is dependent of the change of the expression of PGE2 receptors in Saos-2 cells
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Chansi, Kengni Hurette Junie. "Régulation et expression de la prostaglandine D synthétase (PGDS) et de la prostacycline synthétase (PGIS) dans l'endomètre de rat gestant, non gestant et pseudogestant /." Trois-Rivières : Université du Québec à Trois-Rivières, 2006. http://www.uqtr.ca/biblio/notice/resume/24760974R.pdf.

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Chansi, Kengni Hurette Junie. "Régulation et expression de la prostaglandine D synthétase (PGDS) et de la prostacycline synthétase (PGIS) dans l'endomètre de rat gestant, non gestant et pseudogestant." Thèse, Université du Québec à Trois-Rivières, 2006. http://depot-e.uqtr.ca/1907/1/000134642.pdf.

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Nowak, Katharina [Verfasser], Hans-Georg [Akademischer Betreuer] Schaible, Hans-Christoph [Akademischer Betreuer] Scholle, and Karl [Akademischer Betreuer] MeßLinger. "Bedeutung spinaler Prostaglandine für die zentrale Sensibilisierung bei akuter und chronischer Kniegelenksarthritis bei Ratten / Katharina Nowak. Gutachter: Hans-Georg Schaible ; Hans-Christoph Scholle ; Karl Meßlinger." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2015. http://d-nb.info/1075492785/34.

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Gallant, Maxime. "Production de prostaglandine D[indice inférieur 2] par les ostéoblastes humains[ressource électronique] : augmentation de la chimiotaxie et diminution de la production d'ostéoprotégérine par la liaison aux récepteurs CRTH2 et DP." Mémoire, Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/3369.

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Les effets des prostaglandines sur le métabolisme osseux sont définis principalement par les actions de la prostaglandine E[indice inférieur 2] sur les cellules osseuses. Cependant, peu de données existent sur les effets possibles des autres prostaglandines sur le métabolisme osseux. Considérant l'hypothèse que d'autres prostaglandines produites lors d'une réaction inflammatoire (ex.: prostaglandine D[indice inférieur 2] ) pourraient jouer un rôle encore inconnu dans le métabolisme osseux, nous avons décidé de caractériser les récepteurs de la PGD[indice inférieur 2] chez les ostéoblastes humains primaires en culture, ainsi que la production de PGD[indice inférieur 2] par ces mêmes cellules, pour finalement caractériser certaines actions physiologiques de l'activation de ces récepteurs sur les ostéoblastes. Nous voulions ensuite démontrer si la PGD[indice inférieur 2] produite par les ostéoblastes pouvait agir directement sur ces cellules. Nous concluons que la PGD[indice inférieur 2] est produite par les ostéoblastes humains primaires, et que ces cellules expriment de façon fonctionnelle les récepteurs DP et CRTH2. Nos résultats démontrent que la PGD[indice inférieur 2] peut agir en tant qu'autacoïde sur les ostéoblastes humains"--Résumé abrégé par UMI.
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May, Julia [Verfasser], and W. [Akademischer Betreuer] Rascher. "Suppression von Interleukin 8, Cyclooxygenase 2, Prostaglandin-E-3-Rezeptor und Prostaglandinen durch Parecoxib und Indometacin im Tiermodell der neonatalen B- Streptokokkensepsis / Julia May. Betreuer: W. Rascher." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/1018801464/34.

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Book chapters on the topic "Prostaglandine D₂"

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Kleine, T. O. "Liquor-Prostaglandin-D-Synthetase." In Springer Reference Medizin, 1507–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1945.

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Kleine, T. O. "Liquor-Prostaglandin-D-Synthetase." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1945-1.

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Hayaishi, Osamu. "Prostaglandin D Synthase, β-Trace and Sleep." In Advances in Experimental Medicine and Biology, 347–50. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1810-9_74.

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Urade, Yoshihiro, and Osamu Hayaishi. "Structure and Function of Two Distinct Types of Prostaglandin D Synthase." In Advances in Prostaglandin and Leukotriene Research, 69–72. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9721-0_12.

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Pettipher, Roy, and Trevor T. Hansel. "Antagonists of the prostaglandin D2 receptor CRTH2." In New Drugs and Targets for Asthma and COPD, 193–98. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320819.

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Binda, Chantal, and Jean-Luc Parent. "Characterization of the Interaction Between the Prostaglandin D2 DP1 Receptor and the Intracellular l-Prostaglandin D Synthase." In Methods in Molecular Biology, 53–67. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1755-6_6.

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Beuckmann, Carsten T., Yoshihiro Urade, and Osamu Hayaishi. "Lipocalin-type Prostaglandin D Synthase (β-Trace) Binds Non- Substrate Lipophilic Ligands." In Advances in Experimental Medicine and Biology, 55–60. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4793-8_9.

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Ikai, K., M. Ujihara, Y. Horiguchi, and Y. Urade. "Prostaglandin D Synthetase Is Localized in Antigen Presenting Cells and Mast Cells." In New Trends in Allergy III, 149–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46717-2_20.

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Post, S., A. P. Gonzalez, M. Rentsch, P. Palma, and M. D. Menger. "Verminderung des Reperfusionsschadens bei Lebertransplantation durch Blockade des Prostaglandin D-Receptors in der Ratte." In Chirurgisches Forum ’92 für experimentelle und klinische Forschung, 317–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77389-1_66.

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Bachmann, G., H. Petereit, U. Djenabi, and O. Michel. "Vorhersagewerte von Beta-trace Protein (Prostaglandin D Synthase) mittels Laser-Nephelometer zur Identifikation von Liquor." In Schädelbasischirurgie, 69–73. Vienna: Springer Vienna, 2004. http://dx.doi.org/10.1007/978-3-7091-0622-8_13.

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Conference papers on the topic "Prostaglandine D₂"

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Fajt, Merritt L., Silvana Balzar, John B. Trudeau, Haizhen Hu, and Sally E. Wenzel. "Epithelial Hematopoietic Prostaglandin (PG) D Synthase Is Increased In Asthma." 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.a1440.

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Türk, Murat, Oğuz Köktürk, Zeynep Işıkdoğan, and Canan Demirtaş. "Urinary biomarkers for obstructive sleep apnea syndrome: Lipocalin type prostaglandin-D synthase and F2-isoprostane." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2535.

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Thill, M., D. Fischer, S. Becker, C. Tim, K. Diedrich, and M. Friedrich. "Expression of prostaglandin metabolizing enzymes in correlation with vitamin D receptor in benign and malignant breast cell lines and breast tissue and regulation of prostaglandin metabolism by calcitriol." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6028.

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Fasano, Serena, Luciana Pierro, Alessia Borgia, Melania Alessia Coscia, Ranieri Formica, Antonella Riccardi, and Francesco Ciccia. "THU0249 URINARY NEUTROPHIL GELATINASE ASSOCIATED LIPOCALCIN AND PROSTAGLANDIN D-SYNTHETASE PREDICT DISEASE FLARES IN SYSTEMIC LUPUS ERYTHEMATOSUS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3472.

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Yashiro, Masakazu, Tatsunari Fukuoka, Haruhito Kinoshita, Go Masuda, Kishu Kitayama, Yuichiro Miki, Tamami Morisaki, Tsuyoshi Hasegawa, and Kosei Hirakawa. "Abstract 1281: Prostaglandin D synthase is a potential novel therapeutic agent for the treatment of gastric carcinomas expressing PPARγ." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1281.

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Martin, J., S. Ulrich-Rückert, and J. Stein. "Untersuchungen zur regulatorischen Wirkung von 15-Deoxy-Delta-12 – 14-prostaglandin J (15-d -PGJ2) in der Regulation der Eisenhomöostase." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605181.

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Chin, Kazuo, Yuichi Chihara, Kousuke Aritake, Yuka Harada, Masanori Azuma, Yoshiro Toyama, Kimihiko Murase, et al. "A Possible Specific Urine Biomarker For Severe Obstructive Sleep Apnea And Cardiovascular Diseases-Lipocalin-Type Prostaglandin D Synthase (L-PGDS)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2179.

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Pascual, Rodolfo M., Susan Foster, Wendy Moore, Deborah A. Meyers, Eugene R. Bleecker, and Stephen P. Peters. "Differential Prostaglandin D2 Signaling Via Chemoattactant Receptors Expressed On Th2 Cells (CRTH2) And D-Prostanoid 1 Receptors (DP1) In Human Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2789.

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Thill, M., H. Friedericke, K. Katharina, C. Dittmer, F. Dorothea, D. Klaus, F. Michael, and S. Becker. "The Antiproliferative Effect of Calcitriol on Breast Cancer Cell Lines Depends on Vitamin D Receptor Status and the Expression of Prostaglandin Metabolizing Enzymes." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5155.

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Wernet, P., M. Haurand, W. Nüsing, E. M. Schneider, K. Jaschonek, and V. Ullrich. "Production and characterization of a murine monoclonal antibody against human thromboxane synthetase." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643382.

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Eicosanoids appear to have an important role in the actual momentary regulation of tissue blood flow. The function of constricting blood vessels by affecting the vascular tone has been assigned to thromboxane. Thromboxane synthetase, the enzyme responsible for the conversion of Prostaglandin-H2 into thromboxane A2, has been shown to be present in platelets, lung fibroblasts and the brain. Recently, thromboxane synthetase has been totally purified. The enzyme isolated from platelets appears to have a molecular weight of 58,800 Dalton and to belong to the group of cytochrome P450 proteins. In order to make a monoclonal antibody against thromboxane synthetase, BALB/c mice were injected four times i.m. with 10, 5, 5 and 4 μg of the platelet purified enzyme in complete Freund's adjuvant. The serum antibody titer against thromboxane synthetase in an ELISA was higher than 1:1000 after the second boost. One mouse received a fifth i.v. injection of 10 μg of the purified enzyme. One monoclonal antibody of the several hundreds of hybridomas screened in an ELISA revealed specific activity against thromboxane synthetase with a titer of 1:512 present in the culture supernatant. After recloning this reagent, called T0300, was used for the preparation of an immunoaffinity column, where it also reacted specifically. In immunoprecipitation experiments T0300 was able to precipitate a 58,000 D molecule. Also the biological activity of thromboxane synthetase could be blocked by monoclonal antibody T0300. In addition this reagent was employed in indirect immunofluorescence on leukemic cells employing a FACS IV cytofluorometer. Here specific staining of two megacaryocytic blast cell populations could be demonstrated. Thus T0300 appears to be a monoclonal antibody against human thromboxane synthetase.
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Reports on the topic "Prostaglandine D₂"

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Moreno, Jacqueline. Vitamin D-Prostaglandin Interactions and Effects on Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada446263.

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Moreno, Jacqueline. Vitamin D-Prostaglandin Interactions and Effects in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada463443.

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