Relevant bibliographies by topics / PTGER1

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'PTGER1'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "PTGER1"

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Chandras, C., T. E. Harris, A. López Bernal, D. R. E. Abayasekara, and A. E. Michael. "PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11β-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa–lutein cells." Journal of Endocrinology 194, no. 3 (September 2007): 595–602. http://dx.doi.org/10.1677/joe-07-0128.

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In luteinizing granulosa cells, prostaglandin E2 (PGE2) can exert luteotrophic actions, apparently via the cAMP signalling pathway. In addition to stimulating progesterone synthesis, PGE2 can also stimulate oxidation of the physiological glucocorticoid, cortisol, to its inactive metabolite, cortisone, by the type 1 11β-hydroxysteroid dehydrogenase (11βHSD1) enzyme in human granulosa–lutein cells. Having previously shown these human ovarian cells to express functional G-protein coupled, E-series prostaglandin (PTGER)1, PTGER2 and PTGER4 receptors, the aim of this study was to delineate the roles of PTGER1 and PTGER2 receptors in mediating the effects of PGE2 on steroidogenesis and cortisol metabolism in human granulosa–lutein cells. PGE2-stimulated concentration-dependent increases in both progesterone production and cAMP accumulation (by 1.9 ± 0.1- and 18.7 ± 6.8-fold respectively at 3000 nM PGE2). While a selective PTGER1 antagonist, SC19220, could partially inhibit the steroidogenic response to PGE2 (by 55.9 ± 4.1% at 1000 nM PGE2), co-treatment with AH6809, a mixed PTGER1/PTGER2 receptor antagonist, completely abolished the stimulation of progesterone synthesis at all tested concentrations of PGE2 and suppressed the stimulation of cAMP accumulation. Both PGE2 and butaprost (a preferential PTGER2 receptor agonist) stimulated concentration-dependent increases in cortisol oxidation by 11βHSD1 (by 42.5 ± 3.1 and 40.0 ± 3.0% respectively, at PGE2 and butaprost concentrations of 1000 nM). Co-treatment with SC19220 enhanced the ability of both PGE2 and butaprost to stimulate 11βHSD1 activity (by 30.2 ± 0.2 and 30.5 ± 0.6% respectively), whereas co-treatment with AH6809 completely abolished the 11βHSD1 responses to PGE2 and butaprost. These findings implicate the PTGER2 receptor–cAMP signalling pathway in the stimulation of progesterone production and 11βHSD1 activity by PGE2 in human granulosa–lutein cells.
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Miyoshi, Moe, Masayuki Sato, Kenji Saito, Lila Otani, Katsuhiko Shirahige, Fumihito Miura, Takashi Ito, Huijuan Jia, and Hisanori Kato. "Maternal Protein Restriction Alters the Renal Ptger1 DNA Methylation State in SHRSP Offspring." Nutrients 10, no. 10 (October 5, 2018): 1436. http://dx.doi.org/10.3390/nu10101436.

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We previously reported that maternal protein restriction (LP) during pregnancy increases salt sensitivity in offspring using the Stroke-Prone Spontaneously Hypertensive Rat (SHRSP). In the present study, we focus on DNA methylation profiles of prostaglandin E receptor 1 gene (ptger1), which is known to be associated with hypertension. We evaluated the ptger1 DNA methylation status via bisulfite sequencing, and analyzed the expression of ptger1-related genes. The results of these analyses showed that, compared to controls, the LP-S offspring exhibited both marked ptger1 hypermethylation, and significantly increased ptger1 expression. Moreover, they also exhibited significantly decreased expression of the downstream gene epithelial Na+ channel alpha (enacα). Interestingly, LP offspring that were provided with a standard water drinking supply (W) also exhibited increased ptger1 methylation and expression. Together, these results suggest that maternal protein restriction during pregnancy modulates the renal ptger1 DNA methylation state in SHRSP offspring, and thereby likely mediates ptger1 and enacα gene expression to induce salt sensitivity.
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González, Luz María, Nicolás Roberto Robles, Sonia Mota-Zamorano, José Manuel Valdivielso, Juan López-Gómez, and Guillermo Gervasini. "Genetic Variants in PGE2 Receptors Modulate the Risk of Nephrosclerosis and Clinical Outcomes in These Patients." Journal of Personalized Medicine 11, no. 8 (August 6, 2021): 772. http://dx.doi.org/10.3390/jpm11080772.

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Prostaglandin E2 (PGE2) is a major actor mediating renal injury. We aimed to determine genetic variability in the genes coding for its receptors (PTGER1-4) and study associations with nephrosclerosis risk and clinical outcomes. We identified 96 tag-SNPs capturing global variability in PTGER1-4 and screened 1209 nephrosclerosis patients and controls. The effect of these variants was evaluated by multivariate regression analyses. Two PTGER3 SNPs, rs11209730 and rs10399704, remained significant in a backward elimination regression model with other non-genetic variables (OR = 1.45 (1.07–1.95), p = 0.016 and OR = 0.71 (0.51–0.99), p = 0.041, respectively). In the nephrosclerosis patients, a proximal region of PTGER3 was tagged as relevant for eGFR (p values for identified SNPs ranged from 0.0003 to 0.038). Two consecutive PTGER3 SNPs, rs2284362 and rs2284363, significantly decreased systolic (p = 0.005 and p = 0.0005), diastolic (p = 0.039 and p = 0.005), and pulse pressure values (p = 0.038 and 0.014). Patients were followed for a median of 47 months (7–54) to evaluate cardiovascular (CV) risk. Cox regression analysis showed that carriers of the PTGER1rs2241360 T variant had better CV event-free survival than wild-type individuals (p = 0.029). In addition, PTGER3rs7533733 GG carriers had lower event-free survival than AA/AG patients (p = 0.011). Our results indicate that genetic variability in PGE2 receptors, particularly EP3, may be clinically relevant for nephrosclerosis and its associated CV risk.
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Kowalewski, Mariusz Pawel, Hakki Bülent Beceriklisoy, Christiane Pfarrer, Selim Aslan, Hans Kindahl, Ibrahim Kücükaslan, and Bernd Hoffmann. "Canine placenta: a source of prepartal prostaglandins during normal and antiprogestin-induced parturition." REPRODUCTION 139, no. 3 (March 2010): 655–64. http://dx.doi.org/10.1530/rep-09-0140.

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Expression of cyclooxygenase 2 (COX2, now known as PTGS2), prostaglandin E2 synthase (PTGES, PGES), and prostaglandin F2α synthase (PGFS), of the respective receptors PTGFR (FP), PTGER2 (EP2), and PTGER4 (EP4) and of the progesterone receptor (PGR, PR) was assessed by real-time PCR, immunohistochemistry (IHC), or in situ hybridization (ISH) in utero/placental tissue samples collected from three to five bitches on days 8–12 (pre-implantation), 18–25 (post-implantation), and 35–40 (mid-gestation) of pregnancy and during the prepartal luteolysis. Additionally, ten mid-pregnant bitches were treated with the antiprogestin aglepristone (10 mg/kg bw (2×/24 h)); ovariohysterectomy was 24 and 72 h after the second treatment. Plasma progesterone and 15-ketodihydro-PGF2α (PGFM) concentrations were determined by RIA. Expression of the PGR was highest before implantation and primarily located to the endometrium; expression in the placenta was restricted to the decidual cells. PTGS2 was constantly low expressed until mid-gestation; a strong upregulation occurred at prepartal luteolysis concomitant with an increase in PGFM. PGFS was upregulated after implantation and significantly elevated through early and mid-gestation. PTGES showed a gradual increase and a strong prepartal upregulation. PTGFR, PTGER2, and PTGER4 were downregulated after implantation; a gradual upregulation of PTGFR and PTGER2 occurred towards parturition. ISH and IHC co-localized PGFS, PTGFR, PTGES, and PTGS2 in the trophoblast and endometrium. The changes following application of aglepristone were in the same direction as those observed from mid-gestation to prepartal luteolysis. These data suggest that the prepartal increase of PGF2α results from a strong upregulation of PTGS2 in the fetal trophoblast with the withdrawal of progesterone having a signalling function and the decidual cells playing a key role in the underlying cell-to-cell crosstalk.
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Zschockelt, Lina, Olga Amelkina, Marta J. Siemieniuch, Mariusz P. Kowalewski, Martin Dehnhard, Katarina Jewgenow, and Beate C. Braun. "Synthesis and reception of prostaglandins in corpora lutea of domestic cat and lynx." Reproduction 152, no. 2 (August 2016): 111–26. http://dx.doi.org/10.1530/rep-16-0180.

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Felids show different reproductive strategies related to the luteal phase. Domestic cats exhibit a seasonal polyoestrus and ovulation is followed by formation ofcorpora lutea(CL). Pregnant and non-pregnant cycles are reflected by diverging plasma progesterone (P4) profiles. Eurasian and Iberian lynxes show a seasonal monooestrus, in which physiologically persistent CL (perCL) support constantly elevated plasma P4 levels. Prostaglandins (PGs) represent key regulators of reproduction, and we aimed to characterise PG synthesis in feline CL to identify their contribution to the luteal lifespan. We assessed mRNA and protein expression of PG synthases (PTGS2/COX2, PTGES, PGFS/AKR1C3) and PG receptors (PTGER2, PTGER4, PTGFR), and intra-luteal levels of PGE2and PGF2α. Therefore, CL of pregnant (pre-implantation, post-implantation, regression stages) and non-pregnant (formation, development/maintenance, early regression, late regression stages) domestic cats, and prooestrous Eurasian (perCL, pre-mating) and metoestrous Iberian (perCL, freshCL, post-mating) lynxes were investigated. Expression ofPTGS2/COX2, PTGES and PTGER4 was independent of the luteal stage in the investigated species. High levels of luteotrophic PGE2in perCL might be associated with persistence of luteal function in lynxes. Signals for PGFS/AKR1C3 expression were weak in mid and late luteal stages of cats but were absent in lynxes, concomitant with low PGF2αlevels in these species. Thus, regulation of CL regression by luteal PGF2αseems negligible. In contrast, expression of PTGFR was evident in nearly all investigated CL of cat and lynxes, implying that luteal regression, e.g. at the end of pregnancy, is triggered by extra-luteal PGF2α.
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Thibodeau, Jean-François, Rania Nasrallah, Anthony Carter, Ying He, Rhian Touyz, Richard L. Hébert, and Christopher R. J. Kennedy. "PTGER1 Deletion Attenuates Renal Injury in Diabetic Mouse Models." American Journal of Pathology 183, no. 6 (December 2013): 1789–802. http://dx.doi.org/10.1016/j.ajpath.2013.08.022.

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Nuttinck, Fabienne, Brigitte Marquant-Le Guienne, Laetitia Clément, Pierrette Reinaud, Gilles Charpigny, and Bénédicte Grimard. "Expression of genes involved in prostaglandin E2 and progesterone production in bovine cumulus–oocyte complexes during in vitro maturation and fertilization." REPRODUCTION 135, no. 5 (May 2008): 593–603. http://dx.doi.org/10.1530/rep-07-0453.

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Prostaglandin E2(PGE2) and progesterone appear to be critical mediators of cumulus expansion and the resumption of oocyte meiosis. The aim of this study was to identify the types of prostaglandin E synthase (PTGES) expressed in the bovine cumulus–oocyte complex (COC), to characterize their temporal expression during the periconceptional interval using anin vitromodel of maturation (IVM) and fertilization (IVF), and to compare their expression with the level of steroidogenic gene expression. Real-time RT-PCR analysis revealed that enzymes related to the PGE2biosynthesis pathway were mainly expressed during IVM. Transcripts encoding PTGES1–3 were detected in bovine COCs. Only the expression of PTGES1 significantly increased during IVM whereas that of PTGES2 and PTGES3 remained unchanged. The induction of PTGES1 expression paralleled the induction of prostaglandin G/H synthase-2 (PTGS2) expression and the amounts of PGE2secreted by maturing COCs. Concomitantly, cholesterol side chain cleavage cytochrome P450 expression was significantly upregulated in maturing COCs and the high level of expression persisted in fertilized COCs. The expression of the StAR protein remained constant during IVM and then decreased significantly during IVF. Expression of the progesterone catabolic-related enzyme, 20α-hydroxysteroid dehydrogenase significantly decreased throughout the periconceptional interval. This was associated with a rising level of progesterone released by COCs in the culture media. In conclusion, our results suggest that the periconceptional differentiation of the bovine COC includes the transient induction of PGE2biosynthetic activity via the PTGS2/PTGES1 pathway during the maturation period and the increasing ability to produce progesterone from the immature to the fertilized stages.
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Waclawik, Agnieszka, Piotr Kaczynski, and Henry N. Jabbour. "Autocrine and Paracrine Mechanisms of Prostaglandin E2 Action on Trophoblast/Conceptus Cells through the Prostaglandin E2 Receptor (PTGER2) during Implantation." Endocrinology 154, no. 10 (October 1, 2013): 3864–76. http://dx.doi.org/10.1210/en.2012-2271.

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The conceptus and endometrium secrete large amounts of prostaglandin E2 (PGE2) into the porcine uterine lumen during the periimplantation period. We hypothesized that PGE2 acts on conceptus/trophoblast cells through auto- and paracrine mechanisms. Real-time RT-PCR analysis revealed that PGE2 receptor (PTGER)2 mRNA was 14-fold greater in conceptuses/trophoblasts on days 14–25 (implantation and early placentation period) vs preimplantation day 10–13 conceptuses (P < .05). Similarly, expression of PTGER2 protein increased during implantation. Conceptus expression of PTGER4 mRNA and protein did not differ on days 10–19. PGE2 stimulated PTGER2 mRNA expression in day 15 trophoblast cells through PTGER2 receptor signaling. PGE2 elevated aromatase expression and estradiol-17β secretion by trophoblast cells. Moreover, PGE2 and the PTGER2 agonist, butaprost, increased the adhesive capacity of both human HTR-8/SVneo trophoblast and primary porcine trophoblast cells to extracellular matrix. This PGE2-induced alteration in trophoblast cell adhesion to extracellular matrix was abolished by incubation of these cells with AH6809 (PTGER2 antagonist), ITGAVB3-directed tetrapeptide arg-gly-asp-ser or integrin ITGAVB3 antibody. PGE2 stimulated adhesion of porcine trophoblast cells via the estrogen receptor and MEK/MAPK signaling pathway. PGE2 induced phosphorylation of MAPK1/MAPK3 through PTGER2 and up-regulated expression of cell adhesion proteins such as focal adhesion kinase and intercellular adhesion molecule-1. Our study indicates that elevated PGE2 in the periimplantation uterine lumen stimulates conceptus PTGER2 expression, which in turn promotes trophoblast adhesion via integrins, and synthesis and secretion of the porcine embryonic signal estradiol-17β. Moreover, the mechanism through which PGE2 increases trophoblast adhesion is not species specific because it is PTGER2- and integrin-dependent in both porcine and human trophoblast cells.
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Jamshed, Laiba, Genevieve A. Perono, Shanza Jamshed, Kim Ann Cheung, Philippe J. Thomas, and Alison Holloway. "The Effects of Naphthenic Acids on Tryptophan Metabolism and Peripheral Serotonin Signalling." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A493. http://dx.doi.org/10.1210/jendso/bvab048.1008.

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Abstract Introduction: Serotonin produced in the periphery has been shown to affect glucose and lipid homeostasis. The availability of the amino acid tryptophan, the precursor of serotonin, affects serotonin availability. In addition, the metabolism of tryptophan via the kynurenine pathway produces physiologically active metabolites which have been shown to be altered under conditions of increased adiposity and dysglycemia. There is now evidence demonstrating some environmental xenobiotics, known to affect glucose and lipid homeostasis, can also alter serotonin production and key components of the kynurenine pathway. Recent evidence suggests that exposure to compounds present in petroleum and wastewaters from oil and gas extraction sites can impact endocrine signaling and result in aberrant lipid accumulation and altered glycemic control. However, whether any of these changes can be causally ascribed to altered serotonin synthesis/signaling or tryptophan metabolism remains unknown. The goal of this study was to determine the effects of exposure to naphthenic acid (NA), a key toxicant found in wastewater from bitumen (thick crude oil present in oil sands deposits) extraction on the enzymes involved in tryptophan metabolism and serotonin production. Methods: McA-RH7777 rat hepatoma cells, were exposed to a technical NA mixture for 48 hours at concentrations within the reported range of NA found in wastewaters from oil extraction. We assessed mRNA expression for key rate-limiting enzymes involved in tryptophan metabolism that lead to either serotonin [Tph1] and/or kynurenine [Ido2 and Tdo2] production, as well as downstream enzymes in the kynurenine pathway [Afmid, Kyat1, Aadat, Kyat3, Kmo, Haao, Acmsd, Qprt]. We also examined the effects of NA on prostaglandin synthesis [Ptgs1, Ptgs2, Ptges] and signalling [Ptger2, Ptger4] as prostaglandins have been shown to be induced by serotonin and are linked to hepatic fat accumulation. Results: NA treatment significantly increased Tph1 and Ido2 expression; this occurred in association with a significant increase in the expression of the inducible prostaglandin synthase Ptgs2 (COX-2), prostaglandin E synthase Ptges, and prostaglandin receptors Ptger2 and Ptger4. Acmsd was the only downstream enzyme in the kynurenine pathway that was significantly altered by NA treatment. Conclusion: These results provide proof-of-concept that compounds associated with oil sands extraction have the potential to perturb key components of serotonin synthesis (Tph1) and tryptophan metabolism (Ido2, Acmsd). Furthermore, we found that the increase in Tph1 expression paralleled expression of Ptgs2. As increased prostaglandin production has been reported in association with nonalcoholic steatohepatitis, these data provide a potential mechanism by which exposure to NA and other petroleum-based compounds may increase the risk of metabolic disease.
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Zhao, Xin-mei, Yuan-Bin Li, Peng Sun, Ya-di Pu, Meng-jie shan, and Yuan-meng Zhang. "Bioinformatics analysis of key biomarkers for retinoblastoma." Journal of International Medical Research 49, no. 6 (June 2021): 030006052110222. http://dx.doi.org/10.1177/03000605211022210.

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Objective To identify key genes involved in occurrence and development of retinoblastoma. Methods The microarray dataset, GSE5222, was downloaded from the gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) between unilateral and bilateral retinoblastoma were identified and functional enrichment analysis performed. The protein–protein interaction (PPI) network was constructed and analysed by STRING and Cytoscape. Results DEGs were mainly associated with activation of cysteine-type endopeptidase activity involved in apoptotic process and small molecule catabolic process. Seven genes (WAS, GNB3, PTGER1, TACR1, GPR143, NPFF and CDKN2A) were identified as HUB genes. Conclusion Our research provides more understanding of the mechanisms of the disease at a molecular level and may help in the identification of novel biomarkers for retinoblastoma.
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Dissertations / Theses on the topic "PTGER1"

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Heumann, Tina [Verfasser], and Ursula [Akademischer Betreuer] Klingmüller. "Characterization of the novel pericyte receptors S1PR3 and PTGER2 / Tina Heumann ; Betreuer: Ursula Klingmüller." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178010465/34.

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Mesa, Solís Julio. "Human prostaglandin reductase 1 (PTGR1): Substrate specificity, site-directed mutagenesis and catalytic mechanism." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/394081.

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Ello, Serge. "Préparation de catalyseurs bimétalliques PtGe/Al2O3 par voie organométallique pour une application en reformage." Poitiers, 2005. http://www.theses.fr/2005POIT2303.

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L'objectif de ce travail a été axé sur la préparation des catalyseurs bimétalliques Pt-Ge/Al2O3 puis l'évaluation de leurs performances pour une éventuelle application en reformage. Les catalyseurs ont été préparés par greffage organométallique. Cette technique de préparation a permis de déposer de très faible quantité de germanium à la surface du catalyseur parent Pt/Al2O3. Ces catalyseurs ont ensuite subi diverses techniques de caractérisation : microscopie électronique à transmission (MET), chimisorption d'hydrogène, chimisorption de monoxyde de carbone puis des tests de caractérisation : l'hydrogénation du benzène, la déshydrogénation du cyclohexène et la transformation de l'éthylcyclopentane. On a pu obtenir des catalyseurs bimétalliques de différentes structures selon la quantité de germanium déposé. Pour les faibles teneurs on obtient un dépôt (sélectif) du germanium sur les sites de forte coordinance (faces) puis pour les fortes teneurs en germanium, le dépôt devient non sélectif. Au delà d'une demie monocouche en germanium, des composés définis se forment PtxGey. Pour l'évaluation des performances, le réarrangement du n-hexane, et du n-heptane ont été choisis comme réactions modèles. Dans le cas du n-hexane on a obtenu les résultats suivant ; Pour de faible teneurs en germanium (P76Ge1/8, P60Ge1/8, P60Ge1/2), on a une forte sélectivité pour les réactions isomérisation, et de déshydrocyclisation (méthylcyclopentane) et très peu de fragmentation et d'aromatisation. Pour de forte teneur en germanium (P76Ge2, P60Ge1, P60Ge2) on obtient également plus d'aromatiques que les catalyseurs à faible ajout, moins d'isomères, et de produits cyclisés et beaucoup de fragments. Dans le cas du n-heptane, pour les catalyseurs à faible teneur de germanium, on a une diminution de la sélectivité des produits issus de la fragmentation, une augmentation de l'isomérisation et une diminution de la déshydrocyclisation par rapport au catalyseur parent. Les catalyseurs à forte teneur quand à eux, s'avèrent plus réactifs pour les réactions de déshydrocyclisation (aromatisation), de fragmentation, mais moins active pour l'isomérisation. Les catalyseurs PtGe à faible teneur produisent plus d'isomères et moins de fragments ce qui permet d'augmenter l'indice d'octane. En plus ils sont très peu sélectifs en aromatiques ce qui serait intéressant car la législation tend à diminuer la nocivité des essences en abaissant la teneur en aromatique au profit des composés cycliques saturés
The objective of this work was centered on the preparation of bimetallic catalysts Pt-Ge/Al2 O3 and the evaluation of their performances for a possible application in reforming. The catalysts were prepared by organometallic grafting. This technique of preparation made it possible to deposit very small quantity of germanium on the surface of the catalyst Pt/Al2O3. These catalysts then underwent various techniques of characterization: microscopy electronic by transmission (MET), chemisorption of hydrogen, carbon monoxide chemisorption and tests of characterization: the hydrogenation of benzene, the dehydrogenation of cyclohexene and the transformation of the ethylcyclopentane. We have obtained bimetallic catalysts of various structures according to the quantity of gemanium deposited. For the low contents we obtain a deposit (selective) germanium on the sites of high coordination (faces) then for the strong germanium contents, the deposit becomes nonselective. Beyond half monocouche of germanium, compounds definis are formed PtXGey. For the performance evaluation, the rearrangement of n-hexan, and n-heptan were selected for model reaction. In the case of n-hexane one obtained the results according to; For small germanium contents (P76Ge1/8, P60Ge1/8, P60Ge1/2), there is a high selectivity in isomerization, deshydrocyclisation (methyclopentane) and very little fragmentation and aromatization. For strong content (P76Ge2, P60Ge1, P60Ge2) we obtain also more aromatization than catalysts with weak addition, less isomers, and products cyclized and much of fragmentation. For catalysts with low content of germanium, there is a reduction in the selectivity of the products resulting from fragmentation, an increase in isomerization and a reduction in the deshydrocyclisation compared to the catalyst Pt/Al2O3. Catalysts with strong content prove more reactive for the reactions of deshydrocyclisation (aromatization), of fragmentation, but less active for isomerization
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Berry-Mortada, Fadwa. "Stabilité des plasmides recombinés en cellules libres et immobilisées : développement d'un système à double réacteur en continu en vue d'une surproduction de catéchol 2,3-dioxygénase." Compiègne, 1989. http://www.theses.fr/1989COMPD211.

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Dans cette étude, l'effet de certains facteurs, comme les caractéristiques génétiques des vecteurs la concentration de l'inoculum, les conditions de culture, etc. . . . Sur la stabilité de différents vecteurs (portant le gène sous contrôle de différents promoteurs) et la production de catéchol 2,3-dioxygénase en culture de cellules libres et immobilisées a été étudié. Nous avons montré d'une part, qu'en suspension les plasmides sont maintenus avec un degré variable de stabilité dans les souches d'E. Coli. L'instabilité des plasmides pTG201 et pTG205 est surtout attribuée à la forte expression du gène XyIE porté par les plasmides. D'autre part, par opposition au système libre, dans un système immobilisé les plasmides sont maintenus très stables durant plusieurs centaines de générations. L'immobilisation augmente considérablement la stabilité des plasmides pTG201 et pTG205, même dans les conditions de répression. Cette stabilité est d'autant plus importante quand la concentration de l'inoculum est élevée. L'immobilisation des cellules recombinées a permis aussi de maintenir constant le nombre de copies des plasmides et d'empêcher les phénomènes de fluctuations et de modifications géniques observes dans le système libre. Pour surmonter l'impact de la forte expression du gène XyIE sur la stabilité des plasmides pTG201 (contenant le promoteur puissant de Lambda Pr) et pTG205 (contenant le promoteur trp), nous avons développé un système à deux réacteurs. Dans le premier réacteur, les cellules recombinées sont cultivées à l'état immobilisé et dans un état de répression. Cet état permet une meilleure stabilité de l'information génétique. Dans le deuxième réacteur, les cellules sont maintenues dans un état de dérépression. Ce procédé a permis de maintenir très stable les plasmides pTG201 et pTG205 dans le premier réacteur durant l'équivalent de plusieurs centaines de générations et une expression élevée et constante dans le temps du gène XyIE dans le second réacteur. Ce système à double réacteur, qui associe le génie enzymatique (par le biais de l'immobilisation) et le génie génétique (avec l'utilisation de systèmes inductibles) peut être utilisé comme procédé pour la production de produits de haute valeur ajoutée.
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Pasciuto, Giulia [Verfasser], and Stephan [Akademischer Betreuer] Brand. "Neue Krankheitssuszeptibilitätsgene bei chronisch entzündlichen Darmerkrankungen und deren phänotypische Auswirkungen : der Einfluss von Polymorphismen im PTGER4-, PHOX2B-, NCF4- und FAM92B-Gen und in der chromosomalen Region 10q21.1 auf die Suszeptibilität und den Phänotyp von chronisch entzündlichen Darmerkrankungen / Giulia Pasciuto ; Betreuer: Stephan Brand." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1136270590/34.

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WU, PEI-JU, and 吳佩儒. "PTGFRN Expression Correlate with WHO Grades in Gliomas." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/f88244.

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碩士
國防醫學院
病理及寄生蟲學研究所
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Recent studies have shown Prostaglandin F2 Receptor Inhibitor (PTGFRN) is related to angiogenesis and tumor overgrowth in human. De novo glioblastoma multiforme (GBM) is the most common and highly malignant form of brain tumor. It is aggressive and challenging to be treated. Due to their finger-like tentacles, they are difficult to be completely removed by surgery. Median survival time for patients receiving only surgical resection is 4 months. The median survival time is extended to 9 to 10 months with conventional radiation therapy. The current standard treatment for glioblastoma is concurrent chemo-radiation therapy (CCRT) with median survival time of 15 months. 5-year survival rate of GBM ≤ 5% which is less than ideal. The objective of this study is to explore human genes that is associated with GBM. We sincerely hope to achieve better outcomes via pharmacology target therapy in the future. U87MG, LN229 and GBM8401 cell lines were cultured to determine the mRNA and protein expression level of PTGFRN in gliomas. For the immunohistochemistry (IHC) stain, 85 glioma brain tissues and 5 non-neoplastic brain tissues were collected to make the tissue microarray. The expression level of PTGFRN was evaluated by real-time PCR, western blot and IHC. Our results showed mRNA and protein expression level of PTGFRN is up-regulated in glioma cells/tissues as compared to normal brain tissues. The expression level of PTGFRN is thus positively correlated to WHO tumor grades of gliomas. PTGFRN serve as a promising candidate for future research to place upon in observing its inhibition on the effects on cell cycle, growth rate, and invasion ability. This may serve to verify in determining whether PTGFRN can act as new therapeutic target for glioma patients.
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Guo, Chien-Jung, and 郭千榕. "The role of Glucocorticoid receptor(GR) in PTGR2 regulation." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/u2p5xy.

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碩士
國立臺灣大學
分子醫學研究所
105
Adipocyte differentiation is an elegant, complicated process involving sequentially activation of thousands of transcriptional factors. Our group previously discovered a novel enzyme, called prostaglandin reductase 2 (PTGR2) through mRNA differential display. PTGR2 is an oxidoreductase which catalyze 15-keto PGE2 to 13,14-dihydro-15-keto PGE2 as final product. In functional study, overexpression PTGR2 rather than its catalytic mutant inhibited adipocyte differentiation and relatively triacylglycerol content,which suggest a role of PTGR2 in adipogenesis. Additionally, PTGR2 is upregulated in omental fat in obese mouse model. However, the molecular mechanism of PTGR2 expression remains unknown. Results from promoter assay and inhibitors of different signaling pathways indicated that PTGR2 transcriptional regulation is possibly mediated via dexamethasone-GR pathway. Moreover, the predicted TF binding sites also indicated presence of GR binding sites on PTGR2 promoter. With site-direct mutagenesis, we confirmed the proximal GR binding site at -277/-283 is responsible for promoter activation by dexamethasone. We then performed chromatin immunoprecipitation (ChIP) and demonstrated a direct binding of GR on PTGR2 promoter site. To further investigate the regulation of PTGR2 in vivo, we discovered that dexamethasone pulse therapy significantly upregulate PTGR2 mRNA in in inguinal fat tissue. Our findings thus support the dexamethasone-GR pathway that leads to PTGR2 activation in both cell and animal models.
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Chen, Kuan-Ju, and 陳冠如. "Triage of Endometrial Atypical Hyperplasia by DNA Methylation of SOX1, HS3ST2, AJAP1 and PTGDR." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/35059509426421457312.

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碩士
國防醫學院
病理及寄生蟲學研究所
100
Endometrial carcinoma (EC) is the one of the most common cancers in female genital tract worldwide. It can be classified into two major subtypes with respect to histopathology, cell biology and clinical course. Epigenetic aberration is known to be important in human carcinogenesis. Promoter methylation status of SOX1, HS3ST2, AJAP1 and PTGDR, was evaluated in 20 endometrial carcinomas (EC) and normal endometrial tissue by methylation specific PCR. These 4 genes had higher methylation value in patients with EC than in normal controls of AJAP1, PTGDR, HS3ST2, and SOX1 (p < 0.0001, p = 0.0002, p = 0.0004, p = 0.0035, respectively). Atypical hyperplasia (AH) is a premalignant lesion of endometrial pathology. Women with this diagnosis based on endometrial sampling are frequently found to have EC at hysterectomy. The failure of accurately diagnose EC preoperatively in these women can lead to inadequate staging and potentially suboptimal treatment for some women. So, there is a need for other markers to identify women with AH in endometrial sampling harboring an underlying EC. Sixty-one endometrial sampling with pathological diagnosis of AH were analyzed. Fourteen of the sixty-one (23%) AH patients were confirmed to have EC at hysterectomy. Three of 4 genes had higher methylation value in patients with EC hidden in AH compared with AH of AJAP1, HS3ST2 and SOX1 (p = 0.0005, p = 0.014, p = 0.023, respectively). Best cutoff values of the methylation data for different genes were determined to test the sensitivity, specificity, positive predict value (PPV), negative predict value (NPV) and to generate receiver operating characteristic (ROC) curve. ROC curve analysis demonstrated that the sensitivity, specificity, accuracy, PPV and NPV for the best performance for separating EC from AH has a sensitivity of 0.86, 0.71 and 0.71, respectively, and a specificity of 0.72, 0.70 and 0.60, respectively and accuracy of 0.81, 0.72 and 0.70, respectively, and a PPV of 0.48, 0.42 and 0.35, respectively, and a NPV of 0.94, 0.89 and 0.88, respectively. In conclusion, promoter hypermethylation of AJAP1, HS3ST2, PTGDR and SOX1 is found in EC. In addition, we also show for the first time that AJAP1, HS3ST2 and SOX1 hypermethylation analysis may have potential as a EC biomarker for endometrial malignancy.
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Ye, Yan-Ting, and 葉延廷. "Tailoring the Schottky-Barrier Height of a PtGex/Ge Contact by Combining the Experiments and First-principles Calculations." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/32041341404494249416.

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碩士
國立交通大學
電子研究所
105
In this thesis, we combine the first-principles simulations and experiments to study the Pt-germanide/Ge Schottky junction. In experiments, we first investigate how various PDA treatments affect the SBHs of a Pt-germanide/Ge junction. The I-V measurements show that SBHs are slightly reduced and gradually saturated as the annealing temperature increases. As being inspected by GIXRD analysis, the Pt-germanide phase and crystalline plane is found to vary slightly and gradually saturated as the annealing temperature increases. In order to realize the Pt-germanide/Ge interface structure in atomic scale and also to reduce possible computational trials, we use the XPS analysis to eliminate the possibility that the materials surrounding the junctions diffuse in during annealing. Next, we figure out the Pt-germanide compositions and crystalline planes from the GIXRD analysis, and do an initial screening to keep only several crystalline planes of the stronger peak signals for simulation modeling. After further considering the lattice mismatches and their desire computational resources, we finally choose and construct the three interfaces: PtGe(121)/Ge, PtGe(800)/Ge, and PtGe(120)/Ge, corresponding to the junctions formation under different annealing temperatures. By the first-principles calculations, we first investigate how SBH changes with these three single-crystalline PtmGen/Ge interfaces. We find that their SBHs depend on different Pt-germanide phases in a way in agreement with the experiments. In addition, their values differ by less than 0.1eV, consistent with the experiments. This can result from the strong Fermi level pinning. Finally, we compare the SBH-lowering effects under segregation of various dopants. Calculations reveal that they tend to segregate to the interface, and the conventional N-type dopants P and As can both reduce SBH. In addition, we find that the Sc dopant can reduce SBH from 0.671 to 0.388eV. It is the most effective among these dopants, which can be testified in the further experiments. In summary, first-principles calculations can help us explore SBHs of different crystalline planes and dopants, and pursue its reduction for device purposes. We expect that such calculations can provide a better direction for realistic fabrication, and can further shorten process development cycles and lower the cost.
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Hsieh, Meng-Lun, and 謝孟倫. "Identification of small-molecule human PTGR-2 inhibitor through high-throughput compound screening." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/11717556324919987625.

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碩士
國立臺灣大學
基因體暨蛋白體醫學研究所
105
Peroxisome proliferator-activated receptor γ (PPARγ) is a master regulator of whole-body energy metabolism, glucose homeostasis, and insulin resistance mainly expressed in adipose tissue. PPARγ acts through transcriptional regulation of genes involved in glucose and energy homeostasis upon ligand binding. The widely used anti-diabetic agent thiazolidinediones (TZD) are potent synthetic PPARγ agonist. However, most PPARγ agonists are associated with significant side effects, such as water retention, increased adiposity, and osteoporosis. There is an urgent need to develop effective way to modulate PPARγ activity without unwanted side effects. Nowadays, the natural ligands for PPARγ are still not certain (mostly oxidized fatty acids). Our team previously found prostaglandin reductase-2 (PTGR2) can catalyze15-keto-PGE2 to 13,14-dihydro-15-keto-PGE2, and provided further evidence that15-keto-PGE2 is an endogenous PPARγ ligand. Our team further found that Ptgr2 knockout mice are leaner, more insulin sensitive, and more glucose tolerant than control in high-fat high-sucrose (HFHS) diet without fluid retention and osteoporosis, indicating PTGR2 inhibition is a novel therapeutic approach for treating type 2 diabetes and obesity. In this study, we sought to identify PTGR2 small-molecule inhibitor through rational drug design and high-throughput compound screening. We further validated the enzymatic inhibitory activities, the PPARγ transactivating activities, and the cytotoxicity of these hits. Based on this study, we identified potential PTGR2 inhibitors for further optimization and animal experiment.
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Book chapters on the topic "PTGER1"

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"PTGER2." In Encyclopedia of Signaling Molecules, 4286. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103155.

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"Ptgs1." In Encyclopedia of Pain, 3319. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_101923.

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Lea, Robert, Yashvant Jani, GianGuido Rizzotto, Hans Hellendoorn, Toshio Fukuda, Yasuhisa Hasegawa, Jyh-Shing Roger Jang, et al. "Operations Research." In Handbook of Fuzzy Computation. Taylor & Francis, 1998. http://dx.doi.org/10.1201/9781420050394.ptg1.

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Makin-Iniesta, F. "Kinetic Study of pTG201 Plasmid Stability in Escherichia coli." In 1988, 311–18. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112581803-003.

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"Post-Transcriptional Gene Regulation (PTGR)." In Encyclopedia of Systems Biology, 1728. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_101172.

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Conference papers on the topic "PTGER1"

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Bayraktar, Emine, Cristian Rodriguez-Aguayo, Junhua Mai, Cristina Ivan, Cristina Ivan, Arturo Chavez-Reyes, Anil K. Sood, Mauro Ferrari, Haifa Shen, and Gabriel Lopez-Berestein. "Abstract 4668: Silencing PTGER3 enhances chemotherapeutic responses." 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.am2016-4668.

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Dong, Sheng, and Xiaoli Hao. "Statistical Analysis of Ocean Environmental Conditions With PTGEVD." In ASME 2004 23rd International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/omae2004-51615.

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Poisson Trivariate Gumbel Extreme Value Distribution (PTGEVD), a multivariate from of the Compound Extreme Value Distribution, is presented to solve for the ocean environmental design criteria in this paper. The proposed model is combined with a discrete distribution of storm frequency and a continuous trivariate extreme value distribution of environmental conditions simultaneously occurred in storm processes. Different from traditional univariate design method, the proposed design method with PTGEVD can reflect the combined effect of multi-loads on offshore structures and result in reasonable reduction of the design criteria. Validated with the synchronically measured significant wave heights, wind speeds and current velocities of 20 typhoon processes, PTGEVD model shows that it is easy to be applied and has considerable economic potential in the exploitation of ocean oil and gas, especially for marginal field.
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Gui, H., D. Hu, P. Sleiman, A. M. Levin, S. Xiao, M. Yang, J. J. Yang, et al. "Genome-Wide Association Study of Asthma Exacerbation in African Americans Identify PTGER3 as New Susceptibility Gene." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3044.

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Hess, T., L. Hamann, YK Vashist, K. Butterbach, T. Schmidt, I. Krasniuk, A. Höblinger, et al. "Evidence for PTGER4, PSCA and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604759.

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Bayraktar, Emine, Cristian Rodriguez-Aguayo, Zahid Siddik, and Gabriel Lopez-Berestein. "Abstract 2066: Delivery of 2`F-PS2 PTGER3 siRNA-DOPC enhances anti-tumoral activity in cisplatin resistant ovarian cancer model." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2066.

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Schlegel, Anne, Oliver Hasinger, Selina Esche, Melanie Martini, Thomas König, and Gunter Weiss. "Abstract 2260: Classification of patients with lung cancer and benign lung disease via assessment of DNA methylation of SHOX2 and PTGER4 in plasma." 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.am2016-2260.

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Silva, Gustavo Figueiredo da, Bruno Mattei Lopes, Vinicius Moser, and Leslie Ecker Ferreira. "Impact of pharmacogenetics on aspirin resistance: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.663.

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Background: Pharmacogenetics promises better control of diseases, such as Cardiovascular disease (CVD). Acetylsalicylic acid, aspirin, prevents the formation of an activating agent of platelet aggregation and vasoconstriction, and it is used to prevent CVD. Nevertheless, patients may have treatment failure, causing recurrence and increased mortality, due to medication adherence, drug- drug interactions, aspirin-independent thromboxane A2 synthesis or genetic variants. In this sense, genetic variants have been related with aspirin resistance (AR). Objective: To evaluate the evidence of impact of genetic variants on AR through systematic literature review. Design and setting: Systematic review. Methods: Articles published since 2009 in MEDLINE/PubMed, Cochrane, Scopus, LILACS and SCIELO were systematically screened. Results: The genetic variants rs1126643 (ITGA2), rs3842787 (PTGS1), rs20417 (PTGS2) and rs5918 (ITGB3) were the most studied. As for the relevance of the genetic variants studied, of the 64 evaluated, 14 had statistical significance (p <0.05, 95% CI) in at least one article. Among them, the following have had unanimous. Results: rs1371097 (P2RY1), rs1045642 (MDR1), rs1051931 and rs7756935 (PLA2G7), rs2071746 (HO1), rs1131882 and rs4523 (TBXA2R), rs434473 (ALOX12), rs9315042 (ALOX5AP) and rs662 (PON1). While these differ in real interference in AR: rs5918 (ITGB3), rs2243093 (GP1BA), rs1330344 (PTGS1) and rs20417 (PTGS2). Conclusion: As limitations of our study, we highlight the non-uniform methodologies of the analyzed articles, as well as population differences. It is also noteworthy that pharmacogenetics is an expanding area. Therefore, further studies are needed to better understand the association between genetic variants and AR, as well as the practical application.
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Habermann, Nina, Martha L. Slattery, Elizabeth M. Poole, Liren Xiao, Rachel L. Galbraith, David Duggan, Richard J. Kulmacz, et al. "Abstract 3757: PTGS1 and PTGS2 polymorphisms, fatty acid intake, and risk of colon and rectal cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3757.

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Marquez, Jorge, Jianping Dong, Chun Dong, and Ginette Serrero. "Abstract LB116: Prostaglandin F2 Receptor Negative Regulator (PTGFRN) is a novel target to inhibit tumor growth via antibody drug conjugate." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb116.

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Wagner, Michael J., Sanford A. Klein, and Douglas T. Reindl. "Simulation of Utility-Scale Central Receiver System Power Plants." In ASME 2009 3rd International Conference on Energy Sustainability collocated with the Heat Transfer and InterPACK09 Conferences. ASMEDC, 2009. http://dx.doi.org/10.1115/es2009-90132.

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The operation of solar energy systems is necessarily transient. Over the lifetime of a concentrating solar power plant, the system operates at design conditions only occasionally, with the bulk of operation occurring under part-load conditions depending on solar resource availability. Credible economic analyses of solar-electric systems requires versatile models capable of predicting system performance at both design and off-design conditions. This paper introduces new and adapted simulation tools for power tower systems including models for the heliostat field, central receiver, and the power cycle. The design process for solar power tower systems differs from that for other concentrating solar power (CSP) technologies such as the parabolic trough or parabolic dish systems that are nearly modular in their design. The design of an optimum power tower system requires a determination of the heliostat field layout and receiver geometry that results in the greatest long-term energy collection per unit cost. Research presented in this paper makes use of the DELSOL3 code (Kistler, 1986) which provides this capability. An interface program called PTGEN was developed to simplify the combined use of DELSOL3 and TRNSYS. The final product integrates the optimization tool with the detailed component models to provide a comprehensive modeling tool set for the power tower technology.
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