Relevant bibliographies by topics / PDE

Academic literature on the topic 'PDE'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 July 2024

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Journal articles on the topic "PDE"

1

Bloom, Timothy J. "Cyclic nucleotide phosphodiesterase isozymes expressed in mouse skeletal muscle." Canadian Journal of Physiology and Pharmacology 80, no. 12 (December 1, 2002): 1132–35. http://dx.doi.org/10.1139/y02-149.

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To understand changes in cyclic nucleotide metabolism in muscle disease states, the expression of phosphodiesterase (PDE) isozymes in normal mouse leg muscle was examined. Four subcellular fractions were generated by differential centrifugation at 10 000 × g and 100 000 × g. cAMP PDE activity was found predominately in the soluble fractions, while cGMP PDE activity was more evenly distributed amongst soluble and particulate fractions. Pharmacological inhibitors demonstrate that PDE4 represents the major cAMP hydrolyzing activity and PDE2 represents the major cGMP hydrolyzing activity in mouse leg muscle. PDE1 is expressed at low levels, while PDE3 and PDE5 are intermediate. Between 20 and 40% of total PDE activity remained in the presence of inhibitors for PDE1–PDE5, indicating that other PDE families contribute to the total PDE pool. Reverse-transcription PCR with family-specific primers showed expression of mRNA for PDE7–PDE9, supporting this conclusion. Total PDE activity was found to be elevated in tissue extracts from a mouse model of Duchenne's muscular dystrophy.Key words: cyclic nucleotide, phosphodiesterase, skeletal muscle, pharmacological inhibitors, muscular dystrophy.
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DAY, Jonathan P., Julian A. T. DOW, Miles D. HOUSLAY, and Shireen-A. DAVIES. "Cyclic nucleotide phosphodiesterases in Drosophila melanogaster." Biochemical Journal 388, no. 1 (May 10, 2005): 333–42. http://dx.doi.org/10.1042/bj20050057.

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Cyclic nucleotide PDEs (phosphodiesterases) are important enzymes that regulate intracellular levels of cAMP and cGMP. In the present study, we identify and characterize novel PDEs in the genetic model, Drosophila melanogaster. The Drosophila genome encodes five novel PDE genes in addition to dunce. Predicted PDE sequences of Drosophila show highly conserved critical domains when compared with human PDEs. Thus PDE-encoding genes of D. melanogaster are CG14940-PDE1C, CG8279-PDE6β, CG5411-PDE8A, CG32648-PDE9 and CG10231-PDE11. Reverse transcriptase–PCRs of adult tissues reveal widespread expression of PDE genes. Drosophila Malpighian (renal) tubules express all the six PDEs: Drosophila PDE1, dunce (PDE4), PDE6, PDE8, PDE9 and PDE11. Antipeptide antibodies were raised against PDE1, PDE6, PDE9 and PDE11. Verification of antibody specificity by Western blotting of cloned and expressed PDE constructs allowed the immunoprecipitation studies of adult Drosophila lysates. Biochemical characterization of immunoprecipitated endogenous PDEs showed that PDE1 is a dual-specificity PDE (Michaelis constant Km for cGMP: 15.3±1 μM; Km cAMP: 20.5±1.5 μM), PDE6 is a cGMP-specific PDE (Km cGMP: 37±13 μM) and PDE11 is a dual-specificity PDE (Km cGMP: 6±2 μM; Km cAMP: 18.5±5.5 μM). Drosophila PDE1, PDE6 and PDE11 display sensitivity to vertebrate PDE inhibitors, zaprinast (IC50 was 71±39 μM for PDE1, 0.65±0.015 μM for PDE6 and 1.6±0.5 μM for PDE11) and sildenafil (IC50 was 1.3±0.9 μM for PDE1, 0.025±0.005 μM for PDE6 and 0.12±0.06 μM for PDE11). We provide the first characterization of a cGMP-specific PDE and two dual-specificity PDEs in Drosophila, and show a high degree of similarity in structure and function between human and Drosophila PDEs.
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Wright, Lyndon C., Joachim Seybold, Annette Robichaud, Ian M. Adcock, and Peter J. Barnes. "Phosphodiesterase expression in human epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 4 (October 1, 1998): L694—L700. http://dx.doi.org/10.1152/ajplung.1998.275.4.l694.

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Epithelial cells play a critical role in airway inflammation and have the capacity to produce many inflammatory mediators, including bioactive lipids and proinflammatory cytokines. Intracellular levels of cAMP and cGMP are important in the control of inflammatory cell function. These cyclic nucleotides are inactivated via a family of phosphodiesterase (PDE) enzymes, providing a possible site for drug intervention in chronic inflammatory conditions. We studied the expression of PDE activity in an epithelial cell line (A549) and in primary human airway epithelial cells (HAECs). We measured PDE function using specific inhibitors to identify the PDE families present and used RT-PCR to elucidate the expression of PDE isogenes. Both A549 cells and HAECs predominantly expressed PDE4 activity, with lesser PDE1, PDE3, and PDE5 activity. RT-PCR identified HSPDE4A5 and HSPDE4D3 together with HSPDE7. Inhibition of PDE4 and PDE3 reduced secretion by these cells. Epithelial PDE may be an important target for PDE4 inhibitors in the development of the control of asthmatic inflammation, particularly when delivered via the inhaled route.
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Sasseville, M., F. K. Albuz, F. J. Richard, and R. B. Gilchrist. "254. Evidences for a novel cAMP-phosphodiesterase expressed in the bovine ovarian follicle." Reproduction, Fertility and Development 20, no. 9 (2008): 54. http://dx.doi.org/10.1071/srb08abs254.

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3′5’-Cyclic adenosine monophosphate (cAMP) is an important second messenger in the mammalian ovarian follicle implicated in gonadotrophin signalling as well as oocyte meiotic arrest. Cyclic AMP-degrading phosphodiesterases (PDE) modulate cAMP levels in the ovarian follicle, but the specific PDE subtypes responsible for this degradation in the different cellular compartments within the bovine follicle remain unknown. The current dogma, established principally in rodent, presents PDE3A as the ‘oocyte PDE’, while PDE4D is the ‘granulosa/cumulus PDE’. Our PDE activity measurements suggested that a PDE3 (cilostamide-sensitive, 10µM) was representing 79% of the total cAMP-PDE activity in the bovine oocyte, in agreement with the dogma. However, our results suggested that PDE4 (rolipram-sensitive, 10µM) is representing only 19% of the cAMP-PDE activity in the cumulus cells, while 65% of the activity was due to PDE8 (IBMX-insensitive, 500µM), a result in direct opposition with the accepted PDE distribution in the ovarian follicle. Mural granulosa cells were displaying equal amounts of PDE4 (31%) and PDE8 (30%) cAMP-PDE activities. Interestingly, cAMP-PDE activities were not varying during the first 9 h of IVM in the bovine cumulus-oocyte complexes (COC), as seen in rat. COCs treated with an adenylyl cyclase stimulator (forkolin 100µM) in combinaison with the only known inhibitor for the PDE8 family, dipyridamole, are showing a dose-dependant increase of cAMP levels and a significant delay nuclear maturation, whereas a potent PDE4 inhibitor, rolipram (up to 100µM), was ineffective. This study provides the first insight into subtype-specific PDE cAMP degrading activities in the bovine ovarian follicle, especially around oocyte nuclear maturation. It demonstrates dramatic differential PDE subtype compartmentalisation between ovarian somatic cells and the germ cell, including the important contribution of a new PDE family member in the ovarian follicle, PDE8. PDE8 could be a novel pharmacological target to improve bovine oocyte IVM conditions and to increase developmental competence.
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Neumann, Joachim, Rafaela Voss, Ulrich Laufs, Christian Werner, and Ulrich Gergs. "Phosphodiesterases 2, 3 and 4 can decrease cardiac effects of H2-histamine-receptor activation in isolated atria of transgenic mice." Naunyn-Schmiedeberg's Archives of Pharmacology 394, no. 6 (February 12, 2021): 1215–29. http://dx.doi.org/10.1007/s00210-021-02052-y.

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AbstractHistamine exerts cAMP-dependent positive inotropic effects (PIE) and positive chronotropic effects (PCE) on isolated left and right atria, respectively, of transgenic mice which overexpress the human H2-receptor in the heart (=H2-TG). To determine whether these effects are antagonized by phosphodiesterases (PDEs), contractile studies were done in isolated left and right atrial preparations of H2-TG. The contractile effects of histamine were tested in the additional presence of the PDE-inhibitorserythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA, 1 μM, PDE2-inhibitor) or cilostamide (1 μM, PDE3-inhibitor), rolipram (10 μM, a PDE4-inhibitor), and their combinations. Cilostamide (1 μM) and EHNA (1 μM), rolipram (1 μM), and EHNA (1 μM) and the combination of rolipram (0.1 μM) and cilostamide (1 μM) each increased the potency of histamine to elevate the force of contraction (FOC) in H2-TG. Cilostamide (1 μM) and rolipram (10 μM) alone increased and EHNA (1 μM) decreased alone, and their combination increased the potency of histamine to increase the FOC in H2-TG indicating that PDE3 and PDE4 regulate the inotropic effects of histamine in H2-TG. The PDE inhibitors (EHNA, cilostamide, rolipram) alone did not alter the potency of histamine to increase the heart beat in H2-TG whereas a combination of rolipram, cilostamide, and EHNA, or of rolipram and EHNA increased the potency of histamine to act on the beating rate. In summary, the data suggest that the PCE of histamine in H2-TG atrium involves PDE 2 and 4 activities, whereas the PIE of histamine are diminished by activity of PDE 3 and 4.
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Tarpey, Siobhán B., Darrell R. Sawmiller, Claire Kelly, W. Joseph Thompson, and Mary I. Townsley. "Phosphodiesterase 3 activity is reduced in dog lung following pacing-induced heart failure." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 5 (May 1, 2003): L766—L773. http://dx.doi.org/10.1152/ajplung.00373.2002.

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We hypothesized that decreases in expression and/or activity of cAMP-specific phosphodiesterases (PDE) contribute to protective adaptations observed in lung after heart failure. In this study, we compared PDE activity in lung parenchyma isolated from control dogs and those paced to heart failure by assaying cyclic nucleotide hydrolysis in fractions of homogenate supernatant eluted from DEAE-Trisacryl columns. Cyclic nucleotide hydrolysis due to PDE3, PDE4, and PDE5 isoforms was predominant in both control and paced groups. The ratio of PDE3 activity to total cAMP PDE activity was decreased in the paced group compared with control ( P< 0.05), whereas PDE4 or PDE5 activity ratios were not different between the two groups. With the use of RT-PCR, message expression for PDE3A or PDE3B did not differ between the two groups. Cilostamide, a selective PDE3 inhibitor, and forskolin, a nonspecific agonist for adenylyl cyclase, both inhibited thapsigargin-induced increases in endothelial permeability in control lung. We conclude that PDE3 activity, but not mRNA expression, is reduced in lung from dogs paced to heart failure, a change that could contribute to heart failure-induced attenuation of the lung endothelial permeability response to injury.
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Phillips, Peter G., Lu Long, Martin R. Wilkins, and Nicholas W. Morrell. "cAMP phosphodiesterase inhibitors potentiate effects of prostacyclin analogs in hypoxic pulmonary vascular remodeling." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 1 (January 2005): L103—L115. http://dx.doi.org/10.1152/ajplung.00095.2004.

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We investigated the effects of prostacyclin analogs and isoform-selective phosphodiesterase (PDE) inhibitors, alone and in combination, on pulmonary vascular remodeling in vitro and in vivo. Vascular smooth muscle cells (VSMC) isolated from pulmonary (proximal and distal) and systemic circulations demonstrated subtle variations in expression of PDE isoform mRNA. However, using biochemical assays, we found PDE3 and PDE4 isoforms to be responsible for the majority of cAMP hydrolysis in all VSMC. In growth assays, the prostacyclin analogs cicaprost and iloprost inhibited mitogen-induced proliferation of VSMC in a cAMP-dependent manner. In addition, isoform-selective antagonists of PDEs 1, 3, or 4 inhibited VSMC proliferation, an effect that synergized with the effect of prostacyclin analogs. The inhibitory effects were greater in cells isolated from pulmonary circulation. In an in situ perfused rat lung preparation, administration of prostacyclin analogs or the PDE inhibitors vinpocetine (PDE1), cilostamide (PDE3), or rolipram (PDE4), but not EHNA (PDE2), attenuated acute hypoxic vasoconstriction (HPV). Combinations of agents led to a greater reduction in HPV. Furthermore, during exposure to hypoxia for 13 days, Wistar rats were treated with iloprost, rolipram, cilostamide, or combinations of these agents. Compared with normoxic controls, hypoxic animals developed pulmonary hypertension and distal pulmonary artery muscularization. These parameters were attenuated by iloprost+cilostamide, iloprost+rolipram, and cilostamide+rolipram but were not significantly affected by single agents. Together, these findings provide a greater understanding of the role of cAMP PDEs in VSMC proliferation and provide rationale for combined use of prostacylcin analogs plus PDE3/4 inhibitors in treatment of pulmonary vascular remodeling.
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ERDOGAN, Suat, and Miles D. HOUSLAY. "Challenge of human Jurkat T-cells with the adenylate cyclase activator forskolin elicits major changes in cAMP phosphodiesterase (PDE) expression by up-regulating PDE3 and inducing PDE4D1 and PDE4D2 splice variants as well as down-regulating a novel PDE4A splice variant." Biochemical Journal 321, no. 1 (January 1, 1997): 165–75. http://dx.doi.org/10.1042/bj3210165.

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The cAMP phosphodiesterase (PDE) 3 and PDE4 isoforms provide the major cAMP-hydrolysing PDE activities in Jurkat T-cells, with additional contributions from the PDE1 and PDE2 isoforms. Challenge of cells with the adenylate cyclase activator forskolin led to a rapid, albeit transient, increase in PDE3 activity occurring over the first 45 min, followed by a sustained increase in PDE3 activity which began after ∼3 h and continued for at least 24 h. Only this second phase of increase in PDE3 activity was blocked by the transcriptional inhibitor actinomycin D. After ∼3 h of exposure to forskolin, PDE4 activity had increased, via a process that could be inhibited by actinomycin D, and it remained elevated for at least a 24 h period. Such actions of forskolin were mimicked by cholera toxin and 8-bromo-cAMP. Forskolin increased intracellular cAMP concentrations in a time-dependent fashion and its action was enhanced when PDE induction was blocked with actinomycin D. Reverse transcription (RT)-PCR analysis, using generic primers designed to detect transcripts representing enzymically active products of the four PDE4 genes, identified transcripts for PDE4A and PDE4D but not for PDE4B or PDE4C in untreated Jurkat T-cells. Forskolin treatment did not induce transcripts for either PDE4B or PDE4C; however, it reduced the RT-PCR signal for PDE4A transcripts and markedly enhanced that for PDE4D transcripts. Using RT-PCR primers for PDE4 splice variants, a weak signal for PDE4D1 was evident in control cells whereas, in forskolin-treated cells, clear signals for both PDE4D1 and PDE4D2 were detected. RT-PCR analysis of the PDE4A species indicated that it was not the PDE4A isoform PDE-46 (PDE4A4B). Immunoblotting of control cells for PDE4 forms identified a single PDE4A species of ∼118 kDa, which migrated distinctly from the PDE4A4B isoform PDE-46, with immunoprecipitation analyses showing that it provided all of the PDE4 activity in control cells. Forskolin treatment led to a marked decrease of this novel PDE4A species and allowed the detection of a strong signal for an ∼67 kDa PDE4D species, suggested to be PDE4D1, but did not induce PDE4B and PDE4C isoforms. Elevation of intracellular cAMP concentrations in Jurkat T-cells thus exerts a highly selective effect on the transcriptional activity of the genes encoding the various PDE4 isoforms. This leads to the down-regulation of a novel PDE4A splice variant and the induction of PDE4D1 and PDE4D2 splice variants, leading to a net increase in the total PDE4 activity of Jurkat T-cells.
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Szczypka, Marianna. "Role of Phosphodiesterase 7 (PDE7) in T Cell Activity. Effects of Selective PDE7 Inhibitors and Dual PDE4/7 Inhibitors on T Cell Functions." International Journal of Molecular Sciences 21, no. 17 (August 25, 2020): 6118. http://dx.doi.org/10.3390/ijms21176118.

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Phosphodiesterase 7 (PDE7), a cAMP-specific PDE family, insensitive to rolipram, is present in many immune cells, including T lymphocytes. Two genes of PDE7 have been identified: PDE7A and PDE7B with three or four splice variants, respectively. Both PDE7A and PDE7B are expressed in T cells, and the predominant splice variant in these cells is PDE7A1. PDE7 is one of several PDE families that terminates biological functions of cAMP—a major regulating intracellular factor. However, the precise role of PDE7 in T cell activation and function is still ambiguous. Some authors reported its crucial role in T cell activation, while according to other studies PDE7 activity was not pivotal to T cells. Several studies showed that inhibition of PDE7 by its selective or dual PDE4/7 inhibitors suppresses T cell activity, and consequently T-mediated immune response. Taken together, it seems quite likely that simultaneous inhibition of PDE4 and PDE7 by dual PDE4/7 inhibitors or a combination of selective PDE4 and PDE7 remains the most interesting therapeutic target for the treatment of some immune-related disorders, such as autoimmune diseases, or selected respiratory diseases. An interesting direction of future studies could also be using a combination of selective PDE7 and PDE3 inhibitors.
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Teng, Bunyan, Daniel N. Darlington, and Andrew P. Cap. "Adenosine Regulation of cAMP through Phosphodiesterases." Blood 132, Supplement 1 (November 29, 2018): 2424. http://dx.doi.org/10.1182/blood-2018-99-114929.

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Abstract Introduction: Adenosine, an autacoid and metabolite of ATP, has been known to have anti-platelet properties. Of the 4 adenosine receptors (ARs), only A2A AR have been implicated in adenosines anti-platelet properties in human. A2A AR is a G-Protein Coupled Receptors associated with a stimulatory G-Protein (Gs) that can activate adenylyl cyclase (AC) and increase intracellular cAMP. An elevation of cAMP has been shown to inhibit platelet aggregation to natural stimuli. Regulation of intracellular cAMP is balanced between synthesis by adenylate cyclase and degradation by phosphdiesterases (PDE). There are 3 PDE subtypes found in platelets: PDE2, PDE3, and PDE5. However, it is not know which subtype(s) is (are) responsible for regulating cAMP level in human platelets after adenosine stimulation. Materials and Methods: Platelet-rich plasma (PRP) was isolated from whole blood of human volunteers, and centrifuged at 200g for 10min. Light transmission aggregometry was performed after stimulation of platelets with 100uM ADP, with or without NECA (non-specific AR agonist), DPCPX (A1 AR antagonist), and Sch 58261 (A2A AR antagonist). PRP treated with NECA, DPCPX, Sch 58261, and PDE inhibitors (EHNA, E in figures, for PDE2, Trequinsin, T in figures, for PDE3, and 4-{[3'4'-(methylenedioxy) benzyl]amino}-6-methoxyqunazolin, 4 in figures, for PDE 5). Cyclic AMP was measured in platelets after treatment by liquid chromatography/ Tandem Mass Spectroscopy (Quantiva, ThrermoFisher) after treated with these drugs. Results: ADP-induced platelet aggregation was inhibited in a dose dependent manner by the non-specific adenosine agonist, NECA (Figure 1) and the effect was blocked by A2A specific antagonist Sch 58261, not by the A1 AR antagonist, DPCPX (Figure 2). NECA inhibition of platelet aggregation was likely due to an elevation of intracellular cAMP (1 uM, 5min incubation, Figure 3). Inhibition of PDE3 alone, significantly increased intracellular cAMP, suggesting that basal PDE3 activity is present. PDE 3 inhibition combined with NECA elevated cAMP even higher than PDE inhibition or NECA alone (Figure 3), suggesting that NECA (A2A stimulation) effects PDE activity. Inhibition of PDE2 or 5 had no effect on basal or NECA stimulated cAMP (Figure 3). Inhibition of all 3 PDE (2,3,5) combined with NECA elevated cAMP to levels higher then NECA+ PDE3 inhibition, again suggesting that NECA maybe effecting the activity of the PDEs (Figure 3). The potentiation of cAMP by PDE3 inhibition + NECA was block by A2A, but not A1 antagonist (Figure 4) suggesting that the nonspecific adenosine agonist is elevating cAMP through A2A. Conclusion: 1. In human platelets, NECA stimulates cAMP through A2A receptors and this elevation is likely due to an elevation in adenylate cyclase via Gs coupled to A2A. PDE3 is basally active and likely regulated by adenosine receptors. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "PDE"

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Ugail, Hassan. "On the spine of a PDE surface." Springer, 2003. http://hdl.handle.net/10454/2687.

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The spine of an object is an entity that can characterise the object¿s topology and describes the object by a lower dimension. It has an intuitive appeal for supporting geometric modelling operations. The aim of this paper is to show how a spine for a PDE surface can be generated. For the purpose of the work presented here an analytic solution form for the chosen PDE is utilised. It is shown that the spine of the PDE surface is then computed as a by-product of this analytic solution. This paper also discusses how the of a PDE surface can be used to manipulate the shape. The solution technique adopted here caters for periodic surfaces with general boundary conditions allowing the possibility of the spine based shape manipulation for a wide variety of free-form PDE surface shapes.
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Öhrnell, Carl. "Lie Groups and PDE." Thesis, Uppsala universitet, Analys och sannolikhetsteori, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-420706.

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Tsui, Ka Cheung. "A networked PDE solving environment /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?MATH%202003%20TSUI.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 56-58). Also available in electronic version. Access restricted to campus users.
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Ugail, Hassan. "Method of trimming PDE surfaces." Elsevier, 2006. http://hdl.handle.net/10454/2648.

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A method for trimming surfaces generated as solutions to Partial Differential Equations (PDEs) is presented. The work we present here utilises the 2D parameter space on which the trim curves are defined whose projection on the parametrically represented PDE surface is then trimmed out. To do this we define the trim curves to be a set of boundary conditions which enable us to solve a low order elliptic PDE on the parameter space. The chosen elliptic PDE is solved analytically, even in the case of a very general complex trim, allowing the design process to be carried out interactively in real time. To demonstrate the capability for this technique we discuss a series of examples where trimmed PDE surfaces may be applicable.
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Bolzonella, Nicolo' <1989&gt. "MLPG solution of elliptic PDE." Master's Degree Thesis, Università Ca' Foscari Venezia, 2017. http://hdl.handle.net/10579/10509.

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Meshless methods for the numerical solution of Partial Differential Equations (PDE) are emerging techniques. Nowadays their efficiency is not comparable to Finite Element methods. Among the ample literature on meshless methods, we focus on Meshless Petrov--Galerkin (MLPG) methods.In many variants they pervade the Research on meshless methods for solving PDE. This thesis aims at implementing a MATLAB code allowing for the numerical approximation of Poisson problems. The accuracy and efficiency of the code is tested. Moreover, strategies for using GPU devices are analyzed, developed and implemented. A discussion of the their efficiency is conducted on test problems.
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Ugail, Hassan, and N. Kirmani. "Method of surface reconstruction using partial differential equations." WSEAS, 2006. http://hdl.handle.net/10454/2750.

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Seidel, Cathleen. "Integration externer PDE-Löser in Mathcad." Universitätsbibliothek Chemnitz, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-201000672.

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Mathcad gilt in den unterschiedlichsten Bereichen, z.B. in den Ingenieurwissenschaften, der Mathematik, der Physik, der Biologie oder sogar der Qualitätssicherung als hervorragendes Werkzeug zur übersichtlichen Darstellung komplexer Berechnungen. Sollten die enthaltenen Funktionalitäten nicht mehr ausreichen, besteht die Möglichkeit, Mathcad mit Hilfe von User-DLLs zu erweitern. Diese Erweiterung kann perfekt als Schnittstelle zwischen Mathcad und anderen Softwarepaketen genutzt werden. Die von der inuTech GmbH entwickelte Klassenbibliothek Diffpack zur Simulation und numerischen Lösung von Differentialgleichungen aus den verschiedensten Bereichen eignet sich hervorragend, erforderliche Funktionalitäten für Mathcad zu implementieren. Mathcad kann somit zur Parametrisierung, für Berechnungen und zur Darstellung der Ergebnisse verwendet werden, während Diffpack die Lösung der partiellen Differentialgleichung, z.B. mittels FEM, übernimmt.
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Dascaliuc, Radu. "Backward time behavior of dissipative PDE." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4940.

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We study behavior for negative times t of the 2D periodic Navier-Stokes equations and Burgers' original model for turbulence. Both systems are proved to have rich sets of solutions that exist for all t - R and increase exponentially as t -> -(Infinity) However, our study shows that the behavior of these solutions as well as the geometrical structure of the sets of their initial data are very different. As a consequence, Burgers original model for turbulence becomes the first known dissipative system that despite possessing a rich set of backward-time exponentially growing solutions, does not display any similarities, as t -> -(Infinity), to the linear case.
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Broomé, Sofia, and Jonathan Ridenour. "A PDE PERSPECTIVE ON CLIMATE MODELING." Thesis, KTH, Matematik (Inst.), 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-147765.

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This report will provide an overview of climate modeling from a mathematical perspective, particularly with respect to the use of partial differential equations. A visit to the Swedish Meterological and Hydrological Institute's Rossby Center for climate research in Norrkoping, Sweden, is at the foundation of our investigations. An introduction and a brief history section will be followed by a description of the Navier-Stokes equations, which are at the heart of climate-related mathematics, as well as a survey of many of the popular approximations and modeling techniques in use by climate researchers today. Subsequently, a boundary value problem based on the one dimensional compressible Euler equations will be discussed from an analytical as well as a numerical point of view, especially with concern to the well-posedness of the same.
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Zhu, Kangping. "Two problems in applications of PDE." Thesis, New York University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3635320.

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This thesis contains two different parts. For part I, we develop a PDE perspective on a model problem from the machine learning literature. The problem involves ''prediction" via ''regret minimization". Our PDE approach identifies the optimal strategies and the associated outcomes in a scaling limit where the number of time steps tends to 1. While our PDE is very nonlinear, explicit solutions are available in many cases due to a surprising and convenient link to the linear heat equation.

For part II, We consider H–αgradient flow of the Modica-Mortola energy. The evolution law can be viewed as a nonlocal analogue of the Cahn-Hilliard equation for α > 0; the limit as α= 0 is (formally at least) the volume preserving Allen-Cahn flow. When α > ½ , we prove a time-averaged upper bound on the typical length scale, of order t < 1/( 1 +2α) We also argue that for α > ½ the true time scale of the evolution is the original time scale (and that the case α < ½ is different). Finally, we derive the sharp interface limit of the flow using heuristic arguments.

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Books on the topic "PDE"

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Schiesser, William E. Moving Boundary PDE Analysis. Boca Raton : Taylor & Francis, [2019]: CRC Press, 2019. http://dx.doi.org/10.1201/9780429275128.

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De los Reyes, Juan Carlos. Numerical PDE-Constrained Optimization. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13395-9.

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Hoppe, Ronald, ed. Optimization with PDE Constraints. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08025-3.

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Reinhard, Laubenbacher, Lowen R. (Robert), Pinnau Rene, Stevens A, Ulbrich Michael, Ulbrich Stefan, and SpringerLink (Online service), eds. Optimization with PDE Constraints. Dordrecht: Springer Netherlands, 2009.

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Kuehn, Christian. PDE Dynamics: An Introduction. Philadelphia, PA: Society for Industrial and Applied Mathematics, 2019. http://dx.doi.org/10.1137/1.9781611975666.

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Taylor, Michael E. Pseudodifferential Operators and Nonlinear PDE. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4612-0431-2.

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Biegler, Lorenz T., Matthias Heinkenschloss, Omar Ghattas, and Bart van Bloemen Waanders, eds. Large-Scale PDE-Constrained Optimization. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55508-4.

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Leugering, Günter, Peter Benner, Sebastian Engell, Andreas Griewank, Helmut Harbrecht, Michael Hinze, Rolf Rannacher, and Stefan Ulbrich, eds. Trends in PDE Constrained Optimization. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05083-6.

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Antil, Harbir, Drew P. Kouri, Martin-D. Lacasse, and Denis Ridzal, eds. Frontiers in PDE-Constrained Optimization. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8636-1.

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Pseudodifferential operators and nonlinear PDE. Boston: Birkhäuser, 1991.

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Book chapters on the topic "PDE"

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Karafyllis, Iasson, and Miroslav Krstic. "Parabolic PDE-PDE Loops." In Input-to-State Stability for PDEs, 235–61. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91011-6_10.

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Karafyllis, Iasson, and Miroslav Krstic. "Hyperbolic PDE-PDE Loops." In Input-to-State Stability for PDEs, 215–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91011-6_9.

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Krstic, Miroslav. "Other PDE-PDE Cascades." In Delay Compensation for Nonlinear, Adaptive, and PDE Systems, 385–91. Boston: Birkhäuser Boston, 2009. http://dx.doi.org/10.1007/978-0-8176-4877-0_20.

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Beyna, Ingo. "PDE Valuation." In Lecture Notes in Economics and Mathematical Systems, 101–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-34925-6_7.

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McAllister-Williams, R. Hamish, Daniel Bertrand, Hans Rollema, Raymond S. Hurst, Linda P. Spear, Tim C. Kirkham, Thomas Steckler, et al. "PDE Inhibitors." In Encyclopedia of Psychopharmacology, 976. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3466.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "PDE 1." In Encyclopedia of Signaling Molecules, 1353. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101009.

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Barles, Guy, and Emmanuel Chasseigne. "PDE Tools." In On Modern Approaches of Hamilton-Jacobi Equations and Control Problems with Discontinuities, 23–87. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-49371-3_2.

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Efendiev, Messoud. "The Spatial Evolution of Mitochondria: PDE-PDE Systems." In Mathematical Modeling of Mitochondrial Swelling, 207–23. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99100-9_7.

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Cossali, Gianpietro Elvio, and Simona Tonini. "Separability of PDE." In Drop Heating and Evaporation: Analytical Solutions in Curvilinear Coordinate Systems, 73–88. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49274-8_3.

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Petroianu, Georg, and Peter Michael Osswald. "Phosphodiesterase(PDE)-Inhibitoren." In Anästhesie in Frage und Antwort, 155–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-05715-5_54.

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Conference papers on the topic "PDE"

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Aarsnes, Ulf Jakob F., Rafael Vazquez, Florent Di Meglio, and Miroslav Krstic. "Delay robust control design of under-actuated PDE-ODE-PDE systems." In 2019 American Control Conference (ACC). IEEE, 2019. http://dx.doi.org/10.23919/acc.2019.8814788.

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Kornprobst, Pierre, Rachid Deriche, and Gilles Aubert. "Image restoration via PDE." In Enabling Technologies for Law Enforcement and Security, edited by Leonid I. Rudin and Simon K. Bramble. SPIE, 1997. http://dx.doi.org/10.1117/12.267177.

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Ghattas, Omar. "Session details: PDE applications." In SC '07: International Conference for High Performance Computing, Networking, Storage and Analysis. New York, NY, USA: ACM, 2007. http://dx.doi.org/10.1145/3246899.

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Jun Tan, Lai Jin-mei, Ren Jun-yan, and Wing. "A fast PDE solver for numerical solution of coupled ODE-PDE-AE." In 2003 5th International Conference on ASIC Proceedings (IEEE Cat No 03TH8690) ICASIC-03. IEEE, 2003. http://dx.doi.org/10.1109/icasic.2003.1277510.

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Paunonen, Lassi, and Jukka-Pekka Humaloja. "On Robust Regulation of PDEs: from Abstract Methods to PDE Controllers." In 2022 IEEE 61st Conference on Decision and Control (CDC). IEEE, 2022. http://dx.doi.org/10.1109/cdc51059.2022.9993119.

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Weisenberger, H., and W. Haarmann. "CORRELATION BETWEEN INHIBITION OF PLATELET PHOSPHODIESTERASES (PDEs) AND PLATELET FUNCTION TESTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643433.

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Abstract:
A systematic investigation of over 100 PDE inhibiting pyrimidopyrimidines was performed regarding a possible correlation between influence on platelet function tests and inhibition of platelet PDEs. Basically, the compounds tested were congeners of Dipyridamole but lack substitution in position 6. The concentration necessary for a 50% inhibition of PDE activity in platelet homogenates ranged between 0.000045 and 35 μmoles/L.The inhibition of platelet PDEs was measured in freeze-thaw homogenates of human platelets using 3H-cAMP as substrate. Intraplatelet cAMP changes were measured by prelabelling the ATP pool with 3H-adenine and isolation of 3H-cAMP. Inhibition of platelet retention was determined using Morris' method (rotating citrated whole blood with glass beads) and the aggregation tests were performed according to Born and Cross in citrated platelet rich plasma.The rather large number of compounds allowed the application of correlation analysis. The results of linear regression tests (IC50 and EC200 values) are shown in the table.It appears that increased intracellular cAMP caused by PDE inhibition shows a strong correlation to the inhibition of the above mentioned platelet function tests. A weaker relation exists between inhibition of isolated PDEs and platelet function. Thus, determination of intrinsic PDE inhibitory potency is not sufficient to predict the influence of a given compound on platelet function tests.
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Saito, Takahiro, Hiroyuki Harada, and Takashi Komatsu. "Model-based PDE method and model-free PDE method for motion de-blurring." In Visual Communications and Image Processing 2005. SPIE, 2005. http://dx.doi.org/10.1117/12.633209.

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Yezzi, Anthony, Ganesh Sundaramoorthi, and Minas Benyamin. "PDE Acceleration for Active Contours." In 2019 IEEE/CVF Conference on Computer Vision and Pattern Recognition (CVPR). IEEE, 2019. http://dx.doi.org/10.1109/cvpr.2019.01260.

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Baravdish, George, Gianpaolo Evangelista, Oloj Svensson, and Faten Sofya. "PDE-SVD based audio denoising." In 2012 5th International Symposium on Communications, Control and Signal Processing (ISCCSP). IEEE, 2012. http://dx.doi.org/10.1109/isccsp.2012.6217853.

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Lisle, Ian G., S. L. Tracy Huang, and Greg J. Reid. "Structure of symmetry of PDE." In the 2014 Symposium. New York, New York, USA: ACM Press, 2014. http://dx.doi.org/10.1145/2631948.2631962.

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Reports on the topic "PDE"

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Hwang, Kai. Supercomputers for Solving PDE Problems. Fort Belvoir, VA: Defense Technical Information Center, November 1988. http://dx.doi.org/10.21236/ada204611.

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Rice, John R. Parallel Algorithms for PDE Solvers. Fort Belvoir, VA: Defense Technical Information Center, July 1988. http://dx.doi.org/10.21236/ada199625.

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Chan, Tony F., Jianhong Shen, and Luminita Vese. Variational PDE Models in Image Processing. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada437477.

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Pothen, Alex. Terascale Optimal PDE Simulations (TOPS) Center. Office of Scientific and Technical Information (OSTI), August 2006. http://dx.doi.org/10.2172/890547.

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Smith, B. Extensible PDE Solvers package users manual. Office of Scientific and Technical Information (OSTI), September 1994. http://dx.doi.org/10.2172/10194934.

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Rice, John R. Parallel PDE Algorithms and Supercomputer Architecture. Fort Belvoir, VA: Defense Technical Information Center, January 1985. http://dx.doi.org/10.21236/ada185589.

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Goldschneider, Jill, Lydia Ng, and Vikram Chalana. PDE Software for Digital Image Management. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384519.

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Turner, Daniel Z., Richard B. Lehoucq, and Carlos A. Garavito-Garzon. PDE Constrained Optimization for Digital Image Correlation. Office of Scientific and Technical Information (OSTI), October 2015. http://dx.doi.org/10.2172/1494349.

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Tucker, K. C., Paul I. King, Frederick R. Schauer, and John L. Hoke. Branched Detonation in a Multi-Tube PDE. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada453067.

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Barles, G., L. C. Evans, and P. E. Souganidis. Wavefront Propagation for Reaction-Diffusion Systems of PDE. Fort Belvoir, VA: Defense Technical Information Center, March 1989. http://dx.doi.org/10.21236/ada210862.

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