Relevant bibliographies by topics / LPAR

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  2. Dissertations / Theses
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  5. Conference papers
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Academic literature on the topic 'LPAR'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "LPAR"

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Park, Hoyong, Sungmin Kim, Jeehae Rhee, Hyeon-Joong Kim, Jung-Soo Han, Seung-Yeol Nah, and ChiHye Chung. "Synaptic enhancement induced by gintonin via lysophosphatidic acid receptor activation in central synapses." Journal of Neurophysiology 113, no. 5 (March 1, 2015): 1493–500. http://dx.doi.org/10.1152/jn.00667.2014.

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Lysophosphatidic acid (LPA) is one of the well-characterized, ubiquitous phospholipid molecules. LPA exerts its effect by activating G protein-coupled receptors known as LPA receptors (LPARs). So far, LPAR signaling has been critically implicated during early development stages, including the regulation of synapse formation and the morphology of cortical and hippocampal neurons. In adult brains, LPARs seem to participate in cognitive as well as emotional learning and memory. Recent studies using LPAR1-deficient mice reported impaired performances in a number of behavioral tasks, including the hippocampus-dependent spatial memory and fear conditioning tests. Nevertheless, the effect of LPAR activation in the synaptic transmission of central synapses after the completion of embryonic development has not been investigated. In this study, we took advantage of a novel extracellular agonist for LPARs called gintonin to activate LPARs in adult brain systems. Gintonin, a recently identified active ingredient in ginseng, has been shown to activate LPARs and mobilize Ca2+ in an artificial cell system. We found that the activation of LPARs by application of gintonin acutely enhanced both excitatory and inhibitory transmission in central synapses, albeit through tentatively distinct mechanisms. Gintonin-mediated LPAR activation primarily resulted in synaptic enhancement and an increase in neuronal excitability in a phospholipase C-dependent manner. Our findings suggest that LPARs are able to directly potentiate synaptic transmission in central synapses when stimulated exogenously. Therefore, LPARs could serve as a useful target to modulate synaptic activity under pathological conditions, including neurodegenerative diseases.
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Headen, Karmel V., Afolabi O. Ogunleye, and David E. Williams. "A High-resolution Immunohistochemical Method for studying Receptor Expression on the Periodontal Ligament of Whole-mount Human Tooth Roots." International Journal of Experimental Dental Science 5, no. 2 (2016): 99–103. http://dx.doi.org/10.5005/jp-journals-10029-1134.

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ABSTRACT Aims Our laboratory has found that lysophosphatidic acid (LPA) and its cognate receptors [LPARs, (LPA1–6)] expressed by human gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) play key roles in oral fibroblast homeostasis and are implicated in the inflammation seen in periodontal disease. We have reported that PDLF express LPA1 and LPA3; however, information on the gross topographic distribution of LPARs in the periodontal ligament (PDL) was lacking, and therefore, we developed a simple method for in situ labeling of LPARs in the PDL of extracted teeth. Materials and methods Sectioning or grinding thin sections of demineralized or native teeth and periodontium have long been the standard methodologies used to assess biomarker distribution in the PDL; however, we modified traditional immunohistochemical labeling and used whole teeth with fixed, solvent permeabilized PDLs. Results LPA1 and LPA3 were specifically labeled in the PDL and could be visualized at both the macroand micro-levels. Conclusion This technique effectively labeled LPARs, and it can serve as a basis for the in situ visualization of other biomolecules expressed in the PDL. Clinical Significance The ability to observe PDL LPAR distribution at the macro-level complements the microscopic data, and it is useful for detecting and documenting molecular changes in the PDL/PDLF that were brought about by age, experimental treatments, or pathologies like periodontal disease. How to cite this article Cerutis DR, Headen KV, Ogunleye AO, Williams DE. A High-resolution Immunohistochemical Method for studying Receptor Expression on the Periodontal Ligament of Whole-mount Human Tooth Roots. Int J Experiment Dent Sci 2016;5(2):99-103.
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Balijepalli, Pravita, Ciera C. Sitton, and Kathryn E. Meier. "Lysophosphatidic Acid Signaling in Cancer Cells: What Makes LPA So Special?" Cells 10, no. 8 (August 11, 2021): 2059. http://dx.doi.org/10.3390/cells10082059.

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Lysophosphatidic acid (LPA) refers to a family of simple phospholipids that act as ligands for G protein-coupled receptors. While LPA exerts effects throughout the body in normal physiological circumstances, its pathological role in cancer is of great interest from a therapeutic viewpoint. The numerous LPA receptors (LPARs) are coupled to a variety of G proteins, and more than one LPAR is typically expressed on any given cell. While the individual receptors signal through conventional GPCR pathways, LPA is particularly efficacious in stimulating cancer cell proliferation and migration. This review addresses the mechanistic aspects underlying these pro-tumorigenic effects. We provide examples of LPA signaling responses in various types of cancers, with an emphasis on those where roles have been identified for specific LPARs. While providing an overview of LPAR signaling, these examples also reveal gaps in our knowledge regarding the mechanisms of LPA action at the receptor level. The current understanding of the LPAR structure and the roles of LPAR interactions with other receptors are discussed. Overall, LPARs provide insight into the potential molecular mechanisms that underlie the ability of individual GPCRs (or combinations of GPCRs) to elicit a unique spectrum of responses from their agonist ligands. Further knowledge of these mechanisms will inform drug discovery, since GPCRs are promising therapeutic targets for cancer.
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Lee, Jong, Donghee Kim, Yoon Oh, and Hee-Sook Jun. "Lysophosphatidic Acid Signaling in Diabetic Nephropathy." International Journal of Molecular Sciences 20, no. 11 (June 11, 2019): 2850. http://dx.doi.org/10.3390/ijms20112850.

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Lysophosphatidic acid (LPA) is a bioactive phospholipid present in most tissues and body fluids. LPA acts through specific LPA receptors (LPAR1 to LPAR6) coupled with G protein. LPA binds to receptors and activates multiple cellular signaling pathways, subsequently exerting various biological functions, such as cell proliferation, migration, and apoptosis. LPA also induces cell damage through complex overlapping pathways, including the generation of reactive oxygen species, inflammatory cytokines, and fibrosis. Several reports indicate that the LPA–LPAR axis plays an important role in various diseases, including kidney disease, lung fibrosis, and cancer. Diabetic nephropathy (DN) is one of the most common diabetic complications and the main risk factor for chronic kidney diseases, which mostly progress to end-stage renal disease. There is also growing evidence indicating that the LPA–LPAR axis also plays an important role in inducing pathological alterations of cell structure and function in the kidneys. In this review, we will discuss key mediators or signaling pathways activated by LPA and summarize recent research findings associated with DN.
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Okusa, Mark D., Hong Ye, Liping Huang, Laura Sigismund, Timothy Macdonald, and Kevin R. Lynch. "Selective blockade of lysophosphatidic acid LPA3 receptors reduces murine renal ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 285, no. 3 (September 2003): F565—F574. http://dx.doi.org/10.1152/ajprenal.00023.2003.

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Lysophosphatidic acid (LPA) released during ischemia has diverse physiological effects via its G protein-coupled receptors, LPA1, LPA2, and LPA3 (formerly Edg-2, -4, and -7). We tested the hypothesis that selective blockade of LPA receptors affords protection from renal ischemia-reperfusion (I/R) injury. By real-time PCR, LPA1-3 receptor mRNAs were expressed in mouse renal cortex, outer medulla, and inner medulla with the following rank order LPA3 = LPA2 > LPA1. In C57BL/6 mice whose kidneys were subjected to ischemia and reperfusion, treatment with a selective LPA3 agonist, oleoyl-methoxy phosphothionate (OMPT), enhanced injury. In contrast, a dual LPA1/LPA3-receptor antagonist, VPC-12249, reduced I/R injury, but this protective effect was lost when the antagonist was coadministered with OMPT. Interestingly, delaying administration of VPC-12249 until 30 min after the start of reperfusion did not alter its efficacy significantly. We conclude that VPC-12249 reduces renal I/R injury predominantly by LPA3 receptor blockade and could serve as a novel compound in the treatment of ischemia acute renal failure.
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Chen, Min, L. Nicole Towers, and Kathleen L. O'Connor. "LPA2 (EDG4) mediates Rho-dependent chemotaxis with lower efficacy than LPA1 (EDG2) in breast carcinoma cells." American Journal of Physiology-Cell Physiology 292, no. 5 (May 2007): C1927—C1933. http://dx.doi.org/10.1152/ajpcell.00400.2006.

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Lysophosphatidic acid (LPA) acts via binding to specific G protein-coupled receptors and has been implicated in the biology of breast cancer. Here, we characterize LPA receptor expression patterns in common established breast cancer cell lines and their contribution to breast cancer cell motility. By measuring expression of the LPA receptors LPA1, LPA2, and LPA3 with real-time quantitative PCR, we show that the breast cancer cell lines tested can be clustered into three main groups: cells that predominantly express LPA1 (BT-549, Hs578T, MDA-MB-157, MDA-MB-231, and T47D), cells that predominantly express LPA2 (BT-20, MCF-7, MDA-MB-453, and MDA-MB-468), and a third group that shows comparable expression level of these two receptors (MDA-MB-175 and MDA-MB-435). LPA3 expression was detected primarily in MDA-MB-157 cells. Using a Transwell chemotaxis assay to monitor dose response, we find that cells predominantly expressing LPA1 have a peak migration rate at 100 nM LPA that drops off dramatically at 1 μM LPA, whereas cells predominantly expressing LPA2 show the peak migration rate at 1 μM LPA, which remains high at 10 μM. Using BT-20 cells, LPA2-specific small interfering RNA, and C3 exotransferase, we demonstrate that LPA2 can mediate LPA-stimulated cell migration and activation of the small GTPase RhoA. Using LPA2 small interfering RNA, exogenous expression of LPA1, and treatment with Ki16425 LPA receptor antagonist in the BT-20 cells, we further find that LPA1 and LPA2 cooperate to promote LPA-stimulated chemotaxis. In summary, our results suggest that the expression of both LPA1 and LPA2 may contribute to chemotaxis and may permit cells to respond optimally to a wider range of LPA concentrations, thus revealing a new aspect of LPA signaling.
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Turgut, Ali, Emre Bilgin, Mert Filibeli, İbrahim Kuşak, Mert Kumbaracı, and Önder Kalenderer. "A New Reference to Evaluate Syndesmosis in Sagittal Plane Radiographs of the Ankle: The Lateral Posterior Ankle Ratio." Journal of the American Podiatric Medical Association 109, no. 6 (November 1, 2019): 426–30. http://dx.doi.org/10.7547/17-134.

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Background: Confirmation of anatomical reduction of ankle syndesmosis is mandatory because improper reduction leads to poor functional results. Coronal plane evaluation of syndesmosis is well described in the literature, but there is little information about sagittal plane evaluation. We sought to evaluate the relationship of fibula and tibia in the sagittal plane and create a new reference that can be applied easily and reliably. Methods: Lateral ankle radiographs of 337 individuals with no history of ankle fracture were evaluated. A line was drawn between the anterior and posterior cortices of the distal lateral tibia, and the length of this line was measured (line 1). The distance between the anterior and posterior cortices of the fibula on this line was measured, and the center of this second distance was identified and marked. The posterior half of the fibular width was divided by line 1 and was named the lateral posterior ankle ratio (LPAR). Statistical analysis was performed by side and sex. Results: Mean patient age was 38.6 years; mean LPAR was 0.48. There was a significant difference between men and women by age (P < .001) and LPAR (P = .01). There was no significant difference between right and left ankles by age (P = .63) and LPAR (P = .64). The LPAR was less than 0.40 in 6.8% of the radiographs, 0.40 to 0.50 in 57.9%, and greater than 0.50 to 0.60 in 32.9%. Conclusions: The LPAR should approximate 50% in normal lateral ankle images and, by extrapolation, after syndesmotic reduction.
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Stope, Matthias B., Robert Mandelkow, Daniela Brunnert, Martin Weiss, and Martin Burchardt. "Lysophosphatidic acid receptor isoforms expression in prostate cancer cells is differentially regulated by the CYP17A1 inhibitor abiraterone and depends on the androgen receptor." Advances in Modern Oncology Research 2, no. 1 (February 19, 2016): 57. http://dx.doi.org/10.18282/amor.v2.i1.83.

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<p>Prostate cancer (PC) treatment with steroid synthesis inhibitor, abiraterone acetate (AA) provides substantial survival advantages in advanced PC therapy. Owing to AA's anti-proliferative efficacy, even in the absence of androgen receptor (AR), the molecular mode of action is suspected to be a result of simultaneously targeted cellular factors. The present study demonstrated a differentially regulated expression of proliferative lysophosphatidic acid receptor (LPAR) isoforms in androgen receptor AR-positive LNCaP cells incubated with AA. Since LPAR regulation in AR-negative PC-3 cells is unaffected, it could be assumed that AA’s anticancer activity on LPAR expression depends on AR signaling cascades.</p>
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Contos, James J. A., Isao Ishii, Nobuyuki Fukushima, Marcy A. Kingsbury, Xiaoqin Ye, Shuji Kawamura, Joan Heller Brown, and Jerold Chun. "Characterization of lpa2 (Edg4) and lpa1/lpa2 (Edg2/Edg4) Lysophosphatidic Acid Receptor Knockout Mice: Signaling Deficits without Obvious Phenotypic Abnormality Attributable to lpa2." Molecular and Cellular Biology 22, no. 19 (October 1, 2002): 6921–29. http://dx.doi.org/10.1128/mcb.22.19.6921-6929.2002.

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ABSTRACT Lysophosphatidic acid (LPA), a bioactive lipid produced by several cell types including postmitotic neurons and activated platelets, is thought to be involved in various biological processes, including brain development. Three cognate G protein-coupled receptors encoded by lpa1 /lp A1/Edg-2/Gpcr26, lpa2 /lp A2/Edg-4, and lpa3 /lp A3/Edg-7 mediate the cellular effects of LPA. We have previously shown that deletion of lpa1 in mice results in craniofacial dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of pups with frontal hematoma. To further investigate the role of these receptors and LPA signaling in the organism, we deleted lpa2 in mice. Homozygous knockout (lpa2 (−/−)) mice were born at the expected frequency and displayed no obvious phenotypic abnormalities. Intercrosses allowed generation of lpa1 (−/−) lpa2 (−/−) double knockout mice, which displayed no additional phenotypic abnormalities relative to lpa1 (−/−) mice except for an increased incidence of perinatal frontal hematoma. Histological analyses of lpa1 (−/−) lpa2 (−/−) embryonic cerebral cortices did not reveal obvious differences in the proliferating cell population. However, many LPA-induced responses, including phospholipase C activation, Ca2+ mobilization, adenylyl cyclase activation, proliferation, JNK activation, Akt activation, and stress fiber formation, were absent or severely reduced in embryonic fibroblasts derived from lpa1 (−/−) lpa2 (−/−) mice. Except for adenylyl cyclase activation [which was nearly abolished in lpa1 (−/−) fibroblasts], these responses were only partially affected in lpa1 (−/−) and lpa2 (−/−) fibroblasts. Thus, although LPA2 is not essential for normal mouse development, it does act redundantly with LPA1 to mediate most LPA responses in fibroblasts.
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Tucker, B. J., C. A. Mundy, and R. C. Blantz. "Can causality be determined from proximal tubular reabsorption and peritubular physical factors?" American Journal of Physiology-Renal Physiology 250, no. 1 (January 1, 1986): F169—F175. http://dx.doi.org/10.1152/ajprenal.1986.250.1.f169.

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Many studies in the literature have drawn conclusions regarding the mechanism of change in absolute proximal tubular reabsorption (APR) based on steady-state measurements of proximal reabsorptive rates and the peritubular capillary. The proximal reabsorptive rate, APR, is the product of the effective reabsorptive pressure (ERP) and the peritubular capillary reabsorptive coefficient (LpAR) (APR = ERP . LpAR). The ERP is defined by the net hydrostatic and oncotic pressure gradient acting across the capillary wall from interstitium to peritubular capillary flow. The relationship APR = ERP . LpAR is predefined, and steady-state measurements do not permit determination of causality because primary changes in any variable obligate a proportional change in a second variable. As an example of the difficulties in interpretation of this type of analysis, we have examined the APR and factors contributing to ERP and LpAR before and after the administration of benzolamide, a carbonic anhydrase inhibitor, to saline-expanded Munich-Wistar rats. Alterations in peritubular capillary fluid uptake cannot always be interpreted as casual mechanisms for changes in absolute fluid reabsorption but may result from primary alterations in epithelial transport.
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Dissertations / Theses on the topic "LPAR"

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Burgess, R. Alan. "Elucidating Molecular Interactions of Shigella Type Three Secretion System Components Critical for Pathogenesis." DigitalCommons@USU, 2018. https://digitalcommons.usu.edu/etd/6968.

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Shigella spp. are Gram-negative, non-motile bacterial pathogens that are the causative agent of bacillary dysentery in humans. During infection, Shigella utilize a complex type three secretion system (T3SS) to inject effector proteins and take over host cell functions. With the rise of multi-antibiotic resistant Shigella strains, the T3SS is a promising alternative therapeutic target. While the needle and syringe-like apparatus of the T3SS has been extensively studied in Shigella, several components and mechanisms of this system remain unclear. The research presented here addresses two major knowledge gaps in the current understanding of the T3SS ATPase, Spa47, and the initial host-pathogen interaction at the tip of the apparatus. In this work, high resolution crystal structures of Spa47 guided the creation of an oligomer model which suggested ATP hydrolysis may be supported by specific side chain contributions from adjacent protomers within the complex. Mutagenesis experiments targeting predicted active site residues and the oligomerization domain revealed that active site residues alone are not responsible for Spa47 oligomerization while protein oligomerization is crucial for ATPase activity. Together with in vivo experiments, we show that ATP hydrolysis and proper Spa47 oligomer formation is critical for T3SS apparatus formation, effector secretion, and overall Shigella virulence. Additionally, we have combined the Langmuir Blodgett technique with fluorescent microscopy to visualize the interaction between key T3SS tip proteins with defined artificial phospholipid membranes. These membranes were generated using Langmuir Blodgett which provided control over lipid phase and composition. Lipid phase and protein localization were monitored using lipophilic dyes and selective fluorescent protein labeling. These experiments suggest a differential interaction between the tip protein IpaB with the membrane components cholesterol and sphingomyelin based on IpaB oligomerization. IpaC, another T3SS tip protein, was found to destabilize membranes when alone, but was stabilized in the presence of IpaB. These experiments suggest that IpaB confers IpaC stability within membranes and that tip protein localization is dependent on lipid phase and composition. Overall, these new insights into the T3SS ATPase and tip proteins provide a more complete understanding of Shigella virulence that will aid in future endeavors to identify alternative therapeutic targets for treatment.
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David, Marion. "Rôle de l’axe Autotaxine (ATX)- Acide Lysophosphatidique (LPA) et récepteur LPA1 dans la dissémination métastatique des cancers du sein." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10314/document.

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Les métastases sont des conséquences dramatiques lors de la progression des cancers. Malgré les traitements actuels la médiane de survie de patients atteints de métastases osseuses n’est que de 24 mois. Donc l’identification de nouvelles cibles thérapeutiques dans le traitement ou la prévention des métastases revêt un caractère crucial. L’objectif de ce travail de thèse est d’étudier le rôle de l’acide lysophosphatidique (LPA) et de l’autotaxine (ATX) dans la dissémination métastatique des cancers du sein. Notre laboratoire a montré que le LPA contrôle la croissance tumorale et la progression des métastases osseuses dans le contexte des cancers du sein. On sait depuis peu qu’en raison de son activité lysophospholipase D, ATX produit du LPA à partir de la lysophosphatidylcholine et contrôle les niveaux de LPA dans la circulation sanguine. ATX est une protéine sécrétée présentant des propriétés métastatiques. Les travaux présentés dans cette thèse montrent que l'expression d'ATX par les cellules tumorales contrôle les événements précoces de la dissémination métastatique des cancers du sein ainsi que le processus plus tardif de formation et de progression des métastases osseuses en agissant sur la fonction ostéoclastique. Il existe un grand nombre de récepteurs capables de transmettre l’activation cellulaire par le LPA (LPA1-6). Ce travail de thèse montre également que le niveau d’expression du récepteur LPA1 au niveau de la tumeur primaire est un facteur prédictif de la rechute métastatique chez les patientes ayant un cancer du sein. D’autre part dans un modèle animal préclinique, nous avons observé que le ciblage thérapeutique précoce de LPA1 par le DEBIO-0719 bloque efficacement la dissémination métastatique des cellules de cancer du sein. En conclusion, nos résultats montrent que le ciblage de l’axe ATX/LPA/LPA1 présente un haut potentiel thérapeutique chez des patientes atteintes d’un cancer du sein à fort risque métastatique
Metastases consist of poor disease progression for patients with cancers. Bone metastases are frequently found in multiple cancers. Despite the improvement of current therapies, the survival of bone metastasis patients is only 24 months. The aim of this work consisted in understanding the role of lysophosphatidic acid (LPA), autotaxin (ATX) and the LPA receptor LPA1 in the metastatic dissemination of breast cancers. Our laboratory showed previously that LPA produced tumor growth and the progression of osteolytic bone metastases of breast cancer cells. Due to its lysophospholipase D activity, ATX generates LPA from lysophosphatidylcholine and controls LPA levels in the blood. ATX is a secreted protein with metastatic properties. In the present thesis, we first demonstrated that ATX expressed by tumors cells controls early events of metastatic dissemination of breast cancer cells and latter bone metastases formation and progression by acting on osteoclastic function. There is a large number of receptors mediating the cellular activation of LPA (LPA1-6). This work showed additionally that the LPA1 expression level at the primary tumor site is predictive for the metastatic relapse of breast cancers. On the other hand, in a preclinical animal model, we observed that targeting LPA1 at early stage of tumor development with the DEBIO-0719 decreased efficiently the metastatic dissemination of breast cancer cells. Altogether, these results indicate that targeting the ATX/LPA/LPA1 track has a high therapeutic potential against metastasis formation for patients with breast cancer
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Boucharaba, Ahmed. "Rôle de l'acide lysophosphatidique (LPA) et du récepteur LPA1 dans la formation des métastases osseuses." Paris 7, 2006. http://www.theses.fr/2006PA077219.

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Les cancers du sein induisent fréquemment la formation de métastases osseuses. Les cellules tumorales présentes aux sites osseux produisent de nombreux facteurs (cytokines, PTHrP) qui stimulent l'activité de résorption des ostéoclastes entraînant la dégradation de l'os et libérant les facteurs de croissance piégés dans la matrice osseuse. Les traitements actuels permettent seulement de ralentir la progression de la destruction osseuse. Il est donc important de mieux comprendre les mécanismes moléculaires impliqués dans le développement des métastases osseuses. Parmi les facteurs présentant un fort potentiel dans la régulation du développement tumoral, l'acide lysophosphatidique (LPA) est un lipide biologique libéré massivement par les plaquettes sanguines au moment de leur activation. Mes travaux, ont pour but de comprendre le rôle de l'acide lysophosphatidique (LPA) in vitro et in vivo dans les processus du développement tumoral au tissu osseux et d'évaluer si le LPA et/ou ses récepteurs sont des cibles thérapeutiques potentielles dans le traitement des patients atteints de métastases osseuses. Mes résultats montrent que le LPA est produit au site même des métastases osseuses et qu'il y joue un rôle stimulateur de leur progression en agissant sur la croissance tumorale et sur la sécrétion des interleukines stimulatrices de la résorption osseuse (IL-6 et IL-8), que l'interaction entre les plaquettes sanguines et les cellules tumorales est à l'origine de la production de LPA par le: plaquettes activées, et enfin de montrer que le récepteur LPA1 est une cible thérapeutique prometteuse dans le traitement des métastases osseuses
Breast cancers frequently metastasize to bone. Bonemetastases are associated with hypercalcemia due to bone destruction, intractable bone pain, and pathological fractures. In bone metastasis, there is a vicious cycle wherein bone-residing tumor cells stimulate osteoclast-mediated bone résorption and bone-derived growth factors released from resorbed bone promote tumor growth. However, current treatments aimed to inhibit bone resorption (bisphosphonates) only delay the progression of osteolytic lesions in metastatic patients. Therefore, in addition to bone-derived growth factors, other endogenous sources of growth factors are probably involved in promoting skeletal tumor growth. In this respect, human blood platelets activation is an important source of LPA, and platelet aggregation plays a primordial role in the metastatic spreading of melanoma and Lewis lung carcinoma cells in bone and lungs, respectively. Here we provide experimental evidence for a direct role of LPA in the progression of bone metastasis in breast cancer. We identify platelet-derived LPA as an endogenous source that, in the bone microenvironment, stimulates both tumor growth and bone destruction. Although a role for LPA in cancer was emerging, there was a paucity of experimental evidence to support it. This study is to the best of our knowledge, the first to demonstrate a role for LPA and its receptor LPA1 in thé growth of breast cancer bone metastasis
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Alioli, Adebayo Candide. "Etude du rôle du récepteur LPA1 dans l'ostéogénèse au cours de la croissance du squelette : implication dans l'acquisition de masse osseuse." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30254.

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L'os est un organe dynamique qui se renouvelle constamment grâce à une activité coordonnée des ostéoblastes et des ostéocytes qui forment la matrice osseuse nouvelle, et des ostéoclastes qui la dégradent. De la naissance à la fin de l'adolescence, le squelette subit une croissance rapide, médiée par une activité de formation osseuse intense, encore appelée modelage osseux. Cette acquisition de masse osseuse est finement régulée grâce à l'action de nombreux facteurs systémiques et locaux. L'acide lysophosphatidique (LPA) est un médiateur lipidique naturel dont les fonctions biologiques affectent de nombreux organes et de nombreux types cellulaires, y compris les cellules osseuses, ostéoblastes, ostéocytes ostéoclastes. L'action du LPA sur le tissu osseux a été mise en évidence pour la première fois dans notre laboratoire, dans un modèle murin dans lequel l'expression de son récepteur LPA1 a été désactivée de façon globale (Lpar1-/-). Ces animaux présentent un défaut de croissance ainsi que des anomalies osseuses sévères. Cependant, en raison de l'expression ubiquitaire du récepteur LPA1, ce modèle ne permet pas de déterminer l'effet spécifique du LPA dans cellules ostéoblastiques dont l'action est majoritaire au cours de la croissance. L'objectif de mon travail de thèse a été d'étudier le rôle spécifique du LPA et de son récepteur LPA1 dans la lignée ostéoblastique, afin de déterminer son importance pendant le modelage de l'os. Pour ce faire, j'ai étudié des souris Lpar1-ΔOb, générées au laboratoire, et dont l'expression du récepteur LPA1 a été spécifiquement supprimée dans la lignée ostéoblastique. Ces souris ont présenté une baisse de la minéralisation osseuse et une réduction de l'épaisseur de l'os corticale, ainsi qu'une augmentation de la porosité osseuse. In vitro, les ostéoblastes primaires Lpar1-ΔOb et cl1-Ob-Lpar1-/- immortalisés ont révélé une prolifération cellulaire réduite, une altération de la différentiation et une activité de minéralisation réduite. De plus, j'ai mis en évidence chez les souris Lpar1-ΔOb une nette altération de la fonction des ostéocytes. Enfin, j'ai pu montrer in vitro, à la fois dans les ostéoblastes primaires Lpar1-ΔOb et immortalisés cl1-Ob-Lpar1-/-, que l'absence du récepteur LPA1 induit une altération importante de la formation des dendrites, processus précoce et déterminant dans leur différenciation en ostéocyte (ostéocytogenèse). Ces résultats suggèrent un nouveau rôle pour le LPA dans le contrôle de la masse osseuse via la minéralisation osseuse et la fonction des ostéocytes. Ils représentent une piste intéressante à explorer en physiopathologies pour résoudre des problématiques de minéralisation. Ils pourraient également ouvrir des perspectives dans l'exploration de certaines anomalies d'acquisition de masse osseuse comme la scoliose idiopathique de l'adolescent, qui est une pathologie rare dans laquelle des défauts de fonction ostéocytaire similaires à ceux des souris Lpar1-ΔOb ont été rapportés
Bone is a complex and dynamic organ that is constantly renewing by the coordinated activity of osteoblasts and osteocytes which form the new bone matrix, and osteoclasts responsible for bone resorption. During normal childhood and adolescence, the skeleton undergoes rapid growth, mediated by intense bone-forming activity, also called bone modeling. This acquisition of bone mass requires the proper interaction of numerous systemic and local factors. Lysophosphatidic acid (LPA) is a natural lipid mediator whose biological functions affect multiple organs and multiple cell types, including bone cells. The action of LPA on bone tissue was demonstrated for the first time in our laboratory, in a global Lpar1-knockout mice. These animals present a growth defect as well as severe bone abnormalities. However, due to the large expression of LPA1 in the cells, including bone cells, the Lpar1-/- mice are not suitable to understand the specific effect of LPA in osteoblastic cells, that have the predominant action during growth. The objective of my thesis work was to study the specific role of LPA and its receptor LPA1 in the osteoblastic lineage, in order to determine its importance during bone modeling. Thus, I studied the osteoblast-specific Lpar1 knockout mice (Lpar1-ΔOb) that we generated in the laboratory. These mice revealed reduced bone mineralization and decreased cortical thickness, as well as increased bone cortical porosity. In vitro, primary Lpar1-ΔOb and immortalized cl1-Ob-Lpar1-/- osteoblasts revealed a reduced cell proliferation associated with alterations in differentiation markers, and reduced mineralization activity. Furthermore, I highlighted in Lpar1-ΔOb mice a markedly impaired osteocyte specification. Finally, I was able to show in vitro, both in primary Lpar1-ΔOb and immortalized cl1-Ob-Lpar1-/- osteoblasts that the absence of LPA1 receptor leads to a significant alteration in the dendrites formation, an early and decisive process in their differentiation into osteocytes (Osteocytogenesis). These results suggest a new role for LPA in the control of bone mass via bone mineralization and osteocyte function. They will certainly be helpful in pathophysiology to solve mineralization problems. They could also open perspectives in the exploration of certain abnormalities in bone mass acquisition such as adolescent's idiopathic scoliosis, which is a rare pathology in which defects in osteocyte function similar to those in Lpar1-ΔOb mice have been reported
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Spruth, Wilhelm G. "Enterprise Computing." Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-126859.

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Das vorliegende Buch entstand aus einer zweisemestrigen Vorlesung „Enterprise Computing“, die wir gemeinsam über viele Jahre als Teil des Bachelor- oder Master-Studienganges an der Universität Leipzig gehalten haben. Das Buch führt ein in die Welt des Mainframe und soll dem Leser einen einführenden Überblick geben. Band 1 ist der Einführung in z/OS gewidmet, während sich Band 2 mit der Internet Integration beschäftigt. Ergänzend werden in Band 3 praktische Übungen unter z/OS dargestellt.
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Jones, Joanna L. "The involvement and regulation of ARF6 in agonist-induced internalization of the β₂-adrenoceptor and the LPA2 and LPA3 receptors." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422551.

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David, Marion. "Rôle de l'axe Autotaxine (ATX)- Acide Lysophosphatidique (LPA) et récepteur LPA1 dans la dissémination métastatique des cancers du sein." Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00878970.

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Les métastases sont des conséquences dramatiques lors de la progression des cancers. Malgré les traitements actuels la médiane de survie de patients atteints de métastases osseuses n'est que de 24 mois. Donc l'identification de nouvelles cibles thérapeutiques dans le traitement ou la prévention des métastases revêt un caractère crucial. L'objectif de ce travail de thèse est d'étudier le rôle de l'acide lysophosphatidique (LPA) et de l'autotaxine (ATX) dans la dissémination métastatique des cancers du sein. Notre laboratoire a montré que le LPA contrôle la croissance tumorale et la progression des métastases osseuses dans le contexte des cancers du sein. On sait depuis peu qu'en raison de son activité lysophospholipase D, ATX produit du LPA à partir de la lysophosphatidylcholine et contrôle les niveaux de LPA dans la circulation sanguine. ATX est une protéine sécrétée présentant des propriétés métastatiques. Les travaux présentés dans cette thèse montrent que l'expression d'ATX par les cellules tumorales contrôle les événements précoces de la dissémination métastatique des cancers du sein ainsi que le processus plus tardif de formation et de progression des métastases osseuses en agissant sur la fonction ostéoclastique. Il existe un grand nombre de récepteurs capables de transmettre l'activation cellulaire par le LPA (LPA1-6). Ce travail de thèse montre également que le niveau d'expression du récepteur LPA1 au niveau de la tumeur primaire est un facteur prédictif de la rechute métastatique chez les patientes ayant un cancer du sein. D'autre part dans un modèle animal préclinique, nous avons observé que le ciblage thérapeutique précoce de LPA1 par le DEBIO-0719 bloque efficacement la dissémination métastatique des cellules de cancer du sein. En conclusion, nos résultats montrent que le ciblage de l'axe ATX/LPA/LPA1 présente un haut potentiel thérapeutique chez des patientes atteintes d'un cancer du sein à fort risque métastatique
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Sahay, Debashish. "Identification of genes activated and biological markers involved in lysophosphatidic acid (LPA)-induced breast cancer metastasis through its receptor LPA1." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10012/document.

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L'acide lysophosphatique est un biolipide naturel actif capable de réguler diverses fonctions biologiques et d'agir en tant que facteur de croissance, via l'activation de six différents récepteurs de surfaces couplées aux protéines G (LPA1-6). Notre laboratoire a montré que le ciblage thérapeutique du récepteur LPA1 bloque de façon remarquable la dissémination métastatique des cellules de cancer du sein. Les mécanismes moléculaires et génétiques impliqués dans ce processus sont cependant encore inconnus. De plus, la plupart des cellules de mammifères co-expriment plusieurs formes de récepteurs du LPA. La réponse cellulaire est la résultante de l'activation de multiples voies de signalisation, parfois synergiques ou opposées, compromettant la validation chez le patient de l'efficacité des thérapies ciblant ces récepteurs. Au cours de cette thèse, nous avons dans un premier temps montré que HB-EGF est un marqueur spécifique de l'activité de LPA1. Le blocage pharmacologique de ce récepteur via des antagonistes des récepteurs LPA1-3 (Ki16425/Debio0719) ou l'invalidation de son expression par une technique d'ARN interférence entraine une inhibition de la surexpression en HB-EGF. Le ciblage thérapeutique de LPA1 via l'antagoniste Ki16425, dans notre modèle animal préclinique de xénogreffe de cancer de la prostate PC3, conduit également à une diminution de l'expression en ARNm de HB-EGF au niveau de la tumeur primaire et à une diminution des concentrations en HB-EGF humain circulants dans le sérum. Dans un deuxième temps, nous nous sommes intéressé au rôle des miRNAs, qui sont impliqués dans la régulation de l'expression de gènes. Grâce à l'analyse de 1488 patients atteins de cancers du sein référencés sur des bases de données publiques, nous avons pu établir une corrélation entre le gène LPA1 et le gène ZEB1. Nous avons également trouvé que le coefficient de corrélation entre ZEB1 et LPA1 était supérieur au niveau des tumeurs mammaires basales
Lysophosphatidic acid (LPA) is a natural bioactive lipid with growth factor-like functions due to activation of a series of six G protein-coupled receptors (LPA1-6). It has been demonstrated that blocking LPA1 activity in vivo inhibits breast cancer cell metastasis, however, activated genes involved in LPA-induced metastasis have not been defined yet. In addition most mammalian cells co-express multiple LPA receptors, resulting in the co-activation of multiple intracellular signaling pathways with potential redundant or opposite effects impairing the validation of target inhibition in patients because of missing LPA receptor-specific biomarkers. In the first part of this thesis I found that HB-EGF is a specific biomarker of LPA1 activity. HB-EGF upregulation was inhibited by LPA1-3 antagonists (Ki16425, Debio0719) and by stably silencing LPA1. Using a human xenograft prostate tumors mouse model with PC3 cells, we found that a five-day treatment with Ki16425 significantly decreased both HB-EGF mRNA expression at the primary tumor site and circulating human HB-EGF concentrations in serum. In the second part of experimental work, we focused our attention on miRNAs that are master gene regulators. We carried out correlation studies in 1488 human primary breast tumors from publically available databases and found ZEB1 as the most correlated gene with LPAR1. The coefficient of correlation between ZEB1 and LPAR1 was higher in human basal tumors than in non basal tumors. In three different basal cell lines LPA up-regulated ZEB1 through an LPA1/Phosphatidylinositol-3-Kinase (Pi3K)/AKT-dependent pathway. Based on microarray and real-time PCR analyses we found that LPA up-regulated the oncomiR miR-21 through an LPA1/Pi3K/AKT/ZEB1-dependent mechanism. MirVana miR-21 inhibitor, silencing LPA1 or silencing ZEB1 totally blocked in vitro LPA-induced cell migration and invasion, and in vivo tumor cell bone colonization. In all cases, basal breast cancer cell functions were rescued with mirVana miR-21 mimic. All together our results identify HB-EGF as a new and relevant biomarker with potentially high value in quantifying LPA1 activation state in patients receiving anti-LPA1 therapies
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Urs, Nikhil Mahabir. "The regulation of cellular trafficking of the human lysophosphatidic acid receptor 1: identification of the molecular determinants required for receptor trafficking." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/16177.

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The following thesis research was undertaken to gain a better understanding of the mechanisms that regulate the cellular trafficking and signaling of the endothelial differentiation gene (EDG) family of G-protein coupled receptors, LPA1, LPA2, and LPA3. This thesis will specifically focus on the regulation of the trafficking of the LPA1 Lysophosphatidic acid receptor, which is the most widely expressed and has been shown to be a major regulator of migration of cells expressing it. The initial studies undertaken in this project were aimed at understanding the endocytic pathway followed by the LPA1 receptor. Lysophosphatidic acid (LPA), an abundant serum phospholipid, stimulates heterotrimeric G protein signaling by activating three closely related receptors, termed LPA1, LPA2 and LPA3. In the first part of the project we show that in addition to promoting LPA1 signaling, membrane cholesterol is essential for the association of LPA1 with β-arrestin, which leads to signal attenuation and clathrin dependent endocytosis of LPA1. The second phase of the project was aimed at elucidating the different structural motifs required for the trafficking and signaling of the LPA1 receptor and helping us gain a more mechanistic view of the processes involved in its regulation. In the second part of the project we show that agonist-independent internalization of the LPA1 receptor is clathrin adaptor, AP-2 dependent and PKC-dependent and that it requires a distal dileucine motif, whereas agonist-dependent internalization of the LPA1 receptor is β-arrestin and clathrin-dependent and requires a cluster of serine residues in the tail region, which is upstream of the dileucine motif. These studies collectively vastly enhance our understanding of mechanisms that regulate LPA1 trafficking and signaling. These studies can also be applied to other G-protein coupled receptors making the task easier for other scientists to understand this vast family of receptors.
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Murph, Mandi Michelle. "A characterization of the human G protein-coupled receptor, lysophosphatidic acid1 its intracellular trafficking and signaling consequences on the tumor suppressor, P53 /." Diss., Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-03222005-105717/unrestricted/murph%5Fmandi%5Fm%5F200505%5Fphd.pdf.

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Thesis (Ph. D.)--Biology, Georgia Institute of Technology, 2005.
Merrill, Alfred, Committee Member ; Mills, Gordon, Committee Member ; McCarty, Nael, Committee Member ; Kubanek, Julia, Committee Member ; Radhakrishna, Harish, Committee Chair. Includes bibliographical references.
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Books on the topic "LPAR"

1

Frank, Pfenning, ed. Logic programming and automated reasoning: 5th International Conference, LPAR '94, Kiev, Ukraine, July 16-22, 1994 : proceedings. Berlin: Springer-Verlag, 1994.

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LPAR '92 (1992 Saint Petersburg, Russia). Logic programming and automated reasoning: International conference, LPAR '92, St. Petersburg, Russia, July 15-20, 1992 : proceedings. Berlin: Springer-Verlag, 1992.

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1959-, Voronkov A., ed. Logic programming and automated reasoning: 4th international conference, LPAR '93, St. Petersburg, Russia, July 13-20, 1993 : proceedings. Berlin: Springer-Verlag, 1993.

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LPAR (Conference) (17th 2010 Yogyakarta, Indonesia). Logic for programming, artificial intelligence, and reasoning: 17th international conference, LPAR-17, Yogyakarta, Indonesia, October 10-15, 2010 : proceedings. Berlin: Springer, 2010.

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1956-, Parigot Michel, and Voronkov A. 1959-, eds. Logic for programming and automated reasoning: 7th International Conference, LPAR 2000, Reunion Island, France, November 6-10, 2000 : proceedings. Berlin: Springer, 2000.

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1959-, Voronkov A. (Andreĭ), and SpringerLink (Online service), eds. Logic for Programming, Artificial Intelligence, and Reasoning: 18th International Conference, LPAR-18, Mérida, Venezuela, March 11-15, 2012. Proceedings. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012.

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Robert, Nieuwenhuis, and Voronkov A. 1959-, eds. Logic for programming, artificial intelligence, and reasoning: 8th international conference, LPAR 2001, Havana, Cuba, December 3-7, 2001 : proceedings. Berlin: Springer, 2001.

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Nachum, Dershowitz, and Voronkov A. 1959-, eds. Logic for programming, artificial intelligence, and reasoning: 14th international conference, LPAR 2007, Yerevan, Armenia, October 15-19, 2007 : proceedings. Berlin: Springer, 2007.

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Franz, Baader, and Voronkov A. 1959-, eds. Logic for programming, artificial intelligence, and reasoning: 11th international conference, LPAR 2004, Montevideo, Uruguay, March 14-18, 2005 : proceedings. Berlin: Springer, 2005.

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Geoff, Sutcliffe, Voronkov A. 1959-, and LINK (Online service), eds. Logic for programming, artificial intelligence, and reasoning: 12th international conference, LPAR 2005, Montego Bay, Jamaica, December 2-6, 2005 : proceedings. Berlin: Springer, 2005.

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Book chapters on the topic "LPAR"

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Falsafi, Babak, Samuel Midkiff, JackB Dennis, JackB Dennis, Amol Ghoting, Roy H. Campbell, Christof Klausecker, et al. "Dynamic LPAR." In Encyclopedia of Parallel Computing, 592. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-09766-4_2253.

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Zeller, Elmar. "LPA-Checklisten, LPA-Fragen und LPA-Visualisierung." In Layered Process Audit (LPA), 57–110. München: Carl Hanser Verlag GmbH & Co. KG, 2018. http://dx.doi.org/10.3139/9783446449527.004.

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Murph, Mandi. "LPA." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7121-6.

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Murph, Mandi. "LPA." In Encyclopedia of Cancer, 2539–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7121.

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Lackner, K. J., and D. Peetz. "LpA-I." In Springer Reference Medizin, 1533. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1973.

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Lackner, K. J., and D. Peetz. "LpA-I." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1973-1.

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Zeller, Elmar. "LPA umsetzen." In Layered Process Audit (LPA), 43–52. München: Carl Hanser Verlag GmbH & Co. KG, 2013. http://dx.doi.org/10.3139/9783446437456.003.

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Lackner, K. J., and D. Peetz. "LpA-I:A-II." In Springer Reference Medizin, 1533. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1974.

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Lackner, K. J., and D. Peetz. "LpA-I:A-II." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1974-1.

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Zeller, Elmar. "LPA und Prozessmanagement." In Layered Process Audit (LPA), 143–65. München: Carl Hanser Verlag GmbH & Co. KG, 2013. http://dx.doi.org/10.3139/9783446437456.008.

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Conference papers on the topic "LPAR"

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Xia, Liang, Jiangping Yang, Hanzhong Wang, and Xiaodong Hou. "Safety Analysis and Risk Assessment of LPAR Software System." In 2018 12th International Conference on Reliability, Maintainability, and Safety (ICRMS). IEEE, 2018. http://dx.doi.org/10.1109/icrms.2018.00037.

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Wu, C. Eric, and William P. Horn. "A J2EE application for process accounting, LPAR accounting, and transaction accounting." In the 5th international workshop. New York, New York, USA: ACM Press, 2005. http://dx.doi.org/10.1145/1071021.1071049.

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Lee, Sue-Chin, Yuko Fujiwara, Jianxiong Liu, Junming Yue, Ryoko Tsukahara, Erzsebet Szabo, Renukadevi Patil, et al. "Abstract B28: Autotaxin, LPA1 and LPA5 receptors in the tumor microenvironment determine melanoma invasion and metastasis." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b28.

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Aldabbas, Hamza. "LPBR." In ICFNDS'18: International Conference on Future Networks and Distributed Systems. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3231053.3231059.

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Windt, D. L., and R. C. Catura. "Multilayer Characterization At LPARL." In 32nd Annual Technical Symposium, edited by Finn E. Christensen. SPIE, 1988. http://dx.doi.org/10.1117/12.948773.

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Gregg, Michael L., Sean M. Van Andel, and Steven E. Saylor. "Lean+ manufacturing process analysis simulation (LPAS+)." In 2011 Winter Simulation Conference - (WSC 2011). IEEE, 2011. http://dx.doi.org/10.1109/wsc.2011.6147929.

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García Marchena, Nuria, María Flores-López, Nerea Requena-Ocaña, Antonia Serrano, Fracisco Javier Pavón, Juan Suárez, Roberto Muga, and Fernando Rodríguez de Fonseca. "Evaluación de especies de LPA en plasma de pacientes con trastornos por uso de alcohol: potencial asociación con déficits cognitivos." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p079.

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Descripción de los objetivos Los trastornos por uso de alcohol (TUA) se relacionan con problemas cognitivos, específicamente con dificultades en funciones ejecutivas y memoria. El ácido lisofosfatídico (LPA) es un lípido bioactivo estrechamente vinculado a procesos de desarrollo neurológico. El objetivo consiste en evaluar cambios en niveles circulantes de las especies relevantes de LPA asociadas con las características clínicas y neuropsicológicas de los TUA. Material y métodos Un total de 55 pacientes con TUA en abstinencia que fueron evaluados clínica y cognitivamente y pareados en edad sexo e IMC con 34 controles sanos. Se cuantificaron las medias de LPA total, y de las siguientes especies: 16:0-, 18:0-, 18:1-, 18:2- y 20:4- y se compararon con medidas de factores de crecimiento asociados a neuroplasticidad: brain derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and -2 (IGF-2). Resultado y conclusiones Los pacientes con TUA mostraron síndrome disejecutivo (22,4%) y déficit en la memoria (32,6%). Las concentraciones plasmáticas de LPA total, 18:0- y 18:1-LPA estaban disminuidos en pacientes TUA comparados con el grupo control. El 22,4% de los pacientes TUA mostró déficit en funciones ejecutivas y un 32,6% déficits relacionados con la memoria. Las puntuaciones en tareas ejecutivas en pacientes con TUA correlacionan positivamente con las especies de LPA en plasma. Además, las concentraciones del LPA total y las especies LPA 18:2- y 20:4- correlacionaron positivamente con niveles plasmáticos de BDNF. Por el contrario, se encuentra correlación negativa entre IGF-1 y la mayoría de las especies LPA, así como entre IGF-2 y 18:1-. Estos resultados sugieren que los déficits cognitivos evaluados en los TUA pueden estar relacionados con la desregulación de especies LPA, especialmente 18:0- y 18:1-LPA. Se propone estudiar la relación entre 18:1-LPA y BDNF en plasticidad y neurogénesis en la búsqueda de marcadores biológicos de deterioro cognitivo.
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Wu, Tao, Leiting Chen, Yayong Guan, Xin Li, and Yuxiao Guo. "LPA Based Hierarchical Community Detection." In 2014 IEEE 17th International Conference on Computational Science and Engineering (CSE). IEEE, 2014. http://dx.doi.org/10.1109/cse.2014.65.

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Zhang, Tianyu, Tiantian Han, Lu Tian, Yi Li, Xijie Jia, Guangdong Liu, Pingbo An, et al. "LPAC: A Low-Precision Accelerator for CNN on FPGAs." In FPGA '20: The 2020 ACM/SIGDA International Symposium on Field-Programmable Gate Arrays. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3373087.3375343.

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Harutunian, Vigain, Anne Harutunian, Kegham A. Harutunian, and Shant Harutunian. "Evaluating Functional Coupling in Aeration Basin Air Distribution Systems." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-51211.

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Axiomatic Design provides a set of axioms and corollaries to help make system design decisions. In this paper, the independence axiom is applied to evaluate alternate low pressure air (LPA) distribution system designs to serve the aeration basins of a wastewater treatment plant. The airflow to each air zone is defined as a functional requirement (FR) in the functional domain. A design parameter (DP) in the physical domain is selected to achieve each FR. The DPs include the LPA motor operated valve (MOV) damper positions and a process air blower inlet guide vane (IGV) position. Three design alternatives are developed and evaluated with the respect to the independence axiom. Each subsequent alternative attempts to reduce the amount of functional coupling. Reduced functional coupling in an LPA system results in a more stable treatment process and greater system longevity through reduced component wear.
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Reports on the topic "LPAR"

1

Padfield, Jon, Ted Boehm, and Jim Handy. INDOT-JTRP LPA Process Improvement. Purdue University, December 2016. http://dx.doi.org/10.5703/1288284316351.

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Mathews, Bruce D., Steven Walker, and Robert A. Swirbalus. LPCR Wind Vector Profile Mode for Precision Air Delivery in Adverse Weather. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada387639.

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Lammers, Gary, and Mel Lammers. Technical Raster Transfer Installation Drawing: Waveguide LPCR-130-2 Radar. Submitted By: Lockheed Aeronautical Systems. Supporting: WR-ALC/TILCA's EDCARS Program Contract Number F33657-90-C-0071-P000l3BL2. MIL-STD-1840A, MIL-R-28002A (Raster). Quick Short Test Report. Fort Belvoir, VA: Defense Technical Information Center, August 1994. http://dx.doi.org/10.21236/ada312997.

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Inverse Cerenkov LPA experiments. 1986 Annual report. Office of Scientific and Technical Information (OSTI), December 1986. http://dx.doi.org/10.2172/10107162.

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