Relevant bibliographies by topics / Cyclic GMP

Academic literature on the topic 'Cyclic GMP'

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Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Cyclic GMP"

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Sager, Georg. "Cyclic GMP transporters." Neurochemistry International 45, no. 6 (November 2004): 865–73. http://dx.doi.org/10.1016/j.neuint.2004.03.017.

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Takemoto, Dolores J., Karen Gonzalez, Igor Udovichenko, and Jess Cunnick. "Cyclic GMP-regulated cyclic nucleotide phosphodiesterases." Cellular Signalling 5, no. 5 (September 1993): 549–53. http://dx.doi.org/10.1016/0898-6568(93)90050-v.

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Souness, J. E., B. K. Diocee, W. Martin, and S. A. Moodie. "Pig aortic endothelial-cell cyclic nucleotide phosphodiesterases. Use of phosphodiesterase inhibitors to evaluate their roles in regulating cyclic nucleotide levels in intact cells." Biochemical Journal 266, no. 1 (February 15, 1990): 127–32. http://dx.doi.org/10.1042/bj2660127.

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Two cyclic nucleotide phosphodiesterase (PDE) activities were identified in pig aortic endothelial cells, a cyclic GMP-stimulated PDE and a cyclic AMP PDE. Cyclic GMP-stimulated PDE had Km values of 367 microM for cyclic AMP and 24 microM for cyclic GMP, and low concentrations (1 microM) of cyclic GMP increased the affinity of the enzyme for cyclic AMP (Km = 13 microM) without changing the Vmax. This isoenzyme was inhibited by trequinsin [IC50 (concn. giving 50% inhibition of substrate hydrolysis) = 0.6 microM for cyclic AMP hydrolysis in the presence of cyclic GMP; IC50 = 0.6 microM for cyclic GMP hydrolysis] and dipyridamole (IC50 = 5 microM for cyclic AMP hydrolysis in the presence of cyclic GMP; IC50 = 3 microM for cyclic GMP hydrolysis). Cyclic AMP PDE exhibited a Km of 2 microM for cyclic AMP and did not hydrolyse cyclic GMP. This activity was inhibited by trequinsin (IC50 = 0.2 microM), dipyridamole (IC50 = 6 microM) and, selectively, by rolipram (IC50 = 3 microM). Inhibitors of cyclic GMP PDE (M&B 22948) and of low Km (Type III) cyclic AMP PDE (SK&F 94120) only weakly inhibited the two endothelial PDEs. Incubation of intact cells with trequinsin and dipyridamole induced large increases in cyclic GMP, which were completely blocked by LY-83583. Rolipram, SK&F 94120 and M&B 22948 did not significantly influence cyclic GMP accumulation. Dipyridamole enhanced the increase in cyclic GMP induced by sodium nitroprusside. Cyclic AMP accumulation was stimulated by dipyridamole and trequinsin with and without forskolin. Rolipram, although without effect alone, increased cyclic AMP in the presence of forskolin, whereas M&B 22948 and SK&F 94120 had no effects on resting or forskolin-stimulated levels. These results suggest that cyclic GMP-stimulated PDE regulates cyclic GMP levels and that both endothelial PDE isoenzymes contribute to the control of cyclic AMP.
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Srivastava, D., D. A. Fox, and R. L. Hurwitz. "Effects of magnesium on cyclic GMP hydrolysis by the bovine retinal rod cyclic GMP phosphodiesterase." Biochemical Journal 308, no. 2 (June 1, 1995): 653–58. http://dx.doi.org/10.1042/bj3080653.

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Knowledge of the kinetics of the rod cyclic GMP phosphodiesterase is essential for understanding the kinetics and gain of the light response. Therefore, the interactions between Mg2+, cyclic GMP, and purified, trypsin-activated bovine rod cyclic GMP phosphodiesterase (EC 3.1.4.17) were examined. The effects of Mg2+ and of cyclic GMP on the rod phosphodiesterase activity were mutually concentration-dependent. Formation of a free Mg-cyclic GMP complex is unlikely due to its high dissociation constant (Kd = 19 mM). Plots of 1/velocity versus 1/[cyclic GMP] as a function of [Mg2+] and 1/velocity versus 1/[Mg2+] as a function of [cyclic GMP] intersected to the left of the 1/velocity axis. This is consistent with the formation of a ternary complex between the phosphodiesterase, Mg2+, and cyclic GMP. A competitive inhibitor of the phosphodiesterase relative to cyclic GMP, 3-isobutyl-1-methylxanthine, non-competitively inhibited the enzyme relative to Mg2+, Pb2+, a competitive inhibitor of the phosphodiesterase relative to Mg2+ [D. Srivastava, R.L. Hurwitz and D. A. Fox (1995) Toxicol. Appl. Pharmacol, in the press] non-competitively inhibited the enzyme relative to cyclic GMP. Collectively these results are suggestive of a rapid equilibrium random binding order of Mg2+ and cyclic GMP to the rod phosphodiesterase.
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Wahler, Gordon M., Nancy J. Rusch, and Nicholas Sperelakis. "8-Bromo-cyclic GMP inhibits the calcium channel current in embryonic chick ventricular myocytes." Canadian Journal of Physiology and Pharmacology 68, no. 4 (April 1, 1990): 531–34. http://dx.doi.org/10.1139/y90-076.

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Superfusion with 8-bromo-cyclic GMP or intracellular injection of cyclic GMP inhibits calcium-dependent slow action potentials in embryonic chick or guinea pig ventricular cells, suggesting that cyclic GMP inhibits calcium currents. Recently, cyclic GMP has been shown to reduce cyclic AMP-stimulated calcium currents in voltage-clamped ventricular myocytes. Since earlier results in intact cells had suggested that cyclic GMP might inhibit basal (i.e., unstimulated by cyclic AMP) calcium currents, we directly investigated the effect of 8-bromo-cyclic GMP on basal calcium channel currents (using barium as the charge carrier) in voltage-clamped ventricular myocytes isolated from embryonic chick hearts. Superfusion with 1 mM 8-bromo-cyclic GMP (without prior cyclic AMP elevation) progressively decreased peak calcium channel currents (−68% at 15 min after the onset of drug exposure). In contrast, the currents were unchanged during 15 min superfusion with control solution, or 1 mM 8-bromo-GMP (the noncyclic inactive analog of 8-bromo-cyclic GMP). The present results in voltage-clamped embryonic chick heart cells indicate that cyclic GMP can inhibit basal calcium channel currents, apparently through a cyclic AMP-independent mechanism.Key words: cyclic GMP, calcium channels, calcium current, heart.
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Houslay, Miles D. "Renaissance for cyclic GMP?" Trends in Biochemical Sciences 10, no. 12 (December 1985): 465–66. http://dx.doi.org/10.1016/0968-0004(85)90199-9.

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Okada, D. "Cyclic GMP binding regulates the catalytic activity of cyclic GMP-specific phosphodiesterase." Neuroscience Research 38 (2000): S48. http://dx.doi.org/10.1016/s0168-0102(00)81135-9.

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Zhang, Qihang, Michael Lazar, Lin Yan, Yiqi He, James Tse, Harvey R. Weiss, and Peter M. Scholz. "Cyclic GMP Reduces Myocardial Stunning Through Non-Cyclic GMP Protein Kinase Mechanisms." Journal of Cardiovascular Pharmacology 44, no. 2 (August 2004): 235–43. http://dx.doi.org/10.1097/00005344-200408000-00014.

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Biswas, Kabir H., and Sandhya S. Visweswariah. "Distinct Allostery Induced in the Cyclic GMP-binding, Cyclic GMP-specific Phosphodiesterase (PDE5) by Cyclic GMP, Sildenafil, and Metal Ions." Journal of Biological Chemistry 286, no. 10 (December 29, 2010): 8545–54. http://dx.doi.org/10.1074/jbc.m110.193185.

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Miller, Herman T., W. Yesus, T. Cooper, and S. Harwell. "Cyclic AMP and cyclic GMP in hyperresponsiveness." Life Sciences 43, no. 24 (January 1988): 1991–97. http://dx.doi.org/10.1016/0024-3205(88)90572-3.

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Dissertations / Theses on the topic "Cyclic GMP"

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Tang, Katherine Mary. "Targets of cyclic GMP in blood platelets, photolabelling, mutagenesis and pharmacological analysis of the cyclic GMP-inhibited phosphodiesterase." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0016/NQ30173.pdf.

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Günay-Esiyok, Özlem. "Cyclic GMP signaling during the lytic cycle of Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20740.

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Der cGMP-Signalweg ist als einer der Hauptregulatoren von diversen Funktionen in Eukaryoten bekannt; allerdings ist seine Funktionsweise in Protozoen wenig verstanden. Im Rahmen dieser Arbeit wurde eine Guanylatcyclase, gekoppelt mit N-terminalen P4-ATPase, in intrazellulären Parasiten Toxoplasma gondii gemeldet. Eine in silico-Analyse wies auf eine Aktivierung der Guanylatcyclase durch Heterodimerisierung ihrer Cyclasedomänen hin und ermöglichte wertvolle Einsichten in mögliche Funktionen ihrer ATPase-Domäne. Dieses Protein (477-kDa) bezeichnet als TgATPaseP-GC in dieser Studie, lokalisiert in der Plasmamembran am apikalen Pol des Parasiten. TgATPaseP-GC ist unempfänglich gegenüber genetischer Deletion und seine CRISPR/Cas9 unterstützte Spaltung beendet den lytischen Zyklus von T. gondii vorzeitig. Darüber hinaus reduzierte ein Cre/loxP-vermittelter Knockdown von TgATPaseP-GC die Synthese von cGMP im Tachyzoiten und inhibierte das Parasitenwachstum aufgrund von Beeinträchtigungen Motilitäts-abhängiger Prozesse des Austretens und Eindringens. Trotz seiner zeitlich beschränkten Funktion ist TgATPaseP-GC konstitutiv während des ganzen lytischen Zyklus exprimiert, welches eine post-translationale Regulierung des cGMP-Signalweges bedingt. Nicht zuletzt impliziert das Vorhandensein von TgATPaseP-GC-Orthologen in anderen Alveolata eine divergente Umfunktionierung der cGMP-Signalwege in Protozoen. Darüber hinaus wurde ein optogenetischer Ansatz verwendet, um den cGMP-Weg durch eine photo-aktivierte Rhodopsin-Guanylat-Cyclase (RhoGC) in T. gondii zu exprimiert. Dieses System erlaubte eine kontrollierte Erhöhung von cGMP durch Licht in einer schnellen und reversiblen Weise. Die Anregung von RhoGC stimulierte signifikant die Parasitenmotilität, deren Auswirkung auch mit erhöhten Eindringen und Austreten überwacht wurde; im Gegensatz zum genetischen Knockdown von TgATPaseP-GC. Das System ermöglicht die Vermittler des cGMP-Signalwegs durch Phosphoproteomics zu identifizieren.
cGMP signaling is known as one of the master regulators of diverse functions in eukaryotes; however, its architecture and functioning in protozoans remain poorly understood. In the scope of this thesis, an exclusive guanylate cyclase coupled with N-terminal P4-ATPase was reported in an obligate intracellular parasite Toxoplasma gondii. In silico analysis indicated an activation of the guanylate cyclase by heterodimerization of its two cyclase domains and offered valuable insights into possible functions of its ATPase domain. This bulky protein (477-kDa), termed in this study as TgATPaseP-GC to reflect its envisaged multifunctionality, localizes in the plasma membrane at the apical pole of the parasite. TgATPaseP-GC is refractory to genetic deletion, and its CRISPR/Cas9-assisted disruption aborts the lytic cycle of T. gondii. Besides, Cre/loxP-mediated knockdown of TgATPaseP-GC reduced the synthesis of cGMP in tachyzoites and inhibited the parasite growth due to impairments of motility-dependent egress and invasion events. Notably, despite its temporally restricted function, TgATPaseP-GC is expressed constitutively throughout the lytic cycle, entailing a post-translational regulation of cGMP signaling. Not least, the occurrence of TgATPaseP-GC orthologs in several other alveolates implies a divergent functional repurposing of cGMP signaling in protozoans. Furthermore, an optogenetic approach was utilized to induce cGMP pathway by a photo-activated rhodopsin-guanylate cyclase (RhoGC) in T. gondii. The system enabled a light-control of cGMP elevation on crucial steps of lytic cycle in a fast, spatial and reversible manner. Excitation of RhoGC significantly stimulated the parasite motility of which impact was also monitored with an increased host-cell invasion and egress; as opposed to the genetic knockdown of TgATPaseP-GC. Having an established optogenetic system in the parasite allows to identify downstream targets of cGMP signaling via phosphoproteomic analysis.
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Engelhardt, Thomas. "The regulation of cyclic GMP during anaesthesia." Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409272.

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The glutamate-NO-cyclic GMP pathway has previously been identified as a potential major target for general anaesthetic agents. An animal model of type I NOS gene disrupted mice was employed to investigate in vivo effects of the general anaesthetic agents isoflurane, ketamine, pentobarbital, and propofol on cyclic GMP in the presence or absence of the isoform specific NOS inhibitor, 7-nitroindazole. G protein function was studied ex vivo in whole brains. Primary neuronal cell cultures were employed to investigate the effects of anaesthetic agents on glutamate stimulated cyclic GMP production. The influence of anaesthetic agents on the metabolism of cyclic GMP via phosphodiesterases was studied in vitro. The effects of anaesthetic agents on the regulation of cyclic GMP in humans are unknown. Cyclic GMP was measured in human oral mucosal transudate in volunteers and patients undergoing short general anaesthesia. A prospective double-blind placebo controlled crossover trial was conducted assessing the effects of selective PDE5 inhibition on propofol sedation requirements in healthy volunteers. Both studies indicate a potential role of cyclic GMP mediating consciousness in humans. The work presented in this thesis indicates substantial effects of anaesthetic agents on the regulation of cyclic GMP in in vivo, ex vivo, in vitro and human studies and provides new insights into the mechanisms involved in modulating general anaesthesia. However, a great deal of further work remains before the complex processes underlying general anaesthesia are fully elucidated.
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Hennan, James Kenneth. "Role of cyclic GMP, cyclic GMP-dependent protein kinase and protein phosphorylation in the control of smooth muscle tension." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0017/NQ56558.pdf.

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Zolle, Lapuente Olga C. "Cyclic GMP and calcium homeostasis in endothelial cells." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367654.

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Park, Ji S. "CYCLIC GMP: A SATIETY SIGNAL IN C. ELEGANS." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3851.

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Appetite control and satiety mechanisms help animals maintain energy homeostasis; however, these mechanisms can be misregulated, leading to overweight and obesity. Caenorhabditis elegans is an excellent model system to study appetite and satiety because of its conserved behavioral aspects of satiety and conserved molecular mechanisms. ASI senses nutrition and its activity is required for the behavioral state of satiety quiescence. The purpose of this thesis project was to elucidate the function of cGMP signaling in ASI by looking at behavioral effects from the pharmacological use of sildenafil (Viagra), a PDE inhibitor, and the effects on ASI activation from mutating guanylyl cyclase DAF-11. Sildenafil treatment increases satiety quiescence and decreases fat storage in a PDE-dependent manner. The daf-11 mutation decreased overall fluorescence intensity of ASI activation and the frequency at which ASI activated by about 50% compared to wild-type worms, suggesting that DAF-11 plays an important role in ASI to promote satiety.
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Freedman, John. "Cyclic-di-GMP Signaling in the Borrelia Spirochetes." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/269.

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Lyme disease is the most common tick-borne disease in North America, with approximately 35,000 cases reported to the Centers for Disease Control in 2008. The genome of its causative agent, Borrelia burgdorferi, encodes for a set of genes involved in the metabolism and regulatory activities of the second messenger nucleotide, cyclic-di-GMP (c-di-GMP). Rrp1 is a response regulatory-diguanylate cyclase, and its regulatory capability is likely mediated via production of c-di-GMP, as it lacks a DNA-binding domain. One known class of c-di-GMP effector/binding proteins are those that harbor a PIlZ domain. The genome of B. burgdorferi strain 5A4 encodes for one chromosomally-carried PilZ domain, which we have designated PlzA. Additionally, certain B. burgdorferi strains encode for a second PilZ domain-containing protein (PlzB) which is plasmid-carried. Both PlzA and PlzB were found to bind specifically to c-di-GMP, and c-di-GMP binding by PlzA was found to be dependant upon arginine residues in the c-di-GMP binding region. Additionally, expression of PlzA was found to be upregulated by tick feeding and was constitutive in the mammalian host. We next constructed two deletion/allelic exchange mutants – one with the targeted deletion of PlzA, and on ethat replaced PlzA with PlzB in a strain lacking the plzB gene. Our studies demonstrated that ΔplzA was deficient in motility and was also non-infectious in the mouse model of B. burgdorferi infection. Additionally, this strain remained viable in larval Ixodes ticks. Also, B31-plzB KI was deficient in motility, as well as infectivity, demonstrating that PlzB is unable to complement for functions fo PlzA in vitro and in vivo and that it may play other roles in the biology of B. burgdorferi strains carrying the plzB gene. These studies represent the first identification of a c-di-GMP binding protein in any spirochete, but also represent the first demonstration of the importance of PilZ domain proteins in a spirochetal system. We additionally examined the effects of c-di-GMP synthesis and breakdown in the related bacterium, B. hermsii, a causative agent of tick-borne relapsing fever (TBRF). Deletion mutants in Rrp1 (B. hermsii’s sole diguanylate cyclase) and PdeA (B. hermsii’s only EAL domain-containing phosphodiesterase) were created. These strains were analyzed in order to determine: 1) the effect(s) of the losse of Rrp1/PdeA on intracellular spirochete c-di-GMP levels, and 2) the effects of Rrp1/PdeA on the establishment of murine infection and on gross motility/chemotaxis. It was demonstrated that c-di-GMP accumulates intracellularly in the cells lacking PdeA. Additionally, spirochetes were shown to chemotax towards N-acetyl-glucosamine (NAG) and they did not form soft agar swarms. In contrast, cells lacking Rrp1 did not accumulate detectable levels of c-di-GMP, demonstrated a reduced ability to chemotax towards NAG, and swarmed on soft agar in a fashion indistinguishable from wild type. Despite these differences in phenotype, both mutant strains display an attenuated murine infectivity. These results indicate that c-di-GMP is indeed important in the TBRF spirochete, B. hermsii and this vital second messenger plays key roles in virulence, motility, and chemotaxis. These studies also pave the way for future investigation of B. hermsii through use of targeted genetic manipulation.
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Williams, A. C. "The importance of cyclic nucleotides (cyclic GMP and cyclic AMP) in the development of malignant disease." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379348.

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Broderick, Kate Elizabeth. "Cyclic GMP - dependent signalling in D. melanogaster Malpighian tubules." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252518.

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Deal, Justin. "Second Messenger Cyclic-di-GMP Regulation in Acinetobacter baumannii." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/honors/534.

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Over time, “superbugs,” or bacteria that have become resistant to antibiotics, have become a great concern in modern medicine. Viable alternates are currently being looked into as effective and safe ways to prevent or treat infections caused by these superbugs. One such method is through the utilization of the second messenger molecule cyclic-di-GMP (c-di-GMP) that has been shown to regulate phenotypes within other bacteria that may control surface colonization in Acinetobacter baumannii. Through a series of experiments, the active enzymes that create c-di-GMP - diguanylate cyclases - and break down c-di- GMP - phosphodiesterases - have been inactivated in mutants to test phenotypes including biofilm formation, motility, antibiotic resistance, and desiccation survival. The research’s objective is to show that manipulation of c-di-GMP within the multi-drug resistant strain of Acinetobacter baumannii may serve as a means to control this bacteria.
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Books on the topic "Cyclic GMP"

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Krieg, Thomas, and Robert Lukowski, eds. Guanylate Cyclase and Cyclic GMP. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-459-3.

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Cyclic GMP: Biochemistry, physiology and pathophysiology. Austin: R.G. Landes, 1994.

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Wolfe, Alan J., and Karen L. Visick, eds. The Second Messenger Cyclic Di-GMP. Washington, DC, USA: ASM Press, 2010. http://dx.doi.org/10.1128/9781555816667.

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J, Wolfe Alan, Visick Karen L, and American Society for Microbiology, eds. The second messenger cyclic Di-GMP. Washington, DC: ASM Press, 2010.

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J, Wolfe Alan, Visick Karen L, and American Society for Microbiology, eds. The second messenger cyclic Di-GMP. Washington, DC: ASM Press, 2010.

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D, Corbin Jackie, and Johnson Roger A, eds. Initiation and termination of cyclic nucleotide action. San Diego: Academic Press, 1988.

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Krzysztof, Palczewski, ed. Vertebrate phototransduction and the visual cycle. San Diego, CA: Academic Press, 2000.

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1935-, Gingell Clive, ed. Management of ED: Focus on sildenafil : a urologist's approach. Chicago: PharmaLibri, 1998.

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J, Fowler Clare, ed. Management of ED: Focus on sildenafil : a neurologist's approach. Montreal: PharmaLibri, 1999.

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E, Morgensen C., ed. Management of ED: Focus on sildenafil : a diabetologist's/endocrinologist's approach. Montreal: PharmaLibri, 1999.

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Book chapters on the topic "Cyclic GMP"

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Wilson, John Fawcett. "Cyclic GMP." In The Immunoassay Kit Directory, 1835–42. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_92.

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Gao, Yuansheng. "Cyclic GMP Signaling." In Biology of Vascular Smooth Muscle: Vasoconstriction and Dilatation, 181–95. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4810-4_14.

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Gao, Yuansheng. "Cyclic GMP Signaling." In Biology of Vascular Smooth Muscle, 247–66. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7122-8_14.

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Francis, Sharron H., Jackie D. Corbin, and Erwin Bischoff. "Cyclic GMP-Hydrolyzing Phosphodiesterases." In cGMP: Generators, Effectors and Therapeutic Implications, 367–408. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-68964-5_16.

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Du, Xiao-Xia, and Xiao-Dong Su. "Detection of Cyclic Dinucleotides by STING." In c-di-GMP Signaling, 59–69. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7240-1_6.

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Schomburg, Dietmar, and Margit Salzmann. "3′, 5′-Cyclic-GMP phosphodiesterase." In Enzyme Handbook 3, 599–603. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76463-9_125.

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Chambers, Jacob R., and Karin Sauer. "Detection of Cyclic di-GMP Binding Proteins Utilizing a Biotinylated Cyclic di-GMP Pull-Down Assay." In c-di-GMP Signaling, 317–29. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7240-1_25.

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Römling, Ute, and Michael Y. Galperin. "Discovery of the Second Messenger Cyclic di-GMP." In c-di-GMP Signaling, 1–8. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7240-1_1.

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Miller, Samuel I., and Erik Petersen. "Measuring Individual Cell Cyclic di-GMP: Identifying Population Diversity and Cyclic di-GMP Heterogeneity." In Microbial Cyclic Di-Nucleotide Signaling, 193–207. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_12.

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Borlee, Grace I., Mihnea R. Mangalea, and Bradley R. Borlee. "Cyclic di-GMP in Burkholderia spp." In Microbial Cyclic Di-Nucleotide Signaling, 519–43. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_30.

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Conference papers on the topic "Cyclic GMP"

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Li, Tuo, and Zhijian J. Chen. "Abstract B003: Developing an analytical method for second messenger cyclic GMP-AMP." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b003.

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Brill, Alexander G., Gregory E. Brill, Boris Shenkman, Ilya Tamarin, Rima Dardik, David Varon, and Naphtali Savion. "Low-power laser irradiation of blood inhibits platelet function: role of cyclic GMP." In BiOS Europe '98, edited by Giovanni F. Bottiroli, Tiina I. Karu, and Rachel Lubart. SPIE, 1998. http://dx.doi.org/10.1117/12.334392.

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Islam, Bianca N., Yali Hou, Namratha Mylarapu, Kaylin A. Browning, Kenneth J. Vega, and Darren D. Browning. "Abstract 2978: Cyclic GMP-independent inhibition of colon cancer cell growth by phosphodiesterase inhibitors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2978.

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Polito, Carmine P. "Constant-Volume Cyclic Testing to Determine Input Parameters for the GMP Pore Pressure Generation Model." In Geotechnical Frontiers 2017. Reston, VA: American Society of Civil Engineers, 2017. http://dx.doi.org/10.1061/9780784480489.008.

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Edgecombe, M., M. C. Scrutton, and R. Kerry. "RELATIONSHIP BETWEEN ELEVATION OF CYCLIC-3∲,5∲-GMP (cGMP) AND AGGREGATE FORMATION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644534.

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Maximal 3- to 5-fold increases in platelet cGMP levels as measured by specific radioimmunoassay are observed on stimulation of aspirin-treated platelet-rich plasma with saturating doses of ADP, adrenaline, 5HT, PAF, thrombin, 9,11-epoxymethano-PGH2 (U44069), collagen, ristocetin and the Ca2+-ionophore ionomycin. The dose/response curves for the elevation in cGMP induced by these agents are either superimposable on, or lie to the right of, those describing the rate or extent of the aggregatory response as measured by an increase in light transmittance. The increase in cGMP induced by ADP is totally inhibited by addition of PGI2 or forskolin with dose/response relationships superimposable on those observed for inhibition of the aggregatory response. No increase in cGMP is observed if platelets are stimulated by PAF or ionomycin in an unstirred system or when aggregation induced by ADP is prevented by addition of a monoclonal antibody which recognises the glycoprotein IIb/IIIa complex.Addition of the fibrinogen γ-chain C-terminal decapeptide (γ402-411) or α-Chain tetrapeptide ARG-GLY-ASP-SER prevents aggregation and the increase in cGMP induced by PAF. The γ-chain decapeptide also completely prevents the increase in cGMP induced by ristocetin, but the a-chain tetrapeptide is ineffective in this respect. Both peptides inhibit to some extent aggregate formation induced by ristocetin.The data demonstrates a strong correlation between aggregate formaticfn and the increase in the platelet cGMP levels and support the previous postulate that platelet-platelet contact causes, activation of guanylate cyclase. No relationship is apparent between the effects of the various agents tested on cGMP levels and their known ability to increase cytosolic Ca2+ concentration. (Supported by SERC and Ciba-Geigy.)
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Drndarski, S., A. De Silva, PI Aaronson, and JP Ward. "Evidence for a Key Role of Phosphodiesterase III and Cyclic AMP in the Response of Intrapulmonary Arteries to Cyclic GMP-Dependent Stimuli." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6259.

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Yan, F., Y. Han, L. Chen, and H. Liu. "The Cytosolic DNA Sensor Cyclic-GMP-AMP Synthase Is Critical in Experimental Models of Allergic Airway Inflammation." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1049.

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SIMON, M. F., H. CHAP, and L. DOUSTE-BLAZY. "EFFECTS OF SIN 1 ON PLATELET ACTIVATION INDUCED BY THROMBIN IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643423.

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The mechanism of platelet activation is well known. The interaction of agonist such as thrombin, on specific membrane receptor induces phosphatidylinositol-specific phospholipase C activation, with a concomitant formation of two second messengers (from PIP2): inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 is able to induce a rapid discharge of Ca2+ from internal stores and Ca2+ influx through plasma membrane by unidentified Ca2+ channels linked to receptor activation. The increase of cytoplasmic free calcium concentration leads to the activation of the calcium calmodulin dependent myosine light chain kinase which phosphoryla-tes 20 kD proteins (myosine light chain). DAG is a potent activator of protein kinase C, which phosphorylates 40 kD proteins. These different pathways act in synergism.Sin 1 is a platelet aggregating inhibitor. This compound is an active metabolite of molsidomine, which activates platelet guany-late cyclase, inducing a rapid rise in cyclic GMP level. The precise role of cyclic GMP in platelet activation is not yet known. In order to study the mechanism of action of this drug, we tried to determine the effect of Sin 1 on the different steps described above. We measured Ca2+ fluxes and phospholipase C activation in thrombin (0,5 U/ml) stimulated platelets in the presence of different doses of Sin 1 (10™7-10™3M). Serotonin secretion was inhibited by 30 % with Sin 1 (10™4M-10™5m). A parallel inhibition of phospholipase C was detected by measurement of [32P)-PA level. Platelets loaded with Quin 2 and stimulated by thrombin showed a 70 % inhibition of external Ca2+ influx as soon as a concentration of 10™7M of Sin 1 was added. A study on platelet loaded with [45Ca2+) and Quin 2 confirmed these results. On the contrary, discharge of internal Ca2+ store seemed to be unaffected.In conclusion, the major effect of Sin 1 on platelet phospholipase C pathway is an inhibition of Ca2+ influx through plasma membrane. Some further experiments are necessary to shown whether this inhibition is correlated with cyclic GMP formation (the major effect of Sin 1) and try to establish a relation between this inhibition and that exerted on phospholipase C.Sin 1 was a generous gift of Hoechst.
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Gao, Pu. "Abstract B145: Small molecule inhibition of cyclic GMP-AMP synthase reduces interferon expression in macrophages from an autoimmune mouse model." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b145.

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Fini, M. A., M. Li, and K. R. Stenmark. "Targeting Cyclic GMP-Activated PKG (Protein Kinase G)-1α Oxidation in Left Heart Disease; Implications in Pulmonary Hypertension Due To HFpEF." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3691.

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Reports on the topic "Cyclic GMP"

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Nataro, James P., and David K. Karaolis. Host Immune Response to Bacterial Cyclic Diguanylic Acid (c-di-GMP). Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada533324.

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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Cristiano-Botia, Deicy J., Manuel Dario Hernandez-Bejarano, and Mario A. Ramos-Veloza. Labor Market Indicator for Colombia (LMI). Banco de la República de Colombia, December 2020. http://dx.doi.org/10.32468/be.1152.

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We construct the Labor Market Indicator (LMI) focusing on the cyclical similarities of eighteen time series from household, industrial, and opinion surveys between 2001 and 2019. The LMI summarizes the growth cycle of the labor market as defined by \cite{mintz} and is connected to the evolution of the traditional business cycle indicators as well as to that of the GDP and the Unemployment rate GAP. The evolution of the indicator provide useful information to policy makers, as it complements the characterization of expansions and turning points. Thus, improving the analysis of the current momentum of the labor market.
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Wang, Chih-Hao, and Na Chen. Do Multi-Use-Path Accessibility and Clustering Effect Play a Role in Residents' Choice of Walking and Cycling? Mineta Transportation Institute, June 2021. http://dx.doi.org/10.31979/mti.2021.2011.

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The transportation studies literature recognizes the relationship between accessibility and active travel. However, there is limited research on the specific impact of walking and cycling accessibility to multi-use paths on active travel behavior. Combined with the culture of automobile dependency in the US, this knowledge gap has been making it difficult for policy-makers to encourage walking and cycling mode choices, highlighting the need to promote a walking and cycling culture in cities. In this case, a clustering effect (“you bike, I bike”) can be used as leverage to initiate such a trend. This project contributes to the literature as one of the few published research projects that considers all typical categories of explanatory variables (individual and household socioeconomics, local built environment features, and travel and residential choice attitudes) as well as two new variables (accessibility to multi-use paths calculated by ArcGIS and a clustering effect represented by spatial autocorrelation) at two levels (level 1: binary choice of cycling/waking; level 2: cycling/walking time if yes at level 1) to better understand active travel demand. We use data from the 2012 Utah Travel Survey. At the first level, we use a spatial probit model to identify whether and why Salt Lake City residents walked or cycled. The second level is the development of a spatial autoregressive model for walkers and cyclists to examine what factors affect their travel time when using walking or cycling modes. The results from both levels, obtained while controlling for individual, attitudinal, and built-environment variables, show that accessibility to multi-use paths and a clustering effect (spatial autocorrelation) influence active travel behavior in different ways. Specifically, a cyclist is likely to cycle more when seeing more cyclists around. These findings provide analytical evidence to decision-makers for efficiently evaluating and deciding between plans and policies to enhance active transportation based on the two modeling approaches to assessing travel behavior described above.
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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
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Arumugam, Udayansankar, Mimoun Elboujdaini, Ming Gao, and Ramiro Vanoye. PR-328-133702-R02 F-S Fatigue Testing of Crack-in-Dent with Framework for Life Prediction. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), October 2019. http://dx.doi.org/10.55274/r0011628.

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ASME B31.8 states that "Dents that contain stress corrosion cracking or other cracks are injurious to the pipeline" and therefore, requires immediate attention by the Operators. Dent containing crack fields (colonies) are often observed in liquid pipelines. The recently completed PRCI research project MD-1N "Study of the Mechanism for Cracking in Dents in a Crude Oil Pipeline" showed evidence of a mechanism for fatigue cracking. The crack growth rate as a function of stress intensity factor was estimated using the measured spacings of fatigue striations from fracture surfaces based on the assumption that the formation of fatigue striations on a cycle-by-cycle basis. However, due to the lack of full-scale fatigue crack growth data, the success was limited. This gap prompted PRCI to launch a full-scale experimental investigation of crack growth rates of cracks in dents under cyclic pressure load in the simulated groundwater NS4 environment (PRC-328-133702, MD-1Q). The objective of the study was to determine the crack growth rate as a function of stress intensity factor, the number of cycles to failure, and the failure modes of cracks in dents. The test results would be used to evaluate the validity of cycle-by-cycle based assumption for crack growth rate estimation from the measured fatigue-striation-spacing. The investigation was also aimed at establishing a framework for remaining fatigue life prediction of cracks in dents in liquid pipelines. This framework would benefit liquid pipeline Operators to manage better the integrity of dents associated with corrosion fatigue cracking in groundwater. A total of six pipe samples containing cracks in shallow dents excavated from a retired 24-inch diameter liquid transmission pipeline were available and used for the full-scale fatigue tests. The test system developed under the project consisted of four components: (1) a computer-controlled hydraulic pressure cycling system, (2) an environment chamber containing a simulated groundwater NS4 solution mounted on the pipe in around the dent region to provide a simulated field environment condition; (3) real-time crack growth monitoring systems including direct cur-rent potential drop (DCPD), Clip gage and Strain gage; (4) data acquisition system. The cyclic pressure range used in the fatigue tests was 78 to 780 psig (72%SMYS) with R=0.1, which was based on historical operational pressure data and the Rain flow analysis. A constant frequency of 0.0526 Hz was selected for the testing to ensure the frequency requirement for corrosion fatigue is met. The remaining fatigue life of cracks-in-dents and failure modes were evaluated using the full-scale fatigue test results. Further, fatigue crack growth rates were established. Finally, a framework was developed for the life prediction of cracks in shallow dents based on the findings from six full-scale fatigue cyclic tests. This framework will assist liquid pipeline operators to estimate the remaining fatigue life for cracks in shallow dents utilizing inputs from ILI and pipeline's historical operational pressure fluctuation data and to mitigate the threat of cracks in dents in a timely manner. There is a related webinar.
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Blonigen, Bruce, Jeremy Piger, and Nicholas Sly. Comovement in GDP Trends and Cycles Among Trading Partners. Cambridge, MA: National Bureau of Economic Research, May 2012. http://dx.doi.org/10.3386/w18032.

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Christiano, Lawrence, and Wouter J. Den Haan. Small Sample Properties of GMM for Business Cycle Analysis. Cambridge, MA: National Bureau of Economic Research, March 1995. http://dx.doi.org/10.3386/t0177.

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Nelson, Charles. Implicit Estimates of Natural, Trend, and Cyclical Components of Real GNP. Cambridge, MA: National Bureau of Economic Research, May 1987. http://dx.doi.org/10.3386/w2253.

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Batyr, A. V., Володимир Миколайович Соловйов, and E. P. Sedov. The Cyclic Surgings as One of the Reasons of the Modern Economical Crisis. Information Systems Management Institute, April 2009. http://dx.doi.org/10.31812/0564/1130.

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Since the problem of the world economical crisis is gaming importance nowadays, it becomes necessary to reveal its real nature and reasons, in order to act in the most adequate way. The cycle theory is a possible explanation for the current situation in the economy.We have carried out our own investigation, during which the economies of USA, United Kingdom and France in 1961-2007 were compared. The real GDP and unemployment dynamics were taken into consideration. We also paid attention to historical events of the period and Kondratiev’s empiric truths, in order to explain both the most powerful crises and the modern one.
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