Relevant bibliographies by topics / Activated

Academic literature on the topic 'Activated'

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Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Activated"

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Kuspiel, Sven, Dominik Wiemuth, and Stefan Gründer. "The Neuropeptide Nocistatin Is Not a Direct Agonist of Acid-Sensing Ion Channel 1a (ASIC1a)." Biomolecules 11, no. 4 (April 13, 2021): 571. http://dx.doi.org/10.3390/biom11040571.

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Acid-sensing ion channels (ASICs) are ionotropic receptors that are directly activated by protons. Although protons have been shown to act as a neurotransmitter and to activate ASICs during synaptic transmission, it remains a possibility that other ligands directly activate ASICs as well. Neuropeptides are attractive candidates for alternative agonists of ASICs, because related ionotropic receptors are directly activated by neuropeptides and because diverse neuropeptides modulate ASICs. Recently, it has been reported that the neuropeptide nocistatin directly activates ASICs, including ASIC1a. Here we show that nocistatin does not directly activate ASIC1a expressed in Xenopus oocytes or CHO cells. Moreover, we show that nocistatin acidifies the bath solution to an extent that can fully explain the previously reported activation by this highly acidic peptide. In summary, we conclude that nocistatin only indirectly activates ASIC1a via acidification of the bath solution.
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Schonhoff, Christopher M., Se Won Park, Cynthia R. L. Webster, and M. Sawkat Anwer. "p38 MAPK α and β isoforms differentially regulate plasma membrane localization of MRP2." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 11 (June 1, 2016): G999—G1005. http://dx.doi.org/10.1152/ajpgi.00005.2016.

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In hepatocytes, cAMP both activates p38 mitogen-activated protein kinase (MAPK) and increases the amount of multidrug resistance-associated protein-2 (MRP2) in the plasma membrane (PM-MRP2). Paradoxically, taurolithocholate (TLC) activates p38 MAPK but decreases PM-MRP2 in hepatocytes. These opposing effects of cAMP and TLC could be mediated via different p38 MAPK isoforms (α and β) that are activated differentially by upstream kinases (MKK3, MKK4, and MKK6). Thus we tested the hypothesis that p38α MAPK and p38β MAPK mediate increases and decreases in PM-MRP2 by cAMP and TLC, respectively. Studies were conducted in hepatocytes isolated from C57BL/6 wild-type (WT) and MKK3-knockout (MKK3−/−) mice and in a hepatoma cell line (HuH7) that overexpresses sodium-taurocholate cotransporting polypeptide (NTCP) (HuH-NTCP). Cyclic AMP activated MKK3, p38 MAPK, and p38α MAPK and increased PM-MRP2 in WT hepatocytes, but failed to activate p38α MAPK or increase PM-MRP2 in MKK3−/− hepatocytes. In contrast to cAMP, TLC activated total p38 MAPK but decreased PM-MRP2, and did not activate MKK3 or p38α MAPK in WT hepatocytes. In MKK3−/− hepatocytes, TLC still decreased PM-MRP2 and activated p38 MAPK, indicating that these effects are not MKK3-dependent. Additionally, TLC activated MKK6 in MKK3−/− hepatocytes, and small interfering RNA knockdown of p38β MAPK abrogated TLC-mediated decreases in PM-MRP2 in HuH-NTCP cells. Taken together, these results suggest that p38α MAPK facilitates plasma membrane insertion of MRP2 by cAMP, whereas p38β MAPK mediates retrieval of PM-MRP2 by TLC.
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Barger, Philip M., Alyssa C. Browning, Ashley N. Garner, and Daniel P. Kelly. "p38 Mitogen-activated Protein Kinase Activates Peroxisome Proliferator-activated Receptor α." Journal of Biological Chemistry 276, no. 48 (September 27, 2001): 44495–501. http://dx.doi.org/10.1074/jbc.m105945200.

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Yeh, Yi-Chun, and Anant B. Parekh. "Distinct Structural Domains of Caveolin-1 Independently Regulate Ca2+Release-Activated Ca2+Channels and Ca2+Microdomain-Dependent Gene Expression." Molecular and Cellular Biology 35, no. 8 (February 2, 2015): 1341–49. http://dx.doi.org/10.1128/mcb.01068-14.

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In eukaryotic cells, calcium entry across the cell surface activates nuclear gene expression, a process critically important for cell growth and differentiation, learning, and memory and immune cell functions. In immune cells, calcium entry occurs through store-operated Ca2+release-activated Ca2+(CRAC) channels, comprised of STIM1 and Orai1 proteins. Local calcium entry through CRAC channels activates expression of c-fos- and nuclear factor of activated T cells (NFAT)-dependent genes. Although c-fos and NFAT often interact to activate gene expression synergistically, they can be activated independently of one another to regulate distinct genes. This raises the question of how one transcription factor can be activated and not the other when both are stimulated by the same trigger. Here, we show that the lipid raft scaffolding protein caveolin-1 interacts with the STIM1-Orai1 complex to increase channel activity. Phosphorylation of tyrosine 14 on caveolin-1 regulates CRAC channel-evoked c-fos activation without impacting the NFAT pathway or Orai1 activity. Our results reveal that structurally distinct domains of caveolin-1 selectively regulate the ability of local calcium to activate distinct transcription factors. More generally, our findings reveal that modular regulation by a scaffolding protein provides a simple, yet effective, mechanism to tunnel a local signal down a specific pathway.
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Shiozaki, Kazuhiro, Mitsue Shiozaki, and Paul Russell. "Heat Stress Activates Fission Yeast Spc1/StyI MAPK by a MEKK-Independent Mechanism." Molecular Biology of the Cell 9, no. 6 (June 1998): 1339–49. http://dx.doi.org/10.1091/mbc.9.6.1339.

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Fission yeast Spc1/StyI MAPK is activated by many environmental insults including high osmolarity, oxidative stress, and heat shock. Spc1/StyI is activated by Wis1, a MAPK kinase (MEK), which is itself activated by Wik1/Wak1/Wis4, a MEK kinase (MEKK). Spc1/StyI is inactivated by the tyrosine phosphatases Pyp1 and Pyp2. Inhibition of Pyp1 was recently reported to play a crucial role in the oxidative stress and heat shock responses. These conclusions were based on three findings: 1) osmotic, oxidative, and heat stresses activate Spc1/StyI in wis4 cells; 2) oxidative stress and heat shock activate Spc1/StyI in cells that express Wis1AA, in which MEKK consensus phosphorylation sites were replaced with alanine; and 3) Spc1/StyI is maximally activated in Δpyp1 cells. Contrary to these findings, we report: 1) Spc1/StyI activation by osmotic stress is greatly reduced in wis4 cells; 2)wis1-AA and Δwis1 cells have identical phenotypes; and 3) all forms of stress activate Spc1/StyI inΔpyp1 cells. We also report that heat shock, but not osmotic or oxidative stress, activate Spc1 in wis1-DDcells, which express Wis1 protein that has the MEKK consensus phosphorylation sites replaced with aspartic acid. Thus osmotic and oxidative stress activate Spc1/StyI by a MEKK-dependent process, whereas heat shock activates Spc1/StyI by a novel mechanism that does not require MEKK activation or Pyp1 inhibition.
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DeFea, K. A., J. Zalevsky, M. S. Thoma, O. Déry, R. D. Mullins, and N. W. Bunnett. "β-Arrestin–Dependent Endocytosis of Proteinase-Activated Receptor 2 Is Required for Intracellular Targeting of Activated Erk1/2." Journal of Cell Biology 148, no. 6 (March 20, 2000): 1267–82. http://dx.doi.org/10.1083/jcb.148.6.1267.

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Recently, a requirement for β-arrestin–mediated endocytosis in the activation of extracellular signal–regulated kinases 1 and 2 (ERK1/2) by several G protein–coupled receptors (GPCRs) has been proposed. However, the importance of this requirement for function of ERK1/2 is unknown. We report that agonists of Gαq-coupled proteinase–activated receptor 2 (PAR2) stimulate formation of a multiprotein signaling complex, as detected by gel filtration, immunoprecipitation and immunofluorescence. The complex, which contains internalized receptor, β-arrestin, raf-1, and activated ERK, is required for ERK1/2 activation. However, ERK1/2 activity is retained in the cytosol and neither translocates to the nucleus nor causes proliferation. In contrast, a mutant PAR2 (PAR2δST363/6A), which is unable to interact with β-arrestin and, thus, does not desensitize or internalize, activates ERK1/2 by a distinct pathway, and fails to promote both complex formation and cytosolic retention of the activated ERK1/2. Whereas wild-type PAR2 activates ERK1/2 by a PKC-dependent and probably a ras-independent pathway, PAR2(δST363/6A) appears to activate ERK1/2 by a ras-dependent pathway, resulting in increased cell proliferation. Thus, formation of a signaling complex comprising PAR2, β-arrestin, raf-1, and activated ERK1/2 might ensure appropriate subcellular localization of PAR2-mediated ERK activity, and thereby determine the mitogenic potential of receptor agonists.
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Rao, LV, SI Rapaport, and SP Bajaj. "Activation of human factor VII in the initiation of tissue factor- dependent coagulation." Blood 68, no. 3 (September 1, 1986): 685–91. http://dx.doi.org/10.1182/blood.v68.3.685.685.

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Abstract We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.
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Rao, LV, SI Rapaport, and SP Bajaj. "Activation of human factor VII in the initiation of tissue factor- dependent coagulation." Blood 68, no. 3 (September 1, 1986): 685–91. http://dx.doi.org/10.1182/blood.v68.3.685.bloodjournal683685.

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We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.
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Quayle, J. M., M. R. Turner, H. E. Burrell, and T. Kamishima. "Effects of hypoxia, anoxia, and metabolic inhibitors on KATP channels in rat femoral artery myocytes." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (July 2006): H71—H80. http://dx.doi.org/10.1152/ajpheart.01107.2005.

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Vascular ATP-sensitive potassium (KATP) channels have an important role in hypoxic vasodilation. Because KATP channel activity depends on intracellular nucleotide concentration, one hypothesis is that hypoxia activates channels by reducing cellular ATP production. However, this has not been rigorously tested. In this study we measured KATP current in response to hypoxia and modulators of cellular metabolism in single smooth muscle cells from the rat femoral artery by using the whole cell patch-clamp technique. KATP current was not activated by exposure of cells to hypoxic solutions (Po2 ∼35 mmHg). In contrast, voltage-dependent calcium current and the depolarization-induced rise in intracellular calcium concentration ([Ca2+]i) was inhibited by hypoxia. Blocking mitochondrial ATP production by using the ATP synthase inhibitor oligomycin B (3 μM) did not activate current. Blocking glycolytic ATP production by using 2-deoxy-d-glucose (5 mM) also did not activate current. The protonophore carbonyl cyanide m-chlorophenylhydrazone (1 μM) depolarized the mitochondrial membrane potential and activated KATP current. This activation was reversed by oligomycin B, suggesting it occurred as a consequence of mitochondrial ATP consumption by ATP synthase working in reverse mode. Finally, anoxia induced by dithionite (0.5 mM) also depolarized the mitochondrial membrane potential and activated KATP current. Our data show that: 1) anoxia but not hypoxia activates KATP current in femoral artery myocytes; and 2) inhibition of cellular energy production is insufficient to activate KATP current and that energy consumption is required for current activation. These results suggest that vascular KATP channels are not activated during hypoxia via changes in cell metabolism. Furthermore, part of the relaxant effect of hypoxia on rat femoral artery may be mediated by changes in [Ca2+]i through modulation of calcium channel activity.
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Izumi, T., and J. L. Maller. "Phosphorylation and activation of the Xenopus Cdc25 phosphatase in the absence of Cdc2 and Cdk2 kinase activity." Molecular Biology of the Cell 6, no. 2 (February 1995): 215–26. http://dx.doi.org/10.1091/mbc.6.2.215.

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The M-phase inducer, Cdc25C, is a dual-specificity phosphatase that directly phosphorylates and activates the cyclin B/Cdc2 kinase complex, leading to initiation of mitosis. Cdc25 itself is activated at the G2/M transition by phosphorylation on serine and threonine residues. Previously, it was demonstrated that Cdc2 kinase is capable of phosphorylating and activating Cdc25, suggesting the existence of a positive feedback loop. In the present study, kinases other than Cdc2 that can phosphorylate and activate Cdc25 were investigated. Cdc25 was found to be phosphorylated and activated by cyclin A/Cdk2 and cyclin E/Cdk2 in vitro. However, in interphase Xenopus egg extracts with no detectable Cdc2 and Cdk2, treatment with the phosphatase inhibitor microcystin activated a distinct kinase that could phosphorylate and activate Cdc25. Microcystin also induced other mitotic phenomena such as chromosome condensation and nuclear envelope breakdown in extracts containing less than 5% of the mitotic level of Cdc2 kinase activity. These findings implicate a kinase other than Cdc2 and Cdk2 that may initially activate Cdc25 in vivo and suggest that this kinase may also phosphorylate M-phase substrates even in the absence of Cdc2 kinase.
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Dissertations / Theses on the topic "Activated"

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Downward, Alan Murray. "Photo-activated Cytotoxins." Thesis, University of Canterbury. Chemistry, 2010. http://hdl.handle.net/10092/4179.

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The thesis addresses the potential application of ruthenium(II)-cobalt(III) heterodinuclear complexes as a new selective cancer treatment. The selectivity is to be achieved through the use of visible light to trigger activation of the drug. The majority of work conducted relates to the design and synthesis of the bridging ligand for the final ruthenium(II)-cobalt(III) heterodinuclear complex. In Chapter 2, a potential bridging ligand based on a functionalised terpyridine is described. The intention was to bind the ruthenium(II) metal centre to the terpyridine end of the bridging ligand and have a secondary binding domain available for coordination of the cobalt(III) metal centre. However, a reductive step in the synthetic pathway failed to produce the desired product and this potential bridging ligand had to be abandoned. In Chapter 3, two series of bridging ligands are described. The first of these series is based on Jurgen Sauer’s ‘LEGO’ system. In addition to describing the free synthesis of these ligands, their synthesis on a ruthenium(II) metal centre is described. The second series is based on disubstituted-1,2,4,5-tetrazines. These compounds are only able to be directly synthesised as the non-coordinated ligand. Coordination of these ligands to a single ruthenium(II) metal centre is then described. Ruthenium(II) complexes of both ligand series are then exposed to several transition metals and their ability to coordinate a second metal centre investigated. The formation of ruthenium(II)-cobalt(III) heterodinuclear complexes, using the ligand series detailed in Chapter 3, is described in Chapter 4. These complexes are formed by reacting the ruthenium(II) complex of the bridging ligand with either [Co(en)₂(OTf)₂](OTf) or [Co(tren)(OTf)₂](OTf). These heterodinuclear complexes exhibit photo-activated ligand release, which makes them candidates for development as a potential cancer treatment. The non-bridging ligands coordinated to the cobalt(III) metal centre in Chapter 4 were not cytotoxic. In order to make the system biologically active these ligands need to be changed. Chapter 5 describes how nitrogen mustards (a class of cytotoxic DNA alkylators) could be introduced as the non-bridging ligands. This involves the synthetic strategy of forming the cobalt(III) complex of the alcohol precursor of a nitrogen mustard. This precursor complex is then converted into the nitrogen mustard complex and coordinated to the ruthenium(II) bound bridging ligand. The synthetic strategies outlined in this thesis can be applied to a wide range of potential bridging ligands and could potentially lead to a large number of ruthenium(II)-cobalt(III) heterodinuclear complexes being synthesised. One journal article based on this research has been accepted for publication, in the Australian Journal of Chemistry. Three more articles are in preparation.
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Chinni, Carla. "Proteolytically activated receptors." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627093.

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Jones, Dale. "Light activated inteins." Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/382905/.

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The ability to control posttranslational assembly of proteins would be a powerful research tool that would allow researchers to selectively control and induce the function of a targeted protein. Several approaches have utilized inteins, protein domains that when inserted into a given protein sequence, excise themselves from the host protein, ligating the host protein fragments together to leave the excised intein and a mature protein. This process, known as protein splicing, would be a useful tool for studying protein function if it was selectively inducible. Herein we detail our efforts towards the development of a light activated intein that preferentially undergoes protein splicing in the presence of blue light. Our design combines the LOV2 domain from Avena sativa and the Npu DnaE trans intein from Nostoc punctiforme PCC73102 to yield a light activated intein. It was observed by western blot that this light activated intein demonstrated a 1.74 fold increase in intein mediated protein splicing when exposed to blue light. Mutations to eliminate the protein splicing ability of the light activated intein demonstrated that the extein products observed were the result of intein mediated protein splicing. Mutations to render the LOV2 domain insensitive to light indicated that the LOV2 domain influenced the protein splicing ability of the light activated intein, allowing it to progress at a higher rate in the presence of blue light.
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Svingala, Forrest R. "Alkali activated aerogels /." Online version of thesis, 2009. http://hdl.handle.net/1850/10097.

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Liu, Xiaoling. "Laboratory evaluation of microbial aggregation in activated in activated [sic] sludge." Connect to this title online, 2007. http://etd.lib.clemson.edu/documents/1202501487/.

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Kawamoto, Takahiro. "Endothelin-1 activates Homer 1a expression via mitogen-activated protein kinase in cardiac myocytes." Kyoto University, 2006. http://hdl.handle.net/2433/135882.

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González, León Oriol. "Light activated gas nanosensors." Doctoral thesis, Universitat Rovira i Virgili, 2018. http://hdl.handle.net/10803/665617.

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Aquesta tesi està centrada en explorar la utilitat de la llum ultraviolada per tal d'activar els sensors de gasos basats òxids metàl·lics (MOX), i comparar els resultats amb l'activació per temperatura. Mitjançant l'aplicació d'UV, i més concretament el sistema proposat en aquesta tesi, aplicant llum polsada, hem obtingut resultats prometedors. Per una banda, hem reduït la temperatura necessària per a la detecció dels gasos, possibilitant que puguin treballar fins i tot a temperatura ambient, amb el consequent estalvi energètic. La metodologia proposada consisteix en irradiar el material sensible mitjançant UV polsada, això crea uns transitoris dintre dels cicles de llum i no llum (arrissat en el senyal de la resistència mesurada) on hem observat que aquests transitoris estan relacionats amb la concentració dels gasos a detectar. Durant la il·lumincació UV, es generen en el MOX portadors de càrrega, es modifica la quantitat i/o naturalesa de les espècies d’oxigen ionoadsorbides i s'afavoreix la desorbció d’altres espècies presents en la superficie del material sensible. El fet de polsar la il·luminació sotmet el MOX a treballar en una successió d’estats transitoris. Aquesta metodologia s’ha aplicat a dos òxids metàlics diferents: In2O3 (nanooctahedres) i WO3 (en forma de nanoagulles). Els gasos amb els que s’ha treballat han estat NO2, NH3, Acetona i Etanol, amb diferents condicions d´humitat. Com a conclusió podem dir que amb aquesta metodologia podem millorar el temps de resposta, reduir el consum (temperatura a utilitzar) i millorar la sensibilitat i selectivitat, tant per gasos reductors com oxidants.
Esta tesis está centrada en explorar la utilidad de la luz ultravioleta para activar los sensores de gases basados en óxidos metálicos (MOX), y comparar los resultados con la activación por temperatura. Los MOX necesitan subir en temperatura para activar sus propiedades como semiconductores y también propiciar las reacciones con los gases a detectar, donde medimos la variación de la conductividad como respuesta a ese gas. Mediante la aplicación de UV, y más concretamente para el sistema propuesto en esta tesis aplicando pulsos de luz, hemos obtenido resultados prometedores. Por un lado hemos reducido la temperatura de detección de los gases y hemos propiciado reacciones e interacciones con el material que nos permiten discriminar mejor entre los gases. También hemos mejorado el tiempo de respuesta a RT con UV pulsada respecto activación sólo con temperatura. La metodología propuesta consiste en irradiar el material sensible mediante UV pulsada, esto crea unos transitorios dentro de los ciclos de luz y no luz (rizado en la señal) donde hemos observado que estos transitorios están relacionados con la concentración de los gases a detectar. Durante esta tesis hemos estudiado el comportamiento del IN2O3 (octahedros) y WO3 (nanoagujas) para la detección del NO2, NH3, Acetona y Ethanol, también bajo condiciones de humedad. Como conclusión podemos decir que con esta metodología podemos mejorar el tiempo de respuesta, reducir el consumo (temperatura) y mejorar la sensitibilidad y selectividad, tanto para gases reductores como oxidantes.
This thesis is focused on exploring the potential of ultraviolet light to activate metal oxide gas sensors (MOX), and to compare the results obtained against those when only temperature activation is used. MOXs need to be heated in order to show their properties as semiconductors and also react, on their surface, with the target gases, where we measure conductivity variations as a response towards those gases. In this thesis we have obtained promising results applying pulses of UV light. First of all, we have reduced the temperature for gas detection, then we have noticed that other kind of interactions appeared when the material is at low temperatures under UV excitation, which allows us to discriminate better between gases. We have also improved the response time at room temperature with pulsed UV in contrast to temperature alone. The proposed methodology consists of irradiating the sensitive material with on and off cycles of UV light, creating transients ( a ripple) in sensor resistance. What we have observed is that these transients are related to the concentration of the pollutant gases. This allows to design strategies to improve selectivity. During this thesis, we have studied In2O3 (octahedra) and WO3 (nanoneedles) as sensing layers for the detection of NO2, NH3, acetone, and ethanol, also under humid conditions. In conclusion we can say that with this methodology we can improve response time, reduce consumption (operation temperature can be lowered significantly) and improve sensitivity and selectivity, both for reducing and oxidizing gases.
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Bechwati, Fouad. "Acoustics of activated carbon." Thesis, University of Salford, 2008. http://usir.salford.ac.uk/26573/.

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This thesis describes a study into how sound interacts with activated carbon, a material that exhibits adsorbing and desorbing properties. Adsorption is where molecules from the surrounding gas are attracted to the material microstructure and held in place by a weak physical attraction force named after the scientist van der Waals\ desorption is the opposite process. Activated carbons include a complex porous structure, with a large internal surface area, and a considerable adsorption capacity caused by free electrons in the deformed graphene layers. The process of adsorption and desorption is usually associated with energy exchanges, caused by transfers of heat between the adsorbate molecules and the adsorbent surface. The study of acoustic interactions with granular activated carbons at normal conditions makes the subject of this doctoral thesis. Two main physical phenomena were seen to accompany sound propagation through the material: (i) an increase in volume compliance which is assumed to be caused by a change in the density of the interacting gas, and (ii) excess absorption at low frequencies thought to be due to the energy lost in the adsorption/desorption hysteresis. For the former, measurements on the impedance of low frequency Helmholtz resonators reveal significant shifts in resonance when activated carbon is used as a porous liner in the backing volume. At constant aperture dimensions, these shifts are attributed to a larger apparent volume of the resonator as compared to an empty backing volume. This phenomenon is in direct contravention of the physical theory associated with Helmholtz resonators as the resonant frequency of a device increases slightly when a porous solid is placed in the backing volume. An upper frequency limit of SOOHz is also determined where sorption effects in activated carbon are assumed to become almost negligible in relation to sound propagation. For the latter, the excess absorption at low frequency, a series of experiments to reveal the physical cause of the phenomenon have been undertaken. Hysteresis was observed during the sorption of humid air onto activated carbon at room temperature. At such conditions, the different rates of adsorption and desorption lead to a disturbance in the system equilibrium and cause a change in entropy. The return of the system to equilibrium is an exothermic process hence involves energy losses between activated carbon and the surrounding gas. This is suggested as a possible cause of the excess attenuation. However,the relaxation times are rather long for acoustic propagation, and further work is needed to examine this. An experimental apparatus to explore sound propagation through the material was devised. Results showed a violation of the equation of state for the relationship between volume and pressure: as the volume in a sealed chamber was reduced at constant temperature, the measured pressure change was found to be lower for a sample of activated carbon than when the chamber was empty; a phenomenon assumed due to the differences between adsorption and desorption rates. A new method for determining the porosity of a material exhibiting adsorption at acoustic pressures has been devised and found to be 81 ±7% for the granular sample examined. BET analysis and examination of electron microscope pictures allowed the pore size distribution to be found. Although the activated carbon sample has many very small pores (0.7nm in width), the BET isotherm showed that these will be saturated with water vapour in normal conditions. Consequently, the pores that affect sound propagation are those between the grains of the activated carbon, and the macropores (>50nm) on the surface of the grains. A theoretical model is developed and outlined based on the Langmuir isotherm. This was used to predict the sound propagation within the material and is compared to acoustic impedance measured in a large low frequency impedance tube, which was constructed especially for this project. The match between theory and measurement is rather poor, thought to be due to the lack of modelling the hysteresis effects in the adsorption- desorption cycle. Two applications of the material are examined, within a Helmholtz resonator and the cups of hearing defenders. In both cases, improved performance is seen. For instance, the use of the material in hearing defenders showed that activated carbon could be used to improve the attenuation at low frequencies in comparison to conventional foam liners.
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Shah, Samit Friedman Simon H. "Light activated RNA interference." Diss., UMK access, 2007.

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Thesis (Ph. D.)--School of Pharmacy and Dept. of Chemistry. University of Missouri--Kansas City, 2007.
"A dissertation in pharmaceutical science and chemistry." Advisor: Simon H. Friedman. Typescript. Vita. Description based on contents viewed July 16, 2008; title from "catalog record" of the print edition. Includes bibliographical references (leaves 206-220). Online version of the print edition.
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Moorcroft, Matthew James. "Electroanalysis at activated electrodes." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:6089e63c-3db2-4627-90e7-13763efcbd07.

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This thesis details advances made within the field of electroanalytical chemistry through the use of working electrodes that have been activated through application of ultrasound, heat, geometry, chemical modification or composition. Initially the thesis reports the enhanced analytical utility of chemically and compositionally modified working electrodes when directed towards the detection and determination of NO3¯ and NO2¯ anions in environmental samples. This has been achieved through the use of electrodes that have been a) modified with a Cu deposit and b) fashioned from a Cu-Ni alloy. Nitrate and nitrite anions have been successfully determined in a variety of passivating matrices, at analytically relevant detection limits of the order of 10-6 M with a dynamic linear range extending from 10 to 200 μM. The methods presented have been shown to surpass existing electrochemical techniques in terms of nitrate/nitrite speciation through separation of the voltammetric signals, where existing analyses have reported the intereference of both species when present in the same solution. The use of ultrasound as a further enhancement to the sensitivity and versatility of the electrochemical detection of nitrate at a chemically modified electrode is then presented. The influence of ultrasound is shown to remove a portion of the deposited copper, but a significant catalytic layer remains, resulting in greater sensitivity during insonation. The effect of temperature on electrochemical systems involving one- and two-electron redox reactions of K4Fe(CN)6, Ru(NH3)6Cl3, Fe(C5H5)2, N,N,N',N'tetramethylphenylenediamine, N,N'dimethylphenylenediamine and tris(4- bromophenyl)amine have been studied under hydrothermal conditions using a novel hydrodynamic method based on a conventional channel flow cell where the working electrode is heated by radio frequency radiation. The diffusion activation parameters obtained with the radio frequency channel cell and computer simulation were compared with independent data from microelectrode high temperature experiments. The application of the heated flow cell as a tool for mechanistic studies is discussed with the investigation of the well characterised ECE reaction of m-iodo-nitrobenzene in acetonitrile, giving a value of 80 ± 5 kJ mol-1 for the activation energy of the rate constant for the decomposition of the m-iodo-nitrobenzene radical anion. This represents the first observation of an ECE or mechanistically complex reaction at a locally heated electrode. The work presented in the final two chapters of this thesis examines the enhanced activation achieved from modification of the electrode geometry, and in particular the application of microelectrodes to the development of electroanalytical techniques. The electrochemical reduction of the inhalation anaesthetic agent enflurane (2-chloro-1,1,2- trifluoroethyl difluoromethyl ether) is reported at a variety of microelectrode substrates (Au, Ag, Cu, Pt and glassy carbon) with electrode dimensions varying from 5 to 60 μm. The solvents water, dimethylsulfoxide and acetonitrile were investigated along with the supporting electrolytes potassium chloride, tetrabutylammonium hexafluorophosphate and various tetraalkylammonium perchlorates. The use of a gold microelectrode with dimethyl sulfoxide solvent and tetraethylammonium perchlorate as the supporting electrolyte was found to give well-defined voltammetry. Linear calibration curves were obtained between 0 and 2 % v/v (gaseous additions) or up to 135 mM (gravimetric additions), offering scope for the development of a rapid, inexpensive electrochemical gas sensor. The analytical utility of the system has been investigated in the presence of oxygen and nitrous oxide in DMSO solvent. The superoxide anion radical, formed from the electro-reduction of dissolved oxygen, is shown to react with enflurane complicating their simultaneous detection. The kinetics of the enflurane / superoxide reaction are found to be first order with respect to both superoxide and enflurane with a rate constant of 0.25 M-1 s-1 determined by three independent methods: steady-state voltammetry, digital simulation of cyclic voltammetric data and UV/Vis spectroscopic analysis.
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Books on the topic "Activated"

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J, Thiel Donald, Water Environment Federation. Activated Sludge Task Force., and Water Environment Federation. Municipal Subcommittee., eds. Activated sludge. 2nd ed. Alexandria, VA: Water Environment Federation, 2002.

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1941-, Rodríguez-Reinoso F., ed. Activated carbon. Amsterdam: Elsevier, 2006.

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Water Pollution Control Federation. Task Force on Activated Sludge. and Water Pollution Control Federation. O & M Subcommittee., eds. Activated sludge. Alexandria, VA: Water Pollution Control Federation, 1987.

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Henze, M. Activated sludge model. London: International Association on Water Quality, 1995.

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Heitz, James R., and Kelsey R. Downum, eds. Light-Activated Pesticides. Washington, DC: American Chemical Society, 1987. http://dx.doi.org/10.1021/bk-1987-0339.

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Provis, John L., and Jannie S. J. van Deventer, eds. Alkali Activated Materials. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7672-2.

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Chartered Institution of Water and Environmental Management., ed. Activated-sludge treatment. London: Chartered Institution of Water and Environmental Management, 1997.

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Richard, Michael G. Activated sludge microbiology. Alexandria, VA: Water Pollution Control Federation, 1989.

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Mordechai, Liscovitch, ed. Signal-activated phospholipases. Austin: R.G. Landes Co., 1994.

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Kwiatkowski, James F. Activated carbon: Classifications, properties and applications. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Book chapters on the topic "Activated"

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Gooch, Jan W. "Activated." In Encyclopedic Dictionary of Polymers, 17. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_217.

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Ehsassi, Marjan H. "Canada." In Activated Citizenship, 154–89. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-5.

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Ehsassi, Marjan H. "France." In Activated Citizenship, 71–118. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-3.

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Ehsassi, Marjan H. "Democratic Malaise and Voice Insecurity." In Activated Citizenship, 1–13. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-1.

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Ehsassi, Marjan H. "United States." In Activated Citizenship, 190–215. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-6.

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Ehsassi, Marjan H. "Democratic Deficits, Citizens' Assemblies, and Activated Citizenship." In Activated Citizenship, 14–70. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-2.

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Ehsassi, Marjan H. "A Blueprint for Activated Citizenship." In Activated Citizenship, 216–58. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-7.

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Ehsassi, Marjan H. "Belgium." In Activated Citizenship, 119–53. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-4.

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Ehsassi, Marjan H. "Afterword." In Activated Citizenship, 259–66. New York: Routledge, 2024. http://dx.doi.org/10.4324/9781003494201-8.

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Guler, Sibel Deren, Madeline Gannon, and Kate Sicchio. "Activated Garments." In Crafting Wearables, 161–73. Berkeley, CA: Apress, 2016. http://dx.doi.org/10.1007/978-1-4842-1808-2_14.

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Conference papers on the topic "Activated"

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Bray, Liam. "Activated." In OzCHI '18: 30th Australian Computer-Human Interaction Conference. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3292147.3292205.

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Exner, T. "CONCENTRATION DEPENDENCE OF ACTIVATION OF ACARBOXYPROTEIN C BY THE CONTORTRIX ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644301.

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The protein C activator in Southern Copperhead (Agkistrodon Contortrix Contortrix) venom was isolated by sequential chromatographies on SP�Sephadex, Con A Sepharose and hydroxylapatite. It was found to be a single chain glycoprotein with an apparent molecular weight of 36,000 and an enzymatic specificity on chromogenic substrates resembling kallikein.This "contortrix activator" was used in a solid-phase immunochromometric assay (ICMA) for functional protein C in which heterologous antibody against protein C was passively coated onto microtitre wells and used to immoblize protein C. This was then activated, easily freed of excess activator by washing and assessed by its subsequent overnight cleavage of chromogenic substrates sensitive to activated protein C.Correlation between protein C results obtained by ICMA and immunoradiometric assay (IRMA) on a variety of patient samples was excellent when relatively high concentrations of the venom activator was used. However with lower concentration of activator plasmas from patients deficient in vitamin K gave lower protein C values by ICMA then obtained by IRMA.Normal protein C and "acarboxy" protein C from a patient on oral anticoagulant therapy were immuno-immobilized and studied by the ICMA technique using varying concentrations of the venom activator. The acarboxy-protein C, although completely activatable by high concentrationa of activator, was found to activate much more slowly than normal protein C at low concentrations of the contortrix activator. Thus by reducing the intensity of the activation step, the ICMA protein C results were increased in their sensitivity for functional protein C.
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Wang, Guangzhi, Weiguang Li, and Likun Huang. "Ecological Variation of High Activated Bacteria on Bioaugmentation Activated Carbon." In 2008 2nd International Conference on Bioinformatics and Biomedical Engineering (ICBBE '08). IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.1062.

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Højfeldt, Grith W., Christine Dethlefsen, Bente K. Pedersen, and Pernille Hojman. "Abstract 5400: Exercise activates AMP-activated protein kinase in breast cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5400.

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Kim, Sungho, Ece Isenbike Ozalp, Mohamed Darwish, and Jeffrey A. Weldon. "Electrically activated nanofluidic diodes." In 2017 IEEE 17th International Conference on Nanotechnology (IEEE-NANO). IEEE, 2017. http://dx.doi.org/10.1109/nano.2017.8117500.

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Kim, Jaehwan, Yung B. Seo, and Sang H. Choi. "Electrically-activated paper actuators." In SPIE's International Symposium on Smart Materials, Nano-, and Micro- Smart Systems, edited by Alan R. Wilson. SPIE, 2002. http://dx.doi.org/10.1117/12.469358.

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Moldovan, Dan. "VOICE-ACTIVATED QUESTION ANSWERING." In 2006 IEEE Spoken Language Technology Workshop. IEEE, 2006. http://dx.doi.org/10.1109/slt.2006.326782.

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Baborowski, J., C. Bourgeois, A. Pezous, C. Muller, and M. A. Dubois. "Piezoelectrically Activated Silicon Resonators." In 2007 IEEE International Frequency Control Symposium Joint with the 21st European Frequency and Time Forum. IEEE, 2007. http://dx.doi.org/10.1109/freq.2007.4319269.

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Gunay, A. Alperen. "ACTIVATED CARBON HEAT SINKS." In Proceedings of CONV-22: Int. Symp. on Convective Heat and Mass Transfer June 5 – 10, 2022, Turkey. Connecticut: Begellhouse, 2022. http://dx.doi.org/10.1615/ichmt.2022.conv22.180.

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Manocha, S., L. M. Manocha, Parth Joshi, Bhavesh Patel, Gaurav Dangi, and Narendra Verma. "Activated carbon from biomass." In CARBON MATERIALS 2012 (CCM12): Carbon Materials for Energy Harvesting, Environment, Nanoscience and Technology. AIP, 2013. http://dx.doi.org/10.1063/1.4810041.

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Reports on the topic "Activated"

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McLaughlin, H. Solvent-regenerated activated carbon. Office of Scientific and Technical Information (OSTI), July 1988. http://dx.doi.org/10.2172/6294679.

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Mullin, Amy S. Dynamics of Activated Molecules. Office of Scientific and Technical Information (OSTI), November 2016. http://dx.doi.org/10.2172/1332395.

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Michael A. Romano. PRESSURE ACTIVATED SEALANT TECHNOLOGY. Office of Scientific and Technical Information (OSTI), April 2004. http://dx.doi.org/10.2172/823486.

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Bender, T. R., and J. J. Zimmerman. Demand Activated Manufacturing Architecture. Office of Scientific and Technical Information (OSTI), February 2001. http://dx.doi.org/10.2172/774610.

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None, None. Thermally activated technologies: Technology Roadmap. Office of Scientific and Technical Information (OSTI), May 2003. http://dx.doi.org/10.2172/1216242.

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Del Cul, G. D., L. D. Trowbridge, D. W. Simmons, D. F. Williams, and L. M. Toth. Passivation of fluorinated activated charcoal. Office of Scientific and Technical Information (OSTI), October 1997. http://dx.doi.org/10.2172/658250.

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Kuriyama, K., and M. S. Dresselhaus. Photoconductivity of activated carbon fibers. Office of Scientific and Technical Information (OSTI), August 1990. http://dx.doi.org/10.2172/6824682.

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Jones, Graham B. Prostate Activated Prodrugs and Imaging Agents. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada442972.

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Jones, Graham B. Prostate Activated Prodrugs and Imaging Agents. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada443080.

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Jones, Graham B. Prostate Activated Prodrugs and Imaging Agents. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada443084.

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