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Journal articles on the topic 'Reactive oxygen species'

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Published: 4 June 2021
Last updated: 27 July 2024

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1

Drobot, L. B. "Reactive oxygen species in signal transduction." Ukrainian Biochemical Journal 85, no. 6 (December 27, 2013): 207–17. http://dx.doi.org/10.15407/ubj85.06.209.

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2

Kumar, Vishnu, and Abdus Salam. "A REVIEW ON REACTIVE OXYGEN AND NITROGEN SPECIES." ERA'S JOURNAL OF MEDICAL RESEARCH 5, no. 1 (June 2018): 59–66. http://dx.doi.org/10.24041/ejmr2018.63.

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3

Jadko, S. I. "Histone deacetylase activity and reactive oxygen species content." Ukrainian Biochemical Journal 87, no. 3 (June 27, 2015): 57–62. http://dx.doi.org/10.15407/ubj87.03.057.

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4

Bayr, Hülya. "Reactive oxygen species." Critical Care Medicine 33, Suppl (December 2005): S498—S501. http://dx.doi.org/10.1097/01.ccm.0000186787.64500.12.

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5

Morrell, Craig N. "Reactive Oxygen Species." Circulation Research 103, no. 6 (September 12, 2008): 571–72. http://dx.doi.org/10.1161/circresaha.108.184325.

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6

Bukoski, Richard D. "Reactive oxygen species." Journal of Hypertension 20, no. 11 (November 2002): 2141–43. http://dx.doi.org/10.1097/00004872-200211000-00009.

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7

Krötz, Florian, Hae-Young Sohn, and Ulrich Pohl. "Reactive Oxygen Species." Arteriosclerosis, Thrombosis, and Vascular Biology 24, no. 11 (November 2004): 1988–96. http://dx.doi.org/10.1161/01.atv.0000145574.90840.7d.

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8

SURI, R. K., M. S. RATNA, V. DHAWAN, A. GUPTA, R. GUPTA, K. SHARMA, S. K. S. THINGNAM, G. D. PURI, S. MADHULIKA, and N. K. GANGULY. "Reactive Oxygen Species." Annals of the New York Academy of Sciences 793, no. 1 Myocardial Pr (September 1996): 366–70. http://dx.doi.org/10.1111/j.1749-6632.1996.tb33528.x.

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9

N. Agbedanu, Prince, Troy B. Puga, Joshua Schafer, Pearce Harris, Gary Branum, and Nora Strasser. "Investigation of Reactive Oxygen Species production in Human Hepatocytes." Gastroenterology Pancreatology and Hepatobilary Disorders 6, no. 2 (January 12, 2022): 01–06. http://dx.doi.org/10.31579/2641-5194/058.

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1. Aim/Background: Reactive oxygen species (ROS) have been identified as compounds responsible for producing cellular damage. The purpose of this research is to examine if there is production of reactive oxygen species through free radical intermediates within human hepatocytes treated with morphine, bilirubin, or furosemide. The investigation examines the early stages of biotransformation by measuring the levels of reactive oxygen species produced inside of the treated hepatocytes within the first and second hours of treatment. The experiment was designed upon a case of a jaundiced (elevated bilirubin) infant who received morphine and furosemide and later died through unknown mechanisms. The experiment looks to examine if these drug compounds could contribute to cellular damage. This can help to further understand the potential interactions and complications of free radical intermediates produced during the phases of biotransformation. 2. Method: Previously cultured human hepatocytes were washed by centrifugation and re-suspended in 1x supplemental buffer to a concentration of 1x106 cells/mL and seeded in a dark clear bottom 96-well microplate at 100,000 stained cells/well. The cells were treated with either furosemide, morphine, bilirubin, a Tert-Butyl hydro peroxide (TBHP) positive control, or left as a background. Reactive oxygen generated in the presence of these agents were quantified by fluorescence excitation/emission measurement at 495nm/529nm. Fluorescence was measured at one and two hours. ROS generated convert 2',7'-dichlorodihydrofluorescein diacetate to 2',7'-dichlorodihydrofluorescein within the cells, which fluoresces. The fluorescence intensity detected is equivalent to the level of ROS generated. Wells that were untreated were used as blanks and subtracted from background and TBPH. 3. Results: Furosemide and Morphine did not produce statistically significant levels of ROS (p >0.05) above the background in both hours 1 and 2 of biotransformation and ROS measurement (Figure 1). Although Bilirubin did not produce statistically significant (p >0.05) levels of ROS above the background (Figure 2) during the first hour, it did produce statistically significant levels in the second hour of biotransformation. Each compound’s level of ROS was reduced during the second hour, signaling the removal of intermediate ROS metabolites (Figure 2). The production of ROS in each compound signifies that there is biotransformation to an intermediate that produces ROS. 4. Conclusion: The production of ROS above the background by each of the compounds shows there is an intermediate free radical compound that is produced during the biotransformation of each compound [21]. In this study, although furosemide and morphine did not produce statistically significant levels of ROS in both hours of biotransformation, bilirubin did produce significant levels of ROS in the second hour of biotransformation. This finding is in line with previous studies that shows morphine to offer protective effects against ROS production [16, 17]; and bilirubin demonstrating deleterious production of ROS at high doses [18]. Further work must be done to examine the correlation between the levels of ROS and extent of hepatocellular damage.
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10

TANAKA, Katsuya, and David C. WARLTIER. "Mechanism of Anesthetic Preconditioning: A Role for Reactive Oxygen Species." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 25, no. 2 (2005): 206–12. http://dx.doi.org/10.2199/jjsca.25.206.

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11

Lushchak, V. I. "Free radicals, reactive oxygen species, oxidative stresses and their classifications." Ukrainian Biochemical Journal 87, no. 6 (December 25, 2015): 11–18. http://dx.doi.org/10.15407/ubj87.06.011.

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12

Tykhomyrov, A. A., D. D. Zhernosekov, M. M. Guzyk, V. V. Korsa, and T. V. Grinenko. "Plasminogen modulates formation of reactive oxygen species in human platelets." Ukrainian Biochemical Journal 90, no. 6 (November 19, 2018): 31–40. http://dx.doi.org/10.15407/ubj90.06.031.

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13

Hill, Bradford G., and Aruni Bhatnagar. "Beyond Reactive Oxygen Species." Circulation Research 105, no. 11 (November 20, 2009): 1044–46. http://dx.doi.org/10.1161/circresaha.109.209791.

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14

Brown, G. C., and V. Borutaite. "Interactions between nitric oxide, oxygen, reactive oxygen species and reactive nitrogen species." Biochemical Society Transactions 34, no. 5 (October 1, 2006): 953–56. http://dx.doi.org/10.1042/bst0340953.

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ROS (reactive oxygen species) and RNS (reactive nitrogen species) are central to the innate immunity that protects us from infection, but also contribute to degenerative diseases and possibly aging. However, ROS and RNS are increasingly recognized to contribute to physiological signalling. This review briefly describes the main interactions between ROS and RNS and shows how their origins, chemistry, metabolism and biological actions are intimately linked.
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15

Olson, Kenneth R. "Are Reactive Sulfur Species the New Reactive Oxygen Species?" Antioxidants & Redox Signaling 33, no. 16 (December 1, 2020): 1125–42. http://dx.doi.org/10.1089/ars.2020.8132.

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16

Schwager, Patrick, Saustin Dongmo, Daniela Fenske, and Gunther Wittstock. "Reactive oxygen species formed in organic lithium–oxygen batteries." Physical Chemistry Chemical Physics 18, no. 16 (2016): 10774–80. http://dx.doi.org/10.1039/c5cp07145c.

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The generation of reactive oxygen species has been assumed to occur during the charging reaction of lithium-oxygen batteries with organic electrolytes. Here we show independently by fluorescence microscopy and scanning electrochemical microscopy that superoxide is also formed and released into the solution during the discharge reaction.
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17

Tauffenberger, Arnaud, and Pierre J. Magistretti. "Reactive Oxygen Species: Beyond Their Reactive Behavior." Neurochemical Research 46, no. 1 (January 2021): 77–87. http://dx.doi.org/10.1007/s11064-020-03208-7.

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AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.
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18

Bergamini, Carlo, Stefania Gambetti, Alessia Dondi, and Carlo Cervellati. "Oxygen, Reactive Oxygen Species and Tissue Damage." Current Pharmaceutical Design 10, no. 14 (May 1, 2004): 1611–26. http://dx.doi.org/10.2174/1381612043384664.

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19

Cash, Timothy P., Yi Pan, and M. Celeste Simon. "Reactive oxygen species and cellular oxygen sensing." Free Radical Biology and Medicine 43, no. 9 (November 2007): 1219–25. http://dx.doi.org/10.1016/j.freeradbiomed.2007.07.001.

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20

Delaney, M., L. Underhill, and J. C. Robins. "Low oxygen decreases intracellular reactive oxygen species." Fertility and Sterility 96, no. 3 (September 2011): S108. http://dx.doi.org/10.1016/j.fertnstert.2011.07.422.

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21

Nagano, Tetsuo. "Bioimaging Probes for Reactive Oxygen Species and Reactive Nitrogen Species." Journal of Clinical Biochemistry and Nutrition 45, no. 2 (2009): 111–24. http://dx.doi.org/10.3164/jcbn.r09-66.

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22

Yamaoka-Tojo, Minako, Taiki Tojo, Naonobu Takahira, Takashi Masuda, and Tohru Izumi. "Ezetimibe and Reactive Oxygen Species." Current Vascular Pharmacology 9, no. 1 (January 1, 2011): 109–20. http://dx.doi.org/10.2174/157016111793744652.

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23

Choi, Inpyo. "Reactive Oxygen Species and Cancer." Hanyang Medical Reviews 33, no. 2 (2013): 118. http://dx.doi.org/10.7599/hmr.2013.33.2.118.

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24

Dahiya, Parveen, Rohit Bhardwaj, Karun Chaudhary, Reet Kamal, Rajan Gupta, and Simerpreet Kaur. "Reactive oxygen species in periodontitis." Journal of Indian Society of Periodontology 17, no. 4 (2013): 411. http://dx.doi.org/10.4103/0972-124x.118306.

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25

Niess, Andreas M. "Reactive Oxygen Species and Inflammation." Medicine & Science in Sports & Exercise 39, Supplement (May 2007): 37. http://dx.doi.org/10.1249/01.mss.0000272256.65493.bb.

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26

Leeuwenburgh, Christiaan. "Reactive Oxygen Species and Apoptosis." Medicine & Science in Sports & Exercise 39, Supplement (May 2007): 37. http://dx.doi.org/10.1249/01.mss.0000272257.42622.6c.

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27

Diplock, Anthony T. "Defence against reactive oxygen species." Free Radical Research 29, no. 6 (January 1998): 463–67. http://dx.doi.org/10.1080/10715769800300521.

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28

Waters, Christopher M. "Reactive oxygen species in mechanotransduction." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 3 (September 2004): L484—L485. http://dx.doi.org/10.1152/ajplung.00161.2004.

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29

Fluhr, Robert, Moshe Sagi, Olga Davydov, and Cher Ashtamker. "Signals from reactive oxygen species." BMC Plant Biology 5, Suppl 1 (2005): S15. http://dx.doi.org/10.1186/1471-2229-5-s1-s15.

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30

Mikawa, K., H. Akamatsu, K. Nishina, T. Uesugi, and Y. Niwa. "Naloxone scavenges reactive oxygen species." Acta Anaesthesiologica Scandinavica 50, no. 9 (October 2006): 1171–73. http://dx.doi.org/10.1111/j.1399-6576.2006.01104.x.

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31

Bonnefont-Rousselot, Dominique. "Glucose and reactive oxygen species." Current Opinion in Clinical Nutrition and Metabolic Care 5, no. 5 (September 2002): 561–68. http://dx.doi.org/10.1097/00075197-200209000-00016.

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32

Ochsendorf, F. R. "Infection and reactive oxygen species." Andrologia 30, S1 (April 27, 2009): 81–86. http://dx.doi.org/10.1111/j.1439-0272.1998.tb02830.x.

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33

Addabbo, Francesco, Monica Montagnani, and Michael S. Goligorsky. "Mitochondria and Reactive Oxygen Species." Hypertension 53, no. 6 (June 2009): 885–92. http://dx.doi.org/10.1161/hypertensionaha.109.130054.

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34

Degli Esposti, M. "Measuring mitochondrial reactive oxygen species." Methods 26, no. 4 (April 2, 2002): 335–40. http://dx.doi.org/10.1016/s1046-2023(02)00039-7.

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35

Kowaltowski, Alicia J., Nadja C. de Souza-Pinto, Roger F. Castilho, and Anibal E. Vercesi. "Mitochondria and reactive oxygen species." Free Radical Biology and Medicine 47, no. 4 (August 2009): 333–43. http://dx.doi.org/10.1016/j.freeradbiomed.2009.05.004.

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36

Liou, Geou-Yarh, and Peter Storz. "Reactive oxygen species in cancer." Free Radical Research 44, no. 5 (January 2010): 479–96. http://dx.doi.org/10.3109/10715761003667554.

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37

Ford, W. Chris L. "Reactive oxygen species and sperm." Human Fertility 4, no. 2 (January 2001): 77–78. http://dx.doi.org/10.1080/1464727012000199321.

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38

Salisbury, Dereck, and Ulf Bronas. "Reactive Oxygen and Nitrogen Species." Nursing Research 64, no. 1 (2015): 53–66. http://dx.doi.org/10.1097/nnr.0000000000000068.

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39

Gutterman, David D. "Mitochondria and Reactive Oxygen Species." Circulation Research 97, no. 4 (August 19, 2005): 302–4. http://dx.doi.org/10.1161/01.res.0000179773.18195.12.

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40

Bennett, Martin R. "Reactive Oxygen Species and Death." Circulation Research 88, no. 7 (April 13, 2001): 648–50. http://dx.doi.org/10.1161/hh0701.089955.

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41

Rani, Shikha, and Deepak Chawla. "Preeclampsia and Reactive Oxygen Species." Indian Journal of Pediatrics 85, no. 5 (March 14, 2018): 333–34. http://dx.doi.org/10.1007/s12098-018-2657-5.

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42

Heiser, I., and E. F. Elstner. "Biochemical mechanisms of plant defense a central role for reactive oxygen species." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S76—S86. http://dx.doi.org/10.17221/10325-pps.

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In general mechanics stress is clearly defined as the point or degree of bending of an elastic system at the very point of just symptomless reversibility and irreversible deformation or break. In medicine and botany, stress is supposed to indicate all situations beyond normal, defined by the observer. All organs of higher plants (with some exceptions) perform aerobic metabolism and are thus subject to activated oxygen species. Oxygen oversaturation and thus oxygen stress may occur under various different conditions. Since most abiotic and biotic stress situations in plants result in the accelerated production of ROS oxidative stress is a common signaling event in plant stress and redox regulation therefore plays a central role in the stress signaling network (PASTORI & FOYER 2002). In this review basic reactions operating during stress and defence will be discussed where certain prooxidative situations and antioxidative processes in plants will be dealt with.
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43

Turčan, Pavel, Pavel Pokorný, Peter Kepič, Jozef Hambálek, Pavla Entnerová, Jana Kvintová, Martin Sigmund, Eva Sedlatá Jurásková, and Tomáš Fait. "Reactive oxygen species and their role in the andrological factor of couple fertility." Česká gynekologie 89, no. 2 (April 22, 2024): 139–43. http://dx.doi.org/10.48095/cccg2024139.

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Reactive oxygen species play a significant role in male fertility and infertility. They are essential for physiological processes, but when their concentration becomes excessive, they can be a cause of various sperm pathologies. Seminal leukocytes and pathologically abnormal sperm are the primary sources of oxygen radicals in ejaculate. They negatively affect sperm quality, including DNA fragmentation and sperm motility impairment. Addressing increased concentrations of reactive oxygen species involves various appropriate lifestyle modifications and measures, including the use of antioxidants, treatment of urogenital infections, management of varicocele, weight reduction, and others. In many cases, these interventions can lead to adjustments in the condition and improvement in sperm quality. Such improvements can subsequently lead to enhanced outcomes in assisted reproduction or even an increased likelihood of natural conception. In some instances, the need for donor sperm may be eliminated. However, a key factor is adhering to a sufficiently prolonged treatment, which requires patience on the part of both, the physician and the patient. Key words: reactive oxygen species – infertility – male infertility – spermatocytes pathology – DNA fragmentation
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44

Lindermayr, Christian, and Jörg Durner. "Interplay of Reactive Oxygen Species and Nitric Oxide: Nitric Oxide Coordinates Reactive Oxygen Species Homeostasis." Plant Physiology 167, no. 4 (March 27, 2015): 1209–10. http://dx.doi.org/10.1104/pp.15.00293.

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45

Riley, J. C. M., and H. R. Behrman. "Oxygen Radicals and Reactive Oxygen Species in Reproduction." Experimental Biology and Medicine 198, no. 3 (December 1, 1991): 781–91. http://dx.doi.org/10.3181/00379727-198-43321c.

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46

Olson, Kenneth R. "Hydrogen sulfide, reactive sulfur species and coping with reactive oxygen species." Free Radical Biology and Medicine 140 (August 2019): 74–83. http://dx.doi.org/10.1016/j.freeradbiomed.2019.01.020.

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47

Ryazantsev, V. V. "THE GENERATION OF REACTIVE OXYGEN SPECIES BY CORD BLOOD NUCLEATED CELLS DURING CRYOPRESERVATION." Biotechnologia Acta 7, no. 4 (2014): 100–106. http://dx.doi.org/10.15407/biotech7.04.100.

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48

Panus, Peter C., John Shearer, and Bruce A. Freeman. "Pulmonary Metabolism of Reactive Oxygen Species." Experimental Lung Research 14, sup1 (January 1988): 959–76. http://dx.doi.org/10.3109/01902148809064186.

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49

Kao, Mei-Chung, and Chiu-Sen Wang. "Reactive Oxygen Species in Incense Smoke." Aerosol and Air Quality Research 2, no. 1 (2002): 61–69. http://dx.doi.org/10.4209/aaqr.2002.06.0007.

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50

Ngô, Charlotte, Christiane Chéreau, Carole Nicco, Bernard Weill, Charles Chapron, and Frédéric Batteux. "Reactive Oxygen Species Controls Endometriosis Progression." American Journal of Pathology 175, no. 1 (July 2009): 225–34. http://dx.doi.org/10.2353/ajpath.2009.080804.

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