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Journal articles on the topic '5O2'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Yongnan, P., F. Daiichiro, S. Shoichiro, O. Akira, S. Eime, and T. Nagai. "320 EFFECT OF OXYGEN TENSION AND FOLLICLE CELLS DURING IN VITRO CULTURE OF PORCINE OOCYTES IN FOLLICULAR FLUID ON THEIR MATURATION AND FERTILIZATION." Reproduction, Fertility and Development 19, no. 1 (2007): 275. http://dx.doi.org/10.1071/rdv19n1ab320.

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If we could use porcine follicular fluid (pFF) as a solo in vitro maturation (IVM) medium, the preparation of complicated medium wouldn't be necessary. In this study, we investigated the effects on nuclear maturation and subsequent IVF of oxygen tension and follicle cells (FC) during IVM of porcine oocytes in pFF using static (S) and rotating (R) systems. In Experiment 1, all of the cumulus–oocyte complexes (COCs) in pFF were collected, and COCs with compact cumulus cells were selected for IVM. Also, small clusters of FC were collected by centrifugation of the pFF after filtration through 212 µm mesh, and pFF without any cells was prepared by centrifugation and used as a maturation medium (MpFF) after supplementation with FSH and antibiotics. The COCs were transferred to 2 mL (in a 35-mm petri dish) or 3.5 mL (in a 15-mL test tube) of MpFF with or without FC (5.2 × 106 cells mL−1) added and were cultured for 48 h at 38.5°C in 5% CO2 and 20% O2 (in air) or 5% O2 using the S or R culture systems (5O2/FC−/S, 5O2/FC+/S, 20O2/FC−/S, 20O2/FC+/S, 5O2/FC−/R, 5O2/FC+/R, 20O2/FC−/R, and 20O2/FC+/R groups). The oxygen tension had no effect on nuclear maturation except for the FC−/R groups. In the FC−/R groups, cumulus cells were detached from oocytes and their maturation rates were so low that it was difficult to discuss the effect of oxygen tension. When cultured with FC, oocytes were surrounded with expanded cumulus cells and matured to metaphase II (MII) at higher rates in 5O2/FC+/R (67.7%) and 20O2/FC+/R (65.9%) than those in 5O2/FC+/S (17.5%) and 20O2/FC+/S (35.7%) (chi-squared test; P < 0.05). In contrast, when cultured without FC, oocytes matured to MII at higher rates in 5O2/FC−/S (78.3%) and 20O2/FC−/S (76.5%) than those in 5O2/FC−/R (32.7%) and 20O2/FC−/R (11.4%) (P < 0.05). In Experiment 2, oocytes were cultured in 5O2/FC−/S, 20O2/FC−/S, 5O2/FC+/R, or 20O2/FC+/R; fertilized in vitro, as reported previously (Kikuchi et al. 2002 Biol. Reprod. 66, 1033–1041), and fixed 10 h after IVF. Oocytes cultured in 20O2/FC+/R showed a significantly higher sperm penetration rate (95.9%) than those cultured in 5O2/FC−/S and 20O2/FC−/S (88.0% and 88.4%, respectively), but were similar to those cultured in 5O2/FC+/R (90.9%) (P < 0.05). Oocytes cultured in 5O2/FC+/R formed a male pronucleus at a higher rate (77.1%) than those cultured in 5O2/FC−/S, 20O2/FC−/S, and 20O2/FC+/R (52.8, 51.6, and 63.3%, respectively) (P < 0.05). These results indicate that oxygen tension had no effect on IVM and IVF, except for a higher male pronucleus formation rate in 5O2/FC+/R than in 20O2/FC+/R, for porcine oocytes cultured in pFF, and that the addition of FC to pFF in the rotating culture system promoted nuclear maturation and a high male pronucleus formation rate after IVF, especially under 5% O2. In contrast, when the static culture system was used for IVM, the addition of FC was found to be detrimental to oocyte maturation in pFF.
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2

Othman, Norinsan Kamil, A. Jalar, N. Othman, and David J. Young. "Effects of Lanthanum on Fe-25Cr Alloys under Cyclic Oxidation." Advanced Materials Research 97-101 (March 2010): 1212–15. http://dx.doi.org/10.4028/www.scientific.net/amr.97-101.1212.

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Fe-Cr binary model alloys (Cr: 25 wt %) with additions of 0.09 wt% lanthanum were subjected to cyclic oxidation experiments at 700oC. All model alloys were exposed in five different gases; Ar-20O2, Ar-20O2-5H2O, Ar-5O2-20H2O, Ar-10H2-5H2O (pO2 = 3.64 x 10-22 atm) and Ar-10H2-20H2O (pO2 = 7.37 x 10-21 atm) all in volume %. Very low weight gains were observed in all gases of Fe-25Cr-0.09La. However, breakaway oxidation occurred on La-free alloy experienced increased weight gain in Ar-5O2-20H2O due to formation of iron-rich oxide. The addition of La (<0.1 wt%) to the Fe25Cr retarded the growth of iron-rich oxide in Ar-5O2-20H2O.
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3

Chitsazan, A., M. Monajjemi, and H. Aghaei. "Increased efficiency of a fuel cell using h-BN electrodes and Teflon polymer electrolyte [-C2F4-]n." Revista de la Universidad del Zulia 11, no. 29 (February 8, 2020): 60–78. http://dx.doi.org/10.46925//rdluz.29.05.

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Graphene and h-BN have been theoretically simulated for hydrogen storage and oxygen diffusion in a single fuel cell unit. Obviously, the efficiency of the PEM hydrogen fuel cells was significantly related to the amount of H2 concentration, the water activities in catalyst substrates and the polymer of the electrolyte membranes, the temperature and the dependence of such variables in the direction of the fuel and air currents between the anode path and the cathode. The single PEM parameter has been estimated and the results show greater fuel cell efficiency using graphene sheets and h-BN. Maximum efficiency is observed with the stoichiometry of the 5H2, 5O2 and 3 C2F4 molecules during adsorption.
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4

Tong, Miaohui, Yujun Liang, Guogang Li, Zhanggen Xia, Mengfei Zhang, Fan Yang, and Qiang Wang. "Luminescent properties of single Dy3+ ions activated Ca3Gd7(PO4)(SiO4)5O2 phosphor." Optical Materials 36, no. 9 (July 2014): 1566–70. http://dx.doi.org/10.1016/j.optmat.2014.04.026.

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5

Эренбург, С. Б., С. В. Трубина, К. О. Квашнина, В. Н. Кручинин, В. В. ГРИЦЕНКО, А. Г. Черникова, and А. М. Маркеев. "БЛИЖНИЙ ПОРЯДОК В АМОРФНОМ И КРИСТАЛЛИЧЕСКОМ СЕГНЕТОЭЛЕКТРИЧЕСКОМ Hfo.5Zro.5O2, "Журнал экспериментальной и теоретической физики"." Журнал экспериментальной и теоретической физики, no. 6 (2018): 982–91. http://dx.doi.org/10.7868/s0044451018060135.

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6

Zhang, Yang, Guogang Li, Dongling Geng, Mengmeng Shang, Chong Peng, and Jun Lin. "Color-Tunable Emission and Energy Transfer in Ca3Gd7(PO4)(SiO4)5O2: Ce3+/Tb3+/Mn2+Phosphors." Inorganic Chemistry 51, no. 21 (October 17, 2012): 11655–64. http://dx.doi.org/10.1021/ic3015578.

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7

Zhang, Yang, Guogang Li, Dongling Geng, Mengmeng Shang, Chong Peng, and Jun Lin. "ChemInform Abstract: Color-Tunable Emission and Energy Transfer in Ca3Gd7(PO4) (SiO4)5O2: Ce3+/Tb3+/Mn2+Phosphors." ChemInform 44, no. 7 (February 12, 2013): no. http://dx.doi.org/10.1002/chin.201307007.

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8

Перевалов, Т. В., В. А. Гриценко, Д. Р. Исламов, and И. П. Просвирин. "Электронная структура вакансий кислорода в орторомбической нецентросимметричной фазе Hfo.5Zro.5O2, "Письма в Журнал экспериментальной и теоретической физики"." Письма в Журнал экспериментальной и теоретической физики, no. 1-2 (2018): 62–67. http://dx.doi.org/10.7868/s0370274x18010113.

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9

Gauthier, Nicolas, Cécile Courrèges, Julien Demeaux, Cécile Tessier, and Hervé Martinez. "Influence of the Cathode Potential on Electrode Interactions within a Li4Ti5O12 vs LiNi3/5Mn1/5Co1/5O2 Li-Ion Battery." Journal of The Electrochemical Society 167, no. 4 (February 11, 2020): 040504. http://dx.doi.org/10.1149/1945-7111/ab7116.

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10

Lagercrantz, Carl. "Formation of the paramagnetic complex [Cr(OH)5O2]5− in the reaction between chromium(VI) oxide, and hydrogen peroxide or superoxide anion radicals studied by EPR spectroscopy." Free Radical Biology and Medicine 26, no. 9-10 (May 1999): 1134–37. http://dx.doi.org/10.1016/s0891-5849(98)00294-9.

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11

Elton, Hugh, and Geoffrey Greatrex. "Rome and Persia at War, 502-532." Phoenix 53, no. 3/4 (1999): 388. http://dx.doi.org/10.2307/1089014.

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12

Wheeler, Everett L., and Geoffrey Greatrex. "Rome and Persia at War, 502-532." Journal of Military History 63, no. 2 (April 1999): 435. http://dx.doi.org/10.2307/120656.

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13

Whitby, Michael. "Book Review: Rome and Persia at War, 502-532." War in History 7, no. 3 (July 2000): 354–56. http://dx.doi.org/10.1177/096834450000700306.

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14

Шпакова, Е. А., К. В. Деркач, and А. О. Шпаков. "Биологическая активность липофильных производных пептида 562–572 рецептора лютеинзирующего гормона крысы." Доклады Академии наук 452, no. 4 (2013): 453–56. http://dx.doi.org/10.7868/s0869565213290240.

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15

Da Costa, Bruno, Christophe Chevalier, Celine Henry, Jean-Claude Huet, Stéphanie Petit, Jean Lepault, Hein Boot, and Bernard Delmas. "The Capsid of Infectious Bursal Disease Virus Contains Several Small Peptides Arising from the Maturation Process of pVP2." Journal of Virology 76, no. 5 (March 1, 2002): 2393–402. http://dx.doi.org/10.1128/jvi.76.5.2393-2402.2002.

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ABSTRACT The capsid proteins VP2 and VP3 of infectious bursal disease virus, a birnavirus, are derived from the processing of a large polyprotein: NH2-pVP2-VP4-VP3-COOH. Although the primary cleavage sites at the pVP2-VP4 and VP4-VP3 junctions have been identified, the proteolytic cascade involved in the processing of this polyprotein is not yet fully understood, particularly the maturation of pVP2. By using different approaches, we showed that the processing of pVP2 (residues 1 to 512) generated VP2 and four small peptides (residues 442 to 487, 488 to 494, 495 to 501, and 502 to 512). We also showed that in addition to VP2, at least three of these peptides (residues 442 to 487, 488 to 494, and 502 to 512) were associated with the viral particles. The importance of the small peptides in the virus cycle was assessed by reverse genetics. Our results showed that the mutants lacking the two smaller peptides were viable, although the virus growth was affected. In contrast, deletions of the domain 442 to 487 or 502 to 512 did not allow virus recovery. Several amino acids of the peptide 502 to 512 appeared essential for virus viability. Substitutions of the P1 and/or P1" position were engineered at each of the cleavage sites (P1-P1": 441-442, 487-488, 494-495, 501-502, and 512-513). Most substitutions at the pVP2-VP4 junction (512-513) and at the final VP2 maturation cleavage site (441-442) were lethal. Mutations of intermediate cleavage sites (487-488, 494-495, and 501-502) led to viable viruses showing different but efficient pVP2 processing. Our data suggested that while peptides 488 to 494 and 495 to 501 play an accessory role, peptides 442 to 487 and 502 to 512 have an unknown but important function within the virus cycle.
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16

Evans, John K. "Rome and Persia at War, 502-532, by Geoffrey GreatrexRome and Persia at War, 502-532, by Geoffrey Greatrex. Leeds, England, Francis Cairns, 1998. xvi, 301 pp. $70.00." Canadian Journal of History 34, no. 3 (December 1999): 429–30. http://dx.doi.org/10.3138/cjh.34.3.429.

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17

Abdel-Rahman, Abdel-Fattah M. "Chlorites in a spectrum of igneous rocks: mineral chemistry and paragenesis." Mineralogical Magazine 59, no. 394 (March 1995): 129–41. http://dx.doi.org/10.1180/minmag.1995.59.394.13.

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AbstractThe chlorite data presented are from four igneous complexes covering the compositional spectrum of igneous rocks (gabbro to granite) of orogenic and anorogenic settings. The four igneous complexes are; early orogenic gabbro-diorite-tonalite (D-T) suite, late orogenic granodiorite-adamellite (G-A) suite (both are calc-alkaline suites), high-alumina trondhjemite (TR), and anorogenic peralkaline granite (PGR).Chlorites in these igneous rocks show characteristic compositional fields. The Mg vs Fe plot provides the best discriminant, as data points define three compositionally different groups. Phases in the PGR are Fe-rich, siliceous, interlayered chlorite-smectite (Fe/Mg = 8.6), and differ significantly from those in the calc-alkaline D-T and G-A rocks which are Mg-rich chlorites (Fe/Mg = 0.6–0.8). The X-ray diffraction data for the peralkaline granite samples show superlattice reflections at approximately 31 Å (air-dried) and 34 Å (ethylene glycollated), thus suggesting the presence of an expandable (smectite-like) component in this interlayered (chlorite-smectite) phyllosilicate phase. Chlorites in the peraluminous TR rocks contain Fe/Mg values intermediate between the other two types (Fe/Mg = 1.3). Tetrahedral Al (AlZ) values are remarkably low (0–0.5) in phyllosilicates in the PGR, but vary from 1.9–2.5 in chlorites from the other suites. Yet, these chlorite groups with their generally low AlZ values are distinct from the more stable (type IIb) metamorphic chlorites. Sedimentary chlorites are somewhat similar, in their low AlZ values and metastable structural type, to chlorites in igneous rocks.In the calc-alkaline rocks, chlorite may have been formed at the expense of both biotite [biotite + 3M + 3H2O = chlorite + A], and calcic amphibole [2 Ca-amphibole + 6H2O + 5O2 + 1.8Al = 1 chlorite + 8SiO2 + A], where M = Fe, Mg, Al, and A = K, Na, Ca. The alteration of alkali amphibole in the peralkaline rocks may have produced interlayered chlorite-smectite via this reaction; [1 Na-amphibole + 7H2O + 2.5O2 + M = 1 chlorite-smectite + A]. The presence of such interlayered chlorite-smectite which typically form at low T (150–200°C) suggests that the region was not affected by any major reheating events, which is consistent with the nature of the feldspars.
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18

Mao, W., R. B. Carroll, and D. P. Whittington. "Association of Phoma terrestris, Pythium irregulare, and Fusarium acuminatum in Causing Red Root Rot of Corn." Plant Disease 82, no. 3 (March 1998): 337–42. http://dx.doi.org/10.1094/pdis.1998.82.3.337.

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Greenhouse and field tests were conducted in 1992 and 1993 to determine the causal pathogen(s) of red root rot (RRR) of corn. Corn hybrids Dekalb DK 522, DK 572, DK 677, and DK 582 were utilized. Phoma terrestris, Pythium irregulare, and Fusarium acuminatum were used alone or in combination to infest potting mix in greenhouse tests or soil in field tests. Results indicated that P. terrestris is the primary pathogen in the RRR complex of corn in Delaware. When P. terrestris and Pythium irregulare were associated, the disease progressed faster and was more severe, resulting in significantly higher (P ≤ 0.01) root rot, basal stalk rot, and wilt. F. acuminatum played a minor role in causing the disease, with little additional symptom development when combined with P. terrestris or Pythium irregulare.
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19

Shpakova, E. A., K. V. Derkach, and A. O. Shpakov. "Biological activity of lipophilic derivatives of peptide 562–572 of rat luteinizing hormone receptor." Doklady Biochemistry and Biophysics 452, no. 1 (September 2013): 248–50. http://dx.doi.org/10.1134/s1607672913050116.

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20

Derkach, K. V., E. A. Shpakova, and A. O. Shpakov. "Palmitoylated Peptide 562-572 of Luteinizing Hormone Receptor Increases Testosterone Level in Male Rats." Bulletin of Experimental Biology and Medicine 158, no. 2 (November 29, 2014): 209–12. http://dx.doi.org/10.1007/s10517-014-2724-5.

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21

Zou, Xuan, Minghui Li, Zebo Huang, Xin Zhou, Qingxie Liu, Tiansong Xia, and Wei Zhu. "Circulating miR-532-502 cluster derived from chromosome X as biomarkers for diagnosis of breast cancer." Gene 722 (January 2020): 144104. http://dx.doi.org/10.1016/j.gene.2019.144104.

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22

De Luca, Mariagrazia, David A. Facey, Emmanuel J. Favaloro, Mark S. Hertzberg, James C. Whisstock, Tracy McNally, Robert K. Andrews, and Michael C. Berndt. "Structure and function of the von Willebrand factor A1 domain: analysis with monoclonal antibodies reveals distinct binding sites involved in recognition of the platelet membrane glycoprotein Ib-IX-V complex and ristocetin-dependent activation." Blood 95, no. 1 (January 1, 2000): 164–72. http://dx.doi.org/10.1182/blood.v95.1.164.

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Abstract Binding of the adhesive glycoprotein, von Willebrand factor (vWf), to the platelet membrane glycoprotein (GP) Ib-IX-V complex initiates platelet adhesion and aggregation at high shear stress in hemostasis and thrombosis. In this study, the GP Ib-IX-V binding site within the vWf A1 domain was analyzed using a panel of murine monoclonal antibodies raised against a 39/34-kd vWf fragment (Leu-480/Val-481–Gly-718) encompassing the A1 domain. One antibody, 6G1, strongly inhibited ristocetin-dependent vWf binding to platelets, but had no effect on botrocetin- or jaracetin-dependent binding, or asialo-vWf–dependent platelet aggregation. The 6G1 epitope was mapped to Glu-700–Asp-709, confirming the importance of this region for modulation of vWf by ristocetin. Like ristocetin, 6G1 activated the vWf A1 domain, because it enhanced binding of the 39/34-kd fragment to platelets. In contrast, 5D2 and CR1 completely inhibited asialo-vWf–induced platelet aggregation and ristocetin-induced vWf binding to GP Ib-IX-V. However, only 5D2 blocked botrocetin- and jaracetin-induced vWf binding to platelets and binding of vWf to botrocetin- and jaracetin-coated beads. Epitopes for 5D2 and CR1 were conformationally dependent, but not congruent. Other antibodies mapped to epitopes within the A1 domain (CR2 and CR15, Leu-494–Leu-512; CR2, Phe-536–Ala-554; CR3, Arg-578–Glu-596; CR11 and CR15, Ala-564–Ser-582) were not functional, identifying regions of the vWf A1 domain not directly involved in vWf-GP Ib-IX-V interaction. The combined results provide evidence that the proline-rich sequence Glu-700–Asp-709 constitutes a regulatory site for ristocetin, and that ristocetin and botrocetin induce, at least in part, separate receptor-recognition sites on vWf. (Blood. 2000;95:164-172)
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23

De Luca, Mariagrazia, David A. Facey, Emmanuel J. Favaloro, Mark S. Hertzberg, James C. Whisstock, Tracy McNally, Robert K. Andrews, and Michael C. Berndt. "Structure and function of the von Willebrand factor A1 domain: analysis with monoclonal antibodies reveals distinct binding sites involved in recognition of the platelet membrane glycoprotein Ib-IX-V complex and ristocetin-dependent activation." Blood 95, no. 1 (January 1, 2000): 164–72. http://dx.doi.org/10.1182/blood.v95.1.164.001k35_164_172.

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Binding of the adhesive glycoprotein, von Willebrand factor (vWf), to the platelet membrane glycoprotein (GP) Ib-IX-V complex initiates platelet adhesion and aggregation at high shear stress in hemostasis and thrombosis. In this study, the GP Ib-IX-V binding site within the vWf A1 domain was analyzed using a panel of murine monoclonal antibodies raised against a 39/34-kd vWf fragment (Leu-480/Val-481–Gly-718) encompassing the A1 domain. One antibody, 6G1, strongly inhibited ristocetin-dependent vWf binding to platelets, but had no effect on botrocetin- or jaracetin-dependent binding, or asialo-vWf–dependent platelet aggregation. The 6G1 epitope was mapped to Glu-700–Asp-709, confirming the importance of this region for modulation of vWf by ristocetin. Like ristocetin, 6G1 activated the vWf A1 domain, because it enhanced binding of the 39/34-kd fragment to platelets. In contrast, 5D2 and CR1 completely inhibited asialo-vWf–induced platelet aggregation and ristocetin-induced vWf binding to GP Ib-IX-V. However, only 5D2 blocked botrocetin- and jaracetin-induced vWf binding to platelets and binding of vWf to botrocetin- and jaracetin-coated beads. Epitopes for 5D2 and CR1 were conformationally dependent, but not congruent. Other antibodies mapped to epitopes within the A1 domain (CR2 and CR15, Leu-494–Leu-512; CR2, Phe-536–Ala-554; CR3, Arg-578–Glu-596; CR11 and CR15, Ala-564–Ser-582) were not functional, identifying regions of the vWf A1 domain not directly involved in vWf-GP Ib-IX-V interaction. The combined results provide evidence that the proline-rich sequence Glu-700–Asp-709 constitutes a regulatory site for ristocetin, and that ristocetin and botrocetin induce, at least in part, separate receptor-recognition sites on vWf. (Blood. 2000;95:164-172)
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24

Cavallo, Bice. "Corrigendum to “Computing random consistency indices and assessing priority vectors reliability” [Inf. Sci. 420 (2017) 532–542]." Information Sciences 430-431 (March 2018): 282–86. http://dx.doi.org/10.1016/j.ins.2017.11.017.

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25

Crochet, P., F. Rami, R. Donà, J. P. Coffin, P. Fintz, G. Guillaume, F. Jundt, et al. "Erratum to “Azimuthal anisotropies as stringent test for nuclear transport models” [Nucl. Phys. A 627 (1997) 522–542]." Nuclear Physics A 628, no. 4 (January 1998): 687–88. http://dx.doi.org/10.1016/s0375-9474(98)00112-2.

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Boynton, H., E. Winslow, R. Ling, and D. Mehlman. "502." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S84. http://dx.doi.org/10.1249/00005768-198704001-00502.

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Moore, T., and J. K. Barclay. "512." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S86. http://dx.doi.org/10.1249/00005768-198704001-00512.

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Pollock, M. L., J. E. Graves, A. E. Jones, A. Colvin, and S. Leggett. "522." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S87. http://dx.doi.org/10.1249/00005768-198704001-00522.

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Parry, A. C., P. F. Mosher, M. S. Realatad, and A. Lapersiero. "532." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S89. http://dx.doi.org/10.1249/00005768-198704001-00532.

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Zoltick, J. M., R. Virmani, J. Kishel, W. Fitzgerald, M. Kobinowitz, and J. Bedynek. "542." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S91. http://dx.doi.org/10.1249/00005768-198704001-00542.

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Chase, P. B., M. J. Reiling, J. A. Taylor, and D. R. Seals. "552." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S92. http://dx.doi.org/10.1249/00005768-198704001-00552.

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P??ronnet, F., D. Hassicotte, J. E. P??quet, G. Brisson, and J. de Champlain. "562." Medicine & Science in Sports & Exercise 19, Supplement (April 1987): S94. http://dx.doi.org/10.1249/00005768-198704001-00562.

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Berrios, Ronaldo Sevilla, John OʼHoro, Jennifer Elmer, Rahul Kashyap, Jeff Jensen, and Sean Caples. "502." Critical Care Medicine 41 (December 2013): A122. http://dx.doi.org/10.1097/01.ccm.0000439645.92228.e7.

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Feih, Joel, Michael Katz, and Kate Schaafsma. "512." Critical Care Medicine 41 (December 2013): A125. http://dx.doi.org/10.1097/01.ccm.0000439655.45594.57.

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Tran, Sheri, Rebecca Sell, Ruth Chappell, Sheri Reiakvam, Anushirvan Minokadeh, and Daniel Davis. "522." Critical Care Medicine 41 (December 2013): A127. http://dx.doi.org/10.1097/01.ccm.0000439665.70251.12.

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Tegtmeyer, Ken, Sheryl Bloomer, and Barbara Hagan. "532." Critical Care Medicine 41 (December 2013): A130. http://dx.doi.org/10.1097/01.ccm.0000439675.31240.ab.

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Raisdana, Behnam, and Gus Slotman. "542." Critical Care Medicine 41 (December 2013): A132—A133. http://dx.doi.org/10.1097/01.ccm.0000439785.04944.d2.

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Spaeder, Michael, Jason Custer, Alison Miles, Lisa Razzi, Nicholas Morin, Susanna Scafidi, Melania Bembea, and Xiaoyan Song. "552." Critical Care Medicine 41 (December 2013): A135. http://dx.doi.org/10.1097/01.ccm.0000439794.81179.ae.

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Fitzgerald, Julie, Scott Weiss, Vinay Nadkarni, Jenny Bush, and Neal Thomas. "562." Critical Care Medicine 41 (December 2013): A137. http://dx.doi.org/10.1097/01.ccm.0000439803.96426.12.

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Duffett, Mark, Karen Choong, Lisa Hartling, Kusum Menon, Lehana Thabane, and Deborah Cook. "572." Critical Care Medicine 41 (December 2013): A139—A140. http://dx.doi.org/10.1097/01.ccm.0000439813.13460.c2.

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Schneider, James, Meredith Akerman, Gabrielle Pollack, and Todd Sweberg. "582." Critical Care Medicine 41 (December 2013): A142—A143. http://dx.doi.org/10.1097/01.ccm.0000439823.66825.38.

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Markovitz, Barry, Gerardo Soto-Campos, and Robinder Khemani. "592." Critical Care Medicine 41 (December 2013): A145. http://dx.doi.org/10.1097/01.ccm.0000439833.42993.65.

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Hashemian, Reza, Payam Tabarsi, Hosein Khadem Sadeghi, Seyed Amir Mohajerani, Navid Nooraei, and Hamidreza Jamaati. "502." Critical Care Medicine 42 (December 2014): A1481. http://dx.doi.org/10.1097/01.ccm.0000457999.37518.3c.

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Ammar, Abdalla, Simon Lam, Elizabeth Neuner, Stephanie Bass, Abhijit Duggal, Jorge Guzman, Michael Adams, and Seth Bauer. "512." Critical Care Medicine 42 (December 2014): A1483. http://dx.doi.org/10.1097/01.ccm.0000458009.90883.73.

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MIYAMOTO, KAZUYUKI, Hirokazu Ohtaki, Sachiko Tanaka, Tomoyuki Yamashita, Shunsuke Nakamura, Yasufumi Miyake, Seiji Shioda, and Tohru Aruga. "522." Critical Care Medicine 42 (December 2014): A1485—A1486. http://dx.doi.org/10.1097/01.ccm.0000458019.30788.26.

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rodriguez, Raquel Gutiérrez, Ines Macias Guarasa, and Maria Dolores Arias Verdu. "532." Critical Care Medicine 42 (December 2014): A1488. http://dx.doi.org/10.1097/01.ccm.0000458029.84152.2e.

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Yousef, Khalil, Elizabeth Crago, Thomas Price, Theodore Lagattuta, and Paula Sherwood. "542." Critical Care Medicine 42 (December 2014): A1490. http://dx.doi.org/10.1097/01.ccm.0000458039.63999.a4.

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de la Cruz, J. Salvador, Mitchell Sally, Madhukar Patel, Megan Crutchfield, and Darren Malinoski. "552." Critical Care Medicine 42 (December 2014): A1492—A1493. http://dx.doi.org/10.1097/01.ccm.0000458049.31719.16.

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Tigges, Cody, Alex Fedinec, and Charles Leffler. "562." Critical Care Medicine 42 (December 2014): A1495. http://dx.doi.org/10.1097/01.ccm.0000458059.15579.b0.

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Brockman, Erik, Travis Jackson, C. Dixon, Hulya Bayir, Robert Clark, Li Ma, Carelton Hsia, and Patrick Kochanek. "572." Critical Care Medicine 42 (December 2014): A1497. http://dx.doi.org/10.1097/01.ccm.0000458069.24988.23.

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