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Plasma VAP-1/SSAO Activity Predicts Intracranial Hemorrhages and Adverse Neurological Outcome After Tissue Plasminogen Activator Treatment in Stroke by Mar Hernandez-Guillamon, Lidia Garcia-Bonilla, Montse Solé, Victoria Sosti, Mireia Parés, Mireia Campos, Arantxa Ortega-Aznar, Carmen Domínguez, Marta Rubiera, Marc Ribó, Manolo Quintana, Carlos A. Molina, José Alvarez-Sabín, Anna Rosell, Mercedes Unzeta, and Joan Montaner Stroke Volume 41(7): July 1, 2010 Copyright © American Heart Association, Inc. All rights reserved.
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Figure I. VAP-1/SSAO activity in healthy controls (n=30) and stroke patients (n=140) upon arrival to the emergency department (within 3 h). Figure I. VAP-1/SSAO activity in healthy controls (n=30) and stroke patients (n=140) upon arrival to the emergency department (within 3 h). Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure 1. A, VAP-1/SSAO activity according to the presence of HT (B) and main HT subtypes of patterns. Figure 1. A, VAP-1/SSAO activity according to the presence of HT (B) and main HT subtypes of patterns. C, Baseline VAP-1/SSAO activity relates to all CT-based HT subtypes. Broken line indicates the reference interval for healthy controls. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure 2. Plasma VAP-1/SSAO activity temporal profile according to HT presence or absence after stroke. Figure 2. Plasma VAP-1/SSAO activity temporal profile according to HT presence or absence after stroke. Broken line indicates the reference interval for healthy controls. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure 3. Neurological outcome was determined in the acute phase (48 hours).
Figure 3. Neurological outcome was determined in the acute phase (48 hours). Broken line indicates the reference interval for healthy controls. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure 4. Representative brain VAP-1/SSAO immunostaining of a patient with stroke who had an HT; infarcted areas (A, C) compared with the corresponding contralateral (B; A–B bars=50 μm; C bar=10 μm). Figure 4. Representative brain VAP-1/SSAO immunostaining of a patient with stroke who had an HT; infarcted areas (A, C) compared with the corresponding contralateral (B; A–B bars=50 μm; C bar=10 μm). D, VAP-1/SSAO activity in infarcted areas (I) of human brain homogenates compared with contralateral areas (CL) or healthy control subjects. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure II. Plasma VAP-1/SSAO activity of ischemic rats treated with delayed-tPA and saline or semicarbazide. Figure II. Plasma VAP-1/SSAO activity of ischemic rats treated with delayed-tPA and saline or semicarbazide. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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Figure 5. A, Infarct volume of rats treated with tPA at 2, 3, or 4 hours after clot embolism.
Figure 5. A, Infarct volume of rats treated with tPA at 2, 3, or 4 hours after clot embolism. B, Infarct volume of ischemic rats cotreated with delayed tPA and either saline or semicarbazide. C, Representative images of 2–3-5-triphenyl tetrazolium chloride staining, (D) mortality rate, and (E) systemic bleeding. Mar Hernandez-Guillamon et al. Stroke. 2010;41: Copyright © American Heart Association, Inc. All rights reserved.
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