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Kurumi Y. Horiuchi - One of the best experts on this subject based on the ideXlab platform.
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Sickling in vitro at venous and arterial oxygen tensions of reticulocytes from patients with sickle cell disease.
Biochemical and Biophysical Research Communications, 1995Co-Authors: A.e. Onyike, K. Ohenefrempong, Kurumi Y. HoriuchiAbstract:Sickling of reticulocytes and mature erythrocytes from patients with sickle cell disease was compared at venous and arterial oxygen tensions (PO2 = 30 and 90 mm Hg). Reticulocyte-rich fractions (d < 1.06) were partially deoxygenated in two ways after incubation at PO2 = 180 mm Hg: (1) PO2 of 30 mm Hg for 1 hour, and Reoxygenation to 90 mm Hg for 2 hours and (2) PO2 of 90 mm Hg and kept for 2 hours. Percentages of sickled cells were always higher (3 - 5 times) in reticulocytes than in mature erythrocytes. Percentage of sickled reticulocytes measured at PO2 = 90 mm Hg after partial deoxygenation to PO2 = 30 mm Hg was 2 times higher than that obtained directly at PO2 = 90 mm Hg. In contrast, there was no difference in percentage of sickled cells in the mature erythrocyte population under the two experimental conditions. These results suggest that reticulocytes are more susceptible to sickling under venous oxygen tension and less likely than mature erythrocytes to resume discoidal shape even at arterial oxygen tension.
Marianne S. Wright - One of the best experts on this subject based on the ideXlab platform.
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Transcriptome profiling of the newborn mouse brain after hypoxia–Reoxygenation: hyperoxic Reoxygenation induces inflammatory and energy failure responsive genes
Pediatric research, 2013Co-Authors: Embjørg J. Wollen, Yngve Sejersted, Marianne S. Wright, Miroslaw Bik-multanowski, Anna Madetko-talowska, Clara-cecilie Günther, Ståle Nygård, Przemko Kwinta, Else Marit Løberg, Martin Bogale YstgaardAbstract:Transcriptome profiling of the newborn mouse brain after hypoxia–Reoxygenation: hyperoxic Reoxygenation induces inflammatory and energy failure responsive genes
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Transcriptome profiling of the newborn mouse lung after hypoxia and Reoxygenation: hyperoxic Reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation.
Pediatric research, 2013Co-Authors: Embjørg J. Wollen, Yngve Sejersted, Marianne S. Wright, Miroslaw Bik-multanowski, Anna Madetko-talowska, Clara-cecilie Günther, Ståle Nygård, Przemko Kwinta, Jacek J Pietrzyk, Ola Didrik SaugstadAbstract:The use of oxygen in acute treatment of asphyxiated term newborns is associated with increased mortality. It is unclear how hyperoxic Reoxygenation after hypoxia affects transcriptional changes in the newborn lung. On postnatal day 7, C57BL/6 mice (n = 62) were randomized to 120-min hypoxia (fraction of inspired oxygen (FiO2) 0.08) or normoxia. The hypoxia group was further randomized to Reoxygenation for 30 min with FiO2 0.21, 0.40, 0.60, or 1.00, and the normoxia group to FiO2 0.21 or 1.00. Transcriptome profiling was performed on homogenized lung tissue using the Affymetrix 750k expression array, and validation was carried out by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The hypoxia–Reoxygenation model induced hypoxia-inducible factor 1 (HIF-1) targets like Vegfc, Adm, and Aqp1. In total, ~70% of the significantly differentially expressed genes were detected in the two high hyperoxic groups (FiO2 0.60 and 1.00). Reoxygenation with 100% oxygen after hypoxia uniquely upregulated Gadd45g, Dusp1, Peg3, and Tgm2. Pathway analysis identified mammalian target of rapamycin (mTOR) signaling pathway, DNA repair, c-jun N-terminal kinase (JNK)-pathway regulation, and cell cycle after hyperoxic Reoxygenation was applied. Acute hypoxia induces HIF-1 targets independent of the Reoxygenation regime applied. Hyperoxic Reoxygenation affects pathways regulating cell growth and survival. DNA-damage–responsive genes are restricted to Reoxygenation with 100% oxygen.
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Acidosis has opposite effects on neuronal survival during hypoxia and Reoxygenation.
Journal of neurochemistry, 2003Co-Authors: Runar Almaas, Julie K. Lindstad, Marianne S. Wright, Ola Didrik Saugstad, Morten Pytte, David E Pleasure, Terje RootweltAbstract:To study the effect of extracellular acidosis on apoptosis and necrosis during ischemia and Reoxygenation, we exposed human post-mitotic NT2-N neurones to oxygen and glucose deprivation (OGD) followed by Reoxygenation. In some experiments, pH of the cell medium was lowered to 5.9 during either OGD or Reoxygenation or both. Staurosporine, used as a positive control for apoptosis, caused Poly(ADP-ribose)-polymerase (PARP) cleavage and nuclear fragmentation, but no PARP cleavage and little fragmentation were seen after OGD. Low molecular weight DNA fragments were found after staurosporine treatment, but not after OGD. No protective effect of caspase inhibitors was seen after 3 h of OGD and 21 h of Reoxygenation, but after 45 h of Reoxygenation caspase inhibition induced a modest improvement in 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) cleavage. While acidosis during OGD accompanied by neutral medium during Reoxygenation protected the neurones (MTT: 228 ± 117% of neutral medium, p
H. De Groot - One of the best experts on this subject based on the ideXlab platform.
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O2-. release by activated Kupffer cells upon hypoxia-Reoxygenation
American Journal of Physiology-Gastrointestinal and Liver Physiology, 1991Co-Authors: B. Rymsa, Ji-feng Wang, H. De GrootAbstract:Primary cultures of rat liver Kupffer cells generated large amounts of superoxide anion radical (O2-.) when subjected to Reoxygenation after a hypoxic period of at least 2 h. O2-. formation reached its maximum rate of approximately 25 nmol/10(6) cells within 1 h after Reoxygenation. Two to four hours after Reoxygenation, the number of injured cells began to increase and after 10 h approximately 60% of the cells were dead. During the period of O2-. release no significant difference in cell viability was observed between reoxygenated and hypoxically incubated cells, indicating a distinct time lag between O2-. release and onset of cell damage. Addition of diphenyliodonium, a specific inhibitor of the neutrophilic NADPH oxidase, to the Kupffer cells just before Reoxygenation diminished both O2-. formation and cell injury up to 70%. Reoxygenation injury was completely prevented when superoxide dismutase and catalase were added immediately before Reoxygenation. The results indicate that Kupffer cells subjected to hypoxia-Reoxygenation generate a burst of reactive oxygen species and that this kind of "activation," probably by activating the NADPH oxidase, contributes to the self-destruction of the cells.
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Hypoxia/Reoxygenation injury in liver: Kupffer cells are much more vulnerable to Reoxygenation than to hypoxia.
Research communications in chemical pathology and pharmacology, 1990Co-Authors: B. Rymsa, H. D. Becker, W. Lauchart, H. De GrootAbstract:Cell injury due to hypoxia and Reoxygenation was studied in primary cultured rat Kupffer cells. Under hypoxic conditions only 20% of the cells had lost their viability after 12 h of incubation. In contrast, almost complete losses of cell viability were observed when Reoxygenation was performed after 2, 4 or 6 h of hypoxia. The time-course of Reoxygenation injury in Kupffer cells was characterized by a lag phase of 2 h during which no difference between reoxygenated and hypoxically incubated cells was apparent; during the next 4 h, there was an increase of up to 100% in the amount of nonviable cells in the reoxygenated cultures. These results indicate that Kupffer cells were much more vulnerable to Reoxygenation than to hypoxia. The time-course of cell damage upon hypoxia/Reoxygenation may indicate a self-destruction mechanism caused by an oxygen-triggered activation of these cells.
L’ubica Derková - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of hippocampal Reoxygenation injury. Treatment with antioxidants
Neuropharmacology, 1997Co-Authors: Lubica Horakova, Svorad Štolc, Z Chromíková, A Pekárová, L’ubica DerkováAbstract:Abstract The effects of hypoxia of different durations (8, 12 or 15 min) and of subsequent Reoxygenation were studied in rat hippocampal slices by measuring enzyme activities related to oxidative stress: superoxide dismutase (SOD), cytochrome c oxidase and lactate dehydrogenase (LDH). Simultaneously the degree of lipid peroxidation was estimated by measuring conjugated dienes (CD). Reoxygenation after 8-min of hypoxia induced general cell injury indicated by increased LDH activity. Reoxygenation after 12-min of hypoxia started lipid peroxidation assessed by an increase in CD, and after 15-min of hypoxia followed by Reoxygenation CD were found to be significantly decreased, suggesting lipid degradation. The injury induced by a hypoxia of 12 min and Reoxygenation was reduced by SOD and catalase, indicating that oxygen radicals were involved in this process. The oxygen radicals originated from the xanthine/xanthine oxidase system, from the synthesis of prostaglandins, as well as from the mitochondrial respiratory chain, since allopurinol, indomethacin and rotenone decreased while antimycin increased Reoxygenation injury. An increase in ATP may also have been involved as cyanide, an inhibitor of ATP synthesis, decreased the Reoxygenation injury. The chain-breaking antioxidants trolox, alpha tocopherol and the pyridoindole stobadine were effective in preventing Reoxygenation injury, indicating the involvement of lipid peroxidation in this process. © 1997 Elsevier Science Ltd. All rights reserved.
Embjørg J. Wollen - One of the best experts on this subject based on the ideXlab platform.
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Transcriptome profiling of the newborn mouse brain after hypoxia–Reoxygenation: hyperoxic Reoxygenation induces inflammatory and energy failure responsive genes
Pediatric research, 2013Co-Authors: Embjørg J. Wollen, Yngve Sejersted, Marianne S. Wright, Miroslaw Bik-multanowski, Anna Madetko-talowska, Clara-cecilie Günther, Ståle Nygård, Przemko Kwinta, Else Marit Løberg, Martin Bogale YstgaardAbstract:Transcriptome profiling of the newborn mouse brain after hypoxia–Reoxygenation: hyperoxic Reoxygenation induces inflammatory and energy failure responsive genes
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Transcriptome profiling of the newborn mouse lung after hypoxia and Reoxygenation: hyperoxic Reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation.
Pediatric research, 2013Co-Authors: Embjørg J. Wollen, Yngve Sejersted, Marianne S. Wright, Miroslaw Bik-multanowski, Anna Madetko-talowska, Clara-cecilie Günther, Ståle Nygård, Przemko Kwinta, Jacek J Pietrzyk, Ola Didrik SaugstadAbstract:The use of oxygen in acute treatment of asphyxiated term newborns is associated with increased mortality. It is unclear how hyperoxic Reoxygenation after hypoxia affects transcriptional changes in the newborn lung. On postnatal day 7, C57BL/6 mice (n = 62) were randomized to 120-min hypoxia (fraction of inspired oxygen (FiO2) 0.08) or normoxia. The hypoxia group was further randomized to Reoxygenation for 30 min with FiO2 0.21, 0.40, 0.60, or 1.00, and the normoxia group to FiO2 0.21 or 1.00. Transcriptome profiling was performed on homogenized lung tissue using the Affymetrix 750k expression array, and validation was carried out by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The hypoxia–Reoxygenation model induced hypoxia-inducible factor 1 (HIF-1) targets like Vegfc, Adm, and Aqp1. In total, ~70% of the significantly differentially expressed genes were detected in the two high hyperoxic groups (FiO2 0.60 and 1.00). Reoxygenation with 100% oxygen after hypoxia uniquely upregulated Gadd45g, Dusp1, Peg3, and Tgm2. Pathway analysis identified mammalian target of rapamycin (mTOR) signaling pathway, DNA repair, c-jun N-terminal kinase (JNK)-pathway regulation, and cell cycle after hyperoxic Reoxygenation was applied. Acute hypoxia induces HIF-1 targets independent of the Reoxygenation regime applied. Hyperoxic Reoxygenation affects pathways regulating cell growth and survival. DNA-damage–responsive genes are restricted to Reoxygenation with 100% oxygen.
