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Bo K Siesjo - One of the best experts on this subject based on the ideXlab platform.
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CHANGES IN PYRUVATE DEHYDROGENASE COMPLEX ACTIVITY DURING AND FOLLOWING SEVERE INSULIN-INDUCED HYPOGLYCEMIA
Journal of Cerebral Blood Flow and Metabolism, 2016Co-Authors: Monika Cardell, Bo K Siesjo, Tadeusz WielochAbstract:The effect of severe insulin-induced hypoglycemia on the activity of the pyruvate dehydrogenase enzyme complex (PDHC) was investigated in homogenates of frozen rat cerebral cortex during burst suppression EEG, after 10, 30, and 60 min of isoelectric EEG, and after 30 and 180 min and 24 h of recovery following 30 min of Hypoglycemic Coma. Changes in PDHC activity were correlated to levels of labile organic phosphates and glycolytic metabolites. In cortex from control animals, the rate of [1-14C]pyruvate decarboxylation was 7.1 ± 1.3 U/mg of protein, or 35% of the total PDHC activity. The activity was unchanged during burst suppression EEG whereas the active fraction increased to 81-87% during Hypoglycemic Coma. Thirty minutes after glucose-induced recovery, the PDHC activity had decreased by 33% compared to control levels, and remained significantly depressed after 3 h of recovery. This decrease in activity was not due to a decrease in the total PDHC activity. At 24 h of recovery, PDHC activity had returned to control levels. We conclude that the activation of PDHC during Hypoglycemic Coma is probably the result of an increased PDH phosphatase activity following depolarization and calcium influx, and allosteric inhibition of PDH kinase due to increased ADP/ATP ratio. The depression of PDHC activity following Hypoglycemic Coma is probably due to an increased phosphorylation of the enzyme, as a consequence of an imbalance between PDH phosphatase and kinase activities. Since some reduction of the ATP/ADP ratio persisted and since the lactate pyruvate ratio had normalized by 3 h of recovery, the depression of PDHC most likely reflects a decrease in PDH phosphatase activity, probably due to a decrease in intramitochondrial Ca2+. (Less)
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alteration of cyclic adenosine monophosphate response element binding protein in rat brain after Hypoglycemic Coma
Journal of Cerebral Blood Flow and Metabolism, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:In the current study, the temporal and regional changes of the transcription factor cyclic adenosine monophosphate response element binding protein (CREB) were investigated in rat brains subjected to 30 minutes of Hypoglycemic Coma followed by varied periods of recovery using Western blot and confocal microscopy. The total amount of CREB was not altered in any area examined after Coma. The level of the phosphorylated form of CREB decreased during Coma but rebounded after recovery. In the relatively resistant areas, such as the inner layers of the neocortex and the inner and outer blades of the dentate gyrus (DG), phospho-CREB increased greater than the control level after 30 minutes of recovery and continued to increase up to 3 hours of recovery. In contrast, little or no increase of phospho-CREB was observed during the recovery period in the outer layers of the neocortex and at the tip of the DG, that is, regions that are selectively vulnerable to Hypoglycemic insults. The current findings suggest that a neuroprotective signaling pathway may be more activated in the resistant regions than in the vulnerable ones after Hypoglycemic Coma.
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differential phosphorylation at ser473 and thr308 of akt 1 in rat brain following Hypoglycemic Coma
Brain Research, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:Abstract We analyzed both total Akt-1 and phosphorylation of Akt-1 at residues Ser473 and Thr308 (phospho-Akt-1 Ser474 and phospho-Akt-1 Thr308 , respectively) in the outer and inner layers of cortex following 30 min of Hypoglycemic Coma by Western blot analyses and confocal microscopy. The total amount of Akt-1 was not altered in any area examined. Phospho-Akt-1 Ser474 , however, increased significantly in both layers of cortex at 0 and 30 min of recovery, but returned to control level at 3 h of recovery. In the vulnerable area (outer layer of cortex), no upregulation of phospho-Akt-1 Thr308 was observed at any time points examined. In the resistant area like inner layer of cortex, however, phospho-Akt-1 Thr308 was significantly over the control level at 3 h of recovery. Confocal microscopy result indicates that most of phospho-Akt-1 Thr308 had already moved into nucleus at 3 h of recovery. Our results suggest that Akt-1, when phosphorlyted at Thr308, may play a protective role for neurons in the resistant regions of the brain.
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is neuronal injury caused by Hypoglycemic Coma of the necrotic or apoptotic type
Neurochemical Research, 2000Co-Authors: Yi Bing Ouyang, Qingping He, Pingan Li, Shorena Janelidze, Guixia Wang, Bo K SiesjoAbstract:In this study, we explored if a 30 minute period of Hypoglycemic Coma yields damage which shows some features associated with apoptosis. To that end, we induced insulin-Hypoglycemic Coma of 30 min duration, and studied brain tissues after the Coma period, and after recovery period of 30 min, 3 h, and 6 h. Histopathological data confirmed neuronal damage in all of the vulnerable neuronal populations. Release of cytochrome c (cyt c), assessed by Western Blot, was observed in the neocortex and caudoputamen after 3 and 6 h of recovery. In these regions, the caspase-like activity increased above control after 6 h of recovery. By laser-scanning confocal microscopy, a clear expression of Bax was observed after 30 min of Coma in the superficial layers of the neocortex, reaching a peak after 30 min of recovery. Punctuate immunolabeling surrounding nuclei in soma and dendrites in cortical pyramidal neurons likely represents mitochondria, which suggests that Bax protein assembled at the surface of mitochondria in vulnerable neocortical neurons. It is concluded that although previous morphological data have suggested that cells die by necrosis, neuronal damage after Hypoglycemic Coma shows some features of apoptosis.
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influence of Hypoglycemic Coma on brain water and osmolality
Experimental Brain Research, 1998Co-Authors: Lars Gisselsson, Majlis Smith, Bo K SiesjoAbstract:To study the effects of pronounced hypoglycemia on brain osmolality and brain edema formation, fasted rats were rendered Hypoglycemic by injection of insulin, and subjected to 30 min of Hypoglycemic Coma. Recovery was accomplished by glucose administration. The change in water content in different brain regions was measured as a change in specific gravity after 30 min of Hypoglycemic Coma, or 30, 60, and 180 min after glucose administration. Plasma and brain tissue osmolality were measured in separate animals. The results show a significant decrease in specific gravity (increase in water content) in all structures measured (caudoputamen, neocortex, hippocampus, and cerebellum) at the end of the period of Coma, as well as after 30 min and 60 min of recovery. At 180 min of recovery, brain water was normalized. The edema affected all structures to the same degree regardless of their vulnerability to Hypoglycemic damage. Brain tissue osmolality showed a tendency to decrease with decreasing tissue glucose content. The decrease was significant (P<0.01) at 30 min of isoelectric Coma. In the recovery phase, normal brain osmolality was restored within 30 min. Measurements of blood-brain barrier (BBB) permeability after 30 min of Hypoglycemic Coma showed no extravasation of Evan’s blue, though a small but significant increase in the permeability for aminoisobutyric acid (AIB) in caudoputamen and in cerebellum was found. To analyze the importance of tissue acidosis for formation of edema, Hypoglycemic animals were made acidotic by increasing the CO2 concentration in inspired air to produce an arterial plasma pH of 6.8–6.9. In these animals the edema was of a similar degree to the normocapnic animals, and the permeability for AIB was normal. We conclude that osmolytic mechanisms are not the primary cause of the selective neuronal vulnerability in Hypoglycemic Coma. Furthermore, the BBB is largely intact during a Hypoglycemic insult.
Bing Ren Hu - One of the best experts on this subject based on the ideXlab platform.
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protein ubiquitination in rat brain following Hypoglycemic Coma
Neuroscience Letters, 2001Co-Authors: Yi Bing Ouyang, Bing Ren HuAbstract:Hypoglycemic Coma of 30 min duration selectively damages CA1 pyramidal neurons and the crest of dentate gyrus (DG) granule cells in hippocampus. Here, we show by high-resolution confocal microscopy and biochemical analysis that 30 min of Hypoglycemic Coma induces the ubiquitination and aggregation of several proteins in rat brain tissues. Protein ubiquitination and aggregation occurred in the CA1 and DG regions as early as the end of 30 min of Hypoglycemic Coma and lasted until neuronal death in the late recovery period after hypoglycemia. In comparison, the neurons surviving hypoglycemia were less affected. On western blots, ubiquitinated proteins (ubi-proteins) were present mainly in Triton-insoluble pellets, indicating that they are irreversibly aggregated. We conclude that proteins are ubiquitinated and aggregated in neurons after hypoglycemia prior to their death. We hypothesize that protein ubiquitination and aggregation may contribute to neuronal damage after hypoglycemia.
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alteration of cyclic adenosine monophosphate response element binding protein in rat brain after Hypoglycemic Coma
Journal of Cerebral Blood Flow and Metabolism, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:In the current study, the temporal and regional changes of the transcription factor cyclic adenosine monophosphate response element binding protein (CREB) were investigated in rat brains subjected to 30 minutes of Hypoglycemic Coma followed by varied periods of recovery using Western blot and confocal microscopy. The total amount of CREB was not altered in any area examined after Coma. The level of the phosphorylated form of CREB decreased during Coma but rebounded after recovery. In the relatively resistant areas, such as the inner layers of the neocortex and the inner and outer blades of the dentate gyrus (DG), phospho-CREB increased greater than the control level after 30 minutes of recovery and continued to increase up to 3 hours of recovery. In contrast, little or no increase of phospho-CREB was observed during the recovery period in the outer layers of the neocortex and at the tip of the DG, that is, regions that are selectively vulnerable to Hypoglycemic insults. The current findings suggest that a neuroprotective signaling pathway may be more activated in the resistant regions than in the vulnerable ones after Hypoglycemic Coma.
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differential phosphorylation at ser473 and thr308 of akt 1 in rat brain following Hypoglycemic Coma
Brain Research, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:Abstract We analyzed both total Akt-1 and phosphorylation of Akt-1 at residues Ser473 and Thr308 (phospho-Akt-1 Ser474 and phospho-Akt-1 Thr308 , respectively) in the outer and inner layers of cortex following 30 min of Hypoglycemic Coma by Western blot analyses and confocal microscopy. The total amount of Akt-1 was not altered in any area examined. Phospho-Akt-1 Ser474 , however, increased significantly in both layers of cortex at 0 and 30 min of recovery, but returned to control level at 3 h of recovery. In the vulnerable area (outer layer of cortex), no upregulation of phospho-Akt-1 Thr308 was observed at any time points examined. In the resistant area like inner layer of cortex, however, phospho-Akt-1 Thr308 was significantly over the control level at 3 h of recovery. Confocal microscopy result indicates that most of phospho-Akt-1 Thr308 had already moved into nucleus at 3 h of recovery. Our results suggest that Akt-1, when phosphorlyted at Thr308, may play a protective role for neurons in the resistant regions of the brain.
Yi Bing Ouyang - One of the best experts on this subject based on the ideXlab platform.
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protein ubiquitination in rat brain following Hypoglycemic Coma
Neuroscience Letters, 2001Co-Authors: Yi Bing Ouyang, Bing Ren HuAbstract:Hypoglycemic Coma of 30 min duration selectively damages CA1 pyramidal neurons and the crest of dentate gyrus (DG) granule cells in hippocampus. Here, we show by high-resolution confocal microscopy and biochemical analysis that 30 min of Hypoglycemic Coma induces the ubiquitination and aggregation of several proteins in rat brain tissues. Protein ubiquitination and aggregation occurred in the CA1 and DG regions as early as the end of 30 min of Hypoglycemic Coma and lasted until neuronal death in the late recovery period after hypoglycemia. In comparison, the neurons surviving hypoglycemia were less affected. On western blots, ubiquitinated proteins (ubi-proteins) were present mainly in Triton-insoluble pellets, indicating that they are irreversibly aggregated. We conclude that proteins are ubiquitinated and aggregated in neurons after hypoglycemia prior to their death. We hypothesize that protein ubiquitination and aggregation may contribute to neuronal damage after hypoglycemia.
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alteration of cyclic adenosine monophosphate response element binding protein in rat brain after Hypoglycemic Coma
Journal of Cerebral Blood Flow and Metabolism, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:In the current study, the temporal and regional changes of the transcription factor cyclic adenosine monophosphate response element binding protein (CREB) were investigated in rat brains subjected to 30 minutes of Hypoglycemic Coma followed by varied periods of recovery using Western blot and confocal microscopy. The total amount of CREB was not altered in any area examined after Coma. The level of the phosphorylated form of CREB decreased during Coma but rebounded after recovery. In the relatively resistant areas, such as the inner layers of the neocortex and the inner and outer blades of the dentate gyrus (DG), phospho-CREB increased greater than the control level after 30 minutes of recovery and continued to increase up to 3 hours of recovery. In contrast, little or no increase of phospho-CREB was observed during the recovery period in the outer layers of the neocortex and at the tip of the DG, that is, regions that are selectively vulnerable to Hypoglycemic insults. The current findings suggest that a neuroprotective signaling pathway may be more activated in the resistant regions than in the vulnerable ones after Hypoglycemic Coma.
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differential phosphorylation at ser473 and thr308 of akt 1 in rat brain following Hypoglycemic Coma
Brain Research, 2000Co-Authors: Yi Bing Ouyang, Bo K Siesjo, Qingping He, Guixia Wang, Xiaohu Zhang, Bing Ren HuAbstract:Abstract We analyzed both total Akt-1 and phosphorylation of Akt-1 at residues Ser473 and Thr308 (phospho-Akt-1 Ser474 and phospho-Akt-1 Thr308 , respectively) in the outer and inner layers of cortex following 30 min of Hypoglycemic Coma by Western blot analyses and confocal microscopy. The total amount of Akt-1 was not altered in any area examined. Phospho-Akt-1 Ser474 , however, increased significantly in both layers of cortex at 0 and 30 min of recovery, but returned to control level at 3 h of recovery. In the vulnerable area (outer layer of cortex), no upregulation of phospho-Akt-1 Thr308 was observed at any time points examined. In the resistant area like inner layer of cortex, however, phospho-Akt-1 Thr308 was significantly over the control level at 3 h of recovery. Confocal microscopy result indicates that most of phospho-Akt-1 Thr308 had already moved into nucleus at 3 h of recovery. Our results suggest that Akt-1, when phosphorlyted at Thr308, may play a protective role for neurons in the resistant regions of the brain.
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is neuronal injury caused by Hypoglycemic Coma of the necrotic or apoptotic type
Neurochemical Research, 2000Co-Authors: Yi Bing Ouyang, Qingping He, Pingan Li, Shorena Janelidze, Guixia Wang, Bo K SiesjoAbstract:In this study, we explored if a 30 minute period of Hypoglycemic Coma yields damage which shows some features associated with apoptosis. To that end, we induced insulin-Hypoglycemic Coma of 30 min duration, and studied brain tissues after the Coma period, and after recovery period of 30 min, 3 h, and 6 h. Histopathological data confirmed neuronal damage in all of the vulnerable neuronal populations. Release of cytochrome c (cyt c), assessed by Western Blot, was observed in the neocortex and caudoputamen after 3 and 6 h of recovery. In these regions, the caspase-like activity increased above control after 6 h of recovery. By laser-scanning confocal microscopy, a clear expression of Bax was observed after 30 min of Coma in the superficial layers of the neocortex, reaching a peak after 30 min of recovery. Punctuate immunolabeling surrounding nuclei in soma and dendrites in cortical pyramidal neurons likely represents mitochondria, which suggests that Bax protein assembled at the surface of mitochondria in vulnerable neocortical neurons. It is concluded that although previous morphological data have suggested that cells die by necrosis, neuronal damage after Hypoglycemic Coma shows some features of apoptosis.
Sergio Fanconi - One of the best experts on this subject based on the ideXlab platform.
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adrenal crisis presenting as Hypoglycemic Coma
Intensive Care Medicine, 2000Co-Authors: Joachim E Fischer, T Stallmach, Sergio FanconiAbstract:An 18-month-old male infant presented with Hypoglycemic Coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. Plasma levels of ACTH and cortisol remained undetectable. Renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. Intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.
Erino A Rendina - One of the best experts on this subject based on the ideXlab platform.
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the evolution of a pleural nodule into a giant fibrous tumor associated with Hypoglycemic Coma
European Journal of Cardio-Thoracic Surgery, 2007Co-Authors: Antonio Dandrilli, Claudio Andreetti, Mohsen Ibrahim, Erino A RendinaAbstract:We hereby present the exceptional case of Hypoglycemic Coma associated with a giant benign localized fibrous tumor of the pleura (LFTP). A 79-year-old woman was found to have a small peripheral nodular lesion in the right hemithorax 7 years ago. A fine needle aspiration biopsy provided a diagnosis of LFTP, but the patient refused surgery. Six years later Hypoglycemic Coma and respiratory insufficiency appeared in association with a giant mass completely filling the right chest and shifting the mediastinum contralaterally. The tumor was completely resected, and complete relief of the Hypoglycemic and respiratory symptoms was achieved. The patient is in good metabolic and respiratory conditions and disease-free 14 months after the operation.