The Experts below are selected from a list of 306 Experts worldwide ranked by ideXlab platform
Robert C Vannucci - One of the best experts on this subject based on the ideXlab platform.
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rat model of perinatal hypoxic ischemic Brain Damage
Journal of Neuroscience Research, 1999Co-Authors: Robert C Vannucci, Javad Towfighi, James R Connor, David T Mauger, C Palmer, Michael B Smith, Susan J VannucciAbstract:To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic Brain Damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces permanent hypoxic-ischemic Brain Damage limited to the cerebral hemisphere ipsilateral to the carotid artery occlusion. The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia. Future research will focus on molecular mechanisms of neuronal injury with a continuing focus on therapeutic strategies to prevent or minimize hypoxic-ischemic Brain Damage.
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a model of perinatal hypoxic ischemic Brain Damage
Annals of the New York Academy of Sciences, 1997Co-Authors: Robert C Vannucci, Susan J VannucciAbstract:In conclusion, our immature rat model has gained wide acceptance as the animal model of choice to study basic physiologic, biochemical, and molecular mechanisms of perinatal hypoxic-ischemic Brain Damage. In addition, the model has been used extensively to study those physiologic and therapeutic variables which either are deleterious or beneficial to the perinatal Brain undergoing hypoxia-ischemia. As therapeutic interventions are tested in the animal setting, the results will provide important information regarding the effect of these agents in the human setting.
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measuring the accentuation of the Brain Damage that arises from perinatal cerebral hypoxia ischemia
Neonatology, 1997Co-Authors: Robert C Vannucci, Anthony Rossini, Javad Towfighi, Susan J VannucciAbstract:To ascertain the manner in which the severity of perinatal Brain Damage occurs as a result of hypoxia-ischemia, 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed thereafter by exposure to 8% oxygen for up to 2.5 h. Following the hypoxic-ischemic exposure, the rat pups were reared with their dams until 30 days of postnatal age, at which time their Brains underwent pathologic analysis. The severity of Brain Damage at each of four specific intervals of hypoxia-ischemia was determined and statistically compared by linear polynomial and nonparametric regression procedures. The data indicated that the accentuation of Brain Damage with increasing duration of hypoxia-ischemia was linear rather than curvilinear.
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cerebral carbohydrate and energy metabolism in perinatal hypoxic ischemic Brain Damage
Brain Pathology, 1992Co-Authors: Robert C VannucciAbstract:Cerebral hypoxia-ischemia remains a major cause of acute perinatal Brain injury. Research in experimental animals over the past decade has greatly expanded our knowledge of those oxidative events which occur during a hypoxic-ischemic insult to the Brain, as well as those metabolic alterations which evolve during the recovery period following resuscitation. The available evidence suggests that hypoxia alone does not lead to Brain Damage, but rather a combination of hypoxia-ischemia or isolated cerebral ischemia is a necessary prerequisite for tissue injury to occur. Furthermore, hypoxia-ischemia severe enough to produce irreversible tissue injury is always associated with major perturbations in the energy status of the perinatal Brain which persists well into the recovery period. The lingering energy depletion sets in motion a cascade of biochemical alterations that are initiated during the course of the insult and proceed well into the recovery period to culminate in either neuronal necrosis or infarction. Unlike the adult, where glucose supplementation prior to or during hypoxia-ischemia accentuates tissue injury, glucose treatment of perinatal animals subjected to a similar insult substantially reduces the extent of tissue injury. The mechanism for the age-specific effect of glucose on hypoxic-ischemic Brain Damage is discussed in relation to pathogenetic mechanisms responsible for the occurrence of permanent Brain Damage.
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glucose lactic acid and perinatal hypoxic ischemic Brain Damage
Pediatric Neurology, 1992Co-Authors: Robert C Vannucci, Jerome Y YagerAbstract:Investigations suggest that hyperglycemia, superimposed on hypoxia-ischemia or cerebral ischemia, accentuates Brain Damage in adult experimental animals and humans, but not in immature animals. Fundamental differences in the immature and adult Brain, which account for the age-specific paradox, are discussed. Based on currently available data, we recommend that glucose supplementation not be curtailed during labor and delivery of asphyxiated human infants; on the contrary, glucose therapy may substantially reduce hypoxic-ischemic Brain Damage.
Susan J Vannucci - One of the best experts on this subject based on the ideXlab platform.
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rat model of perinatal hypoxic ischemic Brain Damage
Journal of Neuroscience Research, 1999Co-Authors: Robert C Vannucci, Javad Towfighi, James R Connor, David T Mauger, C Palmer, Michael B Smith, Susan J VannucciAbstract:To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic Brain Damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces permanent hypoxic-ischemic Brain Damage limited to the cerebral hemisphere ipsilateral to the carotid artery occlusion. The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia. Future research will focus on molecular mechanisms of neuronal injury with a continuing focus on therapeutic strategies to prevent or minimize hypoxic-ischemic Brain Damage.
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a model of perinatal hypoxic ischemic Brain Damage
Annals of the New York Academy of Sciences, 1997Co-Authors: Robert C Vannucci, Susan J VannucciAbstract:In conclusion, our immature rat model has gained wide acceptance as the animal model of choice to study basic physiologic, biochemical, and molecular mechanisms of perinatal hypoxic-ischemic Brain Damage. In addition, the model has been used extensively to study those physiologic and therapeutic variables which either are deleterious or beneficial to the perinatal Brain undergoing hypoxia-ischemia. As therapeutic interventions are tested in the animal setting, the results will provide important information regarding the effect of these agents in the human setting.
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measuring the accentuation of the Brain Damage that arises from perinatal cerebral hypoxia ischemia
Neonatology, 1997Co-Authors: Robert C Vannucci, Anthony Rossini, Javad Towfighi, Susan J VannucciAbstract:To ascertain the manner in which the severity of perinatal Brain Damage occurs as a result of hypoxia-ischemia, 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed thereafter by exposure to 8% oxygen for up to 2.5 h. Following the hypoxic-ischemic exposure, the rat pups were reared with their dams until 30 days of postnatal age, at which time their Brains underwent pathologic analysis. The severity of Brain Damage at each of four specific intervals of hypoxia-ischemia was determined and statistically compared by linear polynomial and nonparametric regression procedures. The data indicated that the accentuation of Brain Damage with increasing duration of hypoxia-ischemia was linear rather than curvilinear.
Clive Harper - One of the best experts on this subject based on the ideXlab platform.
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The neuropathology of alcohol-related Brain Damage
Alcohol and Alcoholism, 2009Co-Authors: Clive HarperAbstract:Excessive alcohol use can cause structural and functional abnormalities of the Brain and this has significant health, social and economic implications for most countries in the world. Even heavy social drinkers who have no specific neurological or hepatic problems show signs of regional Brain Damage and cognitive dysfunction. Changes are more severe and other Brain regions are Damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke-Korsakoff syndrome). Quantitative studies and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the Damage are not understood. A human Brain bank targeting alcohol cases has been established in Sydney, Australia, and tissues can be used for structural and molecular studies and to test hypotheses developed from animal models and in vivo studies. The recognition of potentially reversible changes and preventative medical approaches are important public health issues.
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ethanol and Brain Damage
Current Opinion in Pharmacology, 2005Co-Authors: Clive Harper, Izuru MatsumotoAbstract:It is now well established that even uncomplicated alcoholics who have no specific neurological or hepatic problems show signs of regional Brain Damage and cognitive dysfunction. Improvements in neuroimaging technology, magnetic resonance imaging, magnetic resonance spectroscopy and positron emission tomography have contributed significantly, revealing alcoholic-specific changes in the CNS associated with neuropsychological abnormalities. Although greater efforts are needed, a human Brain bank specifically targeting alcohol cases is now able to provide fresh and frozen tissue for alcohol researchers. These tissues can be used to test hypotheses developed using animal models and/or in vitro studies. The aim is to delineate mechanisms underlying alcohol-related Brain Damage in humans. The development of high-throughput, non-hypothesis-driven approaches using DNA microarrays and proteomics might also provide clues to this important problem.
Javad Towfighi - One of the best experts on this subject based on the ideXlab platform.
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rat model of perinatal hypoxic ischemic Brain Damage
Journal of Neuroscience Research, 1999Co-Authors: Robert C Vannucci, Javad Towfighi, James R Connor, David T Mauger, C Palmer, Michael B Smith, Susan J VannucciAbstract:To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic Brain Damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces permanent hypoxic-ischemic Brain Damage limited to the cerebral hemisphere ipsilateral to the carotid artery occlusion. The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia. Future research will focus on molecular mechanisms of neuronal injury with a continuing focus on therapeutic strategies to prevent or minimize hypoxic-ischemic Brain Damage.
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measuring the accentuation of the Brain Damage that arises from perinatal cerebral hypoxia ischemia
Neonatology, 1997Co-Authors: Robert C Vannucci, Anthony Rossini, Javad Towfighi, Susan J VannucciAbstract:To ascertain the manner in which the severity of perinatal Brain Damage occurs as a result of hypoxia-ischemia, 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed thereafter by exposure to 8% oxygen for up to 2.5 h. Following the hypoxic-ischemic exposure, the rat pups were reared with their dams until 30 days of postnatal age, at which time their Brains underwent pathologic analysis. The severity of Brain Damage at each of four specific intervals of hypoxia-ischemia was determined and statistically compared by linear polynomial and nonparametric regression procedures. The data indicated that the accentuation of Brain Damage with increasing duration of hypoxia-ischemia was linear rather than curvilinear.
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effect of insulin induced and fasting hypoglycemia on perinatal hypoxic ischemic Brain Damage
Pediatric Research, 1992Co-Authors: Jerome Y Yager, Javad Towfighi, Daniel F Heitjan, Robert C VannucciAbstract:Experiments in adult animals have indicated that hyperglycemia accentuates whereas hypoglycemia ameliorates hypoxic-ischemic Brain Damage. To determine whether hypoglycemia is protective or deleterious to the perinatal Brain subjected to hypoxia-ischemia, 7-d postnatal rats were rendered hypoglycemic either by receiving an s.c. injection of insulin or fasting for 12 h. All rat pups underwent unilateral common carotid artery ligation followed by exposure to 8% oxygen-balance nitrogen at 37 degrees C for 2 h. Control animals (no insulin or fasting) received s.c. injections of normal saline. Mean blood glucose concentrations were 5.4 +/- 0.1, 4.3 +/- 0.2, and 3.4 +/- 0.1 mmol/L for control, insulin, and fasted animals, respectively. Blood beta-hydroxybutyrate concentrations were identical (0.5 +/- 0.1 mmol/L) for control and insulin-treated animals, but more than doubled in concentration in the fasted animals (p less than 0.001). Mortality rates during hypoxia-ischemia were higher in the insulin-treated animals (30%) than in either the fasted (4%) or control (0%) animals (p less than 0.05). Fasted animals showed a significant reduction in hypoxic-ischemic Brain Damage as compared with either the insulin-treated or control animals. Insulin-treated animals were not significantly different from controls. The findings indicate that 1) insulin induced hypoglycemia does not provide a protective effect on perinatal hypoxic-ischemic Brain Damage, as in adults; and 2) fasting adequate to produce hypoglycemia and ketonemia improved neuropathologic outcome.
E. Martin - One of the best experts on this subject based on the ideXlab platform.
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astroglial protein s 100 is an early and sensitive marker of hypoxic Brain Damage and outcome after cardiac arrest in humans
Circulation, 2001Co-Authors: Bernd W Bottiger, Stefan Mobes, Rolf Glatzer, Harald Bauer, André Gries, Jean Motsch, Peter Bartsch, E. MartinAbstract:BACKGROUND: The results of early conventional tests do not correlate with cerebral outcome after cardiac arrest. We investigated the serum levels of astroglial protein S-100 as an early marker of Brain Damage and outcome after cardiac arrest. METHODS AND RESULTS: In 66 patients undergoing cardiopulmonary resuscitation after nontraumatic cardiac arrest, blood samples for the evaluation of S-100 were drawn immediately after and 15, 30, 45, and 60 minutes; 2, 8, 24, 48, and 72 hours; and 7 days after initiation of cardiopulmonary resuscitation. Moreover, the serum levels of neuron-specific enolase were determined between 2 hours and 7 days. If patients survived for >48 hours, Brain Damage was assessed by a combination of neurological, cranial CT, and electrophysiological examinations. Overall, 343 blood samples were taken for the determination of S-100. Maximum S-100 levels within 2 hours after cardiac arrest were significantly higher in patients with documented Brain Damage (survivors and nonsurvivors, 3.70+/-0.77 microg/L) than in patients without Brain Damage (0.90+/-0.29 microg/L). Significant differences between these 2 groups were observed from 30 minutes until 7 days after cardiac arrest. In addition, the positive predictive value of the S-100 test at 24 hours for fatal outcome within 14 days was 87%, and the negative predictive value was 100% (P<0.001). With regard to neuron-specific enolase, significant differences between patients with documented Brain Damage and those with no Brain Damage were found at 24, 48, and 72 hours and 7 days. CONCLUSIONS: Astroglial protein S-100 is an early and sensitive marker of hypoxic Brain Damage and short-term outcome after cardiac arrest in humans.
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astroglial protein s 100 is an early and sensitive marker of hypoxic Brain Damage and outcome after cardiac arrest in humans
Circulation, 2001Co-Authors: Bernd W Bottiger, Stefan Mobes, Rolf Glatzer, Harald Bauer, André Gries, Jean Motsch, Peter Bartsch, E. MartinAbstract:Background—The results of early conventional tests do not correlate with cerebral outcome after cardiac arrest. We investigated the serum levels of astroglial protein S-100 as an early marker of Brain Damage and outcome after cardiac arrest. Methods and Results—In 66 patients undergoing cardiopulmonary resuscitation after nontraumatic cardiac arrest, blood samples for the evaluation of S-100 were drawn immediately after and 15, 30, 45, and 60 minutes; 2, 8, 24, 48, and 72 hours; and 7 days after initiation of cardiopulmonary resuscitation. Moreover, the serum levels of neuron-specific enolase were determined between 2 hours and 7 days. If patients survived for >48 hours, Brain Damage was assessed by a combination of neurological, cranial CT, and electrophysiological examinations. Overall, 343 blood samples were taken for the determination of S-100. Maximum S-100 levels within 2 hours after cardiac arrest were significantly higher in patients with documented Brain Damage (survivors and nonsurvivors, 3.70±0...
