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_a10.1007/9780387791128 _2doi |
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050 | 4 | _aRC321-580 | |
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_aMcCandless, David W. _eeditor. _9303385 |
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_aMetabolic Encephalopathy / _cedited by David W. McCandless. |
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_aNew York, NY : _bSpringer New York : _bImprint: Springer, _c2009. |
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_axvI, 601 páginas _brecurso en línea. |
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_atexto _btxt _2rdacontent |
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_acomputadora _bc _2rdamedia |
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_aarchivo de texto _bPDF _2rda |
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505 | 0 | _aFunctional Anatomy of the Brain -- Brain Metabolic Adaptations to Hypoxia -- Hypoglycemic Brain Damage -- Experimental Ischemia: Summary of Metabolic Encephalopathy -- Metabolic Encephalopathy Stroke – Clinical Features -- The Role of Animal Models in the Study of Epileptogenesis -- Seizure-Induced Neuronal Plasticity and Metabolic Effects -- Metabolic Encephalopathies in Children -- Pathophysiology of Hepatic Encephalopathy: Studies in Animal Models -- Hepatic Encephalopathy -- Uremic and Dialysis Encephalopathies -- Thiamine Deficiency: A Model of Metabolic Encephalopathy and of Selective Neuronal Vulnerability -- Alcohol, Neuron Apoptosis, and Oxidative Stress -- Wernicke’s Encephalopathy -- The Genetics of Myelination in Metabolic Brain Disease: The Leukodystrophies -- Bilirubin Encephalopathy -- Infectious and Inflammatory Metabolic Encephalopathies -- Major Depression and Metabolic Encephalopathy: Syndromes More Alike Than Not? -- Attention-Deficit/Hyperactivity Disorder as a Metabolic Encephalopathy -- Retracted: Brain Damage in Phenylalanine, Homocysteine and Galactose Metabolic Disorders -- Wilson Disease -- Metabolic Abnormalities in Alzheimer Disease -- Prions and the Transmissible Spongiform Encephalopathies -- Lead Encephalopathy -- Retracted: Brain Damage in Phenylalanine, Homocysteine and Galactose Metabolic Disorders. | |
520 | _aMetabolic Encephalopathy is meant to combine and correlate animal and human studies. In many cases, alterations in the neurochemistry of humans and experimental animal models is similar. It is hoped that increased awareness of the importance of early diagnosis and treatment of these disorders may result in a lowering of the incidence of structural changes and morbidity. These metabolic encephalopathies hold a special fascination for both basic scientists and clinical investigators because they are accessible, treatable, and there exist good animal models for further study. Therefore, this book assembles both basic and clinical neuroscience issues in the treatment of specific metabolic encephalopathies such as uremia, Wernicke’s disease, epilepsy, stroke, hepatic encephalopathy, pediatric encephalopathies, inborn errors of metabolism, toxins such as lead, depression, cerebral infections, kernicterus, Wilson disease, and many others. About the Editor: Dr. David W. McCandless is the John J. Sheinin Professor of Anatomy in the Department of Cell Biology and Anatomy at The Chicago Medical School, Rosalind Franklin University, North Chicago, IL. He has over 35 years of laboratory research into basic mechanisms of various metabolic encephalopathies. He serves as Editor-in Chief of the journal Metabolic Brain Disease (Springer), now in its 23rd year. Dr. McCandless has been on the faculty or research staff at The University of Vermont College of Medicine, NIH-NINCDS, University of Texas Medical School at Houston, and The Chicago Medical School, and was a visiting professor at Washington University School of Medicine. Dr. McCandless has published in journals such as The J. Clinical Investigation, Nature, Proc. National Academy of Sciences, Amer. J. of Physiology, Brain Research, J. Neurochemistry, Teratology, Epilepsia, Stroke, and many others. This is his third edited book. | ||
590 | _aPara consulta fuera de la UANL se requiere clave de acceso remoto. | ||
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_aSpringerLink (Servicio en línea) _9299170 |
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_iEdición impresa: _z9780387791098 |
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_uhttp://remoto.dgb.uanl.mx/login?url=http://dx.doi.org/10.1007/978-0-387-79112-8 _zConectar a Springer E-Books (Para consulta externa se requiere previa autentificación en Biblioteca Digital UANL) |
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