Neurobiology of diabetic neuropathy /
This volume of International Review of Neurobiology defines primary biochemical causation of diabetic complications, identifies cellular glucose transducers, balancing roles of protein kinase C and MAP kinases, and sets in context the role of apoptosis and the interactive roles of neurons and Schwan...
| Other Authors: | |
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| Format: | Book |
| Language: | English |
| Published: |
Amsterdam ; Boston :
Academic Press,
c2002
Amsterdam ; Boston : [2002] |
| Series: | International review of neurobiology,
v. 50 International review of neurobiology v. 50 |
| Subjects: |
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| 245 | 0 | 0 | |a Neurobiology of diabetic neuropathy / |c edited by David Tomlinson |
| 260 | |a Amsterdam ; |a Boston : |b Academic Press, |c c2002 | ||
| 264 | 1 | |a Amsterdam ; |a Boston : |b Academic Press, |c [2002] | |
| 264 | 4 | |c ©2002 | |
| 300 | |a xxiii, 482 p., [8] p. of plates : |b ill. (some col.) ; |c 24 cm | ||
| 300 | |a xxiii, 482 pages, 8 unnumbered pages of plates : |b illustrations (some color) ; |c 24 cm | ||
| 336 | |a text |b txt |2 rdacontent | ||
| 337 | |a unmediated |b n |2 rdamedia | ||
| 338 | |a volume |b nc |2 rdacarrier | ||
| 440 | 0 | |a International review of neurobiology, |x 0074-7742 ; |v v. 50 | |
| 490 | 1 | |a International review of neurobiology, |x 0074-7742 ; |v v. 50 | |
| 500 | |a This WorldCat-derived record is shareable under Open Data Commons ODC-BY, with attribution to OCLC |5 CTY | ||
| 504 | |a Includes bibliographical references and index | ||
| 505 | 0 | 0 | |g Part I |t Primary Mechanisms -- |t How Does Glucose Generate Oxidative Stress In Peripheral Nerve? / |r Irina G. Obrosova -- |g I |t Manifestations of Diabetes-Associated Oxidative Stress in the Peripheral Nervous System (PNS) |g 4 -- |g II. |t Role for Oxidative Stress in Peripheral Diabetic Neuropathy |g 6 -- |g III. |t Origin of Diabetes-Induced Oxidative Stress in PNS |g 9 -- |g IV. |t Interactions between Oxidative Stress and Other Hyperglycemia-Initiated Factors in Pathogenesis of Diabetic Peripheral Neuropathy |g 12 -- |g V. |t Role for Aldose Reductase (AR) in Diabetes-Induced Oxidative Stress in Peripheral Nerve and Endothelium |g 14 -- |t Glycation in Diabetic Neuropathy: Characteristics, Consequences, Causes, and Therapeutic Options / |r Paul J. Thornalley -- |g I. |t Glycation: A Definition |g 38 -- |g II. |t Nomenclature: Early and Advanced Glycation |g 38 -- |g III. |t Evidence for Increased Glycation in Diabetic Neuropathy |g 40 -- |g IV. |t Indirect Evidence for Involvement of Increased Glycation in Diabetic Neuropathy: Effects of Antiglycation Agents |g 42 -- |g V. |t Glycation-Related Correlates in Risk Analysis of Clinical Diabetic Neuropathy |g 43 -- |g VI. |t Functional Effects of Increased Glycation in Diabetic Nerve |g 44 -- |g VII. |t Receptor for Advanced Glycation End Products |g 45 -- |g VIII. |t Raised Intracellular Glucose: Trigger for Increased Glycation by [alpha]-Oxoaldehydes |g 47 -- |g IX. |t Therapeutic Options |g 48 -- |g Part II |t Secondary Changes -- |t Protein Kinase C Changes in Diabetes: Is the Concept Relevant to Neuropathy? / |r Joseph Eichberg -- |g II. |t Molecular Features of Protein Kinase C (PKC) |g 62 -- |g III. |t Activation and Regulation of PKC |g 65 -- |g IV. |t PKC and Nonneural Diabetic Complications |g 66 -- |g V. |t PKC and 1,2-Diacylglycerol in Normal and Diabetic Nerve |g 68 -- |g VI. |t PKC and Na[superscript +],K[superscript +]-ATPase |g 70 -- |g VII. |t PKC Actions: Neural versus Neurovascular? |g 72 -- |g VIII. |t Emerging and Potential Roles for PKC in Nerve |g 73 -- |g IX. |t Conclusions and Future Directions |g 75 -- |t Are Mitogen-Activated Protein Kinases Glucose Transducers for Diabetic Neuropathies? / |r Tertia D. Purves, David R. Tomlinson -- |g II. |t Mitogen-Activated Protein (MAP) Kinases |g 84 -- |g III. |t Glucose, Diabetes, and MAP Kinases |g 86 -- |g IV. |t MAP Kinase Activation in Primary Sensory Neurons |g 90 -- |g V. |t MAP Kinases and Neuropathy in the Streptozotocin Rat Model of Diabetes |g 95 -- |g VI. |t MAP Kinase Activation in Sural Nerve from Type I and Type II Diabetic Patients |g 101 -- |g VII. |t Role of MAP Kinase Activation |g 101 -- |g VIII. |t What Is the Molecular Basis for the Development of Nerve Conduction Deficits and Structural Abnormalities in Diabetes? |g 106 -- |t Neurofilaments in Diabetic Neuropathy / |r Paul Fernyhough, Robert E. Schmidt -- |g II. |t Neurofilament Structure |g 116 -- |g III. |t Phosphorylation of Neurofilament |g 118 -- |g IV. |t Axonal Transport of Neurofilament |g 120 -- |g V. |t Neurofilaments and Axonal Cytoskeleton: Regulation of Axonal Caliber and Slow Transport |g 121 -- |g VI. |t Neurofilament Pathology in Diabetic Sensory and Autonomic Neuropathy |g 121 -- |g VII. |t Possible Pathogenetic Mechanisms |g 128 -- |g VIII. |t Future Directions |g 136 -- |t Apoptosis in Diabetic Neuropathy / |r Aviva Tolkovsky -- |g II. |t Apoptotic Pathways |g 146 -- |g III. |t Apoptotic Indicators in Diabetic Neuropathy |g 153 -- |t Nerve and Ganglion Blood Flow in Diabetes: An Appraisal / |r Douglas W. Zochodne -- |g II. |t Anatomy and Physiology of Peripheral Nerve and Spinal Ganglia Vascular Supply |g 162 -- |g III. |t Measurements of Local Blood Flow |g 166 -- |g IV. |t Changes in Nerve Blood Flow with Ischemia and Injury |g 171 -- |g V. |t Nerve and Ganglia Blood Flow in Experimental and Human Diabetes |g 175 -- |g Part III |t Manifestations -- |t Potential Mechanisms of Neuropathic Pain in Diabetes / |r Nigel A. Calcutt -- |g I. |t Diabetic Neuropathy and Painful Diabetic Neuropathy |g 206 -- |g II. |t Clinical Clues to Potential Mechanisms of Painful Diabetic Neuropathy |g 207 -- |g III. |t Sensory Dysfunction in Diabetic Animals |g 208 -- |g IV. |t Using Animal Models to Predict Therapeutic Efficacy of Experimental Agents |g 211 -- |g V. |t Contribution of Peripheral Nerves to Hyperalgesia in Diabetic Animals |g 214 -- |g VI. |t A Potential Role for Altered Spinal Processing in Diabetic Hyperalgesia |g 217 -- |t Electrophysiologic Measures of Diabetic Neuropathy: Mechanism and Meaning / |r Joseph C. Arezzo, Elena Zotova -- |g II. |t Functional and Structural Deficits Associated with Diabetic Neuropathy |g 231 -- |g III. |t Whole Nerve Neural Response |g 232 -- |g IV. |t Maximal Nerve Conduction Velocity |g 236 -- |g V. |t F-Wave Responses |g 240 -- |g VI. |t Distribution of Velocities |g 241 -- |g VII. |t Amplitude and Area |g 242 -- |g VIII. |t Refractory Periods and Neural Fatigue |g 245 -- |g IX. |t Measures of Excitability |g 248 -- |t Neuropathology and Pathogenesis of Diabetic Autonomic Neuropathy / |r Robert E. Schmidt -- |g II. |t Neuropathology of Clinical Diabetic Autonomic Neuropathy |g 259 -- |g III. |t Experimental Diabetic Autonomic Neuropathy |g 263 -- |g IV. |t Proposed Pathogenetic Mechanisms of Diabetic Autonomic Neuropathy |g 271 -- |t Role of the Schwann Cell in Diabetic Neuropathy / |r Luke Eckersley -- |g I. |t Peripheral Nervous System Development |g 294 -- |g II. |t Function of Schwann Cells |g 296 -- |g III. |t Schwann Cells in Diabetic Neuropathy |g 300 -- |g IV. |t Neuropathy in Diabetic Patients |g 301 -- |g V. |t Etiological Models for Nerve Dysfunction |g 301 -- |g VI. |t Paranodal Structure and Axoglial Dysjunction |g 310 -- |g VII. |t Is Regeneration Abnormal in Diabetic Neuropathy? |g 311 -- |g VIII. |t Reversible or Irreversible Schwann Cell Injury? |g 313 -- |g Part IV |t Potential Treatment -- |t Polyol Pathway and Diabetic Peripheral Neuropathy / |r Peter J. Oates -- |g II. |t Polyol Pathway |g 331 -- |g III. |t Enzymes of the Polyol Pathway |g 333 -- |g IV. |t Physiological Role of Polyol Pathway Enzymes |g 345 -- |g V. |t Localization of AR and SDH in Peripheral Nerve |g 348 -- |g VI. |t Inhibitors of Polyol Pathway Enzymes |g 351 -- |g VII. |t Polyol Pathway Inhibition in Models of Diabetic Neuropathy |g 353 -- |g VIII. |t Effects of Polyol Pathway Inhibitors in Human Diabetic Neuropathy |g 362 -- |g IX. |t Inhibition of Nerve Sorbitol versus AR Metabolic Flux |g 366 -- |g X. |t Future Research Directions |g 375 -- |t Nerve Growth Factor for the Treatment of Diabetic Neuropathy: What Went Wrong, What Went Right, and What Does the Future Hold? / |r Stuart C. Apfel -- |g II. |t Rationale for the Application of Nerve Growth Factor to Diabetic Polyneuropathy |g 397 -- |g III. |t Early Clinical Studies |g 402 -- |g IV. |t Phase III Clinical Trial of Recombinant Human Nerve Growth Factor in Diabetic Polyneuropathy |g 405 -- |g V. |t What Does the Future Hold? |g 410 -- |t Angiotensin-Converting Enzyme Inhibitors: Are there Credible Mechanisms for Beneficial Effects in Diabetic Neuropathy? / |r Rayaz A. Malik, David R. Tomlinson -- |g II. |t Vascular Basis for Diabetic Neuropathy |g 416 -- |g III. |t Interventions |g 418 -- |g IV. |t Physiology of Angiotensin II |g 421 -- |g V. |t Nonvascular Effects of Angiotensin II |g 422 -- |g VI. |t Pharmacology of Angiotensin-Converting Enzyme Inhibition |g 423 -- |g VII. |t Tissue Renin/Angiotensin |g 423 -- |g VIII. |t Alternative Pathways of Angiotensin II Formation |g 424 -- |t Clinical Trials for Drugs Against Diabetic Neuropathy: Can We Combine Scientific Needs With Clinical Practicalities? / |r Dan Ziegler, Dieter Luft -- |g I. |t Clinical Impact of Diabetic Polyneuropathy |g 432 -- |g II. |t Role of Drug Treatment in Diabetic Polyneuropathy |g 433 -- |g III. |t Classification, Diagnosis, and Staging |g 435 -- |g IV. |t Outcome Measures |g 437 -- |g V. |t Natural History and Risk Factors |g 440 -- |g VI. |t Sample Size and Duration of Trials |g 442 -- |g VII. |t Reproducibility of Outcome Measures |g 443 -- |g VIII. |t Nonspecific Effects of Treatment |g 445 -- |g IX. |t Measures of Treatment Effects |g 447 -- |g X. |t Generalizability of Overall Results of Randomized Clinical Trials (External Validity) |g 449 -- |g XI. |t Reporting of Randomized Clinical Trials |g 451 -- |g XII. |t Current State of Pharmacological Treatments Based on Pathogenetic Concepts |g 451. |
| 520 | |a This volume of International Review of Neurobiology defines primary biochemical causation of diabetic complications, identifies cellular glucose transducers, balancing roles of protein kinase C and MAP kinases, and sets in context the role of apoptosis and the interactive roles of neurons and Schwann cells. It also defines the cell biology of autonomic neuropathy, considers the balanced needs of science, clinical practice, and economics in clinical trial design, provides the definitive evaluation of aldose reductase inhibitors, and explains the failure of nerve growth factor. One of the most successful series in the field of neuroscience continues its standard of excellence with this newest edition. Published since 1959, International Review of Neurobiology is a well-known series appealing to neuroscientists, clinicians, psychologists, physiologists, and pharmacologists | ||
| 630 | 0 | 7 | |a Pathogenesis |2 fast |
| 650 | 0 | |a Diabetic neuropathies |x Pathogenesis | |
| 650 | 0 | |a Diabetic neuropathies |x Pathophysiology | |
| 650 | 7 | |a Diabetic neuropathies |2 fast | |
| 650 | 7 | |a Physiology, Pathological |2 fast | |
| 650 | 1 | 2 | |a Diabetic Neuropathies |x pathology |
| 650 | 1 | 2 | |a Diabetic Neuropathies |x physiopathology |
| 700 | 1 | |a Tomlinson, David R | |
| 830 | 0 | |a International review of neurobiology |x 0074-7742 ; |v v. 50 | |
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