Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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V. Neutrophil-Mediated Tissue Injury 343 Endotoxin CD14 Macrophage TNF IL-1 ICAM E-selectin Activated endothelial cell PAF IL-8 C LBT4 TF TF TM↓ ADP ase↓ Activated endothelial cell PECAM VWF PGI2↓ PAF Neutrophil adhesion Neutrophil activation Procoagulant Platelet adhesion Platelet activation FIGURE 11-5 The activation of endothelial cells at a site of inflammation. At sites of inflammation, activated macrophages release proinflammatory mediators including tumor necrosis factor- α (TNF- α ) and interleukin-1 (IL-1). These cytokines activate endothelial cells, converting their surface from antiadhesive and anticoagulant to proadhesive and procoagulant. Activated endothelium express intercellular adhesion molecules (ICAM) and selectin molecules that promote neutrophil adhesion. Activated endothelium also express platelet-activating factor (PAF), interleukin-8 (IL-8), and leukotriene-B4 (LTB4) and may bind complement , all of which will activate neutrophils while attached to endothelium. Decreased expression of adenosine diphosphatase and thrombomodulin as well as increased expression of platelet-endothelial cell adhesion molecules (PECAM) and von Willebrand’s factor promote platelet adhesion. Decreased production of prostaglandin I 2 (PGI2) and expression of PAF promotes platelet activation. Finally, tissue factor (TF), a potent activator of the extrinsic clotting pathway, may be expressed on activated endothelium. B . Ischemia/Reperfusion Injury Prolonged ischemia results in numerous metabolic and ultrastructural changes within cells. Ischemia decreases cellular oxidative phosphorylation resulting in failure to resynthesize high-energy phosphate compounds such as adenosine 5 -triphosphate. Adenosine 5 -triphosphate catabolism during ischemia results in accumulation of hypoxanthine. Hypoxanthine is subsequently converted to oxygen radicals upon reperfusion of the tissue. Ischemia also promotes expression of leukocyte and platelet adhesion receptors on the cell surface; promotes expression of proinflammatory cytokines (e.g., IL-8) and bioactive agents (e.g., platelet-activating agents, endothelin, thromboxane A2); and suppresses certain gene products including nitric oxide, nitric oxide synthase, thrombomodulin, and prostacyclin. Restoration of blood flow after a period of ischemia places tissues at risk of further cellular necrosis ( Carden and Granger, 2000 ; Eltzschig and Collard, 2004). Reperfusion injury is primarily directed at the endothelial cells lining the microvasculature and is manifest as accelerated production of a variety of bioactive agents and expression of adhesion molecules for neutrophils. Neutrophils appear to become activated while attached to endothelium-releasing oxygen radicals and granule contents directly onto the endothelial surface. In addition to production of superoxide by neutrophils, superoxide is generated from hypoxanthine within endothelial cells and is produced by mast cells and macrophages. Neutrophils may also contribute to tissue hypoperfusion after blood flow is reestablished. Activated neutrophils are rigid and tend to lodge in capillaries, obstructing blood flow. Neutrophil-neutrophil aggregates and plateletneutrophil aggregates also may contribute to capillary malperfusion by plugging capillaries resulting in prolonged maldistribution of blood flow. Platelet-neutrophil aggregates may also contribute to microthrombus formation.
344 Chapter | 11 Neutrophil Function The observation that blood flow to an ischemic organ is not fully restored after release of a vascular occlusion has been termed the no-reflow phenomenon. Experimental studies, using leukocyte depletion models, have demonstrated a central role of neutrophils in the no-reflow phenomenon. C . Neutrophil-Mediated Injury at Distant Sites Neutrophils become activated within the circulation during a variety of physiological and pathological conditions in domestic animals. Circulating activated neutrophils have been documented during strenuous exercise, inflammatory disease, equine colic, and equine laminitis. At least in some circumstances, there is evidence to suggest that these activated neutrophils may contribute to the pathogenesis of the disease process. 1 . Exercise Strenuous exercise has been associated with up-regulation of neutrophil surface-associated integrin receptors in dogs undergoing short duration sled-pulling activity ( Moritz et al. , 2003 ). Additionally, decreased neutrophil granularity was observed postexercise. Because CD11b/CD18 integrin is stored in neutrophil granules and transported to the cell surface when neutrophils degranulate, the combination of increased cell surface integrin concentration and decreased granularity postrace is consistent with exercise-associated neutrophil degranulation. 2 . Infl ammatory Disease Neutrophils circulate in an activated state in a variety of inflammatory conditions. Dogs with naturally occurring septic and nonseptic inflammatory diseases had increased cell surface expression of CD11b ( Weiss et al. , 2004 ). Neutrophils from dogs with septic inflammatory diseases and those with evidence of multiple organ dysfunction also had decreased neutrophil granularity and increased neutrophil size. However, neutrophil activation markers may not predict neutrophil function. In a study by Gosset et al. (1983/1984) , neutrophils from dogs with severe inflammatory disease were reported to have a defect in bactericidal activity. Monocytes and lymphocytes from dogs with septic and nonseptic inflammation and multiple organ dysfunction had decreased expression of major histocompatibility factor class-II suggesting impaired immune responsiveness ( Weiss et al. , 2004 ). Leukocyte deformability, neutrophil CD11b expression, and neutrophil size were evaluated in calves experimentally inoculated intrabronchially with Mannheimia haemolytica organisms ( McClenahan et al. , 1999 ). Infected calves had decreased leukocyte deformability and increased neutrophil size by 1h and increased CD11b expression by 6h after organism inoculation. Decreased neutrophil deformability and increased size may contribute to sequestration of neutrophils in alveolar capillary beds during sepsis. 3 . Colic The activation status of circulating neutrophils was evaluated in horses with naturally occurring colic ( Weiss and Evanson, 2003 ). Activated neutrophils were not detected in healthy horses or horses with impaction or gas colic. Conversely, horses with inflammatory bowel disease consistently had increased neutrophil cell membrane CD11/ CD18 expression, increased neutrophil size, and decreased neutrophil granularity consistent with circulating activated and degranulated neutrophils. These horses also had decreased leukocyte deformability indicating that neutrophils were rigid. Horses with strangulating colic had variable results. Among horses with strangulating colic, changes in leukocyte deformability, neutrophil size, and neutrophil granularity correlated directly with adverse outcome. 4 . Equine Laminitis Neutrophils may become activated in the prodromal stages of equine laminitis. At various times during the first 12 h after induction of black walnut-induced laminitis, horse neutrophils had increased oxygen radical production, and some horses had increased phagocytosis of bacteria ( Black et al. , 2006 ). These changes were associated with neutropenia and were presumed to be due to a systemic inflammatory response resulting from absorption of inflammatory mediators from the intestine. These activated neutrophils have been incriminated in the pathogenesis of the laminar injury ( Black et al. , 2006 ). 5 . Adult Respiratory Distress Syndrome and Multiple Organ Failure A ctivated neutrophils are central to the pathogenesis of ARDS and MODS associated with sepsis and endotoxemia (Lehr et al. , 2000 ). As in ischemia/reperfusion injury, microvascular injury is a major site of injury in these conditions. The lungs are particularly sensitive to neutrophil-induced vascular injury. The process of lung involvement has been divided into four sequential stages: (1) sequestration of neutrophils in pulmonary capillaries, (2) adhesion, (3) activation, and (4) release of oxygen radicals and proteases ( Lee and Downey, 2001 ). The process of neutrophil sequestration in the lungs differs from that of other tissues. In other tissues, neutrophil sequestration occurs predominately in postcapillary venules and is dependent on selectin and integrin adhesion molecules. Alternatively, neutrophil sequestration in the lungs occurs primarily in pulmonary capillaries and is largely independent of adhesion molecules. Sequestration
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Preface It has been more than a dec
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viii Contributors Björn P. Meij (5
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2 Chapter | 1 Concepts of Normality
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10 Chapter | 1 Concepts of Normalit
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Chapter 2 Comparative Medical Genet
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I. Introduction 29 Green Red Green
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I. Introduction 31 A1 genetic map d
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I. Introduction 33 of genomes of va
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36 Chapter | 2 Comparative Medical
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46 Chapter | 3 Carbohydrate Metabol
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IX. Disorders of Carbohydrate Metab
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X. Disorders of Ruminants Associate
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X. Disorders of Ruminants Associate
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References 79 Kaneko , J. J. , Luic
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Chapter 4 Lipids and Ketones Michae
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II. Long Chain Fatty Acids 83 FIGUR
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II. Long Chain Fatty Acids 85 Plasm
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IV. Phospholipids 87 The regulation
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V. Cholesterol 89 V. CHOLESTEROL A.
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VI. Lipoproteins 91 TABLE 4-1 Compo
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VI. Lipoproteins 93 TABLE 4-2 Apoli
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96 Chapter | 4 Lipids and Ketones B
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98 Chapter | 4 Lipids and Ketones
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Chapter 5 Proteins, Proteomics, and
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III. Metabolism of Proteins 119 C .
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IV. Plasma Proteins 121 NH 4 HCO
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V. Methodology 123 molecule. The gl
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V. Methodology 125 has occurred wil
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V. Methodology 127 Although attempt
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V. Methodology 129 kD 94 67 43 2 2
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V. Methodology 131 D . Specific Pro
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VI. Normal Plasma and Serum Protein
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VII. Interpretation of Serum Protei
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References 149 Andersson , M. , Ste
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References 151 response of haptoglo
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References 153 dogs with metastasiz
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References 155 Watson , T. D. G. (
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158 Chapter | 6 Clinical Veterinary
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V. Methods for Evaluation of the Im
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VI. Laboratory Diagnosis of Disease
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Chapter 7 The Erythrocyte: Physiolo
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II. Hematopoiesis 175 progenitor ce
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III. Developing Erythroid Cells 177
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IV. Mature RBC 185 immune-mediated
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IV. Mature RBC 187 TABLE 7-3 Erythr
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IV. Mature RBC 189 TABLE 7.5 Erythr
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IV. Mature RBC 191 Echinocyte forma
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IV. Mature RBC 193 Pig RBC isoantig
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IV. Mature RBC 195 occurs in chicke
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IV. Mature RBC 197 inorganic phosph
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IV. Mature RBC 199 (a) FIGURE 7-6 T
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IV. Mature RBC 201 RBC 2,3DPG incre
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IV. Mature RBC 203 mechanisms would
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IV. Mature RBC 205 released during
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IV. Mature RBC 207 reduced by ascor
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V. Determinants of RBC Survival 209
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V. Determinants of RBC Survival 211
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VI. Inherited Disorders of RBCs 213
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described in people. They include a
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References 221 Boas , F. E. , Forma
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References 223 Della Rovere , F. ,
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References 225 Gedde , M. M. , Davi
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References 227 phosphofructokinase-
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References 229 Knight , A. P. , Las
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References 231 Martinovich , D. , a
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References 233 Pearson , W. , Boerm
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References 235 Shadduck , R. K. ( 1
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References 237 Tennant , B. , Dill
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References 239 Williams , D. M. , L
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Chapter 8 Porphyrins and the Porphy
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II. Porphyrins 243 two vinyl groups
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II. Porphyrins 245 TABLE 8-2 Nomenc
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IV. Porphyrias 247 6. Uroporphyrins
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IV. Porphyrias 249 i . Urine It is
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IV. Porphyrias 251 to localize the
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IV. Porphyrias 253 FIGURE 8-6 Metab
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IV. Porphyrias 255 estrogens. The d
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References 257 and hexachlorobenzen
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Chapter 9 Iron Metabolism and Its D
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II. Iron Distribution 261 plasma of
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IV. Plasma Iron Transport 263 pathw
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VI. Iron Metabolism in Cells 265 of
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VI. Iron Metabolism in Cells 267 in
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VII. Tests for Evaluating Iron Meta
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VII. Tests for Evaluating Iron Meta
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VIII. Disorders of Iron Metabolism
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References 279 ( Norrdin et al ., 2
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References 281 Fresco , R. ( 1981 )
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References 283 Moore , C. V. , Duba
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References 285 Weiden , P. L. , Hac
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288 Chapter | 10 Hemostasis TABLE 1
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290 Chapter | 10 Hemostasis TABLE 1
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394 Chapter | 13 Hepatic Function 2
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396 Chapter | 13 Hepatic Function u
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398 Chapter | 13 Hepatic Function 2
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400 Chapter | 13 Hepatic Function c
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402 Chapter | 13 Hepatic Function F
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404 Chapter | 13 Hepatic Function A
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406 Chapter | 13 Hepatic Function E
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408 Chapter | 13 Hepatic Function K
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410 Chapter | 13 Hepatic Function R
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412 Chapter | 13 Hepatic Function W
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414 Chapter | 14 Gastrointestinal F
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Chapter 15 Skeletal Muscle Function
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II. Specialization of the Sarcolemm
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II. Specialization of the Sarcolemm
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III. Heterogeneity of Skeletal Musc
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III. Heterogeneity of Skeletal Musc
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V. Exercise and Adaptations to Trai
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VI. Diagnostic Laboratory Methods f
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VI. Diagnostic Laboratory Methods f
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IX. Selected Neuromuscular Disorder
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IX. Selected Neuromuscular Disorder
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References 479 and, recently, there
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References 481 Engel , A. G. ( 2004
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References 483 Paciello , O. , Maio
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Chapter 16 Kidney Function and Dama
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II. Kidney Morphology and Function
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II. Kidney Morphology and Function
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III. Tests of Kidney Function 491 (
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III. Tests of Kidney Function 493 T
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III. Tests of Kidney Function 495 B
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6 5 4 3 2 1 0 Dog Cat Equine Cattle
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III. Tests of Kidney Function 499 d
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IV. Tests of Kidney Damage 501 1000
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IV. Tests of Kidney Damage 503 and
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IV. Tests of Kidney Damage 505 Enzy
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V. Biochemical Changes in Kidney Di
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V. Biochemical Changes in Kidney Di
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References 511 were reported to occ
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References 513 Bovee , K. C. ( 1969
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References 515 Deguchi , E. , and A
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References 519 Harvey , D. G. ( 197
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References 521 Kühl , S. , Mischke
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References 523 creatinine measureme
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References 525 Reusch , C. , Vochez
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References 527 Terry , R. , Hawkins
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Chapter 17 Fluid, Electrolyte, and
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532 Chapter | 17 Fluid, Electrolyte
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VIII. Clinicopathological Indicator
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References 555 plasma water, electr
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References 557 Krzywanek , H. ( 197
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References 559 Strombeck , D. R. (1
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562 Chapter | 18 Pituitary Function
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606 Chapter | 19 Adrenocortical Fun
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624 Chapter | 20 Thyroid Function a
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626 Chapter | 20 Thyroid Function t
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628 Chapter | 20 Thyroid Function A
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630 Chapter | 20 Thyroid Function S
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632 Chapter | 20 Thyroid Function a
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634 Chapter | 20 Thyroid Function O
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636 Chapter | 21 Clinical Reproduct
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664 Chapter | 22 Trace Minerals the
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666 Chapter | 22 Trace Minerals the
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668 Chapter | 22 Trace Minerals P i
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670 Chapter | 22 Trace Minerals be
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Copper Cuproreductase Cytochromes C
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674 Chapter | 22 Trace Minerals 2 .
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676 Chapter | 22 Trace Minerals Cor
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678 Chapter | 22 Trace Minerals inf
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680 Chapter | 22 Trace Minerals tis
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682 Chapter | 22 Trace Minerals VI
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684 Chapter | 22 Trace Minerals red
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686 Chapter | 22 Trace Minerals of
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688 Chapter | 22 Trace Minerals Per
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692 Chapter | 22 Trace Minerals Liu
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Chapter 23 Vitamins Robert B. Rucke
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III. Fat-Soluble Vitamins 697 TABLE
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III. Fat-Soluble Vitamins 699 Carot
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III. Fat-Soluble Vitamins 701 Major
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III. Fat-Soluble Vitamins 703 doses
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III. Fat-Soluble Vitamins 705 Diet
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III. Fat-Soluble Vitamins 707 conta
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III. Fat-Soluble Vitamins 709 immun
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IV. Water-Soluble Vitamins 711 are
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IV. Water-Soluble Vitamins 713 abil
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IV. Water-Soluble Vitamins 715 5’
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IV. Water-Soluble Vitamins 717 H 2
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IV. Water-Soluble Vitamins 719 Enzy
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722 Chapter | 23 Vitamins When biot
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724 Chapter | 23 Vitamins Cyanocoba
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726 Chapter | 23 Vitamins V . VITAM
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728 Chapter | 23 Vitamins nature, r
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730 Chapter | 23 Vitamins Stites ,
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732 Chapter | 24 Lysosomal Storage
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Chapter 25 Tumor Markers Michael D.
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II. Serum Tumor Markers 753 also be
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III. Flow Cytometry 755 cancer of t
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V. Immunohistochemistry/Immunocytoc
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V. Immunohistochemistry/Immunocytoc
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References 761 analysis will facili
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References 763 Fernandez , N. J. ,
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References 765 Meinecke , B. , and
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References 767 Walter , J. ( 2000 )
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770 Chapter | 26 Cerebrospinal Flui
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TABLE 26-7 Continued Constituent Ro
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Chapter 27 Clinical Biochemistry in
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II. Hepatotoxicity 823 Therefore, A
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III. Nephrotoxicity 825 suggested a
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IV. Toxins Affecting Skeletal and C
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VII. Toxins Affecting Erythrocytes
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VIII. Toxins Affecting Hemoglobin a
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IX. Toxins Affecting the Nervous Sy
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References 835 Plants classified as
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References 837 Solaiman , S. G. , M
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840 Chapter | 28 Avian Clinical Bio
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Budgerigar ALAT (IU/g tissue) Budge
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874 Appendix | I SI Units TABLE E S
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Appendix II Conversion Factors of S
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Appendix IV Stability of Serum Enzy
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Appendix VI Nomogram for Computing
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t0100 Appendix VIII Blood Analyte R
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884 Appendix | VIII Blood Analyte R
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890 Appendix | IX Blood Analyte Ref
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Appendix X Blood Analyte Reference
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Appendix XI Blood Analyte Reference
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Appendix XII Urine Analyte Referenc
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902 Appendix | XIII Cerebrospinal F
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904 Appendix | XIV Cerebrospinal Fl
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