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

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III. Copper 671 Tocopherol Mitochondrial electron transport O 2 A Reduced substrates Cytochrome system H 2 O O 2 . - MnSOD H 2 O 2 1/2 O 2 H 2 O 2 Catalase Tocopherol SOD Catalase B 2H Cu(II) Fe(II) O 2 O 2 •- H 2 O 2 H 2 O • OH HO- O 2 H 2 O Fe 2 or Cu 1 D NADH/NADPH oxidase Xanthine oxidase Lipoxygenase Cycloxygenase P-450 monooxygenase Mitochondrial oxidative- Phosphorylation Electron transport NO• Fenton reaction ONOO- •OH OH- • OH HO- Metal Chaperones Metal Complexes (e.g. MT, Ferritin) "RH" "RH" "RH" Organic and Lipid peroxides (ROOH) Glutathione Peroxidase GSH ROH H 2 O Glutathione Reductase NADP Hexode GSSG C Monophosphate Shunt NADPH Tocopherol FIGURE 22-3 Major sources and regulation of reactive oxidant species (ROSs) in cells. Depending on the stage of development and condition, on a per mole basis ROSs are normally generated at rates of 1% to 4% of the oxygen consumed or greater when ROS regulation is disrupted. A major source of ROS is derived from superoxide anion (O 2 ) generated in the mitochondrion (A) because of uncoupling from the cytochrome oxidase system during mitochondrial electron transport. In addition to water and oxidized metabolites as products, superoxide anion and H 2 O 2 are produced. Enzymes, such as catalase and MnSOD (localized in the mitochondria) control excess production of O 2 and H 2 O 2 . When there is subsequent leakage from mitochondria, an increase in the cellular pool of ROS occurs owing both to ROSs from mitochondria and production from other organelles and cytosol (B). Sources of ROSs from other organelles and cytosol are the products from reactions catalyzed by NADH and NAPH oxidases, xanthine oxidase (activated during ischemic injury), lipoxygenase, and P450 monooxygenase enzymes (localized mainly in the smooth endoplasmic reticulum and responsible for the metabolism of xenobiotics, drugs, and secondary metabolites). In addition, excess ROS can potentially alter nitric oxide metabolism (e.g., formation of peroxynitrites) and cause the generation of organic and lipid peroxides and so-called Fenton products (C). For example, “ RH, ” used to depict numerous aromatic and lipid-derived possibilities as potential reactants, can be converted to ROOH, potential organic peroxide-containing products. Excess superoxide anion, ROOH, OH-, OH · , and other ROSs can then damage proteins, nucleic acids, and lipids, particularly lipid structures in cell and organelle membranes. Important to this discussion, metals can act as both catalysts for ROS formation and cofactors for antioxidant enzymes that modulate influence ROS metabolism. For example, (1) MnSOD and CuZn SOD (superoxide dismutases) cause the dismutation of excess superoxide anion to peroxide, (2) catalase (contains Fe) and glutathione peroxidase (contains Se) can control excess of both hydrogen and organic peroxides. As an additional defense, metal chaperones (see text), metallothionein (MT), or ferritin control “ free ” metal ion concentrations in cells that are capable of redox (D). Redox metals (Fe or Cu) can act as Fenton catalysts and promote the homolytic cleavage of H 2 O 2 to OH · and OH-, which are highly damaging oxidants. Reduction in the concentration or sequestration of metals (depicted by the dashed line) markedly reduces potential Fenton products. As a final line of defense, tocopherols and polyphenolic and related phytochemicals, which localize to lipid membranes, provide additional ROS defense.
Copper Cuproreductase Cytochromes Cytochromes (a) Cp, Albumin, Others CRT1 DCT1 DMT1/Nramp2 Cu Cytochromes Metallothionein Yeast ATOX, Homologue CuZnSOD Cu Cu Cu Cu Cu Manganese TfR Yeast Homologue of Mtm 1 P Mn SOD Mn SOD Metal Oxyanion Transporters Transferrin[Mn] DCT1 DMT1/Nramp2 Ca/Mn ATPase Metal Oxyanion Transporters (b) Selenium Selenomethionine and Amino Se-Methylselenocysteine Selenoprotein-P Mn SOD Ferritin Se-Met Acid Transporters CH 3 SeH Se-Cys Mn SOD Protein Se-Cystathionine [-CH 3 ] (c) Sodium Selenite Metal Oxyanion Transporters Selenite GSSeSG GSH Selenite/Sulfite Reduction Pathways GSSG HSe - HSePO 4 - Ser-tRNA UGA Sec-tRNA Se-Specific Proteins Zinc Zn-Protein Zn-Amino Acid Complexes ZIP Family [n] L-type calcium channels (LTCC) Zn ZnT[n] ZnT[n] ZnT[n] DCT1 DMT1/Nramp2 Metallothionein ZnT[n] (d) FIGURE 22-4 Cellular transport. Features important to the transport of copper, manganese, selenium, and zinc are summarized. For features related to cobalt (and vitamin B 12 ), refer to the vitamin chapter and for molybdate see Figure 22-5. (a) Dietary copper is presented to intestinal cells in the form of protein and amino acid complexes, and in plasma, Cu is bound to a number of proteins; however, it is most often associated with albumin and ceruloplasmin. The transport and cellular metabolism of Cu depend on a series of membrane proteins and smaller soluble peptides that constitute a functionally integrated system for maintaining cellular Cu homeostasis. The high-affinity copper transporter (CTR1) of the plasma membrane mediates
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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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292 Chapter | 10 Hemostasis The pro
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294 Chapter | 10 Hemostasis exhibit
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298 Chapter | 10 Hemostasis that is
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302 Chapter | 10 Hemostasis However
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304 Chapter | 10 Hemostasis 2. Comp
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306 Chapter | 10 Hemostasis is a re
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308 Chapter | 10 Hemostasis 2. Asse
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310 Chapter | 10 Hemostasis necessi
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312 Chapter | 10 Hemostasis disease
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314 Chapter | 10 Hemostasis concent
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316 Chapter | 10 Hemostasis the rol
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318 Chapter | 10 Hemostasis proport
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320 Chapter | 10 Hemostasis a consi
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322 Chapter | 10 Hemostasis Bakhtia
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324 Chapter | 10 Hemostasis Dowd ,
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326 Chapter | 10 Hemostasis Kier ,
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328 Chapter | 10 Hemostasis Nielsen
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330 Chapter | 10 Hemostasis Tablin
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332 Chapter | 11 Neutrophil Functio
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352 Chapter | 12 Diagnostic Enzymol
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380 Chapter | 13 Hepatic Function L
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382 Chapter | 13 Hepatic Function e
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384 Chapter | 13 Hepatic Function p
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386 Chapter | 13 Hepatic Function m
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388 Chapter | 13 Hepatic Function s
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390 Chapter | 13 Hepatic Function f
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392 Chapter | 13 Hepatic Function T
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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 521 Kühl , S. , Mischke
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References 523 creatinine measureme
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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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562 Chapter | 18 Pituitary Function
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606 Chapter | 19 Adrenocortical Fun
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Page 617 and 618: 620 Chapter | 19 Adrenocortical Fun
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Page 691 and 692: Chapter 23 Vitamins Robert B. Rucke
Page 693 and 694: III. Fat-Soluble Vitamins 697 TABLE
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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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