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

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I. Introduction 665 The stability of calcium complexes of ethylenediamine tetraacetic acid (EDTA) and its homologues with increasing number of C atoms in the bridge between N atoms is as follows: Although a further discussion of ligand basicity and steric effects is beyond the scope of this chapter, knowledge of the following relationship can be useful where various coordinating groups are compared in order of decreasing affinity for given metal ions: N Atom in Bridge Carbon Log K a 2 5 10.5 3 6 7.1 4 7 5.2 5 8 4.6 Such complexes are called chelates. Note that the stability also increases as the number of rings increases: Ligand Number of Rings Log K a H 2 NCH 2 COOH 1 5.2 CH 2 COOH NHCH 2 COOH 2 7.0 CH 2 COOH NCH 2 COOH CH 2 COOH 3 10.6 CCO > NH2 > NN> N > COO > O>> CO Enolates > Amino > Azo > Ring N > Carboxylate > Ether >> Carbonyl These relationships are important to the types and shapes of complexes that metal ions form, their stabilities, and their redox potentials. C . Biological Perspectives 1 . Trace Elements as Essential Components in Evolution and Animal Diversity A reasonable question to ask is why are certain elements more nutritionally important than others From an evolutionary perspective, relative abundance and, in many cases, the ability to form complexes with catalytic (redox) potential are among the most important reasons. Figure 22-1 shows the distribution of elements in seawater, bacteria, fungi, plants, and animals ( Banin and Navrot, 1975 ). That 3.6 Bacteria G N 3.6 Fungi G N 0 12 24 Log 36 Enrichment Factor 48 60 72 84 K Na Sea water CuMg Sr Ca Cd Zn Cu Mg Mn Cr Fa Cd Si B Ma Mo P S C N Log Enrichment Factor 1.2 0 1.2 3.6 3.6 K Na 0.0 Cu Zn Mg Ca Mn Plants Mo Fa AJ Si B P S 0.5 1.0 1.5 G N 1.2 0 1.2 3.6 3.6 K Na 0.0 Cd Zn Sr Cu Ca Ma Animals Mg Ni Cr Fa Mo B Si AJ P S 0.5 1.0 1.5 G N 0.0 0.5 1.0 1.5 Log ionic potential Log Enrichment Factor 1.2 0 1.2 3.6 S Cd B P K Zn Mo Ca Mg Na Sr Mn Cu Ca Ni Si Fa Cr AJ Co 1.2 0 1.2 3.6 K Za P Zn Ca Mo Cd B Sr Md Ni Si Cu Fa Cr Mn Ag S 0.0 0.5 1.0 1.5 Log ionic potential 0.0 0.5 1.0 1.5 Log ionic potential FIGURE 22-1 Distribution of elements in seawater, bacteria, fungi, plants, and animals relative to the earth’s crust plotted as a function of the ionic potential (see text).
666 Chapter | 22 Trace Minerals the patterns are similar suggests common chemical principles have persisted as a part of natural selection. To the extent that the ionic potential of an element is related to its relative abundance in seawater, one can argue that evolutionary choice as it relates to metal utilization is based in part on chemical properties that dictate its interaction with water. For example, when the ionic potential is high ( 10), the positive ion appropriates one or more oxygen ions, freeing the hydrogen and forming an oxyanion. Oxyanions are generally soluble; thus, relative to the earth’s crust, the log enrichment is high. This is a characteristic of the nonmetals in the upper right corner of the periodic table (e.g., C, N, O, S, P). Such elements are also the smallest in size to form stable multiple bonds. With time carbon can become a carbonate ion in water and eventually CO 2 (O C O, a gas) when oxidized further. Contrast that with silicon, carbon’s tetravalent homologue in period 4 of the periodic table. Silicon in water forms silicates, which easily polymerize and are oxidized to the end product silicon dioxide or quartz, a solid, because of the inability to form stable multiple bonds: | | | | | -Si-O-Si-O-Si-O-Si-O-Si- | | | | | O O O O O | | | | | -Si-O-Si-O-Si-O-Si-O-Si- | | | | | For elements with low to intermediate ionic potential values, such as silicon (IP log 0.5), the log of the enrichment factor is often in the range of 1 to 1, indicating small enrichment or even depletion relative to the crust. Metals with low, but positive, intermediate, or slightly negative ionic potentials tend to form hydroxides in water, most with low solubility. Many of the essential trace elements fall in this category. Finally, elements with negative ionic potentials tend to form hydrated shells and interact by organizing water structure, a role that is important to understanding the functions of Na, K, Mg, and Ca in cells. 2 . Utilization of Trace Elements and Metabolic Regulation and Metabolism As an additional perspective, it can be generalized that dietary requirements across species ( Table 22-2 and Fig. 22-2 ) are more similar than dissimilar ( Rucker, 2007 ). This is particularly the case when given requirements are expressed per unit of energy consumed or per unit weight of ration. Figure 22-2 shows the relationship for selected mineral requirements and metabolic body size. The requirements of trace elements scale allometrically in a manner that is similar in principle to scaling algorithms (e.g., kWt 3/4 ) for basal metabolism. If a set of common principles was involved in Log Approx. Daily Need In Mg 2 1 0 Approx. 1 Daily 25 Need X In Mg 0 0 25 50 75 100 X Body weight in Kg 2 2 1 0 1 2 3 Log body weight in Kg FIGURE 22-2 Relationship of mineral requirements and metabolic body size. Log plots of the daily intake of selected minerals for mice, rats, chickens, dogs, humans, and pigs versus their respective body weights in kilograms. The data for individual minerals plotted in this fashion result in reasonably linear plots with slopes that range from 0.6 to 0.8. For any given mineral, plots of daily intake versus units of body weight are not linear and require polynomial equations to describe the function (insert). the selection of the elements important to life, it follows that nutrition requirements would be influenced by the same principles (e.g., all cells utilize in principle the same metabolic strategies). Indeed, a strong case can be made that when expressed per unit of food-derived energy or relative to metabolic body size, requirements for essential elements are similar for a diverse array of species. As substances important to catalyst and entasis, it follows consequently that their relative nutritional needs are also driven by factors and principles important to energy utilization. Why do deficiencies or excess occur Nutritional deficiencies obviously result when the intake of essential nutrients consistently falls below the minimal requirement (i.e., a primary deficiency). In animal nutrition this is regrettably common given the tendency to feed monotonous diets or foods common to a given region. Secondary mineral deficiencies can also arise through a variety of mechanisms that include poor bioavailability, interactions with other competing substances, and genetic influences (e.g., polymorphisms that dictate an increased need for given nutrients; Keen, 1996 ). Table 22-3 provides a list of several mechanisms underlying the development of deficiencies and common interactions that will be amplified in each of the sections that follow. II . COBALT A large animal (50 to 100 kg) can contain 1 to 2 mg of Co with liver containing about 0.1 mg (1.7 μmol), skeletal muscle 0.2 mg (3.4 μmol), bone and hair 0.3 mg (5.1 μmol) each, and adipose tissue 0.4 mg (6.8 μ mol) ( Smith et al. , 1987 ). X 50 X Mn Zn Zinc Cu X
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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 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 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 691 and 692: Chapter 23 Vitamins Robert B. Rucke
Page 693 and 694: III. Fat-Soluble Vitamins 697 TABLE
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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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