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

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702 Chapter | 23 Vitamins H CH H 3 C CH 3 H 3 cis-configuration C C 8 C 10 C H 1 7 9 11 H 2 C 2 6 C C C 12 C 3 5 13 H 2 C 4 C H H C H C CH 3 H 3 C C 14 H 2 11-cis-retinal C 15 H O Capillary all-transretinol Retinal Pigment Epithelium 11-cis-retinal 11-cis-retinol all-trans-retinyl ester all-trans-retinol Interphotoreceptor Matrix Photoreceptor (Rod) Cell 11-cis-retinal Rhodopsin Opsin Opsin + all-trans-retinal all-trans-retinol LIGHT Neuronal signaling VISION Visible light P-Opsin II-CIS Retinal ATP Opsin Rhodopsin h H CH H 3 C CH 3 H CH 3 3 C C 8 C 10 C 12 C 14 1 7 9 11 13 H 2 C 2 6 C C C C C 3 5 H 2 C 4 C H H H H C CH 3 H 2 trans-configuration all-trans-retinal H C 15 O all-trans Retinal GTP + Transducin-GDP Membrane hyperpolarization Pi GTP Metarhodopsin II + Transducin-GTP + GDP + Phosphodiesterase cGMP Na uptake + GMP FIGURE 23-7 Vitamin A and vision. Retinal, as a component of rhodopsin, facilitates the transfer of energy from photons of light to electrochemical signals. The series of events includes the cis - trans isomerization, which results in a highly strained form of rhodopsin that is converted to metarhodopsin with subsequent deprotonation. The deprotonated metarhodopsin interacts with transducin, one of the proteins in the transmembrane G-protein family. This interaction stimulates cGMP phosphodiesterase activity, which results in a decrease in cGMP and signal amplification. The local changes in cGMP concentration result in turn in changes in cation flux (Na and Ca ions) across rod cell membranes to initiate firing of cells of the optic nerve. Retinyl Ester Retinol Retinyl esters mRNA Retinoic Acid Retinol Retinal RAR X 9cRAR PPAR X 9cRAR VDR X 9cRAR Retinoic Acid 9-cis or 13-cis Retinoic Acid FIGURE 23-8 Vitamin A and cell regulation. Within cells all- trans retinol associates with cytosolic retinol-specific binding proteins, and the resulting complex become vehicles for subsequent processing. For example, all- trans retinol may be oxidized and isomerized to all- trans, 9- cis, or 13- cis retinoic acid, which subsequently binds to retinoic acid-specific binding proteins that act as transcription factors in protein regulation and cellular differentiation. The nature of the metabolic control has many facets including the regulation of specific receptor concentrations and their combination to form specific signaling complexes. The figure shows duplexes for the retinoic acid receptor (RAR) with (1) an isomeric form, (2) complexes with peroxisomal activation receptors, and (3) receptors under the control of vitamin D derivatives.
III. Fat-Soluble Vitamins 703 doses of retinoids, epithelial cells undergo a “ terminal differentiation. ” Epithelial cells lose their normal columnar shape, become flattened or squamous, and increase their cytosolic content of keratin (stabilized by transglutaminase catalyzed cross-links). In dermis, this process normally results in a protective outer layer, scales, and other specialized surfaces. With a deficiency, however, the skin can thicken and become hyperkeratinized. If the primary function of the epithelial cell is the provision of a moist surface or absorption (e.g., an enterocyte or lung secretory cell), squamous hyperkeratinization leads to loss of functional integrity. Lack of protective mucus secretions sets the stage for infections of the lungs and other tissues that depend on a mucus barrier. In the intestine, hyperkeratinization induces premature sloughing of enterocytes and malabsorption. The gradient delivery of retinoids to epithelial cells helps to explain why some epithelial cells undergo terminal differentiation, whereas others undergo cell cycling and periodic turnover, although important details need to be resolved. Other cells that are responsive to retinoids include phagocytic cells and cells associated with the immune response (e.g., the normal proliferation of the B cells and T cells requires vitamin A) ( Ross et al., 2000 ). 6 . Requirements For any given animal, the requirement for vitamin A depends on age, sex, rate of growth, and reproductive status. For optimal maintenance, the allowance for many animals ranges from 100 to 200 international units per kilogram of body weight per day (one international unit is equal to 0.3 μg of retinol). In young growing animals, a more precise method of expressing the vitamin A requirement is on an energetic basis. In animal feeds, 4000 to 10,000 international units per kilogram of feed is considered adequate in the United States to provide vitamin A requirements for most animals. Pathological conditions that influence vitamin A status include malabsorption, including pancreatic insufficiency and cholestatic disease, cystic fibrosis, liver disease, and kidney disease. Many forms of liver disease interfere with the production or release of RBP, which results in a lower plasma level of vitamin A. Renal failure can result in loss of RBP in urine. Factors that impair lipid absorption and transport might also be expected to influence vitamin A status. 7 . Evaluation of Vitamin A Status of Animals The vitamin A status of animals may be evaluated on the basis of physiological, clinical, and biochemical procedures. Clinical testing for night blindness and the elevation of CSF pressure has been used to indicate vitamin A status. The concentration of retinol and its esters is readily measured in biological samples by HPLC using various detectors and indicates the vitamin A status. As the concentration of retinol in plasma is well maintained until liver reserves are depleted, plasma retinol is not an index of vitamin A reserves. The latter is best provided by analysis of liver biopsy samples. In many carnivores, the plasma contains, in addition to retinol, equal or greater concentrations of retinyl palmitate and retinyl stearate bound to albumin, the immunoglobulin fraction, or to VLDL. Plasma retinol concentrations in excess of 30 μ g/dl generally indicate that vitamin A is not limiting. In most species, liver concentrations of 100 μ g of retinol/g liver are generally adequate. 8 . Pharmacology and Toxicity Vitamin A and various retinoids are used increasingly to treat skin disorders (acne and psoriasis) and certain forms of cancer. A vitamin A responsive dermatosis in cocker spaniels is well recognized and has been previously described ( Scott, 1986 ). Retinyl- β -glucuronide and hydroxyethyl retinamide are commercial preparations of retinoids that have such activity but are less toxic than retinoic acid. The mechanisms by which these agents function most probably relate to the complex pathways involved in epithelial and epidermal cell differentiation. Vitamin toxicities may be classified under three broad categories: acute, chronic, and teratogenic. When a single dose of vitamin A (greater than 100 mg) is injected into animals (20 to 50-kg weight range), symptoms such as nausea, vomiting, increased cerebral spinal fluid pressure, and impaired muscular coordination result. A lethal dose of vitamin A (100 mg) given to young monkeys has been reported to cause coma, convulsions, and eventual respiratory failure. Chronic toxicity may be induced by intakes of vitamin A in amounts 10 times the normal requirements. Doses of vitamin A in this range can lead to alopecia, ataxia, bone and muscle pain, and purities. Although cats have a high tolerance to excessive intakes of vitamin A, hypervitaminosis A occurs in cats that are given a diet largely of liver. Affected cats exhibit skeletal deformations, particularly exostoses of the cervical vertebra, which precludes effective grooming. Vitamin A is also a powerful teratogen. A single large dose during pregnancy (in the 50- to 100-mg range) for an animal weighing 20 to 50 kg can result in fetal malformations. Chronic intakes (exceeding 10 times the requirements for given animals) can also be teratogenic. Carotenoids, unlike retinoids, are generally nontoxic, and many animals routinely ingest gram amounts of carotenoids on a daily basis with no deleterious effects (old world primates, herbivores, etc.). 9 . Other Carotenoids In addition to β -carotene, of the other carotenoids, the most information is available for α -carotene, lycopene, lutein, zeaxanthin, and cryptoxanthin. To reiterate, these carotenoids along with hundreds of others are the natural pigments in
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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 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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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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Page 647 and 648: 650 Chapter | 21 Clinical Reproduct
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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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Page 746 and 747: 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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