No description available.

Thesis (doctoral)--Tartu Riiklik Ülikool, 1994. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--Lehigh University, 2005. / Includes bibliographical references and vita.

Restricting dietary protein may reduce endogenous acid load. Horses were fed diets with 10% supplemental corn oil in experiment one and either 0% or 10% supplemental corn oil in experiment two. Also, low protein (7.5% crude protein, LP) fortified with .5% lysine and .3% threonine or high protein (14.5% crude protein, HP) was fed. Horses underwent similar interval training and standard exercise tests. In experiment two, horses performed an SET prior to conditioning. The SET consisted of warm ups at the walk and trot followed by six repeated sprints and concluding with a 30 minute recovery at the walk. All sprints were at 10 m/s except the SET prior to conditioning in experiment two, which were at 7 m/s. Blood samples were taken every two weeks and as part of SETs. Samples were analyzed for pH, pCO₂, pO2, Na⁺, K⁺, Cl⁻, lactate, total protein (TP), albumin, creatinine and plasma urea-N (PUN). Bicarbonate, strong ion difference (SID) and total weak acids (Atot) were calculated. Plasma urea-N concentrations were higher in the HP group. Plasma creatinine was not different in experiment one but was higher in the LPHF group in experiment two. Also, the LPHF group had a low body condition score and the same weight therefore had a higher lean body mass. Plasma albumin was not different in either experiment and TP was not different in experiment one. Total protein was higher in the HF groups in experiment two. Protein moderated acid-base responses to SETs in both experiments. The LP group had higher pH and bicarbonate levels as well as a tendency for a higher SID in experiment one and in the SET prior to conditioning for experiment two. Lower lactate levels were observed in the LP group in experiment one. Following conditioning in experiment two, the LP group had higher pH and bicarbonate levels but only combined with HF. Restricting dietary protein can increase pH and bicarbonate levels and high fat has been shown to improve fatty acid oxidation and spare muscle glycogen. Therefore, restricting dietary protein especially in combination with high fat may be beneficial for the exercising horse. / Ph. D.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 1994. / Vita. Abstract. Includes bibliographical references. Also available via the Internet.

Thesis (Ph. D.)--University of Liverpool, 1977. / Includes bibliographical references (leaves 245-261).

Reptiles can often experience perturbations that greatly influence their metabolic status (e.g., temperature, exercise, digestion, and ontogeny). The most common cause of fluctuations in metabolic status in post-embryonic reptiles is arguably digestion and physical activity (which will be further referred to as exercise). The objective of this thesis is to determine the mechanisms involved in CO2 transport during digestion, determine the mechanisms that allow for the maintenance of acid-base homeostasis during digestion, and observing the effect of an understudied form of exercise in semi-aquatic reptiles on the regulation of metabolic acidosis and base deficit. This dissertation provided evidence for potentially novel and under investigated mechanisms for acid-base homeostasis (e.g., small intestine and tissue buffering capacity; Chapters 3 & 4), while also debunking a proposed hypothesis for the function of an anatomical feature that still remains a mystery to comparative physiologist (Chapter 2). This thesis is far from systematic and exhaustive in its approach, however, the work accomplished in this dissertation has become the foundation for multiple distinct paths for ecologically relevant investigations of the regulation of metabolic acidosis/alkalosis in reptiles.

Increased cancer risk is associated with select dietary factors. Dietary lifestyles can alter systemic acid-base balance over time. Acidogenic diets, which are typically high in animal protein and salt and low in fruits and vegetables, can lead to a sub-clinical or low-grade state of metabolic acidosis. The relationship between diet and cancer risk prompts questions about the role of acidosis in the initiation and progression of cancer. Cancer is triggered by genetic and epigenetic perturbations in the normal cell, but it has become clear that microenvironmental and systemic factors exert modifying effects on cancer cell development. While there are no studies showing a direct link between diet-induced acidosis and cancer, acid-base disequilibrium has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion. In short, diet-induced acidosis may influence molecular activities at the cellular level that promote carcinogenesis or tumor progression. This review defines the relationship between dietary lifestyle and acid-base balance and discusses the potential consequences of diet-induced acidosis and cancer occurrence or progression.

Acid-base regulation is vital for animals and while the inorganic carbon system largely determines body fluid pH, another potentially valuable acid-base pair is ammonia (NH4+/NH3). This study focuses on the American horseshoe crab (Limulus polyphemus), a phylogenetically ancient marine chelicerate with no published studies on its acid-base physiology. Physiological and molecular analyses indicate that Na+/K+-ATPase, Rhesus-protein (Rh), and carbonic anhydrase (CA) are involved in acid-base homeostasis and/or ammonia regulation. This likely occurs in the book gills, which consist of ultrastructurally distinct regions. The ventral half-lamella is ion-leaky and displayed high Rh-protein, cytoplasmic CA, and hyperpolarization-activated cyclic nucleotide-gated K+ channel mRNA expression levels, suggesting a specialization in facilitated CO2 and/or ammonia diffusion compared to the dorsal half-lamella. During hypercapnia acclimation, hemolymph acid-base status exhibited a compensated respiratory acidosis accompanied with signs of metabolic depression. Ammonia influx associated with high environmental ammonia acclimation was successfully counteracted, but induced modifications in acid-base homeostasis. / October 2016

by Wang, Wei Vivian. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 237-266). / ACKNOWLEDGEMENTS --- p.viii / SUMMARY --- p.ix / PUBLICATION --- p.xiv / STATEMENT OF ORIGINALITY --- p.xv / LIST OF ABBREVIATIONS --- p.xvi / Chapter CHAPTER 1 --- INTRODUCTION --- p.3 / Chapter 1.1 --- Preamble --- p.3 / Chapter 1.2 --- Free oxygen radicals --- p.7 / Chapter 1.2.1 --- Free oxygen radicals and mechanism of radical damage / Chapter 1.2.1.1 --- What is a free radical? / Chapter 1.2.1.2 --- Mechanism of free radical damage / Chapter 1.2.2 --- Detection and characterisation of free radical species / Chapter 1.2.2.1 --- Direct methods / Chapter 1.2.2.1.1 --- Electron spin resonance (ESR) spectroscopy / Chapter 1.2.2.1.2 --- Chemiluminescence / Chapter 1.2.2.2 --- Indirect methods / Chapter 1.2.2.2.1 --- Lipid peroxidation / Chapter 1.2.2.2.2 --- Protein and DNA oxidation / Chapter 1.2.2.2.3 --- Purine and pyrimidine metabolites / Chapter 1.2.3 --- Free oxygen radicals and major disease / Chapter 1.2.4 --- Oxygen-derived free radicals and fetal hypoxia / Chapter 1.3 --- Acid-base status in cord blood --- p.41 / Chapter 1.3.1 --- Correlation between obstetric clinical events and cord blood acid-base / Chapter 1.3.2 --- Practical implications of cord blood acid-base studies / Chapter 1.4 --- Intrapartum cardiotocography (CTG) analysis --- p.58 / Chapter 1.4.1 --- Base line / Chapter 1.4.1.1 --- Baseline rate / Chapter 1.4.1.2 --- Baseline variability / Chapter 1.4.2 --- Accelerations and decelerations / Chapter 1.4.3 --- Fetal outcome of labour / Chapter 1.4.3.1 --- Fetal heart rate (FHR) changes during labour / Chapter 1.4.3.2 --- Acidaemia during labour / Chapter 1.4.4 --- Computerised analysis of cardiotocogram / Chapter 1.5 --- Intrapartum complications --- p.83 / Chapter 1.5.1 --- Meconium stained amniotic fluid / Chapter 1.5.2 --- Nuchal cord entanglement / Chapter 1.5.3 --- Prolonged 1st and 2nd stage of labour / Chapter 1.6 --- Objectives of project --- p.93 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.98 / Chapter 2.1 --- Materials --- p.98 / Chapter 2.1.1 --- Clinical materials / Chapter 2.1.2 --- Chemicals and reagents / Chapter 2.1.2.1 --- The measurement of malondialdehyde (MDA) / Chapter 2.1.2.2 --- The measurement of organic hydroperoxides (OHP) / Chapter 2.1.2.3 --- The measurement of purine and pyrimidine metabolites / Chapter 2.1.3 --- Equipment / Chapter 2.1.3.1 --- Fetal monitor / Chapter 2.1.3.2 --- Fetal heart rate analysis system / Chapter 2.1.3.3 --- Blood gas analyser / Chapter 2.1.3.4 --- UV-VIS Spectrophotometer / Chapter 2.1.3.5 --- Fluorescence Spectrophotometer / Chapter 2.1.3.6 --- High Performance Liquid Chromatography (HPLC) / Chapter 2.2 --- Investigation Methods --- p.105 / Chapter 2.2.1 --- Blood gas / Chapter 2.2.2 --- Lipid peroxidation in umbilical cord blood / Chapter 2.2.2.1 --- The measurement of MDA / Chapter 2.2.2.2 --- The measurement of OHP / Chapter 2.2.3 --- Purine and pyrimidine metabolites in umbilical cord blood / Chapter 2.2.4 --- Computer analysis of CTG / Chapter 2.2.4.1 --- Data and signal processing / Chapter 2.2.4.2 --- The algorithm / Chapter 2.3 --- Statistical analysis --- p.112 / Chapter CHAPTER 3 --- RESULTS --- p.116 / Chapter 3.1 --- Umbilical blood pH and gas measurements --- p.118 / Chapter 3.2 --- Lipid peroxidation in cord blood plasma --- p.121 / Chapter 3.2.1 --- Validation of assay / Chapter 3.2.1.1 --- Performance characteristics of the MDA assay / Chapter 3.2.1.2 --- Performance characteristics of the OHP assay / Chapter 3.2.2 --- "Inter-relationship among MDA, OHP and acid-base status" / Chapter 3.3 --- Nucleotide metabolites in cord blood plasma --- p.142 / Chapter 3.3.1 --- Calibration of assay / Chapter 3.3.2 --- Inter-relationship among nucleotides and acid-base status / Chapter 3.4 --- Analysis of FHR patterns --- p.150 / Chapter 3.4.1 --- Umbilical blood gas and CTG analysis / Chapter 3.4.2 --- Biochemical parameters and CTG analysis / Chapter 3.5 --- "Relations of umbilical arterial blood pH and gas, lipid peroxidation, purine or pyrimidine metabolites and FHR patterns with intrapartum complications" --- p.166 / Chapter 3.5.1 --- Meconium stained amniotic fluid / Chapter 3.5.1.1 --- Clinical features / Chapter 3.5.1.2 --- Relationship between meconium stained amniotic fluid and biochemical parameters / Chapter 3.5.1.3 --- Relationship between meconium stained amniotic fluid and FHR patterns / Chapter 3.5.2 --- Nuchal cord / Chapter 3.5.2.1 --- Clinical features / Chapter 3.5.2.2 --- Relationship between nuchal cord and biochemical parameters / Chapter 3.5.2.3 --- Relationship between nuchal cord and FHR patterns / Chapter 3.5.3 --- The length of second stage of labour / Chapter 3.5.3.1 --- Clinical features / Chapter 3.5.3.2 --- Relationship between the length of second stage and acidaemia or FHR patterns / Chapter 3.5.4 --- Apgar scores / Chapter 3.5.4.1 --- Clinical features / Chapter 3.5.4.2 --- Relationship between Apgar scores and biochemical parameters / Chapter 3.5.4.3 --- Relationship between Apgar scores and FHR patterns / Chapter 3.5.4.4 --- "Relationship between Apgar scores and nuchal cord, meconium or second stage of labour" / Chapter CHAPTER 4 --- DISCUSSION --- p.189 / Chapter 4.1 --- Blood pH and gas in fetal asphyxia --- p.189 / Chapter 4.2 --- Lipid peroxidation in cord blood at birth --- p.194 / Chapter 4.2.1 --- Method for measurement of the cord plasma MDA / Chapter 4.2.2 --- Method for measurement of the cord plasma OHP / Chapter 4.2.3 --- Relationship between the fetal asphyxia and lipid peroxidation in cord plasma / Chapter 4.3 --- Purine and pyrimidine metabolites in cord blood at birth --- p.203 / Chapter 4.3.1 --- Limitations imposed by the tcchniqucs used / Chapter 4.3.2 --- Relationship between the fetal asphyxia and purine and pyrimidine metabolites in cord plasma / Chapter 4.4 --- Computerised analysis of CTG --- p.210 / Chapter 4.4.1 --- CTG patterns and cord blood acid base balance / Chapter 4.4.2 --- CTG patterns and cord blood biochemical parameters / Chapter 4.5 --- "Intrapartum complications 2,9" / Chapter 4.5.1 --- Meconium stained amniotic fluid / Chapter 4.5.2 --- Nuchal cord / Chapter 4.5.3 --- The length of second stage / Chapter 4.5.4 --- Apgar scores / Chapter CHAPTER 5 --- CONCLUSION --- p.233 / REFERENCES --- p.237