Thesis (doctoral)--Ludwig Maximilians-Universität zu München, 1979.

No description available.

The effect of exercise on the total ketone body (acetoacetate + D-3-hydroxybutyrate) concentrations in the blood was studied to find out whether the susceptibility of non-athletes, compared with athletes, to develop post-exercise ketosis is the result of the former's increased reliance on glycolysis during exercise. In the first experiments, use was made of the diving reflex to induce peripheral vasoconstriction during exercise in both physically trained and untrained subjects. It was hoped that under these circumstances athletes and non-athletes would utilize similar amounts of muscle glycogen during exercise, and therefore develop similar degrees of ketosis after exercise, if the glycogen content of the muscles was in fact the factor which determined post-exercise ketosis. Ten non-athletic subjects, six long-distance runners, and three competitive swimmers were therefore studied before, and for 9½ hours after swimming in the early morning. The last meal was eaten during the evening before the swim. On the first test day the subjects swam underwater for as far as they could go three times in succession. A week later the same distance was swum on the surface without breath-holding. There was no increase in the post-exercise blood ketone body concentrations in any of the subjects after either form of the exercise, compared with control day values (when the subjects fasted, but did not swim at 07h30). Similar results were obtained when healthy young medical students (aged 18 - 23 years; trained and untrained) performed maximal exercise for 15 minutes, or moderate exercise for up to 90 minutes, on a bicycle ergometer. When six older subjects (aged 30 - 51 years) exercised at 75 W for 90 minutes, three of them developed ketonaemia, which reached its maximum intensity about three hours after exercise. The exercising heart rates of these older subjects were similar to those of the younger non-athletic subjects who had performed the same exercise, but had not developed post-exercise ketosis., An extra 60 - 90 g sucrose in the diet of the subject who had developed the most marked post-exercise ketonaemia, abolished the response, whereas carbohydrate restriction intensified it. A protein-fat diet caused two well trained marathon runners to develop the highest post-exercise blood ketone body levels yet recorded (3,88 mmoles/l). Free fatty acid, glucose, growth hormone and insulin concentrations in the serum followed patterns different from the ketone body levels during, and for 7 ½ hours after exercise, but were also affected more by diet than by training. Post-exercise ketosis, previously ascribed to a lack of athletic training, could equally well be ascribed to the lower carbohydrate intake of sedentary subjects compared with athletes: the two marathon runners were estimated to eat about twice as much carbohydrate in their regular diet than the sedentary subject who had developed post-exercise ketonaemia without carbohydrate restriction. The final experiments were designed to find out whether post-exercise ketosis was the result of the low levels of glycogen in the body, or of the gluconeogenesis which occurs after exercise to replenish the carbohydrate stores. Twenty-four highly trained athletes were therefore studied after prolonged exercise following a protein-fat diet to induce post-exercise ketosis. Six of them were then given 100 g alanine to take by mouth, six ingested 100 g glucose, six ingested 100 g starch, and the remaining six acted as controls. It was found that both alanine and glucose ingestion reduced the blood ketone body concentration from about 2 mmoles/l to less than 0,4 mmoles/l in 3 hours. Starch had a minimal effect on the blood ketone body levels during the 5-hour observation period. Alanine and glucose exerted their antiketogenic effects in the context of widely different serum insulin, glucagon and growth hormone concentrations. Similar results were obtained in starvational ketosis, and even in normoketonaemic subjects. The results indicate that ketogenesis is not the result of gluconeogenesis, nor of a low insulin/glucagon (+ growth hormone) ratio in the blood. It is concluded that low levels of glycogen, or of a metabolic intermediary of glycogen metabolism (such as glucose-1-phosphate, or glucose-6-phosphate) in the liver is probably the single most important stimulus for ketogenesis after exercise and starvation.

M. Pharm., Faculty of Health Sciences, University of the Witwatersrand, 2011 / Background: According to the 2010 edition of the UNAIDS Report on the global AIDS epidemic, an estimated 320 000 (20%) fewer people died of AIDS-related causes in South Africa in 2009 than in 2004 due to the increase in availability of anti-retroviral medicines.(2) With this positive trend, the mindset should be shifted towards reducing adverse effects of ART. The need for permanent ART treatment and the significant increase in life expectancy have led to the observation of new, frequent, and sometimes severe drug-related adverse effects.(4) One of the most challenging and potentially dangerous side-effects is hyperlactataemia (Hlac) that may evolve to lactic acidosis (LA)(5) ART–associated Hlac may be asymptomatic, or symptomatic which in the extreme case can progress to life threatening acidosis. The latter, i.e. lactic acidosis is a fairly frequent and often misdiagnosed or under diagnosed and potentially fatal side effect of ARTs. (6) Objectives: To explore the relationship between Hlac/LA and gender, weight, dosage CD4 and regimen alterations in HIV patients on ARTs and to compare the earlier regimens to the revised regimens as independent risk factors for Hlac and LA. Sample size would be based on the hypothesis that newer regimens would reduce the incidence of Hlac and LA. Methods: A Retrospective study was conducted by reviewing 3 741 patient files from August 2004 to December 2007. This study was to assess the incidence and risk factors of Hlac/LA. Hlac was defined as a venous lactate measurement of ≥2.3mmol/L and LA was ≥5mmol/L. Immunological, virological, haemotological and biochemical results were recorded for all the patients. A second phase involved a Prospective study. Patients who were on treatment for >12 months were randomly selected from the queue at the clinic between the September 2008 and December 2009. Immunological, virological, haematological and biochemical information was recorded for all patients selected. Analysis involved descriptive statistics, comparison of means, frequency analysis and multivariate analysis. Results: Two-hundred and thirty two patients were identified with elevated lactate levels in the retrospective study. The incidence was 6.2% in this population, with gastro-intestinal symptoms, peripheral neuropathy, abdominal tenderness, rash and upper respiratory tract infection being the significant symptoms. The major risk factor was a low CD4 count. The prospective study included 292 patients with 24.3% with Hlac/LA with peripheral neuropathy (p 0.209), gastrointestinal symptoms (nausea, vomiting) (p 0.148) and abdominal tenderness (p 0.214) were the most significant symptoms. In terms of the hypothesis that newer regimens would lower the incidence of elevated lactate levels by 50%, the observed incidence of 24.3% is no different from previously reported rates. This therefore shows that although regimen changes have been implemented the overall incidence of Hlac appears to be unchanged but the LA rate was found to be significantly lower than before, 6.8 cases per 1000 patient years vs ±19 cases per 1000 person years.(16) Gastro-intestinal symptoms but not peripheral iv neuropathy; with low CD4 count, weight loss and low weight on entry were the significant risk factors, which is most likely representative of advanced disease. Conclusions: Although newer regimens have been introduced, Hlac/LA still exist. Healthworkers need to be on high alert for Hlac/LA particularly if a patient enters into the ART program with a low CD4 count and a low weight

Two experiments were conducted. In experiment 1, the objectives were: 1) to develop and evaluate the accuracy and precision of a new continuous ruminal pH measurement system 2) to determine the required frequency for pH electrode standardization and 3) to determine the effect of additional pre-partum concentrate when compared to NRC (2001) recommendations on post-partum ruminal acidosis in primiparous cows. Accuracy and precision of the Lethbridge Research Centre Ruminal pH measurement system (LRCpH) was determined by comparing LRCpH derived values against manual measurement. To determine the required frequency of electrode standardization, three treatments were imposed (24, 48, or 72 h of continuous measurement) and arranged in a repeated 3×3 Latin square design. The LRCpH accurately and precisely measured ruminal pH (repeated measures correlation coefficient = 0.97 and concordance correlation coefficient = 0.97 for 5-min averages). Changes in baseline mV readings for pH readings after 24, 48 or 72 h of ruminal incubation were not significantly different than zero, indicating that daily standardization of new electrodes was not essential. Using the LRCpH to measure ruminal pH overcomes animal mobility restrictions of previous systems. <p>In experiment 2, the effect of additional concentrate allocation during the pre-partum period was evaluated using 14 ruminally cannulated Holstein heifers. The heifers were assigned to one of two feeding regimes pre-calving: 1) control treatment or 2) an intensive high concentrate feeding treatment (HC). All cows received the same lactation diet post-partum. Ruminal pH was measured continuously from d -5 to d +5, and for 3-consecutive days starting on d +17 ± 1.2, d +37 ± 1.4, and d +58 ± 1.5 relative to parturition. Feeding additional concentrate pre-partum did not reduce post-partum ruminal acidosis. In fact, animals fed the HC treatment had more daily episodes of acute acidosis and lower dry matter intake and body condition score than animals fed the control treatment. Day relative to parturition affected the occurrence and severity of ruminal acidosis with a dramatic increase in ruminal acidosis after parturition. This study demonstrates that feeding addition concentrate pre-partum did not reduce post-partum acidosis which emphasized the need to develop and implement feeding strategies that reduce this risk.

Two experiments were conducted. In experiment 1, the objectives were: 1) to develop and evaluate the accuracy and precision of a new continuous ruminal pH measurement system 2) to determine the required frequency for pH electrode standardization and 3) to determine the effect of additional pre-partum concentrate when compared to NRC (2001) recommendations on post-partum ruminal acidosis in primiparous cows. Accuracy and precision of the Lethbridge Research Centre Ruminal pH measurement system (LRCpH) was determined by comparing LRCpH derived values against manual measurement. To determine the required frequency of electrode standardization, three treatments were imposed (24, 48, or 72 h of continuous measurement) and arranged in a repeated 3×3 Latin square design. The LRCpH accurately and precisely measured ruminal pH (repeated measures correlation coefficient = 0.97 and concordance correlation coefficient = 0.97 for 5-min averages). Changes in baseline mV readings for pH readings after 24, 48 or 72 h of ruminal incubation were not significantly different than zero, indicating that daily standardization of new electrodes was not essential. Using the LRCpH to measure ruminal pH overcomes animal mobility restrictions of previous systems. <p>In experiment 2, the effect of additional concentrate allocation during the pre-partum period was evaluated using 14 ruminally cannulated Holstein heifers. The heifers were assigned to one of two feeding regimes pre-calving: 1) control treatment or 2) an intensive high concentrate feeding treatment (HC). All cows received the same lactation diet post-partum. Ruminal pH was measured continuously from d -5 to d +5, and for 3-consecutive days starting on d +17 ± 1.2, d +37 ± 1.4, and d +58 ± 1.5 relative to parturition. Feeding additional concentrate pre-partum did not reduce post-partum ruminal acidosis. In fact, animals fed the HC treatment had more daily episodes of acute acidosis and lower dry matter intake and body condition score than animals fed the control treatment. Day relative to parturition affected the occurrence and severity of ruminal acidosis with a dramatic increase in ruminal acidosis after parturition. This study demonstrates that feeding addition concentrate pre-partum did not reduce post-partum acidosis which emphasized the need to develop and implement feeding strategies that reduce this risk.

Thesis (Ph. D.)--University of Alberta, 2010. / Title from pdf file main screen (viewed on Jan. 18, 2010). A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Department of Biochemistry, University of Alberta. Includes bibliographical references.

No description available.

The effects of induced subacute ruminal acidosis (SARA) using grain pellet-based (GPI) and alfalfa pellet-based diet models on systemic immunological parameters were evaluated in nonlactating Holstein cows. The systemic immunological parameters analysed in this study included rectal temperature, blood cell leukogram, expression of lipopolysaccharide (LPS) recognition receptors on leukocytic cells, and plasma and serum proteins. Also, blood biochemistry was analysed. There were no significant differences in rectal temperature, blood cell leukogram, expression of LPS recognition receptors and fibrinogen or haptoglobin concentrations between control and SARA induction treatments. Concentrations of serum amyloid A and lipopolysaccharide-binding protein increased while total protein concentrations decreased in response to GPI SARA compared to control. Blood glucose and urea concentrations increased and decreased, respectively, with GPI SARA treatment. Grain pellet-induced SARA resulted in changes to serum proteins and acute phase proteins but did not affect other systemic immunological parameters suggesting a localized inflammatory response was initiated.

The effects of induced subacute ruminal acidosis (SARA) using grain pellet-based (GPI) and alfalfa pellet-based diet models on systemic immunological parameters were evaluated in nonlactating Holstein cows. The systemic immunological parameters analysed in this study included rectal temperature, blood cell leukogram, expression of lipopolysaccharide (LPS) recognition receptors on leukocytic cells, and plasma and serum proteins. Also, blood biochemistry was analysed. There were no significant differences in rectal temperature, blood cell leukogram, expression of LPS recognition receptors and fibrinogen or haptoglobin concentrations between control and SARA induction treatments. Concentrations of serum amyloid A and lipopolysaccharide-binding protein increased while total protein concentrations decreased in response to GPI SARA compared to control. Blood glucose and urea concentrations increased and decreased, respectively, with GPI SARA treatment. Grain pellet-induced SARA resulted in changes to serum proteins and acute phase proteins but did not affect other systemic immunological parameters suggesting a localized inflammatory response was initiated.