With the alarming prevalence of overweight and obesity, it is important to explore new approaches and strategies to improve dietary quality and weight status. Recently, a neuropsychological model of obesity was proposed. This new model illustrates an evidencebased relationship between a chronically activated hypothalamic-pituitary-adrenal (HPA) axis, due to chronic psychological stress and mood disturbance, and the food reward-related mechanisms within the brain. Intensive mindfulness-based training programs, such as Jon Kabat-Zinn's Mindfulness-Based Stress Reduction have demonstrated impressive results with a variety of populations. Given the relationship of stress to eating behavior and the capacity of mindfulness in managing stress, a relationship between mindfulness and eating is expected. The goal of this dissertation research was to help understand the concept of mindful eating and the relationship between stress and eating behavior for mothers of young children in order to inform the development of a mindfulness-based stress management and dietary intervention. The research consisted of three components: 1) an informative photo-elicitation study with working mothers of young children aiming to understand how mothers define, perceive, and experience mindful eating; 2) a crosssectional study investigating the relationship between mindful eating, dietary quality, and stress; and 3) the development and mixed-methods pilot intervention of the Slow Down Program, a mindfulness-based stress management and nutrition program for mothers of young children. Results from these studies give further evidence on how mindfulness can be utilized in nutrition research and they further confirm the success of mindfulness-based training on health and dietary outcomes. This research can inform public health programs and practice to encourage mindfulness, as it relates to dietary behavior, for families and other audiences, as well as future research studies that explore the interaction between mindfulness and eating behaviors. / Ph. D.

The purpose of the present study is to determine the nitrogen intake and output (in both urine and feces) of two groups of Texas college women living in the Home Management House at North Texas State College.

Background Chronic kidney disease (CKD) is a condition characterized by gradual loss of kidney function over time. Millions of adults have CKD and those who have diabetes, hypertension, and family history of kidney failure are at highest risk of its development. Patients may develop comorbidities, such as cardiovascular disease, anemia, mineral and bone disorders, and peripheral nervous system diseases. Those with kidney failure require dialysis or kidney transplantation, as well as medications, diet therapy, restriction of fluid intake, and lifestyle modifications. The cost for such treatment represents an enormous burden on healthcare systems worldwide, costing about 8% of the Medicare budget in the U.S. Literature review findings Chronic kidney disease is now described based on internationally accepted definitions and diagnosed, when structural or functional abnormalities of the kidneys persist for more than 3 months. End-stage kidney disease is the last stage of chronic kidney disease and is associated with a decreased quality of life and life expectancy. This comprehensive literature review focuses on the effectiveness of dietary therapy in delaying the progression of CKD to end stage kidney disease (ESKD). Current evidence provides guidelines to manage ESRD with the general population. However, despite this, many clinicians do not know how to use diet as part of clinical management. Proposed methods Given the broad spectrum of different dietary therapies to decelerate progression of CKD, many providers do not utilize this information in clinical practice. A workshop hosted by registered dieticians, summarizing the most up-to-date literature on the topic of dietary interventions to slow down CKD progression would be beneficial. The workshop will measure mid-level and high-level practitioner’s knowledge on dietary therapy for CKD and assess this post-workshop. The goal is to expand the knowledge of providers and equip them with the resources necessary to educate patients on healthy dietary modifications, in order to minimize progressive CKD. Conclusions Despite the availability of dialysis and recent advancements in post-transplant care, there is a benefit to lifestyle modification. There is promising evidence that a diet low in protein, potassium, or salt and following certain diets, such as the Mediterranean diet, is beneficial in the deceleration of CKD to end stage renal disease (ESRD). A diet containing processed foods, high protein, high salt, and high potassium content has been associated with an increased risk of transition from late-stage CKD to ESRD. It is possible that these dietary recommendations may apply to prevention of CKD or ESRD. The workshop will present the most up-to-date knowledge in the area of dietary therapies for CKD. A curriculum for mid- and advanced-level health care providers will provide them with the tools necessary to provide their patients with nutrition and lifestyle management.

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / The mechanisms by which diets high in saturated fat (HFD) contribute to intestinal adaptation and obesity are unknown. The hypothesis that functional changes in distal portions of small intestine are induced by HFD was tested in C57B1/6 mice. Specifically, it was examined whether the putative fatty acid translocase CD36 was phosphorylated in mouse intestinal epithelial cells and whether dephosphorylation of CD36 increased long chain fatty acid (LCFA) absorption. Co-immunoprecipitation was used to investigate specific intestinal alkaline phosphatases that might interact with CD36. It was also examined whether chronic ingestion of an HFD would lead to upregulation of the CD36 and/or one or more intestinal alkaline phosphatases that may activate CD36. CD36 was found to be phosphorylated on the surface of mouse enterocytes, indicating that there may be a phosphatase-sensitive pool of phospho-CD36 (pCD36) in mouse small intestinal tissue. CD36 was dephosphorylated by alkaline phosphatase and this treatment increased long chain but not short chain fatty acid uptake. Long chain fatty acid uptake was blocked with a specific CD36 inhibitor. CD36 from mouse small intestines physically interacted specifically with global intestinal alkaline phosphatase (gIAP) but not duodenal alkaline phosphatase (dIAP). As expected, HFD increased body weight, adiposity, and plasma triglycerides compared to control mice. CD36 and gIAP but not dIAP protein levels were significantly increased in distal but not proximal regions of intestines of HFD mice. Finally, HFD increased the absorptive capacity of the distal small intestine for LCFA in a CD36-dependent manner. It is concluded that HFD specifically upregulates gIAP protein in epithelial cells of the distal regions of the small intestine of mice, and that one of its substrates is pCD36, which has been implicated in transcellular fat transport. This diet also increases the absorptive capacity of the distal small intestine for LCFAs. Taken together, these results suggest that HFD causes intestinal adaptation that results in an increased capacity to absorb dietary fat. This effect is mediated in part by increasing the expression and activity of the fatty acid transporter CD36 and its regulatory enzyme gIAP. / 2999-01-01

Koon Chi Man. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 158-174). / Abstracts in English and Chinese. / Acknowledgment --- p.i / Abbreviations --- p.ii / Abstract --- p.v / Chinese Abstract --- p.viii / Table of Content --- p.x / Chapter Chapter one: --- Introduction --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Classification of Plant Polysaccharides --- p.2 / Chapter 1.2.1 --- Definition of Dietary Fiber --- p.3 / Chapter 1.2.2 --- Types of Soluble Dietary Fiber --- p.3 / Chapter 1.3 --- Physiological Effect of Fiber --- p.6 / Chapter 1.3.1 --- Reduction in Absorption by Viscous Polysaccharides --- p.7 / Chapter 1.3.2 --- Gastric Emptying --- p.7 / Chapter 1.3.3 --- Effect of Viscous Polysaccharides on Intraluminal Mixing --- p.8 / Chapter 1.3.4 --- Effect of Luminal Secretions on Viscosity --- p.9 / Chapter 1.4 --- Physicochemical Qualities and Hypocholesterolemic Effects --- p.9 / Chapter 1.5 --- Gastrointestinal Events and Hypocholesterolemic Effects --- p.11 / Chapter 1.5.1 --- Mouth --- p.11 / Chapter 1.5.2 --- Stomach --- p.12 / Chapter 1.5.3 --- Small intestine --- p.12 / Chapter 1.5.4 --- Large intestine --- p.13 / Chapter 1.6 --- Proposed Mechanisms for Hypocholesterolemic Effects --- p.13 / Chapter 1.6.1 --- Altered Bile Acid Absorption and Metabolism --- p.14 / Chapter 1.6.2 --- Modified Lipid Absorption and Metabolism --- p.15 / Chapter 1.6.3 --- Effects of SCFA on Lipid Metabolism --- p.15 / Chapter 1.6.4 --- Changed Hormone Concentrations --- p.16 / Chapter Chapter Two: --- Materials and Methods --- p.17 / Chapter 2.1 --- Materials --- p.17 / Chapter 2.1.1 --- Fungus --- p.17 / Chapter 2.1.2 --- Animals --- p.17 / Chapter 2.1.2.1 --- Golden Syrian Hamster --- p.17 / Chapter 2.1.2.2 --- Rabbit --- p.18 / Chapter 2.1.3 --- Characterization of Auricularia Polytricha --- p.18 / Chapter 2.1.4 --- Chromatographic materials --- p.22 / Chapter 2.1.5 --- "Determination of Plasma TC，HDL-C, LDL-C，TG，AST and ALT" --- p.24 / Chapter 2.1.6 --- HMG-CoA Reductase Activity Assay --- p.26 / Chapter 2.1.7 --- "Quantitative Determination of Liver Cholesterol, Acidic and Neutral Sterol" --- p.27 / Chapter 2.1.8 --- Animal Diets --- p.29 / Chapter 2.1.8.1 --- Hamster Diets --- p.29 / Chapter 2.1.8.2 --- Rabbit Diets --- p.29 / Chapter 2.2 --- Methods --- p.33 / Chapter 2.2.1. --- Extraction of Water-Soluble AP Polysaccharide (APP) --- p.33 / Chapter 2.2.2. --- Characterization of Auricularia Polytricha --- p.34 / Chapter 2.2.2.1 --- Determination of carbohydrate content of AP Polysaccharide --- p.34 / Chapter 2.2.2.2 --- Determination of uronic acid content of AP Polysaccharide --- p.34 / Chapter 2.2.2.3 --- Determination of protein content of AP Polysaccharide by BCA protein assay --- p.35 / Chapter 2.2.2.4 --- Determination of component sugar units of AP Polysaccharide --- p.35 / Chapter 2.2.2.5 --- Fractionation of AP Polysaccharide --- p.36 / Chapter 2.2.2.6 --- Determination of monosaccharides of AP Polysaccharide by HPLC --- p.37 / Chapter 2.2.3 --- "Determination of plasma TC, HDL-C, LDL-C,TG,AST and ALT" --- p.39 / Chapter 2.2.3.1 --- Plasma Total Cholesterol --- p.39 / Chapter 2.2.3.2 --- Plasma HDL-Cholesterol --- p.40 / Chapter 2.2.3.3 --- Plasma LDL-Cholesterol --- p.40 / Chapter 2.2.3.4 --- Plasma Triglyceride --- p.41 / Chapter 2.2.3.5 --- Plasma Aspartate Aminotransferase --- p.41 / Chapter 2.2.3.6 --- Plasma Alanine Aminotransferase --- p.42 / Chapter 2.2.4 --- HMG-CoA Reductase Activity Assay --- p.42 / Chapter 2.2.4.1 --- Preparation of Hepatic Microsome --- p.42 / Chapter 2.2.4.2 --- HMG-CoA Activity Assay --- p.43 / Chapter 2.2.5 --- Quantitative Determination of Liver Cholesterol --- p.44 / Chapter 2.2.5.1 --- Cholesterol Extraction and its Silylation --- p.44 / Chapter 2.2.5.2 --- GLC Analysis of TMS-Ether Derivative of Cholesterol --- p.45 / Chapter 2.2.6 --- Quantitative Determination of Neutral and Acidic Sterols --- p.45 / Chapter 2.2.6.1 --- Separation of Neutral and Acidic Sterols --- p.45 / Chapter 2.2.6.2 --- Conversion of Neutral Sterols to its TMS-Ether Derivative --- p.46 / Chapter 2.2.6.3 --- Conversion of Acidic Sterols to its TMS-Ether Derivatives --- p.46 / Chapter 2.2.6.4 --- GLC Analysis of Neutral and Acidic Sterols --- p.47 / Chapter 2.2.7 --- Study of Atherosclerosis of Rabbit --- p.48 / Chapter 2.2.7.1 --- Sudan III staining of the thoracic aorta --- p.48 / Chapter 2.2.7.2 --- Measurement of atheroma formation in the aorta --- p.49 / Chapter 2.2.8 --- Animal Experiments --- p.51 / Chapter 2.2.8.1 --- Protective Effect of APP in Hyperlipidemic Study (Exp. 1) --- p.51 / Chapter 2.2.8.2 --- Therapeutic Effect of APP in Hyperlipidemic Study (Exp. 2) --- p.52 / Chapter 2.2.8.3 --- Dose Response of APP in Hyperlipidemic Study (Exp. 3) --- p.52 / Chapter 2.2.8.4 --- Hypolipidemic Effect of Short Chain Fatty Acid (Exp. 4) --- p.53 / Chapter 2.2.8.5 --- Effect of APP and SCFA on HMG-CoA Reductase Activity (Exp5） --- p.53 / Chapter 2.2.8.6 --- Hypolipidemic and Anti-atherosclerotic Effect of APP (Exp. 6) ´Ø… --- p.54 / Chapter 2.3 --- Statistical analysis --- p.54 / Chapter Chapter Three: --- Fractionation and Characterization of Auricularia Polytricha Polysaccharide --- p.55 / Chapter 3.1 --- Introduction --- p.55 / Chapter 3.2 --- Fungal polysaccharides from Auricularia Polytricha --- p.55 / Chapter 3.3 --- Results --- p.57 / Chapter 3.3.1 --- Extraction and Fractionation of Auricularia Polytricha --- p.57 / Chapter 3.3.2 --- Determination of Carbohydrates Content --- p.58 / Chapter 3.3.3 --- Determination of Protein Content --- p.61 / Chapter 3.3.4 --- Determination of Uronic Acid Content --- p.61 / Chapter 3.3.5 --- Determination of component sugars of AP Polysaccharide --- p.65 / Chapter 3.3.6 --- Fractionation of AP Polysaccharide --- p.67 / Chapter 3.3.7 --- Determination of monosaccharide components of AP Polysaccharide by HPLC --- p.72 / Chapter 3.4 --- Discussion --- p.79 / Chapter Chapter Four: --- "Protective, Therapeutic and Dose Effect of Auricularia Polytricha Polysaccharide (APP) on Hyperlipidemia" --- p.83 / Chapter 4.1 --- Introduction --- p.83 / Chapter 4.2 --- Results (Exp. 1) --- p.86 / Chapter 4.2.1 --- Body Weight and Food Intake --- p.86 / Chapter 4.2.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.86 / Chapter 4.2.3 --- "Effect of APP Supplementation on Plasma TC, HDL-C and TG" --- p.87 / Chapter 4.2.4 --- Effect of APP Supplementation on Fecal Output of Neutral Sterols --- p.94 / Chapter 4.2.5 --- Effect of APP Supplementation on Fecal Output of Acidic Sterols --- p.94 / Chapter 4.3 --- Discussion (Exp. 1) --- p.99 / Chapter 4.4 --- Results (Exp. 2) --- p.102 / Chapter 4.4.1 --- Body Weight and Food Intake --- p.102 / Chapter 4.4.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.102 / Chapter 4.4.3 --- Effect of APP Supplementation on Plasma TC and TG --- p.103 / Chapter 4.4.4 --- Effect of APP Supplementation on Plasma HDL-C and LDL-C --- p.104 / Chapter 4.5 --- Discussion (Exp. 2) --- p.109 / Chapter 4.6 --- Results (Exp. 3) --- p.111 / Chapter 4.6.1 --- Body Weight and Food Intake --- p.111 / Chapter 4.6.2 --- Dose Response of APP Supplementation on Hepatic Cholesterol --- p.111 / Chapter 4.6.3 --- Dose Response of APP Supplementation on Plasma TG --- p.112 / Chapter 4.6.4 --- Dose Response of APP Supplementation on Plasma HDL-C and LDL-C --- p.112 / Chapter 4.6.5 --- Dose Response of APP Supplementation on ALT and AST Activity --- p.113 / Chapter 4.6.6 --- Dose Response of APP Supplementation on Fecal Output of Neutral and Acidic Sterols --- p.113 / Chapter 4.7 --- Discussion --- p.121 / Chapter Chapter Five: --- Hypolipidemic Effect of Short Chain Fatty Acids --- p.123 / Chapter 5.1 --- "Introduction (Exp. 4,5)" --- p.123 / Chapter 5.2 --- "Results (Exp. 4,5)" --- p.125 / Chapter 5.2.1 --- Body Weight and Food Intake --- p.125 / Chapter 5.2.2 --- Effect of SCFA Supplementation on Hepatic Cholesterol --- p.125 / Chapter 5.2.3 --- "Effect of SCFA Supplementation on Plasma TG, HDL-C and LDL-C" --- p.128 / Chapter 5.2.4 --- Effect of SCFA Supplementation on AST and ALT Activity --- p.128 / Chapter 5.2.5 --- Effect of SCFA supplementation on HMG-CoA Reductase Activity --- p.133 / Chapter 5.3 --- "Discussion (Exp. 4,5)" --- p.135 / Chapter Chapter Six: --- Hypolipidemic and Antiatherosclerotic Effect of APP --- p.137 / Chapter 6.1 --- Introduction (Exp. 6) --- p.137 / Chapter 6.2 --- Results (Exp. 6) --- p.139 / Chapter 6.2.1 --- Body Weight and Food Intake --- p.139 / Chapter 6.2.2 --- Effect of APP Supplementation on Hepatic Cholesterol --- p.139 / Chapter 6.2.3 --- "Effect of APP Supplementation on Plasma TG, HDL- and LDL-C" --- p.141 / Chapter 6.2.3 --- Effect of APP Supplementation on AST and ALT Activity --- p.142 / Chapter 6.2.5 --- Effect of APP supplementation on HMG-CoA Reductase Activity --- p.146 / Chapter 6.2.6 --- Effect of APP supplementation on the Formation of Atheroma --- p.146 / Chapter 6.3 --- Discussion (Exp. 6) --- p.151 / Chapter Chapter Seven: --- General Discussion and Future Perspectives --- p.153 / References --- p.158

Sit Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 135-150). / Abstracts in English and Chinese. / Acknowledgment --- p.i / Abbreviations --- p.ii / Abstract --- p.v / Chinese Abstract --- p.vii / Table of Content --- p.ix / Chapter Chapter one: --- General Introduction --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Definition of Dietary Fiber --- p.1 / Chapter 1.3 --- Classification of Dietary Fiber --- p.2 / Chapter 1.4 --- Hypocholesterolemic Effects of Soluble Dietary Fibers --- p.3 / Chapter 1.5 --- Proposed Mechanisms for Hypocholesterolemic Effects --- p.4 / Chapter 1.5.1 --- Alter Eating Pattern --- p.4 / Chapter 1.5.2 --- Delay Gastric Emptying --- p.4 / Chapter 1.5.3 --- Modify Lipid Digestion and Absorption --- p.5 / Chapter 1.5.4 --- Effects of SCFA on Lipid Metabolism --- p.6 / Chapter 1.5.5 --- Enhance Bile Acid Excretion --- p.7 / Chapter 1.6 --- Auricularia polytricha --- p.8 / Chapter Chapter Two: --- Chemical Analysis of Auricularia polytrica --- p.11 / Chapter 2.1 --- Introduction --- p.11 / Chapter 2.2 --- Materials and Methods --- p.12 / Chapter 2.2.1 --- Extraction and Fractionation of Auricularia polytricha --- p.12 / Chapter 2.2.2 --- Determination of Carbohydrate Content --- p.12 / Chapter 2.2.3 --- Determination of Protein Content --- p.13 / Chapter 2.2.4 --- Determination of Uronic Acid Content --- p.13 / Chapter 2.2.5 --- Determination of Molecular Weight by Gel Filtration Chromatography --- p.14 / Chapter 2.2.6 --- Determination of Monosaccharide Components by HPLC --- p.15 / Chapter 2.3 --- Results --- p.18 / Chapter 2.3.1 --- Yield of Auricularia polytricha polysaccharides --- p.18 / Chapter 2.3.2 --- Carbohydrate Content of APPs --- p.18 / Chapter 2.3.3 --- Protein Content of APPs --- p.18 / Chapter 2.3.4 --- Uronic Acid Content of APPs --- p.19 / Chapter 2.3.5 --- Molecular Weight of APPs --- p.22 / Chapter 2.3.6 --- Monosaccharide Components of APPs --- p.27 / Chapter 2.4 --- Discussion --- p.33 / Chapter Chapter Three: --- Hypolipidemic Effects of APPs --- p.36 / Chapter 3.1 --- Introduction --- p.36 / Chapter 3.2 --- Materials and Methods --- p.38 / Chapter 3.2.1 --- Golden Syrian Hamster --- p.38 / Chapter 3.2.2 --- Animal Experiments --- p.40 / Chapter 3.2.2.1 --- Protective Effect and Dose Response of APPs (Exp. 1) --- p.40 / Chapter 3.2.2.2 --- Therapeutic Effect of APPs (High-cholesterol Diet) (Exp. 2) --- p.40 / Chapter 3.2.2.3 --- Therapeutic Effect of APPII (Normal Diet) (Exp. 3) --- p.41 / Chapter 3.2.2.4 --- Effect of APPs on HMG-CoA Reductase and AC AT Activity (Exp. 4) --- p.42 / Chapter 3.2.3 --- Determination of Plasma AST and ALT --- p.42 / Chapter 3.2.4 --- "Determination of Plasma TC, LDL-C, HDL-C and TG" --- p.43 / Chapter 3.2.5 --- Quantitative Determination of Hepatic and Heart Cholesterol --- p.43 / Chapter 3.2.6 --- Quantitative Determination of Perirenal Adipose Tissue Triglyceride --- p.44 / Chapter 3.2.7 --- Statistical analysis --- p.45 / Chapter 3.3 --- Results (Exp. 1) --- p.47 / Chapter 3.3.1 --- Food Intake and Growth --- p.47 / Chapter 3.3.2 --- Effect of APPs on Plasma AST and ALT --- p.47 / Chapter 3.3.3 --- "Effect of APPs on Plasma TC, LDL-C, HDL-C and TG" --- p.53 / Chapter 3.3.4 --- Effect of APPs on Hepatic and Heart Cholesterol --- p.59 / Chapter 3.4 --- Discussion (Exp. 1) --- p.64 / Chapter 3.5 --- Results (Exp. 2) --- p.67 / Chapter 3.5.1 --- Food Intake and Growth --- p.67 / Chapter 3.5.2 --- Effect of APPs on Plasma AST and ALT --- p.67 / Chapter 3.5.3 --- "Effect of APPs on Plasma TC, LDL-C, HDL-C and TG" --- p.67 / Chapter 3.5.4 --- Effect of APPs on Hepatic and Heart Cholesterol --- p.71 / Chapter 3.6 --- Discussion (Exp. 2) --- p.74 / Chapter 3.7 --- Results (Exp. 3) --- p.76 / Chapter 3.7.1 --- Food Intake and Growth --- p.76 / Chapter 3.3.2 --- Effect of APPII on Plasma AST and ALT --- p.76 / Chapter 3.7.3 --- "Effect of APPII on Plasma TC, LDL-C, HDL-C and TG" --- p.76 / Chapter 3.7.4 --- Effect of APPII on Hepatic and Heart Cholesterol --- p.80 / Chapter 3.8 --- Discussion (Exp. 3) --- p.83 / Chapter Chapter Four: --- Influences of APPs on Cholesterol Homeostasis --- p.84 / Chapter 4.1 --- Introduction --- p.84 / Chapter 4.2. --- Materials and Methods --- p.87 / Chapter 4.2.1 --- HMG-CoA Reductase Activity Assay --- p.87 / Chapter 4.2.1.1 --- Preparation of Hepatic Microsome --- p.87 / Chapter 4.2.1.2 --- HMG-CoA Reductase Activity Assay --- p.87 / Chapter 4.2.2 --- ACAT Activity Assay --- p.88 / Chapter 4.2.2.1 --- Preparation of Hepatic and Intestinal Microsome --- p.89 / Chapter 4.2.2.2 --- ACAT Activity Assay --- p.89 / Chapter 4.2.3 --- Quantitative Determination of Neutral and Acidic Sterols --- p.90 / Chapter 4.2.3.1 --- Extraction of Neutral and Acidic Sterols --- p.90 / Chapter 4.2.3.2 --- Conversion of Neutral Sterols to its TMS-Ether Derivative --- p.91 / Chapter 4.2.3.3 --- Conversion of Acidic Sterols to its TMS-Ether Derivatives --- p.91 / Chapter 4.2.3.4 --- GLC Analysis of Neutral and Acidic Sterols --- p.92 / Chapter 4.3 --- Statistic Analysis --- p.93 / Chapter 4.4 --- Results (Exp. 4) --- p.94 / Chapter 4.4.1 --- Effect of APPs on Hepatic HMG-CoA Reductase Activity --- p.94 / Chapter 4.4.2 --- Effect of APPs on Hepatic and Intestinal AC AT Activity --- p.94 / Chapter 4.4.3 --- Effect of APPs on Fecal Excretion (Exp. 1 & 4) --- p.98 / Chapter 4.5 --- Discussion (Exp. 4) --- p.105 / Chapter Chapter Five: --- Hypolipidemic and Antiatherosclerotic Effect of APPII in Rabbit --- p.110 / Chapter 5.1 --- Introduction --- p.110 / Chapter 5.2 --- Materials and Methods --- p.113 / Chapter 5.2.1 --- New Zealant White Rabbit --- p.113 / Chapter 5.2.2 --- Hypolipidemic and Anitatherosclerosis Effect of APPII (Exp. 5) --- p.113 / Chapter 5.2.3 --- Measurement of Atheroma Formation --- p.115 / Chapter 5.3 --- Results (Exp. 5) --- p.117 / Chapter 5.3.1 --- Food Intake and Growth --- p.117 / Chapter 5.3.2 --- Effect of APPII on Plasma AST and ALT --- p.117 / Chapter 5.3.3 --- "Effect of APPII on Plasma TC, LDL-C, HDL-C and TG" --- p.117 / Chapter 5.3.4 --- Effect of APPII on Hepatic and Heart Cholesterol --- p.125 / Chapter 5.3.5 --- Effect of APPII on Perirenal Adipose Tissue Triglycerige Composition --- p.125 / Chapter 5.3.6 --- Effect of APPII on the Formation of Atheroma --- p.125 / Chapter 5.4 --- Discussion (Exp. 5) --- p.130 / Chapter Chapter Six: --- Conclusion --- p.132 / References --- p.135

by Annie Chi Kwan Lam. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 112-119). / Abstracts in English and Chinese ; questionnaires also in Chinese. / Acknowledgements --- p.i / Abstract --- p.ii-vi / List of Figures --- p.vii / List of Tables --- p.vii-x / List of Abbreviations --- p.xi / Table of Contents --- p.xii-xvi / Chapter Chapter One: --- Background / Chapter 1.1 --- Diabetes Mellitus: A public health burden / Chapter 1.1.1 --- Definition and Health Consequences --- p.2 / Chapter 1.1.2 --- Prevalence of Type 2 Diabetes Mellitus in Asia --- p.3 / Chapter 1.1.3 --- Prevalence of Type 2 Diabetes Mellitus in the Hong Kong Chinese Population --- p.4 / Chapter 1.1.4 --- Medical Burden of Diabetes Mellitus in Hong Kong --- p.7 / Chapter 1.2 --- Clinical Intervention To Improve Glycemic Control / Chapter 1.2.1 --- The United Kingdom Prospective Studies (UKPDS) --- p.8 / Chapter 1.2.2 --- The Diabetes and Complications Trial (DCCT) --- p.9 / Chapter 1.2.3 --- Another Clinical Trial of Lifestyle Intervention --- p.10 / Chapter 1.2.4 --- Physical Activity in Diabetes Management --- p.12 / Chapter 1.3 --- Dietetic Situation in Hong Kong / Chapter 1.3.1 --- Survey of the Hong Kong Dietetics Situation --- p.15 / Chapter 1.3.2 --- Current Situation of Prince of Wales Hospital --- p.17 / Chapter 1.3.3 --- Diabetes Knowledge and Compliance Level in Hong Kong Patients --- p.22 / Chapter 1.4 --- Medical Nutrition Therapy and Practice Guidelines / Chapter 1.4.1 --- Definition --- p.24 / Chapter 1.4.2 --- Development of the Practice Guidelines --- p.24 / Chapter 1.4.3 --- Recommended Procedure for the Practice Guidelines in Type 2 Diabetic Patients --- p.28 / Chapter 1.5 --- Study Purpose and Objectives --- p.32 / Chapter Chapter Two: --- Study Design and Method / Chapter 2.1 --- Research Design --- p.34 / Chapter 2.2 --- Sample Selection --- p.34 / Chapter 2.2.1 --- Method of Randomization --- p.35 / Chapter 2.2.2 --- Sample Size Calculation --- p.36 / Chapter 2.2.3 --- Inclusion Criteria --- p.37 / Chapter 2.2.4 --- Exclusion Criteria --- p.38 / Chapter 2.3 --- Summary of Patient Procedure --- p.38 / Chapter 2.3.1 --- Definition Of The Two Treatments --- p.41 / Chapter 2.3.2 --- Research Procedure For PGC Group --- p.43 / Chapter 2.3.3 --- Research Procedure For CC Group --- p.49 / Chapter 2.4 --- Outcome Measures / Chapter 2.4.1 --- Anthropometrics Variable --- p.50 / Chapter 2.4.2 --- Laboratory Data --- p.51 / Chapter 2.4.3 --- Pre-testing For Questionnaires --- p.51 / Chapter 2.4.4 --- Dietary Variables --- p.52 / Chapter 2.4.5 --- Measurement of Diabetes Knowledge --- p.53 / Chapter 2.4.6 --- Measurement of Barriers To Diet Compliance --- p.54 / Chapter 2.4.7 --- Measurement of Physical Activity --- p.54 / Chapter 2.4.8 --- Measurement of Barriers To Exercise Compliance --- p.54 / Chapter 2.4.9 --- Measurement of Overall Compliance in MNT --- p.55 / Chapter 2.5 --- Statistical Analysis --- p.57 / Chapter 2.6 --- Ethics --- p.58 / Chapter Chapter Three: --- Results / Chapter 3.1 --- Subjects and Response Rate --- p.60 / Chapter 3.1.1 --- Baseline Characteristics of the PGC and CC Group --- p.61 / Chapter 3.2 --- Results of Intervention Process Between PGC and CC Group / Chapter 3.2.1 --- Attendance Rate --- p.67 / Chapter 3.2.2 --- Total Patient-Dietitian Contact Time --- p.67 / Chapter 3.2.3 --- Satisfaction With Dietetic Services --- p.68 / Chapter 3.2.4 --- Other Alternatives Treatment --- p.69 / Chapter 3.2.5 --- Changes In Medical Therapy After Intervention --- p.69 / Chapter 3.2.6 --- Hospital Admission --- p.71 / Chapter 3.3 --- Outcomes - Questionnaires Results Between PGC and CC Group / Chapter 3.3.1 --- Food Frequency Questionnaire --- p.72 / Chapter 3.3.2 --- Physical Activity Questionnaire --- p.72 / Chapter 3.3.3 --- Diabetes Knowledge --- p.72 / Chapter 3.3.4 --- Barrier To Diet Compliance --- p.72 / Chapter 3.3.5 --- Barrier To Exercise Compliance --- p.73 / Chapter 3.3.6 --- Overall Medical Nutrition Therapy Compliance --- p.78 / Chapter 3.4 --- Outcomes - Anthropometry Results Between PGC and CC Group --- p.79 / Chapter 3.5 --- Outcomes - Laboratory Results Between PGC and CC Group / Chapter 3.5.1 --- Glycemic Control --- p.83 / Chapter 3.5.2 --- Lipid --- p.84 / Chapter Chapter four: --- Discussion and Conclusion / Chapter 4.1 --- Enrollment / Chapter 4.1.1 --- Response Rates --- p.91 / Chapter 4.1.2 --- Behavior Change Model --- p.92 / Chapter 4.1.3 --- Participation of Subjects --- p.93 / Chapter 4.1.4 --- Randomization --- p.93 / Chapter 4.2 --- Measurements / Chapter 4.2.1 --- Questionnaire --- p.94 / Chapter 4.2.2 --- Blinding Process --- p.94 / Chapter 4.2.3 --- Laboratory --- p.94 / Chapter 4.3 --- Outcomes / Chapter 4.3.1 --- Questionnaire Outcomes --- p.95 / Chapter 4.3.2 --- Anthropometry Outcomes --- p.100 / Chapter 4.3.3 --- Glycemic Outcomes --- p.102 / Chapter 4.3.4 --- MNT Process Outcomes --- p.103 / Chapter 4.3.5 --- Limitations --- p.104 / Chapter 4.4 --- Clinical Significance and Implications --- p.104 / Chapter 4.5 --- Conclusions and Recommendations --- p.110 / References --- p.112 / Appendices --- p.120

Diet is mentioned by many seamen as a subject of joy and aims to give nutritional value and sufficient energy to manage a long working day at sea. The purpose with this investigation is to examine if there is a need among seamen to receive more information about diet regulations onboard and if they wish that it was shaped differently to meet their demands. The study is based on a literature part where diet regulations are examined and an interview part with semi structured qualitative interviews with five seamen. The conclusion of the study indicates that seamen have limited knowledge about the enunciation of the regulation, where it is to be found and consider it to be imprecise. Interviews showed that seamen believe that variety is the most important factor in diet intake and it was this expression that they primarily wanted stated in the regulations. There are legitimate reasons to assume that Livsmedelsverket´s (compare NFA) recommendations also are applicable regarding diet at sea. A good diet is not only good for the individual’s health but also gains including safety and quality of work performed. / Kosten anges av många sjömän som ett glädjeämne ombord och ska ge den näring och energi som krävs för att orka med en lång arbetsdag på sjön. Syftet med denna studie var att undersöka om det finns ett behov hos sjömän att få mera information om kostregleringen ombord och om de önskar att den vore utformad annorlunda för att möta deras krav. Arbetet baseras på en litteraturdel där kostregleringen undersöks och en intervjudel med semistrukturerade kvalitativa intervjuer med fem sjömän.  Sammanfattningsvis tyder vår undersökning på att sjömän har bristande kännedom om regleringens utformning, var den återfinns samt anser att den är oprecis. Intervjuerna visade att sjömän anser att variation är den viktigaste faktorn i kostintaget och det var också detta uttryck som främst önskades framgå av regleringen. Det finns välmotiverade skäl att utgå från Livsmedelsverkets rekommendationer även på sjön. Ett bra kostintag är inte bara bra för individens hälsa utan ger också vinster i bland annat säkerheten och kvaliteten på utfört arbete.

OBJECTIVES: This dissertation was divided into two studies. The aim of the first study was to investigate whether there is an association between diet quality of preschool children and their caregivers. The aim of the second study was to examine the relationship of children diet quality and dental caries risk. METHODS: The study utilized a longitudinal population-based data of a representative sample of low-income African American families in Detroit, Michigan. Analyses were limited to 522 children aged 3-5 years old and their primary caregivers. For caregivers, dietary histories were obtained at wave I using the Block 98.2 food frequency questionnaire. For children, dietary histories were obtained at wave I and wave II using the Block Kids Food Questionnaire. Healthy Eating Index-2005 was used to evaluate overall diet quality. Dental caries in primary teeth were measured by the ICDAS criteria. The mean number of decayed surfaces (noncavitated and cavitated), missing, and filled surfaces for each child was estimated. Statistical analyses were conducted using SAS 9.4 and STATA 14 to account for the complex sampling design. RESULTS: The first study found that the mean total HEI-2005 scores were 57.47 for caregivers at wave I, 56.04 for children at wave I, and 57.39 for children at wave II indicating that the diet quality of this population needs improvement. Significant, positive relationship was found between caregivers-child overall diet quality at wave I (β=0.35; p <0.0001) and wave II (β=0.31; p <0.0001). The second study found that children who had high diet quality or improved their diet quality throughout the study period had significantly lower dental caries incidence compared to those with low diet quality scores (IRR = 0.59 and 0.55, respectively) (CI = 0.36-0.96 and 0.35-0.86 , respectively). CONCLUSION: Our findings suggest that caregiver’s and children’s diet quality are associated. Therefore, caregiver’s diet quality should be considered in efforts to improve diets of their children. Additionally, preschooler children in our study with improved diet quality showed lower caries incidence. These results suggest that strategies and intervention to prevent dental caries among children should focus on improving overall diet quality. / 2018-09-28T00:00:00Z

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