A dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the degree of Master of Science in Medicine. / Introduction Despite the availability of several antifungal drugs, Candida infections remain a major health threat worldwide. The Candida infections problem has been amplified by the emergence of multidrug resistant Candida species towards the conventional antifungal drugs. In addition, activation of antioxidant defense system by Candida species has been known to be forefront mechanism to escape drug toxicity.This indicates an urgent need for the development of new therapeutic strategies and antifungal drugs. Natural products have served for centuries for the treatment of infectious diseases and are among the major sources for finding new antifungal drugs. Berberine (BER), an isoquinoline alkaloid found in a variety of plant species, has been shown to possess multiple biological and pharmacological properties including antimicrobial activity against C. albicans and other Candida species. However, the mechanism of action exerted by BER and its effect on Candida cells is not yet fully elucidated. Therefore, this study was conducted to evaluate the role of antioxidant enzymes in the susceptibility to fluconazole (FLC) in C. albicans. Another aspect was to determine the effect of BER on growth, antioxidant enzymes and their gene expression in C. albicans. Materials and methods Candida albicans clinical isolates (10 FLC susceptible and 10 FLC resistant) and one ATCC strain were obtained from the Department of Clinical Microbiology and Infectious Diseases, University of the Witwatersrand. Species identification was confirmed using API 20C AUX. Antifungal susceptibility was determined following CLSI M27-A3 guidelines. Gene expression of SOD1, SOD2, GPx2, GLR1, GTT11, and CAT1 in untreated and BER treated C. albicans cells was measured by RT-qPCR. The activity level of the corresponding enzymes in the presence of BER was determined using a spectrophotometer. Results Gene expression analysis showed an increase in mRNA expression level of SOD1, SOD2, GPx2, GLR1 and GTT11 genes in FLC resistant isolates than in the susceptible group. The most significantly expressed gene was SOD1 with 50.69-fold increase. The other genes showed moderate increase in the expression with fold change ranging from 1.2 to 4.2. The susceptibility test showed MICs ranging from 125 to 500 μg/ml with a significant difference in the activity of BER between FLC susceptible and resistant C. albicans. BER treatment induced upregulation in the mRNA expression and enzymatic activities of major antioxidants. In FLC resistant C. albicans, treatment with ½ MIC value of BER caused downregulation of the targeted antioxidant genes indicating that BER at this concentration induced an intense oxidative stress, therefore, surpassing the antioxidant capacity of the cells. Conclusion The findings in this study showed that drug resistance is not only caused by mutations in a particular gene but could also arise from proteomic modulations. The study . The study also demonstrated that C. albicans activates several antioxidant enzymes that form an integral component of the cell’s response against oxidative stress. Candida albicans showed efficient antioxidant response at lower concentrations of BER. However, BER at ½ MIC value induced robust oxidative stress, especially in FLC resistant C. albicans, surpassing the antioxidant capacity of the cells. This demonstrates that BER at sub-inhibitory concentrations is able to render C. albicans avirulent by suppressing its antioxidant defense response without compromising cell viability of the fungi. Therefore, BER has a potential to be developed into BER has a potential to be developed into a therapeutic agent a therapeutic agent for for the the treatment oftreatment of C. albicansC. albicans infections and other pathogenic fungi to infections and other pathogenic fungi to overcome drug resistance. overcome drug resistance. / E.K. 2019

Thesis (Ph.D.)--Aberdeen University, 2008. / Title from web page (viewed on Apr. 14, 2009). Includes bibliographical references.

Thesis (M.Nurs.)--Washington State University, December 2008. / Title from PDF title page (viewed on Mar. 4, 2009). "Intercollegiate College of Nursing." Includes bibliographical references (p. 71-87).

The study investigated whether dietary flavonoid intake and dietary patterns were associated with bone mineral density (BMD) and bone turnover in postmenopausal Scottish women. The subjects were recruited in 1990-3, and the majority of them returned 6.3 ± 0.6 y later (mean age (SD) at baseline 54.7 (2.2) y). At the both visits they had bone density scans of the lumbar spine (LS) and hip (FN) and at the second visit they provided urine samples for analysis of bone resorption markers. Flavonoid intakes were calculated using food frequency questionnaires, “validated” for flavonoid intakes using 4-day food diaries. (R=0.76, p≤0.001 for energy adjusted total flavonoids). FN BMD was associated with flavonoid intakes at baseline and follow up (p=0.012, p=0.001 respectively after adjusting for confounders) and LS BMD at follow up only (p=0.038). Dietary flavanones had a negative correlation with bone resorption markers; catechins and procyanidins were associated with annual change in FN and LS BMD. Principal components analysis was used to identify five important patterns in the diets. The “healthy” diet, rich in fruit and vegetables, was negatively associated with bone resorption markers and the nutrient diets were both negatively associated with FN and LS BMD. Partial least squares analysis identified that tinned fruit and root vegetables were associated with greater bone resorption, and berries, tomatoes and juice with decreasing bone resorption. Tomato intakes were the most important when predicting bone resorption marker excretion. Tomatoes, salad, berries, and green vegetables were associated with increased BMD. Berries, applies, root vegetables and salad were the most important fruit and vegetables for predicting BMD. Results from this work confirm that fruit and vegetables are important in bone health.

Background Polycystic ovary syndrome (PCOS) is a common endocrine condition in women associated with obesity, reproductive and metabolic abnormalities. It improves with weight loss, however currently no specific dietary recommendations exist and there may be abnormalities in appetite regulation in PCOS that contribute to difficulty in weight management. Aims To assess the effect of 1) short and long-term weight loss and weight maintenance strategies on weight loss, reproductive and metabolic parameters in overweight women with PCOS and to 2) assess the relative effect of weight loss on cardiovascular risk factors and 3) postprandial appetite, appetite hormones (ghrelin, CCK, PYY) and food intake in overweight women with and without PCOS. Results Overweight women with PCOS followed an 8-week weight loss (2 meal replacements/day, 4904.4±127 kJ, n=32) followed by a 6 month carbohydrate (<120 g/day) or fat restricted (<50 g/day) weight maintenance regime (n=23). Reductions in weight (5.6±2.4 kg) and improvements in body composition, insulin, reproductive hormones and menstrual cyclicity occurred and were sustained equivalently for both diet groups. We then assessed the effect of weight loss (4.2±0.7 kg over 8 weeks as described above) in overweight women with (n=15) and without (n=17) PCOS on cardiovascular risk factors. All subjects had similar improvements in body composition, triglycerides, reproductive hormones and fasting and post-prandial insulin. C-reactive protein decreased with weight loss for non-PCOS women (-1.2±0.5 mg/L, P=0.025) but not for PCOS women. We finally assessed appetite regulation in PCOS. Women with (n=20) and without (n=12) PCOS followed a standard protein (55% carbohydrate, 15% protein) or high protein diet (40% carbohydrate, 30% protein) for 16 weeks (~6000 kJ/day). Non-PCOS subjects were more satiated (P=0.001) and less hungry (P=0.007) after the test meals and had a 70% higher fasting baseline ghrelin (P=0.011), a greater increase in fasting ghrelin (57.5 versus 34.0%, P=0.033), a greater post-prandial ghrelin decrease at week 16 (113.5±46.3 versus 49.3±12.2 pg/mL, P=0.05) and a greater maximal decrease in post-prandial ghrelin (-144.1±58.4 versus -28.9±14.2 pg/mL, P=0.02) following weight loss than subjects with PCOS. Lastly, women with (n=14) and without (n=14) PCOS undertook an 8-week weight loss regime (4.2±0.7 kg as described above). At week 0 and 8, women with PCOS again displayed lower ghrelin levels (P=0.01 and P=0.097 respectively) and a lesser post-prandial ghrelin decrease (P=0.048 and P=0.069 respectively) but similar post-prandial appetite, buffet consumption and fasting or post-prandial peptide YY and cholecystokinin compared to women without PCOS. Conclusion Meal replacements and moderate macronutrient restriction are effective strategies for the dietary management of PCOS. Equivalent weight losses improved cardiovascular risk factors similarly for overweight women with and without PCOS with the exception of CRP which did not decrease with weight loss for overweight women with PCOS. PCOS status is associated with altered fasting and post-prandial ghrelin levels but is not consistently associated with other impairments in post-prandial gut peptides or food intake. Further investigation is required to assess if appetite regulation is impaired in PCOS and the optimal strategies and amount of weight loss for improvement of reproductive and metabolic parameters in PCOS. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1282329 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2007

Thesis (M.S.)--University of North Carolina at Greensboro, 2007. / Title from PDF title page screen. Advisor: Allan H.Goldfarb; submitted to the School of Health and Human Performance. Includes bibliographical references (p. 49-57).

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

A procedure for preparing an enteral formula was developed, using Pakistani indigenous food items. The basis of development was that it would be nutritionally effective, easy to prepare and relatively cheap. 100 indigenous enteral diets were formulated using a computer aided master sheet in which various combinations were analysed. In order to prove the efficacy of these diets, a modified PER was carried out on 6 diets and results indicated a higher PER for the experimental diet. 29 formulations were shortlisted for preparation trials, and 2 main techniques were applied: incubation and cooking techniques. Physical and chemical analyses were carried out to assess the effect of preparation, the cooking methodologies were tried on various diets and 2 diets were shortlisted for human trials. To compare the efficacy of the indigenous enteral formula versus commercial formulae, a pilot study was carried out. Patient nutritional outcomes were assessed using biochemical parameters, and preliminary findings indicated that the experimental diet performed as well as the control diet. / Doctor of Philosophy (PhD)

Thesis (Ph. D.)--Rutgers University, 2009. / "Graduate Program in Food Science." Includes bibliographical references.