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1
Samiayah, Ganesh Kumar School of Physiology & Pharmacology UNSW. "Pharmacokinetics, Cerebrovascular Permeability & Biotransformation of the Neurotoxic Plasticiser N-butylbenzenesulfonamide (NBBS)". Awarded by:University of New South Wales. School of Physiology & Pharmacology, 1997. http://handle.unsw.edu.au/1959.4/17597.
Testo completoAbstract (sommario):
The pharmacokinetics, oral bioavailability, cerebrovascular permeability and biotransformation of the neurotoxic plasticiser n-butylbenzenesulfonamide (NBBS) were studied in order that the human health risk due to environmental exposure to NBBS could be evaluated. The pharmacokinetics of NBBS was determined in Wistar rats, following intravenous administration of the isotopomer [13C6] NBBS (1 mg/kg in 0.9% saline). [13C6] NBBS is cleared from plasma at a rate of 5 ml/min by the liver. The plasticiser has a short distribution phase (t1/2 of 47 seconds) and a long terminal phase (t1/2 of 17 hours). Plasma [13C6] NBBS concentrations, 24 hours after administration, represented 0.04% of the administered dose. These data indicated rapid uptake into tissue, which was subsequently confirmed by monitoring tissue concentrations of [13C6] NBBS for upto 8 hours following administration. [13C6] NBBS was not accumulated by any of the tissues studied (brain, liver, kidney, muscle and adipose tissue). Oral bioavailability was determined by simultaneously administering native NBBS orally and [13C6] NBBS intravenously to Wistar rats. The plasticiser was found to be absorbed erratically and subject to first pass metabolism. Plasma concentrations of orally administered NBBS fluctuated over the duration of the experiment. Furthermore, limitations posed by the assay resulted in truncated oral curves. These factors precluded estimation of areas under the oral NBBS curves to infinity and partial area ratios were instead used to calculate absolute bioavailability (mean of 19%). Cerebrovascular permeability of NBBS was determined with [13C6] NBBS, in Sprague-Dawley rats, using the in-situ brain perfusion technique of Takasato et al. (1984). The uptake of [13C6] NBBS into brain was very rapid and flow limited. Assuming an average cerebral perfusion fluid flow rate of 0.11 ml/s/g, the calculated single pass extraction value for [13C6] NBBS is 99.9% with a Kin of 0.11 ml/s/g. This is in close agreement with experimental values for the 15 second saline perfusions (extraction = 98% - 125% and Kin = 0.108 - 0.137). Differences in regional brain distribution of the plasticiser were not found. In-vitro biotransformation studies revealed one phase I metabolite in incubates of NBBS containing human, rabbit and rat post-mitochondrial supernatant (S9 fraction). This metabolite is 2-hydroxy-n-butylbenzenesulfonamide (NBBS-OH hydroxylated in the Based on these data, environmental exposure to NBBS does not pose a significant human health risk.
2
Fincher, Cynthia Ellen. "The Use of Single Photon Emission Computed Tomography to Indicate Neurotoxicity in Cases of Pesticide and Solvent Exposures". Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc277747/.
Testo completoAbstract (sommario):
This study examined the effect of neurotoxic chemical exposures on brain processes using Single Photon Emission Computed Tomography (SPECT). A control group carefully screened for good health and minimal chemical exposures was compared to two groups of patients diagnosed with health problems following exposure to pesticides or to organic solvents.
3
Palvie, Stefanie Michelle. "An investigation into the neuroprotective effects of dehydroepiandrosterone". Thesis, Rhodes University, 2006. http://hdl.handle.net/10962/d1003260.
Testo completoAbstract (sommario):
Dehydroepiandrosterone, a C-19 steroid, is found endogenously with the highest circulating serum levels. It is converted to important steroids such as the sex hormones oestrogen and testosterone. DHEA has come under the spotlight as a purported “fountain of youth” due to its well-characterised age-related decline. The supplementation of DHEA in both the elderly and those with a pathophysiological deficiency has been shown to be of benefit, particularly with regard to wellbeing and depression. The role of DHEA in the periphery has not been elucidated beyond its role as a precursor hormone in sex steroid biosynthesis, though it has been established as a neuroactive neurosteroid, capable of exerting neuroprotective effects in the brain. Since the importance of free radicals in aging and neurodegeneration is well established, investigations were conducted on the ability of DHEA to inhibit free radical generation or scavenge existing free radicals. DHEA was able to significantly inhibit quinolinic acid-induced lipid peroxidation, a measure of membrane damage, over a range of concentrations, although the reduction did not appear to be dose-dependent. This was observed in both in vitro and in vivo studies. Thus, the ability of a compound to reduce the degree of lipid peroxidation may indicate its value as a neuroprotectant. However, DHEA did not significantly reduce cyanide induced generation of the superoxide free radical, suggesting that DHEA is not an effective free radical scavenger of the superoxide anion and that the reduction in lipid peroxidation does not occur through a scavenging mechanism. Apoptosis is a physiological process which is necessary for development and homeostasis. However, this form of programmed cell death can be initiated through various mechanisms and too much apoptotic cell death results in deleterious effects in the body. DHEA was shown not to induce apoptosis. Even the lowest concentration of DHEA investigated in this thesis shows a remarkable decrease in the degree of apoptosis caused by intrahippocampal chemical insult by the neurotoxin quinolinic acid. Cresyl violet was used to visualise tissue for histological examination which revealed that DHEA is able to preserve the normal healthy morphology of hippocampal cells which have been exposed to quinolinic acid. Cells maintained their integrity and showed little evidence of swelling associated with necrosis. Organ culture studies were performed by assessing the impact of DHEA on several pineal metabolites. The study revealed that DHEA exerted an effect on the metabolism of indoleamines in the pineal gland. Melatonin, the chief pineal hormone, did not appear to be affected while the concentrations of N-acetylserotonin, serotonin and methoxytryptamine showed significant alterations. Thus, the neuroprotective mechanism of DHEA does not appear to be mediated by an increase in the presence of melatonin. The biological importance of metal ions in neurodegeneration is also well established and thus the potential interaction between DHEA and metal ions was considered as a mechanism of action. Spectroscopic and electrochemical analyses were performed to determine whether DHEA is able to interact with metal ions as a ligand. These reveal that DHEA does not form a strong bond with the metals investigated, namely copper (II) and iron (III), but that a weak interaction is evident. These investigations were conducted in a rodent model, which has neither large amounts of endogenous DHEA, nor the enzymatic infrastructure present in humans. Thus, the theory that DHEA exerts its effects through downstream metabolic products is unlikely. However, these investigations reveal that there is merit in the statement that DHEA itself is a neuroprotective molecule, and confirm that the further investigation of DHEA is an advisable strategy in the war against neurodegeneration and aging.
4
Shabani, Fariba. "Regulation of matrix metalloproteinases, their inhibitors and IL-8 in inflammatory rheumatic diseases : effects of cytokines and anti-rheumatic agents /". Title page and contents only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phs524.pdf.
Testo completo
5
Davis, Christopher John. "Neuropharmacological investigations into the mechanisms of emesis caused by cytotoxic drugs and radiation". Thesis, University of Oxford, 1988. https://ora.ox.ac.uk/objects/uuid:b9afefde-a43e-415e-8754-ed2a8eaac620.
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6
Liu, Xiaoling. "Determination of whether the effects of statin drugs are mediated by phosphoinostide 3-kinase". Virtual Press, 2004. http://liblink.bsu.edu/uhtbin/catkey/1306853.
Testo completoAbstract (sommario):
Phosphoinositide 3-kinases (PI3Ks) are a family of proteins involved in many different aspects of cell signaling. To date, eight different human PI3K isoforms have been identified, and distinct roles are beginning to emerge for each family member. Statins, HMG co-A reductase inhibitors used clinically to lower LDL cholesterol levels, also act through the PI3K signaling pathway to regulate cholesterol independent of their lipid-lowering effects. In an effort to discover the role of pl 10f3 in mediating non-lipid lowering effects of pravastatin, a mutant of p110(3 was overexpressed in human coronary artery endothelial cells (HCAEC) to form a dominant negative model (p110(3 DN). Silence si-RNA as an alterative tool was also optimized to diminish p110(3 protein expression successfully. HepG2 3: RE was used to monitor statins function by assaying luciferase expression. Results from these studies will determine the contribution of p110f3 in mediating selective cellular responses to statin.Department of Biology
7
Oliva, Jean L. (Jean Louise). "The Teratogenic Effects of Nocodazole and Acrylamide in Mus Musculus". Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc500254/.
Testo completoAbstract (sommario):
In two separate experiments, weight adjusted doses of nocodazole and acrylamide were injected intraperitoneally at various time intervals into twelve week old female mice. Within the nocodazole experiment, the doses were injected at varying time intervals before and after mating. On day seventeen of gestation, the female mice were sacrificed and their uterine contents examined. Nocodazole induced a significant increase in reproductive pathology per total implants when administered one hour after mating to the (SECxC57BL)F, stock: 5.00% total deads, 70.23% moles, and 3.41% abnormal fetuses. Acrylamide treatment produced a significant reduction in live births when administered six hours after mating: 50.86% moles and 46.46% living fetuses per total implants.
8
Wong, Suk-yu, e 黃淑如. "Study of anti-cancer and anti-viral activities of lanthanide and vanadium complexes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37674547.
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Yoshida, Makiko. "Plant sterols and glucomannan as hypocholesterolemic and hypoglycemic agents in subjects with and without type 2 diabetes". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80900.
Testo completoAbstract (sommario):
The objective of this research was to examine the effects of plant sterols and glucomannan on lipid profiles, plasma plant sterol levels and glycemic control in mildly hypercholesterolemic subjects. Thirteen type 2 diabetic and sixteen non-diabetic individuals participated in a randomized crossover trial consisting of 4 phases, of 21 days each. During the study period, subjects were supplemented with plant sterols and/or glucomannan. Overall reductions of total cholesterol and low-density lipoprotein (LDL) cholesterol concentrations were greater after consumption of plant sterols and glucomannan compared to plant sterol or glucomannan supplementation alone. Plasma lathosterol levels, indicators of cholesterol biosynthesis, were decreased after combination treatment. The results suggest that a combination of glucomannan and plant sterols substantially improve plasma lipids by reducing cholesterol absorption and synthesis simultaneously. Supplementation of plant sterols and glucomannan can thus be used as an effective treatment for management of circulating cholesterol levels and prevention of cardiovascular disease.
10
Xu, Yang, e 徐阳. "Proteomic and biochemical characterization of the anti-cancer mechanism of tubeimoside-1 extracted from the Chinese herbalmedicine "Tu bei mu"". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44135968.
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11
Das, Kumuda C. "Amelioration of oxidative lung injury by antiarrhythmic agents". Diss., Virginia Tech, 1992. http://hdl.handle.net/10919/39844.
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12
Fisher, Kim Noël. "Behavioural and physiological effects of two aniracetam analogues". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22585.
Testo completoAbstract (sommario):
The behavioural and electrophysiological consequences of two newly developed aniracetam analogues were investigated in male Long-Evans rats. Results indicate that an intraperitoneal (i.p.) injection of LD38.2 significantly improved retention in a two odour olfactory discrimination task. However, three different dosages of LN1 did not facilitate memory in the task. In rats with chronically implanted electrodes, both compounds rapidly crossed the blood brain barrier (BBB) after an i.p. injection and influenced several parameters of the field excitatory postsynaptic potential (EPSP) in the CA1 and dentate gyrus regions of the hippocampus. The enhancement of the field EPSP following LD38.2 administration may be related to the drug's ability to facilitate memory in the olfactory discrimination task. Compounds, like LD38.2, that enhance both hippocampal transmission and performance in learning/memory tasks in laboratory rodents may have implications for the treatment of clinical memory disorders.
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Urbano, Charissa M. "Potentiating effects of caffeine on the teratogenicity of acetazolamide in two strains of mice". Virtual Press, 1988. http://liblink.bsu.edu/uhtbin/catkey/552944.
Testo completoAbstract (sommario):
This study was designed to determine the effect of caffeine on the teratogenicity of acetazolamide in susceptible and resistant strains of inbred mice. The highly susceptible C57BL/6J and more resistant SWV strain were used. Pregnant C57BL/6J and SWV mice were treated with caffeine, low or high dose acetazolamide, or a combination of both agents during the sensitive period of development. Untreated and vehicle-treated groups served as controls. Individual fetuses were examined for gross morphological abnormalities and skeletal variations.Findings1. A highly significant (P<.001) increase in fetal malformations, especially right forelimb ectrodactyly, was evident in C57BL/6J litters exposed on day 9 of gestation to both agents when contrasted with those exposed to either agent alone. Both frequency and severity of ectrodactyly was potentiated by caffeine.2. The SWV strain was resistant to the interaction of caffeine and acetazolamide when treated on day 9 of gestation. However, a highly significant (P<.001) increase in the rate of fetal malformation was found in litters whose dams were treated with high dose acetazolamide and caffeine on day 8 of gestation. The most common malformations observed were exencephaly and umbilical hernia.3. No differences in maternal mortality, fetal weight, litter size, or embryo mortality could be attributed to treatment in either strain.4. Skeletal examination of the number of ossified cervical and caudal vertebral centra revealed a reduction in ossification among C57BL/6J litters exposed to high dose acetazolamide or acetazolamide plus caffeine. These same centers of ossification were mildly affected by treatment in the SWV strain. In both strains the first cervical vertebrae (Cl) appeared to provide the most sensitive index of teratogenic exposure.ConclusionsThis study provides evidence that a subteratogenic dose of caffeine can potentiate the teratogenic effect of acetazolamide in both C57BL/6J and SWV mice. However, strain associated, and therefore genetically based, differences in sensitivity were confirmed. Skeletal examinations provided evidence that treatment with both agents delayed fetal development in the more susceptible C57BL/6J strain, while reduction of ossification was less evident in the SWV strain. Thus, this parameter also reflects the greater resistance of the SWV strain to the interaction of acetazolamide and caffeine. Finally, these experiments support the idea that chemical interactions may, in part, be responsible for many birth defects of unknown etiology--a claim worthy of further investigation.Department of Biology
14
Barake, Roula. "Effects of plant sterols and glucomannan on parameters of cholesterol kinetics in hyperlipidemic individuals with and without type 2 diabetes". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=83964.
Testo completoAbstract (sommario):
The objective of this study was to examine the effects of plant sterols and/or glucomannan on lipid profiles and cholesterol kinetics in hyperlipidemic individuals with or without type 2 diabetes. It was hypothesized that plant sterols and glucomannan reduce circulating cholesterol levels and may have an additive or synergistic effect when combined by reducing cholesterol absorption. Thirteen type 2 diabetics and sixteen non-diabetics all mildly hypercholesterolemic free living subjects participated in a randomized crossover trial consisting of 4 phases, 21 days each. Subjects consumed plant sterols and glucomannan during the trial. Overall reductions in total and LDL-cholesterol levels were greater (P<0.05) after consumption of the combination supplement. Effects of supplements were not different between diabetics and non-diabetics. No significant changes were observed in cholesterol absorption or synthesis in both diabetics and non-diabetics. The intake of plant sterols and glucomannan together may be an alternative approach in reducing blood cholesterol levels.
15
Liby, Tiera A. "The role of phosphoinositide 3-kinase (PI3K) in mediating mitogen and Simvastatin induced effects in the vasculature". Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1315171.
Testo completoAbstract (sommario):
Statins induce beneficial vascular effects. How statins induce beneficial vascular effects is yet to be determined. Here we examine Simvastatin and vascular endothelial growth factor (VEGF) acting through the phosphoinositide 3-kinase (PI3K) pathway in human coronary artery endothelial cells (HCAEC). While Simvastatin and VEGF both activated mediators in the PI3K pathway, the proteins and the rates of activation were not always consistent. This suggests that although Simvastatin and VEGF share a common PI3K pathway in HCAEC and similar vascular effects, the agonists diverge in the induction of cellular signaling cascades. Simvastatin also was shown to induce phosphoinositide 3, 4, 5-triphosphate (PIPS) organization and PI3K p110 gamma (y) perinuclear localization. Beneficial, non-lipid lowering effects of statins may occur through the PI3K pathway through activation of distinct mediators from those of VEGF. Better understanding of the pathways associated with statins is necessary for the discovery of better treatments for cardiovascular disease (CVD).Department of Biology
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Varady, Kristina A. "Effect of plant sterol supplementation and endurance training on cardiovascular disease risk parameters and cholesterol kinetics in previously sedentary hypercholesterolemic adults". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111831.
Testo completoAbstract (sommario):
Background. A high ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol, in addition to increased levels of small low-density lipoprotein (LDL) particles, are important indicators of cardiovascular disease risk. Therefore, interventions that combine the lowering of total cholesterol and raising of HDL cholesterol concentrations that also increase LDL particle size, may be preventive against cardiovascular disease. Plant sterols decrease total cholesterol and LDL cholesterol levels by 10-15%, while exercise increases HDL cholesterol levels by 4-22%. In view of their complementary effects, combining plant sterols with exercise would appear to be an effective lifestyle therapy to decrease the risk of future cardiovascular disease.Objective. The aim of this study was to examine the independent and combined effects of plant sterols and exercise on blood lipid levels, and LDL particle size in previously sedentary, hypercholesterolemic adults. An additional objective of this trial was to assess the underlying mechanism by which this combination therapy modulates whole body cholesterol metabolism, to in turn improve lipid profiles.
Methods. In an 8-week, parallel-arm trial, 84 subjects were randomized to 1 of 4 interventions: (1) plant sterols and exercise,(2) plant sterols alone, (3) exercise alone, or (4) control. Blood lipid concentrations were measured using enzymatic kits, and LDL particle size was assessed using polyacrylamide gel electrophoresis. Cholesterol absorption and synthesis were determined using the single isotope single tracer technique and the deuterium incorporation approach, respectively.
Results. Plant sterol supplementation decreased (P < 0.01) total cholesterol concentrations by 8.2% when compared to baseline. Exercise increased (P < 0.01) HDL cholesterol levels by 7.5% while decreasing (P < 0.01) triglyceride concentrations by 13.3% when compared to baseline. Exercise reduced (P < 0.05) post-treatment LDL peak particle size from 255 to 253 A, and decreased (P < 0.05) the proportion of large LDL particles by 13.1%. Plant sterols had no effect on particle size distribution. Plant sterol supplementation decreased (P < 0.01) intestinal cholesterol absorption by 18%, while exercise had no effect on cholesterol absorption. Non-significant increases in cholesterol synthesis rates of 63%, 59%, and 57%, were observed in the combination, exercise, and plant sterol groups, respectively, relative to control.
Conclusion. These findings suggest that this combination therapy yields the most favourable alterations in lipid profiles when compared to each intervention alone. This combined intervention exerts its beneficial effects on lipid profiles by suppressing intestinal cholesterol absorption. Therefore, this lifestyle therapy may be an effective means of decreasing the risk of cardiovascular disease in hypercholesterolemic adults.
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Palenske, Nicole Marie. "Effects of Triclosan, Triclocarban, and Caffeine Exposure on the Development of Amphibian Larvae". Thesis, University of North Texas, 2009. https://digital.library.unt.edu/ark:/67531/metadc11016/.
Testo completoAbstract (sommario):
Triclosan and triclocarban are antimicrobials found in numerous consumer products, while caffeine is the most commonly consumed stimulant by humans. This study was undertaken to determine the effects of triclosan, triclocarban, and caffeine on the development and physiology of amphibian larvae. LC50 values of triclosan and triclocarban were determined after 96 hours for three North American larval species: Acris crepitans blanchardii, Bufo woodhousii woodhousii, Rana sphenocephala, and for a common amphibian developmental model: Xenopus laevis. Amphibian larvae were most sensitive to triclosan and triclocarban exposure during early development based upon 96-hour LC50 values. Heart rates for X. laevis and North American larvae exposed to triclosan were variable throughout development. However, significantly lower heart rates were observed in all larvae exposed to triclocarban. Metabolic rates of X. laevis and R. sphenocephala larvae exposed to triclosan were significantly affected in larvae exposed to ½ LC50 and the LC50 concentration. Metabolic rates of X. laevis larvae exposed to triclocarban were significantly affected by exposure to ½ LC50 concentrations in three of four stages investigated. No significant differences were observed in North American larvae exposed to triclocarban. Tissue uptake, lipid uptake, tissue bioconcentration factor (BCF) and lipid BCF of triclosan and triclocarban were investigated in three developmental stages of X. laevis, and in one developmental stage of B. woodhousii woodhousii, and R. sphenocephala. For most tissue and lipid uptake values, a significant increase was observed as exposure concentration increased. Tissue and lipid BCF values were dependent upon both stage and species. Chronic and acute effects of caffeine were determined in X. laevis larvae. Acute 96-hour LC50 values in four developmental stages were > 75,000 ug L-1 caffeine and heart rates were significantly different at the two earliest developmental stages. Larvae chronically exposed to caffeine reached metamorphosis at the same time as controls. Changes in chronic heart rate were dependent upon stage of development and exposure concentration. This research indicates that the toxicity of amphibian larvae exposed to triclosan, triclocarban, and caffeine appears to be dependent upon species and developmental stage, with early developmental stages being most sensitive to contaminant exposure.
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Lau, Vivian Wai Yan 1977. "Effects of plant sterols on plasma lipid profiles, glycemic control of hypercholesterolemic individuals with and without type 2 diabetes". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80312.
Testo completoAbstract (sommario):
Plant sterols (PS) are effective in reducing plasma lipid concentrations, however, few studies have examined their cholesterol lowering effects in type 2 diabetics. The objective was to assess whether PS consumption alters blood lipid profile in hypercholesterolemic subjects with and without type 2 diabetes. Fifteen control subjects (age = 55.1 +/- 8.5 yr and BMI = 26.9 +/- 3.0kg/m2) and fourteen diabetic subjects (age = 54.5 +/- 6.7 yr and BMI = 30.2 +/- 3.0kg/m2) participated in a double-blinded, randomized, crossover, placebo-controlled feeding trial. The Western diet included either 1.8g/d of PS or cornstarch placebo each provided over 21 d separated by a 28 d washout period. Subjects consumed only foods prepared in Mary Emily Clinical Nutrition Research Unit of McGill University. Total cholesterol (TC) decreased (p < 0.05) from baseline with PS for control and diabetic subjects by 9.7% and 13.6%, respectively. TC decreased (P < 0.05) from baseline with placebo for control and diabetic subjects by 10.9% and 11.6%, respectively. Non high density lipoprotein cholesterol (non-HDL-C) decreased (p < 0.05) from baseline with PS for diabetic subjects by 18.5%. Low density lipoprotein cholesterol (LDL-C) levels were reduced (p < 0.05) from baseline with PS for control and diabetic subjects by 14.9% and 29.8%, respectively. The reduction of LDL-C due to PS alone is greater with type 2 diabetics. There were no significant changes in HDL-C and TG across diets or treatments. It is thus concluded that PS consumption with diet enhances non-HDL-C and LDL-C reduction compared with diet alone in hypercholesterolemic individuals with and without type 2 diabetes. Demonstration for the first time that PS alone are more efficacious in lowering LDL-C and non-HDL-C in diabetic individuals compared to non-diabetics confirm the beneficial effects of PS to help prevent cardiovascular disease (CVD) for this high risk population.
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Horn, Mary P. "The effects of simvastatin on Staphyloccus aureus infection in endothelial cells". Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1366299.
Testo completoAbstract (sommario):
Simvastatin, a commonly prescribed statin, has exhibited several unexpected non-cholesterol lowering benefits. For example, patients taking statins have a decreased mortality rate due to bactereamia, a systemic bacterial infection commonly caused by Staphylococcus aureus (S. aureus). To investigate statin protection during bactereamia, human umbilical vein endothelial cells (HUVEC) were pre-treated with simvastatin followed by infection with S. aureus, and infection was significantly decreased. Simvastatin inhibits the cholesterol biosynthesis pathway. Therefore, the protective effect of simvastatin may be due to isoprenoid inhibition, specifically, farnesyl pyrophosphate (Fpp) and geranylgeranyl pyrophosphate (GGpp). Fpp and GGpp prenylate small G-proteins that function in cytoskeletal rearrangement and endocytosis. When Fpp and GGpp were replenished, infection was not significantly reduced. Furthermore, when farnesyl transferase and geranylgeranyl transferase, enzymes essential to transfer isoprenoid group during prenylation, were inhibited a significant decrease in infection was observed. The data indicates that Fpp and GGpp are essential for S. aureus infection.Department of Biology
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Kalis, Joni Kathryn. "THE EFFECT OF BETA-ADRENERGIC BLOCKADE ON THE DRIFT IN OXYGEN CONSUMPTION WITH PROLONGED EXERCISE". Thesis, The University of Arizona, 1985. http://hdl.handle.net/10150/292014.
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Lum, Ching-tung, e 林菁潼. "Treatment of hepatocellular carcinoma with a novel gold compound". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B30699927.
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Penny, Daniel James. "Changes in integrated cardiovascular physiology during inotropic stimulation in the early postnatal period". Monash University, Institute of Reproduction and Development, 2004. http://arrow.monash.edu.au/hdl/1959.1/9661.
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Burns, Erin M. "Simvastatin treatment modulates the immune response, increasing the survival of mice infected with Staphylococcus aureus". Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/612.
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Journoud, Mélanie. "The effect of plant sterols on lipid profiles and cholesterol kinetics of hypercholesterolemic individuals with type 2 diabetes compared with non-diabetic controls /". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80296.
Testo completoAbstract (sommario):
The objective of this study was to compare the effect of phytosterols (PS) on lipid profiles and cholesterol kinetics of hypercholesterolemic individuals with or without type 2 diabetes. It was hypothesised that the response to PS would differ between both groups due to different lipid metabolism. During this randomised, double blind, crossover trial, participants consumed a controlled diet with placebo or PS for 21 days.Plasma total cholesterol (TC) decreased with placebo and PS (10.9% and 9.7% in non-diabetic versus 11.6% and 13.6% in diabetic participants, p < 0.05). Plasma low-density lipoprotein cholesterol (LDL) significantly decreased with PS in both groups. The reduction in LDL with PS was greater in diabetic compared to non-diabetic individuals (29.8% versus 14.9%, p < 0.05). Cholesterol absorption decreased on average (p = 0.06) by 26.5% with PS compared with placebo in the diabetic group only. Therefore, a controlled heart healthy diet reduced TC and LDL concentrations in non-diabetic and diabetic individuals. Adding PS as adjuncts to a hypocholesterolemic dietary treatment was associated with lower LDL concentrations and cholesterol absorption in hypercholesterolemic participants with type 2 diabetes.
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Van, Eeden Simon Peter. "The effect of a topical combined anti-inflammatory antibiotic preparation on the outcome of third molar surgery". Diss., Pretoria : [s.n.], 2000. http://upetd.up.ac.za/thesis/available/etd-01052007-123151/.
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Pan, Beiqing. "Molecular and cellular studies of zoledronic acid : a potent inhibitor of multiple myeloma-induced osteolysis". Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09MSM/09msmp187.pdf.
Testo completoAbstract (sommario):
Bibliography: leaves 86-103. Investigates the effect of zoledronic acid on myeloma cells and osteoblast-like cells to establish the molecular and cellular mechanisms responsible for the clinical effectiveness of bisphosphonates in the treatment of patients with myelomatosis. Concludes that zoledronic acid inhibits myelomatosis-induced osteolysis thorugh the mechanisms of myeloma cell death and proliferation and maturation of osteoblasts.
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Volk, Catherine B. "Role of inhibition of protein prenylation in the cholesterol-dependent and cholesterol-independent effects of simvastatin". Virtual Press, 2006. http://liblink.bsu.edu/uhtbin/catkey/1339597.
Testo completoAbstract (sommario):
Statins are widely used to treat hypercholesterolemia. Statins inhibit cholesterol biosynthesis, thereby activating genes involved in cholesterol homeostasis, which are under the control of the Sterol Regulatory Element (SRE). Statins also have cholesterol-independent beneficial cardiovascular effects mediated through the phosphoinositide 3-kinase (PI3-K) / Akt signaling pathway and by inhibition of protein prenylation. Because statins inhibit the synthesis of isoprenoids, they can act by inhibiting the small signaling GTPases Ras and Rho, which require post-translational prenylation to become membrane-anchored and functional. We showed that simvastatin-mediated inhibition of protein prenylation does not appear to play a role in activation of SRE transcriptional activity in HepG2 cells. We also found that when isoprenoids were replenished, basal phospho-Akt decreased, suggesting that inhibition of prenylation by simvastatin mediates Akt phosphorylation. Future studies will be needed to investigate the role that inhibition of protein prenylation plays in the activation of the PI3-K/Akt pathway by simvastatin.Department of Biology
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Garrett, Ian Ross. "Studies of the effect of metal containing drugs on acute and chronic inflammation /". Title page, table of contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phg2386.pdf.
Testo completo
29
Kohutek, Jodi Lynn. "Long-term effects of 3,4- Methylenedioxymethamphetamine (MDMA) on serotonergic and dopaminergic functioning". CSUSB ScholarWorks, 2003. https://scholarworks.lib.csusb.edu/etd-project/2305.
Testo completoAbstract (sommario):
Methylenedioxymethamphetamine (MDMA) popularly known as "Ecstasy" continues to gain popularity as a recreational drug that has been shown to increase serotonin and dopamine levels. The present study has demonstrated that repeated exposure to MDMA produces long-term damage to serotonergic and dopaminergic neurons in various regions of the rat brain.
30
Kenney, Shelby R. "Development of a high throughput small molecule screen using Staphylococcus aureus invasion of cells". Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/404.
Testo completo
31
Demasi, Maryanne. "The effects of hypoxia on cyclooxygenase-2 expression and eicosanoid synthesis /". Title page, table of contents and summary only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phd3729.pdf.
Testo completoAbstract (sommario):
Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine and Royal Adelaide Hospital, Rheumatology Unit, 2004.Includes list of publications arising from this thesis. Erratum attached to inside back cover. "25/03/2004." Includes bibliographical references (leaves 185-257).
32
Liu, Chia-chi. "Oxidation of ascorbate by protein radicals in simple systems and in cells". Phd thesis, Australia : Macquarie University, 2007. http://hdl.handle.net/1959.14/16746.
Testo completoAbstract (sommario):
Thesis (PhD) -- Macquarie University, Division of Environmental and Life Sciences, Dept. of Chemistry and Biomolecular Sciences, 2007.Bibliography: leaves 295-322.
Generation of peroxide groups in proteins exposed to a wide variety of reactive oxygen species (ROS) requires an initial formation of protein carbon-centred or peroxyl free radicals, which can be reduced to hydroperoxides. Both protein radicals and protein hydroperoxides are capable of oxidizing important biomolecules and thus initiate biological damage. In this study, we investigated the inhibition of protein hydroperoxide formation by ascorbate and GSH in gamma-irradiated HL-60 cells.--We used HL-60 cells as a model for general protection of living organisms by ascorbate (Asc) and glutathione (GSH) from the deleterious effects of protein hydroperoxides generated by radicals produced by gamma radiation. Measurement by HPLC indicated that incubation of HL-60 cells with Asc in the presence of ascorbate oxidase resulted in the accumulation of intracellular Asc. The intracellular Asc levels were lowered by irradiation, demonstrating intracellular consumption of Asc by the radiation-generated radicals. Exposure of HL-60 cells to increasing gamma irradiation doses resulted in increasing accumulation of protein peroxides in the cells. This was measured by the FOX assay. A significant decrease in intracellular protein hydroperoxides was noted when the cells were treated with ascorbic acid before irradiation. A dose-dependent protective effect of Asc was observed. Asc loading also provided strong protection from radiation-generated protein hydroperoxides independently of the composition of the external medium, showing that only the radicals formed within the cells were effective in oxidizing the cell proteins. Similarly, protein peroxidation was inhibited in cells with enhanced levels of GSH and increased when the intracellular GSH concentration was reduced. These findings indicate that ascorbate and GSH are important antioxidants in protecting cells from oxidative stress associated with the generation of protein hydroperoxide.
Mode of access: World Wide Web.
xxix, 322 leaves ill
33
Hutton, Peter. "Antimicrobial plants of Australia have the potential to prevent lactic acidosis in ruminants". University of Western Australia. School of Animal Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0159.
Testo completoAbstract (sommario):
[Truncated abstract] Antimicrobial growth promoters are added to feed to prevent lactic acidosis in ruminant animals by selectively inhibiting rumen bacteria that produce lactic acid. However, recently imposed or impending bans on the use of antimicrobial growth promoters in animal production have lead to a critical need to find practical alternatives that are safe for the animal and consumer and that obtain similar production benefits. I investigated bioactive plants of Australia for their potential to prevent lactic acidosis in ruminants. The unifying hypothesis tested was that plants would be identified that selectively inhibit lactic acid-producing bacteria and consequently protect against lactic acidosis. This hypothesis was tested in a three phase process: phase 1, plant selection and collection; phase 2, a three stage protocol for screening plants and essential oils; phase 3, in vivo experiments and chemical fractionation of the most promising plant. I developed an in vitro bioassay that simulated acidosis by adding glucose to rumen fluid in Bellco tubes and incubating for 5 h (Chapter 4). The pH and gas production were used as indicators of acidosis and fermentation activity. I used this bioassay to screen ninety-five plants (dried and ground material from 79 species) and ten essential oils and included a negative control (oaten chaff) and a positive control (virginiamycin). One plant, Eremophila glabra, produced a similar pH (5.63) to the positive control (5.43) although it inhibited gas production to a moderate extent (P < 0.05). ... Seven serrulatane diterpenes were identified to be the major secondary metabolites in E. glabra. The metabolites were screened using a broth dilution and microtitre spectrophotometry method and were selective against S. bovis at between 320 and 1077 [mu]g/ mL. The serrulatanes from E. glabra were probably responsible for the activity against acidosis that I observed in vitro, because they selectively inhibited lactateproducing bacteria. It is also possible that a synergy between serrulatanes and possibly other metabolites are responsible for the activity observed in vitro. The results from my experiments support the role that bioactive plants may have to replace the antibiotics that are added to livestock feed. Australian plants were identified containing compounds that were active against the bacterial processes responsible for ruminant acidosis. To my knowledge this is the first work undertaken to identify bioactive plants of Australia for their potential to prevent acidosis. I developed in vitro screening bioassays that targeted key indicators of acidosis. These bioassays enabled me to identify 5 plants from the 104 screened that could potentially control acidosis. One of these plants in particular, E. glabra, showed a level of activity in vitro that was comparable to antibiotic protection against acidosis. The exciting in vitro results were not demonstrated in vivo but only one dose level of E. glabra was used, which was based on the in vitro work. In contrast to the in vitro system the rumen is a continuous flow system with greater complexity and it is possible that the concentration of E. glabra that I used in vivo was not optimum. This places importance on future dose response experiments to confirm the efficacy of E. glabra in vivo.
34
Almasri, Hanine. "Toxicologie des mélanges de pesticides chez des abeilles exposées à un agent pathogène : action combinée de l'agent pathogène Nosema ceranae, de l'insecticide imidaclopride, du fongicide difénoconazole et de l'herbicide glyphosate Mixtures of an insecticide, a fungicide and a herbicide induce high toxicities and systemic physiological disturbances in winter Apis mellifera honey bees Toxicity of the pesticides imidacloprid, difenoconazole and glyphosate alone and in binary and ternary mixtures to winter honey bees: effects on survival and antioxidative defenses Toxicological status changes the susceptibility of the honey bee Apis mellifera to a single fungicidal spray application Physiological effects of the interaction between Nosema ceranae and sequential and overlapping exposure to glyphosate and difenoconazole in the honey bee Apis mellifera". Thesis, Avignon, 2020. http://www.theses.fr/2020AVIG0722.
Testo completoAbstract (sommario):
Les données scientifiques actuelles suggèrent un déclin de la diversité et de l’abondance des insectes, y compris les abeilles domestiques Apis mellifera. Ces dernières sont confrontées à de fortes pertes de colonies dans plusieurs régions du monde telles que l’ouest de l’Europe et les États-Unis. De nombreuses études suggèrent que l’origine du déclin des colonies d’abeilles est multicausale et identifient les pesticides et les agents pathogènes comme étant les principaux contributeurs à ce déclin. La co-exposition des abeilles à de multiples pesticides et l’infection par plusieurs pathogènes constituent un phénomène courant. Cependant, les recherches sur les effets des mélanges de pesticides n’ont pas fait l’objet d’un intense développement. Ainsi, les travaux conduits dans le cadre de cette thèse ont été focalisés sur la détermination de la toxicité des mélanges de pesticides, appliqués à des niveaux d’exposition environnementaux, en présence d’un agent pathogène. Le choix s’est porté sur l’étude des interactions entre un insecticide néonicotinoïde, l’imidaclopride, un fongicide azole, le difénoconazole, et un herbicide, le glyphosate, en présence de l’agent pathogène Nosema ceranae. Les résultats des différentes études effectuées durant cette thèse, révèlent la complexité des études sur les mélanges de pesticides. Ces travaux nous ont permis de constater que les effets d’un mélange de pesticides peuvent fortement varier en fonction des concentrations des pesticides constituant le mélange. L’augmentation du nombre de substances et du niveau d’exposition, n’induit pas nécessairement une augmentation de la toxicité du mélange. De plus, les effets du mélange peuvent varier en fonction de la séquence d’exposition aux pesticides et de l’état sanitaire des abeilles. Les mélanges de pesticides affectent l’état physiologique des abeilles suite à une réponse systémique liée à des perturbations de mécanisme généraux tels que le stress oxydant. Cependant, ces trois pesticides, seuls et en mélanges n’ont aucun effet sur l’installation du microbiote intestinal à des niveaux d’exposition environnementauxCurrent scientific findings suggest a decline in the diversity and abundance of insects, including the honey bee Apis mellifera. The latter are facing high colony losses in several regions of the world such as Western Europe and the United States. Numerous studies suggest that the origin of bee colony decline is multi-causal and identify pesticides and pathogens as the main contributors to this decline. Co-exposure of honey bees to multiple pesticides and infection by multiple pathogens are common phenomena. However, research on the effects of pesticide mixtures has not been extensively developed. Thus, the thesis work has focused on determining the toxicity of pesticide mixtures, applied at environmental exposure levels, in the presence of pathogens. The choice was made to study the interactions between a neonicotinoid insecticide, imidacloprid, an azole fungicide, difenoconazole, and a herbicide, glyphosate, in the presence of the pathogen Nosema ceranae. The results of the different studies, carried out during this thesis, reveal the complexity of the studies on pesticide mixtures. The work allowed us to notice that the effects of a pesticide mixture can vary according to the concentrations of the pesticides constituting the mixture. The increase of the number of substances and the level of exposure does not necessarily induce an increase of the toxicity of the mixture. Furthermore, the effects of the mixture may vary depending on the sequence of exposure to the different pesticides and the health status of the honey bees. Pesticide mixtures affect the physiological state of individuals as a result of a systemic response related to disturbances of general mechanisms such as oxidative stress. However, these three pesticides, alone and in mixtures, have no effect on the installation of the intestinal microbiota at environmental exposure levels
35
De, Bruto Petro C. "ART-related body composition changes in adult women in a semi-rural South African context". Thesis, Stellenbosch : Stellenbosch University, 2006. http://hdl.handle.net/10019.1/17445.
Testo completoAbstract (sommario):
Assignment (MPhil)--University of Stellenbosch, 2006.ENGLISH ABSTRACT: The aim of this study was to investigate practical methods of monitoring AIDS related wasting and lipodystrophy in a resource-poor clinical setting with HIV infected women as the population group of interest. Measurement of body composition changes using anthropometry is both cost- and time-efficient. Various different skinfolds were taken and two different equations (the equations of Pollock et al. (1975) and Durnin and Womersley (1974) for calculating body fat were used to determine the most promising method or methods of monitoring body composition changes in a clinical setting. Detailed anthropometric measurements were performed, as well as selected measurements for haematological parameters and quality of life (QoL) for a group of 8 participants on antiretroviral medication (ART group) and 6 participants who were not on treatment (TN group). New variables namely, intra-abdominal indicator (IAI) and a percent of ideal body mass to percent of ideal arm circumference ratio (%IBW:%IAC) were investigated as possible indicators of lipodystrophy. Although measurements were taken at various timepoints, three specific time-points were chosen for data-analysis for the ART group and two time points for the TN group. These three time-points were, baseline (on the day of recruitment for TN participants and within one month before the initiation of treatment for ART participants), short-term (2 to 12 weeks after treatment initiation or the baseline measurement or for the ART and the TN participants) and long-term (within one and a half year of treatment initiation for the ART group). ART and TN participants did not differ for many variables at baseline. The major differences between ART and TN were in measured and derived variables of the arm, especially percent of ideal arm circumference (%IAC) and upper arm fat area (UAFA), which were significantly lower in the ART group. CD4+ and QoL improved significantly for the ART participants from baseline to long-term. This was not associated with changes in muscle mass, but rather some fat mass variables. Participants on antiretroviral medication exhibited changes relating to abdominal obesity. It was concluded that antiretroviral therapy contributed greatly to the QoL of the participants and it probably aided in the recovery from wasting for at least one participant in this study. Measures of the arm can be used in a rural clinical setting to effectively monitor patients with regard to AIDS related wasting. The new variables IAI and %IBW:%IAC could be helpful in the monitoring of lipodystrophy and should be investigated in future research.
AFRIKAANSE OPSOMMING: Die doelwit van hierdie studie is om praktiese metodes te ondersoek om VIGS-verwante uittering en lipodistrofie te meet in ‘n plattelandse kliniese omgewing (waar hulpbronne dikwels beperk is) met MIV ge-infekteerde vroue as populasiegroep. Die gebruik van antropometrie om veranderinge in liggaamssamestelling te meet is beide koste- en tydeffektief. Verskeie velvoumetings is geneem en twee verskillende vergelykings (die vergelykings van Pollock et al. (1975) en Durnin en Womersley (1974)) is gebruik om liggaamsvetinhoud te bereken, met die doel om ‘n belowende metode te vind om veranderinge in liggaamssamestelling te meet in ‘n kliniese omgewing. Verskeie antropometriese metings is geneem, sowel as uitgesoekte hematologiese en lewenskwaliteitmetings (QoL) vir ‘n groep van agt deelnemers wat antiretrovirale medikasie ontvang het (ART groep) en ses deelnemers wat nie hierdie behandeling ontvang het nie (TN groep). Nuwe veranderlikes (binnebuikindikator (IAI) en die verhouding van persentasie van ideale liggaamsmassa tot persentasie van ideale armomtrek (%IBW:%IAC)) is ondersoek as moontlike aanwysers van lipodistrofie. Drie spesifieke tydpunte vir die ART groep en twee tydpunte vir die TN groep is gekies uit die verskeie tydpunte waarby metings geneem is, nl. basislyn (gedefinieer as die dag wat TN deelnemers in die studie opgeneem is en 0 tot 4 weke voor die begin van behandeling vir die ART deelnemers), korttermyn (2 tot 12 weke nadat behandeling begin is of na die basislyn meting) en lang-termyn (binne een en ‘n half jaar nadat behandeling begin is vir die ART groep). By die basislyn tydpunt het min van die ART en TN deelnemers se gemete veranderlikes verskil. Die ART en TN groepe het hoofsaaklik verskil ten opsigte van veranderlikes wat betrekking het op die arm, veral persentasie van ideale armomtrek (%IAC) en bo-arm vetarea (UAFA). Hierdie twee veranderlikes was beduidend laer in die ART groep as in die TN groep. CD4+ seltelling en lewenskwaliteit tellings het beduidend verbeter vir die ART deelnemers van die basislyn tot die lang-termyn tydpunt. Hierdie veranderinge is nie samehangend met veranderinge in spiermassa nie, maar eerder met sommige vetmassa veranderlikes. Deelnemers wat antiretrovirale medikasie ontvang het, het veranderinge getoon wat gedui het op ‘n verhoogde neerlegging van vet in die buikarea. Ten slotte is bevind dat antiretrovirale medikasie bygedra het tot die verbeterde lewenskwaliteit van die deelnemers en dat dit waarskynlik ook die omkeer van uittering van ten minste een deelnemer aangehelp het. Daar is ook bevind dat armverwante metinge gebruik kan word in die plattelandse kliniese omgewing om pasiënte suksesvol te monitor ten opsigte van VIGSverwante uittering. Die nuwe veranderlikes, IAI en %IBW:%IAC kan moontlik gebruik word om lipodistrofie-verwante veranderings te meet en die gebruik van hierdie veranderlikes behoort ondersoek te word in verdere navorsing.
36
Taylor, Matthew Craig. "Parkinson's disease and xenobiotic metabolism". Master's thesis, 2001. http://hdl.handle.net/1885/147421.
Testo completo
37
"Mechanism of the hypocholesterolemic effect of water-soluble non-starch polysaccharides from jelly mushroom". 2006. http://library.cuhk.edu.hk/record=b5892916.
Testo completoAbstract (sommario):
Lam Wai Yee.Thesis (M.Phil.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (leaves 124-148).
Abstracts in English and Chinese.
Chapter Chapter 1: --- Introduction --- p.1
Chapter 1.1 --- Lipoproteins --- p.1
Chapter 1.1.1 --- General structure --- p.1
Chapter 1.1.2 --- Chylomicrons --- p.2
Chapter 1.1.3 --- Very-low-density lipoprotein (VLDL) --- p.3
Chapter 1.1.4 --- Low-density lipoprotein (LDL) --- p.4
Chapter 1.1.5 --- High-density lipoprotein (HDL) --- p.4
Chapter 1.1.6 --- Lipoprotein metabolism --- p.5
Chapter 1.1.6.1 --- Exogenous pathway --- p.5
Chapter 1.1.6.2 --- LDL receptor pathway --- p.6
Chapter 1.1.6.3 --- Reverse cholesterol transport --- p.6
Chapter 1.2 --- Cholesterol homeostasis --- p.8
Chapter 1.2.1 --- Role of Acyl-CoA: Cholesterol Acyltransferase (ACAT) in intracellular cholesterol regulation --- p.8
Chapter 1.2.2 --- Cholesterol biosynthesis --- p.9
Chapter 1.2.3 --- Bile acid metabolism --- p.10
Chapter 1.3 --- Coronary heart disease (CHD) --- p.14
Chapter 1.3.1 --- Risk factors of CHD --- p.16
Chapter 1.3.2 --- Lipoprotein cholesterol and CHD --- p.18
Chapter 1.4 --- Animal models for hypercholesterolemic study --- p.20
Chapter 1.5 --- Physico-chemical properties of water-soluble dietary fiber (SDF) --- p.22
Chapter 1.5.1 --- Water-holding capacity --- p.23
Chapter 1.5.2 --- Viscosity --- p.24
Chapter 1.5.3 --- Adsorption or entrapment of organic molecules --- p.25
Chapter 1.5.4 --- Fermentability --- p.25
Chapter 1.6 --- Hypocholesterolemic effect of SDF and proposed mechanisms --- p.26
Chapter 1.7 --- Medicinal properties of edible mushrooms --- p.28
Chapter 1.7.1 --- Background information --- p.28
Chapter 1.7.2 --- Hypocholesterolemic effect of edible mushrooms --- p.29
Chapter 1.7.3 --- Previous studies on edible jelly mushrooms --- p.31
Chapter 1.8 --- Objectives
Chapter Chapter 2: --- Materials and Methods --- p.34
Chapter 2.1 --- Materials --- p.34
Chapter 2.1.1 --- Sample preparation --- p.34
Chapter 2.1.2 --- Animal model --- p.35
Chapter 2.2 --- Methods --- p.35
Chapter 2.2.1 --- Extraction scheme of mushroom water-soluble non-starch polysaccharides (SNSPs) --- p.35
Chapter 2.2.2 --- Proximate analyses of samples --- p.36
Chapter 2.2.2.1 --- Crude protein --- p.36
Chapter 2.2.2.2 --- Fat --- p.37
Chapter 2.2.2.3 --- Total dietary fiber --- p.38
Chapter 2.2.2.4 --- Soluble and insoluble dietary fiber --- p.39
Chapter 2.2.2.5 --- Ash --- p.40
Chapter 2.2.2.6 --- Moisture --- p.41
Chapter 2.2.3 --- Chemical characterization of mushroom SNSPs --- p.41
Chapter 2.2.3.1 --- Monosaccharide composition by gas chromatography --- p.41
Chapter 2.2.3.2 --- Total carbohydrate content --- p.44
Chapter 2.2.3.3 --- Uronic acid content --- p.44
Chapter 2.2.3.4 --- Soluble protein content --- p.45
Chapter 2.2.4 --- Rheological study of mushroom SNSPs --- p.46
Chapter 2.2.4.1 --- Determination of intrinsic viscosity [ η] of mushroom SNSPs --- p.46
Chapter 2.2.4.2 --- Determination of apparent viscosity [ηap] of mushroom SNSPs --- p.48
Chapter 2.2.5 --- In vivo study --- p.50
Chapter 2.2.5.1 --- Animal diets --- p.50
Chapter 2.2.5.1.1 --- Study for hypocholesterolemic potential of mushroom SNSPs --- p.50
Chapter 2.2.5.1.2 --- Study for dose-dependent effect on hypocholesteolemic potential of Auricularia polytricha (AP) SNSP --- p.50
Chapter 2.2.5.2 --- Feeding experiments --- p.51
Chapter 2.2.5.2.1 --- Screening for hypocholesterolemic potential of mushroom SNSPs --- p.51
Chapter 2.2.5.2.2 --- Dose-dependent effect on hypocholesterolemic potential of AP SNSP --- p.52
Chapter 2.2.5.3 --- Blood samples collection --- p.52
Chapter 2.2.5.4 --- Plasma preparation --- p.53
Chapter 2.2.5.5 --- Liver samples collection and preparation --- p.53
Chapter 2.2.5.6 --- Fecal samples collection and preparation --- p.53
Chapter 2.2.5.7 --- Determination of plasma lipid profiles --- p.54
Chapter 2.2.5.7.1 --- Plasma total cholesterol (TC) analysis --- p.54
Chapter 2.2.5.7.2 --- Plasma high-density lipoprotein cholesterol (HDL-C) analysis --- p.54
Chapter 2.2.5.7.3 --- Plasma triglycerides (TG) analysis --- p.55
Chapter 2.2.5.8 --- Determination of hepatic cholesterol profile by gas chromatography --- p.56
Chapter 2.2.5.9 --- Determination of hepatic enzymes activity --- p.58
Chapter 2.2.5.9.1 --- Preparation of hepatic microsomes --- p.58
Chapter 2.2.5.9.2 --- Determination of 3-hydroxy-3-methyl- glutaryl-Coenzyme A reductase (HMG-CoA reductase) activity --- p.58
Chapter 2.2.5.10 --- Determination of fecal lipid profiles by gas chromatography --- p.61
Chapter 2.2.5.10.1 --- Separation of fecal neutral and acidic sterols --- p.61
Chapter 2.2.5.10.2 --- Fecal neutral sterol analysis --- p.61
Chapter 2.2.5.10.3 --- Fecal acidic sterol analysis --- p.62
Chapter 2.2.6 --- Statistical analysis --- p.63
Chapter Chapter 3: --- Results and Discussion --- p.65
Chapter 3.1 --- Proximate analysis of edible jelly mushrooms --- p.65
Chapter 3.2 --- Yield of mushroom SNSP crude extracts --- p.67
Chapter 3.3 --- Chemical characterization of mushroom SNSPs --- p.68
Chapter 3.3.1 --- Total carbohydrate content --- p.68
Chapter 3.3.2 --- Uronic acid content --- p.68
Chapter 3.3.3 --- Soluble protein content --- p.68
Chapter 3.3.4 --- Monosaccharide composition --- p.69
Chapter 3.4 --- Rheological behavior of mushroom SNSPs --- p.71
Chapter 3.4.1 --- Intrinsic viscosity [η] --- p.71
Chapter 3.4.2 --- Apparent viscosity [ηap] --- p.75
Chapter 3.5 --- In vivo hypocholesterolemic potential of mushroom SNSPs --- p.78
Chapter 3.5.1 --- Effect on body weight and diet intake --- p.79
Chapter 3.5.2 --- Effect on plasma TC concentration --- p.81
Chapter 3.5.3 --- Effect on plasma HDL-C concentration --- p.84
Chapter 3.5.4 --- Effect on plasma TG concentration --- p.86
Chapter 3.5.5 --- Effect on hepatic cholesterol profile --- p.89
Chapter 3.5.6 --- Effect on HMG-CoA reductase activity by AA and AP SNSPs --- p.92
Chapter 3.5.7 --- Effect on neutral and acidic sterols excretion by AA and AP SNSPs --- p.93
Chapter 3.5.8 --- Correlation between hypocholesterolemic potential and viscosity of mushroom SNSPs --- p.97
Chapter 3.6 --- In vivo dose-dependent effect on hypocholesterolemic potential of AP SNSP --- p.99
Chapter 3.6.1 --- Effect on body weight and diet intake --- p.100
Chapter 3.6.2 --- Effect on plasma TC concentration --- p.102
Chapter 3.6.3 --- Effect on plasma HDL-C concentration --- p.105
Chapter 3.6.4 --- Effect on plasma TG concentration --- p.107
Chapter 3.6.5 --- Effect on hepatic cholesterol profile --- p.110
Chapter 3.6.6 --- Effect on HMG-CoA reductase activity --- p.113
Chapter 3.6.7 --- Effect on neutral and acidic sterols excretion --- p.114
Chapter 3.6.8 --- Correlation between dosage and hypocholesterolemic effect of AP SNSP --- p.119
Chapter Chapter 4: --- Conclusions and Future works --- p.121
List of References --- p.124
Related Publications --- p.149
38
"In vitro and in vivo antioxidant activity and hypocholesterolemic effect in extracts of Agrocybe aegerita". 2005. http://library.cuhk.edu.hk/record=b5896402.
Testo completoAbstract (sommario):
Ng Yuk Fan.Thesis (M.Phil.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (leaves 145-162).
Abstracts in English and Chinese.
Thesis Committee: --- p.i
Acknowledgements --- p.ii
Abstract --- p.iii
摘要 --- p.v
Content --- p.vii
List of Tables --- p.xiii
List of Figures --- p.xvi
Abbreviations --- p.xviii
Chapter Chapter 1: --- Introduction --- p.1
Chapter 1.1 --- Antioxidants --- p.1
Chapter 1.1.1 --- Definition and mode of actions of antioxidants --- p.1
Chapter 1.1.2 --- Synthetic antioxidants --- p.2
Chapter 1.1.3 --- Natural antioxidants --- p.3
Chapter 1.2 --- Changes of antioxidant activity in food processing --- p.4
Chapter 1.2.1 --- Blanching --- p.4
Chapter 1.2.2 --- Drying --- p.5
Chapter 1.2.3 --- Microwave and Infrared energy --- p.7
Chapter 1.2.4 --- Freezing --- p.8
Chapter 1.3 --- Lipid oxidation and antioxidant --- p.8
Chapter 1.3.1 --- Free radicals --- p.8
Chapter 1.3.1.1 --- Superoxide --- p.10
Chapter 1.3.1.2 --- Hydrogen peroxide --- p.11
Chapter 1.3.1.3 --- Hydroxyl radical --- p.13
Chapter 1.3.2 --- Mechanism of lipid oxidation --- p.14
Chapter 1.3.3 --- Oxidation of low-density-liporoproteins (LDLs) and coronary heart disease --- p.15
Chapter 1.3.4 --- Role of antioxidants in inhibiting lipid oxidation --- p.16
Chapter 1.4 --- Hypocholesterolemic and antioxidant activity of phenolics --- p.19
Chapter 1.5 --- Medicinal properties of mushrooms --- p.21
Chapter 1.5.1 --- Background information of mushrooms --- p.21
Chapter 1.5.2 --- Phenolics in mushrooms --- p.22
Chapter 1.5.3 --- Hypocholesterolemic effect in mushroom --- p.23
Chapter 1.5.4 --- Previous studies in Agrocybe aegerita --- p.25
Chapter 1.6 --- Animal model for hypocholesteroliemic study --- p.27
Chapter 1.6.1 --- General requirements --- p.27
Chapter 1.6.2 --- Hamster model --- p.27
Chapter 1.7 --- Principles of assays that involved in antioxidant activity --- p.30
Chapter 1.7.1 --- ABTS + radical cation scavenging activity --- p.30
Chapter 1.7.2 --- Beta carotene bleaching method --- p.31
Chapter 1.7.3 --- Ferric reducing antioxidant power (FRAP) --- p.31
Chapter 1.7.4 --- Scavenging activity of hydroxyl radical --- p.32
Chapter 1.7.5 --- Inhibition of low-density lipoproteins (LDLs) oxidation --- p.33
Chapter 1.7.6 --- Total phenolic content determination --- p.33
Chapter 1.8 --- Principles of assays in hypocholesterolemic study --- p.34
Chapter 1.8.1 --- HDL-Cholesterol determination --- p.34
Chapter 1.8.2 --- Total cholesterol determination --- p.34
Chapter 1.8.3 --- Determination of plasma total triglyceride --- p.35
Chapter 1.9 --- Objectives --- p.36
Chapter Chapter 2: --- Materials and Methods --- p.37
Chapter 2.1 --- Sample preparation --- p.37
Chapter 2.2 --- Proximate Analysis of FAa and DAa --- p.38
Chapter 2.2.1 --- Determination of crude protein --- p.38
Chapter 2.2.2 --- Determination of ash --- p.39
Chapter 2.2.3 --- Total dietary fiber --- p.39
Chapter 2.2.4 --- Determination of fat --- p.41
Chapter 2.2.5 --- Moisture content --- p.42
Chapter 2.3 --- Sample extraction --- p.42
Chapter 2.3.1 --- Small-scale extraction --- p.42
Chapter 2.3.2 --- Large-scale extraction --- p.43
Chapter 2.4 --- Total phenolic content of DAa and FAa extract --- p.44
Chapter 2.5 --- Chemical assays for in vitro antioxidative properties determination --- p.45
Chapter 2.5.1 --- Hydroxyl free radical scavenging activity --- p.45
Chapter 2.5.2 --- Beta-carotene bleaching method --- p.46
Chapter 2.5.3 --- Inhibition of human low-density-lipoproteins (LDLs) oxidation --- p.47
Chapter 2.5.4 --- Scavenging activity of ABTS+radical cation --- p.50
Chapter 2.6 --- In vivo tests for antioxidative and hypocholesterolemic effect of DAa --- p.51
Chapter 2.6.1 --- Feeding experiments --- p.51
Chapter 2.6.2 --- Collection of plasma --- p.52
Chapter 2.6.3 --- Liver sample preparation --- p.52
Chapter 2.6.4 --- Determination of in vivo antioxidative effect --- p.54
Chapter 2.6.4.1 --- FRPA assay --- p.54
Chapter 2.6.4.2 --- ABTS + radical cation scavenging activity --- p.55
Chapter 2.6.5 --- Determination of plasma lipid profiles --- p.55
Chapter 2.6.5.1 --- Plasma total cholesterol (TC) --- p.55
Chapter 2.6.5.2 --- Plasma total triglyceride (TG) --- p.56
Chapter 2.6.5.3 --- Plasma high density lipoprotein cholesterol (HDL-C) determination --- p.57
Chapter 2.6.5.4 --- Hepatic cholesterol determination by gas chromatography analysis --- p.57
Chapter 2.7 --- Statistical analysis --- p.59
Chapter Chapter 3: --- Results and discussion --- p.61
Chapter 3.1 --- Proximate analysis --- p.61
Chapter 3.2 --- Small-scale extraction scheme --- p.63
Chapter 3.2.1 --- Extraction yield --- p.63
Chapter 3.2.2 --- Antioxidant assays --- p.65
Chapter 3.2.2.1 --- Hydroxyl free radical scavenging activity --- p.65
Chapter 3.2.2.2 --- Beta-carotene bleaching method --- p.68
Chapter 3.2.2.3 --- The formation of TBARS in human LDL oxidation --- p.75
Chapter 3.2.2.4 --- Total phenolic content (TPC) in DAa and FAa ethanolic and water extracts --- p.81
Chapter 3.2.2.5 --- Correlation between total phenolic content and antioxidant activity of mushroom extracts --- p.84
Chapter 3.2.2.6 --- Comparison of antioxidant activity and TPC in DAa and FAa ethanolic and water extracts in the small-scale extraction scheme --- p.88
Chapter 3.3 --- Large-scale extraction scheme --- p.91
Chapter 3.3.1 --- Extraction yield --- p.91
Chapter 3.3.2 --- Antioxidant assays --- p.91
Chapter 3.3.2.1 --- Hydroxyl free radical scavenging activity --- p.91
Chapter 3.3.2.2 --- Beta-carotene bleaching method --- p.94
Chapter 3.3.2.3 --- ABTS + radical cation scavenging activity --- p.96
Chapter 3.3.2.4 --- Formation of TBARS in human LDL oxidation in the DAa_E_l and Daa_W_1 --- p.97
Chapter 3.3.2.5 --- Total phenolic content (TPC) of DAa_E_l and DAa_W_l --- p.97
Chapter 3.3.2.6 --- Correlation between total phenolic content and antioxidant activity --- p.101
Chapter 3.3.2.7 --- Summary of large-scale extraction scheme --- p.103
Chapter 3.4 --- In vivo antioxidant activity and hypocholesterolemic effect of DAa studied by animal model --- p.104
Chapter 3.4.1 --- Effect of DAa´ؤE_1 and DAa_W_l on body weight and food intake --- p.105
Chapter 3.4.2 --- Effect of DAa一E´ؤ1 and DAa_W_l on plasma total cholesterol (TC) in hamsters --- p.108
Chapter 3.4.3 --- Effect of DAa´ؤE_1 and DAa W l on plasma total triglycerides (TG) in hamsters --- p.114
Chapter 3.4.4 --- Effect of DAa_E_l and DAa_W_l on plasma high-density-lipoprotein cholesterol (HDL-C) in hamsters --- p.119
Chapter 3.4.5 --- Effect of DAa_E_l and DAa一W_1 on hepatic cholesterol (HC) profile in hamsters --- p.124
Chapter 3.4.6 --- Effect of DAa_E_l and DAa W l on ferric reducing antioxidant power (FRAP) in hamsters (FRAP) --- p.128
Chapter 3.4.7 --- Effect of DAa_E_l and DAa_W_l on ABTS + cation radical scavenging activity --- p.131
Chapter 3.4.8 --- The antioxidant activity and hypocholesterolemic effect of DAa extracts --- p.134
Chapter 3.4.9 --- Summary of in vivo antioxidant activity and hypocholesterolemic effect of DAa studied by animal model --- p.140
Chapter Chapter 4: --- Conclusions --- p.142
References --- p.145
39
Wood, Philip (Philip Gregory) 1967. "Control of pulmonary surfactant secretion : an evolutionary perspective". 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phw878.pdf.
Testo completoAbstract (sommario):
Bibliography: leaves 209-254. Attempts to construct an evolutionary overview of the regulation of surfactant secretion among the vertebrates. A detailed whole animal and in vitro study of the factors that control surfactant secretion and function in the central Australian agamid lizard Pogona vitticeps was undertaken. Type II pneumocytes were also isolated and cultured from Australian lungfish, North American bullfrogs and fat-tailed dunnarts.
40
Yeh, Jun-Yen 1970. "Cost-effectiveness analyses of anti-resorptive agents for management of glucocorticoid-induced osteoporosis and fractures: empirical estimates from the 1996-2004 MEPS data and longitudinal projection from Markov modeling". Thesis, 2007. http://hdl.handle.net/2152/3366.
Testo completoAbstract (sommario):
Long-term glucocorticoid use leads to glucocorticoid-induced osteoporosis (GIOP) and fractures which require proper management. Little is known about the "real-world," long-term costs and effectiveness of anti-osteoporotic treatments. A retrospective analysis of data from the 1996-2004 Medical Expenditure Panel Survey was conducted to evaluate the "real-world" outcomes. Markov modeling with Monte Carlo simulations was used to yield long-term estimates of these outcomes. A total of 5,461 subjects met the study criteria for long-term glucocorticoid users (LTGS, average prednisone-equivalent dose=11.0 mg/day, average length=237 days), which represents 2.3% of the non-institutional U.S. population. The study subjects tended to be middle-aged (49.7 years old), female (61.4%) and white (86.2%). Overall 22.4% of LTGS users reported use of any anti-osteoporotic agent. Hormone replacement therapy (HRT) was the most frequently used in women followed by bisphosphonates, while bisphosphonates and calcitonin were used by men. Analyses of variance indicated some significant differences in characteristics of LTGS users among treatment groups which suggest a selection bias. Female LTGS users had higher prevalence rates (6.8%) of osteoporosis than males (1.0%), but the prevalence rates of osteoporotic fractures were similar (3.0%). The logistic regression analyses indicated that the use of oral glucocorticoid tablets does not significantly change the odds of osteoporotic fractures in study subjects (relative risk (RR)=1.146, 95% confidence interval (CI) 0.901-1.458 for subjects in the WELL state; RR=0.55, 95% CI 0.188-1.621 for subjects in the GIOP state; RR=1.241, 95% CI 0.532-2.893 for subjects in the GIFX state). The estimated 10-year and lifetime incremental cost per osteoporotic fracture avoided are $27,253-$35,692 (10-year) and $84,942-$91,075 (lifetime) in hypothetical female glucocorticoid users. HRT is the most cost-effective option for hypothetical females except that calcitonin is preferred for 65-year-old females receiving lifetime treatments. When HRT is excluded, calcitonin is the next most cost-effective option except that raloxifene is preferred for 30- and 50-year-old females receiving 10-year treatments. Calcitonin is the most cost-effective option for male glucocorticoid users. Bisphosphonates are less cost-effective which may be due to selection bias. Anti-osteoporotic treatments are recommended for all long-term glucocorticoid users, but the preferred option depends on gender, age, length of treatments and budgets.
41
"TRPV4-TRPC1-KCa1.1 complex: its function in vascular tone regulation". 2014. http://library.cuhk.edu.hk/record=b6115563.
Testo completoAbstract (sommario):
一氧化氮（NO）和內皮源性超極化因子（EDHFs）是內皮衍生的血管舒張因子兩大類。 EETs是構成EDHFs的主要類型，這是由花生四烯酸通過細胞色素P450 （CYP）表氧化酶的催化活性得到。雖然這兩個EET和NO誘導血管舒張，從而降低血壓，許多報告表明，NO對EET引起的血管舒張起抑製作用。然而，不管它的重要性，有關一氧化氮對EETs的抑制作用的機理尚未完全了解。在本研究中，我調查了一氧化氮對EET的負調控。通過膜電位和動脈張力測量，我們發現， 11,12-EET可引起內皮剝脫豬冠狀動脈平滑肌細胞膜超極化和血管舒張。該反應被S-亞硝基-N-乙酰青黴胺（SNAP）和8-Br-cGMP，一個NO的供體和cGMP的膜穿透物類似物，分別抑制。 SNAP和8-Br-cGMP對11,12-EET引起的細胞膜超極化和血管舒張的抑製作用被羥鈷胺，一氧化氮清除劑; ODQ ，鳥苷酸環化酶抑製劑;和KT5823 ，蛋白激酶G（PKG）抑製劑逆轉。 SNAP和8-Br-cGMP對EET反應的抑製作用也被過度供應外源性激酶底物， TAT-TRPC1S¹⁷²和TAT -TRPC1T³¹³廢除。羥鈷胺，ODQ， KT5823， TAT -TRPC1，和TAT -scrambled獨自使用不影響11,12-EET引起的細胞膜超極化和血管舒張作用。然而，獨自使用14，15-EEZE（EET的拮抗劑）抑制了11,12-EET的作用。 此外，磷酸化試驗表明， PKG可以直接在Ser172和Thr313位點磷酸化TRPC1 。此外，TRPV4 ， TRPC1 ，或KCa1.1被選擇性地抑制時，11,12-EET未能引起細胞膜超極化和血管舒張。免疫共沉澱研究表明， TRPV4 ， TRPC1和KCa1.1物理上彼此相關聯。
以上結果表明，NO-cGMP-PKG通路可通過TRPC1的磷酸化來抑制11,12- EETs在冠狀動脈血管平滑肌細胞上的作用。此外，TRPV4，TRPC1和KCa1.1參與11,12-EET誘導平滑肌超極化和血管舒張，他們可能互相關聯。從本研究的結果表明，NO和cGMP可通過PKG-介導的TRPC1的磷酸化，抑製EET誘導的平滑肌超極化和血管舒張。
Nitric oxide (NO) and endothelium-derived hyperpolarizing factors (EDHFs) are two main classes of endothelium-derived vascular relaxant factors. EETs constitute a major type of EDHFs, which are derived from arachidonic acids via the catalytic activity of cytochrome P450 (CYP) epoxygenases. Although both EET and NO induce vascular relaxation, thus reduce blood pressure, numerous reports demonstrated that NO exerts an inhibitory action on EET-induced vascular relaxation. However, despite of its importance, the mechanisms related to the inhibitory effects of NO on EETs are incompletely understood.
In the present study, I investigated the scheme for negative regulation of NO on EET action. Through measurements of membrane potential and arterial tension, we showed that 11,12-EET could induce membrane hyperpolarization and vascular relaxation in endothelium-denuded porcine coronary arteries. The responses were suppressed by S-nitroso-N-acetylpenicillamine (SNAP) and 8-Br-cGMP, a NO donor and a membrane-permeant analogue of cGMP, respectively. The inhibitory actions of SNAP and 8-Br-cGMP on 11,12-EET-induced membrane hyperpolarization and vascular relaxation were reversed by hydroxocobalamin, a NO scavenger; ODQ, a guanylyl cyclase inhibitor; and KT5823, a protein kinase G (PKG) inhibitor. The inhibitory actions of SNAP and 8-Br-cGMP on EET responses were also abrogated by shielding TRPC1-PKG phosphorylation sites with excessive supply of exogenous PKG substrates, TAT-TRPC1S¹⁷² and TAT-TRPC1T³¹³. Hydroxocobalamin, ODQ, KT5823, TAT-TRPC1 and TAT-scrambled alone has no effect on 11,12-EET-induced membrane hyperpolarization and vascular relaxation. However, 14,15-EEZE (a selective EET antagonist) alone inhibits the action of 11,12-EET. Furthermore, phosphorylation assay was performed and it demonstrated that PKG could directly phosphorylate TRPC1 at Ser¹⁷² and Thr³¹³. In addition, 11,12-EET failed to induce membrane hyperpolarization and vascular relaxation when TRPV4, TRPC1, or KCa1.1 was selectively inhibited. Co-immunoprecipitation studies demonstrated that TRPV4, TRPC1 and KCa1.1 physically associated with each other in smooth muscle cells.
Taking together, our findings demonstrated that the NO-cGMP-PKG pathway may act through the phosphorylation of TRPC1 to inhibit the action of 11,12-EETs in coronary arterial smooth muscle cells. Furthermore, TRPV4, TRPC1 and KCa1.1 are critically involved in the 11,12-EET-induced smooth muscle hyperpolarization and relaxation and that they may physically associate with each other. The results from this study demonstrated that NO and cGMP could lead to PKG-mediated phosphorylation of TRPC1, resulting in an inhibition of EET-induced smooth muscle hyperpolarization and vascular relaxation.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Zhang, Peng.
"Ca" on title page is subscript.
Thesis (Ph.D.) Chinese University of Hong Kong, 2014.
Includes bibliographical references (leaves 115-133).
Abstracts also in Chinese.
42
"Effect of oxidized and hyperoxidized guanine on DNA primer-template structures". 2009. http://library.cuhk.edu.hk/record=b5896585.
Testo completoAbstract (sommario):
Fenn, Dickson.Thesis (M.Phil.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 74-81).
Abstract also in Chinese.
Title Page --- p.i
Thesis Committee --- p.ii
Acknowledgement --- p.iii
Table of Contents --- p.v
List of Tables --- p.ix
List of Figures --- p.x
List of Abbreviations and Symbols --- p.xv
Abstract --- p.xvii
Chapter 1.Chapter One: --- Introduction --- p.1
Chapter 1.1 --- Oxidation and Hyperoxidation of Guanine --- p.1
Chapter 1.2. --- DNA Replication --- p.2
Chapter 1.3 --- Mutagenesis --- p.3
Chapter 1.4 --- Literature Survey on Spiroiminodihydantoin (Sp) --- p.4
Chapter 1.5 --- Purpose of This Work --- p.5
Chapter 1.6 --- DNA Structure --- p.6
Chapter 1.6.1 --- Nomenclature --- p.6
Chapter 1.6.2 --- Torsion Angles --- p.6
Chapter 1.6.3 --- Sugar Pucker Conformation --- p.7
Chapter 1.6.4 --- Secondary Structures of DNA --- p.8
Chapter 2.Chapter Two: --- Materials and Methodology --- p.10
Chapter 2.1 --- Sample Design --- p.10
Chapter 2.2 --- Sample Preparation --- p.11
Chapter 2.2.1 --- DNA Synthesis and Purification --- p.11
Chapter 2.2.2 --- HPLC Separation --- p.11
Chapter 2.2.3 --- NMR Samples Preparation --- p.12
Chapter 2.3 --- NMR Analysis --- p.12
Chapter 2.3.1 --- Resonance Assignment --- p.14
Chapter 2.3.1.1 --- Proton --- p.14
Chapter 2.3.1.2 --- Phosphorous --- p.16
Chapter 2.3.2 --- Sugar Pucker Conformation --- p.17
Chapter 2.3.3 --- Backbone Conformation --- p.18
Chapter 2.4 --- UV Melting Analysis --- p.19
Chapter 3.Chapter Three: --- "HPLC, NMR and UV Results" --- p.21
Chapter 3.1 --- HPLC Separation of Sp Diastereoisomers --- p.21
Chapter 3.2 --- NMR Resonance Assignments --- p.24
Chapter 3.2.1 --- 5'-GG Sample --- p.24
Chapter 3.2.2 --- 5'-G(oG) Sample --- p.26
Chapter 3.2.3 --- 5'-G(Sp) Sample --- p.29
Chapter 3.2.4 --- 5'-T(oG) Sample --- p.31
Chapter 3.2.5 --- 5'-T(Sp) Sample --- p.34
Chapter 3.3 --- Sugar Pucker Conformation --- p.38
Chapter 3.4 --- Backbone Conformation --- p.41
Chapter 3.5 --- UV Melting --- p.43
Chapter 4.Chapter Four: --- Effect of Spiroiminodihydantoin and 7-hydro-8-oxoguanine on Primer-Template Structures --- p.44
Chapter 4.1 --- Overview --- p.42
Chapter 4.2 --- NMR Investigations of the Primer-Template Models --- p.45
Chapter 4.2.1 --- Incorporation of a dCTP Opposite a 5'-GG Template --- p.45
Chapter 4.2.2 --- Incorporation of a dCTP Opposite a 5'-G(oG) Template --- p.46
Chapter 4.2.3 --- Incorporation of a dCTP Opposite a 5'-G(Sp) Template --- p.48
Chapter 4.2.4 --- Incorporation of a dATP Opposite a 5'-T(oG) Template --- p.50
Chapter 4.2.5 --- Incorporation of a dATP Opposite a 5'-T(Sp) Template --- p.51
Chapter 4.3 --- Effect of Sp and oG on Primer-Template Structures --- p.52
Chapter 4.3.1 --- Misaligned Structure with a Sp-Bulge --- p.52
Chapter 4.3.2 --- C·oG Base Pair in 5'-G(oG) --- p.54
Chapter 4.3.3 --- Biological Implications --- p.54
Chapter 5. --- Chapter Five: Preliminary Structural Calculations on Primer- Template Structures --- p.56
Chapter 5.1 --- Experimental Restraints Extraction --- p.56
Chapter 5.2 --- Experimental Restraints Distribution --- p.58
Chapter 5.3 --- Structural Calculations --- p.60
Chapter 5.4 --- Structural Results --- p.62
Chapter 5.4.1 --- 5'-GG --- p.63
Chapter 5.4.2 --- 5'-G(oG) --- p.64
Chapter 5.4.3 --- 5'-T(oG) --- p.65
Chapter 5.4.4 --- 5'-T(SpR) with 5'-T(Spl) Restraints --- p.66
Chapter 5.4.5 --- 5'-T(SpR) with 5'-T(Sp2) Restraints --- p.67
Chapter 5.4.6 --- 5'-T(SpS) with 5'-T(Spl) Restraints --- p.68
Chapter 5.4.7 --- 5'-T(SpS) with 5'-T(Sp2) Restraints --- p.69
Chapter 5.6 --- Structural Analysis --- p.70
Chapter 6. --- Chapter Six: Conclusions and Future Work --- p.72
Appendix --- p.73
References --- p.74
43
Glassburn, Jenny E. "The effects of simvastatin pretreatment on innate immune responses to Staphylococcus aureus infection". 2011. http://liblink.bsu.edu/uhtbin/catkey/1640179.
Testo completoAbstract (sommario):
Sepsis is a systemic inflammatory response that causes, increased heart rate, respirations, fever, and inadequate blood flow to organs. One of the most prevalent causes of sepsis is Staphylococcus aureus (S. aureus). With increasing numbers of strains of bacteria becoming antibiotic resistant, new methods for the treatment and clearance of sepsis are needed. Studies have shown that the lipid lowering drug simvastatin is protective for incidence of sepsis, having immunomodulatory effects and anti-inflammatory properties, specifically. Thus, it may be an alternative way to prevent sepsis due to S. aureus infections. Studies in our laboratory have shown that simvastatin pretreatment increases survival of mice infected with S. aureus and alters the adaptive immune response such that levels of IgG2c are reduced to the level of uninfected controls. Our studies have demonstrated that while simvastatin does not enhance bacterial clearance, or affect serum C5a levels, it does decrease serum levels of TNF.Department of Biology
44
Moodley, Nivrithi. "Antimicrobial activity of ciprofloxacin-coated gold nanoparticles on selected pathogens". Thesis, 2014. http://hdl.handle.net/10321/1120.
Testo completoAbstract (sommario):
Submitted in complete fulfillment for the Degree of Master of Technology: Biotechnology, Durban University of Technology, Durban, South Africa, 2014.Antibiotic resistance amongst bacterial pathogens is a crisis that has been worsening over recent decades, resulting in serious and often fatal infections that cannot be treated by conventional means. Diseases caused by these drug resistant agents result in protracted illnesses, greater mortality rates and increases in treatment costs. Improvements to existing therapies and the development of novel treatments are urgently required to deal with this escalating threat to human health. One of the more promising strategies to combat antibiotic resistance is the use of metallic nanoparticles. Research into this area has shown that the binding of antibiotics to nanoparticles enhances their antimicrobial effects, reduces side-effects due to requirement of lower dosages of the drug, concentrates the drug at the interaction site with bacterial cells and in certain cases, has re-introduced susceptibility into bacterial strains that have developed drug resistance. Furthermore, these nanoparticles can be used in cancer treatment in similar drug delivery roles. Based on the promising data that demonstrated the synergistic effects of antimicrobial agents with nanoparticles, the aim of our research is to determine the effect of ciprofloxacin-conjugated gold nanoparticles as antimicrobial agents. To achieve this aim our objectives were: (i) to synthesize citrate-capped and ciprofloxacin-conjugated gold nanoparticles; (ii) to determine the physical and chemical characteristics of the ciprofloxacin-nanoparticle hybrid molecule; (iii) to investigate the antimicrobial activity of the conjugated nanoparticles against various species of common pathogens and (iv) to investigate the anti-cancer potential of the citrate-capped nanoparticles against a Caco-2 cell line. In this study, citrate-capped gold nanoparticles were conjugated to the antibiotic, ciprofloxacin, and their antibacterial and anti-cancer activity was evaluated. Initial experiments involved the synthesis and characterization of gold nanoparticles and ciprofloxacin conjugated nanoparticles. The gold nanoparticles were synthesized using the Turkevich citrate reduction technique which has been extensively used in studies thus far. The synthesized nanoparticles were characterized for specific absorbance using a UV-Spectrophotometer. The bond between the nanoparticles and ciprofloxacin was characterized by FTIR. Ultra structural details of the gold nanoparticles were established by TEM. The colloidal stability of the nanoparticles was determined by spectroscopic analysis. The antibacterial activity of the ciprofloxacin-conjugated gold nanoparticles was studied by exposure to pathogenic bacteria (Staphyloccocus aureus, E. coli, Klebsiella pneumoniae, Enterocococcus spp., Enterobacter spp., and Psuedomonas spp.). MIC values were measured to give indication of antimicrobial effect. These bactericidal properties of the conjugate nanoparticles were further investigated by electron microscopy. To evaluate the action of the citrate capped gold nanoparticles on cancer cells, we exposed Caco-2 cells to various concentrations of the nanoparticles and its effect was evaluated by measuring the viability of the cells. The results showed that 0.5 mM trisodium citrate reduced gold chloride to yield gold nanoparticles, which were spherical and 15 to 30 nm (by TEM characterization) and had an absorption maxima of 530 nm. The ciprofloxacin conjugated nanoparticles had an absorption maxima of 667nm. The colloidal stability, which is used to assess whether the synthesized particles will retain their integrity in solution showed that citrate-capped GNPs were most stable at 37°C over a 14 day storage period while ciprofloxacin-conjugated GNPs were found to be most stable at 4°C over a 14 day period. The FTIR results showed that chemical bonding in the conjugated nanoparticles occurs between the pyridone moiety of ciprofloxacin and the nanoparticle surface. The antimicrobial results of ciprofloxacin-conjugated GNPs had a significantly improved killing response compared to ciprofloxacin on both Gram positive and Gram negative bacteria. The citrate-capped GNPs are shown to exert a similar cytotoxic effect to gemcitabine on the Caco-2 cell line at a concentration of 0.5 mM. These results indicate that combining gold nanoparticles and ciprofloxacin enhances the antimicrobial effect of the antibiotic. The conjugate nanoparticles increase the concentration of antibiotics at the site of bacterium-antibiotic interaction, and thus enhance the binding and entry of antibiotics into bacteria. This has great implications for treatment of infection, as these antibiotic-conjugated nanoparticles can be incorporated into wound dressings, be administered intravenously as drug delivery agents, be engineered to possess multiple functionalities in addition to antibacterial activity and act as dual infection tracking and antimicrobial agents. Likewise, in this study, gemcitabine, an anticancer drug and gold nanoparticles were shown to kill cancer cells. In addition to their use in photothermal therapy and as drug delivery agents, the nanoparticles themselves possess anti-cancer activity against the Caco-2 cells. Thus, they have potential to act alone as a form of cancer treatment if functionalized with certain targeting agents that are specific to cancer cells, reducing the side-effects that come with regular chemotherapeutic drugs. It can be concluded that ciprofloxacin-conjugated gold nanoparticles enhance antibacterial effects of the antibiotic ciprofloxacin against bacterial cells and citrate-capped gold nanoparticles have anti-cancer activity against the Caco-2 cell line.
45
Nelson, Matthew Jay. "Impact of N-2-mercaptopropionylglycine (MPG) and simvastatin on exercise-induced cardiac adaptations". 2008. http://hdl.handle.net/2152/17945.
Testo completoAbstract (sommario):
Experiments were conducted to investigate the role of free radicals in exercise induced cardiac adaptations and to determine if statin administration would adversely affect cardiac adaptations to exercise. In the first experiment myocardial antioxidant enzymes, cardiac function and cardiac hypertrophy were assessed following a chronic exercise protocol previously used by our lab. MPG effectively reduced myocardial oxidative stress and activation of the signaling proteins Akt and S6 following an exercise bout. Skeletal muscle mitochondria content increased to similar levels in E and E+MPG. Similar increases (P<0.05) in both exercised groups were observed for heart wt and heart wt to body wt ratio. Cardiac function at the high workload improved in E vs S as indicated by higher (P<0.05) peak systolic pressure (SP), cardiac output (CO), coronary flow, COxSP and mechanical efficiency (COxSP/VO2). MPG prevented these exercise-induced functional improvements. This study provides evidence that free radicals do not play a role in the development of exercise-induced cardiac hypertrophy, however, they are involved in functional cardiac adaptations, which may be mediated through the PI3K/Akt pathway. In the second experiment a similar exercise protocol was used to determine if statins which have been shown to prevent pathological forms of cardiac hypertrophy, would be detrimental to exercise induced cardiac adaptations. In addition to the sedentary and exercise groups sedentary+statin and exercise+statin groups were assessed. Hearts were isolated and perfused and assessed for function at low and high workloads. Exercise treatment resulted in cardiac hypertrophy in absolute and relative terms to a similar extent in statin-treated and untreated exercised rats. Additionally it resulted in significant functional increases for SP, CO, COxSP, VO₂, and EFF in both exercised groups. In conclusion, these studies provide evidence that exercise in the cold is a valid model for physiological cardiac hypertrophy and that pathological and physiological cardiac hypertrophy signal through different pathways due to the fact that two well established treatments (mpg and statins) that prevent pathological cardiac hypertrophy did not affect exercise induced cardiac hypertrophy.text
46
"Modulatory effects of antimicrobials on Panton-Valentine Leukocidin gene expression in community-associated methicillin-resistant staphylococcus aureus in vitro and disease severity in vivo in a murine model". 2011. http://library.cuhk.edu.hk/record=b5894719.
Testo completoAbstract (sommario):
Wong, Kai Yi.Thesis (M.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 101-110).
Abstracts in English and Chinese.
Abstract --- p.4
摘要 --- p.7
Acknowledgements --- p.9
List of Tables --- p.10
List of Figures --- p.11
List of Abbreviations and Symbols --- p.12
Chapter Chapter 1 --- Introduction --- p.14
Chapter 1.1 --- Staphylococcus aureus --- p.14
Chapter 1.2 --- Methicillin-resistant Staphylococcus aureus (MRSA) --- p.14
Chapter 1.2.1 --- Methicillin resistance of MRSA --- p.15
Chapter 1.2.2 --- Staphylococcal Chromosomal Cassette mec (SCCmec) --- p.16
Chapter 1.2.3 --- Hospital-associated MRSA (HA-MRSA) and Community-associated MRSA (CA-MRSA) --- p.22
Chapter 1.2.3.1 --- Hospital-associated MRSA (HA-MRSA) --- p.23
Chapter 1.2.3.2 --- Community-associated MRSA (CA-MRSA) --- p.23
Chapter 1.2.4 --- Pathogenesis of MRSA infection --- p.27
Chapter 1.2.4.1 --- Possible virulence genes contributing to necrotizing pneumonia --- p.29
Chapter 1.2.4.1.1 --- Panton-Valentine Leukocidin (PVL) --- p.29
Chapter 1.2.4.1.2 --- Phenol-soluble modulins (PSMs) --- p.36
Chapter 1.3 --- Evolution of MRSA --- p.36
Chapter 1.4 --- Epidemiology of MRSA --- p.38
Chapter 1.4.1 --- Epidemiology of MRSA worldwide --- p.38
Chapter 1.4.1.1 --- Epidemiology of HA-MRSA worldwide --- p.38
Chapter 1.4.1.2 --- Epidemiology of CA-MRSA worldwide --- p.39
Chapter 1.4.2 --- Epidemiology of MRSA in Hong Kong --- p.40
Chapter 1.5 --- Clinical significance of MRSA --- p.41
Chapter 1.6 --- Antibiotics --- p.43
Chapter 1.6.1 --- Beta-lactams --- p.43
Chapter 1.6.2 --- Fluoroquinolone --- p.44
Chapter 1.6.3 --- Linezolid --- p.45
Chapter 1.6.4 --- Glycopeptides --- p.45
Chapter 1.6.5 --- Aminoglycosides --- p.46
Chapter 1.6.6 --- Fusidic acid --- p.46
Chapter 1.6.7 --- Clindamycin --- p.47
Chapter 1.7 --- Hypothesis --- p.47
Chapter Chapter 2 --- Methods and Materials --- p.50
Chapter 2.1 --- Bacterial isolate --- p.50
Chapter 2.2 --- Effect of subinhibitory antibiotics on the expression of mRNA in MRSA in vitro --- p.53
Chapter 2.2.1 --- Collection of bacterial fraction --- p.53
Chapter 2.2.2 --- RNA extraction and DNA digestion --- p.53
Chapter 2.2.3 --- Reverse transcription for cDNA synthesis --- p.54
Chapter 2.2.4 --- Quantitative real-time PCR (qPCR) analysis (pvl and psma\-A expression) --- p.55
Chapter 2.2.5 --- Preparation of standard controls for quantification of DNA copy number in qPCR reactions... --- p.58
Chapter 2.3 --- Effect of subinhibitory concentration of antibiotics on MRSA pneumonia in a murine model --- p.60
Chapter 2.4 --- Statistical Analysis --- p.62
Chapter Chapter 3 --- Results --- p.63
Chapter 3.1 --- Effect of subinhibitory antibiotics on the expression ofmRNA in MRSA in vitro --- p.63
Chapter 3.2 --- Effect of subinhibitory concentration of antibiotics on MRSA pneumonia in a murine model --- p.74
Chapter Chapter 4 --- Discussion --- p.80
Chapter 4.1 --- Effect of subinhibitory antibiotics on the expression of mRNA in MRSA in vitro --- p.81
Chapter 4.2 --- Effect of subinhibitory concentration of antibiotics on MRSA pneumonia in a murine model --- p.87
Chapter 4.3 --- Correlation of effects of subinhibitory antibiotics on the expression ofmRNA in MRSA in vitro and on MRSA pneumonia in a murine model --- p.91
Chapter 4.4 --- Limitations of Study --- p.95
Chapter 4.5 --- Future Work --- p.95
Chapter Chapter 5 --- Conclusions --- p.97
References --- p.99
Chapter Appendix I- --- Materials and Reagents --- p.109
Chapter Appendix II- --- Average and standard deviation of the copy number ratio (pvl or psmal-4 copy number/JdiS1 copy number) --- p.111
Chapter Appendix III- --- In-vivo experimental data for infected control group and seven antibiotic groups --- p.116
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Han, Xu. "Identification and mechanistic investigation of clinically important myopathic drug-drug interactions". Thesis, 2014. http://hdl.handle.net/1805/5275.
Testo completoAbstract (sommario):
Indiana University-Purdue University Indianapolis (IUPUI)Drug-drug interactions (DDIs) refer to situations where one drug affects the pharmacokinetics or pharmacodynamics of another. DDIs represent a major cause of morbidity and mortality. A common adverse drug reaction (ADR) that can result from, or be exacerbated by DDIs is drug-induced myopathy. Identifying DDIs and understanding their underlying mechanisms is key to the prevention of undesirable effects of DDIs and to efforts to optimize therapeutic outcomes. This dissertation is dedicated to identification of clinically important myopathic DDIs and to elucidation of their underlying mechanisms. Using data mined from the published cytochrome P450 (CYP) drug interaction literature, 13,197 drug pairs were predicted to potentially interact by pairing a substrate and an inhibitor of a major CYP isoform in humans. Prescribing data for these drug pairs and their associations with myopathy were then examined in a large electronic medical record database. The analyses identified fifteen drug pairs as DDIs significantly associated with an increased risk of myopathy. These significant myopathic DDIs involved clinically important drugs including alprazolam, chloroquine, duloxetine, hydroxychloroquine, loratadine, omeprazole, promethazine, quetiapine, risperidone, ropinirole, trazodone and simvastatin. Data from in vitro experiments indicated that the interaction between quetiapine and chloroquine (risk ratio, RR, 2.17, p-value 5.29E-05) may result from the inhibitory effects of quetiapine on chloroquine metabolism by cytochrome P450s (CYPs). The in vitro data also suggested that the interaction between simvastatin and loratadine (RR 1.6, p-value 4.75E-07) may result from synergistic toxicity of simvastatin and desloratadine, the major metabolite of loratadine, to muscle cells, and from the inhibitory effect of simvastatin acid, the active metabolite of simvastatin, on the hepatic uptake of desloratadine via OATP1B1/1B3. Our data not only identified unknown myopathic DDIs of clinical consequence, but also shed light on their underlying pharmacokinetic and pharmacodynamic mechanisms. More importantly, our approach exemplified a new strategy for identification and investigation of DDIs, one that combined literature mining using bioinformatic algorithms, ADR detection using a pharmacoepidemiologic design, and mechanistic studies employing in vitro experimental models.
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Mbili, Nokwazi Carol. "Evaluation of integrated control of postharvest grey mould and blue mould of pome fruit using yeast, potassium silicate and hot water treatments". Thesis, 2012. http://hdl.handle.net/10413/7984.
Testo completoAbstract (sommario):
The public concern over synthetic pesticides in foods and the environment has created an interest to find effective and safe non-fungicide means of controlling postharvest pathogens. The overall objective of this thesis was to evaluate the effect of potassium silicate, yeast antagonists and hot water dip treatment to control postharvest grey mould and blue mould of pome fruits, caused by Botrytis cinerea and Penicillium expansum, respectively. Botrytis cinerea and Penicillium expansum were isolated from infected strawberry and pear fruits, respectively. These isolates were found to be non-resistant to YieldPlus® (Anchor yeast, Cape Town, South Africa), a biofungicide containing a yeast Cryptococcus albidus. A total of 100 epiphytic yeast isolates were obtained from the fruit surface of “Golden Delicious” apples and “Packham’s Triumph” pears, and screened against B. cinerea and P. expansum. Fifteen yeast isolates reduced grey mould incidence by > 50%, when applied four hours before inoculation with B. cinerea. Similarly, seven yeast isolates reduced blue mould incidence by > 50%, when applied four hours before inoculation with P. expansum. YieldPlus® and yeast Isolate YP25 provided the best control of B. cinerea, while Isolate YP60 and YieldPlus® provided the best control of P. expansum on “Golden Delicious” apples. A mixture of YP25 and YP60 provided complete control of both B. cinerea and P. expansum, when applied to “Golden Delicious” apples before inoculation with either B. cinerea or P. expansum. Electron microscopy studies showed that yeast Isolates YP25 and YP60 inhibited the mycelial growth of B. cinerea and P. expansum, respectively. Preventative and curative application of potassium silicate resulted in reduced incidence of B. cinerea or P. expansum of “Golden Delicious” apples. Electron microscopy studies indicated that potassium silicate inhibited the growth of B. cinerea and P. expansum. Furthermore, treatment of “Golden Delicious” apples with either potassium chloride or potassium hydroxide resulted in reduced incidence of both B. cinerea and P. expansum. In vivo tests showed that the disease incidence of P. expansum and B. cinerea on “Golden Delicious” apples was reduced by hot water dip treatments at 58-60°C for 60 to 120 seconds, compared with the control fruit treated with sterile distilled water, without causing skin damage. The use of potassium silicate, yeasts (Isolates YP25 and YP60), YieldPlus® and the antagonists mixture (YP25+YP60) in combination, resulted in the control of B. cinerea and P. expansum of “Golden Delicious” apples compared with Imazalil® treated fruit.Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2012.
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Shembe, Zamakhosi Thina. "The effects of whoonga on the learning of affected youth in Kwa-Dabeka township". Diss., 2013. http://hdl.handle.net/10500/13827.
Testo completoAbstract (sommario):
Whoonga is a relatively new addition into the drug market. The need for this study was prompted by the devastating effects this new arrival has had in the lives of young people addicted to it. The purpose of this study was to investigate the effects of whoonga on the learning of affected youth in Kwa-Dabeka Township. This study adopted a qualitative method and employed a phenomenological approach to explore the experiences of participants with regard to whoonga use and their learning. Data was collected through purposive sampling. Interviews were conducted, using semi-structured and unstructured questions with the help of an interview guide. Observations were also conducted to collect more data. This was done in the classroom during teaching and learning, as well as outside the classroom during recess. The study employed a social learning theoretical framework on the experiences of participants with regard to the use of whoonga. Four participants from one high school in Kwa-Dabeka Township were involved in the study.
Themes that emerged from the study were that all the participants were totally ignorant of what they were getting themselves into before they started using whoonga. Peer pressure, coupled with curiosity made their decision to use whoonga easy. Challenges that participants face now on daily basis are far beyond their young age. The findings have indicated that learning is a situation of near impossibility for the participants. The findings have also depicted a picture of young people who are trapped in a vicious cycle of one of life‟s harshest living conditions in terms of their encounters with parents, school and the communities they come from. Despite their hopes for a brighter future one day, participants see no end in sight for their suffering at the hands of this unforgiving, destructive drug at this point in time.Educational Studies
M. Ed. (Socio-Education)
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Turner, Dee Ann. "Monitoring, characterizing, and preventing microbial degradation of ignitable liquids on soil". Thesis, 2013. http://hdl.handle.net/1805/5046.
Testo completoAbstract (sommario):
Indiana University-Purdue University Indianapolis (IUPUI)Organic-rich substrates such as soil provide an excellent carbon source for bacteria. However, hydrocarbons such as those found in various ignitable liquids can also serve as a source of carbon to support bacterial growth. This is problematic for fire debris analysis as samples may be stored at room temperature for extended periods before they are analyzed due to case backlog. As a result, selective loss of key components due to bacterial metabolism can make identifying and classifying ignitable liquid residues by their chemical composition and boiling point range very difficult. The ultimate goal of this project is to preserve ignitable liquid residues against microbial degradation as efficiently and quickly as possible. Field and laboratory studies were conducted to monitor microbial degradation of gasoline and other ignitable liquids in soil samples. In addition to monitoring degradation in potting soil, as a worst case scenario, the effect of soil type and season were also studied. The effect of microbial action was also compared to the effect of weathering by evaporation (under nitrogen in the laboratory and by the passive headspace analysis of the glass fragments from the incendiary devices in the field studies). All studies showed that microbial degradation resulted in the significant loss of n-alkanes and lesser substituted alkylbenzenes predominantly and quickly, while more highly substituted alkanes and aromatics were not significantly affected. Additionally, the residential soil during the fall season showed the most significant loss of these compounds over the course of 30 days. To combat this problem, a chemical solution is to be immediately applied to the samples as they are collected. Various household and commercial products were tested for their efficacy at low concentrations to eliminate all living bacteria in the soil. Triclosan (2% (w/v) in NaOH) proved to be the most effective at preserving ignitable liquid residues for at least 30 days.