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Membrane lipid composition and its effect on sodium pump molecular activity a comparative study /Turner, Nigel. January 2003 (has links)
Thesis (Ph.D.)--University of Wollongong, 2003. / Typescript. Includes bibliographical references: leaf 168-188.
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Kinetics and regulation of mitochondrial cation transport systems /Jaburek, Martin, January 1999 (has links)
Thesis, (Ph. D.)--Oregon Graduate Institute, 1999.
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Functional characterisation an developmental expression of Caveolin /Nixon, Susan Jane. January 2004 (has links) (PDF)
Thesis (PhD) - University of Queensland, 2004. / Includes bibliography.
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Enantioselective, potentiometric membrane electrodes for enantioanalysis of amino acids of clinical and pharmaceutical importance /Holo, Luxolo. January 2005 (has links)
Thesis (M.Sc.(Chemistry))--University of Pretoria, 2005. / Includes abstract in English. Includes bibliographical references. Electronic copy also available.
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Morphometry of hair cell bundles and otoconial membranes in the utricle of a turtle, Trachemys scriptaXue, Jingbing. January 2006 (has links)
Thesis (Ph.D.)--Ohio University, August, 2006. / Title from PDF t.p. Includes bibliographical references.
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Solid-state NMR studies of phospholipid model membranes and membrane-associated macromoleculesLu, Jun-xia. January 2007 (has links)
Thesis (Ph. D.)--Miami University, Dept. of Chemistry and Biochemistry, 2007. / Title from second page of PDF document. Includes bibliographical references.
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The role of N-6 and N-3 pufa ratios in the aetiology of multiple sclerosisHon, Gloudina Maria January 2009 (has links)
Thesis (MTech (BioMedical Technology))--Cape Peninsula University of Technology, 2006 / In multiple sclerosis (MS) the myelin sheaths surrounding the axons in the brain are mainly
affected by the disease process. Myelin consists for the most part of lipids and proteins. An
abnormality in essential fatty acid metabolism is known to be present in patients with MS
(Horrobin, 1979), reflected in a high ratio of n-6 to n-3 fatty acids in cell membranes. It has
also been established previously that the pathogenesis of inflammatory disorders is
aggravated by excessive consumption of n-6 fatty acids relative to n-3 fatty acids (Guesnet et
al., 2005),and it has been shown that ingesting a larger proportion of n-3 fatty acids could be
crucial in the regulation of cellular physiology and in the prevention of pathologies such as
autoimmune and inflammatory diseases.
Modern Western medical treatment for autoimmune diseases, which includes MS, involves
the administration of immunosuppressive drugs, such as beta interferon, cortisone
(prednisone), methotrexate and cytoxan, which reduce the effectiveness of the entire
Immune system, and can have serious, sometimes life threatening, side effec1s (Perlmutter,
2006, htlp:/Iwww.msfac1s.org). It would therefore be of interest to investigate other options
for treatment
Although there is an extensive literature on fatly acids in MS, the actual details of the
mechanisms of fatly add imbalances in MS have not been established. It would therefore be
advisable to Investigate the abnormality of the MS cell membrane fatly acid profile. Previous
studies focused on individual fatty acids, but it would be more relevant to investigate the
relationships within and between the n-6 and n-3 series, and their effect on outcome, and to
establish any possible cumulative effects, because the metabolism of fatty adds within the
two series does have an effect on one another.
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Membrane fluidity and fatty acids in multiple sclerosis patientsHon, Gloudina Maria January 2009 (has links)
Thesis (DTech (Biomedical Technology))--Cape Peninsula University of Technology, 2009 / Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system
(CNS), which leads to neuronal demyelination, and eventually to oligodendrocyte and axon
loss, with subsequent lesion formation. The wide distribution of lesions in the CNS results in
a variety of clinical features, such as cognitive impairment, vertigo, spasticity, ataxia tremors,
progressive quadriparesis, pain and depression. Currently no cure exists for CNS disorders,
resulting in a decline in quality of life, and an economic burden on society. Metabolic
disturbances, especially lipid metabolic abnormalities, have been implicated in the
development of MS. Although the disease cannot be cured, disease-modifiers, such as
interferon beta, glatiramer acetate and mitoxantrone, as well as fatty acid supplementatlon
have been used to delay the progression of the disease. Membrane fatty acids are
precursors for mediators of inflammation, the eicosanoids, which are produced soon after
stimulation and which regulate a number of inflammatory effects, such as the induction of
fever, vasodilation and production of macrophage- and Iymphocyte-derived cytokines.
Eicosanoids, in contrast to their fatty acid precursors, have a short half-life and are therefore
difficult to measure.
The objective in the present study was to determine the role of fatty acids from South African
MS patients, by measuring the fatty acid composition of phosphatidylcholine (PC),
phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI) and
sphingomyelin (SM) phospholipids in the plasma, red blood cell (RBC) and peripheral blood
mononuclear cell (PBMC) membranes and correlate abnormalities with the neurological
outcome as measured by the Kurtzke Expanded Disability Status Scale (EDSS) and
inflammation assessed by C-reactive protein (CRP). A second objective was to establish
whether possible changes in membrane lipids (phospholipids, fatty acids and cholesterol)
would have an effect on membrane fluidity, and whether this would correlate with the EDSS
and CRP.
The plasma, RBC and PBMC membrane lipid composition from 31 white female patients with
MS and 30 age- and gender-matched control subjects were assessed. Fatty acids were
quanflfied by gas chromatography (GC), phospholipids by colorimetric and cholesterol by
enzymatic assays. Membrane fluidity, as measured by the membrane lipid composition, was
calculated, using previously established formulae, and includes the following: the saturated
nature of the membrane was measured by the phospholipid PC+PS/PE+PS ratio, fluidity and
permeability were measured by the cholesterol concentratlon and the cholesterol to total
phospholipid ratio and membrane deformability was measured by the phospholipid PE to PS
ratio. Membrane fluidity was also measured by the ordered-erystalline-phase to liquidcrystalline-
phase lipid composition, which correlates with the phospholipid PE to PC ratio.
The membrane saturated (SATS) to polyunsaturated fatty acid (PUFA) ratio was further used
as an indication- of the fluidity status of the membranes. CRP was measured in all
participants using a Beckman nephelometer.
In MS, the n-6 fatty acids, particularly C18:2n-6, C20:4n-6 and C22:4n-6, were significantly
decreased in plasma, RBC and/or PBMC membranes. In addition, the relationship between
C20:3n-6 and C20:4n-6 showed a metabolic disturbance in both RBC and PBMC
membranes from patients with MS, as compared to the control group. C20:4n-6 showed
significant inverse correlations with the EDSS and CRP in MS patients, indicating that loss of
these fatty acids from membranes correlated with higher disability as well as with increased
inflammation. There were significant increases in free fatty acids C18:2n-6 and C20:4n-6 in
plasma from MS patients. Saturated fatty acids, SM C14:0 and PI C22:0 were significantly
increased in PBMC membranes from MS patients, and SM C14:0, C16:0 and C20:0 showed
inverse correlations with the Functional System Scores. In contrast, the longer-ehain SATS,
C22:0 and C24:0 showed positive correlations with the Functional System Scores. Red blood
cell membrane fluidity as measured by the SATS to PUFA ratio was significantly higher in
patients than in controls. In patients with CRP ~ 5.00 Ilglml the ratio showed significant
inverse correlation with disease outcome. The saturated nature correlated positively, whilst
the .ordered-erystalline-phase to liquid-crystalline-phase lipid ratio correlated inversely with
the Functional System Scores.
In this study it was consistently shown that C20:4n-6, or its precursor and elongation
products, C18:2n-6 and C22:4n-6 respectively, was lower in plasma, RBC and/or PBMC
membranes from MS patients. Red blood cells lack the desaturase enzymes and depend on
fatty acids sourced from the plasma. Therefore, lower C20:4n-6 in the RBC membranes from
MS patients may be due to depleted plasma stores, or an indication of an increased demand
of this fatty acid elsewhere. Furthermore, this study has demonstrated that lower RBC
C20:4n-6, with an increase in plasma FFA C20:4n6, resulted in worse disease outcome,
perhaps due to the pro-inflammatory effect of eicosanoid production. This. study also
characterized the specific SATS, that is, longer-ehain SATS that may increase the risk of
developing MS, as higher shorter-ehain SATS, C14:0 and C16:0 reflected better disease
outcome, demonstrated by the inverse correlation with the EDSS and FSS. Lastly, this study
has shown that in the presence of uncontrolled inflammation such as in MS, the altered lipid
composition indirectly compromised cell membrane, structure and fluidity, and thereby
contributed to the disease progression in MS patients.
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Electrical Conductivity of Thin Lecithin-cholesterol Membranes due to 2,4-D, 2,4-DB, 2,4,5-T and 2,4-DCPPaulis, Malkanthi 27 July 1976 (has links)
The effect of the following pesticides on DC electrical conductivity of lecithin-cholesterol membranes has been studied: endothall, paraquat, diquat, 2,4-D, 2,4-DB, 2,4,5-T, 2,4-DCP. It has been found that the ions of endothall, paraquat and diquat are essentially membrane impermeable and that they do not bind to the membrane surface. In contrast, 2,4-D, 2,4-DB, 2,4,5-T and 2,4-DCP induce electrical conductivity in lecithincholesterol membranes and in addition they also cause an increase in the nonactin-K+ membrane conductivity.
The compounds 2,4-D, 2,4-DB, 2,4,5-T and 2,4-DCP basically behave as class II uncouplers. The kinetic scheme of charge transfer across the membrane, based on the assumption that the membrane is permeable both to the negatively charged dimers and to the neutral molecules of pesticides, satisfactorily explains the basic features of the experimental results: the concentration dependence of pesticide-induced membrane conductance, effect of proton concentration on membrane conductance, and the effect of pesticide concentration on the voltage dependence of membrane conductance. It fails to predict the effect of proton concentration on the voltage dependence of membrane conductance.
The enhancement of nonactin-K+ membrane conductance by the pesticide is presumably due to the adsorption of the ionized form of the pesticide at the membrane surface. It was found that the Gouy-Chapman diffuse double layer theory was not applicable for the calculation of surface membrane potential due to the adsorbed ions.
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Relationships between drug-induced perturbation of Na+/K+-ATPase activity and synaptic plasma membrane structureCarfagna, Mark Anthony January 1990 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
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