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Effect of heparin on lipid metabolism and its significance in atherosclerosisDay, Allan John January 1956 (has links)
Typewritten copy / 246 p. : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, Dept. of Medicine, 1957
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Metabolism of sulphate in wheatAscano, Annabelle Francisco. January 1978 (has links) (PDF)
No description available.
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Effects of cadmium on the hepatic microsomal drug metabolizing systemPeters, Peter George. January 1978 (has links) (PDF)
Typescript (photocopy)
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Sulphate metabolism in normal and cancerous tissueMeaney, Maxwell Francis. January 1972 (has links) (PDF)
No description available.
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Metabolism of dichloroethenes by the butane-oxidizing bacterium 'Pseudomonas butanovora'Doughty, David M. 06 January 2003 (has links)
Reductive dechlorination of chlorinated ethenes is dependent upon suitable
substrates promoting microbial activity and creating anaerobic conditions. At the
periphery of active reductive dechlorinating zones combinations of lesser
chlorinated ethenes should exist along with end products of the anaerobic
metabolism that is driving reductive dechlorination. Potential end-products of
anaerobic metabolism were investigated for their ability to stimulate oxidative
cometabolism of dichloro ethenes (DCEs) by the butane-degrading bacterium,
Pseudomonas butanovora. Organic acids that supported butane-monooxygenase
(BMO) activity were acetate, propionate, lactate, and butyrate. Lactate
consistently supported and sustained greater rates of cooxidation than did the other
organic acids. When propane replaced butane as the growth substrate, lactate
remained the superior electron donor, while the ability of butyrate and acetate to
support BMO activity decreased. In contrast, propionate-supported cooxidation
was only observed in propane-grown cells.
Lactate supported the degradation of 1,2-trans dichloroethylene (1,2-trans
DCE), 1,2-cis dichloroethylene (1,2-cis DCE) and 1,1-dichloroethylene (1,1-DCE)
in butane-grown P. butanovora. 78 nmoles (25 μM) of 1,2-cis DCE were
completely degraded by butane-grown P. butanovora. In contrast, smaller
amounts of 1,1-DCE and 1,2-trans DCE were degraded over the twenty minute
time course. Decreasing rates of cooxidation over time were observed for of all
three DCEs, and 50% of BMO activity was irreversibly lost after 15 min, 6 min,
and 0.5 min exposures to 1,2-cis DCE, 1,2 trans-DCE, and 1,1-DCE respectively.
Cell viability decreased by over 90, 95, and 99.95% during the transformation of
25 nmoles/mg protein of 1,2-cis DCE, 1,2-trans DCE and 1,1-DCE. These results
indicate that cellular viability was more sensitive to cooxidation of 1,2-cis DCE
and 1,2-trans DCE than was BMO.
1,2-cis DCE and 1,2-trans DCE induced BMO activity to 25 and 45% of
the butane control, respectively. Induction by 1,2-trans DCE was observed at a
threshold of about 20 μM and higher concentrations did not increase BMO
activity. Fusion of lacZ to the BMO catabolic promoter, with consequent knock
out of BMO activity, provided the opportunity to assess substrate induction
without the confounding effects of enzyme inactivation and product induction.
While BMO substrates, butane, 1,2-cis DCE, and ethylene, were unable to induce
lacZ activity the BMO products, 1-butanol, and ethylene oxide, effectively induced
lacZ activity. 1,2-trans DCE was unique among the BMO substrates tested in it's
ability to induce expression of lacZ, 2-fold above background, in the reporter strain. A wide range of concentrations induced lacZ activities (10 to 100 μM), and
low levels of 1,2-trans DCE achieved high levels of induction after 4 hrs.
However, lacZ activities were limited to an induction of about four-fold above
background and this limit allowed lower concentrations of 1,2-trans DCE to
eventually produce equal levels of beta-galactosidease. These data provide proof-of-
concept that BMO-dependent cometabolism can occur independently of butane
as an inducer and electron donor for BMO gene expression and activity. / Graduation date: 2004
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Cloning and characterization of GRASP, a novel retinoic acid-induced gene from P19 embryonal carcinoma cellsNevrivy, Daniel 05 December 2001 (has links)
Retinoic acid (RA) exerts important effects in the processes of vertebrate
development, cellular growth and differentiation, and homeostasis. However, the
mechanisms of action of RA in the control of cellular and developmental processes are
incompletely understood, as the retinoid target genes have not been fully characterized.
The goal of these studies described herein was to contribute towards a greater
understanding of the cellular effects of retinoids through the identification and
characterization of an RA-induced gene from mouse P19 embryonal carcinoma cells.
The predicted amino acid sequence of GRASP is characterized by several
putative protein-protein interaction motifs, suggesting that GRASP may function in cell
signaling pathways. Towards the goal of identifying which signaling pathways GRASP
may participate in, a yeast two-hybrid screen was performed using GRASP as a bait to
identify protein interaction partners. The general receptor for phosphinositides 1
(GRP1), a guanine nucleotide exchange factor for the ADP-ribosylation factor 6
(ARF6) GTPase, was identified as a GRASP interaction partner. GRASP was shown to
colocalize with endogenous ARFs in cells and enhance GRP1 association with the
plasma membrane, suggesting that GRASP may function as a scaffold protein in the
recruitment of GRP1 and ARF6 to plasma membrane loci.
Overexpression of GRASP was observed to induce accumulation of GRASP in
the endosomal compartment where GTP-binding deficient mutants of ARF6 reside,
suggesting that GRASP induced a block in an ARF6 plasma membrane recycling
pathway. Coexpression of GRP1, but not a catalytically inactive mutant, dramatically
reduced the accumulation of GRASP in this compartment. Furthermore, GRP1 mutants
that lack the region of interaction with GRASP failed to prevent accumulation of
GRASP in the endosomal compartment, suggesting that GRASP recruits GRP1 to the
endosomal compartment where GRP1 stimulates nucleotide exchange on ARF6 and
recycling.
Results described herein demonstrate that GRASP functions in the ARF6
regulated plasma membrane recycling pathway, and that upon overexpression, induces a
block in recycling. Our results suggest a role for GRASP as an adapter or scaffold
protein that may link cell surface receptors to the ARF6 recycling pathway, resulting in
modulation of signal transduction events at the cell surface. / Graduation date: 2002
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Regulation of ribonucleotide reductase analyzed by simultaneous measurement of the four enzyme activitiesHendricks, Stephen P. 12 March 1998 (has links)
The first committed step in DNA biosynthesis occurs by direct reduction of
ribonucleotides. This reduction is catalyzed by ribonucleotide reductase (RNR), an
enzyme which uses a unique radical mechanism to facilitate the transformation. All four
DNA precursors are synthesized by a single enzyme. Therefore, an intricate pattern of
regulation has evolved to insure that RNR generates the proper quantity of each
deoxyribonucleotide. It is this regulation, and conditions that influence this regulation,
that are the central focal points of this dissertation.
The studies described in this thesis have been aided by the development of a novel
RNR assay. Unlike the traditional assay, this new procedure permits the simultaneous
monitoring of all four RNR activities. This four-substrate assay was used to investigate
whether the four enzyme activities of RNR were differentially sensitive to inhibition by the
radical scavenger, hydroxyurea. The assay results, along with the results of a technique
that measured enzyme inhibition as a function of radical decay, suggest that all activities of
RNR are equally inhibited by hydroxyurea. Instead of differential inhibition, it appears
that the activity level of RNR determines the relative sensitivity to hydroxyurea.
The effects of nucleotide effectors and substrates on the relative turnover rates of the
vaccinia virus and T4 phage RNR were also investigated by use of the four-substrate
assay. When physiological concentrations of the allosteric effectors and substrates were
added to the reaction mixtures, both enzyme forms produced dNDPs in ratios that
approximate the nucleotide composition of their respective genomes. Non-physiological
nucleotide concentrations generated significantly different product profiles, indicating that
RNR has evolved to function within a defined nucleotide environment. Interestingly, the
substrate component of the nucleotide environment proved to be as important as the
allosteric effectors in modulating the reaction rates. Although the allosteric effects of
nucleoside triphosphates have been known for some time, little attention has been given to
the potential role that substrates play in the regulation of RNR. The results from my
research suggest that the regulation of RNR in vivo results from a complex interplay
between the enzyme and its substrates, products, and allosteric effectors. / Graduation date: 1998
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Control of muscle protein degradation and steady-state poly(ADP-ribose) polymerase concentration by calpainHuang, Jing, 1961- 13 April 1998 (has links)
The first goal of this study was to understand the role of calpains in skeletal muscle
protein degradation in cultured cells. We have developed a genetic approach to inhibit
endogenous calpain activity through over-expressing dominant negative m-calpain (DN),
antisense m-calpain (AS) and calpastatin inhibitory domain (CID). We observed that,
under conditions of accelerated degradation (serum withdrawal), inhibition of m-calpain
through DN-m-calpain over-expression caused a 30% inhibition of total protein
degradation whereas CID over-expression reduced degradation by 63%. These
constructs did not significantly affect degradation in the presence of serum. These data
indicate that calpains participate in the accelerated degradation associated with serum
withdrawal. Inhibition of calpain also stabilized nebulin, a major structural protein of the
sarcomere. These observations indicate that calpains play significant roles in muscle
protein turnover. Finally, over-expression of antisense m-calpain caused a transient
reduction in m-calpain concentration after which normal m-calpain concentration was
quickly re-established. These observations indicate that m-calpain is a short half-life
protein in muscle cells.
The second goal of this study is to investigate the role of calpain in the mediation
of PARP protein level in differentiating myoblasts. Poly(ADP-ribosyl)ation, catalyzed by
PARP, is involved in various physiological events, such as DNA excision repair, DNA
recombination, DNA replication, cell differentiation, cell growth and transformation, and
apoptosis. A protease participating in PARP turnover could be a significant regulator to the events which PARP is involved. A relationship between apoptosis and myofibrillar
protein degradation via a common protease might suggest the basis for muscle wasting
and atrophy which characterize in many muscle diseases. We established a genetic
approach to inhibit endogenous calpain activity through over-expressing calpastatin
inhibitory domain (CID). We observed that (1) inhibition of calpain activity increased
PARP concentration when post-confluent myoblasts were cultured with 2% HS medium,
an inducer of differentiation and (2) inhibition of calpain activity prevented PARP
degradation induced by A23187 and etoposide in differentiating myoblasts. These data
demonstrate that calpain is involved in regulation of PARP in cultured cells. / Graduation date: 1998
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Fundamentals and application of metabolic engineering /Wong, Kelvin Wai Wah. January 2006 (has links)
Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2006. / Includes bibliographical references (leaves 228-239). Also available in electronic version.
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Obesity a growing concern about fetal nutrition /Coe, Benjamin Lloyd, January 2006 (has links)
Thesis (M.A.)--University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file viewed on (February 6, 2007) Vita. Includes bibliographical references.
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