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1
Smit, B. S. "Cellular radiotoxicity of iodine-123." Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51646.
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Thesis (MSc)--University of Stellenbosch, 2000.ENGLISH ABSTRACT: The Auger electron emitter iodine-123 was examined in the form of 4- [12311iodoantipyrineand as [12311Nal for its effectiveness in killing cells of different sensitivity to photon irradiation. Micronucleus assays showed that 4- [12311iodoantipyrineis two to three times more effective in cell inactivation than C2311Nai.This can be attributed to the fact that antipyrine, for reason of its lipid solubility, can enter cells and can reach the cell nucleus, whereas C231]Nai is excluded from the cytoplasm. The differential targeting of intra- and extracellular compartments was confirmed by radionuclide uptake experiments. In the nucleus, Auger decay conceivably is located on the DNA where it may invoke high-LET irradiation damage. Irradiation damage by [12311Naisl by long range y-irradiation and hence low-LET. Results of the present study demonstrate however that the enhancement of MN-frequency seen with 4-[123I]iodoantipyrine over [12311Nalis similar for all cell lines and that the narrowing of MN-response expected for 4- [12311iodoantipyrinedoes not occur. Experiments with the free radical scavenger, DMSO, indicated nearly identical dose reduction factors for both iodine-123 carriers. These two observations strongly suggest that the cell inactivation by 4- [12311iodoantipyrine is not by high-LET direct ionisation of DNA, but due to an indirect effect. The indirect radiation effect of Auger decay in the nucleus is attributed to shielding of DNA by histones. Such a protection mechanism is not unrealistic if it is realised that histones and DNA associate in a 1: 1 weight ratio and that higher order folding of the nucleosome chain into solenoids, loops, and chromatids generates considerable protein density. In the nucleosome core, the histone acta mer measures 7 nm and closely approximates the 10 nm dimention of the Auger electron range. It is suggested that the interlacing of protein density with DNA density suppresses direct ionisation from Auger decay at the DNA and directs the majority of Auger decay to the histones.
AFRIKAANSE OPSOMMING: Die Auger-elektron-uitstraler, jodium-123, is ondersoek in die vorm van 4- [123l]jodoantipirien en [12311Nal om die effektiwiteit te bepaal waarmee dit selle met verskillende grade van sensitiwiteit vir fotonbestraling doodmaak. Mikrokerntellings toon aan dat 4-[123I]jodoantipirien selle twee tot drie maal meer effektief inaktiveer as [12311Nal.Dit kan toegeskryf word aan die feit dat antipirien, as gevolg van sy vetoplosbaarheidseienskappe, die selle kan binnedring en die kern bereik, teenoor [12311Nalwat uitgesluit word uit die sitoplasma. Die differensiële blootstelling van intra- en ekstrasellulere gebiede is bevestig deur radionukliedopname eksperimente. In die selkern vind Auger verval waarskynlik by die DNA plaas waar dit hoë-LET stralingskade veroorsaak. Stralingskade afkomstig van [1231]Nalis deur langafstand y-strale en dus lae-LET. Die resultate van die huidige studie bewys egter dat die verhoogde mikrokernfrekwensie van 4-[12311jodoantipirienteenoor [1231]Nal dieselfde is vir al die sellyne en dat die vernouïng van mikrokernreaksie soos verwag met 4- [12311jodoantipirien, nie plaasvind nie. Eksperimente met die vryradikaalopruimer, DMSO, dui op feitlik identiese dosis-modifiseringsfaktore vir beide jodium-123 draers. Hierdie twee waarnemings is 'n besliste aanduiding dat die selinaktivering deur 4-[12311jodoantipiriennie deur hoë-LET direkte ionisering van DNA plaasvind nie, maar eerder deur indirekte stralingsaksie. Die indirekte stralingseffek van Augerverval in die kern kan toegeskryf word aan afskerming van DNA deur histone. So 'n beskermingsmeganisme is nie onrealisties nie, as in ag geneem word dat histone en DNA in 'n 1: 1 gewigsverhouding assosieer en dat hoër orde vouïng van die nukleosoomketting tot solenoïede, lusse en chromatiede 'n beduidende protïendigtheid genereer. In die nukleosoomkern is die histoon-oktameer ongeveer 7 nm in deursnit en dus vergelykbaar met die 10 nm reikafstand van die Auger elektrone. Dit word voorgestel dat die ineengeweefdheid van die protien-digtheid met die DNA-digtheid die direkte ionisering van die DNA tydens Auger verval onderdruk en dat die meeste van die Auger verval in die histone plaasvind.
2
Muhamad, Nur Airina. "Cellular basis of magnetic sensation." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610344.
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Willcocks, James Peter. "Magnesium in cellular energetics." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:f4f5de76-8c72-4b42-8bd4-eb151485d47e.
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Most cellular magnesium is bound, yet it is the concentration of free magnesium, [Mg2+]free, in red blood cells that is vital in the regulation of enzyme activity and ion transport. It is unknown how changes in total blood magnesium affect the [Mg2+]free within red blood cells or in tissue, because the presence of other cations, especially H+ and potassium, K+ , affects the degree to which Mg2+ is bound. Consequently, this Thesis presents a new 31P NMR spectroscopic method to measure [Mg2+]free in blood, which analyses the changes in the phosphorus chemical shifts of ATP and 2,3-DPG using theoretical equations expressing the observed chemical shift as a function of pH, K+ and [Mg2+]free, over the pH range of 5.75 to 8.5 and [Mg2+]free range 0 to 5 mM. The equations were adjusted for the binding of haemoglobin to ATP and DPG, which required knowledge of the intracellular concentrations of ATP, DPG, K+ and Hb. These equations enabled, for the first time, the simultaneous analyses of the chemical shifts of 3P-DPG and β-ATP to measure both intracellular 04- pH and [Mg2+]free in normal and sickle blood. To simulate in vivo 100% oxygenated blood, samples were prepared for analysis by equilibration with a mixture of O2 and CO2, adjusted to give a pCO2 of 40 mmHg and pO2 > 150 mmHg. Under these conditions, normal whole blood had an intracellular pH of 7.20 ± 0.02 and a [Mg2+]free of 0.41 ± 0.03 mM (n = 33). Further work determined blood pH and [Mg2+]free for several clinical conditions including sickle cell anaemia, pre-eclampsia, hypoxia, patients with sub-arachnoid haemorrhage and chronic fatigue syndrome. This Thesis has demonstrated the potential of this new technique to evaluate the importance of [Mg2+]free in the regulation of metabolite concentration and metabolic function, and to elucidate some of the properties of magnesium transport across the erythrocyte cell membrane.
4
Hashimoto, Kyoichi. "Cellular context-dependent consequences of Apc mutations on gene regulation and cellular behavior." Kyoto University, 2018. http://hdl.handle.net/2433/230974.
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Khan, Abrar Ul Haq. "Cellular Metabolism Regulates Anti-Oxidant Response Through ERK5-MEF2 Pathway." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT036/document.
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Le métabolisme cellulaire est la source principale d’énergie et les cellules cancéreuses ont un métabolisme différent des cellules non transformées. La cellule tumorale a tendance à éviter l’activité mitochondriale et ainsi la phosphorylation oxydative, pour lui préférer la voie de la glycolyse pour la production d’énergie (Effet Warburg). Cette altération du métabolisme est si bénéfique pour les cellules en croissance que cela favorise la croissance tumorale et supprime la réponse immunitaire anticancéreuse. La spécificité de ce métabolisme en fait une cible intéressante pour le développement de thérapies anticancéreuses. Mon travail de thèse comporte deux parties. La première partie décrit que lorsque les cellules cancéreuses sont forcées à utiliser la voie mitochondriale comme source d’énergie à travers l’oxydation phosphorylative, elles initient un mécanisme antioxydant pour tolérer les effets délétères des espèces oxygénées réactives (EOR ou ROS pour reactive oxygene species) produites au cours de l’activité mitochondriale. La stimulation mitochondriale entraîne l’activation de la voie de signalisation ERK5-MEF2, et cette dernière engendre un mécanisme antioxydant de deux façons.Initialement, nous avons observé que MEF2 régule positivement l’expression de miR23a, et ce dernier inhibe l’expression de KEAP1. Cette protéine est responsable de la dégradation ubiquitine dépendante de NRF2, un régulateur clé de la réponse antioxydante cellulaire. L’inhibition de KEAP1 empêche la dégradation cytoplasmique de NRF2. Consécutivement à cela la concentration cytoplasmique en NRF2 augmente ce qui engendre sa translocation dans le noyau où il se lie à une séquence élément de réponse antioxydant (ARE) dans la région promotrice de nombreux gènes antioxydants, initiant ainsi leur transcription. Plus tard nous avons observé que l’activation de la voie ERK5-MEF2 induisait directement la synthèse de novo de NRF2, induisant sa translocation nucléaire et un mécanisme antioxydant. L’inhibition de la voie ERK5-MEF2 altère la réponse antioxydante, sensibilisant ainsi les cellules au stress oxydant.La seconde partie de mon travail a exploré les mécanismes à l’origine des effets hypolipémiants du dichloroacétate (DCA). Le DCA est une petite molécule qui inhibe la PDK1 et permet au pyruvate d’entrer dans la mitochondrie. Il a été utilisé en clinique dans le passé pour baisser les taux plasmatiques de cholestérol mais le mécanisme n’était pas clair et nous l’avons décris. Le DCA force les cellules à entrer en oxydation phosphorylative ce qui active la voie ERK5-MEF2. Cette voie augmente directement l’expression du LDLR (Low Density Lipoprotein Receptor ; récepteur aux lipoprotéines de basse densité) qui permet l’endocytose des LDL riches en cholestérol qui sont responsables de la plupart des maladies cardiovasculaires. L’inhibition de cette voie supprime l’afflux de lipides et par conséquent serait une cible intéressante pour de futures recherches puisque de hauts taux de cholestérols sont directement corrélés avec une augmentation du risque d’athérosclérose et de toutes les complications mortelles qu’il entraine.Notre prochain objectif est d’explorer les autres mécanismes cellulaires régulés par la voie ERK5-MEF2. Sur la base de nos résultats préliminaires, nous proposons que cette voie non seulement régule l’expression du LDLR mais aussi celle de nombreux autres gènes qui sont impliqués directement ou indirectement dans le métabolisme des lipidesCellular metabolism is the main source of energy and cancer cells has different metabolism than non-transformed cells. Tumor cell tends to avoid mitochondrial activity and oxidative phosphorylation (OXPHOS) and prefer glycolysis for energy production (Warburg effect). This alteration in metabolism is beneficial for growing cells in many ways that promote tumor growth and suppress the anti-cancer immune response. This specific metabolism is an auspicious target for the better development of cancers chemotherapies.My thesis work comprises two parts. The first portion describes that when cancer cells are forced to utilize their mitochondria in order to obtain the energy from OXPHOS they initiate an antioxidant mechanism to cope with the deleterious effects of reactive oxygen species (ROS) produced during mitochondrial activity. Mitochondrial stimulation leads to activation of ERK5-MEF2 signaling pathway, which triggers the antioxidant mechanism by at least two ways.Initially we observed that MEF2 up regulates the expression of miR23a, which inhibits KEAP1 expression. This protein is responsible for ubiquitinational degradation of NRF2, a master regulator of the antioxidant response in cells. The inhibition of KEAP1 prevents the NRF2 cytoplasmic degradation. This results in high built up of NRF2 in cytoplasm that translocates to nucleus where it binds to ARE (antioxidant response element) in the upstream promoter region of many antioxidant genes hence initiates their transcription. Latter we observed that activation of ERK5-MEF2 pathway directly results in de novo synthesis of NRF2, resulting in nuclear translocation and triggering of the antioxidative mechanism. Inhibition of ERK5-MEF2 pathway impairs the cellular antioxidant response, thus sensitizing cells towards oxidative stress.The second part of my work explored the mechanism behind the lipid lowering effects of dichloroacetate (DCA). DCA is a small molecule, which inhibits the PDK1 and enables pyruvate to enter the mitochondria. It was used clinically in past to lower the plasma cholesterol level but the underlying mechanism was not clear and we describe it here. DCA forces cells to perform OXPHOS, which activate the ERK5-MEF2 pathway. This pathway directly up-regulates the expression of Low Density Lipoprotein Receptors (LDLR) that are mainly involved in the endocytosis of cholesterol-rich low density lipoproteins, which are responsible for the majority of cardiovascular diseases. Inhibition of this pathway suppresses lipid influx and hence, it would be an interesting target of future investigation since high cholesterol level is the main cause of various life threatening diseases and the development of atherosclerosis.Our next goal is to exploit other possible cellular mechanism regulated by ERK5-MEF2 pathway. Based on our preliminary data, we propose that this pathway not only regulate the LDLR expression but many other genes, which are directly or indirectly involved in lipid metabolism
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Broderick, Peter. "The effect of EBV on host cellular gene expression." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444349.
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Chakravarthy, Usha. "The effect of gamma radiation on intraocular cellular proliferation." Thesis, Queen's University Belfast, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317046.
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Oyman, Sena. "Cellular integrity : its effect on in-vitro starch digestion." Thesis, University of Nottingham, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440288.
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Chu, Yu-Hsuan. "Custom Fluorophores for Investigating the Cellular Uptake Mechanisms and Side-Effects of Pharmaceuticals." PDXScholar, 2015. http://pdxscholar.library.pdx.edu/open_access_etds/2343.
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There is a significant current need to elucidate the molecular mechanisms of the side-effects caused by widely-used pharmaceuticals. Examples include the acute nephrotoxicity and irreversible ototoxicity promoted by the cationic drugs gentamicin and cisplatin. Gentamicin is an aminoglycoside antibiotic used for the prevention and treatment of life-threatening gram-negative bacterial infections, such as tuberculosis and meningitis. Cisplatin is used to treat a broad spectrum of cancers including head and neck, ovarian, cervical, stomach, bladder, sarcoma, lymphoma, testicular cancer and others.
The objective of this study is to design and synthesize rhodamine derivatives that can be used for the construction of geometrically well-defined cationic drug conjugates. The long-term goal is to use the conjugates as tools to aid in elucidating the properties and identities of ion channels involved in the uptake of cationic pharmaceuticals into kidney and cochlear hair cells. This will shed light on the origin and potential prevention of unwanted side effects such as nephrotoxicity and ototoxicity associated with specific cationic drugs.
A series of extended rhodamine analogs with reactive groups for biomolecule conjugation has been synthesized. These fluorophores show similar spectral properties to their prototype, Texas Red succinimidyl ester (TR-SE). However, they contain rigid linkers between the fluorophore and amine-reactive moiety. The resultant gentamicin conjugates of these materials are rigidified enabling one to assess channel pore dimensions without the confounding issue of conjugate folding. Preliminary cell studies are promising, as one observes reduced gentamicin uptake in both kidney and sensory hair cell upon systematically increasing the dimension of the fluorophore. This work has enabled us to tentatively assign the maximum dilated MET channel pore size as between 1.44 nm to 1.56 nm. However, this preliminary finding, though encouraging, needs further validation via ongoing studies with larger diameter fluorophore conjugates,
A cisplatin-Texas Red conjugate has also been synthesized to enable studies of cellular uptake mechanisms. This conjugate preserves not only the spectral properties of Texas Red after conjugation, but also the cytotoxicity of cisplatin. This has been validated in zebrafish. The series of rhodamine probes that have been conjugated to gentamicin should be similarly useful for cisplatin studies. These studies are planned. Additional future work includes the synthesis of semi-flexible (glycol) and flexible (alkyl) linkers to evaluate structure-activity relationships.
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Hendrichsen, Melissa K. "Thermal effect and fault tolerance in quantum dot cellular automata." Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1314329.
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To have a useful QCA device it is first necessary to study how to control data flow in a device, then study how temperature and manufacturing defects will affect the proper output of the device. Theoretically a "quantum wire" of perfectly aligned QCA cells at zero Kelvin temperature has been examined. However, QCA processors will not be operating at a temperature of zero Kelvin and inherently the manufacturing process will introduce defects into the system. Many different types of defects could occur at the device level and the individual cell level, both kinds of defects should be examined. Device defects include but are not limited to linear and/or rotational translation, and missing or extra cell(s). The internal cell defects would include an odd sized cell, and one or more miss-sized or dislocated quantum dot(s). These defects may have little effect on the operation of the QCA device, or could cause a complete failure. In addition, the thermal effect on the QCA devices may also cause a failure of the device or system. The defect and thermal operating limit of a QCA device must be determined.In the present investigation, the thermal and defect tolerance of clocked QCA devices will be studied. In order to study tolerance of QCA devices theoretical models will be developed. In particular, some existing computer simulation programs will be studied and expanded.Department of Physics and Astronomy
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Kanuchok, Jonathan L. "The thermal effect and clocking in quantum-dot cellular automata." Virtual Press, 2004. http://liblink.bsu.edu/uhtbin/catkey/1286605.
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We present a theoretical study of quasi-adiabatic clocking and thermal effect in Quantum-dot Cellular Automata (QCA). Quasi-adiabatic clocking is the modulation of an inter-dot potential barrier in order to keep the QCA cells near the ground state throughout the switching process. A time-dependent electric field is calculated for arrays of charged rods. The electron tunneling between dots is controlled by raising and lowering a potential barrier in the cell.A quantum statistical model has been introduced to obtain the thermal average of polarization of a QCA cell. We have studied the thermal effect on QCA devices. The theoretical analysis has been approximated for a two-state model where the cells are in one of two possible eigenstates of the cell Hamiltonian. In general, the average polarization of each cell decreases with temperature and the distance from the driver cells. The results demonstrate the critical nature of temperature dependence for the operation of QCA.Department of Physics and Astronomy
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Cousins, Brian G. "The effect of a nanoparticulate silica coating on cellular response." Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420280.
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Anderson, David. "Effect of cellular factors on the generation of β-amyloid." Thesis, Sheffield Hallam University, 2003. http://shura.shu.ac.uk/19274/.
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There is considerable interest in the role of aggregated protein in the underlying pathology of human neurodegenerative conditions including Alzheimer's disease (AD), light chain amyloidosis, spongiform encephalopathies, Huntingdon's disease, Parkinson's disease, etc. AD is a progressive neurodegenerative condition responsible for dementia in the elderly. An early onset, familial genetic basis (FAD) for the disease has been established in kindreds, where mutations in the amyloid precursor protein (APP) and the presenilin proteins (PS) cause cerebral deposition and aggregation of the beta-amyloid (Abeta) peptide responsible for the clinical and pathological features of the disease. In order to investigate the cell biology of presenilinl and the effect of AD-causing mutations on intracellular dynamics, constructs of enhanced green fluorescent protein fused to wild type or mutant N-terminal fragment and full-length PS1 were prepared. Immunocytochemical analysis reveals that the fusion proteins display four distinct phenotypes: ER, Golgi, vesicular and 'blob-like aggregates'. Furthermore, removal of the EGFP moiety had no effect on the phenotype. The 'blob-like aggregates', are high copy number, ubiquitinated structures that originate from the nuclear/ER interface, and are not dependent on microtubules for their formation nor are they contained by the intermediate filament vimentin, indicating that they are neither aggresomes nor inclusion bodies. Moderate to high levels of the fusion protein disrupt the endoplasmic reticulum and Golgi compartments, suggesting that the normal trafficking of materials within the cell may be disturbed. Additionally, the N-terminal construct sensitises cells to staurosporine-induced apoptosis. TEM images from cells expressing the fusion protein reveals numerous phagosomes and mutilaminar bodies that fit the profile seen for the blob-like aggregates in terms of dimension, number and general morphology. These data suggest that the blob-like aggregates might be novel membrane-bound structures. These fusion proteins provide a convenient means for studying the consequences of protein aggregation on the ubiquitin-proteasome system (UPS), apoptosis and phagocytosis within the cell.
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Simon, Kathryn D. "Effect of cellular zinc concentration on glucocorticoid induced gene expression." Diss., This resource online, 1996. http://scholar.lib.vt.edu/theses/available/etd-06062008-155344/.
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Prasad, Saurabh. "Radio over fiber for 3G cellular System." Thesis, Kolhapur Institute of Technology College of Engineering, 2010. http://hdl.handle.net/10919/71529.
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The demand for bandwidth is increasing vigorously. Thus wired network is using fiber optic telephone line instead of coaxial cable. The concept of Fiber to the Home (FTTH) is really coming into picture. Few countries like Japan, Korea etc are leading in this technology. But now the major challenge is how to provide the high speed internet connection wirelessly. Thus the change is to integrate the wireless and optical fiber communication.Wireless Optical Communication
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Wang, He. "Cellular regulatory mechanisms in silica-induced lung inflammation and neoplasia." Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27710.
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It is well known that silica exposure results in an initial acute inflammatory
response followed by the persistence of induced inflammation in lung tissue. In
the process of inflammation, which eventually evolves into fibrosis and possibly
predisposes to carcinogenesis, various substances are produced by the involved
cells which have the potential to result in damage to nuclear material in
surrounding cells, manifesting as morphological apoptosis and micronuclei.
Apoptosis of infiltrated leucocytes and subsequent phagocytosis by pulmonary
alveolar macrophages (PAM) may lead to resolution of the inflammation whereas
a defect in this mechanism may contribute to its persistence. Detection of
micronuclei in PAM may provide a desirable tool to evaluate the potential
genotoxic effects induced by silica in vivo, since PAM are exposed to not only
silica particles but also to induced reactants.
In order to examine these hypotheses, a series of experiments were conducted '
by intratracheal instillation of rats with dust suspensions of silica or titanium
dioxide (TiOz). It was found that notable apoptosis of neutrophils did not occur
until 5 days after silica instillation, reaching the highest point 5 days subsequently. The occurrence of apoptosis occurred concurrently with the formation of granulomata in lung tissue. In subsequent experiments, occurrence of neutrophil apoptosis was detected 1 day after TiOz instillation, with-a peak at 3 days and resolving at 5 days. Dose-dependent apoptosis was detected in rats instilled with different amounts of silica and the proportion of PAM with engulfed apoptotic neutrophil in total PAM decreased with increasing silica dose. Administration of ticlopidine and pentoxifylline inhibited the pulmonary inflammatory reaction induced by silica exposure and enhanced the occurrence of neutrophil apoptosis whereas w—nitro-L-arginine methyl ester (L-NAME) administration had no obvious effect on these events. These are all new findings. Based on these results it is concluded that silica exposure can cause delayed neutrophil apoptosis and compromised phagocytosis of the apoptotic cells by PAM. These changes induced by silica may contribute to the perpetuation of silica-induced inflammation and the development of fibrosis. The neutrophil apoptosis in silica—induced inflammation can be influenced by drugs although it is not quite clear if the inhibition of inflammation leads to the enhanced apoptosis or if enhanced apoptosis leads to the inhibition of silica-induced inflammation.
No increased micronucleus formation could be detected in PAM 1 day after silica
instillation although an acute inflammation was induced. Two days after exposure,' however, a significant increase in the proportion of micronucleated PAM was demonstrated and the increase persisted for the whole experimental period of 20 days. The increase in micronucleated PAM was dose-related in low dosed but not in high dosed rats. lntratracheal instillation of TiO2 and ntraperitoneal injection of silica could not induce an increase in micronucleated PAM. These results indicate that silica can induce micronuclei in PAM in vivo and this is not a nonspecific response. This is the first demonstration that silica has such a genotoxic activity and it adds to the body of evidence for the classification of silica as a genotoxic carcinogen.
This study demonstrated that a defective mechanism for inflammatory cell
removal through apoptosis and subsequent phagocytosis may contribute to the
persistence of silica-induced inflammation and that silica can induce micronucleus formation in lung local cells such as PAM in an inflammatory condition. Since apoptosis can be induced by foreign agents and phagocytic capacity may also be modified, selection of drugs to counteract the persistence of silica-induced inflammation could be based on these mechanisms. The enhanced resolution process of inflammation may not only reduce the risk of fibrosis but also carcinogenesis. Since genotoxic carcinogens cause the development of cancer by different mechanisms to nongenotoxic agents, better understanding of silica carcinogenicity mechanisms will assist in the prevention of silica-induced lung cancer.
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Cox, Andrew Graham. "Effect of Bcl-2 on the cellular response to oxidative stress." Thesis, University of Canterbury. Biological Sciences, 2006. http://hdl.handle.net/10092/1322.
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Exposure of cells to hydrogen peroxide can cause oxidative damage to cellular constituents including lipids, protein, and DNA. At elevated concentrations, hydrogen peroxide can trigger cell death by apoptosis or necrosis. Apoptotic cell death can be prevented by overexpression of the oncoprotein Bcl-2. The exact mechanism by which Bcl-2 blocks cell death is controversial. Some researchers believe that Bcl-2 possesses antioxidant properties that protect cells from apoptosis. The purpose of this thesis was to assess oxidative stress and apoptosis following hydrogen peroxide exposure in Jurkat T cells overexpressing Bcl-2. One of the major objectives was to ascertain whether or not Bcl-2 overexpression elevated the antioxidant capacity of Jurkat T cells to provide protection from oxidant-induced cell death. Hydrogen peroxide treated Jurkat cells became apoptotic at moderate levels of oxidant (25-100 uM H2O2), and necrotic at higher doses (greater than 200 uM H2O2). Bcl-2 overexpression prevented caspase activation and cell death at the apoptotic doses of H2O2, but not the necrotic doses. Caspase inhibition studies demonstrated that Bcl-2 overexpression provided a greater level of resistance from H2O2-induced cell death than the broad-spectrum caspase inhibitor z-VAD.fmk. A systematic study was carried out examining the antioxidant status of Jurkat cells overexpressing Bcl-2. Several Bcl-2 transfectants were utilised for the study, so that any differences seen could be correlated to the level of Bcl-2 expression. Surprisingly, there were no statistically significant differences among the Bcl-2 transfectants for any of the antioxidant enzymes. Jurkat cells overexpressing Bcl-2 exhibited the same level of oxidative damage to lipids and protein in response to H2O2 exposure as the parental Jurkat cells. Interestingly, Jurkat cells overexpressing Bcl-2 continued to grow in culture after H2O2 exposure, despite harboring damage to cellular constituents. Consistent with these results, H2O2 treated Jurkat cells overexpressing Bcl-2, which failed to undergo apoptosis, were more prone to genomic instability. Together, these findings suggest that Bcl-2 overexpression protects Jurkat cells from H2O2-induced cell death by blocking apoptosis. Jurkat cells overexpressing Bcl-2 were no better at detoxifying oxidants and showed the same level of oxidative damage following H2O2 exposure. As a result, the overexpression of Bcl-2 considerably enhanced the mutagenicity of H2O2.
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Simpson, Russell Michael Lloyd. "Effect of cellular aging on fibroblastic phenotype and regulation by hyaluronan." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55467/.
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Collectively, the data demonstrated that HA can serve as a signal integrator by facilitating TGF-beta11-mediated CD44-EGF-R-ERK interactions and ultimately regulate fibroblast phenotype. I propose a model to explain this novel mechanism and the functional consequence of age-dependent dysregulation. This mechanism may have direct implications for modifying the wound healing response, particularly for developing therapeutic strategies to improve healing in the elderly.
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Bolton, Peter Andrew. "The effect of light on cellular mechanisms associated with wound healing." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286667.
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The ability of light to affect and modify human activity, both physiologically and psychologically has been known for many centuries. The treatment of wounds with light with varying properties has seen a dramatic rise over the last twenty years, from initial reports of the "magic laser" in the 1970's, to recent well controlled clinical trials. However, one of the major problems facing researchers and clinicians in elucidating the mechanisms by which light can modulate wound repair, is that of the different parameters of the light sources used, be they true laser devices, monochromatic light sources or. broadband wavelength units. This thesis describes a series of in vitro studies of the effects of varying the parameters of three light sources a) directly on fibroblast proliferation and b) indirectly, via supernatant from light-irradiated macrophage-like U-937 cells. The effect of U-937 cells was investigated because, as well as playing a pivotal role in wound debridement, macrophages playa central role in mediating the body's inflammatory and immune responses, mainly through the release of various polypeptide growth factors and cytokines and these can modulate wound healing. The experiments reported here show that there is a clear dose-response effect on the proliferation of fibroblasts when grown in macrophage-conditioned medium in which U-937 cells had been subjected to energy densities of 2.4, 4.B and 7.2J/cm2 using a monochromatic light source of 660nm at a frequency of 5kHz. Earlier work had shown that of a number of wavelengths examined, this wavelength evoked the greatest response. 2.4, 4.Band 7.2J/cm2 produced an increase in fibroblast proliferation above that of the sham-irradiated sample, 7.2J/cm2 producing the greatest effect. 9.6 J/cm2 was found to be inhibitory. The relationship between energy density and power density was investigated using the same model, but with a pure laser light source (820nm, frequency 5kHz). The U-937 cells were exposed to either 400mW/cm2 or 800mW/cm2 at energy densities of either 2.4 or 7.2J/cm2 (the doses giving the lowest and highest response in the previous experiment). There was a statistically significant difference in fibroblast proliferation between the 400mw/cm2 and Boomw/cm2 treatments, BoomW/cm2 producing the greatest cell proliferation at an energy density of 2.4J/cm2• There was no significant difference between the sham-irradiated sample and the 400mw/cm2 treated group. In contrast, using an energy density of 7.2J/cm2, the 400mW/cm2 treatment produced a greater increase in fibroblast proliferation than the sham-irradiated sample and there was no significant difference in cell number between the sham irradiated sample and 800mw/cm2 sample. The 400mW/cm2 sample produced a greater increase in cell proliferation than the 800mW/cm2 sample. Using the same model as above, the effects of two broadband (400-2000nm, continuous wave) light sources, of which one was 95% and the other 14% polarised, were investigated using energy densities of 1.44 and 2.88 Jjcm2• The proliferative response was greatest in the cultures exposed to supernatants from macrophages treated with the 95% polarised light source for both the energy densities used. The direct effect of 860 nm laser light (continuous wave) on the proliferation and succinic dehydrogenase levels of human forearm fibrobasts was investigated using energy densities of 2 and 16 Jjcm2• At an energy density of 2Jjcm2, succinic dehydrogenase and fibroblast proliferation levels increased to above that of the sham-irradiated sample, however, at an energy density of 16Jjcm2, succinic dehydrogenase levels and fibroblast proliferation were inhibited. The results presented in this thesis indicate either stimulation or inhibition of cellular activity which can be induced by specific levels and types of light irradiation and helps to elucidate the mechanism of action of light-producing devices at the cellular level.
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Barclay, Travis J. "The temperature effect and defect study in quantum-dot cellular automata." Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1319217.
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Quantum-dot Cellular Automata (QCA) is a new paradigm for computation that utilizes polarization states instead of using current switching. It is being studied because of the realization of the quickly approaching limitation of the current CMOS technology. The location of two excess electrons located within four or five quantum dots on a particular cell can transmit the binary information. These dots are located in the corner of a square cell, and if there is a fifth dot it is located in the center. The electrons are allowed to tunnel freely among the dots, but are restricted from tunneling between neighboring cells. Because of the interaction between the electrons, they will anti-align within the cell giving one of two particular configurations. This configuration can be transmitted to neighboring cells. In other words, data is flowing.We present a numerical study of the fabrication defect's influence on Quantum-dot Cellular Automata (QCA) operation. The statistical model that has been introduced simulates the random distribution of positional defects of the dots within cells and of cells within arrays. Missing dots within a QCA cell structure have also been studied.We have studied specific non-clocked QCA devices using the Inter-cellular Hartree Approximation, for different temperatures. Parameters such as success rate and breakdown displacement factor were defined and calculated numerically. Results show the thermal dependence of the breakdown displacement factor of the QCA devices. It has been shown, that the breakdown displacement factor decreases with increasing temperature. As expected, multiple defects within the same QCA array have shown a reduction in success rate greater than that of a single defect influencing the system.Department of Physics and Astronomy
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Powell, Heather Megan. "Nanoscalar modifications to polymeric tissue engineering scaffolds effect on cellular behavior /." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095780106.
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Geraldo, Ângela Margarida Ferreiro. "Substrates effect on Mesenchymal Stem Cells (MSCs) secretome and cellular subproteome." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/16394.
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Mestrado em Biologia Molecular e CelularMesenchymal stem cells (MSCs) are adult multipotent cells that possess self-renewal capacity, have a high proliferative ability and are able to differentiate into mesodermal cell types. MSCs can be isolated from mesenchymal and extraembryonic tissues such as the umbilical cord matrix. The latter constitutes an attractive and alternative source of MSCs since these cells seem to be more naïve and possess higher proliferation capacity. In vivo, MSCs reside in a specialized microenvironment that is essential for the regulation of signaling, proliferation, migration and differentiation. Through mechanotransduction, mechanical forces of microenvironment are transduced into biochemical responses, which can lead to alterations in phenotype and lineage-specific differentiation, and changes in protein synthesis of MSCs. Based on these observations, this study aimed at exploring the effect of physical and biochemical substrate composition on the secretome and cellular subproteomes of MSCs derived from umbilical cord matrix. The present study revealed the modulation of the secretome and cellular subproteome profiles (soluble and membrane fractions) of MSCs cultured on soft substrates, with several proteins being modulated, namely the up-regulation of antioxidant proteins. Hence, we propose that MSCs cultured on soft substrates may constitute a population of cells with increased antioxidant properties, in principle allowing the cells to cope better with the stressful and hostile environments that they may encounter in vivo in a transplantation context.
As células estaminais mesenquimais (MSCs) são células estaminais adultas, multipotentes, capazes de se auto-renovar e diferenciar em diferentes tipos celulares mesodermais. O isolamento destas células pode ser feito a partir tecidos mesenquimais, bem como de extra embrionários, como por exemplo da matriz do cordão umbilical. Este último constitui uma fonte alternativa e atrativa de MSCs uma vez que estas apresentam características mais naïve e uma maior taxa de proliferação. In vivo, as células mesenquimais têm um microambiente especializado que é essencial à regulação da sinalização, proliferação, migração e diferenciação celular. Através da mecanotransdução, as forças mecânicas do ambiente extracelular são traduzidas em respostas bioquímicas que podem conduzir à alteração de fenótipo e diferenciação em diferentes tipos celulares e, além disso, à alteração da síntese de proteínas. A partir destas observações, este trabalho teve como objetivo o estudo do efeito das propriedades do substrato, tais como a rigidez e composição bioquímica, no secretoma e subproteomas de células estaminais mesenquimais isoladas a partir da matriz do cordão umbilical. Este estudo revelou uma modulação do secretoma e subproteomas celulares (frações solúvel e membranar) quando as MSCs foram mantidas em cultura sobre substratos com menor rigidez, demonstrando a modulação de múltiplas proteínas e nomeadamente o aumento dos níveis de proteínas anti-oxidantes. Deste modo, propomos que células cultivadas em substratos com menor rigidez possuam uma maior atividade anti-oxidante, o que irá permitir que estas apresentem uma melhor resposta face a ambientes hostis in vivo num contexto de transplantação.
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Miller, Lana L., and University of Lethbridge Faculty of Arts and Science. "Species differences in selenium toxicity : linking cellular responses to population effects." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2011, 2011. http://hdl.handle.net/10133/2622.
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Model organisms are often used in ecotoxicological studies and environmental risk assessments; however, species differences in responses to toxicants exist. A meta-analysis identified normal biomarker ranges for rainbow trout (RT) and brook trout (BT), and showed that RT had greater whole-body lipids and plasma T4 levels than BT. Exposure to selenium inhibited cortisol secretion of trout adrenocortical cells; however, RT were more sensitive than BT. To investigate species vulnerability at the individual level, RT and BT were stocked into reference and selenium-contaminated pit lakes. Fish accumulated more Se from selenium-contaminated than reference lakes, and selenium accumulation was similar between species. Chronic selenium exposure had a greater energetic cost for RT than BT, but this was mitigated by food availability. Chronic selenium exposure decreased plasma T3 and T4 levels, but did not alter other endocrine or oxidative stress biomarkers. This project highlights the need for both species- and site-specific risk assessments.xiv, 171 leaves : ill., maps ; 29 cm
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Yu, Lok Chiu. "Cellular metabolism in in vitro toxicity and toxicology studies." HKBU Institutional Repository, 2005. http://repository.hkbu.edu.hk/etd_ra/675.
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Prajaneh, Saengsome. "Effect of cellular positional identity on bone regenerative capacity for tissue engineering." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/effect-of-cellular-positional-identity-on-bone-regenerative-capacity-for-tissue-engineering(270579b0-278b-4a3d-9f4a-721f4d38e76e).html.
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The aim of this study was to investigate the stability of positional identity markers and phenotypic differences in isolated osteoblasts from distinct anatomic regions. In addition, the ability of heterotypic co-cultures to reprogramme site-specific Hoxa gene expression also tested. Rat osteoblastic cells from femurs and calvariae were harvested as matched pairs of cultures from 4 male rats. Cells were expanded extensively in medium supplemented with FGF-2, and were shown to maintain their osteoblastic phenotype as characterised by alkaline phosphatase (ALP) staining, osteopontin (OPN), osteocalcin (OCN) expression and osteoblast-associated gene expression in long term culture. Gene expression of cells was determined by quantitative RT-PCR. Differences in Hoxa gene expression as markers of positional identity were maintained for up to at least 10 passages, with calvarial cells remaining Hoxa-ve throughout. The transcription factors Msx2 and Irx5 were consistently more highly expressed in calvarial cells, whereas Tbx3 expression was elevated in femoral cells. Expression of the osteoblast-associated genes Bglap and Sppl were elevated in femoral cells, and also associated with increased osteopontin secretion and bone nodule formation. Runx2 was elevated in calvarial cells. Cells were also pre-labelled with fluorescent vital staining and co-cultured for 7 days prior to separating by fluorescence activated cell sorter to investigate the possibility of re-programming of Hoxa negative cells by direct contact with Hoxa +ve cells. However no evidence was seen of modulation of positional identity genes and phenotypes in these heterotypic cultures. In conclusion, the results demonstrate persistence of expression of positional identity gene markers and phenotypic differences between femoral and calvarial osteoblasts for prolonged periods in culture. These data suggest that these differences in regionally defined osteoblasts are inherently programmed in the cells as a result of their embryological position. The results may have considerable implications when considering the transplantation of autologous cells in tissue engineering.
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Li, Sen, and 李森. "Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46940546.
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Schoeman, Werner. "Cellular stress responses to cadmium contamination as measure of sensitivity in intertidal molluscan species." Thesis, Link to the online version, 2007. http://hdl.handle.net/10019/460.
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El-Sheikh, Medhat. "Studies on the cellular and molecular basis of salt resistance in a halotolerant Arabidopsis thaliana cell line." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274256.
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Padgett, Benjamin David. "Modeling and simulation of fault tolerant properties of quantum-dot cellular automata devices." CardinalScholar 1.0, 2010. http://liblink.bsu.edu/uhtbin/catkey/1569024.
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I present a theoretical study of fault tolerant properties in Quantum-dot Cellular Automata (QCA) devices. The study consists of modeling and simulation of various possible manufacturing, fabrication and operational defects. My focus is to explore the effects of temperature and dot displacement defects at the cell level of various QCA devices. Results of simple devices such as binary wire, logical gates, inverter, cross-over and XOR will be presented. A Hubbard-type Hamiltonian and the inter-cellular Hartree approximation have been used for modeling the QCA devices. Random distribution has been used for defect simulations. In order to show the operational limit of a device, defect parameters have been defined and calculated. Results show fault tolerance of a device is strongly dependent on the temperature as well as on the manufacturing defects.Cell design -- Basic logic gates -- The exclusive or gate.
Department of Physics and Astronomy
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Lomas, Cyprien. "Effect of adenovirus E3/19K protein on cellular processes in the endoplasmic reticulum." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0028/NQ46374.pdf.
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Wing, James Badger. "The effect of mannose-binding lectin on the cellular interactions of Neisseria gonorrhoeae." Thesis, University of Sheffield, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444921.
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Wood, Jennifer Jane. "The effect of Kaposi's sarcoma-associated herpesvirus RTA expression upon the cellular proteome." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6344/.
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Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma (KS). Like all herpesviruses, KSHV has a bi-phasic life cycle, with a dormant latent phase and a productive lytic phase. The switch from viral latency to lytic replication is mediated by the replication and transcription activator protein (RTA). RTA activates KSHV lytic gene expression via direct and indirect binding to lytic promoters. Moreover, it functions as an E3 ubiquitin ligase, actively degrading repressor proteins, such as Hey1, maintaining the virus in the latent state. The first aim of this study was to determine if RTA functions as a SUMOylation targeted ubiquitin ligase (STUbL), which recognises poly-SUMOylated targets via SUMO interacting motifs (SIMs). Results presented herein demonstrate that the Hey1 repressor protein is SUMO2 modified. Furthermore, mutation of SIM domains within RTA resulted in attenuation of RTA-mediated degradation of Hey1 and lytic reactivation. However, SIM mutation also severely reduced RTA-mediated transactivation. These results suggest that RTA may have STUbL activity but additional work is required to reconcile the effect of SIM mutation upon transcriptional activity. The second aim of this investigation was to identify novel points of interaction between RTA and the host cell. In chapter 4, SILAC-based quantitative proteomics identified hundreds of proteins which demonstrated a significant change in abundance upon RTA expression. Abundance of the cellular protein ARID3B was found to increase over 7-fold in the nuclear fraction. Furthermore, ARID3B was shown to re-localise to viral replication centres upon lytic reactivation. In chapter 5 SILAC-based immunoprecipitations were performed to identify novel RTA interaction partners. The cellular co-activator RBM14 was found to be enriched in two independent SILAC data sets and subsequent investigation demonstrated that RBM14 localisation was altered upon RTA expression. These novel observations highlight the potential significance of cellular factors in KSHV infection. Further investigation is required to fully characterise the role of these proteins in viral reactivation.
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Khan, Md Imran Hossen. "Fundamental understanding of cellular water distribution and transport in plant-based food material during drying." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/121217/1/Md%20Imran%20Hossen_Khan_Thesis.pdf.
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This study was conducted to uncover the spatial distribution of cellular water in plant-based food materials and its transport process during drying. A new experimental and analytical method was developed to investigate the cellular water distribution using NMR-T2 relaxometry and X-ray micro CT. It was revealed that at low temperatures cellular water migrates through diffusion whereas at higher temperature cell water mostly migrates through progressive rupturing of the cell walls. This thesis also investigated the impact of process parameters and characteristics of food material on cellular water distribution, transport and associated morphological changes during drying.
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Robinson, L. P. G. "Preliminary investigation of a possible dose rate effect on survival of cells irradiated with low energy protons." Master's thesis, University of Cape Town, 1989. http://hdl.handle.net/11427/26226.
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Apparatus has been developed for the irradiation of V79-379A Chinese hamster lung fibroblast cells with 3.6 MeV protons from the Van de Graaff accelerator at the National Accelerator Centre in Faure. The original intention of this work was to investigate and measure a possible dose rate effect on the survival of V79 cells, in the dose range from zero to 25 Gy, at dose rates of about 3 Gy/s and 300 Gy/s. The survival curves initially obtained were anomalous in that they showed abnormally high levels of survival and a tendency to remain at a constant survival level for doses above 10 Gy. Systematic attempts to correct this observed anomaly, involved the following; apparatus improvements were made, a means of measuring the beam profile was devised, the current measuring device and the dosimetry were improved and a possible dose rate effect on intracellular oxygen was investigated. After these improvements, the anomalous effect was much reduced, but not entirely eliminated. The final results showed no significant difference between the survival of cells irradiated at dose rates of about 3 Gy/s and 300 Gy/s; qualitative differences were however noticeable. After correction for the effect of a non-uniform beam profile, the survival curves were significantly different to published work. This difference suggested a possible dose rate effect between dose rates of about 0.1 Gy/s and dose rates above 3 Gy/s.
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Descoteaux, Albert. "Study on the effect of Leishmania donovani infection on signal transduction in macrophages." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70169.
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The ability of tumor necrosis factor (TNF) and lipopolysaccharide (LPS) to stimulate gene expression in bone marrow-derived macrophages (BMM) was first compared. It is demonstrated that they stimulated gene expression through distinct signal transduction pathways and that TNF stimulated gene expression through a protein kinase C (PKC)-dependent signal transduction pathway. The effect of the intracellular parasite of macrophages Leishmania donovani in BMM was then investigated. It is demonstrated that L. donovani impaired c-fos and TNF gene expression through two distinct mechanisms. The first one is indomethacin-reversible, and the second one involves the inhibition of diacylglycerol-induced PKC-dependent gene expression. A purified cell surface glycoconjugate of the parasite, termed lipophosphoglycan, selectively inhibited PKC-dependent gene expression in BMM. While the translocation of PKC from the cytosol to the membrane was normal, total cellular PKC enzyme activity was inhibited in the U937 human monocyte cell line pretreated with lipophosphoglycan.
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Skornicka, Erin L. "The effect of blood collection methods on the expression of monocyte cellular adhesion molecules /." Connect to online version, 1996. http://hdl.handle.net/1989/3570.
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Zeraia, Magda. "Early effect of xenobiotics on cellular function : a comparison of hepatoma cells and hepatocytes." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428939.
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Meek, Robert Marshall Dominic. "Dupuytren's disease : the effect of steroids on pro-inflammatory cytokine production and cellular apoptosis." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366257.
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Collins, Terry Cordell. "The effect of HSV-2 infection on the expression of cellular mitochondrial aspartate aminotransferase." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266539.
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Kaklamani, Georgia. "The effect of active screen plasma nitriding on the cellular compatibility of polmeric biomaterials." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3844/.
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Active Screen Plasma Nitriding (ASPN) is a novel surface engineering technique, the main advantage of which is the capacity to treat homogeneously all kind of materials surfaces of any shape. Here, ASPN is used to modify the surface properties of ionomer glasses and polymers in order to improve the surface cellular compatibility of these materials. A conventional DC nitriding unit has been used together with an AS experimental arrangement. The materials that were treated were an ionomer glass composition and UHMWPE. All treated/untreated samples were seeded with the 3T3 fibroblasts. In order to identify the effect of the plasma treatment, chemical and mechanical properties characterization was conducted. For the cellular samples, SEM, Interferometry, AFM and MTT assay were conducted in order to observe cells’ behavior on the untreated and treated materials. The inert surface of the untreated glass showed good interaction with fibroblasts only after the ASPN treatment which resulted in enhanced fibroblasts attachment and proliferation. The treatment temperature, the length of treatment and the presence of nitrogen had an influence on the surface properties of glass. UHMWPE treated samples chemical characterization showed the formation of C-N and N-H groups resulting in an increase of the functionality of treated surfaces. 3T3 fibroblasts cell culture studies showed that the ASPN treatment had a positive effect on the adhesion and proliferation of cells according to the time of treatment and the increase of the nitrogen concentration in the gas mixture. As a conclusion ASPN treatment can be a very effective method to modify inorganic and organic polymeric surfaces in order to improve cellular compatibility.
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Yousuf, Ghadah Khaled. "The Effect of Violacein Extracted from Chromobacterium violaceum on Growth of Breast, Colon, Lung, and, Prostate Cancer Cell Lines." Thesis, Tennessee State University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10243226.
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Chromobacterium violaceum (CV) produces a violet color pigment known as Violacein. It has been reported that violacein has anticancer activity. This compound is produced by CV a gram-negative facultatively anaerobic bacterium found in soil and water environmental samples. The purpose of this study was to determine the effect of purified violacein on select cancer cell lines. Violacein used in this study was purified from CV strain (14N23), a strain isolated from environmental samples collected in the Tennessee Copper Basin. The previous reports used a crude extract preparation of violacein; thus, it was of interest to determine the effect of the pure compound on cancer cell growth was similar to that of the crude extracts. The compound purified following the method of Mehta, et al. was exposed to cancer cells and cell death assessed using the Alamar Blue procedure. It was found that violacein had no effect on A549, BT549, and PC3 cancer cell growth; however, there was a significant effect on Colo-320 cancer cells. It was concluded that further studies are required to assess the effect of violacein on enzymes and proteins involved in the cancer cell apoptotic pathways. Such studies will explain why cancer cell death was observed in certain cancer cells and not others.
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Hüfner, Anna. "Gold nanoparticles explore cells : molecular insights into cellular characteristics and processes using surface-enhanced Raman spectroscopy." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708921.
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Daniels, Brodie Belinda. "The effect of human soluble FceRII on the RPMI 8866 B-Lymphoblastoid and the U937 Monocyte cell lines." Thesis, University of Port Elizabeth, 2003. http://hdl.handle.net/10948/322.
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Due to the diverse functions of Fc eRII, such as its roles in cellular adhesion, growth and differentiation of B and T lymphocytes, rescue of B cells from apoptosis and release of cytotoxic mediators, it is clear why it is believed to be a central molecule in allergic response. Because of its important role in the regulation of IgE production, FceRII may be the primary cause of certain allergic conditions. This study attempted to express and purify a recombinant human soluble FceRII to test its effect on a B-lymphoblastoid (RPMI 8866) and a monocytic (U937) cell line. The protein was expressed in Escherichia coli inclusion bodies, before being refolded and purified in a single gel chromatography step. This pure protein was then tested for biological activity by testing its IgE binding func tion. Once proven functional, it was used to test its effect on the cell lines at three concentrations for its apoptotic rescue properties and its cytokine effects. The recombinant protein did not seem to have any significant effect on the apoptotic rescue of either cell line. While the recombinant sFceRII appeared to have a slight effect on the stimulation of IL-1ß and TNFa in the RPMI 8866 cells, there was no apparent effect on the production of NF?B. In U937 cells, the protein did not seem to have any effect on the stimulation of IL-1ß, TNFa or NF?B. However, the cytokine effects of the recombinant protein were tested on isolated PBMCs from a healthy individual and a hyper-IgE syndrome patient. The recombinant protein was able to stimulate the production of cytokines in both individuals’ PBMCs, proving that it has the same effect as the natural protein. The upregulation of these cytokines indicates that the recombinant protein is able to stimulate the immune system. Therefore, this recombinant soluble FceRII protein could possibly be used for immune therapy.
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Gu, Mingyu. "Effect of Nitric Oxide on Myeloid Dendritic Cell Adhesion." Ohio University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1338903998.
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Labib, Sarah. "The effect of LMNA mutations on lamin AC and binding partner interactions and cellular distribution." Thesis, University of Ottawa (Canada), 2011. http://hdl.handle.net/10393/28763.
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Mutations in the LMNA gene, which encodes the nuclear intermediate filament proteins lamin A and lamin C, are associated with over ten tissue-specific diseases, including Dilated Cardiomyopathy (DCM) and lone Atrial Fibrillation (lone AF). There is no clear genotype-phenotype relationship between the location of the mutation and the associated disease phenotype. The general hypothesis of this thesis is that LMNA mutations exert their tissue-specific effects via the perturbation of lamin A and lamin C's specific interacting partners.
Protein kinase C alpha, PKCalpha, is a lamin A/C binding partner implicated in heart failure and cardiac hypertrophy. Furthermore, abnormal PKCalpha function results in IKAch activity associated with chronic AF. My first aim is to identify specific phenotypes associated with three laminopathies: lone AF, DCM, and DCM with AF by a) comparing the cellular phenotype induced by LMNA mutations associated with lone AF, DCM, and DCM with AF and b) determining the effect of the mutations on the cellular distribution of PKCalpha. I found two previously unreported mutant lamin A and C phenotypes -- cytoplasmic lamin A/C extrusion and the formation of intranuclear lamin A/C sickle-shaped aggregates associated with one lone AF mutation and one DCM mutation. I show that PKCalpha is mislocalized to the nucleus in C2C12 cells transfected with the same mutants.
The E2 conjugating enzyme of the Sumo process, Ubc9, is a reported lamin A/C binding partner. Sumo1 is a post-translational modifying protein that is sequestered within mutant lamin A/C aggregates and has increased substrate conjugation in DCM-associated mutant cells. My second aim is to determine how lamin A and C are involved in the Sumo process by a) investigating Ubc9 cellular distribution and lamin A and C binding in the presence of DCM-associated LMNA mutations and b) determining whether lamin A and/or Care Sumo! binding partners. I show that Ubc9 is mislocalized from the inner nuclear membrane to the mutant lamin A/C aggregates. Co-immunoprecipitation did not show lamin A/C sumoylation by Sumo1. Mass spectrometric analysis indicates that heterogeneous ribonucleoprotein U may be a novel lamin A/C binding partner that is sumoylated by Sumo1.
In conclusion, I found that two cellular pathways are perturbed in the presence of LMNA mutations and might account for the specific symptoms observed in the tissue-specific laminopathies. Incorrect activation or deactivation of tissue-specific targets may lead to the wide range of tissue-specific diseases associated with LMNA mutations.
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Deng, Honghua Materials Science & Engineering Faculty of Science UNSW. "Effect of cation addition on cellular response and bone ingrowth into three dimensional porous bioceramics." Awarded by:University of New South Wales. Materials Science & Engineering, 2008. http://handle.unsw.edu.au/1959.4/43733.
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The success of orthopaedic implants fixed in the skeletal system using bone ingrowth into porous surfaces is critically dependent on the extent and quality of the initial bone ingrowth and the subsequent long-term maintenance of the bone within the porous structure. Biologically-significant elements (Ca, Mg, Mn) were incorporated at concentrations up to 5 mol% in solid solution in yttia-stabilised tetragonal zirconia polycrystal (3YTZP), whilst controlling microstructure and phase composition, to investigate the effect of ceramic chemistry on cellular behaviour in vitro and bone ingrowth into porous structures in vivo. Cellular attachment, proliferation, and migration on the ceramics were investigated using in vitro assays using fibroblasts. Cells were able to adhere strongly and proliferate on all ceramic surfaces, exhibiting maximal proliferation and minimal migration on 3YTZP but significantly faster migration on doped-3YTZP. The TZP ceramics were therefore considered to support normal cellular processes and thus were suitable for further study in vivo. A technique based on pressure casting ceramic slurry into a polymer preform of the desire pore structure, followed by polymer burnout and then sintering, was developed for fabricating porous bioceramics containing highly-controlled three-dimensional pore geometries. The ability of a selected pore structure to support bone ingrowth was tested using hydroxyapatite by implanting samples into femoral cortical bone of adult sheep for 4 and 12 weeks. Bone was able to rapidly colonise the porous structure and remodel such that, by 12 weeks implantation time, the majority of the porosity was filled with mature lamellar bone. Porous scaffolds of pure 3YTZP and 3YTZP doped with 1 mol% Mg, 1 mol% Mn, 1 mol% Ca, or 5 mol% Ca were fabricated and tested in the sheep model. Bone ingrowth into the doped compositions was significantly greater than that into pure 3YTZP, and was similar to that into the porous hydroxyapatite, indicating that the dopants significantly promoted osteogenesis within the bioinert scaffolds. This finding has application in clinical applications in that the initial bone ingrowth and, potentially, the long-term maintenance of bone within the porous structure may be improved by the incorporation of small amounts of biologically significant elements.
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Tziampazis, Evangelos. "Engineering functional, insulin-secreting cell systems : effect of entrapment on cellular environment and secretory response." Thesis, Georgia Institute of Technology, 1993. http://hdl.handle.net/1853/10026.
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Peng, Songlin, and 彭松林. "Investigation of the cellular and molecular mechanisms for the dual effect of strontium on bone." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45585167.
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Anduwan, Gabriel A. Y. "The thermal effect and fault tolerance on nanoscale devices : the quantum dot cellular automata (QCA)." Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1369913.
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The defects and fault tolerance study is essential in the QCA devices in order to know its characteristics. Knowing the characteristics, one can understand the flow of information in a QCA system with and without manufacturing and operational defects. The manufacturing defects could be at device level or cell level. At the device level, the cell could be rotated, displaced vertically or horizontally, the cell could be missing or the size of the cell could be different. At the cell level, there could be a missing dot, dot could be displaced from its position or the size of the dots could be different. The operational defects are due to its surrounding, such as temperature or stray charge. Each of these defects and fault tolerances can be studies in detail in order to find the optimum working conditions where the information can be safely transmitted to the appropriate locations in the device.The theoretical studies have shown that at absolute temperature and without any defect, the QCA devices are operational. But it is almost impossible to manufacture a perfect or defect free device, and also it is impractical to think about operating a system at absolute zero temperature environment.Therefore, it is important to investigate the fault tolerant properties with defects and higher temperatures to see how far the QCA device can operate safely. Many studies have been done to investigate the fault tolerant properties in QCA devices. However, these studies have not completely exhausted the study of defects and temperature effects. In this study, the dot displacement and missing dots with temperature effects are investigated for the basic QCA devices and a Full Adder. In order to study fault tolerant properties, the existing theoretical model and computer simulation programs have been expanded and used. The defect characteristics have been simulated using normal distribution.Department of Physics and Astronomy
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Pratt-Marshall, Patricia. "High gravity brewing : an inducer of yeast stress : its effect on cellular morphology and physiology." Thesis, Heriot-Watt University, 2002. http://hdl.handle.net/10399/1175.
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