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Search Results: 1 - 10 of 200708 matches for " Eoin P. Quinlivan "
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Hypomethylation of Serum Blood Clot DNA, but Not Plasma EDTA-Blood Cell Pellet DNA, from Vitamin B12-Deficient Subjects
Eoin P. Quinlivan, Krista S. Crider, Jiang-Hui Zhu, David R. Maneval, Ling Hao, Zhu Li, Sonja A. Rasmussen, R. J. Berry, Lynn B. Bailey
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0065241
Abstract: Vitamin B12, a co-factor in methyl-group transfer, is important in maintaining DNA (deoxycytidine) methylation. Using two independent assays we examined the effect of vitamin B12-deficiency (plasma vitamin B12<148 pmol/L) on DNA methylation in women of childbearing age. Coagulated blood clot DNA from vitamin B12-deficient women had significantly (p<0.001) lower percentage deoxycytidine methylation (3.23±0.66%; n = 248) and greater [3 H]methyl-acceptance (42,859±9,699 cpm; n = 17) than DNA from B12-replete women (4.44±0.18%; n = 128 and 26,049±2,814 cpm; n = 11) [correlation between assays: r = –0.8538; p<0.001; n = 28]. In contrast, uncoagulated EDTA-blood cell pellet DNA from vitamin B12-deficient and B12-replete women exhibited similar percentage methylation (4.45±0.15%; n = 77 vs. 4.47±0.15%; n = 47) and [3 H]methyl-acceptance (27,378±4,094 cpm; n = 17 vs. 26,610±2,292 cpm; n = 11). Therefore, in simultaneously collected paired blood samples, vitamin B12-deficiency was associated with decreased DNA methylation only in coagulated samples. These findings highlight the importance of sample collection methods in epigenetic studies, and the potential impact biological processes can have on DNA methylation during collection.
Genomic DNA Methylation Changes in Response to Folic Acid Supplementation in a Population-Based Intervention Study among Women of Reproductive Age
Krista S. Crider, Eoin P. Quinlivan, Robert J. Berry, Ling Hao, Zhu Li, David Maneval, Thomas P. Yang, Sonja A. Rasmussen, Quanhe Yang, Jiang-Hui Zhu, Dale J. Hu, Lynn B. Bailey
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028144
Abstract: Folate is a source of one-carbons necessary for DNA methylation, a critical epigenetic modification necessary for genomic structure and function. The use of supplemental folic acid is widespread however; the potential influence on DNA methylation is unclear. We measured global DNA methylation using DNA extracted from samples from a population-based, double-blind randomized trial of folic acid supplementation (100, 400, 4000 μg per day) taken for 6 months; including a 3 month post-supplementation sample. We observed no changes in global DNA methylation in response to up to 4,000 μg/day for 6 months supplementation in DNA extracted from uncoagulated blood (approximates circulating blood). However, when DNA methylation was determined in coagulated samples from the same individuals at the same time, significant time, dose, and MTHFR genotype-dependent changes were observed. The baseline level of DNA methylation was the same for uncoagulated and coagulated samples; marked differences between sample types were observed only after intervention. In DNA from coagulated blood, DNA methylation decreased (?14%; P<0.001) after 1 month of supplementation and 3 months after supplement withdrawal, methylation decreased an additional 23% (P<0.001) with significant variation among individuals (max+17%; min-94%). Decreases in methylation of ≥25% (vs. <25%) after discontinuation of supplementation were strongly associated with genotype: MTHFR CC vs. TT (adjusted odds ratio [aOR] 12.9, 95%CI 6.4, 26.0). The unexpected difference in DNA methylation between DNA extracted from coagulated and uncoagulated samples in response to folic acid supplementation is an important finding for evaluating use of folic acid and investigating the potential effects of folic acid supplementation on coagulation.
Sarcoglycanopathies: A clinico-pathological study
Quinlivan R
Neurology India , 2007,
Burkholderia cenocepacia Differential Gene Expression during Host–Pathogen Interactions and Adaptation to the Host Environment
Eoin P. O’Grady,Pamela A. Sokol
Frontiers in Cellular and Infection Microbiology , 2011, DOI: 10.3389/fcimb.2011.00015
Abstract: Members of the Burkholderia cepacia complex (Bcc) are important in medical, biotechnological, and agricultural disciplines. These bacteria naturally occur in soil and water environments and have adapted to survive in association with plants and animals including humans. All Bcc species are opportunistic pathogens including Burkholderia cenocepacia that causes infections in cystic fibrosis and chronic granulomatous disease patients. The adaptation of B. cenocepacia to the host environment was assessed in a rat chronic respiratory infection model and compared to that of high cell-density in vitro grown cultures using transcriptomics. The distribution of genes differentially expressed on chromosomes 1, 2, and 3 was relatively proportional to the size of each genomic element, whereas the proportion of plasmid-encoded genes differentially expressed was much higher relative to its size and most genes were induced in vivo. The majority of genes encoding known virulence factors, components of types II and III secretion systems and chromosome 2-encoded type IV secretion system were similarly expressed between in vitro and in vivo environments. Lower expression in vivo was detected for genes encoding N-acyl-homoserine lactone synthase CepI, orphan LuxR homolog CepR2, zinc metalloproteases ZmpA and ZmpB, LysR-type transcriptional regulator ShvR, nematocidal protein AidA, and genes associated with flagellar motility, Flp type pilus formation, and type VI secretion. Plasmid-encoded type IV secretion genes were markedly induced in vivo. Additional genes induced in vivo included genes predicted to be involved in osmotic stress adaptation or intracellular survival, metal ion, and nutrient transport, as well as those encoding outer membrane proteins. Genes identified in this study are potentially important for virulence during host–pathogen interactions and may be associated with survival and adaptation to the host environment during chronic lung infections.
Atomistic tight-binding study of electronic structure and interband optical transitions in GaBi$_{x}$As$_{1-x}$/GaAs quantum wells
Muhammad Usman,Eoin P. O'Reilly
Physics , 2014, DOI: 10.1063/1.4865827
Abstract: Large-supercell tight-binding calculations are presented for GaBi$_{x}$As$_{1-x}$/GaAs single quantum wells (QWs) with Bi fractions $x$ of 3.125% and 12.5%. Our results highlight significant distortion of the valence band states due to the alloy disorder. A large full-width-half-maximum (FWHM) is estimated in the ground state interband transition energy ($\approx$ 33 meV) at 3.125% Bi, consistent with recent photovoltage measurements for similar Bi compositions. Additionally, the alloy disorder effects are predicted to become more pronounced as the QW width is increased. However, they are less strong at the higher Bi composition (12.5%) required for the design of temperature-stable lasers, with a calculated FWHM of $\approx$ 23.5 meV at $x$=12.5%.
Is PPAR a Prospective Player in HIV-1-Associated Bone Disease?
Eoin J. Cotter,Patrick W. Mallon,Peter P. Doran
PPAR Research , 2009, DOI: 10.1155/2009/421376
Abstract: Currently infection with the human immunodeficiency virus-1 (HIV-1) is in most instances a chronic disease that can be controlled by effective antiretroviral therapy (ART). However, chronic use of ART has been associated with a number of toxicities; including significant reductions in bone mineral density (BMD) and disorders of the fat metabolism. The peroxisome proliferator-activated receptor gamma (PPAR) transcription factor is vital for the development and maintenance of mature and developing adipocytes. Alterations in PPAR expression have been implicated as a factor in the mechanism of HIV-1-associated lipodystrophy. Both reduced BMD and lipodystrophy have been well described as complications of HIV-1 infection and treatment, and a question remains as to their interdependence. Interestingly, both adipocytes and osteoblasts are derived from a common precursor cell type; the mesenchymal stem cell. The possibility that dysregulation of PPAR (and the subsequent effect on both osteoblastogenesis and adipogenesis) is a contributory factor in the lipid- and bone-abnormalities observed in HIV-1 infection and treatment has also been investigated. This review deals with the hypothesis that dysregulation of PPAR may underpin the bone abnormalities associated with HIV-1 infection, and treats the current knowledge and prospective developments, in our understanding of PPAR involvement in HIV-1-associated bone disease.
A Unique Regulator Contributes to Quorum Sensing and Virulence in Burkholderia cenocepacia
Eoin P. O'Grady, Duber F. Viteri, Pamela A. Sokol
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037611
Abstract: Burkholderia cenocepacia causes chronic and life-threatening respiratory infections in immunocompromized people. The B. cenocepacia N-acyl-homoserine lactone (AHL)-dependent quorum sensing system relies on the production of AHLs by the synthases CepI and CciI while CepR, CciR and CepR2 control expression of many genes important for pathogenesis. Downstream from, and co-transcribed with cepI, lies BCAM1871 encoding a hypothetical protein that was uncharacterized prior to this study. Orthologs of B. cenocepacia BCAM1871 are uniquely found in Burkholderia spp and are conserved in their genomic locations in pathogenic Burkholderia. We observed significant effects on AHL activity upon mutation or overexpression of BCAM1871, although these effects were more subtle than those observed for CepI indicating BCAM1871 acts as an enhancer of AHL activity. Transcription of cepI, cepR and cciIR was significantly reduced in the BCAM1871 mutant. Swimming and swarming motilities as well as transcription of fliC, encoding flagellin, were significantly reduced in the BCAM1871 mutant. Protease activity and transcription of zmpA and zmpB, encoding extracellular zinc metalloproteases, were undetectable in the BCAM1871 mutant indicating a more significant effect of mutating BCAM1871 than cepI. Exogenous addition of OHL restored cepI, cepR and fliC transcription but had no effect on motility, protease activity or zmpA or zmpB transcription suggesting AHL-independent effects. The BCAM1871 mutant exhibited significantly reduced virulence in rat chronic respiratory and nematode infection models. Gene expression and phenotypic assays as well as vertebrate and invertebrate infection models showed that BCAM1871 significantly contributes to pathogenesis in B. cenocepacia.
Hypoxia. Regulation of NFκB signalling during inflammation: the role of hydroxylases
Kathryn M Oliver, Cormac T Taylor, Eoin P Cummins
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2575
Abstract: The transcription factor NFκB has been investigated for its diverse range of functions in innate immunity, stress responses, cell survival and development. It is also the master regulator of the inflammatory response [1]. An in-depth review of the NFκB pathway is beyond the scope of the present article, and there are several excellent reviews dedicated specifically to this topic [2,3].Briefly, the NFκB family comprises five members: p65, Rel B, c-Rel, p50 and p52. These proteins share a highly conserved Rel homology domain. In order to bind DNA and modulate gene expression, family members form homodimers or heterodimers – with the exception of Rel B, which will only form heterodimers with p50 or p52 [4]. The most commonly encountered dimer complex is the p50–p65 dimer [5]. There are two primary activation pathways for NFκB: the canonical pathway, which is predominantly dependent on inhibitor of κB kinase (IKK) beta, and the IKKα-dependent noncanonical pathway [6].Under resting conditions, NFκB is bound to its co-repressor molecule IκB in the cytosol, with which it interacts through multiple ankyrin repeats. A nuclear localisation sequence of the p65 protein is masked and it remains predominantly sequestered in the cytosolic compartment. Upon stimulation IκBα is phosphorylated at serine 32 and serine 36, targeted for ubiquitination and thereafter degraded proteolytically by the 26S proteosome [7]. A nuclear localisation sequence of NFκB is then revealed, and this is free to translocate and accumulate in the nucleus where it can become transcriptionally active by binding to specific κB sites within the promoter regions of its target genes [8]. The stimulus for IκBα to release the inhibition of NFκB has been identified as phosphorylation by the 700 kDa IKKα/β/γ protein complex.Genes induced by NFκB include those responsible for encoding inflammatory genes such as TNFα, IL-1, IL-6, IL-8, macrophage inflammatory protein 1 alpha and methyl-accepting chemotaxis protein 1,
Coronal Mass Ejection Mass, Energy, and Force Estimates Using STEREO
Eoin P. Carley,R. T. James McAteer,Peter T. Gallagher
Physics , 2012, DOI: 10.1088/0004-637X/752/1/36
Abstract: Understanding coronal mass ejection (CME) energetics and dynamics has been a long-standing problem, and although previous observational estimates have been made, such studies have been hindered by large uncertainties in CME mass. Here, the two vantage points of the Solar Terrestrial Relations Observatory (STEREO) COR1 and COR2 coronagraphs were used to accurately estimate the mass of the 2008 December 12 CME. Acceleration estimates derived from the position of the CME front in 3-D were combined with the mass estimates to calculate the magnitude of the kinetic energy and driving force at different stages of the CME evolution. The CME asymptotically approaches a mass of 3.4\pm1.0x10^15 g beyond ~10 R_sun. The kinetic energy shows an initial rise towards 6.3\pm3.7x10^29 erg at ~3 R_sun, beyond which it rises steadily to 4.2\pm2.5x10^30 erg at ~18 R_sun. The dynamics are described by an early phase of strong acceleration, dominated by a force of peak magnitude of 3.4\pm2.2x10^14N at ~3 R_sun, after which a force of 3.8\pm5.4x10^13 N takes affect between ~7-18 R_sun. These results are consistent with magnetic (Lorentz) forces acting at heliocentric distances of <7 R_sun, while solar wind drag forces dominate at larger distances (>7 R_sun).
Derivation of 12- and 14-band $\textbf{k}\cdot\textbf{p}$ Hamiltonians for dilute bismide and bismide-nitride semiconductors
Christopher A. Broderick,Muhammad Usman,Eoin P. O'Reilly
Physics , 2013, DOI: 10.1088/0268-1242/28/12/125025
Abstract: Using an $sp^{3}s^{*}$ tight-binding model we demonstrate how the observed strong bowing of the band gap and spin-orbit-splitting with increasing Bi composition in the dilute bismide alloy GaBi$_{x}$As$_{1-x}$ can be described in terms of a band-anticrossing interaction between the extended states of the GaAs valence band edge and highly localised Bi-related resonant states lying below the GaAs valence band edge. We derive a 12-band $\textbf{k}\cdot\textbf{p}$ Hamiltonian to describe the band structure of GaBi$_{x}$As$_{1-x}$ and show that this model is in excellent agreement with full tight-binding calculations of the band structure in the vicinity of the band edges, as well as with experimental measurements of the band gap and spin-orbit-splitting across a large composition range. Based on a tight-binding model of GaBi$_{x}$N$_{y}$As$_{1-x-y}$ we show that to a good approximation N and Bi act independently of one another in disordered GaBi$_{x}$N$_{y}$As$_{1-x-y}$ alloys, indicating that a simple description of the band structure is possible. We present a 14-band $\textbf{k}\cdot\textbf{p}$ Hamiltonian for ordered GaBi$_{x}$N$_{y}$As$_{1-x-y}$ crystals which reproduces accurately the essential features of full tight-binding calculations of the band structure in the vicinity of the band edges. The $\textbf{k}\cdot\textbf{p}$ models we present here are therefore ideally suited to the simulation of the optoelectronic properties of these novel III-V semiconductor alloys.
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