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Search Results: 1 - 10 of 193401 matches for " David B Ramsden "
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Nicotinamide, NAD(P)(H), and Methyl-Group Homeostasis Evolved and Became a Determinant of Ageing Diseases: Hypotheses and Lessons from Pellagra
Adrian C. Williams,Lisa J. Hill,David B. Ramsden
Current Gerontology and Geriatrics Research , 2012, DOI: 10.1155/2012/302875
Abstract: Compartmentalized redox faults are common to ageing diseases. Dietary constituents are catabolized to NAD(H) donating electrons producing proton-based bioenergy in coevolved, cross-species and cross-organ networks. Nicotinamide and NAD deficiency from poor diet or high expenditure causes pellagra, an ageing and dementing disorder with lost robustness to infection and stress. Nicotinamide and stress induce Nicotinamide-N-methyltransferase (NNMT) improving choline retention but consume methyl groups. High NNMT activity is linked to Parkinson’s, cancers, and diseases of affluence. Optimising nicotinamide and choline/methyl group availability is important for brain development and increased during our evolution raising metabolic and methylome ceilings through dietary/metabolic symbiotic means but strict energy constraints remain and life-history tradeoffs are the rule. An optimal energy, NAD and methyl group supply, avoiding hypo and hyper-vitaminoses nicotinamide and choline, is important to healthy ageing and avoids utilising double-edged symbionts or uncontrolled autophagy or reversions to fermentation reactions in inflammatory and cancerous tissue that all redistribute NAD(P)(H), but incur high allostatic costs. 1. Introduction “Progress engenders Leisure whereby Energy is directed toward advancement of the Mind in all parts of Society that in turn receives new Energy.” Turgot, 1750. “In my theory there is no absolute tendency to Progress, except from favourable Circumstances” Darwin, 1838. Mental and neurological disorders are poorly explained yet constitute a good proportion of the global burden of disease, now defined as the inability to adapt homeostatically in the face of social, physical, and emotional challenges [1–3]. Robust brain development in the first place must help and is defined by environmental factors and cell types that evolve in a series of networks to ensure the efficient flow of energy and information [4–6]. Energy supplies from food are a prerequisite for producing the necessary variety of cells and simultaneously act as a major selection force influencing their survival; yet despite its importance to brain evolution and development inequalities of diet, particularly over meat and calorific intake, remain a global issue, as do stress responses such as overeating [7–11]. Bidirectional circuits, from the energy supply to terminal fields, are selected from early exuberant developmental (but evolutionarily constrained) fields by environmental exposures but must have weak links as strong safety factors against every eventuality whether
Aquaporin-4 autoantibodies in neuromyelitis optica spectrum disorders: comparison between tissue-based and cell-based indirect immunofluorescence assays
Koon H Chan, Jason SC Kwan, Philip WL Ho, Jessica WM Ho, Andrew CY Chu, David B Ramsden
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-50
Abstract: Serum of Chinese CNS IDD patients were assayed for AQP4 autoantibodies by tissue-based IIFA using monkey cerebellum and cell-based IIFA using transfected HEK293 cells which express human AQP4 on their cell membranes.In total, 128 CNS IDD patients were studied. We found that 78% of NMO patients were seropositive for AQP4 autoantibodies by cell-based IIFA versus 61% by tissue-based IFA (p = 0.250), 75% of patients having relapsing myelitis (RM) with LETM were seropositive by cell-based IIFA versus 50% by tissue-based IIFA (p = 0.250), and 33% of relapsing ON patients were seropositive by cell-based IIFA versus 22% by tissue-based IIFA (p = 1.000); however the differences were not statistically significant. All patients seropositive by tissue-based IIFA were also seropositive for AQP4 autoantibodies by cell-based IIFA. Among 29 NMOSD patients seropositive for AQP4 autoantibodies by cell-based IIFA, 20 (69%) were seropositive by tissue-based IIFA. The 9 patients seropositive by cell-based IIFA while seronegative by tissue-based IIFA had NMO (3), RM with LETM (3), a single attack of LETM (1), relapsing ON (1) and a single ON attack (1). Among 23 NMO or RM patients seropositive for AQP4 autoantibodies by cell-based IIFA, comparison between those seropositive (n = 17) and seronegative (n = 6) by tissue-based IIFA revealed no differences in clinical and neuroradiological characteristics between the two groups.Cell-based IIFA is slightly more sensitive than tissue-based IIFA in detection of AQP4 autoantibodies, which are highly specific for NMOSD.Neuromyelitis optica (NMO) is a severe central nervous system inflammatory demyelinating disorder (CNS IDD) characterized by monophasic or relapsing optic neuritis (ON) and acute transverse myelitis (ATM) [1-6]. Relapsing NMO is the predominant type, which can mimic relapsing remitting multiple sclerosis (RRMS), the predominant form of classical multiple sclerosis (CMS), on initial presentation [2-8]. Typical relapsing NMO patients
Mitochondrial neuronal uncoupling proteins: a target for potential disease-modification in Parkinson's disease
Philip WL Ho, Jessica WM Ho, Hui-Fang Liu, Danny HF So, Zero HM Tse, Koon-Ho Chan, David B Ramsden, Shu-Leong Ho
Translational Neurodegeneration , 2012, DOI: 10.1186/2047-9158-1-3
Abstract: Parkinson's disease (PD) is a common neurodegenerative disorder and increasingly a major burden in an aging population. Although its pathogenesis is unknown, there is evidence to implicate common pathogenic processes towards eventual cell death in PD. These processes include mitochondrial dysfunction, oxidative stress, neuroinflammation, excitotoxicity, and ubiquitin proteasome dysfunction [1-4].There is considerable evidence to link mitochondrial dysfunction and PD. Mitochondrial Complex I activity is reduced in substantia nigra in PD [5]. Inhibition of Complex I activity using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone (both toxins used in experimental parkinsonian models) produce nigrostriatal dopaminergic degeneration in animal models [6,7]. Cybrid cell lines with normal nuclear genome but with mitochondrial DNA from PD patients have reduced Complex I activity and mitochondrial energy-dependent activities [8], have abnormal mitochondrial morphology [9], and are more susceptible to MPTP-induced toxicity. The process of aging involves the mitochondria [10]. Furthermore, dopamine metabolism and mitochondrial dysfunction generate oxidative stress. High basal levels of oxidative stress in substantia nigra are found in normal brain, and are increased in PD. Furthermore, antioxidant activity, such as glutathione (GSH), is reduced in substantia nigra of PD patients [11,12]. Based on the hypothesis that various genetic and environmental etiological factors converge on these common pathogenic processes in PD, targeting proteins which modulate mitochondria bioenergetics appears to be a logical approach in preserving neurons against mitochondrial dysfunction in PD.Mitochondria are rod-shaped cellular organelles, which range in size from between 1 and 10 microns in length. They provide cellular energy by converting oxygen and nutrients into adenosine triphosphate (ATP) via oxidative phosphorylation. Human cells have hundreds to thousands of mitochondria
Learning with the community. Evolution to transformative action research.
Ramsden VR
Canadian Family Physician , 2003,
Abstract:
Multi-norms and modules over group algebras
Paul Ramsden
Mathematics , 2009,
Abstract: Let G be a locally compact group, and let 1 < p < \infty. In this paper we investigate the injectivity of the left L^1(G)-module L^p(G). We define a family of amenability type conditions called (p,q)-amenability, for any 1 <= p <= q. For a general locally compact group G we show if L^p(G) is injective, then G must be (p,p)-amenable. For a discrete group G we prove that l^p(G) is injective if and only if G is (p,p)-amenable.
Selegiline increases heme oxygenase-1 expression and the cytotoxicity produced by dopamine treatment of neuroblastoma SK-N-SH cells
Rieder, C.R.M.;Williams, A.C.;Ramsden, D.B.;
Brazilian Journal of Medical and Biological Research , 2004, DOI: 10.1590/S0100-879X2004000700015
Abstract: increased dopamine catabolism may be associated with oxidative stress and neuronal cell death in parkinson's disease. the present study was carried out to examine the effect of dopamine on the expression of heme oxygenase-1 and -2 (ho-1 and ho-2) in human neuroblastomas (sk-n-sh cell line) and the effects of selegiline and antioxidants on this expression. cells were kept with close control of ph and were incubated with varying concentrations of dopamine (0.1-100 μm) for 24 h. ho-1 and ho-2 cdna probes were prepared by reverse transcription-polymerase chain reaction amplification. the mrna expression of ho-1 and ho-2 was measured by northern blot analysis. the levels of ho-1 mrna increased after dopamine treatment, in a dose-dependent manner, in all cell lines studied, whereas levels of the two ho-2 transcripts did not. the ho-1 and ho-2 protein expression was analyzed by western blotting. ho-1 protein was undetectable in untreated sk-n-sh cells and increased after treatment with dopamine. in contrast, the ho-2 protein (36 kda) was detected in untreated cells and the levels did not change as a result of treatment. a-tocopherol (10-100 μm) and ascorbic acid (100 μm) did not attenuate the effects of dopamine. selegiline (10 μm) produced significant increase (p < 0.01) in the induction of ho-1 by dopamine (more than six times the control values). the increased expression of ho-1 following dopamine treatment indicates that dopamine produces oxidative stress in this cell line.
Selegiline increases heme oxygenase-1 expression and the cytotoxicity produced by dopamine treatment of neuroblastoma SK-N-SH cells
Rieder C.R.M.,Williams A.C.,Ramsden D.B.
Brazilian Journal of Medical and Biological Research , 2004,
Abstract: Increased dopamine catabolism may be associated with oxidative stress and neuronal cell death in Parkinson's disease. The present study was carried out to examine the effect of dopamine on the expression of heme oxygenase-1 and -2 (HO-1 and HO-2) in human neuroblastomas (SK-N-SH cell line) and the effects of selegiline and antioxidants on this expression. Cells were kept with close control of pH and were incubated with varying concentrations of dopamine (0.1-100 μM) for 24 h. HO-1 and HO-2 cDNA probes were prepared by reverse transcription-polymerase chain reaction amplification. The mRNA expression of HO-1 and HO-2 was measured by Northern blot analysis. The levels of HO-1 mRNA increased after dopamine treatment, in a dose-dependent manner, in all cell lines studied, whereas levels of the two HO-2 transcripts did not. The HO-1 and HO-2 protein expression was analyzed by Western blotting. HO-1 protein was undetectable in untreated SK-N-SH cells and increased after treatment with dopamine. In contrast, the HO-2 protein (36 kDa) was detected in untreated cells and the levels did not change as a result of treatment. alpha-Tocopherol (10-100 μM) and ascorbic acid (100 μM) did not attenuate the effects of dopamine. Selegiline (10 μM) produced significant increase (P < 0.01) in the induction of HO-1 by dopamine (more than six times the control values). The increased expression of HO-1 following dopamine treatment indicates that dopamine produces oxidative stress in this cell line.
Exact time-dependent density-functional potentials for strongly correlated tunneling electrons
Matthew J. P. Hodgson,James D. Ramsden,Jacob B. J. Chapman,Piers Lillystone,Rex W Godby
Physics , 2013, DOI: 10.1103/PhysRevB.88.241102
Abstract: By propagating the many-body Schr\"odinger equation, we determine the exact time-dependent Kohn-Sham potential for a system of strongly correlated electrons which undergo field-induced tunneling. Numerous features are entirely absent from the approximations commonly used in time-dependent density-functional theory. The self-interaction correction is strong and time dependent, owing to electron localization, and prominent dynamic spatial potential steps arise from minima in the charge density, as modified by the Coulomb interaction experienced by the partially tunneled electron.
Hypothesis: the research page. Participatory action research.
Cave AJ,Ramsden VR
Canadian Family Physician , 2002,
Abstract:
On singularities of the inverse problems associated with perfect cuboids
John Ramsden,Ruslan Sharipov
Mathematics , 2012,
Abstract: Two cubic equations and three auxiliary equations for edges and face diagonals of a rational perfect cuboid have been recently derived. They constitute a background for two inverse problems. The coefficients of cubic equations and the right hand sides of auxiliary equations are rational functions of two rational parameters, i. e. they have denominators. Hence the inverse problems have singular points. These singular points are studied in the present paper.
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