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- Abbas, Abdul-Karim, 1959, et al.
(författare)
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Bicarbonate-sensitive cysteine induced elevation of extracellular aspartate and glutamate in rat hippocampus in vitro
- 1997
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Ingår i: Neurochemistry International. - 0197-0186. ; 30:3, s. 253-259
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Tidskriftsartikel (refereegranskat)abstract
- The effect of different concentrations of cysteine (0.125, 0.25, 0.5 and 1 mM) on the net efflux of endogenous amino acids was studied by the incubation of rat hippocampal slices. Addition of cysteine (1 mM) in bicarbonate containing low K+ medium (5 min) selectively increased the basal net efflux of glutamate and aspartate by 370% and 396%, respectively. High K+ media (50 mM) containing cysteine (1 mM) evoked the net efflux of glutamate and aspartate by 1 454% and 1 019%, respectively. The corresponding effects in control slices without cysteine were 669% and 404%, respectively. No changes were observed on the concentrations of GABA, glutamine and taurine. The cysteine oxidation products, cysteine sulfinate (0.5 μM) and cystine (0.25 mM) were without effects. The effect of cysteine (0.5 mM) was dramatically reduced in media with no added bicarbonate/CO2. Thus, cysteine in a bicarbonate-sensitive manner selectively increases the extracellular concentration of excitotoxic amino acids in adult rat brain in vitro, possibly by interfering with the carrier-mediated glutamate uptake/ release
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| 2. |
- Abel, Frida, 1974, et al.
(författare)
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Gain of chromosome arm 17q is associated with unfavourable prognosis in neuroblastoma, but does not involve mutations in the somatostatin receptor 2(SSTR2) gene at 17q24.
- 1999
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Ingår i: British journal of cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 81:8, s. 1402-9
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Tidskriftsartikel (refereegranskat)abstract
- Deletion of chromosome arm 1p and amplification of the MYCN oncogene are well-recognized genetic alterations in neuroblastoma cells. Recently, another alteration has been reported; gain of the distal part of chromosome arm 17q. In this study 48 neuroblastoma tumours were successfully analysed for 17q status in relation to known genetic alterations. Chromosome 17 status was detected by fluorescence in situ hybridization (FISH). Thirty-one of the 48 neuroblastomas (65%) showed 17q gain, and this was significantly associated with poor prognosis. As previously reported, 17q gain was significantly associated with metastatic stage 4 neuroblastoma and more frequently detected than both deletion of chromosome arm 1p and MYCN amplification in tumours of all stages. 17q gain also showed a strong correlation to survival probability (P = 0.0009). However, the most significant correlation between 17q gain and survival probability was observed in children with low-stage tumours (stage 1, 2, 3 and 4S), with a survival probability of 100% at 5 years from diagnosis for children with tumours showing no 17q gain compared to 52.5% for those showing 17q gain (P = 0.0021). This suggests that 17q gain as a prognostic factor plays a more crucial role in low-stage tumours. Expression of the somatostatin receptor 2 (SSTR2), localized in chromosome region 17q24, has in previous studies been shown to be positively related to survival in neuroblastoma. A point mutation in the SSTR2 gene has earlier been reported in a human small-cell lung cancer. In this study, mutation screening of the SSTR2 gene in 43 neuroblastoma tumours was carried out with polymerase chain reaction-based single-stranded conformation polymorphism/heteroduplex (SSCP/HD) and DNA sequencing, and none of the tumours showed any aberrations in the SSTR2 gene. These data suggest that mutations in the SSTR2 gene are uncommon in neuroblastoma tumours and do not correlate with either the 17q gain often seen or the reason some tumours do not express SSTR2 receptors. Overall, this study indicates that gain of chromosome arm 17q is the most frequently occurring genetic alteration, and that it is associated with established prognostic factors.
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| 3. |
- Acke, Filip, et al.
(författare)
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Study of the reduction and reoxidation of a CaO surface
- 1997
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Ingår i: J Phys Chem B. - 1520-5207 .- 1520-6106. ; 101:33
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Tidskriftsartikel (refereegranskat)abstract
- The reduction of NO with CO and H2 is shown to comprise two basic reactions: a surface oxygen abstraction by the reducing agent and a reoxidation of the surface by NO. The former reaction step has been demonstrated by transient CO2 formation during CO exposure of oxidized CaO surfaces, while the latter was demonstrated by N2 and/or N2O transient formation during NO exposure of a prereduced CaO surface. It was shown that at low temperatures (between room temperature and 500 °C) both N2 and N2O were formed, but at temperatures above 500 °C only N2 was observed. The activation energies of the respective steps have been determined using temperature-programmed reaction experiments. The activation energy of the surface oxygen abstraction was determined to be 25 kcal/mol and is similar to the apparent activation energy of the overall reaction. The activation energy of the NO bond breakage was determined to be maximum 10 kcal/mol as measured by N2O formation. The importance of an N2O2- or N2O22- intermediate in the formation of N2O will be discussed, and the importance of N2O decomposition in forming N2 at temperatures above 500 °C will be compared with a N surface diffusion mechanism.
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| 8. |
- Ansell, R, et al.
(författare)
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The two isoenzymes for yeast NAD+-dependent glycerol 3-phosphate dehydrogenase encoded by GPD1 and GPD2 have distinct roles in osmoadaptation and redox regulation.
- 1997
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Ingår i: The EMBO journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 16:9, s. 2179-87
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Tidskriftsartikel (refereegranskat)abstract
- The two homologous genes GPD1 and GPD2 encode the isoenzymes of NAD-dependent glycerol 3-phosphate dehydrogenase in the yeast Saccharomyces cerevisiae. Previous studies showed that GPD1 plays a role in osmoadaptation since its expression is induced by osmotic stress and gpd1 delta mutants are osmosensitive. Here we report that GPD2 has an entirely different physiological role. Expression of GPD2 is not affected by changes in external osmolarity, but is stimulated by anoxic conditions. Mutants lacking GPD2 show poor growth under anaerobic conditions. Mutants deleted for both GPD1 and GPD2 do not produce detectable glycerol, are highly osmosensitive and fail to grow under anoxic conditions. This growth inhibition, which is accompanied by a strong intracellular accumulation of NADH, is relieved by external addition of acetaldehyde, an effective oxidizer of NADH. Thus, glycerol formation is strictly required as a redox sink for excess cytosolic NADH during anaerobic metabolism. The anaerobic induction of GPD2 is independent of the HOG pathway which controls the osmotic induction of GPD1. Expression of GPD2 is also unaffected by ROX1 and ROX3, encoding putative regulators of hypoxic and stress-controlled gene expression. In addition, GPD2 is induced under aerobic conditions by the addition of bisulfite which causes NADH accumulation by inhibiting the final, reductive step in ethanol fermentation and this induction is reversed by addition of acetaldehyde. We conclude that expression of GPD2 is controlled by a novel, oxygen-independent, signalling pathway which is required to regulate metabolism under anoxic conditions.
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| 9. |
- Asadzadeh, Mohammad, 1952
(författare)
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A finite element method for the neutron transport equation in an infinite cylindrical domain
- 1998
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Ingår i: SIAM Journal on Numerical Analysis. ; 35:4, s. 1299-1314
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Tidskriftsartikel (refereegranskat)abstract
- We study the spatial discretization, in a fully discrete scheme, for the numerical solution of a model problem for the neutron transport equation in an infinite cylindrical domain. Based on using an interpolation technique in the discontinuous Galerkin finite element procedure, we derive an almost optimal error estimate for the scalar flux in the L2-norm. Combining a duality argument applied to the above result together with the previous semidiscrete error estimates for the velocity discretizations, we also obtain globally optimal error bounds for the critical eigenvalues.
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| 10. |
- Asadzadeh, Mohammad, 1952
(författare)
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Streamline diffusion methods for the Fermi and Fokker-Planck equations
- 1997
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Ingår i: Transport Theory and Statistical Physics. ; 26:3, s. 319-340
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Tidskriftsartikel (refereegranskat)abstract
- e derive error estimates in certain weighted L2-norms for the streamline diffusion and discontinuous Galerkin finite element methods for steady state, energy dependent, Fermi and Fokker-Planck equations in two space dimensions, giving error bounds of order O(hk+1/2), for the weighted current function J, as in the convection dominated convection-diffusion problems, with J ε Hk+1(Ω) and h being the quasi-uniform mesh size in triangulation of our three dimensional phase-space domain Ω = Iz, times Iy times Iz, with z corresponding to the velocity variable. Our studies, in this paper, contain a priori error estimates for Fermi and Fokker-Planck equations with both piecewise continuous and piecewise discontinuous (in x and xy-directions) trial functions. The analyses are based on stability estimates which relay on an angular symmetry (not isotropy!) assumption. A continuation of this paper, the a posteriori error estimates for Fermi and Fokker-Planck equations, is the subject of a future work.
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