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- Karlsson, Per Erik, 1957, et al.
(author)
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New critical levels for ozone effects on young trees based on AOT40 and simulated cumulative leaf uptake of ozone
- 2004
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In: Atmospheric Environment. - : Elsevier BV. - 1352-2310. ; 38:15, s. 2283-2294
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Journal article (peer-reviewed)abstract
- Leaf or needle ozone uptake was estimated for young trees at seven experimental sites across Europe using a stomatal conductance simulation model. Dose-response relationships based on cumulative leaf uptake of ozone (CUO) were calculated using different hourly ozone flux thresholds and these were compared to dose-response relationships based on daylight AOT40, which is currently used within the UNECE Convention on Long-Range Transboundary Air Pollution (CLRTAP). Regression analysis showed that the CUO-biomass response relationships were highly significant for both coniferous and broadleaf trees, and independent of which ozone flux threshold was applied. On the basis of this regressions analysis, an hourly flux threshold of 1.6 nmol m(-2) s(-1) (COO > 1.6) is proposed as the most appropriate for all species categories in deriving dose-response relationships. The analysis indicated that the current critical level for ozone impacts on European forests of AOT40 10 ppm h may not protect the most sensitive receptors and that critical levels for AOT40 and CUO > 1.6 of 5 ppm h and 4 mmol m(-2), respectively, are more appropriate. The research identified weaker dose-response relationships for the CUO exposure index compared with AOT40. Distinguishing between sensitive and less sensitive species substantially improved the CUO-biomass response relationships although, still, to a lesser extent than when exposure was expressed as AOT40. (C) 2004 Elsevier Ltd. All rights reserved.
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- Novak, R, et al.
(author)
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Extracellular targeting of choline-binding proteins in Streptococcus pneumoniae by a zinc metalloprotease.
- 2000
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In: Molecular Microbiology. - 0950-382X .- 1365-2958. ; 36:2, s. 366-376
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Journal article (peer-reviewed)abstract
- A genetic-based search for surface proteins of Streptococcus pneumoniae involved in adhesion identified a putative zinc metalloprotease (ZmpB). ZmpB shared high amino acid sequence similarities with IgA1 proteases of Gram-positive bacteria, but ZmpB had neither IgA1 nor IgA2 protease activity. Analysis of a family of surface-expressed proteins, the choline-binding proteins (Cbp's), in a zmpB-deficient mutant demonstrated a global loss of surface expression of CbpA, CbpE, CbpF and CbpJ. CbpA was detected within the cytoplasm. The zmpB-deficient mutant also failed to lyse with penicillin, a sign of lack of function of the Cbp LytA. Immunodetection studies revealed that the autolysin (LytA), normally located on the cell wall, was trapped in the cytoplasm colocalized with DNA and the transformation protein CinA. Trafficking of CinA and RecA to the cell membrane during genetic competence was also not observed in the zmpB-deficient mutant. These results suggest a protease dependent regulatory mechanism governing the translocation of CinA and the Cbp's LytA and CbpA of S. pneumoniae.
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- Minkov, Ivaylo, et al.
(author)
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Core-excitations of naphthalene : Vibrational structure versus chemical shifts
- 2004
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In: Journal of Chemical Physics. - : AIP Publishing. - 0021-9606 .- 1089-7690. ; 121:12, s. 5733-5739
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Journal article (peer-reviewed)abstract
- The initial state chemical shifts and vibrational fine structure of core excitations of naphthalene were analyzed using high-resolution x-ray photoelectron emission (XPS) and near-edge x-ray absorption fine structure (NEXAFS) spectra. The carbon atoms at peripheral sites were found to experience a small chemical shift and exhibit similar charge-vibrational coupling. The C-H stretching modes provide significant contributions to overall shape of spectra in the XPS spectra. The results show that vibrational fine structure dominates by particular C-C stretching modes, and in XPS of C2 and C3 sites also by high-energy C-H stretching modes.
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9. |
- Novak, R, et al.
(author)
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Signal transduction by a death signal peptide : uncovering the mechanism of bacterial killing by penicillin.
- 2000
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In: Molecular Cell. - 1097-2765 .- 1097-4164. ; 5:1, s. 49-57
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Journal article (peer-reviewed)abstract
- The binding of bactericidal antibiotics like penicillins, cephalosporins, and glycopeptides to their bacterial targets stops bacterial growth but does not directly cause cell death. A second process arising from the bacteria itself is necessary to trigger endogenous suicidal enzymes that dissolve the cell wall during autolysis. The signal and the trigger pathway for this event are completely unknown. Using S. pneumoniae as a model, we demonstrate that signal transduction via the two-component system VncR/S triggers multiple death pathways. We show that the signal sensed by VncR/S is a secreted peptide, Pep27, that initiates the cell death program. These data depict a novel model for the control of bacterial cell death.
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10. |
- Wendt, Anna, et al.
(author)
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Glucose Inhibition of Glucagon Secretion From Rat alpha-Cells Is Mediated by GABA Released From Neighboring beta-Cells.
- 2004
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In: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 53:4, s. 1038-1045
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Journal article (peer-reviewed)abstract
- γ-Aminobutyric acid (GABA) has been proposed to function as a paracrine signaling molecule in islets of Langerhans. We have shown that rat β-cells release GABA by Ca2+-dependent exocytosis of synaptic-like microvesicles. Here we demonstrate that GABA thus released can diffuse over sufficient distances within the islet interstitium to activate GABAA receptors in neighboring cells. Confocal immunocytochemistry revealed the presence of GABAA receptors in glucagon-secreting α-cells but not in β- and δ-cells. RT-PCR analysis detected transcripts of α1 and α4 as well as β1–3 GABAA receptor subunits in purified α-cells but not in β-cells. In whole-cell voltage-clamp recordings, exogenous application of GABA activated Cl− currents in α-cells. The GABAA receptor antagonist SR95531 was used to investigate the effects of endogenous GABA (released from β-cells) on pancreatic islet hormone secretion. The antagonist increased glucagon secretion at 1 mmol/l glucose twofold and completely abolished the inhibitory action of 20 mmol/l glucose on glucagon release. Basal and glucose-stimulated secretion of insulin and somatostatin were unaffected by SR95531. The L-type Ca2+ channel blocker isradipine evoked a paradoxical stimulation of glucagon secretion. This effect was not observed in the presence of SR95531, and we therefore conclude that isradipine stimulates glucagon secretion by inhibition of GABA release.
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