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Träfflista för sökning "WFRF:(Anna P.) srt2:(1995-1999)"

Sökning: WFRF:(Anna P.) > (1995-1999)

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  • Sohler, D., et al. (författare)
  • Yrast states of the proton drip line nucleus 106 Sb
  • 1999
  • Ingår i: Physical Review C - Nuclear Physics. - 2469-9985 .- 2469-9993 .- 0556-2813 .- 1089-490X. ; 59:3, s. 1324-1327
  • Tidskriftsartikel (refereegranskat)abstract
    • Yrast states of [Formula Presented] have been investigated in the [Formula Presented] reaction using in-beam [Formula Presented]-spectroscopic methods and in the [Formula Presented] reaction performing delayed [Formula Presented] and conversion electron studies. A new isomeric state was found at 103 keV with [Formula Presented] The number of states and transitions in the proposed level scheme have been doubled. The experimental results are discussed within the framework of the shell model. © 1999 The American Physical Society.
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  • Gestblom, C, et al. (författare)
  • The basic helix-loop-helix transcription factor dHAND, a marker gene for the developing human sympathetic nervous system, is expressed in both high- and low-stage neuroblastomas
  • 1999
  • Ingår i: Laboratory Investigation. - 1530-0307 .- 0023-6837. ; 79, s. 67-
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuroblastoma is derived from the sympathetic nervous system and might arise as a result of impaired differentiation, retaining the neuroblastic tumor cells in the cell cycle. Thus, to understand the genesis of neuroblastoma, the study of mechanisms and genes regulating normal sympathetic development is of potential interest. The basic helix-loop-helix transcription factors human achaete-scute homolog-1 (HASH-1) and deciduum, heart, autonomic nervous system, and neural crest derivatives (dHAND) are expressed in the sympathetic nervous system of embryonic mice and chicken, with undetectable postnatal expression. By in situ hybridization technique, we show that dHAND was expressed by human sympathetic neuronal and extra-adrenal chromaffin cells throughout embryonic and fetal life, and was initially expressed in immature chromaffin cells of the adrenal gland. With overt chromaffin differentiation, dHAND was down-regulated. HASH-1, in contrast, was expressed in human sympathetic cells only at the earliest embryonic ages examined (Week 6.5 to 7). All examined neuroblastoma specimens (25/25) and all cell lines (5/5) had detectable dHAND mRNA levels. HASH-1 expression in tumor specimens was more restricted, although all cell lines (5/5) were HASH-1-positive. These results show that neuroblastoma tumors have retained embryonic features, suggesting that many neuroblastomas are blocked at an early stage of normal development when HASH-1 and dHAND are expressed. dHAND also appears to be a reliable and potentially useful clinical diagnostic marker for neuroblastoma, because expression was not dependent on tumor or differentiation stages and other pediatric tumors were dHAND-negative.
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  • Harbecke, Olle, 1966, et al. (författare)
  • Desensitization of formyl peptide receptors is abolished in calcium ionophore-primed neutrophils: an association of the ligand-receptor complex to the cytoskeleton is not required for a rapid termination of the NADPH-oxidase response.
  • 1998
  • Ingår i: Journal of immunology (Baltimore, Md. : 1950). - 0022-1767. ; 160:5, s. 2463-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Binding of ligands to N-formyl peptide chemoattractant receptors exposed on human neutrophils generates signals in the cells that induce an activation of the superoxide anion producing NADPH-oxidase. Ligand binding is followed by a rapid association of the ligand-receptor complex with the cytoskeleton, a process leading to desensitization of the cells with respect to NADPH-oxidase activation. We show that neutrophils that have experienced an intracellular calcium rise obtained through interaction with the calcium-specific ionophore ionomycin are "primed" with respect to the FMLP-induced production of superoxide anions. Mobilization of FMLP receptors from intracellular pools is one well-known mechanism behind the primed response. Based on our finding that ionomycin-treated neutrophils could not be desensitized, we suggest that the lack of association between the ligand-receptor complex and the cytoskeleton is an additional priming mechanism. Since in vivo-exudated neutrophils, which also had mobilized intracellular organelles, could be desensitized, we suggest that the abolished desensitization in ionomycin-treated neutrophils is not due to an inability of newly recruited receptors to couple to the cytoskeleton. We show that a rapid termination of FMLP-induced superoxide anion production is obtained in both desensitizable and nondesensitizable neutrophils, suggesting that the desensitization phenomenon is of limited importance in the oxidase termination process.
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  • Holmes, Janet M, et al. (författare)
  • The effects of the metal ions Mn2+ and Co2+ on muscle contraction in the Norway lobster, Nephrops norvegicus (L.)
  • 1999
  • Ingår i: Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology. - : Springer Science and Business Media LLC. - 0174-1578 .- 1432-136X. ; 169, s. 402-410
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects of the metal ions manganese and cobalt on force production by the abdominal superficial flexor muscle of the Norway lobster, Nephrops norvegicus, have been studied in response to both neuronal stimulation and electrical field stimulation applied to an isolated neuromuscular preparation, and by selectively blocking synaptic transmission with Ivermectin. In response to both forms of stimulation, low concentrations of manganese added to the standard N. norvegicus saline increased the contractile force produced by the muscle, whereas higher concentrations of manganese inhibited both responses in a dose-dependent manner, until force was completely abolished at concentrations above 2.9 mM manganese. Cobalt ions produced similar effects, and no significant difference was found between the concentration of the two ions at 50% force inhibition (K-m) or between the two stimulation methods (manganese: 1.22 mM; cobalt: 1.29 mM, P = 0.86). This suggests that they have a similar mode of action, and a postsynaptic site of inhibition. These K-m values are considerably higher than the concentrations of these ions known to accumulate in the haemolymph of N. norvegicus under eutrophic conditions, and it therefore seems unlikely that accumulations of manganese or cobalt ions under such conditions would cause any significant inhibition of muscle contraction force.
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  • Jensen, T, et al. (författare)
  • Cultured rat and purified human Pneumocystis carinii stimulate intra- but not extracellular free radical production in human neutrophils.
  • 1998
  • Ingår i: The Journal of eukaryotic microbiology. - 1066-5234. ; 45:5, s. 544-7
  • Tidskriftsartikel (refereegranskat)abstract
    • The production of free radicals in human neutrophils was studied in both Pneumocystis carinii derived from cultures of L2 rat lung epithelial-like cells and Pneumocystis carinii purified from human lung. Using the cytochrome C technique, which selectively measured extracellular superoxide generation, hardly any free radical production was observed after stimulation with cultured rat-derived P. carinii. A chemiluminescence technique, which separately measured intra- and extracellular free radical production, was subsequently employed to differentiate the free radical generation. It was established that 1) P. carinii stimulated intra- but not extracellular free radical production in human neutrophils, 2) opsonized cultured rat-derived P. carinii stimulated human neutrophils to a strong intracellular response of superoxide production, and 3) opsonized P. carinii, purified from human lung also stimulated human neutrophils to produce intracellular free radicals.
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  • Karlsson, Anna, 1967, et al. (författare)
  • Galectin-3 activates the NADPH-oxidase in exudated but not peripheral blood neutrophils.
  • 1998
  • Ingår i: Blood. - 0006-4971. ; 91:9, s. 3430-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Galectin-3, a lactose-binding mammalian lectin that is secreted from activated macrophages, basophils, and mast cells, was investigated with respect to its ability to activate the human neutrophil NADPH-oxidase. The galectin-3-induced activity was determined with in vivo exudated cells (obtained from a skin chamber) and compared with that of peripheral blood neutrophils. Galectin-3 was found to be a potent activator of the NADPH-oxidase only in exudated neutrophils and the binding of galectin-3 to the surface of these cells was increased compared with peripheral blood cells. Different in vitro priming protocols resulting in degranulation were used to mimic the exudation process in terms of increasing the receptor exposure on the cell surface. Galectin-3 could induce an oxidative response similar to that in exudated cells only after a significant amount of the intracellular organelles had been mobilized. This increase in oxidative response was paralleled by an increased binding of galectin-3 to the surface of the cells. The major conclusion of the study is that galectin-3 is a potent stimulus of the neutrophil respiratory burst, provided that the cells have first experienced an extravasation process. The results also imply that the neutrophil response to galectin-3 could be mediated through receptors mobilized from intracellular granules, and we report the presence of galectin-3-binding proteins in such organelles.
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  • Karlsson, Anna, 1967, et al. (författare)
  • Neutrophil alkaline phosphatase activity increase in bacterial infections is not associated with a general increase in secretory vesicle membrane components.
  • 1995
  • Ingår i: Infection and immunity. - 0019-9567. ; 63:3, s. 911-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The content of alkaline phosphatase (ALP) was determined in neutrophils isolated from patients with acute bacterial infections by a standard enzyme assay. Compared with control cells, patient cells exhibited about a fivefold increase in ALP activity. There was no difference between the ALP Km values of control and patient cells, which indicates that the elevated activity in patient cells was due to the presence of increased amounts of the enzyme. The ALP isozyme in both cell types was determined to be the tissue-unspecific ALP. The fact that much of the ALP activity was measurable only in the presence of detergent suggested that the enzyme was localized in the secretory vesicles, a putative reservoir of plasma membrane components. The amount and subcellular distribution of two other secretory vesicle membrane proteins, i.e., cytochrome b and complement receptor 3, were not altered; hence, we conclude that there was no general increase in amounts of secretory vesicle membrane constituents in the patient cells.
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