| 1. |
- Keller, H., et al.
(author)
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Search for Forbidden Beta-Decays of the Drip-Line Nucleus Be-12
- 1994
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In: Zeitschrift fur Physik A Hadrons and Nuclei. - 1431-5831 .- 0939-7922. ; 348:1, s. 61-62
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Journal article (peer-reviewed)abstract
- Beta-coincident gamma-rays have been measured from implanted pure samples of Be-12 separated at the LISE3 spectrometer at GANIL. An intensity of 0.040(26)% can be estimated for the branching ratio of the isospin forbidden pure-Fermi transition to the 0+ excited state of B-12 and of 0.008(6) % of the transition to the 1- excited state. Both are taken to represent upper limits. The halflife has been re-measured to be 26.1(2.4) ms.
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| 4. |
- Blume-Jensen, Peter, et al.
(author)
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Activation of the human c-kit product by ligand-induced dimerization mediates circular actin reorganization and chemotaxis
- 1991
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In: EMBO Journal. - 0261-4189 .- 1460-2075. ; 10:13, s. 4121-4128
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Journal article (peer-reviewed)abstract
- The proto-oncogene c-kit is allelic with the murine white spotting (W) locus and encodes a transmembrane protein tyrosine kinase that is structurally related to the receptors for platelet-derived growth factor (PDGF) and colony-stimulating factor-1 (CSF-1). Recently the ligand for the c-kit product, stem cell factor (SCF), was identified in both transmembrane and soluble forms. In order to examine the mechanism for receptor activation by SCF and biological properties of the activated c-kit product, we transfected the wild-type human c-kit cDNA into porcine aortic endothelial cells. We found that the receptor was down-regulated and transmitted a mitogenic signal in response to stimulation with soluble SCF. We also demonstrate that SCF induces dimerization of the c-kit product in intact cells, and that dimerization of the receptor is correlated with activation of its kinase. Activation of the c-kit product by SCF was found to induce circular actin reorganization indistinguishable from that mediated by the PDGF beta-receptor in response to PDGF-BB. Furthermore, soluble SCF was a potent chemotactic agent for cells expressing the c-kit product, a property which might be of importance during embryonic development.
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| 5. |
- Elhassan, I M, et al.
(author)
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Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria
- 1994
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In: American Journal of Tropical Medicine and Hygiene. - : American Society of Tropical Medicine and Hygiene. - 1476-1645 .- 0002-9637. ; 51:3, s. 9-372
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Journal article (peer-reviewed)abstract
- To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplication P. falciparum malaria, as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.
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