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- Markenroth, Karin, 1973, et al.
(author)
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Crossing the dripline to N-11 using elastic resonance scattering
- 2000
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In: Physical Review C - Nuclear Physics. - 2469-9985 .- 2469-9993. ; 6203:3
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Journal article (peer-reviewed)abstract
- The level structure of the unbound nucleus N-11 has been studied by C-10+p elastic resonance scattering in inverse geometry with the LISE3 spectrometer at GANIL, using a C-10 beam with an energy of 9.0 MeV/ nucleon. An additional measurement was done at the A1200 spectrometer at MSU. The excitation function above the C-10+p threshold has been determined up to 5 MeV. A potential-model analysis revealed three resonance states at energies 1.27(-0.05)(+0.18) MeV (Gamma = 1.44 +/- 0.2 MeV), 2.01(-0.05)(+0.15) MeV (Gamma = 0.84 +/- 0.2 MeV), and 3.75 +/- 0.05 MeV (Gamma = 0.60 +/- 0.05 MeV) with the spin-parity assignments I-pi=1/2+,1/2,-,5/2+, respectively. Hence, N-11 is shown to have a ground state parity inversion completely analogous to its mirror partner Be-11. A narrow resonance in the excitation function at 4.33 +/- 0.05 MeV was also observed and assigned spin parity 3/2-.
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- Steiner, H, et al.
(author)
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An autocrine loop for vascular endothelial growth factor is established in prostate cancer cells generated after prolonged treatment with interleukin 6
- 2004
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In: European Journal of Cancer. - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 40:7, s. 1066-1072
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Journal article (peer-reviewed)abstract
- Concentrations of interleukin 6 (IL-6) and its receptor are increased in human prostate cancer. Prostate cancer LNCaP-IL-6+ cells, established after prolonged treatment with IL-6, have been found to acquire a growth advantage. Vascular endothelial growth factor (VEGF) may accelerate the growth of various tumours by stimulation of VEGF receptor 2 (VEGFR-2). To understand better the regulation of proliferation of LNCaP-IL-6+ cells, the expression of VEGF and VEGFR-2 was here investigated in the LNCaP-IL-6+ subline. VEGF was measured in cellular supernatants by enzyme-linked immunoassay. The expression of VEGFR-2 was assessed by Western blot. LNCaP-IL-6+ and control LNCaP-IL-6- cells were treated with a neutralising antibody against VEGFR-2. VEGF concentrations were 20-fold higher in LNCaP-IL-6+ than in LNCaP-IL-6- cells. The stimulatory effect of IL-6 on VEGF production was abolished by an inhibitor of the signalling pathway for phosphoinositol 3 kinase in LNCaP-IL-6+ and LNCaP-IL-6- cells. Exogenous VEGF did not stimulate proliferation in either LNCaP-IL-6+ cells or controls. VEGFR-2 was detected only in LNCaP-IL-6+ cells, in which the neutralising antibody caused a partial inhibition of cell proliferation. It was concluded that a VEGF autocrine loop is established in prostate cancer cells generated after chronic treatment with IL-6. Because of the upregulation of IL-6 in patients with prostate cancer, these findings might be clinically relevant.
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