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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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- Ekengren, Sophia, et al.
(author)
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A humoral stress response in Drosophila.
- 2001
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In: Curr Biol. - 0960-9822. ; 11:9, s. 714-8
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Journal article (peer-reviewed)abstract
- The ability to react to unfavorable environmental changes is crucial for survival and reproduction, and several adaptive responses to stress have been conserved during evolution [1-3]. Specific immune and heat shock responses mediate the elimination of invading pathogens and of damaged proteins or cells [4-6]. Furthermore, MAP kinases and other signaling factors mediate cellular responses to a very broad range of environmental insults [7-9]. Here we describe a novel systemic response to stress in Drosophila. The Turandot A (TotA) gene encodes a humoral factor, which is secreted from the fat body and accumulates in the body fluids. TotA is strongly induced upon bacterial challenge, as well as by other types of stress such as high temperature, mechanical pressure, dehydration, UV irradiation, and oxidative agents. It is also upregulated during metamorphosis and at high age. Strikingly, flies that overexpress TotA show prolonged survival and retain normal activity at otherwise lethal temperatures. Although TotA is only induced by severe stress, it responds to a much wider range of stimuli than heat shock genes such as hsp70 or immune genes such as Cecropin A1.
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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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- Westermark, Gunilla, et al.
(author)
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Islet amyloid development in a mouse strain lacking endogenous islet amyloid polypeptide (IAPP) but expressing human IAPP
- 2000
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In: Molecular Medicine. - 1076-1551 .- 1528-3658. ; 6:12, s. 998-1007
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Journal article (peer-reviewed)abstract
- Background: Several mouse strains expressing human islet amyloid polypeptide (IAPP) have been created to study development of islet amyloid and its impact on islet cell function. The tendency to form islet amyloid has varied strongly among these strains by factors that have not been elucidated. Because some beta cell granule components are known to inhibit IAPP fibril formation in vitro, we wanted to determine whether a mouse strain expressing human IAPP but lacking the nonamyloidogenic mouse IAPP is more prone to develop islet amyloidosis. Materials and Methods: Such a strain was created by cross-breeding a transgenic mouse strain and an IAPP null mouse strain. Results: when fed a fat-enriched diet, male mice expressing only human IAPP developed islet amyloid earlier and to a higher extent than did mice expressing both human and mouse IAPP. Supporting these results, we found that mouse IAPP dose-dependently inhibits formation of fibrils from human IAPP. Conclusions: Female mice did not develop amyloid deposits, although small extracellular amorphous IAPP deposits were found in some islets. When cultivated in vitro, amyloid deposits occurred within 10 days in islets from either male or female mice expressing only human IAPP. The study shows that formation of islet amyloid may be dependent on the environment, including the presence or absence of fibril inhibitors or promoters.
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