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| 2. |
- Ideguchi, E., et al.
(författare)
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Study of high-spin states in 48Ca region induced by secondary fusion reactions
- 2005
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Konferensbidrag (refereegranskat)abstract
- A new method of in-beam gamma-ray spectroscopy induced by secondary fusion reactions, 37P+9Be and 46Ar+9Be is presented. Low-energy secondary beams of 37P and 46Ar ions of ∼5 MeV/A were developed in order to induce fusion evaporation reactions. Excited states of nuclei in the vicinity of 48Ca, 49-52Ti and 46Ca, were studied by the method as well as β decay of the secondary beam 46Ar. Gamma-gamma coincidence and excitation function analysis were performed to study high-spin states of Ti isotopes.
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| 3. |
- Ideguchi, E, et al.
(författare)
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Study of high-spin states in the Ca-48 region by using secondary fusion reactions
- 2005
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Ingår i: European Physical Journal A. - : Springer Science and Business Media LLC. - 1434-6001 .- 1434-601X. ; 25, s. 429-430
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Tidskriftsartikel (refereegranskat)abstract
- An in-beam gamma-ray spectroscopy study, following a fusion reaction induced by a neutronrich secondary beam, Ar-46 + Be-9, is presented. A low-energy secondary beam of Ar-46 at similar to 5 MeV/A was developed in order to induce fusion reactions. Gamma-gamma coincidence and excitation function analysis was performed to study high-spin states in the vicinity of Ca-48, Ti49-52.
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| 4. |
- Oppenheim, Ronald W, et al.
(författare)
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Developing postmitotic mammalian neurons in vivo lacking Apaf-1 undergo programmed cell death by a caspase-independent, nonapoptotic pathway involving autophagy.
- 2008
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Ingår i: The Journal of neuroscience : the official journal of the Society for Neuroscience. - 1529-2401. ; 28:6, s. 1490-7
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies have shown that caspases and Apaf-1 are required for the normal programmed cell death (PCD) in vivo of immature postmitotic neurons and mitotically active neuronal precursor cells. In contrast, caspase activity is not necessary for the normal PCD of more mature postmitotic neurons that are establishing synaptic connections. Although normally these cells use caspases for PCD, in the absence of caspase activity these neurons undergo a distinct nonapoptotic type of degeneration. We examined the survival of these more mature postmitotic neuronal populations in mice in which Apaf-1 has been genetically deleted and find that they exhibit quantitatively normal PCD of developing postmitotic neurons. We next characterized the morphological mode of PCD in these mice and show that the neurons degenerate by a caspase-independent, nonapoptotic pathway that involves autophagy. However, autophagy does not appear to be involved in the normal PCD of postmitotic neurons in which caspases and Apaf-1 are present and functional because quantitatively normal neuronal PCD occurred in the absence of a key gene required for autophagy (ATG7). Finally, we examined the possible role of another caspase-independent type of neuronal PCD involving the apoptosis-inducing factor (AIF). Mice deficient in AIF also exhibit quantitatively normal PCD of postmitotic neurons after caspase inhibition. Together, these data indicate that, when key components of the type 1 apoptotic pathway (i.e., caspases and Apaf-1) are perturbed in vivo, developing postmitotic neurons nonetheless undergo quantitatively normal PCD by a caspase-independent pathway involving autophagy and not requiring AIF.
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