| 1. |
- Galindo-Uribarri, A., et al.
(författare)
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Superdeformation below [Formula Presented]
- 1996
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Ingår i: Physical Review C - Nuclear Physics. - 0556-2813. ; 54:2, s. 454-458
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Tidskriftsartikel (refereegranskat)abstract
- A decoupled rotational band with an average dynamical moment of inertia [Formula Presented] [Formula Presented]/MeV has been observed to high spin in [Formula Presented] [Formula Presented]. The measured quadrupole moment of [Formula Presented] eb is as large as that of the superdeformed band in [Formula Presented]. The large deformation and decoupled character of the band suggests that the odd neutron occupies either the [Formula Presented] orbital or the [Formula Presented] intruder orbital. This is the first example of a superdeformed band extending to high spin below [Formula Presented], a neutron number that has long been considered as the boundary for superdeformation in the [Formula Presented] mass region.
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| 2. |
- Mullins, S. M., et al.
(författare)
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Strong population of a superdeformed band in Eu142
- 1995
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Ingår i: Physical Review C. - 0556-2813. ; 52:1, s. 99-103
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Tidskriftsartikel (refereegranskat)abstract
- A superdeformed band has been found in Eu142. It is populated with 1.2(2)% of the total -ray intensity that decayed into Eu142 via the reaction Sn120(27Al,5n)142Eu at 152 MeV. The strength of the band is similar to that previously reported in Eu143, where the superdeformed band is populated with an intensity of 1.1(1)%. This is unexpected, since both total Routhian surface (TRS) and cranked modified oscillator (MO) calculations predict that the superdeformed band in Eu143 becomes yrast at lower spin than that in Eu142. This difference is 4Latin small letter h with stroke in the MO calculations and 8Latin small letter h with stroke in the TRS. Extrapolation of the normal-deformed yrast states in Eu143 shows, however, that a difference of 8Latin small letter h with stroke in spin corresponds to a change in the relative energy of the superdeformed and normal-deformed yrast lines of only 1 MeV.
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| 3. |
- Drake, M., et al.
(författare)
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The immunosuppressant FK506 ameliorates ischaemic damage in the rat brain
- 1996
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 158:2, s. 155-159
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Tidskriftsartikel (refereegranskat)abstract
- The effect of the immunosuppressant FK506 on ischaemic neuronal damage was studied in a rat model of transient cerebral ischemia induced by occlusion of both common carotid arteries in combination with hypotension for 10 min. Neuronal damage was assessed morphologically after 4 days of recovery. Treatment with FK506, given at a dose of 2 mg kg-1 by intraperitoneal injections 30 min prior to ischemia and once daily during recovery, decreased neuronal damage by 52% in the hippocampal CA1 region and by 48% in the temporal cortex. The protection was not due to diminished body temperature or a marked reduction of ischaemia-induced synaptic overflow of glutamate. We propose that FK506 decreases neuronal damage either by inhibiting calcineurin-mediated events or by preserving mitochondrial function.
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| 4. |
- Ferrand-Drake, M., et al.
(författare)
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Mitochondrial permeability transition induced DNA-fragmentation in the rat hippocampus following hypoglycemia
- 1999
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Ingår i: Neuroscience. - 0306-4522. ; 90:4, s. 1325-1338
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Tidskriftsartikel (refereegranskat)abstract
- In the present study the time-course of DNA fragmentation following insulin-induced hypoglycemia was examined. In situ localization of DNA breaks were studied by the terminal deoxynucleotidyl transferase-mediated biotin- deoxyuridine triphosphate nick-end labelling method, and the temporal profile of DNA-fragmentation by agarose gel electrophoresis. Cell nuclei displayed terminal deoxynucleotidyl transferase-deoxyuridine triphosphate nick-end labelling within 3 h of recovery following 30 min of a hypoglycemic insult, and DNA from the hippocampus displayed oligonucleosomal fragmentation. Ultrastructural examination of the dentate granule cells showed mitochondrial swelling during the acute phase of the hypoglycemic insult, which preceded the DNA fragmentation seen in the recovery phase. Cyclosporin A but not tacrolimus, prevented mitochondrial swelling and subsequent DNA fragmentation. We conclude that during severe energy deprivation following hypoglycemia, mitochondrial swelling occurs due to mitochondrial permeability transition and that factors are released, which upon recovery can activate processes leading to DNA fragmentation and cell death.
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| 5. |
- Ferrand-Drake, M., et al.
(författare)
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The time-course of DNA fragmentation in the choroid plexus and the CA1 region following transient global ischemia in the rat brain. The effect of intra-ischemic hypothermia
- 1999
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Ingår i: Neuroscience. - 0306-4522. ; 93:2, s. 537-549
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Tidskriftsartikel (refereegranskat)abstract
- The time-course of DNA fragmentation in the CA1 region of the hippocampus and the choroid plexus was studied following induction of transient forebrain ischemia under lethal normothermic (37°C), or sublethal hypothermic (33°C) conditions. Oligonucleosomal- and high-molecular-weight DNA fragmentation were analysed by conventional agarose gel electrophoresis and pulsed-field gel electrophoresis, respectively. DNA breaks were visualized by the terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridinetriphosphate nick-end labeling method. At 48h of recovery following normothermic ischemia, in situ labeling of DNA breaks were widespread in medial CA1 and high-molecular-weight DNA cleavage was seen. In contrast, at the same time-point in lateral CA1, many pyknotic but few cells displaying in situ labeling of DNA breaks were observed. Major oligonucleosomal DNA fragmentation was not seen until 72h of recovery. Following hypothermic ischemia, DNA fragmentation was absent in CA1. DNA fragmentation was seen in the choroid plexus at 24h of recovery following normothermic ischemia, which was diminished by 48h of recovery.In conclusion, oligonucleosomal and high-molecular-weight DNA fragmentation at 10-50 kilobase pairs, occur in CA1 after morphological signs, and acidophilia signifying neurodegeneration appear. DNA fragmentation and cell death in the choroid plexus precede neuronal death in CA1 and may play a causative role.
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