| 1. |
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| 2. |
- Hoff, P, et al.
(author)
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Nuclear spectroscopy at Sn-133
- 2000
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In: HYPERFINE INTERACTIONS. - : BALTZER SCI PUBL BV. - 0304-3843. ; 129:1-4, s. 141-148
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Journal article (other academic/artistic)abstract
- It is described how the measurement of n gamma -coincidences can be used to identify single-particle states in Sn-133. This method, in combination with the improved yields at ISOLDE, has facilitated firm determination of three excited single-particle stat
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| 3. |
- Hoff, P, et al.
(author)
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Single-neutron states in Sn-133
- 1996
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In: PHYSICAL REVIEW LETTERS. - : AMER INST PHYSICS. - 0031-9007. ; 77:6, s. 1020-1023
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Journal article (peer-reviewed)abstract
- The location of several single-neutron states in Sn-133 has been identified. The P-3/2, h(9/2), and f(5/2) states were found at 853.7, 1560.9, and 2004.6 keV, respectively, by measuring gamma rays in coincidence with delayed neutrons following the decay o
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| 4. |
- Oinonen, M., et al.
(author)
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Non-analog beta decay of Rb-74
- 2001
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In: Physics Letters, Section B: Nuclear, Elementary Particle and High-Energy Physics. - 0370-2693. ; 511:2-4, s. 145-150
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Journal article (peer-reviewed)abstract
- The magnitude of the Coulomb mixing parameter delta (l)(IM) has been experimentally deduced, for the first time, for the B decay of Rb-74. Th, estimated magnitude is derived from the feeding of the non-analog first excited 0(+) state in Kr-74. The inferred upper Limit of 0.07% is small compared to theoretical predictions. The half-life was measured to be 64.90(9) ms.
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| 5. |
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| 6. |
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| 7. |
- Bjornstad, T., et al.
(author)
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Study of the Giant Gamow-Teller Resonance in Nuclear Beta-Decay - the Case of Ar-32
- 1985
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In: Nuclear Physics A. - : Elsevier BV. - 0375-9474. ; 443:2, s. 283-301
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Journal article (peer-reviewed)abstract
- Delayed proton and gamma emissions following the β-decay of 32Ar have been studied. The half-life of 32Ar is 98 ± 2 ms, and the T = 2 analogue state in 32Cl lies at the excitation energy 5036 ± 12 keV. From the intensity of the feeding to this state the proton intensities can be converted to an absolute scale leading to a total proton branching ratio of (43 ± 3)%. From proton-gamma coincidence measurements it emerges that (1.9 ± 0.2)% of the protons lead to the first-excited state in 31S. A level scheme up to 8.75 MeV excitation in 32Cl has been constructed and the Gamow-Teller strength function has been deduced. The result is a renormalization of the axial-vector strength to (49 ± 5)% of the free-nucleon value.
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| 8. |
- Borge, M. J. G., et al.
(author)
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Study of the Giant Gamow-Teller Resonance in Nuclear Beta-Decay - the Case of Ar-33
- 1987
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In: Physica Scripta. - : IOP Publishing. - 1402-4896 .- 0031-8949. ; 36:2, s. 218-223
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Journal article (peer-reviewed)abstract
- Delayed proton and gamma emissions following the beta decay of 33Ar have been studied. From the calculated intensity of the feeding to the T = 3/2 analogue state in 33C1, the proton intensities have been put on an absolute scale leading to a proton branching ratio of 38.7 ± 1.0%. A proton branch to the first excited state in 32S at 2230.2 keV (1π = 2+) with an intensity of 0.77 ± 0.10% was obtained from gamma singles and proton-gamma coincidence data. The complete spectroscopic information on 33Ar allows the Gamow-Teller (GT) strength function from the gound state and up to 9.25 MeV excitation energy in 33C1 to be deduced. The total strength observed in this interval is 2.90 in absolute units.
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| 9. |
- Aazh, Hashir, et al.
(author)
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Insights from the Third International Conference on Hyperacusis : Causes, Evaluation, Diagnosis, and Treatment
- 2018
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In: Noise & Health. - : Wolters Kluwer. - 1463-1741 .- 1998-4030. ; 20:95, s. 162-170
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Journal article (peer-reviewed)abstract
- Background: Hyperacusis is intolerance of certain everyday sounds that causes significant distress and impairment in social, occupational, recreational, and other day-to-day activities. Objective: The aim of this report is to summarize the key findings and conclusions from the Third International Conference on Hyperacusis.Topics covered: The main topics discussed comprise (1) diagnosis of hyperacusis and audiological evaluations, (2) neurobiological aspect of hyperacusis, (3) misophonia, (4) hyperacusis in autism spectrum disorder, (5) noise sensitivity, (6) hyperacusis-related distress and comorbid psychiatric illness, and (7) audiologist-delivered cognitive behavioral therapy for hyperacusis.Conclusions: Implications for research and clinical practice are summarised.
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| 10. |
- Bauer, K, et al.
(author)
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Perforin deficiency attenuates collagen-induced arthritis
- 2005
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In: Arthritis Research and Therapy. - : Springer Science and Business Media LLC. - 1478-6362 .- 1478-6354. ; 7:4, s. 877-884
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Journal article (peer-reviewed)abstract
- Collagen-induced arthritis ( CIA), an approved animal model for rheumatoid arthritis, is thought to be a T cell-dependent disease. There is evidence that CD8(+) T cells are a major subset controlling the pathogenesis of CIA. They probably contribute to certain features of disease, namely tissue destruction and synovial hyperplasia. In this study we examined the role of perforin (pfp), a key molecule of the cytotoxic death pathway that is expressed mainly in CD8(+) T cells, for the pathogenesis of CIA. We generated DBA/1J mice suffering from mutations of the pfp molecule, DBA/1J-pfp(-/-), and studied their susceptibility to arthritis. As a result, pfp-deficient mice showed a reduced incidence (DBA/1J-pfp(+/+), 64%; DBA/1J-pfp(-/-), 54%), a slightly delayed onset ( onset of disease: DBA/1J-pfp(+/+), 53 +/- 3.6; DBA/1J-pfp(-/-), 59 +/- 4.9 ( mean SEM), and milder form of the disease ( maximum disease score: DBA/1J-pfp(+/+), 7.3 +/- 1.1; DBA/1J-pfp(-/-), 3.4 +/- 1.4 ( mean SEM); P < 0.05). Concomitantly, peripheral T cell proliferation in response to the specific antigen bovine collagen II was increased in pfp(-/-) mice compared with pfp(+/+) mice, arguing for an impaired killing of autoreactive T cells caused by pfp deficiency. Thus, pfp-mediated cytotoxicity is involved in the initiation of tissue damage in arthritis, but pfp-independent cytotoxic death pathways might also contribute to CIA.
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