| 1. |
- Henning, G., et al.
(författare)
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Exploring the stability of super heavy elements: First measurement of the fission barrier of 254No
- 2014
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Ingår i: EPJ Web of Conferences. - : EDP Sciences. - 2101-6275 .- 2100-014X. ; 66
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Konferensbidrag (refereegranskat)abstract
- The gamma-ray multiplicity and total energy emitted by the heavy nucleus 254No have been measured at 2 different beam energies. From these measurements, the initial distributions of spin I and excitation energy E * of 254No were constructed. The distributions display a saturation in excitation energy, which allows a direct determination of the fission barrier. 254No is the heaviest shell-stabilized nucleus with a measured fission barrier. © Owned by the authors, published by EDP Sciences, 2014.
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| 2. |
- Henning, G., et al.
(författare)
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Fission Barrier of Superheavy Nuclei and Persistence of Shell Effects at High Spin: Cases of No-254 and Th-220
- 2014
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Ingår i: Physical Review Letters. - 1079-7114 .- 0031-9007. ; 113:26
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Tidskriftsartikel (refereegranskat)abstract
- We report on the first measurement of the fission barrier height in a heavy shell-stabilized nucleus. The fission barrier height of No-254 is measured to be B-f = 6.0 +/- 0.5 MeV at spin 15 (h) over bar and, by extrapolation, B-f = 6.6 +/- 0.9 MeV at spin 0 (h) over bar. This information is deduced from the measured distribution of entry points in the excitation energy versus spin plane. The same measurement is performed for Th-220 and only a lower limit of the fission barrier height can be determined: B-f (I) > 8 MeV. Comparisons with theoretical fission barriers test theories that predict properties of superheavy elements.
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| 3. |
- Thomson, J., et al.
(författare)
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Competing quasiparticle configurations in W-163
- 2010
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Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 81:1
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Tidskriftsartikel (refereegranskat)abstract
- Excited states in the neutron-deficient nuclide W-163 were investigated using the Cd-106(Ni-60, 2pn)W-163 reaction at a beam energy of 270 MeV. The level scheme for W-163 was extended significantly with the observation of five new band structures. The yrast band based on a 13/2(+) isomeric state is extended up to (57/2(+)). Two band structures were established on the 7/2(-) ground state. Quasiparticle configuration assignments for the new band structures were made on the basis of cranked Woods-Saxon shell-model calculations. The results reported in this article suggest that the negative-parity nu(f(7/2), h(9/2)) orbitals are responsible for the first rotational alignment in the yrast band.
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| 4. |
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| 5. |
- Bendlin, Barbara B, et al.
(författare)
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CSF T-Tau/Aβ42 predicts white matter microstructure in healthy adults at risk for Alzheimer's disease.
- 2012
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Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 7:6
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Tidskriftsartikel (refereegranskat)abstract
- Cerebrospinal fluid (CSF) biomarkers T-Tau and Aβ(42) are linked with Alzheimer's disease (AD), yet little is known about the relationship between CSF biomarkers and structural brain alteration in healthy adults. In this study we examined the extent to which AD biomarkers measured in CSF predict brain microstructure indexed by diffusion tensor imaging (DTI) and volume indexed by T1-weighted imaging. Forty-three middle-aged adults with parental family history of AD received baseline lumbar puncture and MRI approximately 3.5 years later. Voxel-wise image analysis methods were used to test whether baseline CSF Aβ(42), total tau (T-Tau), phosphorylated tau (P-Tau) and neurofilament light protein predicted brain microstructure as indexed by DTI and gray matter volume indexed by T1-weighted imaging. T-Tau and T-Tau/Aβ(42) were widely correlated with indices of brain microstructure (mean, axial, and radial diffusivity), notably in white matter regions adjacent to gray matter structures affected in the earliest stages of AD. None of the CSF biomarkers were related to gray matter volume. Elevated P-Tau and P-Tau/Aβ(42) levels were associated with lower recognition performance on the Rey Auditory Verbal Learning Test. Overall, the results suggest that CSF biomarkers are related to brain microstructure in healthy adults with elevated risk of developing AD. Furthermore, the results clearly suggest that early pathological changes in AD can be detected with DTI and occur not only in cortex, but also in white matter.
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| 6. |
- Croxford, Allyson M., et al.
(författare)
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Chemical changes demonstrated in cartilage by synchrotron infrared microspectroscopy in an antibody-induced murine model of rheumatoid arthritis
- 2011
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Ingår i: Journal of Biomedical Optics. - Bellingham, WA : SPIE - International Society for Optical Engineering. - 1083-3668 .- 1560-2281. ; 16:6
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Tidskriftsartikel (refereegranskat)abstract
- Collagen antibody-induced arthritis develops in mice following passive transfer of monoclonal antibodies (mAbs) to type II collagen (CII) and is attributed to effects of proinflammatory immune complexes, but transferred mAbs may react directly and damagingly with CII. To determine whether such mAbs cause cartilage damage in vivo in the absence of inflammation, mice lacking complement factor 5 that do not develop joint inflammation were injected intravenously with two arthritogenic mAbs to CII, M2139 and CIIC1. Paws were collected at day 3, decalcified, paraffin embedded, and 5-mum sections were examined using standard histology and synchrotron Fourier-transform infrared microspectroscopy (FTIRM). None of the mice injected with mAb showed visual or histological evidence of inflammation but there were histological changes in the articular cartilage including loss of proteoglycan and altered chondrocyte morphology. Findings using FTIRM at high lateral resolution revealed loss of collagen and the appearance of a new peak at 1635 cm(-1) at the surface of the cartilage interpreted as cellular activation. Thus, we demonstrate the utility of synchrotron FTIRM for examining chemical changes in diseased cartilage at the microscopic level and establish that arthritogenic mAbs to CII do cause cartilage damage in vivo in the absence of inflammation. © 2011 Society of Photo-Optical Instrumentation Engineers (SPIE).
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| 7. |
- Croxford, Allyson M., et al.
(författare)
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Specific antibody protection of the extracellular cartilage matrix against collagen antibody-induced damage
- 2010
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Ingår i: Arthritis and Rheumatism. - Hoboken, NJ : John Wiley & Sons. - 0004-3591 .- 1529-0131. ; 62:11, s. 3374-3384
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The type II collagen (CII)-specific monoclonal antibodies (mAb) M2139 and CIIC1 induce arthritis in vivo and degrade bovine cartilage explants in vitro, whereas mAb CIIF4 is nonarthritogenic and prevents arthritis development when given in combination with M2139 and CIIC1. To determine the nature of the protective capacity of CIIF4 antibody, we examined the effects of adding CIIF4 to cartilage explants cultured in vitro with M2139 and CIIC1. METHODS: Bovine cartilage explants were cultured in the presence of M2139 and CIIC1, with or without CIIF4. Histologic changes were examined, and chemical changes to collagens and proteoglycans were assessed by Fourier transform infrared microspectroscopy (FTIRM). Fresh cartilage and cartilage that had been freeze-thawed to kill chondrocytes cultured with or without the addition of GM6001, a broad-spectrum inhibitor of matrix metalloproteinases (MMPs), were compared using FTIRM analysis. RESULTS: M2139 and CIIC1 caused progressive degradation of the cartilage surface and loss of CII, even in the absence of viable chondrocytes. CIIF4 did not cause cartilage damage, and when given with the arthritogenic mAb, it prevented their damage and permitted matrix regeneration, a process that required viable chondrocytes. Inhibition of MMP activity reduced cartilage damage but did not mimic the effects of CIIF4. CONCLUSION: CII-reactive antibodies can cause cartilage damage or can be protective in vivo and in vitro, depending on their epitope specificity. Since CII antibodies of similar specificity also occur in rheumatoid arthritis in humans, more detailed studies should unravel the regulatory mechanisms operating at the effector level of arthritis pathogenesis. © 2010 by the American College of Rheumatology.
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| 8. |
- Croxford, Allyson M., et al.
(författare)
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Type II collagen-specific antibodies induce cartilage damage in mice independent of inflammation
- 2013
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Ingår i: Arthritis and Rheumatism. - Hoboken, NJ : John Wiley & Sons. - 0004-3591 .- 1529-0131. ; 65:3, s. 650-659
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Murine collagen antibody-induced arthritis (CAIA), like collagen-induced arthritis, has clinical and immunopathologic features that parallel those in human rheumatoid arthritis (RA). This study was undertaken to examine the effects of autoantibodies to type II collagen (CII) on articular cartilage in the paws of mice, under conditions in which other factors that may influence joint pathology could be excluded. METHODS: Mice of 2 different strains, B10.QC5delta and the parental strain B10.Q, were injected intravenously with either saline or arthritogenic monoclonal antibodies (mAb) to CII. B10.QC5delta mice lack complement factor C5 and do not develop CAIA when injected with arthritogenic mAb, whereas B10.Q mice have C5 and develop CAIA when administered the mAb and a subsequent injection of lipopolysaccharide. Three days after injection the paws of the mice were examined by standard histologic methods to assess morphologic appearance and proteoglycan loss, and by synchrotron-enhanced Fourier transform infrared microspectroscopy to assess chemical evidence of structural change. RESULTS: No macroscopic or microscopic signs of inflammation were evident in the mice. However, in contrast to the saline-injected controls, all mAb-injected mice exhibited cartilage damage in all joints, with loss of proteoglycans and collagen, chondrocyte hyperplasia and/or loss, and surface damage in the interphalangeal joints. CONCLUSION: The implication of these findings is that an autoimmune response to CII can disrupt articular cartilage, particularly that of the small joints, and the subsequent integrity of the cartilage depends on a balance between breakdown and repair. This has relevance with regard to RA, in which such autoantibodies occur but the inflammatory response may dominate clinically and mask underlying features of the autoimmune response. © 2013 by the American College of Rheumatology
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| 9. |
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| 10. |
- Nandakumar, Kutty Selva, et al.
(författare)
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Dominant suppression of inflammation by glycan-hydrolyzed IgG [Retracted]
- 2013
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Ingår i: Proceedings of the National Academy of Sciences. - : Proceedings of the National Academy of Sciences. - 1091-6490 .- 0027-8424. ; 110:25, s. 10252-10257
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Tidskriftsartikel (refereegranskat)abstract
- A unique anti-inflammatory property of IgG, independent of antigen specificity, is described. IgG with modification of the heavy-chain glycan on asparagine 297 by the streptococcal enzyme endo-beta-N-acetylglucosaminidase (EndoS) induced a dominant suppression of immune complex (IC)-mediated inflammation, such as arthritis, through destabilization of local ICs by fragment crystallizable-fragment crystallizable (Fc-Fc) interactions. Small amounts (250 mu g) of EndoS-hydrolyzed IgG were sufficient to inhibit arthritis in mice and most effective during the formation of ICs in the target tissue. The presence of EndoS-hydrolyzed IgG disrupted larger IC lattice formation both in vitro and in vivo, as visualized with anti-C3b staining. Neither complement binding in vitro nor antigen-antibody binding per se was affected.
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