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| 2. |
- Cederwall, Bo, et al.
(författare)
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NEW OBLATE BAND IN HG-196 WITH QUENCHED M1 STRENGTH
- 1993
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Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 47:6, s. R2443-R2446
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Tidskriftsartikel (refereegranskat)abstract
- High-spin states in the nucleUs Hg-196 were populated in the reaction (Os(Be,5n))-Os-192 at a beam energy of 65 MeV. A regular rotational-like DELTAI = 1 band has been observed up to an excitation energy of E* almost-equal-to 8.7 MeV and spin I almost-equal-to 30hBAR. This is the second observation of a band of this character in a mercury isotope. The experimental results are compared with mean field calculations and semiclassical estimates based on the Donau-Frauendorf formalism. The mercury bands show significantly lower B(M1)/B(E2) branching ratios as compared with similar bands in light lead nuclei. This difference may be more readily explained by a difference in single-particle structure rather than by large differences in deformation between the lead and mercury configurations.
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| 3. |
- HENRY, EA, et al.
(författare)
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COLLECTIVE OBLATE BANDS IN PB NUCLEI
- 1993
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Ingår i: Abstracts of Papers of the American Chemical Society. - 0065-7727. ; 206, s. 58-NUCL
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Hsu, D. S., et al.
(författare)
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FLOW LINEAR DICHROISM AND ELECTRON-MICROSCOPIC ANALYSIS OF PROTEIN-DNA COMPLEXES OF A MUTANT UVRB PROTEIN THAT BINDS TO BUT CANNOT KINK DNA
- 1994
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Ingår i: Journal of Molecular Biology. - : Elsevier BV. - 0022-2836 .- 1089-8638. ; 241:5, s. 645-650
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Tidskriftsartikel (refereegranskat)abstract
- (A)BC excinuclease of Escherichia coli is the enzymatic activity resulting from sequential and partially overlapping actions of UvrA, UvrB, and UvrC protein. UvrA is a molecular matchmaker which promotes the formation of a stable UvrB-damaged DNA complex in which the DNA is kinked by about 130 degrees. The UvrB-DNA complex is then recognized by UvrC) and two incisions are made in the DNA by the joint actions of UvrC and UvrB. A mutant of UvrB (D478A) can be loaded onto the DNA but it does not interact with UvrC to cause a nick 3' to the lesion. Based on the lack of a DNase-I-hypersensitive site in the footprint of the mutant, it was proposed that the lack of incision was due to the inability of the mutant UvrB to kink the DNA. In the current study we have investigated the interaction of the mutant UvrB with DNA using two biophysical methods, flow linear dichroism and electron microscopy. Both methods reveal that the mutant UvrB is unable to bend DNA.
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| 5. |
- Imreh, S, et al.
(författare)
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Hypersomy of chromosome 15 with retrovirally rearranged c-myc, loss of germline c-myc and IgK/c-myc juxtaposition in a macrophage-monocytic tumour line
- 1994
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Ingår i: European Journal of Cancer. - 0959-8049. ; 30A:7, s. 994-1002
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Tidskriftsartikel (refereegranskat)abstract
- From a lymphoid tumour induced by 7,12-dimethylbenz-[a]-anthracene (DMBA) + methyl-N-nitrose-N-urea (MNU) in an [AKR Rb(6.15) x CBAT6T6]F1 mouse, a macrophage- monocyte line (KT-10) was isolated. Following ethyl methanesulfonate (EMS) treatment, a bromodeoxyuridine (BUdR) resistant subline was selected. Serial propagation of this line in vitro in the presence of BUdR (28 months) with periodic cytogenetic and molecular examinations, has led to the definition of four successive stages. During stage I, the cells were trisomic for chromosome 15. They contained Rb(6.15) and Rb(del6.15) of AKR and T(14;15) of CBA origin. Southern blotting showed the presence of both germline (G) and rearranged (R) c-myc. At stage II, Rb(del6.15) has duplicated. Both Rb(6.15) and T(14;15) persisted together with G-myc and R-myc. In stage III, the CBA-derived T(14;15) was lost, in parallel with G-myc. At this stage, a Dic.In(6.15) was detected. One of its arms was cytogenetically identical with the long arm of In(6.15) in the variant IgK/myc translocations. This chromosome carried R-myc and IgK in juxtaposition, as indicated by comigration on pulsed field electrophoresis (PFGE). At stage IV, the R-myc carrying AKR-derived chromosome 15s were present in six copies. Possible relationships between the increasing R/G myc ratio and changed growth characteristics in vivo and in vitro are discussed.
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| 6. |
- OLIVEIRA, JRB, et al.
(författare)
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HIGH-K BANDS IN THE YB-166 REGION
- 1994
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Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 50:3, s. 1360-1369
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Tidskriftsartikel (refereegranskat)abstract
- High-K bands have been observed in the Yb-166,Yb-167,Yb-168 isotopes following the Sn-124(Ca-48,xn gamma) reaction. The nu h(11/2) bend in Yb-167 has been extended to higher spins. The high-K bands in the even-even isotopes were observed for the first time and show very high B(M1)/B(E2) ratios. Configuration assignments for the new bands are proposed. The results are interpreted within the tilted cranking model.
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| 7. |
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| 8. |
- Wang, Y, et al.
(författare)
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Functional homology between N-myc and c-myc in murine plasmacytomagenesis : plasmacytoma development in N-myc transgenic mice
- 1992
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Ingår i: Oncogene. - 0950-9232. ; 7:6, s. 7-1241
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Tidskriftsartikel (refereegranskat)abstract
- Mouse plasmacytomas induced by pristane oil alone, or in combination with Abelson murine leukemia virus (A-MuLV), regularly carry one of three alternative chromosomal translocations that juxtapose c-myc to immunoglobulin heavy- or light-chain loci. E mu-c-myc transgenic mice develop translocation-free plasmacytomas after induction by pristane oil and/or A-MuLV [Sugiyama, H., Silva, S., Wang, Y., Weber, G., Babonits, M., Rosen, A., Wiener, F. & Klein, G. (1990). Int. J. Cancer, 46, 845-852]. In order to test whether another member of the myc family, N-myc, could play a similar role as c-myc, we treated E mu-N-myc transgenic mice with pristane and helper-free A-MuLV. Of 20 mice that received a single pristane injection followed by A-MuLV, 17 developed plasmacytomas with a mean latency period of 54 +/- 20 days. In a corresponding group that only received a single pristane injection, five out of six transgenic mice developed plasmacytomas with a mean latency period of 142 +/- 32 days. However, after three monthly injections of pristane, all 15 transgenic mice developed plasmacytomas with a mean latency period of 128 +/- 20 days. All plasmacytomas expressed the N-myc transgene, while none of them expressed either c-myc or endogenous N-myc. None of the tumors carried the usual plasmacytoma-associated translocations.
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