Theoretical Evaluations of the Fission Cross Section of the 77 eV Isomer of 235-U

We have developed models of the fission barrier (barrier heights and transition state spectra) that reproduce reasonably well the measured fission cross section of $^{235}$U from neutron energy of 1 keV to 2 MeV. From these models we have calculated the fission cross section of the 77 eV isomer of $^{235}$U over the same energy range. We find that the ratio of the isomer cross section to that of the ground state lies between about 0.45 and 0.55 at low neutron energies. The cross sections become approximately equal above 1 MeV. The ratio of the neutron capture cross section to the fission cross section for the isomer is predicted to be about a factor of 3 larger for the isomer than for the ground state of $^{235}$U at keV neutron energies. We have also calculated the cross section for the population of the isomer by inelastic neutron scattering form the $^{235}$U ground state. We find that the isomer is strongly populated, and for $E_n = 1 MeV$ the $(n,n'\gamma)$ cross section leading to the population of the isomer is of the order of 0.5 barn. Thus, neutron reaction network calculations involving the uranium isotopes in a high neutron fluence are likely to be affected by the 77 eV isomer of $^{235}$U. With these same models the fission cross sections of $^{233}$U and $^{237}$U can be reproduced approximately using only minor adjustments to the barrier heights. With the significant lowering of the outer barrier that is expected for the outer barrier the general behavior of the fission cross section of $^{239}$Pu can also be reproduced.Comment: 17 pages including 8 figure

Paucity of FOXP3+ cells in skin and peripheral blood distinguishes Sezary syndrome from other cutaneous T-cell lymphomas.

Cutaneous T-cell lymphomas (CTCL) are mainly comprised of two variants: mycosis fungoides (MF) with CD4(+) tumor cells confined to the skin and the leukemic Sézary syndrome with tumor cell spread to the blood. In this study, we investigated cutaneous expression of the regulatory T-cell (T(reg)) marker FOXP3 in 30 CTCL patients. Immunohistochemical analysis revealed significantly lower numbers of CD4(+)FOXP3(+) cells within the dermal lymphomononuclear infiltrate of Sézary patients (16% FOXP3(+) cells of CD4(+) cells) in contrast to MF (43% FOXP3(+) cells (P<0.05)) and rare types of CTCL (45% FOXP3(+) cells). Furthermore, CD4(+)FOXP3(+) T cells were also markedly reduced in the CD4(+) population within the peripheral blood of Sézary patients compared to controls as determined by fluorescence-activated cell sorter, quantitative PCR and functional analyses. The data support the conclusion that the neoplastic cells in CTCL do not express the T(reg) marker FOXP3. Our data also identify Sézary syndrome as, to our knowledge, the first reported neoplastic disease with a clear reduction in T(reg) numbers within the CD4(+) population. This lack of T(reg) might account for the more aggressive nature of Sézary syndrome compared with other CTCL