Engineering topics
Hu, B.
Publications and source records attributed to Hu, B..
Suppressed electric quadrupole collectivity in Si 32
Lying between O 16 and Ca 40 , the s d shell is well described by robust phenomenological and nuclear theories. In this work, however, we highlight an unexplained reduction in electric-quadrupole strength in the rare isotope Si 32 , studied through sub-barrier Coulomb excitation. It is found that the oblate nature of the deformation is well reproduced, while the absolute scale of quadrupole deformation, however, is inhibited by approximately a factor of 2 compared to theoretical predictions. Through comparison with shell-model and calculations, we present a number of possible explanations for this inhibited E 2 strength. By comparing the results of these calculations to multiple observables, we conclude that there is a reduced role for out-of-space excitations in Si 32 , resulting in a reduction in the corrections normally applied to both models. Published by the American Physical Society 2024
Spectroscopy of A=9 hyperlithium with the $(e,e^{\prime}K^{+})$ reaction
Missing mass spectroscopy with the $(e,e^{\prime}K^{+})$ reaction was performed at JLab Hall C for the neutron rich $\Lambda$ hypernucleus $^{9}_{\Lambda}{\rm Li}$. The ground state energy was obtained to be $B_{\Lambda}^{\rm g.s.}=8.84\pm0.17^{\rm stat.}\pm0.15^{\rm sys.}~{\rm MeV}$ by using shell model calculations of a cross section ratio and an energy separation of the spin doublet states ($3/2^{+}_1$ and $5/2^{+}_1$). In addition, peaks that are considered to be states of [$^{8}{\rm Li}(3^{+})\otimes s_{\Lambda}=3/2^{+}_{2}, 1/2^{+}$] and [$^{8}{\rm Li}(1^{+})\otimes s_{\Lambda}=5/2^{+}_{2}, 7/2^{+}$] were observed at $E_{\Lambda}(\#2)=1.74\pm0.27^{\rm stat.}\pm0.11^{\rm sys.}~{\rm MeV}$ and $E_{\Lambda}(\#3)=3.30\pm0.24^{\rm stat.}\pm0.11^{\rm sys.}~{\rm MeV}$, respectively. The $E_{\Lambda}(\#3)$ is larger than shell model predictions by a few hundred keV, and the difference would indicate that a ${\rm ^{5}He}+t$ structure is more developed for the $3^{+}$ state than those for the $2^{+}$ and $1^{+}$ states in a core nucleus $^{8}{\rm Li}$ as a cluster model calculation suggests.
The radioresistance to killing of A1-5 cells derives from activation of the Chk1 pathway
Checkpoints respond to DNA damage by arresting the cell cycle to provide time for facilitating repair. In mammalian cells, the G(2) checkpoint prevents the Cdc25C phosphatase from removing inhibitory phosphate groups from the mitosis-promoting kinase Cdc2. Both Chk1 and Chk2, the checkpoint kinases, can phosphorylate Cdc25C and inactivate its in vitro phosphatase activity. Therefore, both Chk1 and Chk2 are thought to regulate the activation of the G(2) checkpoint. Here we report that A1-5, a transformed rat embryo fibroblast cell line, shows much more radioresistance associated with a much stronger G(2) arrest response when compared with its counterpart, B4, although A1-5 and B4 cells have a similar capacity for nonhomologous end-joining DNA repair. These phenotypes of A1-5 cells are accompanied by a higher Chk1 expression and a higher phosphorylation of Cdc2. On the other hand, Chk2 expression increases slightly following radiation; however, it has no difference between A1-5 and B4 cells. Caffeine or UCN-01 abolishes the extreme radioresistance with the strong G(2) arrest and at the same time reduces the phosphorylation of Cdc2 in A1-5 cells. In addition, Chk1 but not Chk2 antisense oligonucleotide sensitizes A1-5 cells to radiation-induced killing and reduces the G(2) arrest of the cells. Taken together these results suggest that the Chk1/Cdc25C/Cdc2 pathway is the major player for the radioresistance with G(2) arrest in A1-5 cells.