Observation of Positive-Parity Bands in 109^{109}Pd and 111^{111}Pd: Enhanced γ\gamma-Softness

The neutron-rich nuclei $^{109}$Pd and $^{111}$Pd were produced as fission fragments following the $^{30}$Si + $^{168}$Er reaction at 142 MeV. Using the identification based on the coincidences with the complementary fission fragments, the only positive-parity bands observed so far in $^{109}$Pd and $^{111}$Pd emerged from this work. A band, built on top of the 5/2$^+$ ground state exhibiting $\Delta I$ = 1 energy-level staggering, was observed in each of these nuclei. Both nuclei of interest, $^{109}$Pd and $^{111}$Pd, are suggested to lie in the transitional region of Pd isotopes of maximum $\gamma$-softness. The ground states of both nuclei are predicted by TRS calculations to be extremely $\gamma$-soft with shallow triaxial minima. The first crossing in the new bands is proposed to be due to an alignment of $h^2_{11/2}$ neutrons

Excitation energies of superdeformed states in 196Pb: towards a systematic study of the second well in Pb isotopes

The excitation energy of the lowest-energy superdeformed band in 196Pb is established using the techniques of time-correlated γ-ray spectroscopy. Together with previous measurements on 192Pb and 194Pb, this result allows superdeformed excitation energies, binding energies, and two-proton and two-neutron separation energies to be studied systematically, providing stringent tests for current nuclear models. The results are examined for evidence of a “superdeformed shell gap.

The Role of Atypical Protein Kinase C in CSF-1-Dependent Erk Activation and Proliferation in Myeloid Progenitors and Macrophages

Colony stimulating factor-1 (CSF-1 or M-CSF) is the major physiological regulator of the proliferation, differentiation and survival of cells of the mononuclear phagocyte lineage. CSF-1 binds to a receptor tyrosine kinase, the CSF-1 receptor (CSF-1R). Multiple pathways are activated downstream of the CSF-1R; however, it is not clear which pathways regulate proliferation and survival. Here, we investigated the role of atypical protein kinase Cs (PKCζ) in a myeloid progenitor cell line that expressed CSF-1R (32D.R) and in primary murine bone marrow derived macrophages (BMMs). In 32D.R cells, CSF-1 induced the phosphorylation of PKCζ and increased its kinase activity. PKC inhibitors and transfections with mutant PKCs showed that optimal CSF-1-dependent Erk activation and proliferation depended on the activity of PKCζ. We previously reported that CSF-1 activated the Erk pathway through an A-Raf-dependent and an A-Raf independent pathway (Lee and States, Mol. Cell. Biol. 18, 6779). PKC inhibitors did not affect CSF-1 induced Ras and A-Raf activity but markedly reduced MEK and Erk activity, implying that PKCζ regulated the CSF-1-Erk pathway at the level of MEK. PKCζ has been implicated in activating the NF-κB pathway. However, CSF-1 promoted proliferation in an NF-κB independent manner. We established stable 32D.R cell lines that overexpressed PKCζ. Overexpression of PKCζ increased the intensity and duration of CSF-1 induced Erk activity and rendered cells more responsive to CSF-1 mediated proliferation. In contrast to 32D.R cells, PKCζ inhibition in BMMs had only a modest effect on proliferation. Moreover, PKCζ -specific and pan-PKC inhibitors induced a paradoxical increase in MEK-Erk phosphorylation suggesting that PKCs targeted a common negative regulatory step upstream of MEK. Our results demonstrated that CSF-1 dependent Erk activation and proliferation are regulated differentially in progenitors and differentiated cells

Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks

The role of nucleotides in intracellular energy provision and nucleic acid synthesis has been known for a long time. In the past decade, evidence has been presented that, in addition to these functions, nucleotides are also autocrine and paracrine messenger molecules that initiate and regulate a large number of biological processes. The actions of extracellular nucleotides are mediated by ionotropic P2X and metabotropic P2Y receptors, while hydrolysis by ecto-enzymes modulates the initial signal. An increasing number of studies have been performed to obtain information on the signal transduction pathways activated by nucleotide receptors. The development of specific and stable purinergic receptor agonists and antagonists with therapeutical potential largely contributed to the identification of receptors responsible for nucleotide-activated pathways. This article reviews the signal transduction pathways activated by P2Y receptors, the involved second messenger systems, GTPases and protein kinases, as well as recent findings concerning P2Y receptor signalling in C6 glioma cells. Besides vertical signal transduction, lateral cross-talks with pathways activated by other G protein-coupled receptors and growth factor receptors are discussed

Octupole collectivity in 98,100,102^{98,100,102}Mo

Excited states in 98,100,102Mo have been studied via the 30Si+168Er-induced fission reaction at a beam energy of 142 MeV. Prompt gamma rays were detected with the EUROBALL III multidetector array. The level schemes are extended with more than 20 new transitions and interpreted in the framework of a soft-octupole vibration model