NMR evidence for very slow carrier density fluctuations in the organic metal (TMTSF)2_2ClO4_4

We have investigated the origin of the large increase in spin-echo decay rates for the $^{77}$Se nuclear spins at temperatures near to $T=30K$ in the organic superconductor (TMTSF)$_2$ClO$_4$. The measured angular dependence of $T_2^{-1}$ demonstrates that the source of the spin-echo decays lies with carrier density fluctuations rather than fluctuations in TMTSF molecular orientation. The very long time scales are directly associated with the dynamics of the anion ordering occurring at $T=25K$, and the inhomogeneously broadened spectra at lower temperatures result from finite domain sizes. Our results are similar to observations of line-broadening effects associated with charge-ordering transitions in quasi-two dimensional organic conductors.Comment: 5 pages, 4 figure

Electron-lattice coupling and the broken symmetries of the molecular salt (TMTTF)2_2SbF6_6

(TMTTF)$_2$SbF$_6$ is known to undergo a charge ordering (CO) phase transition at $T_{CO}\approx156K$ and another transition to an antiferromagnetic (AF) state at $T_N\approx 8K$. Applied pressure $P$ causes a decrease in both $T_{CO}$ and $T_N$. When $P>0.5 GPa$, the CO is largely supressed, and there is no remaining signature of AF order. Instead, the ground state is a singlet. In addition to establishing an expanded, general phase diagram for the physics of TMTTF salts, we establish the role of electron-lattice coupling in determining how the system evolves with pressure.Comment: 4 pages, 5 figure

Phase Inhomogeneity of the Itinerant Ferromagnet MnSi at High Pressures

The pressure induced quantum phase transition of the weakly itinerant ferromagnet MnSi is studied using zero-field $^{29}Si$ NMR spectroscopy and relaxation. Below $P^*\approx 1.2GPa$, the intensity of the signal and the nuclear spin-lattice relaxation is independent of pressure, even though the amplitude of the magnetization drops by 20% from the ambient pressure amplitude. For $P>P^*$, the decreasing intensity within the experimentally detectable bandwidth signals the onset of an inhomogeneous phase that persists to the highest pressure measured, $P\ge 1.75GPa$, which is well beyond the known critical pressure $P_c=1.46GPa$. Implications for the non-Fermi Liquid behavior observed for $P>P_c$ are discussed.Comment: 4 pages, 4 figure

Inhomogeneous electronic structure probed by spin-echo experiments in the electron doped high-Tc superconductor Pr_{1.85}Ce_{0.15}CuO_{4-y}

63Cu nuclear magnetic resonance (NMR) spin-echo decay rate (T_2^{-1}) measurements are reported for the normal and superconducting states of a single crystal of Pr_{1.85}Ce_{0.15}CuO_{4-y} (PCCO) in a magnetic field B_0=9T over the temperature range 2K<T<200K. The spin-echo decay rate is temperature-dependent for T<55K, and has a substantial dependence on the radio frequency (rf) pulse parameters below T~25K. This dependence indicates that T_2^{-1} is strongly effected by a local magnetic field distribution that can be modified by the rf pulses, including ones that are not at the nuclear Larmor frequency. The low-temperature results are consistent with the formation of a static inhomogeneous electronic structure that couples to the rf fields of the pulses.Comment: 4 pages, 4 figure

Competition of Dimerization and Charge Ordering in the Spin-Peierls State of Organic Conductors

The effect of the charge ordering on the spin-Peierls (SP) state has been examined by using a Peierls-Hubbard model at quarter-filling with dimerization, on-site and nearest-neighbor repulsive interactions. By taking account of the presence of dimerization, a bond distortion is calculated variationally with the renormalization group method based on bosonization. When the charge ordering appears at V=V_c with increasing the nearest-neighbor interaction (V), the distortion exhibits a maximum due to competition between the dimerization and the charge ordering. It is shown that the second-order phase transition occurs from the SP state with the bond alternation to a mixed state with an additional component of the site alternationat V = V_c.Comment: 11 pages, 13 figures, to be published in J. Phys. Soc. Jpn. 72 No.6 (2003

Loss of BRCA1 or BRCA2 markedly increases the rate of base substitution mutagenesis and has distinct effects on genomic deletions

Loss-of-function mutations in the BRCA1 and BRCA2 genes increase the risk of cancer. Owing to their function in homologous recombination repair, much research has focused on the unstable genomic phenotype of BRCA1/2 mutant cells manifest mainly as large-scale rearrangements. We used whole-genome sequencing of multiple isogenic chicken DT40 cell clones to precisely determine the consequences of BRCA1/2 loss on all types of genomic mutagenesis. Spontaneous base substitution mutation rates increased sevenfold upon the disruption of either BRCA1 or BRCA2, and the arising mutation spectra showed strong and specific correlation with a mutation signature associated with BRCA1/2 mutant tumours. To model endogenous alkylating damage, we determined the mutation spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces more base substitution mutations in BRCA1/2-deficient cells. Spontaneously arising and MMS-induced insertion/deletion mutations and large rearrangements were also more common in BRCA1/2 mutant cells compared with the wild-type control. A difference in the short deletion phenotypes of BRCA1 and BRCA2 suggested distinct roles for the two proteins in the processing of DNA lesions, as BRCA2 mutants contained more short deletions, with a wider size distribution, which frequently showed microhomology near the breakpoints resembling repair by non-homologous end joining. An increased and prolonged gamma-H2AX signal in MMS-treated BRCA1/2 cells suggested an aberrant processing of stalled replication forks as the cause of increased mutagenesis. The high rate of base substitution mutagenesis demonstrated by our experiments is likely to significantly contribute to the oncogenic effect of the inactivation of BRCA1 or BRCA2

Finite-Temperature Phase Diagram of Quasi-One-Dimensional Molecular Conductors: Quantum Monte Carlo Study

Finite-temperature phase transitions in quasi-one-dimensional quarter-filled systems are investigated by the extended Hubbard model with electron-lattice coupling. Using a quantum Monte Carlo method combined with the inter-chain mean-field approximation, we clarify competing and coexisting behaviors among charge ordering, dimer Mott, and spin-Peierls states. It is pointed out that an anharmonicity of lattice distortions plays an important role in multi-critical behaviors. The results are compared with experimental data for quasi-one-dimensional molecular conductors such as DCNQI and TMTTF compounds.Comment: Corrected typo

Entrainment of the Mammalian Cell Cycle by the Circadian Clock: Modeling Two Coupled Cellular Rhythms

The cell division cycle and the circadian clock represent two major cellular rhythms. These two periodic processes are coupled in multiple ways, given that several molecular components of the cell cycle network are controlled in a circadian manner. For example, in the network of cyclin-dependent kinases (Cdks) that governs progression along the successive phases of the cell cycle, the synthesis of the kinase Wee1, which inhibits the G2/M transition, is enhanced by the complex CLOCK-BMAL1 that plays a central role in the circadian clock network. Another component of the latter network, REV-ERBα, inhibits the synthesis of the Cdk inhibitor p21. Moreover, the synthesis of the oncogene c-Myc, which promotes G1 cyclin synthesis, is repressed by CLOCK-BMAL1. Using detailed computational models for the two networks we investigate the conditions in which the mammalian cell cycle can be entrained by the circadian clock. We show that the cell cycle can be brought to oscillate at a period of 24 h or 48 h when its autonomous period prior to coupling is in an appropriate range. The model indicates that the combination of multiple modes of coupling does not necessarily facilitate entrainment of the cell cycle by the circadian clock. Entrainment can also occur as a result of circadian variations in the level of a growth factor controlling entry into G1. Outside the range of entrainment, the coupling to the circadian clock may lead to disconnected oscillations in the cell cycle and the circadian system, or to complex oscillatory dynamics of the cell cycle in the form of endoreplication, complex periodic oscillations or chaos. The model predicts that the transition from entrainment to 24 h or 48 h might occur when the strength of coupling to the circadian clock or the level of growth factor decrease below critical values

Minimum Criteria for DNA Damage-Induced Phase Advances in Circadian Rhythms

Robust oscillatory behaviors are common features of circadian and cell cycle rhythms. These cyclic processes, however, behave distinctively in terms of their periods and phases in response to external influences such as light, temperature, nutrients, etc. Nevertheless, several links have been found between these two oscillators. Cell division cycles gated by the circadian clock have been observed since the late 1950s. On the other hand, ionizing radiation (IR) treatments cause cells to undergo a DNA damage response, which leads to phase shifts (mostly advances) in circadian rhythms. Circadian gating of the cell cycle can be attributed to the cell cycle inhibitor kinase Wee1 (which is regulated by the heterodimeric circadian clock transcription factor, BMAL1/CLK), and possibly in conjunction with other cell cycle components that are known to be regulated by the circadian clock (i.e., c-Myc and cyclin D1). It has also been shown that DNA damage-induced activation of the cell cycle regulator, Chk2, leads to phosphorylation and destruction of a circadian clock component (i.e., PER1 in Mus or FRQ in Neurospora crassa). However, the molecular mechanism underlying how DNA damage causes predominantly phase advances in the circadian clock remains unknown. In order to address this question, we employ mathematical modeling to simulate different phase response curves (PRCs) from either dexamethasone (Dex) or IR treatment experiments. Dex is known to synchronize circadian rhythms in cell culture and may generate both phase advances and delays. We observe unique phase responses with minimum delays of the circadian clock upon DNA damage when two criteria are met: (1) existence of an autocatalytic positive feedback mechanism in addition to the time-delayed negative feedback loop in the clock system and (2) Chk2-dependent phosphorylation and degradation of PERs that are not bound to BMAL1/CLK