Incommensurate Charge and Spin Fluctuations in d-wave Superconductors

We show analytic results for the irreducible charge and spin susceptibilities, $\chi_0 (\omega, {\bf Q})$, where ${\bf Q}$ is the momentum transfer between the nodes in d-wave superconductors. Using the BCS theory and a circular Fermi surface, we find that the singular behavior of the irreducible charge susceptibility leads to the dynamic incommensurate charge collective modes. The peaks in the charge structure factor occur at a set of wave vectors which form an ellipse around ${\bf Q}_{\pi}=(\pi,\pi)$ and ${\bf Q}_0=(0,0)$ in momentum space with momentum dependent spectral weight. It is also found that, due to the non-singular irreducible spin susceptibility, an extremely strong interaction via random phase approximation is required to support the magnetic peaks near ${\bf Q}_{\pi}$. Under certain conditions, the peaks in the magnetic structure factor occur near ${\bf Q}=(\pi,\pi (1 \pm \delta))$ and $(\pi (1 \pm \delta),\pi)$.Comment: 5 pages, 3 figure

Dynamical charge susceptibility in layered cuprates: the influence of screened inter-site Coulomb repulsion

The analytical expression for dynamical charge susceptibility in layered cuprates has been derived in the frame of singlet-correlated band model beyond random-phase-approximation (RPA) scheme. Our calculations performed near optimal doping regime show that there is a peak in real part of the charge susceptibility $\chi({\bf q},\omega)$ at {\bf Q} = ($\pi$, $\pi$) at strong enough inter-site Coulomb repulsion. Together with the strong maximum in the Im $\chi({\bf Q},\omega)$ at 15 meV it confirms the formation of low-energetic plasmons or charge fluctuations. This provides a jsutification that these excitations are important and together with a spin flcutuations can contribute to the Cooper pairing in layered cuprates. Analysing the charge susceptibilitiy with respect to an instability we obtain a new plasmon branch, $\omega_{\bf q}$, along the Brillouin Zone. In particular, we have found that it goes to zero near {\bf Q}$_{CDW} \approx (2\pi/3, 2\pi/3)$

Pseudogap behavior of nuclear spin relaxation in high Tc superconductors in terms of phase separation

We analyze anew experiments on the NMR in cuprates and find an important information on their phase separation and its stripe character hidden in the dependence of $1/^{63}T_{1}$ on degree of doping. In a broad class of materials $1/^{63}T_{1}$ is the sum of two terms: the temperature independent one attributed to ``incommensurate'' stripes that occur at external doping, and an ``universal'' temperature dependent term ascribed to moving metallic and AF sub-phases. We argue that the frustrated first order phase transition in a broad temperature interval bears a dynamical character.Comment: 5 pages, 3 figures; some comments and references added; accepted for publication in JETP Letter

Microscopic theory of weak pseudogap behavior in the underdoped cuprate superconductors I: General theory and quasiparticle properties

We derive in detail a novel solution of the spin fermion model which is valid in the quasi-static limit pi T<<omega_sf, found in the intermediate (pseudoscaling) regime of the magnetic phase diagram of cuprate superconductors, and use it to obtain results for the temperature and doping dependence of the single particle spectral density, the electron-spin fluctuation vertex function, and the low frequency dynamical spin susceptibility. The resulting strong anisotropy of the spectral density and the vertex function lead to the qualitatively different behavior of_hot_ (around k=(pi,0)) and_cold_ (around k=(pi/2,pi/2)) quasiparticles seen in ARPES experiments. We find that the broad high energy features found in ARPES measurements of the spectral density of the underdoped cuprate superconductors are determined by strong antiferromagnetic (AF) correlations and incoherent precursor effects of an SDW state, with reduced renormalized effective coupling constant. The electron spin-fluctuation vertex function, i.e. the effective interaction of low energy quasiparticles and spin degrees of freedom, is found to be strongly anisotropic and enhanced for hot quasiparticles; the corresponding charge-fluctuation vertex is considerably diminished. We thus demonstrate that, once established, strong AF correlations act to reduce substantially the effective electron-phonon coupling constant in cuprate superconductors.Comment: REVTEX with EPS figures, uses multicol.sty, epsfig,sty, psfig.st

Doping Dependence of the Pseudogap in La(2-x)Sr(x)CuO(4)

We report the results of Raman scattering experiments on single crystals of La(2-x)Sr(x)CuO(4) that span the range from underdoped (x = 0.10) to overdoped (x =0.22). The spectra are consistent with the existence of a strong anisotropic quasiparticle interaction that results in a normal state depletion of spectral weight from regions of the Fermi surface located near the zone axes. The strength of the interaction decreases rapidly with increasing hole concentration and the spectral evidence for the pseudogap vanishes when the optimum doping level is reached. The results suggest that the pseudogap and superconducting gap arise from different mechanisms.Comment: 7 pages, 6 eps figures, added new sections, figures, reference

Cytogerontology since 1881: A reappraisal of August Weismann and a review of modern progress

Cytogerontology, the science of cellular ageing, originated in 1881 with the prediction by August Weismann that the somatic cells of higher animals have limited division potential. Weismann's prediction was derived by considering the role of natural selection in regulating the duration of an organism's life. For various reasons, Weismann's ideas on ageing fell into neglect following his death in 1914, and cytogerontology has only reappeared as a major research area following the demonstration by Hayflick and Moorhead in the early 1960s that diploid human fibroblasts are restricted to a finite number of divisions in vitro. In this review we give a detailed account of Weismann's theory, and we reveal that his ideas were both more extensive in their scope and more pertinent to current research than is generally recognised. We also appraise the progress which has been made over the past hundred years in investigating the causes of ageing, with particular emphasis being given to (i) the evolution of ageing, and (ii) ageing at the cellular level. We critically assess the current state of knowledge in these areas and recommend a series of points as primary targets for future research

Renormalized mean-field theory of the neutron scattering in cuprate superconductors

The magnetic excitation spectrum of the t-t'-J-model is studied in mean-field theory and compared to inelastic neutron-scattering (INS) experiments on YBCO and BSCCO superconductors. Within the slave-particle formulation the dynamical spin response is calculated from a renormalized Fermi liquid with an effective interaction ~J in the magnetic particle--hole channel. We obtain the so-called 41meV resonance at wave vector (pi,pi) as a collective spin-1 excitation in the d-wave superconducting state. It appears sharp (undamped), if the underlying Fermi surface is hole-like with a sufficient next-nearest-neighbor hopping t'<0. The double-layer structure of YBCO or BSCCO is not important for the resonance to form. The resonance energy \omega_{res} and spectral weight at optimal doping come out comparable to experiment. The observed qualitative behavior of \omega_{res} with hole filling is reproduced in the underdoped as well as overdoped regime. A second, much broader peak becomes visible in the magnetic excitation spectrum if the 2D wave-vector is integrated over. It is caused by excitations across the maximum gap, and in contrast to the resonance its energy is almost independent of doping. At energies above or below \omega_{res} the commensurate resonance splits into incommensurate peaks, located off (pi,pi). Below \omega_{res} the intensity pattern is of `parallel' type and the dispersion relation of incommensurate peaks has a negative curvature. This is in accordance with recent INS experiments on YBCO.Comment: 17pp including 14 figure

Bax Function in the Absence of Mitochondria in the Primitive Protozoan Giardia lamblia

Bax-induced permeabilization of the mitochondrial outer membrane and release of cytochrome c are key events in apoptosis. Although Bax can compromise mitochondria in primitive unicellular organisms that lack a classical apoptotic machinery, it is still unclear if Bax alone is sufficient for this, or whether additional mitochondrial components are required. The protozoan parasite Giardia lamblia is one of the earliest branching eukaryotes and harbors highly degenerated mitochondrial remnant organelles (mitosomes) that lack a genome. Here we tested whether human Bax expressed in Giardia can be used to ablate mitosomes. We demonstrate that these organelles are neither targeted, nor compromised, by Bax. However, specialized compartments of the regulated secretory pathway are completely ablated by Bax. As a consequence, maturing cyst wall proteins that are sorted into these organelles are released into the cytoplasm, causing a developmental arrest and cell death. Interestingly, this ectopic cargo release is dependent on the carboxy-terminal 22 amino acids of Bax, and can be prevented by the Bax-inhibiting peptide Ku70. A C-terminally truncated Bax variant still localizes to secretory organelles, but is unable to permeabilize these membranes, uncoupling membrane targeting and cargo release. Even though mitosomes are too diverged to be recognized by Bax, off-target membrane permeabilization appears to be conserved and leads to cell death completely independently of mitochondria

Bid Regulates the Pathogenesis of Neurotropic Reovirus

Reovirus infection leads to apoptosis in both cultured cells and the murine central nervous system (CNS). NF-κB-driven transcription of proapoptotic cellular genes is required for the effector phase of the apoptotic response. Although both extrinsic death-receptor signaling pathways and intrinsic pathways involving mitochondrial injury are implicated in reovirus-induced apoptosis, mechanisms by which either of these pathways are activated and their relationship to NF-κB signaling following reovirus infection are unknown. The proapoptotic Bcl-2 family member, Bid, is activated by proteolytic cleavage following reovirus infection. To understand how reovirus integrates host signaling circuits to induce apoptosis, we examined proapoptotic signaling following infection of Bid-deficient cells. Although reovirus growth was not affected by the absence of Bid, cells lacking Bid failed to undergo apoptosis. Furthermore, we found that NF-κB activation is required for Bid cleavage and subsequent proapoptotic signaling. To examine the functional significance of Bid-dependent apoptosis in reovirus disease, we monitored fatal encephalitis caused by reovirus in the presence and absence of Bid. Survival of Bid-deficient mice was significantly enhanced in comparison to wild-type mice following either peroral or intracranial inoculation of reovirus. Decreased reovirus virulence in Bid-null mice was accompanied by a reduction in viral yield. These findings define a role for NF-κB-dependent cleavage of Bid in the cell death program initiated by viral infection and link Bid to viral virulence