Spatial restriction of alpha4 integrin phosphorylation regulates lamellipodial stability and alpha4beta1-dependent cell migration.

Integrins coordinate spatial signaling events essential for cell polarity and directed migration. Such signals from alpha4 integrins regulate cell migration in development and in leukocyte trafficking. Here, we report that efficient alpha4-mediated migration requires spatial control of alpha4 phosphorylation by protein kinase A, and hence localized inhibition of binding of the signaling adaptor, paxillin, to the integrin. In migrating cells, phosphorylated alpha4 accumulated along the leading edge. Blocking alpha4 phosphorylation by mutagenesis or by inhibition of protein kinase A drastically reduced alpha4-dependent migration and lamellipodial stability. alpha4 phosphorylation blocks paxillin binding in vitro; we now find that paxillin and phospho-alpha4 were in distinct clusters at the leading edge of migrating cells, whereas unphosphorylated alpha4 and paxillin colocalized along the lateral edges of those cells. Furthermore, enforced paxillin association with alpha4 inhibits migration and reduced lamellipodial stability. These results show that topographically specific integrin phosphorylation can control cell migration and polarization by spatial segregation of adaptor protein binding

Spatial restriction of α4 integrin phosphorylation regulates lamellipodial stability and α4β1-dependent cell migration

Întegrins coordinate spatial signaling events essential for cell polarity and directed migration. Such signals from α4 integrins regulate cell migration in development and in leukocyte trafficking. Here, we report that efficient α4-mediated migration requires spatial control of α4 phosphorylation by protein kinase A, and hence localized inhibition of binding of the signaling adaptor, paxillin, to the integrin. In migrating cells, phosphorylated α4 accumulated along the leading edge. Blocking α4 phosphorylation by mutagenesis or by inhibition of protein kinase A drastically reduced α4-dependent migration and lamellipodial stability. α4 phosphorylation blocks paxillin binding in vitro; we now find that paxillin and phospho-α4 were in distinct clusters at the leading edge of migrating cells, whereas unphosphorylated α4 and paxillin colocalized along the lateral edges of those cells. Furthermore, enforced paxillin association with α4 inhibits migration and reduced lamellipodial stability. These results show that topographically specific integrin phosphorylation can control cell migration and polarization by spatial segregation of adaptor protein binding

Dynamic Exponent of t-J and t-J-W Model

Drude weight of optical conductivity is calculated at zero temperature by exact diagonalization for the two-dimensional t-J model with the two-particle term, $W$. For the ordinary t-J model with $W$=0, the scaling of the Drude weight $D \propto \delta^2$ for small doping concentration $\delta$ is obtained, which indicates anomalous dynamic exponent $z$=4 of the Mott transition. When $W$ is switched on, the dynamic exponent recovers its conventional value $z$=2. This corresponds to an incoherent-to-coherent transition associated with the switching of the two-particle transfer.Comment: LaTeX, JPSJ-style, 4 pages, 5 eps files, to appear in J. Phys. Soc. Jpn. vol.67, No.6 (1998

Final-State-Interaction Simulation of T-Violation in the Top-Quark Semileptonic Decay

The standard electroweak final-state interaction induces a false T-odd correlation in the top-quark semileptonic decay. The correlation parameter is calculated in the standard model and found to be considerably larger than those that could be produced by genuine T-violation effects in a large class of theoretical models.Comment: 14 pages, 1 diagram (not included

Synergistic effects of traumatic head injury and apolipoprotein 4 in patients with Alzheimer’s disease

The apolipoprotein 4 allele increases the risk of Alzheimer’s disease (AD), but cerebral deposition of B-amyloid with age, a genetic mutation, or head injury may contribute to the pathogenesis of this disease. We examined the risks of AD associated with traumatic head injury and apolipoprotein 4 in 236 community-dwelling elderly persons. A 10-fold increase in the risk of AD was associated with both apolipoprotein 4a nd a history of traumatic head injury, compared with a two-fold increase in risk with apolipoprotein 4 alone. Head injury in the absence of an apolipoprotein 4 allele did not increase risk. These data imply that the biological effects of head injury may increase the risk of AD, but only through a synergistic relationship with apolipoprotein 4

A meta-analysis of state-of-the-art electoral prediction from Twitter data

Electoral prediction from Twitter data is an appealing research topic. It seems relatively straightforward and the prevailing view is overly optimistic. This is problematic because while simple approaches are assumed to be good enough, core problems are not addressed. Thus, this paper aims to (1) provide a balanced and critical review of the state of the art; (2) cast light on the presume predictive power of Twitter data; and (3) depict a roadmap to push forward the field. Hence, a scheme to characterize Twitter prediction methods is proposed. It covers every aspect from data collection to performance evaluation, through data processing and vote inference. Using that scheme, prior research is analyzed and organized to explain the main approaches taken up to date but also their weaknesses. This is the first meta-analysis of the whole body of research regarding electoral prediction from Twitter data. It reveals that its presumed predictive power regarding electoral prediction has been rather exaggerated: although social media may provide a glimpse on electoral outcomes current research does not provide strong evidence to support it can replace traditional polls. Finally, future lines of research along with a set of requirements they must fulfill are provided.Comment: 19 pages, 3 table

Superconductivity of the Sr2Ca12Cu24O41Sr_2 Ca_{12} Cu_{24} O_{41} spin ladder system: Are the superconducting pairing and the spin-gap formation of the same origin?

Pressure-induced superconductivity in a spin-ladder cuprate Sr$_2$Ca$_{12}$Cu$_{24}$O$_{41}$ has not been studied on a microscopic level so far although the superconductivity was already discovered in 1996. We have improved high-pressure technique with using a large high-quality crystal, and succeeded in studying the superconductivity using $^{63}$Cu nuclear magnetic resonance (NMR). We found that anomalous metallic state reflecting the spin-ladder structure is realized and the superconductivity possesses a s-wavelike character in the meaning that a finite gap exists in the quasi-particle excitation: At pressure of 3.5GPa we observed two excitation modes in the normal state from the relaxation rate $T_1^{-1}$. One gives rise to an activation-type component in $T_1^{-1}$, and the other $T$-linear component linking directly with the superconductivity. This gapless mode likely arises from free motion of holon-spinon bound states appearing by hole doping, and the pairing of them likely causes the superconductivity.Comment: to be published in Phys. Rev. Let