Slow Slip Events and Time-Dependent Variations in Locking Beneath Lower Cook Inlet of the Alaska-Aleutian Subduction Zone

We identify a series of abrupt changes in GPS site velocities in Lower Cook Inlet, Alaska, in late 2004, early 2010, and late 2011. The site motions during each time period are nearly linear. The surface deformations inferred from GPS for pre-2004 and 2010–2011 are similar to each other, as are 2004–2010 and post-2011. We estimate the slip distribution on the Alaska-Aleutian subduction plate interface accounting for upper plate block rotations and interpret this toggling between two deformation patterns as caused by transient slip. We find that by allowing negative slip deficit rates (i.e., creep rates in excess of relative plate motion), the data in Lower Cook Inlet are fit significantly better during pre-2004 and 2010–2011, suggesting the occurrence of slow slip events (SSEs) there during those time periods. The earlier SSE lasted at least 9 years (observations in that area began in 1995) with Mw ~7.8. The latter SSE had almost the same area as the earlier one and a duration of ~2 years with Mw ~7.2. During 2004–2010 and post-2011, the inversions result in only positive slip deficit rates (i.e., locking) in Lower Cook Inlet. Slip rates are nearly constant during the Lower Cook Inlet SSEs, and the events start and stop abruptly. Both of these properties contrast with observations of SSEs in Upper Cook Inlet and elsewhere. The Lower Cook Inlet SSEs are consistent with previously proposed duration-magnitude scaling laws and demonstrate that slow slip events can last as long as a decade

JAK inhibition differentially affects NK cell and ILC1 homeostasis

Janus kinase (JAK) inhibitors are widely used in the treatment of multiple autoimmune and inflammatory diseases. Immunologic and transcriptomic profiling have revealed major alterations on natural killer (NK) cell homeostasis associated with JAK inhibitions, while information on other innate lymphoid cells (ILCs) is still lacking. Herein, we observed that, in mice, the homeostatic pool of liver ILC1 was less affected by JAK inhibitors compared to the pool of NK cells present in the liver, spleen and bone marrow. JAK inhibition had overlapping effects on the transcriptome of both subsets, mainly affecting genes regulating cell cycle and apoptosis. However, the differential impact of JAK inhibition was linked to the high levels of the antiapoptotic gene Bcl2 expressed by ILC1. Our findings provide mechanistic explanations for the effects of JAK inhibitors on NK cells and ILC1 which could be of major clinically relevance

A plastidial sodium-dependent pyruvate transporter (vol 476, pg 472, 2011)

Furumoto T, Yamaguchi T, Ohshima-Ichie Y, et al. A plastidial sodium-dependent pyruvate transporter (vol 476, pg 472, 2011). Nature. 2011;478(7368):274

Intermediate-energy Coulomb excitation of 104 Sn: Moderate E2 strength decrease approaching 100 Sn

International audienceThe reduced transition probability B(E2)↑ of the first excited 2 + state in the nucleus 104 Sn was measured via Coulomb excitation in inverse kinematics at intermediate energies. A value of 0.173(28) e 2 b 2 was extracted from the absolute cross section on a Pb target. Feeding contributions in 104 Sn from higher lying states were estimated by a reference measurement of the stable 112 Sn. Corresponding only to a moderate decrease of excitation strength relative to the almost constant values observed in the proton-rich, even-A 106−114 Sn isotopes, present state-of-the-art shell-model predictions, which include proton and neutron excitations across the N = Z = 50 shell closures as well as standard polarization charges, underestimate the experimental findings

In-beam γ-ray spectroscopy of Te 136 at relativistic energies

The reduced transition probability B(E2;01+→21+) to the first excited 2+ state of the neutron-rich nucleus Te136, with two protons and two neutrons outside the doubly magic Sn132 core, was measured via Coulomb excitation at relativistic energies at the RIKEN Radioactive Isotope Beam Factory. A value of B(E2)=0.191(26) e2b2 was extracted from the measured inelastic scattering cross section on an Au target taking into account the contributions from both Coulomb and nuclear excitations. In addition, an upper limit for the transition strength to a 2+ state of mixed-symmetry character in the excitation energy range of 1.5-2.2 MeV was determined and compared to the predictions of various theoretical calculations. Because of the high statistics gathered in the present experiment the error of the deduced B(E2) value is dominated by the systematic uncertainties involved in the analysis of Coulomb excitation experiments at beam energies around 150 MeV/u. Therefore, the latter are for the first time assessed in detail in the present work

Transition strengths in the neutron-rich 73,74,75Ni^73,74,75Ni isotopes

status: publishe

Effects of green tea polyphenol on methylation status of RECK gene and cancer cell invasion in oral squamous cell carcinoma cells

RECK is a novel tumour suppressor gene that negatively regulates matrix metalloproteinases (MMPs) and inhibits tumour invasion, angiogenesis and metastasis. In the present study, we investigated the effects of epigallocatechin-3-gallate (EGCG), a major polyphenol in green tea, on the methylation status of the RECK gene and cancer invasion in oral squamous cell carcinoma cell lines. Our results showed that treatment of oral cancer cells with EGCG partially reversed the hypermethylation status of the RECK gene and significantly enhanced the expression level of RECK mRNA. Inhibition of MMP-2 and MMP-9 levels was also observed in these cells after treatment with EGCG. Interestingly, EGCG significantly suppressed cancer cell-invasive ability by decreasing the number of invasive foci (P<0.0001) as well as invasion depth (P<0.005) in three-dimensional collagen invasion model. Although further investigation is required to assess the extent of contribution of RECK on MMPs to the suppression of invasive behaviour, these results support the conclusion that EGCG plays a key role in suppressing cell invasion through multiple mechanisms, possibly by demethylation effect on MMP inhibitors such as RECK

Anaphylatoxin C3a receptors in asthma

The complement system forms the central core of innate immunity but also mediates a variety of inflammatory responses. Anaphylatoxin C3a, which is generated as a byproduct of complement activation, has long been known to activate mast cells, basophils and eosinophils and to cause smooth muscle contraction. However, the role of C3a in the pathogenesis of allergic asthma remains unclear. In this review, we examine the role of C3a in promoting asthma. Following allergen challenge, C3a is generated in the lung of subjects with asthma but not healthy subjects. Furthermore, deficiency in C3a generation or in G protein coupled receptor for C3a abrogates allergen-induced responses in murine models of pulmonary inflammation and airway hyperresponsiveness. In addition, inhibition of complement activation or administration of small molecule inhibitors of C3a receptor after sensitization but before allergen challenge inhibits airway responses. At a cellular level, C3a stimulates robust mast cell degranulation that is greatly enhanced following cell-cell contact with airway smooth muscle (ASM) cells. Therefore, C3a likely plays an important role in asthma primarily by regulating mast cell-ASM cell interaction