资源环境科技发展态势分析平台

Observed reversals in GNSS surface motions suggests greatly enhanced slab pull in the months preceding the great subduction earthquakes in Maule (Chile, 2010) and Tohoku-oki (Japan, 2011) of moment magnitudes 8.8 and 9.0.

Megathrust earthquakes are responsible for some of the most devastating natural disasters(1). To better understand the physical mechanisms of earthquake generation, subduction zones worldwide are continuously monitored with geophysical instrumentation. One key strategy is to install stations that record signals from Global Navigation Satellite Systems(2,3) (GNSS), enabling us to track the non-steady surface motion of the subducting and overriding plates before, during and after the largest events(4-6). Here we use a recently developed trajectory modelling approach(7) that is designed to isolate secular tectonic motions from the daily GNSS time series to show that the 2010 Maule, Chile (moment magnitude 8.8) and 2011 Tohoku-oki, Japan (moment magnitude 9.0) earthquakes were preceded by reversals of 4-8 millimetres in surface displacement that lasted several months and spanned thousands of kilometres. Modelling of the surface displacement reversal that occurred before the Tohoku-oki earthquake suggests an initial slow slip followed by a sudden pulldown of the Philippine Sea slab so rapid that it caused a viscoelastic rebound across the whole of Japan. Therefore, to understand better when large earthquakes are imminent, we must consider not only the evolution of plate interface frictional processes but also the dynamic boundary conditions from deeper subduction processes, such as sudden densification of metastable slab.

Activation of the non-canonical NF-kappa B signalling pathway by AZD5582 results in the induction of HIV and SIV RNA expression in the blood and tissues of antiretroviral-therapy-treated humanized mice and rhesus macaques.

Long-lasting, latently infected resting CD4(+) T cells are the greatest obstacle to obtaining a cure for HIV infection, as these cells can persist despite decades of treatment with antiretroviral therapy (ART). Estimates indicate that more than 70 years of continuous, fully suppressive ART are needed to eliminate the HIV reservoir(1). Alternatively, induction of HIV from its latent state could accelerate the decrease in the reservoir, thus reducing the time to eradication. Previous attempts to reactivate latent HIV in preclinical animal models and in clinical trials have measured HIV induction in the peripheral blood with minimal focus on tissue reservoirs and have had limited effect(2-9). Here we show that activation of the non-canonical NF-kappa B signalling pathway by AZD5582 results in the induction of HIV and SIV RNA expression in the blood and tissues of ART-suppressed bone-marrow-liver-thymus (BLT) humanized mice and rhesus macaques infected with HIV and SIV, respectively. Analysis of resting CD4(+) T cells from tissues after AZD5582 treatment revealed increased SIV RNA expression in the lymph nodes of macaques and robust induction of HIV in almost all tissues analysed in humanized mice, including the lymph nodes, thymus, bone marrow, liver and lung. This promising approach to latency reversal-in combination with appropriate tools for systemic clearance of persistent HIV infection-greatly increases opportunities for HIV eradication.