We investigate a large geodetic data set of interferometric synthetic aperture radar (InSAR) and GPS measurements to determine the source parameters for the three main shocks of the 2016 Central Italy earthquake sequence on 24 August and 26 and 30 October (Mw 6.1, 5.9, and 6.5, respectively). Our preferred model is consistent with the activation of four main coseismic asperities belonging to the SW dipping normal fault system associated with the Mount Gorzano‐Mount Vettore‐Mount Bove alignment. Additional slip, equivalent to a Mw ~ 6.1–6.2 earthquake, on a secondary (1) NE dipping antithetic fault and/or (2) on a WNW dipping low‐angle fault in the hanging wall of the main system is required to better reproduce the complex deformation pattern associated with the greatest seismic event (the Mw 6.5 earthquake). The recognition of ancillary faults involved in the sequence suggests a complex interaction in the activated crustal volume between the main normal faults and the secondary structures and a partitioning of strain release.

Hematopoietic and endothelial cell lineages share common progenitors. Accordingly, cytokines formerly thought to be specific for the hematopoietic system have been shown to affect several functions in endothelial cells, including angiogenesis. In this study, we investigated the angiogenic potential of erythropoietin (Epo), the main hormone regulating proliferation, differentiation, and survival of erythroid cells. Epo receptors (EpoRs) have been identified in the human EA.hy926 endothelial cell line by Western blot analysis. Also, recombinant human Epo (rHuEpo) stimulates Janus Kinase-2 (JAK-2) phosphorylation, cell proliferation, and matrix metalloproteinase-2 (MMP-2) production in EA.hy926 cells and significantly enhances their differentiation into vascular structures when seeded on Matrigel. In vivo, rHuEpo induces a potent angiogenic response in the chick embryo chorioallantoic membrane (CAM). Accordingly, endothelial cells of the CAM vasculature express EpoRs, as shown by immunostaining with an anti-EpoR antibody. The angiogenic response of CAM blood vessels to rHuEpo was comparable to that elicited by the prototypic angiogenic cytokine basic fibroblast growth factor (FGF2), it occurred in the absence of a significant mononuclear cell infiltrate, and it was not mimicked by endothelin-1 (ET-1) treatment. Taken together, these data demonstrate the ability of Epo to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo and thus act as a bona fide direct angiogenic factor.

S U M M A R YHere we report the preliminary results of GPS data inversions for coseismic and initial afterslip distributions of the M w 6.3 2009 April 6 L'Aquila earthquake. Coseismic displacements of continuous and survey-style GPS sites, show that the earthquake ruptured a planar SW-dipping normal fault with ∼0.6 m average slip and an estimated moment of 3.9 × 10 18 Nm. Geodetic data agree with the seismological and geological information pointing out the Paganica fault, as the causative structure of the main shock. The position of the hypocentre relative to the coseismic slip distribution supports the seismological evidence of southeastward rupture directivity. These results also point out that the main coseismic asperity probably ended downdip of the Paganica village at a depth of few kilometres in agreement with the small (1-10 cm) observed surface breaks. Time-dependent post-seismic displacements have been modelled with an exponential function. The average value of the estimated characteristic times for near-field sites in the hanging-wall of the fault is 23.9 ± 5.4 d. The comparison between coseismic slip and post-seismic displacements for the first 60 d after the main shock, shows that afterslip occurred at the edges of the main coseismic asperity with a maximum estimated slip of ∼25 cm and an equivalent seismic moment of 6.5 × 10 17 Nm. The activation of the Paganica fault, spatially intermediate between the previously recognized main active fault systems, suggests that strain accumulation in the central Apennines may be simultaneously active on distinct parallel fault systems.

14 C-PNU 145156E binds immobilized GST-Tat with a dissociation constant 5 times higher than heparin and is unable to bind GST-Tat R49/52/53/55/56/57A . Although heparin was an antagonist more potent than suramin, modifications of the backbone structure in selected suramin derivatives originated Tat antagonists whose potency was close to that shown by heparin.In conclusion, suramin derivatives bind the basic domain of Tat, prevent Tat/heparin and Tat/cell surface interactions, and inhibit the biological activity of extracellular Tat. Our data demonstrate that tailored polysulfonated compounds represent potent extracellular Tat inhibitors of possible therapeutic value.