Active Faulting and Deep-Seated Gravitational Slope Deformation in Carbonate Rocks (Central Apennines, Italy): A New "Close-Up" View.

Active faulting and deep-seated gravitational slope deformation (DGSD) are common geological hazards in mountain belts worldwide. In the Italian central Apennines, kilometer-thick carbonate sedimentary sequences are cut by major active normal faults that shape the landscape, generating intermontane basins. Geomorphological observations suggest that the DGSDs are commonly located in fault footwalls. We selected five mountain slopes affected by DGSD and exposing the footwall of active seismogenic normal faults exhumed from 2 to 0.5 km depth. Field structural analysis of the slopes shows that DGSDs exploit preexisting surfaces formed both at depth and near the ground surface by tectonic faulting and, locally, by gravitational collapse. Furthermore, the exposure of sharp scarps along mountain slopes in the central Apennines can be enhanced either by surface seismic rupturing or gravitational movements (e.g., DGSD) or by a combination of the two. At the microscale, DGSDs accommodate deformation mechanisms similar to those associated with tectonic faulting. The widespread compaction of micro-grains (e.g., clast indentation), observed in the matrix of both normal faults and DGSD slip zones, is consistent with clast fragmentation, fluid-infiltration, and congruent pressure-solution active at low ambient temperatures (<60°C) and lithostatic pressures (<80 MPa). Although clast comminution is more intense in the slip zones of normal faults because of the larger displacement accommodated, we are not able to find microstructural markers that allow us to uniquely distinguish faults from DGSDs.

New insights into earthquake precursors from InSAR.

We measured ground displacements before and after the 2009 L'Aquila earthquake using multi-temporal InSAR techniques to identify seismic precursor signals. We estimated the ground deformation and its temporal evolution by exploiting a large dataset of SAR imagery that spans seventy-two months before and sixteen months after the mainshock. These satellite data show that up to 15 mm of subsidence occurred beginning three years before the mainshock. This deformation occurred within two Quaternary basins that are located close to the epicentral area and are filled with sediments hosting multi-layer aquifers. After the earthquake, the same basins experienced up to 12 mm of uplift over approximately nine months. Before the earthquake, the rocks at depth dilated, and fractures opened. Consequently, fluids migrated into the dilated volume, thereby lowering the groundwater table in the carbonate hydrostructures and in the hydrologically connected multi-layer aquifers within the basins. This process caused the elastic consolidation of the fine-grained sediments within the basins, resulting in the detected subsidence. After the earthquake, the fractures closed, and the deep fluids were squeezed out. The pre-seismic ground displacements were then recovered because the groundwater table rose and natural recharge of the shallow multi-layer aquifers occurred, which caused the observed uplift.

Gravity-driven postseismic deformation following the Mw 6.3 2009 L'Aquila (Italy) earthquake.

The present work focuses on the postseismic deformation observed in the region of L'Aquila (central Italy) following the Mw 6.3 earthquake that occurred on April 6, 2009. A new, 16-month-long dataset of COSMO-SkyMed SAR images was analysed using the Persistent Scatterer Pairs interferometric technique. The analysis revealed the existence of postseismic ground subsidence in the mountainous rocky area of Mt Ocre ridge, contiguous to the sedimentary plain that experienced coseismic subsidence. The postseismic subsidence was characterized by displacements of 10 to 35 mm along the SAR line of sight. In the Mt Ocre ridge, widespread morphological elements associated with gravitational spreading have been previously mapped. We tested the hypothesis that the postseismic subsidence of the Mt Ocre ridge compensates the loss of equilibrium induced by the nearby coseismic subsidence. Therefore, we simulated the coseismic and postseismic displacement fields via the finite element method. We included the gravitational load and fault slip and accounted for the geometrical and rheological characteristics of the area. We found that the elastoplastic behaviour of the material under gravitational loading best explains the observed postseismic displacement. These findings emphasize the role of gravity in the postseismic processes at the fault scale.

Did the September 2010 (Darfield) earthquake trigger the February 2011 (Christchurch) event?

We have investigated the possible cause-and-effect relationship due to stress transfer between two earthquakes that occurred near Christchurch, New Zealand, in September 2010 and in February 2011. The Mw 7.1 Darfield (Canterbury) event took place along a previously unrecognized fault. The Mw 6.3 Christchurch earthquake, generated by a thrust fault, occurred approximately five months later, 6 km south-east of Christchurch's city center. We have first measured the surface displacement field to retrieve the geometries of the two seismic sources and the slip distribution. In order to assess whether the first earthquake increased the likelihood of occurrence of a second earthquake, we compute the Coulomb Failure Function (CFF). We find that the maximum CFF increase over the second fault plane is reached exactly around the hypocenter of the second earthquake. In this respect, we may conclude that the Darfield earthquake contributed to promote the rupture of the Christchurch fault.

CD127(low) expression in CD4+CD25(high) T cells as immune biomarker of renal function in transplant patients.

BACKGROUND: Noninvasive tests measuring cellular immunity could help predict immunologic risk and subsequent allograft dysfunction in transplant patients. CD25 is a promising marker of activation. Recent descriptions of CD127 expression as a discriminating factor between regulatory and activated T cells suggest its potential utility. METHODS: Expression of CD127 in CD4+CD25 T cells was analyzed by flow cytometry in peripheral blood from 62 renal transplanted patients and 30 healthy controls. Forty patients presented stable graft function and 22 suffered renal failure. RESULTS: Renal transplant patients showed higher levels of CD127(high) and a lower frequency of CD127(low) than healthy controls (0.63% vs. 0.29% [P<0.001] and 1.4% vs. 2.4% [P<0.001], respectively). However, high frequencies of not only CD127(high) but also CD127(low) showed a significant correlation with serum creatinine levels (P=0.012 and P=0.003, respectively). Allogenic stimulation in vitro increased the frequency of CD127(low) subset in a dose dependent manner. Furthermore, in patients with a high frequency of CD127(low) subset, this consisted mostly of FoxP3 negative cells, discarding their regulatory origin. Median frequency of CD127(low), but not CD127(high), cells showed significant differences between patients with stable function and with renal failure (P<0.005), with 16.7% and 53.1% of individuals above the median CD127(low) value (1.4%), respectively. CONCLUSION: Quantification of CD127(low) subset through staining of CD4+ T cells with the combined markers CD127/CD25/CD45RO has been demonstrated to be a significant tool for monitoring the outcome course of renal transplant patients.

The cognitive and histopathological effects of chronic 4-vessel occlusion in rats depend on the set of vessels occluded and the age of the animals.

Continuing previous efforts to develop the 4-vessel occlusion (4-VO) model of chronic cerebral hypoperfusion (CCH), here we evaluated whether permanent, stepwise 4-VO causes both learning deficits, hippocampal neurodegeneration and retinal lesion in young, middle-aged or aged rats. Chronic 4-VO was induced by ligation of different sets of vessels, i.e., the vertebral arteries (VA) plus common carotid arteries (CCA) (4-VO/CCA model) or the VA plus internal carotid arteries (ICA) (4-VO/ICA model) with a 1-week interstage interval. Forty days after the 4-VO, the rats were tested for spatial learning impairment, and then examined for hypoxic/ischemic damage. Young, 4-VO/CCA rats exhibited cognitive impairment, hippocampal neurodegeneration and retinal lesion (p<0.0001-0.05). After 4-VO/ICA, neither young nor middle-aged rats exhibited any learning deficits, hippocampal or retinal damage. In aged rats, chronic 4-VO/ICA caused a mild learning deficit (p<0.05). A significant effect of training was observed for the old, sham-operated rats (p<0.0001-0.001), but not for the aged 4-VO/ICA rats (p>0.05). On average, hippocampal cell density did not change after 4-VO/ICA in aged rats, but 3 of 10 subjects exhibited reduced pyramidal cell counts in all hippocampal subfields. Retinal morphology appeared to be unaffected in the 4-VO/ICA aged rats. These data suggest that the 4-VO/ICA model, but not the 4-VO/CCA model, is a suitable paradigm to study the behavioral outcome of CCH given the preservation of the retina after 4-VO/ICA. Moreover, the age at which 4-VO/ICA occurs seems to be an important factor for determining the behavioral and neuropathological changes.

Casquetes para moldagens unitárias com guias de inserção e limitadores de penetração (casquetes de nóbilo modificados) / Copings for individual impression with insertion guides and penetration stoppage

Este trabalho mostra uma técnica alternativa para a realização de moldagens de preparos protéticos para coroas totais, com casquetes individuais e que apresentam além de abas de retenção, guias de inserção e limitadores de penetração