STATIC AND DYNAMIC STRESS CHANGE AT 27 VOLCANOES OF THE CENTRAL AMERICAN VOLCANIC ARC AFTER THE MW. 7.6 COSTA RICA EARTHQUAKE OF 5 SEPTEMBER 2012

Large earthquakes may strongly influence the activity of volcanoes through static and dynamic processes. In this study, we quantify the static and dynamic stress change on 27 volcanoes in Central America, after the Mw 7.6 Costa Rica earthquake of 5 September 2012. Following this event, 8 volcanoes showed signs of activity. We calculated the static stress change due to the earthquake on hypothetical faults under these volcanoes with Coulomb 3.3. For the dynamic stress change, we computed synthetic seismograms to simulate the waveforms at these volcanoes. We then calculated the Peak Dynamic Stress (PDS) from the modeled peak ground velocities. The resulting values are from moderate to minor changes in stress (10-1-10-2 MPa) with the PDS values generally an order of magnitude larger than the static stress change. Although these values are small, they may be enough to trigger a response by the volcanoes, and are on the order of stress changes implicated in many other studies of volcano and earthquake triggering by large earthquakes. This study provides insight into the poorly-constrained mechanism for remote triggering.

ROLE OF MICRORNA LET-7 IN PANCREATIC BETA CELLS

MicroRNAs (miRNAs) are small non-coding RNAs that inhibit gene expression at transcriptional or post-transcriptional level. Let-7 family is among the first identified human miRNAs and regulates multiple cellular processes including glucose metabolism in multiple organs. It has been reported that overexpression of let-7 resulted in insulin resistance and impaired glucose tolerance through repressing insulin signaling pathway in both muscle and liver. However, the role and mechanism underlying let-7 function in pancreatic beta-cells have yet to be elucidated. Let-7 family contains nine members, which poses a significant challenge in complete deletion of this miRNA family. To study the function of let-7 and to overcome the functional redundancies of various let-7 members in pancreatic beta-cells, the highly expressed let-7a and let-7b were blocked simultaneously using short tandem target mimic (STTM) approach developed in our laboratory. Introducing STTM-let7 into beta-cells markedly increased the expression of Caspase 3, a direct target of let-7, confirming a sufficient functional knockdown of let-7a/b by STTM-let7. STTM-let7 enhanced apoptotic cell death induced by cytokine, indicating that let-7a/b is able to protect from apoptosis through attenuating Caspase 3 expression in pancreatic beta-cells. In contrast to the previous observation that let-7 silencing increases insulin signaling in muscle and liver, inhibition of let-7 with STTM-let7 significantly repressed glucose-stimulated insulin signaling in pancreatic beta-cells, leading to impaired insulin secretion and reduced beta-cell proliferation. Taken together, an appropriate level of let-7 is essential in maintaining beta-cell function and viability. Dysregulation of let-7 may contribute to the pathogenesis of type 2 diabetes.