Search

The Himalayan orogen has produced three thrust earthquakes withmoment magnitude (M[sub w]) 7.8 to 8.5 during the past century, yet nosurface ruptures associated with these great earthquakes have beendocumented. Here, we present paleoseismic evidence from east centralNepal that, since ∼700 A.D., a single earthquake ruptured theFrontal Thrust fault at ∼1100 A.D., with a surface displacement of∼17 (-5/-3) meters and a lateral extent and size that could haveexceeded 240 kilometers and ∼M[sub W] 8.8, respectively. Rupturesassociated with M[sub w] <8.2 events would contribute to the frontalHimalayas folding but would stop before reaching the surface. Thesefindings could require substantial modifications to current regionalseismic hazard models. [ABSTRACT FROM AUTHOR]

New mapping demonstrates that active emergent thrust faulting is occurring within the fold-and-thrust belt north of the deformation thrust front in the NW Himalaya. The >60-km-long Riasi fault system is the southeasternmost segment of a seismically active regional fault system that extends more than 200 km stepwise to the southeast from the Balakot-Bagh fault in Pakistan into northwestern India. Two fault strands, the Main Riasi and Frontal Riasi thrusts, dominate the fault system in the study area. The Main Riasi thrust places Precambrian Sirban Formation over folded unconsolidated Quaternary sediments and fluvial terraces. New age data and crosscutting relationships between the Main Riasi thrust and the Quaternary units demonstrate that the Main Riasi thrust accommodated shortening between 100 and 40 ka at rates of 6-7 mm/yr. Deformation shifted to the southern Frontal Riasi thrust splay after ca. 39 ka. Differential uplift of a 14-7 ka terrace yields a range of shortening rates between 3 and 6 mm/yr. Together, shortening across the two strands indicates that a 6-7 mm/yr shortening rate has characterized the Riasi fault system since 100 ka. Geodetic data indicate that an 11-12 mm/yr arc-normal shortening rate characterizes the interseismic strain accumulation across the plate boundary due to India-Tibet convergence. These data combined with rates of other active faults in the Kashmir Himalaya indicate that the Suruin-Mastgarh anticline at the thrust front accounts for the remainder 40%-50% of the convergence not taken up by the Riasi fault system. Active deformation, and therefore earthquake sources, include both internal faults such the Riasi fault system, as well as rupture of the basal décollement (the Main Himalayan thrust) to the thrust front. Limited paleoseismic data from the Riasi fault system, the historical earthquake record of the past 1000 yr, the high strain rates, and partitioning of slip between the Riasi fault system and the thrust front demonstrate that a substantial slip deficit characterizes both structures and highlights the presence of a regionally important seismic gap in the Kashmir Himalaya. Slip deficit, scaling relationships, and a scenario of rupture and slip on the basal décollement (the Main Himalayan thrust) parsed onto either the Riasi fault system or the thrust front, or both, suggests that great earthquakes (Mw > 8) pose an even greater seismic hazard than the Mw 7.6 2005 earthquake on the Balakot- Bagh fault in Pakistan Azad Kashmir. [ABSTRACT FROM AUTHOR]

It has been observed experimentally that, in many cell types, calcium fluxes across the plasma membrane affect inositol trisphosphate (IP3)-induced calcium oscillations. This is somewhat puzzling; since IP3-induced calcium oscillations involve the cycling of calcium to and from the endoplasmic reticulum it is not well understood how they can be so strongly affected by membrane fluxes. We use a mathematical model to answer this question, a model that relies on the introduction of a slow variable, the Ca2+ load of the cell. We carry out a bifurcation analysis of the model in two time scales, treating the slow variable as a bifurcation parameter, thus simulating a closed-cell model, in which there is no Ca2+ transport to and from the external medium. The presence of a homoclinic bifurcation in the closed-cell model accounts for the existence of a critical value of the Ca2+ load which controls the existence of cytosolic Ca2+ oscillations. Our model predictions are confirmed by experimental results. Since similar behavior is observed in two other models of IP3-induced Ca2+ oscillations, it is possible that this bifurcation structure is a generic feature of Ca2+ oscillation models. [ABSTRACT FROM AUTHOR]

In some cell types, oscillations in the concentration of free intracellular calcium ([Ca2+]) are accompanied by oscillations in the concentration of inositol 1,4,5-trisphosphate ([IP3]). However, in most cell types it is still an open question as to whether oscillations in [IP3] are necessary for Ca2+ oscillations in vivo, or whether they merely follow passively. Using a wide range of models, we show that the response to an artificially applied pulse of IP3 can be used to distinguish between these two cases. Hence, we show that muscarinic receptor-mediated, long-period Ca2+ oscillations in pancreatic acinar cells depend or, [IP3] oscillations, whereas short- period Ca2+ oscillations in airway smooth muscle do not. [ABSTRACT FROM AUTHOR]