Sedimentology and kinematics of a large, retrogressive growth-fault system in Upper Carboniferous deltaic sediments, western Ireland

Growth faulting is a common feature of many deltaic environments and is vital in determining local sediment dispersal and accumulation, and hence in controlling the resultant sedimentary facies distribution and architecture. Growth faults occur on a range of scales, from a few centimetres to hundreds of metres, with the largest growth faults frequently being under-represented in outcrops that are often smaller than the scale of feature under investigation. This paper presents data from the exceptionally large outcrops of the Cliffs of Moher, western Ireland, where a growth-fault complex affects strata up to 60 m in thickness and extends laterally for 3 km. Study of this Namurian (Upper Carboniferous) growth-fault system enables the relationship between growth faulting and sedimentation to be detailed and permits reconstruction of the kinematic history of faulting. Growth faulting was initiated with the onset of sandstone deposition on a succession of silty mudstones that overlie a thin, marine shale. The decollement horizon developed at the top of the marine shale contact for the first nine faults, by which time aggradation in the hangingwall exceeded 60 m in thickness. After this time, failure planes developed at higher stratigraphic levels and were associated with smaller scale faults. The fault complex shows a dominantly landward retrogressive movement, in which only one fault was largely active at any one time. There is no evidence of compressional features at the base of the growth faults, thus suggesting open-ended slides, and the faults display both disintegrative and non-disintegrative structure. Thin-bedded, distal mouth bar facies dominate the hangingwall stratigraphy and, in the final stages of growth-fault movement, erosion of the crests of rollover structures resulted in the highest strata being restricted to the proximity of the fault. These upper erosion surfaces on the fault scarp developed erosive chutes that were cut parallel to flow and are downlapped by the distal hangingwall strata of younger growth faults

Identification of protein kinase D as a novel contraction-activated kinase linked to GLUT4-mediated glucose uptake independent of AMPK

Contraction-induced glucose uptake is only partly mediated by AMPK activation. We examined whether the diacylglycerol-sensitive protein kinase D (PKD; also known as novel PKC isoform mu) is also involved in the regulation of glucose uptake in the contracting heart. As an experimental model, we used suspensions of cardiac myocytes, which were electrically stimulated to contract or treated with the contraction-mimicking agent oligomycin. Induction of contraction at 4 Hz in cardiac myocytes or treatment with 1 mu M oligomycin enhanced (i) autophosphorylation of PKD at Ser916 by 5.1- and 3.8-fold, respectively, (ii) phosphorylation of PKD's downstream target cardiac-troponin-I (cTnI) by 2.9- and 2.1-fold, respectively, and (iii) enzymatic activity of immunoprecipitated PKD towards the substrate peptide syntide-2 each by 1.5-fold. Although AMPK was also activated under these same conditions, in vitro phosphorylation assays and studies with cardiac myocytes from AMPK alpha 2(-/-) mice indicated that activation of PKD occurs independent of AMPK activation. CaMKK beta, and the cardiac-specific PKC isoforms alpha, beta, and epsilon were excluded as upstream kinases for PKD in contraction signaling because none of these kinases were activated by oligomycin. Stimulation of glucose uptake and induction of GLUT4 translocation in cardiac myocytes by contraction and oligomycin each were sensitive to inhibition by the PKC/PKD inhibitors staurosporin and calphostin-C. Together, these data elude to a role of PKD in contraction-induced GLUT4 translocation. Finally, the combined actions of PKD on cTnI phosphorylation and on GLUT4 translocation would efficiently link accelerated contraction mechanics to increased energy production when the heart is forced to increase its contractile activity

Merhaut, Josef

(1863 - 1907), Schriftstelle