Power Line Foundation Design Using the Pressuremeter

During the design phase of a 2000-towers electric power transmission line, a load test program was undertaken to evaluate the accuracy of new design methods for uplift and lateral capacity of drilled shafts. Seven uplift tests and six lateral load tests were performed in three different soil deposits: a medium clay, a very hard clay and a sand. The shafts were 2 ft in diameter and either 10 or 15 ft long. The pressuremeter test results are used together with existing methods to predict the behavior of the shafts

Load-settlement modelling of axially loaded drilled shafts using CPT-based recurrent neural networks

The design of pile foundations requires good estimation of the pile load-carrying capacity and settlement. Design for bearing capacity and design for settlement have been traditionally carried out separately. However, soil resistance and settlement are influenced by each other, and the design of pile foundations should thus consider the bearing capacity and settlement inseparably. This requires the full load–settlement response of piles to be well predicted. However, it is well known that the actual load–settlement response of pile foundations can be obtained only by load tests carried out in situ, which are expensive and time-consuming. In this paper, recurrent neural networks (RNNs) were used to develop a prediction model that can resemble the full load–settlement response of drilled shafts (bored piles) subjected to axial loading. The developed RNN model was calibrated and validated using several in situ full-scale pile load tests, as well as cone penetration test (CPT) data. The results indicate that the developed RNN model has the ability to reliably predict the load–settlement response of axially loaded drilled shafts and can thus be used by geotechnical engineers for routine design practice

Simultaneous determination of thermal conductivity, thermal diffusivity and specific heat in sI methane hydrate

This paper is not subject to U.S. copyright. The definitive version was published in Geophysical Journal International 169 (2007), 767–774, doi:10.1111/j.1365-246X.2007.03382.x.Thermal conductivity, thermal diffusivity and specific heat of sI methane hydrate were measured as functions of temperature and pressure using a needle probe technique. The temperature dependence was measured between −20°C and 17°C at 31.5 MPa. The pressure dependence was measured between 31.5 and 102 MPa at 14.4°C. Only weak temperature and pressure dependencies were observed. Methane hydrate thermal conductivity differs from that of water by less than 10 per cent, too little to provide a sensitive measure of hydrate content in water-saturated systems. Thermal diffusivity of methane hydrate is more than twice that of water, however, and its specific heat is about half that of water. Thus, when drilling into or through hydrate-rich sediment, heat from the borehole can raise the formation temperature more than 20 per cent faster than if the formation's pore space contains only water. Thermal properties of methane hydrate should be considered in safety and economic assessments of hydrate-bearing sediment.Gas Hydrate Project of the U.S. Geological Survey’s Coastal and Marine Geology Program, in addition to Department of Energy contract DE-AI21–92MC2921

Evidence That Ca2+ within the Microdomain of the L-Type Voltage Gated Ca2+ Channel Activates ERK in MIN6 Cells in Response to Glucagon-Like Peptide-1

Glucagon like peptide-1 (GLP-1) is released from intestinal L-cells in response to nutrient ingestion and acts upon pancreatic β-cells potentiating glucose-stimulated insulin secretion and stimulating β-cell proliferation, differentiation, survival and gene transcription. These effects are mediated through the activation of multiple signal transduction pathways including the extracellular regulated kinase (ERK) pathway. We have previously reported that GLP-1 activates ERK through a mechanism dependent upon the influx of extracellular Ca2+ through L-type voltage gated Ca2+ channels (VGCC). However, the mechanism by which L-type VGCCs couple to the ERK signalling pathway in pancreatic β-cells is poorly understood. In this report, we characterise the relationship between L-type VGCC mediated changes in intracellular Ca2+ concentration ([Ca2+]i) and the activation of ERK, and demonstrate that the sustained activation of ERK (up to 30 min) in response to GLP-1 requires the continual activation of the L-type VGCC yet does not require a sustained increase in global [Ca2+]i or Ca2+ efflux from the endoplasmic reticulum. Moreover, sustained elevation of [Ca2+]i induced by ionomycin is insufficient to stimulate the prolonged activation of ERK. Using the cell permeant Ca2+ chelators, EGTA-AM and BAPTA-AM, to determine the spatial dynamics of L-type VGCC-dependent Ca2+ signalling to ERK, we provide evidence that a sustained increase in Ca2+ within the microdomain of the L-type VGCC is sufficient for signalling to ERK and that this plays an important role in GLP-1- stimulated ERK activation

Lipopolysaccharides Impair Insulin Gene Expression in Isolated Islets of Langerhans via Toll-Like Receptor-4 and NF-κB Signalling

BACKGROUND:Type 2 diabetes is characterized by pancreatic β-cell dysfunction and is associated with low-grade inflammation. Recent observations suggest that the signalling cascade activated by lipopolysaccharides (LPS) binding to Toll-Like Receptor 4 (TLR4) exerts deleterious effects on pancreatic β-cell function; however, the molecular mechanisms of these effects are incompletely understood. In this study, we tested the hypothesis that LPS alters insulin gene expression via TLR4 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in islets. METHODOLOGY/PRINCIPAL FINDINGS:A 24-h exposure of isolated human, rat and mouse islets of Langerhans to LPS dose-dependently reduced insulin gene expression. This was associated in mouse and rat islets with decreased mRNA expression of pancreas-duodenum homebox-1 (PDX-1) and mammalian homologue of avian MafA/l-Maf (MafA). Accordingly, LPS exposure also decreased glucose-induced insulin secretion. LPS repression of insulin, PDX-1 and MafA expression, as well as its inhibition of insulin secretion, were not observed in islets from TLR4-deficient mice. LPS inhibition of β-cell gene expression in rat islets was prevented by inhibition of the NF-κB pathway, but not the p38 mitogen-activated protein kinase (p38 MAPK) pathway. CONCLUSIONS/SIGNIFICANCE:Our findings demonstrate that LPS inhibit β-cell gene expression in a TLR4-dependent manner and via NF-κB signaling in pancreatic islets, suggesting a novel mechanism by which the gut microbiota might affect pancreatic β-cell function