Reducing the external environmental costs of pastoral farming in New Zealand: experiences from the Te Arawa lakes, Rotorua

Decades of nutrient pollution have caused water quality to decline in the nationally iconic Te Arawa (Rotorua) lakes in New Zealand. Pastoral agriculture is a major nutrient source, and therefore this degradation represents an external environmental cost to intensive farming. This cost is borne by the wider community, and a major publically funded remediation programme is now under way. This article describes the range of actions being taken to reduce nutrient loads from internal (lake bed sediments) and external (primarily diffuse) sources in the lake catchments. The high economic cost and uncertain efficacy of engineering-based actions to reduce internal nutrient loads is highlighted. Major changes to land management practices to control diffuse nutrient pollution are required throughout New Zealand if the need for costly and lengthy remediation programmes elsewhere is to be avoided. More action to educate farmers and the public about eutrophication issues, development and enforcement of environmental standards, and further consideration of the use of market-based instruments are proposed as ways to correct the current market failure

Reducing the external environmental costs of pastoral farming in New Zealand: experiences from the Te Arawa lakes, Rotorua

Decades of nutrient pollution have caused water quality to decline in the nationally iconic Te Arawa (Rotorua) lakes in New Zealand. Pastoral agriculture is a major nutrient source, and therefore this degradation represents an external environmental cost to intensive farming. This cost is borne by the wider community, and a major publically funded remediation programme is now under way. This article describes the range of actions being taken to reduce nutrient loads from internal (lake bed sediments) and external (primarily diffuse) sources in the lake catchments. The high economic cost and uncertain efficacy of engineering-based actions to reduce internal nutrient loads is highlighted. Major changes to land management practices to control diffuse nutrient pollution are required throughout New Zealand if the need for costly and lengthy remediation programmes elsewhere is to be avoided. More action to educate farmers and the public about eutrophication issues, development and enforcement of environmental standards, and further consideration of the use of market-based instruments are proposed as ways to correct the current market failure

The deformation characteristics of crystalline mercury at 77°K and 4.2°K.

The normal structure of mercury is unique in that it is the only metal having rhombehedral symmetry to possess a single lattice structure. This fact, together with the nearness of the structure to f.c.c., make its deformation behaviour particularly interesting. The present investigation describes the orientation dependence of the deformation characteristics of mercury at two different temperatures. The large standard stereographic triangle associated with the low symmetry structure of mercury occupies one sixth of the full stereogram. Theoretical considerations have shown that, within this one triangle, slip on three different variants of the observed mode is possible, the boundaries between the corresponding regions having two distinct characteristics. These predictions have been tested by experiments on single crystals at 77°K and the role of twinning and kinking in the deformation process assessed. Single crystals tested in tension at 4.2°K have been found to undergo a stress-induced phase transformation. Evidence for this reaction is presented in the form of superconductivity and electrical resistance measurements and the martensitic nature of the transition established. Both the properties of the new phase and the nature of its production served to distinguish this transformation from the previously reported low temperature alpha - beta transition. It has thus been labelled the gamma phase. Detailed metallographic observations determined the shear elements associated with this transformation as {113} , g = 0.47, the indices referring to the f.c.r. cell of alpha-mercury. The morphology of the transformed crystals has been interpreted in terms of the accommodation of the martensitic plates in the parent; matrix and the crystallography of the habit plane and associated shear direction. A marked dependence of the occurrence of the transformation on the orientation of the crystal has been interpreted by regarding the shear process associated with the transformation as a conventional deformation mode. Further explanation of the results using various approaches such as lattice geometry and anisotropic elasticity theory has been attempted. The application of the current theories of martensite crystallography to this transformation based on a product crystal structure predicted using the pseudopotential theory of metals is also reported. Finally, an account of an experimental investigation, using an X-ray diffraction technique, to determine the actual product structure is presented

ERK Activation Requires CaM Kinases in MCF-7 Breast Cancer Cells

Abstract A key signaling pathway involved in regulating cell growth and proliferation throughout the body is the ERK signaling pathway. ERK is activated via numerous pathways including intracellular calcium release downstream of G-Protein Coupled Receptors (GPCRs). Carbachol, a GPCR-agonist, both increases intracellular calcium and ERK activation in MCF-7 cells. ERK activation and control of cell growth may act through the transcription factor Elk-1. Our goal was to elucidate the specific proteins and kinases upstream of ERK in MCF-7 cells treated with carbachol. Secondly, we wanted to investigate the potential involvement of Elk-1 downstream of ERK. Carbachol treatment of MCF-7 cells triggered ERK and Elk-1 phosphorylation within 5 minutes. Interestingly, transfection of cells with shRNAs directed to either CaM KKα or CaM KIγ significantly inhibited carbachol activation of ERK. Phosphorylation of Elk-1, following carbachol stimulation, was also blocked in siERK2 transfected cells, suggesting that ERK2 is required for carbachol\u27s activation of Elk-1. Our results suggest that carbachol treatment of MCF-7 cells activates ERK and cell growth through CaM KK, CaMKI, and an Elk-1-dependent pathway

GPU-OSDDA: A Bit-Vector GPU-based Deadlock Detection Algorithm for Single-Unit Resource Systems

This article presents a GPU-based single-unit deadlock detection methodology and its algorithm, GPU-OSDDA. Our GPU-based design utilizes parallel hardware of GPU to perform computations and thus is able to overcome the major limitation of prior hardware-based approaches by having the capability of handling thousands of processes and resources, whilst achieving real-world run-times. By utilizing a bit-vector technique for storing algorithm ma- trices and designing novel, efficient algorithmic methods, we not only reduce memory usage dramatically but also achieve two orders of magnitude speedup over CPU equivalents. Additionally, GPU-OSDDA acts as an interactive service to the CPU, because all of the aforementioned computations and matrix management techniques take place on the GPU, requiring minimal interaction with the CPU. GPU-OSDDA is implemented on three GPU cards: Tesla C2050, Tesla K20c, and Titan X. Our design shows overall speedups of 6-595X over CPU equivalents

M3-Muscarinic Receptor Activation of ERK and Cell Growth Requires Calcium/Calmodulin-dependent Protein Kinases in MCF-7 Cells

Abstract The extracellular signal-regulated protein kinase (ERK) signaling pathway is found in diverse cells throughout the human body. ERK activation has been implicated in breast cancer cell growth and proliferation. Studies have shown that ERK is activated by carbachol, a G Protein-Coupled Receptor (GPCR) agonist, which increases intracellular calcium in MCF-7 cells. The calcium/calmodulin-dependent protein kinase (CaM K) family of proteins including CaM KK, CaM KI, and CaM KII can be activated by increased intracellular calcium. Our goal was to determine whether CaM Ks may be responsible for ERK activation and cell proliferation in carbachol-treated MCF-7 cells and evaluate which GPCR was responsible for these events. Carbachol treatment of MCF-7 cells triggered ERK 1/2 phosphorylation within 5 minutes. Treatment with KN-93, a general CaM Kinase inhibitor and the MEK inhibitor U0126 blocked ERK activation. Carbachol increased MCF-7 cell growth nearly 4-fold, an effect that was also dependent upon CaM Ks and MEK. Interestingly, CaM KK was responsible for ERK activation and cell growth. Pretreatment of MCF-7 cells with 4-DAMP, a selective M3 receptor antagonist, completely blocked carbachol’s activation of ERK and cell growth. Taken together these results suggest that carbachol stimulated ERK phosphorylation and MCF-7 cell growth by the M3 subtype GPCR receptor perhaps through CaM KK