Religion, Art and Myth-Making: The Halo as an Aesthetic Expression of Ultimate Reality

In recent years there has been an increased interest in questions concerning religion and faith. There have been bestselling books by authors of the so called new-atheist movement, Dawikns, Dennite, Haris and Hitchens, as well as numerous responses given attempting to refute the attacks made on traditional views of religion and faith. Moreover, since September 11th 2001 there has been a heightened awareness of the gulf separating believers and non-believers. Yet, the problem at the heart of this debate often seems to become an inquiry into whether or not religion is good for society rather than a question of the existence of God. This indicates that there may be a new way to look at the question, what is religion? Perhaps we should begin to think of religion as a social thus natural phenomenon; in doing so religion can be understood in aesthetic terms. If it is the case that religion is essentially born from shared relations within a social framework, much in the same mode as aesthetics, then the gulf between believers and non-believers is illusory. Better understanding the dualistic quality of human relationships will likely serve to find common ground within religious dialogues; this involves seeing how both religion and art are modes of myth-making. Historically the aesthetic symbol of the halo has been used by many religions and aesthetic traditions as an expression of enlightenment or reason. Therefore, the halo servers as a fossil of human experience. The intent of this paper is to examine this position through the symbol of the halo and how it has evolved in the Mithraic, Christian and Buddhist traditions

The optical constants of plutonium metal between .7 and 4.3 eV measured by spectroscopic ellipsometry using a double-windowed experimental chamber.

A double-windowed vacuum-tight experimental chamber was developed, and calibrated on the spectroscopic ellipsometer over the energy range from .7 to 4.5 eV using a silicon wafer with approximately 25 nm oxide thickness to remove the multiple-window effects from measurements. The ellipsometric measurements were done such that incident and exit beam were at 65 degree from surface normal. The plutonium sample (3 mm diameter, .1 mm thick) was electro-polished and mounted into the sample chamber in a glove box having a nitrogen atmosphere with less than 100ppm moisture and oxygen content. The index of refraction n and the extinction coefficient k decrease from 3.7 to 1 and 5.5 to 1.1 respectively as the photon energy increases from .7 to 4.3 eV

Using keystroke logging to understand writers’ processes on a reading-into-writing test

Background Integrated reading-into-writing tasks are increasingly used in large-scale language proficiency tests. Such tasks are said to possess higher authenticity as they reflect real-life writing conditions better than independent, writing-only tasks. However, to effectively define the reading-into-writing construct, more empirical evidence regarding how writers compose from sources both in real-life and under test conditions is urgently needed. Most previous process studies used think aloud or questionnaire to collect evidence. These methods rely on participants’ perceptions of their processes, as well as their ability to report them. Findings This paper reports on a small-scale experimental study to explore writers’ processes on a reading-into-writing test by employing keystroke logging. Two L2 postgraduates completed an argumentative essay on computer. Their text production processes were captured by a keystroke logging programme. Students were also interviewed to provide additional information. Keystroke logging like most computing tools provides a range of measures. The study examined the students’ reading-into-writing processes by analysing a selection of the keystroke logging measures in conjunction with students’ final texts and interview protocols. Conclusions The results suggest that the nature of the writers’ reading-into-writing processes might have a major influence on the writer’s final performance. Recommendations for future process studies are provided

The SWELL1-LRRC8 complex regulates endothelial AKT-eNOS signaling and vascular function

The endothelium responds to numerous chemical and mechanical factors in regulating vascular tone, blood pressure, and blood flow. The endothelial volume-regulated anion channel (VRAC) has been proposed to be mechanosensitive and thereby sense fluid flow and hydrostatic pressure to regulate vascular function. Here, we show that the leucine-rich repeat-containing protein 8a, LRRC8A (SWELL1), is required for VRAC in human umbilical vein endothelial cells (HUVECs). Endothelial LRRC8A regulates AKT-endothelial nitric oxide synthase (eNOS) signaling under basal, stretch, and shear-flow stimulation, forms a GRB2-Cav1-eNOS signaling complex, and is required for endothelial cell alignment to laminar shear flow. Endothelium-restricte

Anti-angiogenic effects of VEGF stimulation on endothelium deficient in phosphoinositide recycling

Anti-angiogenic therapies have generated significant interest for their potential to combat tumor growth. However, tumor overproduction of pro-angiogenic ligands can overcome these therapies, hampering success of this approach. To circumvent this problem, we target the resynthesis of phosphoinositides consumed during intracellular transduction of pro-angiogenic signals in endothelial cells (EC), thus harnessing the tumors own production of excess stimulatory ligands to deplete adjacent ECs of the capacity to respond to these signals. Using zebrafish and human endothelial cells in vitro, we show ECs deficient in CDP-diacylglycerol synthase 2 are uniquely sensitive to increased vascular endothelial growth factor (VEGF) stimulation due to a reduced capacity to re-synthesize phosphoinositides, including phosphatidylinositol-(4,5)-bisphosphate (PIP2), resulting in VEGF-exacerbated defects in angiogenesis and angiogenic signaling. Using murine tumor allograft models, we show that systemic or EC specific suppression of phosphoinositide recycling results in reduced tumor growth and tumor angiogenesis. Our results suggest inhibition of phosphoinositide recycling provides a useful anti-angiogenic approach

Changes in γ-secretase activity and specificity caused by the introduction of consensus aspartyl protease active motif in Presenilin 1

Presenilin (PS1 or PS2) is an essential component of the active γ-secretase complex that liberates the Aβ peptides from amyloid precursor protein (APP). PS1 is regarded as an atypical aspartyl protease harboring two essential aspartic acids in the context of the sequence D257LV and D385FI, respectively, rather than the typical DTG...DTG catalytic motif of classical aspartyl proteases. In the present studies, we introduced the sequence DTG in PS1 at and around the catalytic D257 and D385 residues to generate three PS1 mutants: D257TG, D385TG, and the double-mutant D257TG/D385TG. The effects of these changes on the γ-secretase activity in the presence or absence of γ-secretase inhibitors and modulators were investigated. The results showed that PS1 mutants having D385TG robustly enhanced Aβ42 production compared to the wild type (wt), and were more sensitive than wt to inhibition by a classical aspartyl protease transition state mimic, and fenchylamine, a sulfonamide derivative. Unlike wt PS1 and some of its clinical mutants, all three PS1 artificial mutants decreased cleavage of Notch S3-site, suggesting that these artificial mutations may trigger conformational changes at the substrate docking and catalytic site that cause alteration of substrate specificity and inhibition pattern. Consistent with this notion, we have found that NSAID enzymatic inhibitors of COX, known modulators of the γ-secretase activity, cause PS1 mutants containing D385TG to produce higher levels of both Aβ38 and Aβ42, but to reduce levels of Aβ39, showing a pattern of Aβ formation different from that observed with wild type PS1 and its clinical mutants. This study provides an important structural clue for the rational design of drugs to inhibit processing of APP at the γ-site without interfering with Notch processing