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This slim volume offers a thematic exploration of religion and the digital arts. Over the course of six brief sections, this extended essay examines identity and community, authority and authenticity, word and image, ritual and practice, body and space, and myth and faith. Each of these paired sets is explored in concert with technologically inflected correlates. For instance, identity and community are paired with avatars and networks. These twin concepts provide the thematic anchor of each section. Each section looks at four works of digital art with each work employing digital technology in a unique way. The works include virtual and augmented reality pieces, 3D printed sculptures, digital photography, and digitally enabled performance pieces and installations and span the late 1990s to the present. This essay is an introduction to religion and the digital arts and, while no single conclusion can be drawn from such an expansive and diverse field, the reassertion of the religious and theological importance of the body and emotions in the face of digital technology emerges as a recurrent theme.

By leveraging two metaphors central to discussions around the digitization of sacred texts—“books are bodies” and “translation is feeding”—this essay contends that the translation of analog sacred texts into digital formats is a metaphorical gastrointestinal process. This essay accomplishes this through the application of actor-network theory. Central to actor-network theory is the claim that an object, like a book, is the product of a complex network of relationships that together create it and constitute its meaning. Importantly, this includes discourses about the very networks that yield the object in question. As such, this essay incorporates many of the voices that appear elsewhere in this special edition as well as assorted ephemera from my own medical history of gastrointestinal maladies. If books are bodies and translation is feeding, then problems surrounding the digitization of analog sacred texts reside somewhere between ingestion and excretion.

This essay takes up the challenge of unpacking the nature of what Schleiermacher called the “inner affinity” between religion and art. Drawing on the work of philosophers of art such as Susanne Langer and Arthur Danto, and philosophers of religion like Loyal Rue and David Tracy, I suggest that religion and art have at their core a comparable metaphorical structure that lends them this common communion. From this shared structure, I deduce five principal conclusions that I take to be the key avenues of affiliation between religion and art.

The Renaissance marked the emergence of scientific naturalism. Implicit in this naturalism was the replacement of supernatural explanations of the cosmos with the belief that the world could be known and represented through first-hand rational investigation. This in turn inspired the tools and techniques necessary for rendering the visible world with accuracy. One of those techniques was single-point perspective. Single-point perspective placed the individual at the center of a knowable and accurately representable cosmos. For over half a millennia single-point, or linear, perspective and the primacy of the individual perceiver dominated Western art. This is the clearest convergence of humanism and the visual arts. However, beginning in the nineteenth century that primacy began to be challenged as art moved away from the demand for perspectival accuracy and the myth of the autonomous, sovereign subject was dispelled.

We are spending more and more of our lives online. Meanwhile, the combination of constant connectivity and ubiquitous computing is folding the material world itself into an expansive ‘Internet of things’. As a result the line between life online and life off-line has become blurred in an existential equivalence of the digital and the analog. In this networked ecosystem, the old Web 1.0 notion of an anonymous digital persona that is separate from off-line, analog self-identity is no longer applicable. A new paradigm for conceptualizing the dialectic of digital–analog self-identity is needed. To that end, I argue that in our age of networked connectivity, self-identity is being fashioned according to the aesthetics of transmedia production. I conclude that the transmedia paradigm, taken as a model for interpreting self-identity in the liminal space between the virtual and the real, reveals a transmediated self constituted as a browsable story-world that is integrated, dispersed, episodic, and interactive.

The devil is not what he used to be. The mythic villain of the Christian tradition has become a cartoon version of his former terrifying self. And nowhere is this more apparent than in the visual arts. Fearsome images of the devil and his minions once adorned church walls, altars, and holy books. He was the very real incarnation of evil and his image was a lesson in the wages of sin. Today, however, when words like "sin" and "evil" have lost their theological if not cultural resonance, the arts have all but abandoned sincere representations of the devil, trading instead on his image as logo or slur. To image the devil after evil is to reimagine the very idea of evil. The artist Fred Stonehouse has accomplished precisely this.In the year 447 the Council of Toledo set out the first official description of the devil. At the council the devil was described as "a large, black, monstrous apparition with horns on his head, cloven hoofs, or one cloven hoof-ass's ears, hair, claws, fiery eyes, terrible teeth, an immense phallus, and a sulphurous smell" (Hughes 104). Since then the devil has morphed into a caricature of this fierce beast of Christian mythology. More recently the devil has made appearances as the logo for Underwood Deviled Ham and as a regular character on South Park. The reason the devil has ceased to function in the cultural imaginary as the personification of evil is because evil itself has become something of a superstitious relic. As Peter Stanford observes in his book, The Devil: A Biography, "Greater knowledge, less dependency on the idea of a figure of evil, and more on the nega- five within each individual has brought a more precise delineation of the unknown, the darkness, the shadow" (284). Like darkness brought to light, evil has lost its frightful mystery.The notion that evil is the willful product of an external cosmic agent bent on the pain, suffering, and misery of humanity has foundered as a viable theory of evil. Consequently, the devil too has lost much of his historical, theological, and cultural cache. Robert Muchembled argues that "[n]ot only has [the devil] ceased to exist as a terrifying external figure, he no longer even provokes a fear of the self, a dread of the inner demon..." (228). Two centuries of the demystification of evil have enfeebled the once mighty icon of incarnate malevolence.If for nearly two millennia the image of the devil was the didactic embodiment of evil, what then does the devil look like after evil? This article addresses that question by turning to the work of contemporary artist Fred Stonehouse, who has been painting the devil for over three decades with an uncanny awareness of, and artistic reflection on, the tradition of representing the devil in the arts.The following is composed of three sections. The first two form an argument regarding the place of the devil-as-villain in modem art, focusing briefly on the art historical trajectory of the image of the devil before attending to the work of contemporary artist Fred Stonehouse. The third section then turns to Stonehouse himself offering an in depth interview with the artist about his work, his practice, and the place of the devil in his painting.Section one presents the devil as the cosmic archetype for the nemesis-style villain. Here, I attend to how the devil has historically been imaged in the arts and, in anticipation of the work of Fred Stonehouse, the precarious place of that image in contemporary culture where the devil has become more cliche than cosmic villain. Section two turns to the artistry of Fred Stonehouse in a consideration of the figure of the devil in modem art. In this section I propose that Stonehouse offers a rare, sincere figuration of the devil after evil by transforming him from a villain into an icon of vulnerability. Section three is an interview with Stonehouse exploring the evolution of his art practice, the origins of his fascination with the devil, and how he understands this devious character in his work. …

Abstract This article asks after the theological import of the two end of art theses proposed by Arthur Danto and Donald Kuspit respectively. In tribute to the coming thirtieth anniversary of Arthur Danto’s essay “The End of Art” and the tenth anniversary of Donald Kuspit’s book The End of Art, I take up here their respective theories in an attempt to go beyond the surface of their ideas and to ask after the depth of the end(s) of art. Their theses point to a crisis of reflexivity in the respective artworlds they describe and that this crisis is the result of the loss and failed recovery of spiritual depth. Danto’s end of art thesis offers a truth that tells a lie—that there was never depth there to begin with—while Kuspit’s offers a lie that tells the truth—that that depth can be recovered. Danto’s thesis speaks to early postmodern art’s loss of spiritual depth while Kuspit’s addresses late postmodern art’s failure to recover that depth. Taken together, their ends of art present the lying-truth of an irretrievably lost sacred and the true-lie that the sacred in the arts can be recovered.

Howard, R. G. (2011). New York, NY: New York University Press, 213 pp. $24.00 (paperback). Digital Jesus is an ethnographic study of the formation and evolution of a leaderless online fundamentalis...

The endothelium-derived relaxing factor is rapidly inactivated by superoxide radicals, and atherosclerotic vessels generate excess radical species. We tested the hypothesis that an imbalance between intrinsic superoxide dismutase (SOD) activity and the generation of superoxide radicals in atherosclerotic arteries may result in augmented inactivation of endothelium-derived relaxing factor. Vascular SOD was increased in normal and cholesterol-fed (1% cholesterol for 4 months) rabbits approximately twofold by treatment with polyethylene-glycolated SOD (PEG-SOD; 41,000 units/kg/day i.m.) for 1 week. Aortic rings from these animals and nontreated control and atherosclerotic rabbits subsequently were studied in organ chambers. Endothelium-dependent relaxations to acetylcholine and the calcium ionophore A23187 were improved by PEG-SOD in atherosclerotic but not in normal rabbits. PEG-SOD pretreatment did not alter endothelium-independent relaxations to nitroprusside. Thus, treatment with PEG-SOD can partially restore impaired endothelium-dependent relaxation of atherosclerotic arteries. We conclude that generation of oxygen-derived radicals likely contributes to endothelial dysfunction of atherosclerotic arteries.

DRS Sensors & Targeting Systems, under contract to the Space Dynamics Laboratory of Utah State University, is providing the focal plane detector system for NASA's Wide-field Infrared Survey Explorer (WISE). The focal plane detector system consists of two mercury cadmium telluride (MCT) focal plane module assemblies (FPMAs), two arsenic doped silicon (Si:As) Blocked Impurity Band (BIB) FPMAs, electronics to drive the FPMAs and report digital data from them, and the cryogenic and ambient temperature cabling that connect the FPMAs and electronics. The MCT and Si:As BIB focal plane arrays (FPAs) utilized in the WISE FPMAs are both megapixel class indium-bump hybridized devices fabricated by Teledyne Imaging Systems and DRS Sensors & Targeting Systems, respectively. This paper reports performance of the WISE Si:As BIB FPAs that are used for the WISE 12- and 23-μm wavelength bands.

Tirapazamine (TPZ, 3-amino-1,2,4-benzotriazine 1,4-di-N-oxide, SR 4233, WIN 59075) is a bioreductive antitumor agent with a high selective toxicity for hypoxic cells. The selective hypoxic toxicity of TPZ results from the rapid reoxidation of the one-electron reduction product, the TPZ radical, in the presence of molecular oxygen with the concomitant production of superoxide radical. Under hypoxia the TPZ radical kills cells by causing DNA double-strand breaks and chromosome aberrations. However, the mechanism of aerobic cytotoxicity is still a matter of debate. In this study, we investigated the mechanism of aerobic cytotoxicity by adapting human lung adenocarcinoma A549 cells to aerobic TPZ exposure and characterizing the changes associated with drug resistance. The adapted cells were resistant to aerobic TPZ exposures (with dose-modifying factors of up to 9.2), although hypoxic sensitivity was largely unchanged. Relative to the parental A549 cell line, adaptation to continuous aerobic TPZ exposure resulted in increased levels of manganese superoxide dismutase (up to 9.4-fold), moderate increases in glutathione reductase (up to 2.1-fold), and loss of both quinone oxidoreductase (DT-diaphorase) activity and NADPH cytochrome P450 reductase activity. There was essentially no change in the activity of the cytoplasmic form of superoxide dismutase (CuZnSOD), catalase, or glutathione peroxidase. The increased activity of antioxidant enzymes in the resistant cell lines (in particular MnSOD) strongly suggests that reactive oxygen species are, in large part, responsible for the toxicity of TPZ under aerobic conditions, and is consistent with aerobic and hypoxic drug cytotoxicity resulting from different mechanisms.

Tissues from adult Syrian hamsters were studied with immunoperoxidase techniques using polyclonal antibodies to glutathione-S-transferase (rat liver and human placental enzymes) and human erythrocyte glutathione peroxidase. Most tissues immunostained similarly with these antibodies. Most notable was the cytoplasmic staining of mesenchyme tissues, especially smooth muscle, by all three antibodies. Epithelial cells stained distinctively, but usually less intensely than mesenchyme. Epithelial cells from all levels of the gastrointestinal tract, respiratory epithelium, transitional epithelium, and epidermis all showed strong staining with these antibodies. Other epithelial cell types were usually positive but showed less dramatic staining. Most epithelial tissues showed both nuclear and cytoplasmic staining; some also showed cell-surface (eg, cilia) staining. The role of these enzymes in cell differentiation of a stable organ was studied by immunostaining the kidney during its development. Early stroma (13- and 15-day fetuses) of the kidney (metanephric mesenchyme) showed strong cell-surface staining for glutathione transferases and moderate staining for glutathione peroxidase; renal tubules (which are epithelial cells) at this stage were negative for these markers. As renal tubules differentiated, first cytoplasm and then nuclei stained moderately, suggesting that glutathione-S-transferases and glutathione peroxidase are markers of both mesenchymal cells, including embryonic mesenchyme, and terminal differentiation of at least some epithelial cells.

Endothelium-derived relaxing factor (EDRF) is rapidly inactivated by radicals. Endothelial cells possess several antioxidant defense mechanisms. It is not clear which intrinsic antioxidant defense systems are important to preserve the release of biologically active EDRF. We impaired antioxidant defense in normal vascular tissue by inhibiting catalase activity with 3-amino-1,2,4-triazole (AT), superoxide dismutase with diethyldithiocarbamate (DETC), and by reducing glutathione content via inhibiting glutathione synthesis with L-buthionine-(S,R)-sulfoximine (BSO). Pretreatment of rabbit aorta in vitro with DETC markedly reduced endothelium-dependent relaxation in response to acetylcholine and calcium ionophore A23187 and, to a lesser extent, reduced endothelium-independent relaxation in response to nitroprusside. Pretreatment of cultured bovine aortic endothelial cells (BAEC) with DETC did not alter release of nitrogen oxides (measured by chemiluminescence), but, the effluent of pretreated cells showed marked depression in vasodilator activity (measured by bioassay). Pretreatment of rabbit aorta in vitro with AT did not alter endothelium-dependent and -independent relaxations. Pretreatment of BAEC with BSO did not alter the release of nitrogen oxides or the vasodilator activity. These results suggest that endothelial superoxide dismutase activity, but not catalase or glutathione, is necessary for the release of biologically active EDRF. An imbalance of the intrinsic superoxide dismutase and the production of superoxide anions may therefore predispose to impaired endothelium-dependent relaxations and alter vascular reactivity.

The activities of superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione S-transferases, GSSG reductase, thiol transferases, gamma glutamyl-cysteine synthetase, and glucose-6-phosphate dehydrogenase, and the concentrations of H2O2 and reduced and oxidized glutathione were determined in the various developmental stages of houseflies. Housefly development was correlated with a progressive increase of cellular oxidizing equivalents and a loss of cellular reducing capacity. The loss of reducing equivalents appeared to result from a decrease in the activity of enzymes involved in glutathione and NADPH synthesis and a concomitant increase in glutathione-oxidizing enzymes. Relatively little change was observed in SOD activity during housefly development; however, the electrophoretic pattern of MnSOD varied in a manner specific to developmental stage. A striking increase in H2O2 concentration occurred prior to pupation possibly due to changes in substrate catabolism. These results support the hypothesis that the cellular environment becomes progressively more oxidizing during development.

We have shown that interleukin-1 (IL-1) suppresses expression of cartilage-specific types II and IX collagens by cultured human chondrocytes. This inhibition is potentiated by agents which block IL-1-stimulated PGE2 production (J. Clin. Invest. 82:2026, 1988). In contrast, expression of types I and III collagens and fibronectin, matrix components produced by chondrocytes that have lost cartilage-specific phenotype, is increased by IL-1, particularly when IL-1-stimulated synthesis of PGE2 is blocked by a prostaglandin synthetase inhibitor. Etodolac is a new NSAID which is an effective inhibitor of PGE2 synthesis. The enhanced potency of etodolac in chondrocytes (compared with macrophages) suggests that this drug may have selective effects on different target cell types. The present studies were undertaken to compare the effects of etodolac and other nonsteroidal anti-inflammatory drugs (NSAIDs) on IL-1-induced modulation of chondrocyte phenotype. Juvenile human costal chondrocytes or adult articular chondrocytes in primary culture were incubated with etodolac, indomethacin or ketoprofen in the absence or presence of IL-1 beta. After treatment the [3H] proline-labelled collagens were analyzed by SDS-PAGE and type I and type II collagen mRNAs were analyzed by Northern or dot hybridization. Indomethacin (0.3-300 nM) or ketoprofen (2-2000 nM) produced a dose-dependent suppression of type II collagen synthesis associated with decreased levels of type II collagen mRNA in the absence of IL-1, while they potentiated the inhibitory effects of IL-1. In contrast, etodolac (2-2000 nM) maintained expression of type II collagen protein and mRNA. Etodolac unmasked a stimulatory effect of IL-1 on synthesis of type I collagen and fibronectin and levels of type I collagen mRNA, but to a lesser extent than indomethacin. These results suggest that, despite equipotent inhibitory effects of etodolac (IC50 congruent to 10 nM) on PGE2 biosynthesis compared with indomethacin (IC50 congruent to 1.0 nM) or ketoprofen (IC50 congruent to 10 nM), etodolac may be capable of maintaining type II collagen expression by chondrocytes. In vivo this could help to prevent the detrimental effects of mediators such as IL-1 on cartilage matrix synthesis in inflammatory joint diseases.

A microprocessor-based controller that will monitor experiments in the Space Shuttle's Get Away Special (GAS) container is described. The discussion covers electronic designs; outputs and inputs; interfacing with experiments; reprogramming; and the limitations of the design.

Serum levels of phenoxymethyl penicillin (penicillin V; Pen V) were measured following oral administration of two different formulations of the drug to five healthy horses. The mean serum concentration profile was described by a two-compartment model with a first order rate of absorption. Half-lives of the absorption, distribution and elimination phases were, respectively, 0.199 +/- 0.035, 0.362 +/- 0.060 and 3.650 +/- 0.575 hours. The distribution of the drug to body fluid compartments other than serum was examined. Mean peak levels of Pen V in serum, synovial fluid, peritoneal fluid and urine were, respectively, 2.38 +/- 0.18, 0.35 +/- 0.02, 0.25 +/- 0.06 and 472 +/- 80 micrograms/ml with times to achieve peak concentration ranging from 30-360 minutes after oral administration. Steady state pharmacokinetic measurements predicted that minimum serum Pen V concentrations of 0.1 micrograms/ml would be maintained by oral administration of the drug (110,000 I.U./kg) at 8 hour intervals. Our data indicate that oral Pen V is a feasible approach to long-term penicillin therapy in the equine patient.