Modeling the interaction of light between diffuse surfaces

Mary Wollstonecraft and her daughter Mary Shelley are arguably the most important female writers of the eighteenth and nineteenth century, while Wollstonecraft is one of the most significant contributors to the women’s rights movement, with some of her ideas expressed in A Vindication of the Rights of Woman being referenced in the modern-day laws about the rights of women. This paper will analyze the life and work of Mary Wollstonecraft and Mary Shelley, focusing mostly on their most famous and most significant works, A Vindication of the Rights of Woman and Frankenstein; or The Modern Prometheus, respectively. Furthermore, it will analyze the position of women through the biographies of both writers and the autobiographical elements in their works, as well as through the analysis of the female characters in Frankenstein; or, The Modern Prometheus as a representation of more or less typical women of the time. Finally, it will search for and analyze the influence of Mary Shelley’s mother’s works and ideas on her writing in Frankenstein; or, The Modern Prometheus and her work in general. The aim of this BA paper is to analyze the position of women in society and literature through the above mentioned aspects of the life and work of Mary Wollstonecraft and Mary Shelley and to prove the importance of both of these authors, but especially Wollstonecraft, in the female struggle for obtaining the most basic human rights and the still persisting fight for gender equality

Mutations at the flavin binding site of ETF:QO yield a MADD-like severe phenotype in Drosophila

Following a screening on EMS-induced Drosophila mutants defective for formation and morphogenesis of epithelial cells, we have identified three lethal mutants defective for the production of embryonic cuticle. The mutants are allelic to the CG12140 gene, the fly homologue of electron transfer flavoprotein:ubiquinone oxidoreductase (ETF:QO). In humans, inherited defects in this inner membrane protein account for multiple acyl-CoA dehydrogenase deficiency (MADD), a metabolic disease of beta-oxidation, with a broad range of clinical phenotypes, varying from embryonic lethal to mild forms. The three mutant alleles carried distinct missense mutations in ETF:QO (G65E, A68V and S104F) and maternal mutant embryos for ETF:QO showed lethal morphogenetic defects and a significant induction of apoptosis following germ-band elongation. This phenotype is accompanied by an embryonic accumulation of short- and medium-chain acylcarnitines (C4. C8 and 02) as well as long-chain acylcarnitines (C14 and C16:1), whose elevation is also found in severe MADD forms in humans under intense metabolic decompensation. In agreement the ETF:QO activity in the mutant embryos is markedly decreased in relation to wild type activity. Amino acid sequence analysis and structural mapping into a molecular model of ETF:QO show that all mutations map at FAD interacting residues, two of which at the nucleotide-binding Rossmann fold. This structural domain is composed by a beta-strand connected by a short loop to an alpha-helix, and its perturbation results in impaired cofactor association via structural destabilisation and consequently enzymatic inactivation. This work thus pinpoints the molecular origins of a severe MADD-like phenotype in the fruit fly and establishes the proof of concept concerning the suitability of this organism as,a potential model organism for MADD. (C) 2012 Elsevier B.V. All rights reserved.Fundacao para a Ciencia e Tecnologia (FCT/MCTES, Portugal) [PTDC/SAU-GMG/70033/2006, PTDC/QUI-BIQ/113027/2009, PTDC/BIA-BCM/111822/2009, PTDC/SAU-BID/111796/2009, SFRH/BPD/41609/2007, SFRH/BPD/74475/2010, SFRH/BPD/34763/2007]; CLIMB UK; [PEst-OE/EQB/LA0004/2011]info:eu-repo/semantics/publishedVersio

Transglutaminase activation in neurodegenerative diseases

The following review examines the role of calcium in promoting the in vitro and in vivo activation of transglutaminases in neurodegenerative disorders. Diseases such as Alzheimer's disease, Parkinson's disease and Huntington's disease exhibit increased transglutaminase activity and rises in intracellular calcium concentrations, which may be related. The aberrant activation of transglutaminase by calcium is thought to give rise to a variety of pathological moieties in these diseases, and the inhibition has been shown to have therapeutic benefit in animal and cellular models of neurodegeneration. Given the potential clinical relevance of transglutaminase inhibitors, we have also reviewed the recent development of such compounds

Modeling the Interaction of Light Between Diffuse Surfaces

A method is described which models the interaction of light between diffusely reflecting surfaces. Current light reflection models used in computer graphics do not account for the object-to-object reflection between diffuse surfaces, and thus incorrectly compute the global illumination effects. The new procedure, based on methods used in thermal engineering, includes the effects of diffuse light sources of finite area, as well as the "color-bleeding" effects which are caused by the diffuse reflections. A simple environment is used to illustrate these simulated effects and is presented with photographs of a physical model. The procedure is applicable to environments composed of ideal diffuse reflectors and can account for direct illumination from a variety of light sources. The resultant surface intensities are independent of observer position, and thus environments can be preprocessed for dynamic sequences

Characterization of carnitine and fatty acid metabolism in the long-chain acyl-CoA dehydrogenase-deficient mouse

In the present paper, we describe a novel method which enables the analysis of tissue acylcarnitines and carnitine biosynthesis intermediates in the same sample. This method was used to investigate the carnitine and fatty acid metabolism in wild-type and LCAD(−/−) (long-chain acyl-CoA dehydrogenase-deficient) mice. In agreement with previous results in plasma and bile, we found accumulation of the characteristic C(14:1)-acylcarnitine in all investigated tissues from LCAD(−/−) mice. Surprisingly, quantitatively relevant levels of 3-hydroxyacylcarnitines were found to be present in heart, muscle and brain in wild-type mice, suggesting that, in these tissues, long-chain 3-hydroxyacyl-CoA dehydrogenase is rate-limiting for mitochondrial β-oxidation. The 3-hydroxyacylcarnitines were absent in LCAD(−/−) tissues, indicating that, in this situation, the β-oxidation flux is limited by the LCAD deficiency. A profound deficiency of acetylcarnitine was observed in LCAD(−/−) hearts, which most likely corresponds with low cardiac levels of acetyl-CoA. Since there was no carnitine deficiency and only a marginal elevation of potentially cardiotoxic acylcarnitines, we conclude from these data that the cardiomyopathy in the LCAD(−/−) mouse is caused primarily by a severe energy deficiency in the heart, stressing the important role of LCAD in cardiac fatty acid metabolism in the mouse