55 research outputs found

    Seeing death : portraiture in contemporary postmortem photography

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    This thesis focuses on the aesthetics of the photographic representation of the actual dead body in Elizabeth Heyert's The Travelers (2004), Pieter Hugo's The Bereaved (2005) and Walter Schels and Beate Lakotta's Life Before Death: Portraits of the Dying (2004). The use of portraiture in each of these artist's series is crucial as it suggests an interest in the 'subjectness' of the corpse. Katarzyna Majak's (2011) theory of socialization as an attempt to lessen the scandal of the corpse through representation is central throughout this thesis. Majak argues that for the viewer the corpse is a scandal, because it discomfortingly presents the transformation of a body from subject to object. For Majak, socialization is essentially the taming of the dead body, achieved by re-presenting the corpse as an individual. Socialization emphasizes the subject-ness of the deceased individual, rather than the object-ness of the corpse, of pure unadulterated matter. The use of portraiture in each of the above series socializes the corpse by presenting the individual identity of the deceased as a subject, in varying degrees. Death is approached through the recognizable conventions of portraiture itself, thereby to some extent taming or domesticating the corpse. This thesis expands on Majak's valuable theory by establishing a continuum of socialization from subject-ness to object-ness. Importantly, this continuum reveals varying degrees of socialization within the three series. Socialization is used here as an analytical tool with which to explore the photographs, drawing out similarities and differences. I argue that through various aesthetic techniques, these three series encourage the viewer to look at these different images of the corpse with varying degrees of comfort

    A systematic review of group walking in physically healthy people to promote physical activity

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    BACKGROUND: Walking is a good way to meet physical activity guidelines. We examined the effectiveness of walking in groups compared with walking alone or inactive controls in physically healthy adults on physical activity and quality of life. (PROSPERO CRD42016033752). METHODS: We searched Medline, Embase, Cinahl, Web of Knowledge Science Citation Index, and Cochrane CENTRAL until March 2016, for any comparative studies, in physically healthy adults, of walking in groups compared with inactive controls or walking alone, reporting any measure of physical activity. We searched references from recent relevant systematic reviews. Two reviewers checked study eligibility and independently extracted data. Disagreements were resolved through discussion. Quality was assessed using likelihood of selection, performance, attrition, and detection biases. Meta-analysis was conducted using Review Manager 5.3. RESULTS: From 1,404 citations, 18 studies were included in qualitative synthesis and 10 in meta-analyses. Fourteen compared group walking to inactive controls and four to walking alone. Eight reported more than one measure of physical activity, none reported according to current guidelines. Group walking compared with inactive controls increased follow-up physical activity (9 randomized controlled trials, standardized mean difference [SMD] 0.58 [95 percent confidence interval {CI}, 0.34-0.82] to SMD 0.43 [95 percent CI, 0.20-0.66]). Compared with walking alone, studies were too few and too heterogeneous to conduct meta-analysis, but the trend was improved physical activity at follow-up for group walking participants. Seven (all inactive control) reported quality-of-life: five showed statistically significantly improved scores. DISCUSSION: Better evidence may encourage government policy to promote walking in groups. Standardized physical activity outcomes need to be reported in research

    ‘Dr Google’ will see you now! A review of online consumer information about anticoagulant and antithrombotic medication for prevention of recurrent stroke

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    Stroke survivors increasingly use the internet to access health information. The aim of this study was to evaluate the quality of online information about anticoagulant and antiplatelet medication in stroke. 100 online information sources and 50 online news articles about anticoagulants and antiplatelets after stroke were accessed using Google in June-July 2016. Readability, overall quality, and language about prevention, risk, emotive terms, and shared decision-making were evaluated using SMOG and DISCERN tools. Most online information was from national health service (27/100) or charitable (24/100) sources, or from tabloid newspapers’ websites (25/50). Median reading age for materials was 17-18 years. Quality scores were typically 3/5 with only 5 of 16 criteria scoring highly. Stroke risk reduction was typically described in absolute terms with little use of numerical or graphical data. Emotive language was frequently used, particularly in news articles. Shared decision-making was supported mainly by materials from charitable sources. This study has shown that online information about anticoagulant and antiplatelet medication after stroke requires high levels of literacy, and is often unreliable, poor quality and emotionally laden. People working with stroke survivors should facilitate access to accurate, unbiased and readable materials to promote shared decision making about medications

    Mapping Time-course Mitochondrial Adaptations in the Kidney in Experimental Diabetes

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    Abstract Oxidative phosphorylation drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homeostasis. In diabetic kidney disease, mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics, have not been previously documented. Here, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks) a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells of diabetic kidneys were clearly apparent, but no change urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary Kidney injury molecule (Kim)-1 excretion, where an increase in Complex I-linked oxygen consumption rate, in the context of a decrease in kidney ATP, indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of diabetic kidney disease. Summary statement We identified that dysfunction of cellular power stations, mitochondria, may precede the development of kidney disease in diabetes. This suggests that mitochondrial dysfunction is a primary cause of diabetic nephropathy, which could be targeted to improve the burden of this disease. Short title: Mitochondrial adaptations in diabetic nephropath

    Mapping time-course mitochondrial adaptations in the kidney in experimental diabetes

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    Abstract Oxidative phosphorylation (OXPHOS) drives ATP production by mitochondria, which are dynamic organelles, constantly fusing and dividing to maintain kidney homoeostasis. In diabetic kidney disease (DKD), mitochondria appear dysfunctional, but the temporal development of diabetes-induced adaptations in mitochondrial structure and bioenergetics have not been previously documented. In the present study, we map the changes in mitochondrial dynamics and function in rat kidney mitochondria at 4, 8, 16 and 32 weeks of diabetes. Our data reveal that changes in mitochondrial bioenergetics and dynamics precede the development of albuminuria and renal histological changes. Specifically, in early diabetes (4 weeks), a decrease in ATP content and mitochondrial fragmentation within proximal tubule epithelial cells (PTECs) of diabetic kidneys were clearly apparent, but no changes in urinary albumin excretion or glomerular morphology were evident at this time. By 8 weeks of diabetes, there was increased capacity for mitochondrial permeability transition (mPT) by pore opening, which persisted over time and correlated with mitochondrial hydrogen peroxide (H 2 O 2 ) generation and glomerular damage. Late in diabetes, by week 16, tubular damage was evident with increased urinary kidney injury molecule-1 (KIM-1) excretion, where an increase in the Complex I-linked oxygen consumption rate (OCR), in the context of a decrease in kidney ATP , indicated mitochondrial uncoupling. Taken together, these data show that changes in mitochondrial bioenergetics and dynamics may precede the development of the renal lesion in diabetes, and this supports the hypothesis that mitochondrial dysfunction is a primary cause of DKD

    Integrated Approach Reveals Role of Mitochondrial Germ-Line Mutation F18L in Respiratory Chain, Oxidative Alterations, Drug Sensitivity, and Patient Prognosis in Glioblastoma

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    Glioblastoma is the most common and malignant primary brain tumour in adults, with a dismal prognosis. This is partly due to considerable inter- and intra-tumour heterogeneity. Changes in the cellular energy-producing mitochondrial respiratory chain complex (MRC) activities are a hallmark of glioblastoma relative to the normal brain, and associate with differential survival outcomes. Targeting MRC complexes with drugs can also facilitate anti-glioblastoma activity. Whether mutations in the mitochondrial DNA (mtDNA) that encode several components of the MRC contribute to these phenomena remains underexplored. We identified a germ-line mtDNA mutation (m. 14798T > C), enriched in glioblastoma relative to healthy controls, that causes an amino acid substitution F18L within the core mtDNA-encoded cytochrome b subunit of MRC complex III. F18L is predicted to alter corresponding complex III activity, and sensitivity to complex III-targeting drugs. This could in turn alter reactive oxygen species (ROS) production, cell behaviour and, consequently, patient outcomes. Here we show that, despite a heterogeneous mitochondrial background in adult glioblastoma patient biopsy-derived cell cultures, the F18L substitution associates with alterations in individual MRC complex activities, in particular a 75% increase in MRC complex II_III activity, and a 34% reduction in CoQ10, the natural substrate for MRC complex III, levels. Downstream characterisation of an F18L-carrier revealed an 87% increase in intra-cellular ROS, an altered cellular distribution of mitochondrial-specific ROS, and a 64% increased sensitivity to clomipramine, a repurposed MRC complex III-targeting drug. In patients, F18L-carriers that received the current standard of care treatment had a poorer prognosis than non-carriers (373 days vs. 415 days, respectively). Single germ-line mitochondrial mutations could predispose individuals to differential prognoses, and sensitivity to mitochondrial targeted drugs. Thus, F18L, which is present in blood could serve as a useful non-invasive biomarker for the stratification of patients into prognostically relevant groups, one of which requires a lower dose of clomipramine to achieve clinical effect, thus minimising side-effects
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