Heritage and trauma: Reimagining the preservation planning process for the Nova Scotia Home for Colored Children

The literature on trauma acknowledges that the mismanagement of sites associated with difficult experiences puts survivors at considerable risk of retraumatization and disempowerment. However, there are few policy tools available to heritage planners and development professionals to help them navigate heritage designation or redevelopment in sites with difficult histories linked to systemic racism. In this paper, we analyze the contentious redevelopment process and heritage designation related to the Nova Scotia Home for Colored Children, the site of institutional abuse of African Nova Scotian children. We found that there are several gaps in existing heritage and development policies that prevent sites of racialized trauma from being acknowledged in a way that is consistent with the trauma literature. These include a lack of inclusion of difficult sites in designation, biases in scoring processes and a lack of transparent community engagement. From these findings, we provide recommendations for how policy can be improved to address these shortcomings.La littérature sur le traumatisme reconnait que la mauvaise gestion des sites associées avec des expériences difficiles met les survivants en risque considérable, même avec la retraumatisassions et la perte de responsabilisation. Néanmoins, il y a quelques utiles politiques qui sont disponibles au planificateurs et professionnels de développement pour les aider à naviguer la désignation d’héritage ou le redéveloppement des sites avec les histoires difficiles liées au racisme systémique. Ici, on analyse le procédé de redéveloppement contentieux et la désignation d’héritage par rapport à la Nova Scotia Home for Colored Children, le site d’abus institutionnel des enfants. Nous avons trouvé qu’il y a plusieurs lacunes dans la politique de développement et d’héritage qui préviennent les sites de traumatisme racialisé d’être reconnu dans une manière qui conforme à la littérature de traumatisme. Dans ces lacunes il existe un manque d’inclusion de sites difficiles par rapport à la désignation, les préjugés dans le procédé de marquer les points, et un manque d’engagement de la communauté. Avec ces résultats-ci, nous fournissons des recommandations pour améliorer la politique et font face à ces lacunes

Etologens yrkeskodex

Etologi betyder per definition läran om djurens beteende och orsakerna till det. Den generella definitionen av en etolog är således en person som har kunskap om djurens beteende och orsakerna till det. Definitionen är öppen för tolkning och allmänheten har liten eller ingen kännedom om etolog som profession. Dessutom är inte titeln etolog skyddad vilket innebär att i princip vem som helst kan kalla sig etolog. Kunskaps- och kompetensnivån etologer emellan kan således variera, vilket bidrar till gemene mans dåliga kännedom om etologer samt en något splittrad yrkeskår. Etologen med en gedigen vetenskapligt baserad utbildning har en yrkesmässig förmåga och potential att ta sig an vitt spridda arbetsuppgifter. Därigenom ställs etologen inför varierande situationer där vissa kan ses som etiskt känsliga. Dessa situationer kan i viss mån förutsägas, diskuteras, analyseras och således underlättas. Därav idén om att utforma en yrkesetisk kod. Koden skulle upprätta etiska förhållningssätt i form av normer och riktlinjer som underlättar etologens arbetssituation och agerande i etiskt känsliga situationer. Den skulle också formulera en definition av etologens profession och därigenom bidra till en yrkestrygghet. Syftet med denna rapport är att formulera ett första förslag till en yrkeskodex för etologer. För att uppnå detta utfördes en mindre enkätstudie riktad till yrkesverksamma etologer för att kartlägga möjliga etiskt känsliga situationer etologen riskerar att hamna i. Tre centrala problematiska kontexter framlades och analyserades utifrån utilitarismen, plikt- och dygdetiken; 1. Relationen djur – djurägare – etolog 2. Etologens ansvar när djuret far illa samt när djur används i forskningssammanhang 3. Autonomi, etologens självständighet samt kompetensutveckling. En litteraturstudie genomfördes med fokus på yrkeskoders funktion samt en granskning av andra etiska koder. Grundat i ovanstående formulerades en yrkeskodex för etologer. Det kunde fastslås att målet med etologens yrkeskodex är att bidra till etisk diskussion samt reflektion över hur etologens yrkesmässiga framtid kan tänkas se ut. Vidare ska den medverka till att underhålla ett öppet arbetsklimat och samarbete mellan etologer och andra yrkesgrupper, speciellt veterinärer. Den ska också bidra till en ökad yrkestrygghet samt en ökad allmän kännedom om etologi i stort

Photocoagulation of human retinal pigment epithelial cells in vitro: evaluation of necrosis, apoptosis, cell migration, cell proliferation and expression of tissue repairing and cytoprotective genes.

Sight-threatening diabetic retinopathy has been treated with photocoagulation for decades but the mechanisms behind the beneficial clinical effects are poorly understood. One target of irradiation and a potential player in this process is the retinal pigment epithelium (RPE). Here we establish an in vitro model for photocoagulation of human RPE cells

Single nucleotide polymorphisms in the apolipoprotein B and low density lipoprotein receptor genes affect response to antihypertensive treatment

BACKGROUND: Dyslipidemia has been associated with hypertension. The present study explored if polymorphisms in genes encoding proteins in lipid metabolism could be used as predictors for the individual response to antihypertensive treatment. METHODS: Ten single nucleotide polymorphisms (SNP) in genes related to lipid metabolism were analysed by a microarray based minisequencing system in DNA samples from ninety-seven hypertensive subjects randomised to treatment with either 150 mg of the angiotensin II type 1 receptor blocker irbesartan or 50 mg of the β(1)-adrenergic receptor blocker atenolol for twelve weeks. RESULTS: The reduction in blood pressure was similar in both treatment groups. The SNP C711T in the apolipoprotein B gene was associated with the blood pressure response to irbesartan with an average reduction of 19 mmHg in the individuals carrying the C-allele, but not to atenolol. The C16730T polymorphism in the low density lipoprotein receptor gene predicted the change in systolic blood pressure in the atenolol group with an average reduction of 14 mmHg in the individuals carrying the C-allele. CONCLUSIONS: Polymorphisms in genes encoding proteins in the lipid metabolism are associated with the response to antihypertensive treatment in a drug specific pattern. These results highlight the potential use of pharmacogenetics as a guide for individualised antihypertensive treatment, and also the role of lipids in blood pressure control

Pre-commercial thinning in Norway spruce-birch mixed stands can provide abundant forage for ungulates without losing volume production

Mixed stands of Norway spruce and birch have the potential to simultaneously produce timber and provide large ungulates with a significant amount of forage during the regeneration phase. While the growth and yield of such mixtures are well studied, little is known about potential trade-offs between timber and forage production and which management techniques are suitable for meeting both goals. In this study, four different pre-commercial thinning (PCT) strategies were used to study the trade-offs between production and available forage for free-ranging ungulates in a Norway spruce-birch mixture. The four PCT strategies were: 1) retaining 2000 birch stems ha(-1) with 2000 Norway spruce ha(-1), 2) removing all birches within a 0.75 m radius around Norway spruce stems, 3) removing all birches and other broadleaves, and 4) no PCT (control). Growth of Norway spruce was higher in the 2000 birch ha(-1) and full removal treatments compared to the untreated control, but these two treatments did not differ from one another in volume production of Norway spruce. We found a negative effect of PCT on forage availability but no effect on ungulate browsing. Therefore, PCT strategies that provide both sufficient birch forage and maximize volume production of Norway spruce can be implemented

Feeling Small: Exploring the Tactile Perception Limits

The human finger is exquisitely sensitive in perceiving different materials, but the question remains as to what length scales are capable of being distinguished in active touch. We combine material science with psychophysics to manufacture and haptically explore a series of topographically patterned surfaces of controlled wavelength, but identical chemistry. Strain-induced surface wrinkling and subsequent templating produced 16 surfaces with wrinkle wavelengths ranging from 300 nm to 90 μm and amplitudes between 7 nm and 4.5 μm. Perceived similarities of these surfaces (and two blanks) were pairwise scaled by participants, and interdistances among all stimuli were determined by individual differences scaling (INDSCAL). The tactile space thus generated and its two perceptual dimensions were directly linked to surface physical properties – the finger friction coefficient and the wrinkle wavelength. Finally, the lowest amplitude of the wrinkles so distinguished was approximately 10 nm, demonstrating that human tactile discrimination extends to the nanoscale

High glucose enhances store-operated calcium entry by upregulating ORAI/STIM via calcineurin-NFAT signalling

© 2014, Springer-Verlag Berlin Heidelberg. Abstract: ORAI and stromal interaction molecule (STIM) are store-operated channel molecules that play essential roles in human physiology through a coupling mechanism of internal Ca 2+ store to Ca 2+ influx. However, the roles of ORAI and STIM in vascular endothelial cells under diabetic conditions remain unknown. Here, we investigated expression and signalling pathways of ORAI and STIM regulated by high glucose or hyperglycaemia using in vitro cell models, in vivo diabetic mice and tissues from patients. We found that ORAI1-3 and STIM1-2 were ubiquitously expressed in human vasculatures. Their expression was upregulated by chronic treatment with high glucose (HG, 25 mM d-glucose), which was accompanied by enhanced store-operated Ca 2+ influx in vascular endothelial cells. The increased expression was also observed in the aortae from genetically modified Akita diabetic mice (C57BL/6-Ins2 Akita /J) and streptozocin-induced diabetic mice, and aortae from diabetic patients. HG-induced upregulation of ORAI and STIM genes was prevented by the calcineurin inhibitor cyclosporin A and NFATc3 siRNA. Additionally, in vivo treatment with the nuclear factor of activated T cells (NFAT) inhibitor A-285222 prevented the gene upregulation in Akita mice. However, HG had no direct effects on ORAI1-3 currents and the channel activation process through cytosolic STIM1 movement in the cells co-expressing STIM1-EYFP/ORAIs. We concluded that upregulation of STIM/ORAI through Ca 2+ -calcineurin-NFAT pathway is a novel mechanism causing abnormal Ca 2+ homeostasis and endothelial dysfunction under hyperglycaemia. Key message: ORAI1-3 and STIM1-2 are ubiquitously expressed in vasculatures and upregulated by high glucose.Increased expression is confirmed in Akita (Ins2 Akita /J) and STZ diabetic mice and patients.Upregulation mechanism is mediated by Ca 2+ /calcineurin/NFATc3 signalling.High glucose has no direct effects on ORAI1-3 channel activity and channel activation process

An Hsp90 co-chaperone links protein folding and degradation and is part of a conserved protein quality control

In this paper, we show that the essential Hsp90 co-chaperone Sgt1 is a member of a general protein quality control network that links folding and degradation through its participation in the degradation of misfolded proteins both in the cytosol and the endoplasmic reticulum (ER). Sgt1-dependent protein degradation acts in a parallel pathway to the ubiquitin ligase (E3) and ubiquitin chain elongase (E4), Hul5, and overproduction of Hul5 partly suppresses defects in cells with reduced Sgt1 activity. Upon proteostatic stress, Sgt1 accumu- lates transiently, in an Hsp90- and proteasome-dependent manner, with quality control sites (Q-bodies) of both yeast and human cells that co-localize with Vps13, a protein that creates organelle contact sites. Misfolding disease proteins, such as synphilin-1 involved in Parkinson's disease, are also sequestered to these compartments and require Sgt1 for their clearance

NFAT regulates the expression of AIF-1 and IRT-1: Yin and yang splice variants of neointima formation and atherosclerosis.

Aims Alternative transcription and splicing of the allograft inflammatory factor-1 (AIF-1) gene results in the expression of two different proteins: AIF-1 and interferon responsive transcript-1 (IRT-1). Here we explore the impact of AIF-1 and IRT-1 on vascular smooth muscle cell (VSMC) activation and neointima formation, the mechanisms underlying their alternative splicing, and associations of AIF-1 and IRT-1 mRNA with parameters defining human atherosclerotic plaque phenotype.Methods and results Translation of AIF-1 and IRT-1 results in different products with contrasting cellular distribution and functions. Overexpression of AIF-1 stimulates migration and proliferation of human VSMCs, whereas IRT-1 exerts opposite effects. Adenoviral infection of angioplasty-injured rat carotid arteries with AdAIF-1 exacerbates intima hyperplasia, whereas infection with AdIRT-1 reduces neointima. Expression of these variants is modulated by changes in nuclear factor of activated T-cells (NFAT) activity. Pharmacological inhibition of NFAT or targeting of NFATc3 with siRNA lowers the AIF-1/IRT-1 ratio and favors an anti-proliferative outcome. NFAT acts as a repressor on the IRT-1 transcriptional start site, which is also sensitive to interferon-γ stimulation. Expression of AIF-1 mRNA in human carotid plaques associates with less extracellular matrix and a more pro-inflammatory plaque and plasma profile, features that may predispose to plaque rupture. In contrast, expression of IRT-1 mRNA associates with a less aggressive phenotype and less VSMCs at the most stenotic region of the plaque.Conclusions Inhibition of NFAT signaling, by shifting the AIF-1/IRT-1 ratio, may be an attractive target to regulate the VSMC response to injury and manipulate plaque stability in atherosclerosis