The ethics of sociocultural risk research

In socio-cultural risk research, an epistemological tension often follows if real hazards in the world are juxtaposed against the essentially socially constructed nature of all risk. In this editorial, we consider how this paradox is manifest at a practical level in a number of ethical dilemmas for the risk researcher. (1) In terms of strategies for seeking informed consent, and for addressing the power inequalities involved in interpretative and analytical work, researchers can find themselves pushing at the boundaries of standard understandings of ethical practices and ways of engaging informants in their studies. (2) Impact on participants is another key area of concern, since the subject matter on which data are collected in risk research may be a source of uncertainty, anxiety or unwanted self knowledge. (3) Risk researchers also face the possibility of institutional repercussions of raising risk issues with people who usually normalize the risks, thereby stimulating distrust in the institutions or organizations with formal responsibilities for risk management. There are no simple formulae to guide the researcher in dealing with such ethical issues and paradoxes. It is important, though, to recognize their specificity in risk studies, including the ambiguous status of questions about vulnerability since judgements about 'who is vulnerable' and 'in what ways' are themselves influenced by the situational framings and understandings of participants and researchers

Sequence structure emission in The Red Rectangle Bands

We report high resolution (R~37,000) integral field spectroscopy of the central region (r<14arcsec) of the Red Rectangle nebula surrounding HD44179. The observations focus on the 5800A emission feature, the bluest of the yellow/red emission bands in the Red Rectangle. We propose that the emission feature, widely believed to be a molecular emission band, is not a molecular rotation contour, but a vibrational contour caused by overlapping sequence bands from a molecule with an extended chromophore. We model the feature as arising in a Polycyclic Aromatic Hydrocarbon (PAH) with 45-100 carbon atoms.Comment: 13 pages, 9 figures, accepted for publication in ApJ. A version of the paper with full resolution figures is available at: http://www.aao.gov.au/local/www/rgs/Sequence-Structure

The Notch pathway controls fibrotic and regenerative repair in the adult heart.

AIMS: In the adult heart, Notch signalling regulates the response to injury. Notch inhibition leads to increased cardiomyocyte apoptosis, and exacerbates the development of cardiac hypertrophy and fibrosis. The role of Notch in the mesenchymal stromal cell fraction, which contains cardiac fibroblasts and cardiac precursor cells, is, however, largely unknown. In the present study, we evaluate, therefore, whether forced activation of the Notch pathway in mesenchymal stromal cells regulates pathological cardiac remodelling. METHODS AND RESULTS: We generated transgenic mice overexpressing the Notch ligand Jagged1 on the surface of cardiomyocytes to activate Notch signalling in adjacent myocyte and non-myocyte cells. In neonatal transgenic mice, activated Notch sustained cardiac precursor and myocyte proliferation after birth, and led to increased numbers of cardiac myocytes in adult mice. In the adult heart under pressure overload, Notch inhibited the development of cardiomyocyte hypertrophy and transforming growth factor-β/connective tissue growth factor-mediated cardiac fibrosis. Most importantly, Notch activation in the stressed adult heart reduced the proliferation of myofibroblasts and stimulated the expansion of stem cell antigen-1-positive cells, and in particular of Nkx2.5-positive cardiac precursor cells. CONCLUSIONS: We conclude that Notch is pivotal in the healing process of the injured heart. Specifically, Notch regulates key cellular mechanisms in the mesenchymal stromal cell population, and thereby controls the balance between fibrotic and regenerative repair in the adult heart. Altogether, these findings indicate that Notch represents a unique therapeutic target for inducing regeneration in the adult heart via mobilization of cardiac precursor cells

Mediating punitiveness: understanding public attitudes towards work-related fatality cases

This paper concerns an empirical investigation into public attitudes towards work-related fatality cases, where organizational offenders cause the death of workers or members of the public. This issue is particularly relevant following the introduction of the Corporate Manslaughter and Corporate Homicide Act 2007 into UK law. Here, as elsewhere, the use of criminal law against companies reflects governmental concerns over public confidence in the law’s ability to regulate risk. The empirical findings demonstrate that high levels of public concern over these cases do not translate into punitive attitudes. Such cases are viewed rationally and constructively, and lead to instrumental rather than purely expressive enforcement preferences

Resveratrol Reverses Endothelial Colony-Forming Cell Dysfunction in Adulthood in a Rat Model of Intrauterine Growth Restriction.

Individuals born after intrauterine growth restriction (IUGR) are at risk of developing cardiovascular diseases (CVDs). Endothelial dysfunction plays a role in the pathogenesis of CVDs; and endothelial colony-forming cells (ECFCs) have been identified as key factors in endothelial repair. In a rat model of IUGR induced by a maternal low-protein diet, we observed an altered functionality of ECFCs in 6-month-old males, which was associated with arterial hypertension related to oxidative stress and stress-induced premature senescence (SIPS). Resveratrol (R), a polyphenol compound, was found to improve cardiovascular function. In this study, we investigated whether resveratrol could reverse ECFC dysfunctions in the IUGR group. ECFCs were isolated from IUGR and control (CTRL) males and were treated with R (1 μM) or dimethylsulfoxide (DMSO) for 48 h. In the IUGR-ECFCs, R increased proliferation (5'-bromo-2'-deoxyuridine (BrdU) incorporation, p &lt; 0.001) and improved capillary-like outgrowth sprout formation (in Matrigel), nitric oxide (NO) production (fluorescent dye, p &lt; 0.01), and endothelial nitric oxide synthase (eNOS) expression (immunofluorescence, p &lt; 0.001). In addition, R decreased oxidative stress with reduced superoxide anion production (fluorescent dye, p &lt; 0.001); increased Cu/Zn superoxide dismutase expression (Western blot, p &lt; 0.05); and reversed SIPS with decreased beta-galactosidase activity (p &lt; 0.001), and decreased p16 &lt;sup&gt;ink4a&lt;/sup&gt; (p &lt; 0.05) and increased Sirtuin-1 (p &lt; 0.05) expressions (Western blot). No effects of R were observed in the CTRL-ECFCs. These results suggest that R reverses long-term ECFC dysfunctions related to IUGR

A southern hemisphere survey of the 5780 and 6284 {\AA} diffuse interstellar bands: correlation with the extinction

We present a new database of 5780.5 and 6283.8 {\AA} DIB measurements and also study their correlation with the reddening. The database is based on high-resolution, high-quality spectra of early-type nearby stars located in the southern hemisphere at an average distance of 300 pc. Equivalent widths of the two DIBs were determined by means of a realistic continuum fitting and synthetic atmospheric transmissions. For all stars that possess a precise measurement of their color excess, we compare the DIBs and the extinction. We find average linear relationships of the DIBS and the color excess that agree well with those of a previous survey of northern hemisphere stars closer than 550 pc. This similarity shows that there is no significant spatial dependence of the average relationship in the solar neighborhood within $\simeq$ 600 pc. A noticeably different result is our higher degree of correlation of the two DIBs with the extinction. We demonstrate that it is simply due to the lower temperature and intrinsic luminosity of our targets. Using cooler target stars reduces the number of outliers, especially for nearby stars, confirming that the radiation field of UV bright stars has a significant influence on the DIB strength. We have used the cleanest data to compute updated DIB shapes.Comment: Astronomy & Astrophysics (in press

Indirect inguinal hernia masquerading as a Spigelian hernia

Inguinal hernia usually developed and descended into scrotum. The clinical presentation is inguinal or inguino-scrotal swelling. Abdominal wall weakness as it is frequently seen in African tropical zones produces often rare clinical case. We report a case of inguinal hernia presented as an abdominal wall swelling clinically suggestive of a Spigelian hernia and discuss the mechanism

Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.

The adult mammalian heart has poor regenerative capacity. In contrast, the zebrafish heart retains a robust capacity for regeneration into adulthood. These distinct responses are consequences of a differential utilization of evolutionary-conserved gene regulatory networks in the damaged heart. To systematically identify miRNA-dependent networks controlling cardiac repair following injury, we performed comparative gene and miRNA profiling of the cardiac transcriptome in adult mice and zebrafish. Using an integrated approach, we show that 45 miRNA-dependent networks, involved in critical biological pathways, are differentially modulated in the injured zebrafish vs. mouse hearts. We study, more particularly, the miR-26a-dependent response. Therefore, miR-26a is down-regulated in the fish heart after injury, whereas its expression remains constant in the mouse heart. Targets of miR-26a involve activators of the cell cycle and Ezh2, a component of the polycomb repressive complex 2 (PRC2). Importantly, PRC2 exerts repressive functions on negative regulators of the cell cycle. In cultured neonatal cardiomyocytes, inhibition of miR-26a stimulates, therefore, cardiomyocyte proliferation. Accordingly, miR-26a knockdown prolongs the proliferative window of cardiomyocytes in the post-natal mouse heart. This novel strategy identifies a series of miRNAs and associated pathways, in particular miR-26a, which represent attractive therapeutic targets for inducing repair in the injured heart