Massive stars exploding in a He-rich circumstellar medium - V. Observations of the slow-evolving SN Ibn OGLE-2012-SN-006

We present optical observations of the peculiar Type Ibn supernova (SN Ibn) OGLE-2012-SN-006, discovered and monitored by the Optical Gravitational Lensing Experiment-IV survey, and spectroscopically followed by Public ESO Spectroscopic Survey of Transient Objects (PESSTO) at late phases. Stringent pre-discovery limits constrain the explosion epoch with fair precision to JD = 245 6203.8 +/- 4.0. The rise time to the I-band light-curve maximum is about two weeks. The object reaches the peak absolute magnitude M-I = -19.65 +/- 0.19 on JD = 245 6218.1 +/- 1.8. After maximum, the light curve declines for about 25 d with a rate of 4 mag (100 d)(-1). The symmetric I-band peak resembles that of canonical Type Ib/c supernovae (SNe), whereas SNe Ibn usually exhibit asymmetric and narrower early-time light curves. Since 25 d past maximum, the light curve flattens with a decline rate slower than that of the Co-56-Fe-56 decay, although at very late phases it steepens to approach that rate. However, other observables suggest that the match with the Co-56 decay rate is a mere coincidence, and the radioactive decay is not the main mechanism powering the light curve of OGLE-2012-SN-006. An early-time spectrum is dominated by a blue continuum, with only a marginal evidence for the presence of He I lines marking this SN type. This spectrum shows broad absorptions bluewards than 5000 angstrom, likely O II lines, which are similar to spectral features observed in superluminous SNe at early epochs. The object has been spectroscopically monitored by PESSTO from 90 to 180 d after peak, and these spectra show the typical features observed in a number of SN 2006jc-like events, including a blue spectral energy distribution and prominent and narrow (v(FWHM) approximate to 1900 km s(-1)) He I emission lines. This suggests that the ejecta are interacting with He-rich circumstellar material. The detection of broad (10(4) km s(-1)) O I and Ca II features likely produced in the SN ejecta (including the [OI] lambda lambda 6300,6364 doublet in the latest spectra) lends support to the interpretation of OGLE-2012-SN-006 as a core-collapse event.

GeneGrid: Architecture, Implementation and Application

The emergence of Grid computing technology has opened up an unprecedented opportunity for biologists to share and access data, resources and tools in an integrated environment leading to a greater chance of knowledge discovery. GeneGrid is a Grid computing framework that seamlessly integrates a myriad of heterogeneous resources spanning multiple administrative domains and locations. It provides scientists an integrated environment for the streamlined access of a number of bioinformatics programs and databases through a simple and intuitive interface. It acts as a virtual bioinformatics laboratory by allowing scientists to create, execute and manage workflows that represent bioinformatics experiments. A number of cooperating Grid services interact in an orchestrated manner to provide this functionality. This paper gives insight into the details of the architecture, components and implementation of GeneGrid.

Inhibitors of alpha-synuclein oligomerization and toxicity: a future therapeutic strategy for Parkinson's disease and related disorders.

An abundance of genetic, histopathological, and biochemical evidence has implicated the neuronal protein, alpha-synuclein (alpha-syn) as a key player in the development of several neurodegenerative diseases, the so-called synucleinopathies, of which Parkinson's disease (PD) is the most prevalent. Development of disease appears to be linked to events that increase the intracellular concentration of alpha-syn or cause its chemical modification, either of which can accelerate the rate at which it forms aggregates. Examples of such events include increased copy number of genes, decreased rate of degradation via the proteasome or other proteases, or altered forms of alpha-syn, such as truncations, missense mutations, or chemical modifications by oxidative reactions. Aggregated forms of the protein, especially newly formed soluble aggregates, are toxic to cells, so that one therapeutic strategy would be to reduce the rate at which such oligomerization occurs. We have therefore designed several peptides and also identified small molecules that can inhibit alpha-syn oligomerization and toxicity in vitro. These compounds could serve as lead compounds for the design of new drugs for the treatment of PD and related disorders in the future.

Differences in expression of junctional adhesion molecule-A and beta catenin in multiple sclerosis brain tissue: increasing evidence for the role of tight junction pathology

Previously we have employed antibodies to the tight junction (TJ)-associated proteins ZO-1 and occludin to describe endothelial tight junction abnormalities, in lesional and normal appearing white matter, in primary and secondary progressive multiple sclerosis (MS). This work is extended here by use of antibodies to the independent TJ-specific proteins and junctional adhesion molecule A & B (JAM-A, JAM-B). We have also assessed the expression in MS of ß-catenin, a protein specific to the TJ-associated adherens junction. Immunocytochemistry and semiquantitative confocal microscopy for JAM-A and ß-catenin was performed on snap-frozen sections from MS cases (n = 11) and controls (n = 6). Data on 1,443 blood vessels was acquired from active lesions (n = 13), inactive lesions (n = 13), NAWM (n = 20) and control white matter (n = 13). In MS abnormal JAM-A expression was found in active (46%) and inactive lesions (21%), comparable to previous data using ZO-1. However, a lower level of TJ abnormality was found in MS NAWM using JAM-A (3%) compared to ZO-1 (13%). JAM-B was strongly expressed on a small number of large blood vessels in control and MS tissues but at too low a level for quantitative analysis. By comparison with the high levels of abnormality observed with the TJ proteins, the adherens junction protein ß-catenin was normally expressed in all MS and control tissue categories. These results confirm, by use of the independent marker JAM-A, that TJ abnormalities are most frequent in active white matter lesions. Altered expression of JAM-A, in addition to affecting junctional tightness may also both reflect and affect leukocyte trafficking, with implications for immune status within the diseased CNS. Conversely, the adherens junction component of the TJ, as indicated by ß-catenin expression is normally expressed in all MS and control tissue categories.

Ethics in the workplace

The right to request flexible working has been introduced into the UK employment laws against a background of post-fordist work practices, which already allow for employer rather than employee flexibility. This paper posits the idea that for the individual employee to benefit from these new rights what is required is the situation of dialogues within the workplace that take place in an ethical frame that recognises the employee as an individual.

School exclusion, drug use and delinquency in adolescence

Fifty-one young people aged 14�15 years considered to be at a high-risk of substance abuse and exhibiting antisocial behavior, primarily because they longer attended mainstream school, participated in this research by completing a questionnaire to measure drug use and delinquent behaviour. The findings suggest that many of them may have already developed a high propensity to drug abuse and antisocial behaviour compared with their peers in mainstream education. As they were all excluded from school, they were not accessing school based prevention programmes delivered to their contemporaries at school suggesting that additional and specialized resources are required to fully meet their needs.

Accelerated apoptosis in SLE neutrophils cultured with anti-dsDNA antibody isolated from SLE patient serum: a pilot study.

Increased numbers of apoptotic neutrophils are found in SLE, related to disease activity and levels of anti-dsDNA antibody. The mechanism of increased apoptosis is not clear, but anti-dsDNA antibody has been shown to induce apoptosis in neutrophils from normal subjects and in certain cell lines. In this study, polyclonal anti-dsDNA antibody was isolated from the serum of a patient with active SLE, and was shown to substantially accelerate apoptosis in neutrophils from SLE patients as compared with neutrophils from healthy control or rheumatoid arthritis subjects.