Tributyltin (TBT) and the decline of the Norfolk Broads: Hickling Broad and Barton Broad

This study furthers the work of Sayer et al (2001), in which a model was presented regarding the collapse of the plant-dominated state in the aquatic ecosystem of the Norfolk Broads, E. England. The boat antifouling biocide tributyltin (TBT) was implicated as a toxic switching mechanism from evidence gathered in a palaeolimnological study of Wroxham Broad

In vivo study of experimental pneumococcal meningitis using magnetic resonance imaging

<p>Abstract</p> <p>Background</p> <p>Magnetic Resonance Imaging (MRI) methods were evaluated as a tool for the study of experimental meningitis. The identification and characterisation of pathophysiological parameters that vary during the course of the disease could be used as markers for future studies of new treatment strategies.</p> <p>Methods</p> <p>Rats infected intracisternally with <it>S. pneumoniae </it>(n = 29) or saline (n = 13) were randomized for imaging at 6, 12, 24, 30, 36, 42 or 48 hours after infection. T1W, T2W, quantitative diffusion, and post contrast T1W images were acquired at 4.7 T. Dynamic MRI (dMRI) was used to evaluate blood-brain-barrier (BBB) permeability and to obtain a measure of cerebral and muscle perfusion. Clinical- and motor scores, bacterial counts in CSF and blood, and WBC counts in CSF were measured.</p> <p>Results</p> <p>MR images and dMRI revealed the development of a highly significant increase in BBB permeability (P < 0.002) and ventricle size (P < 0.0001) among infected rats. Clinical disease severity was closely related to ventricle expansion (P = 0.024).</p> <p>Changes in brain water distribution, assessed by ADC, and categorization of brain 'perfusion' by cortex ΔSI_(bolus)were subject to increased inter-rat variation as the disease progressed, but without overall differences compared to uninfected rats (P > 0.05). Areas of well-'perfused' muscle decreased with the progression of infection indicative of septicaemia (P = 0.05).</p> <p>Conclusion</p> <p>The evolution of bacterial meningitis was successfully followed <it>in-vivo </it>with MRI. Increasing BBB-breakdown and ventricle size was observed in rats with meningitis whereas changes in brain water distribution were heterogeneous. MRI will be a valuable technique for future studies aiming at evaluating or optimizing adjunctive treatments</p

'Surf's up!':A call to take english soccer fan interactions on the internet more seriously

Soccer fandom practices in England have been significantly impacted by globalization. The creation of the Premier League in 1992, and the way in which satellite television company BSkyB dominated coverage of this, together with other developments, have led to changes in how fans consume top-level English soccer. Whilst such global transformations are well documented in the sociology of soccer literature, the implications of the rise of the most advanced global form of communication - the Internet - on the practices of fans of English soccer clubs, have not been fully taken into account by academics. As such, the significance of the Internet as a site for fans to interact remains under-investigated. This article argues that online interactions between fans of English clubs need to be taken more seriously by academics if they are to more fully understand how soccer contributes to the maintenance of social identities in contemporary England

Activation of N-heterocyclic carbenes by {BeH₂} and {Be(H)(Me)} fragments

A stable three-coordinate dimethylberyllium species coordinated by the 1,3-bis­(2,4,6-trimethylphenyl)­imidazol-2-ylidene (IMes) ligand is readily converted to the corresponding methylhydrido derivative through metathetical reaction with phenylsilane. Attempts to synthesize the corresponding molecular dihydrides are, however, unsuccessful and result in ring opening of an IMes ligand through hydride transfer to the donor carbon atom and the consequent formation of a heterocyclic beryllium organoamide. In agreement with previous calculations, we suggest that this process occurs via a Schlenk-type equilibration process and formation of a four-coordinate bis-NHC beryllium dihydride. These species are not observed, however, as the steric pressure exerted by coordination of the two sterically demanding IMes ligands is sufficient to induce hydride transfer. The latter deduction is supported by the observation that a similar ring-opened product, but derived from methyl and hydride transfer, is available through the introduction of a further equivalent of IMes to the isolated beryllium methyl hydride species. In the latter case the ring-opening process is more facile, which we ascribe to the increased steric pressure achieved upon the formation of four-coordinate beryllium. In a further striking reaction under more forcing thermal conditions, the carbene carbon center of an IMes ligand is observed to be completely eliminated with selective formation of a three-coordinate diamidoberyllium species

Mcph1/brit1 limits ionizing radiation-induced centrosome amplification

Microcephalin (MCPH1/BRIT1) is a potential tumour suppressor that localizes to the centrosome, forms ionizing radiation-induced nuclear foci (IRIF) and is involved in the DNA damage checkpoints that ensure genome stability. Here, we report the impact of Mcph1 disruption in the hyper-recombinogenic DT40 cell line. Mcph1(-/-) cells were viable and proliferated at the same rate as wildtype controls. Mcph1-deficient cells had intact G2-to-M checkpoint responses after ionizing radiation (IR) treatment, but showed moderate radiosensitivity. Light and electron microscopy indicated normal centrosome structures in Mcph1 null cells, but IR induced massive amplification of centrosome numbers in the absence of Mcph1. Mcph1 null cells formed gamma-H2AX and Rad51 IRIF, but resolved them more slowly than wild-type cells. Mcph1 deficiency caused sustained Chk1 phosphorylation after IR, dysregulating Cdk2 activity. These findings show that Mcph1 controls centrosome numbers after DNA damage, which may indicate a novel tumour suppressive mechanism for microcephalin. Oncogene (2010) 29, 5537-5544; doi:10.1038/onc.2010.302; published online 26 July 201