The unexpected origin of plasmaspheric hiss from discrete chorus emissions

Plasmaspheric hiss is a type of electromagnetic wave found ubiquitously in the dense plasma region that encircles the Earth, known as the plasmasphere. This important wave is known to remove the high-energy electrons that are trapped along the Earth's magnetic field lines, and therefore helps to reduce the radiation hazards to satellites and humans in space. Numerous theories to explain the origin of hiss have been proposed over the past four decades, but none have been able to account fully for its observed properties. Here we show that a different wave type called chorus, previously thought to be unrelated to hiss, can propagate into the plasmasphere from tens of thousands of kilometres away, and evolve into hiss. Our new model naturally accounts for the observed frequency band of hiss, its incoherent nature, its day-night asymmetry in intensity, its association with solar activity and its spatial distribution. The connection between chorus and hiss is very interesting because chorus is instrumental in the formation of high-energy electrons outside the plasmasphere, whereas hiss depletes these electrons at lower equatorial altitudes.     

Mortality of the 'Golden Generation': what can the ONS Longitudinal study tell us?

It is well documented that the generations born around 1930 are consistently exhibiting higher rates of mortality improvement than the generations either side of them. There is currently no evidence that these differentials are declining. In current ONS National Population Projections, it is assumed that these cohorts will continue to experience higher rates of improvement. However, it is not yet precisely clear why this is so. This article details preliminary research carried out using the ONS Longitudinal Study to try to understand better why the members of the generation born around 1930 have been enjoying higher rates of mortality improvement throughout their adult life.     

From personality to party: the creation and transmission of Hutchinsonianism, c. 1725-1750

This paper represents a provisional attempt to chart the intellectual construction of Hutchinsonianism over approximately a quarter of a century from the mid-1720s through to the early 1750s. It looks at how Hutchinson’s works were received and fashioned by his first followers, the means they used to communicate their conviction to others, and the extent to which their outlook can be characterised as anti-Newtonian. The paper argues for a slow take up of ‘Hutchinsonian’ views before Spearman and Bate published a collected edition of the master’s works in 1748. This single edition gave Hutchinson’s writings a coherence and a unity they were ill-designed to carry, but it created Hutchinsonianism as an appreciable force in Oxford and elsewhere. The paper concludes that the anti-Newtonian rhetoric of the movement’s founder was increasingly muted in the hands of his followers (with the exception of Bate), and by the 1750s the main bone of contention was less attitudes to Newton than approaches to Hebrew scholarship.     

Identification of loci associated with schizophrenia by genome-wide association and follow-up

We carried out a genome-wide association study of schizophrenia (479 cases, 2,937 controls) and tested loci with P < 10(-5) in up to 16,726 additional subjects. Of 12 loci followed up, 3 had strong independent support (P < 5 x 10(-4)), and the overall pattern of replication was unlikely to occur by chance (P = 9 x 10(-8)). Meta-analysis provided strongest evidence for association around ZNF804A (P = 1.61 x 10(-7)) and this strengthened when the affected phenotype included bipolar disorder (P = 9.96 x 10(-9)).     

Tartrate-resistant acid phosphatase deficiency causes a bone dysplasia with autoimmunity and a type I interferon expression signature

We studied ten individuals from eight families showing features consistent with the immuno-osseous dysplasia spondyloenchondrodysplasia. Of particular note was the diverse spectrum of autoimmune phenotypes observed in these individuals (cases), including systemic lupus erythematosus, Sj?gren's syndrome, hemolytic anemia, thrombocytopenia, hypothyroidism, inflammatory myositis, Raynaud's disease and vitiligo. Haplotype data indicated the disease gene to be on chromosome 19p13, and linkage analysis yielded a combined multipoint log(10) odds (LOD) score of 3.6. Sequencing of ACP5, encoding tartrate-resistant acid phosphatase, identified biallelic mutations in each of the cases studied, and in vivo testing confirmed a loss of expressed protein. All eight cases assayed showed elevated serum interferon alpha activity, and gene expression profiling in whole blood defined a type I interferon signature. Our findings reveal a previously unrecognized link between tartrate-resistant acid phosphatase activity and interferon metabolism and highlight the importance of type I interferon in the genesis of autoimmunity.     

Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1

Multiple self-healing squamous epithelioma (MSSE), also known as Ferguson-Smith disease (FSD), is an autosomal-dominant skin cancer condition characterized by multiple squamous-carcinoma-like locally invasive skin tumors that grow rapidly for a few weeks before spontaneously regressing, leaving scars. High-throughput genomic sequencing of a conservative estimate (24.2 Mb) of the disease locus on chromosome 9 using exon array capture identified independent mutations in TGFBR1 in three unrelated families. Subsequent dideoxy sequencing of TGFBR1 identified 11 distinct monoallelic mutations in 18 affected families, firmly establishing TGFBR1 as the causative gene. The nature of the sequence variants, which include mutations in the extracellular ligand-binding domain and a series of truncating mutations in the kinase domain, indicates a clear genotype-phenotype correlation between loss-of-function TGFBR1 mutations and MSSE. This distinguishes MSSE from the Marfan syndrome-related disorders in which missense mutations in TGFBR1 lead to developmental defects with vascular involvement but no reported predisposition to cancer.     

Control of HIV infection by IFN-α: implications for latency and a cure

Viral infections, including HIV, trigger the production of type I interferons (IFNs), which in turn, activate a signalling cascade that ultimately culminates with the expression of anti-viral proteins. Mounting evidence suggests that type I IFNs, in particular IFN-α, play a pivotal role in limiting acute HIV infection. Highly active anti-retroviral treatment reduces viral load and increases life expectancy in HIV positive patients; however, it fails to fully eliminate latent HIV reservoirs. To revisit HIV as a curable disease, this article reviews a body of literature that highlights type I IFNs as mediators in the control of HIV infection, with particular focus on the anti-HIV restriction factors induced and/or activated by IFN-α. In addition, we discuss the relevance of type I IFN treatment in the context of HIV latency reversal, novel therapeutic intervention strategies and the potential for full HIV clearance.     

Bioadsorption of 4-Chlorophenol to the Activated Sludge

IntroductionChlorinated phenolic compounds,which aregenerated from a number of industrialmanufacturing processes,comprise the bulk of theenvironmental pollutants.Aqueous effluents fromindustrial operations such as polymeric resinproduction,oil refining,iron- steel,petroleum,pesticide,paint,solvent,pharmaceutics,woodpreserving chemicals,coke- oven,and paper andpulp industries contain chlorophenolic compounds.Their fate in the environment is of greatimportance as they are toxic,recalcitrant andb…     

Germline rates of de novo meiotic deletions and duplications causing several genomic disorders

Meiotic recombination between highly similar duplicated sequences (nonallelic homologous recombination, NAHR) generates deletions, duplications, inversions and translocations, and it is responsible for genetic diseases known as 'genomic disorders', most of which are caused by altered copy number of dosage-sensitive genes. NAHR hot spots have been identified within some duplicated sequences. We have developed sperm-based assays to measure the de novo rate of reciprocal deletions and duplications at four NAHR hot spots. We used these assays to dissect the relative rates of NAHR between different pairs of duplicated sequences. We show that (i) these NAHR hot spots are specific to meiosis, (ii) deletions are generated at a higher rate than their reciprocal duplications in the male germline and (iii) some of these genomic disorders are likely to have been underascertained clinically, most notably that resulting from the duplication of 7q11, the reciprocal of the deletion causing Williams-Beuren syndrome.