Two new species of feather mites (Acarina: Psoroptidia) from the blue-throated blue flycatcher,Cyornis rubeculoides (Passeriformes: Muscicapidae)

The paper describes two new species of feather mites collected from the blue-throated blue flycatcher Cyornis rubeculoides (Vigors) (Passeriformes: Muscicapidae) in India (Meghalaya): Trouessartia kharkhanensis Constantinescu et al. sp. nov. (Trouessartiidae) and Proterothrix cyornissimilis Constantinescu et al. sp. nov. (Proctophyllodidae: Pterodectinae). Both sexes of T. kharkhanensis differ from the closest species, T. rubecula Jablonska, 1968 by having setae si and c2 lanceolate and setae c3 and sRIII with acute apex. In males of the new species, the adanal apodemes have a hook-like retroverse apophysis and the internal margins of terminal lamellae have a shallow invagination at the level of setae h3. Both sexes of P. cyornissimilis differ from the closest species, P. cyornis Mironov and Tolstenkov, 2013, mainly by the ornamentation of the dorsal shields: it is absent on the prodorsal shield and poorly expressed on the hysteronothal shield. In males of the new species, the supranal concavity is triangular and the genital arch has a pair of small ovoid sclerites at its tips.

http:/zoobank.org/urn:lsid:zoobank.org:pub:1671D6D4-8895-467B-A124-05EDBB0DF406     

Following evolution of bacterial antibiotic resistance in real time

A new study reports the development of the 'morbidostat', a device that allows for continuous culture of bacteria under a constant drug selection pressure using computer feedback control of antibiotic concentration. This device, together with bacterial whole-genome sequencing, allowed the authors to follow the evolution of resistance-conferring mutations in Escherichia coli populations in real time, providing support for deterministic evolution of resistance in some situations.     

Genome-wide association study of prostate cancer in men of African ancestry identifies a susceptibility locus at 17q21

In search of common risk alleles for prostate cancer that could contribute to high rates of the disease in men of African ancestry, we conducted a genome-wide association study, with 1,047,986 SNP markers examined in 3,425 African-Americans with prostate cancer (cases) and 3,290 African-American male controls. We followed up the most significant 17 new associations from stage 1 in 1,844 cases and 3,269 controls of African ancestry. We identified a new risk variant on chromosome 17q21 (rs7210100, odds ratio per allele = 1.51, P = 3.4 × 10(-13)). The frequency of the risk allele is ～5% in men of African descent, whereas it is rare in other populations (<1%). Further studies are needed to investigate the biological contribution of this allele to prostate cancer risk. These findings emphasize the importance of conducting genome-wide association studies in diverse populations.     

Meta-analysis of genome-wide association study data identifies additional type 1 diabetes risk loci

We carried out a meta-analysis of data from three genome-wide association (GWA) studies of type 1 diabetes (T1D), testing 305,090 SNPs in 3,561 T1D cases and 4,646 controls of European ancestry. We obtained further support for 4q27 (IL2-IL21, P = 1.9 x 10(-8)) and, after genotyping an additional 6,225 cases, 6,946 controls and 2,828 families, convincing evidence for four previously unknown and distinct risk loci in chromosome regions 6q15 (BACH2, P = 4.7 x 10(-12)), 10p15 (PRKCQ, P = 3.7 x 10(-9)), 15q24 (CTSH, P = 3.2 x 10(-15)) and 22q13 (C1QTNF6, P = 2.0 x 10(-8)).     

Bayesian Analysis of a Threshold Stochastic Volatility Model

This paper proposes a parsimonious threshold stochastic volatility (SV) model for financial asset returns. Instead of imposing a threshold value on the dynamics of the latent volatility process of the SV model, we assume that the innovation of the mean equation follows a threshold distribution in which the mean innovation switches between two regimes. In our model, the threshold is treated as an unknown parameter. We show that the proposed threshold SV model can not only capture the time‐varying volatility of returns, but can also accommodate the asymmetric shape of conditional distribution of the returns. Parameter estimation is carried out by using Markov chain Monte Carlo methods. For model selection and volatility forecast, an auxiliary particle filter technique is employed to approximate the filter and prediction distributions of the returns. Several experiments are conducted to assess the robustness of the proposed model and estimation methods. In the empirical study, we apply our threshold SV model to three return time series. The empirical analysis results show that the threshold parameter has a non‐zero value and the mean innovations belong to two separately distinct regimes. We also find that the model with an unknown threshold parameter value consistently outperforms the model with a known threshold parameter value. Copyright © 2016 John Wiley & Sons, Ltd.     

Glioblastoma stem-like cells give rise to tumour endothelium

Glioblastoma (GBM) is among the most aggressive of human cancers. A key feature of GBMs is the extensive network of abnormal vasculature characterized by glomeruloid structures and endothelial hyperplasia. Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined. Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7. We additionally demonstrate that the stem-cell-like CD133(+) fraction includes a subset of vascular endothelial-cadherin (CD144)-expressing cells that show characteristics of endothelial progenitors capable of maturation into endothelial cells. Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell. The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium. Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors. These data may provide new perspectives on the mechanisms of failure of anti-angiogenesis inhibitors currently in use. The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.