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Irritable bowel syndrome (IBS) is a psychosomatic gastrointestinal disorder involving the dysfunctional activation of specific brain regions crucial for interoception and disgust processing. Yet, no study has ever investigated the link between this socio-affective/visceral experience and IBS.The present study investigated whether disgust sensitivity and disgust propensity, which can be socially relevant, relate with IBS symptoms in a nonclinical population.105 healthy participants were asked to complete the Disgust Propensity and Sensitivity Scale-Revised (DPSS-R), the Irritable Bowel Syndrome-Quality of Life Measure (IBS-QOL), and the Chronic Urticaria Quality of Life Measure (CU-Q2OL), as control condition.Results showed higher disgust sensitivity scores in individuals with high IBS-QOL score, compared to individuals with low IBS-QOL score. The correlation analysis corroborates this result by showing a positive relationship between disgust sensitivity and respective IBS-QOL scores.This research provides new insights into understanding the etiopathogenesis of IBS, suggesting the relevance of a socially relevant personality trait such as disgust sensitivity as a potential trigger and / or predisposition factor for this chronic inflammatory disease.

Aims: To compare the genomic signatures of wild-type (WT) and mutated GISTs and the murine inter-stitial cells of Cajal (ICCs) to find markers of celldifferentiation and other functions that may identifycells that give rise to WT tumours.Methods and results: We analysed the gene expressionprofiles of a total of 30 tumour samples (four WT GISTsand 26 mutated GISTs), selected the genes mostdifferentially expressed (P < 0.001:448 probe sets)and validated these results by quantitative polymerasechain reaction (PCR) and immunohistochemistry. Inaddition, we conducted a meta-analysis merging datafrom human GISTs with a genomic data set frommurine ICCs. The gene expression profiles of WT andmutated GISTs differed profoundly, especially in theexpression of those genes restricted primarily to neuraltissues. We found that mature ICCs are more similar tomutated GISTs than WT GISTs.Conclusions: WT GISTs have different genomic profilesfrom both mutated GISTs and murine mature ICCs.Considering that IGF1R expression is common to bothWT GISTs and putative precursor ICCs, this studysuggests that WT GISTs may derive either from ICCs ata different step of differentiation or from a different cellof origin.Keywords: gene expression profiling, GIST, ICC, ICC mature, ICC precursor, IGF1R, KIT, PDGFRAAbbreviations: CDH2, cadherin-2; DMP, deep muscular plexus; ELAVL3, embryonic lethal, abnormal vision,Drosophila-like 3; GIST, gastrointestinal stromal tumours; ICC, interstitial cells of Cajal; IGF1R, insulin-like growthfactor 1 receptor; IHC, immunohistochemistry; KIRREL3, Kin of IRRE-like protein 3; Lhx2, LIM ⁄ homeobox protein;MY, myenteric plexus; NEFL, neurofilament light polypeptide gene; NRCA, neuronal cell adhesion molecule; NSE,neurone-specific enolase; PCR, polymerase chain reaction; PDGFRA, platelet-derived growth factor receptor, alpha;TKI, tyrosine kinase inhibitor; WT, wild-type

A pilot study using Affymetrix Gene Chip(R) Porcine Genome Arrays was set up to evaluate the impact of time lags from death on gene expression profiling of porcine skeletal muscle at four post mortem times (up to 24 h) during the routine processing of fresh thighs. All post chip parameters and data analyses (Average background, Scale Factors, Percent Presence, 3'/5' ratios of beta-actin and glyceraldehyde-3-phosphase dehydrogenase control genes, RNA degradation diagnostics, principal component analysis, hierarchical clustering, mixed regression models with time effects) did not show any effect of post mortem time. Therefore, microarray data obtained from muscle specimens collected in a processing plan over a quite long period have the potential to identify treatments or pre mortem conditions without any potential bias derived from subtle RNA degradation. These results open new perspectives to develop and analyse gene expression biomarkers for pig production and product authentication.

Approximately 10%-15% of gastrointestinal stromal tumors (GISTs) in adults do not harbor any mutation in the KIT or PDGFRA genes (ie, KIT/PDGFRA wild-type GISTs). Recently, mutations in SDHB and SDHC (which encode succinate dehydrogenase subunits B and C, respectively) but not in SDHA and SDHD (which encode subunits A and D, respectively) were identified in KIT/PDGFRA wild-type GISTs. To search for novel pathogenic mutations, we sequenced the tumor transcriptome of two young adult patients who developed sporadic KIT/PDGFRA wild-type GISTs by using a massively parallel sequencing approach. The only variants identified as disease related by computational analysis were in SDHA. One patient carried the homozygous nonsense mutation p.Ser384X, the other patient was a compound heterozygote harboring a p.Arg31X nonsense mutation and a p.Arg589Trp missense mutation. The heterozygous nonsense mutations in both patients were present in germline DNA isolated from peripheral blood. Protein structure analysis indicates that all three mutations lead to functional inactivation of the protein. This is the first report, to our knowle dge, that identifies SDHA inactivation as a common oncogenic event in GISTs that lack a mutation in KIT and PDGFRA.

In the late 1960s, the Australian film industry was in crisis: audiences were turning to television programmes, in part because they offered more Australian content, and the commercially successful screen comedies of the so-called Ocker were perceived to be damaging the image of Australia abroad. In the 1970s, realizing the potential of cinema as a cultural flagship, the government invested heavily in the film industry through the establishment of the Australian Film Commission (AFC) for the purpose of promoting of high-quality productions. This article examines the main polices of the AFC, and argues that its role in transforming the film industry from a ‘cottage industry into a business’ (Murray 1990: 14) has been overestimated by Australian cinema scholars such as Dermody and Jacka, David Stratton and Tom O'Regan. The AFC's role as a government body meant that the Commission was more accountable to the government than to film industry professionals, such as producers and filmmakers. The final s...

In addition to KIT and PDGFRA mutations, sequential accumulation of other genetic events is involved in the development and progression of gastrointestinal stromal tumors (GISTs). Until recently, the significance of these other alterations has not been thoroughly investigated. We report the first study that integrates gene expression profiling and high-resolution genomic copy number analyses in GIST. Fresh tissue specimens from 25 patients with GIST were collected, and gene expression profiling and high-resolution genomic copy number analyses were performed, using Affymetrix U133Plus and SNP array 6.0. We found that all 21 mutant GIST patients showed both macroscopic cytogenetic alterations and cryptic microdeletions or amplifications, whereas 75% (three of four) of wild-type patients with GIST did not show genomic imbalances. The most frequently observed chromosomal alterations in patients with mutant GIST included 14q complete or partial deletion (17 of 25), 1p deletion (14 of 25) and 22q deletion (10 of 25). Genetic targets of the chromosomal aberrations were selected by integrated analysis of copy number and gene expression data. We detected the involvement of known oncogenes and tumor suppressors including KRAS in chr 12p amplification and KIF1B, PPM1A, NF2 in chr 1p, 14q and 22p deletions, respectively. The genomic segment most frequently altered in mutated samples was the 14q23.1 region, which contains potentially novel tumor suppressors, including DAAM1, RTN1 and DACT1. siRNA-mediated RTN1 downregulation showed evidence for the potential role in GIST pathogenesis. The combination of gene expression profiling and high-resolution genomic copy number analysis offers a detailed molecular portrait of GISTs, providing an essential comprehensive knowledge necessary to guide the discovery of novel target genes involved in tumor development and progression.