Transcriptome analysis of skeletal muscle tissue to identify genes involved in pre-slaughter stress response in pigs

The knowledge of genes and molecular processes controlling stress reactions and involved in the genetic system determining resistance to stress in pigs could be important for the improvement of meat quality. This research aimed to compare the expression profiles of skeletal muscle between physically stressed and not stressed pigs of different breeds immediately before slaughter. DNA microarray analysis showed that different functional categories of genes are up-regulated in stressed compared to not stressed pigs and relevant differences among breeds were found. - Utilizzando la tecnica microarray vengono confrontate liste di geni differenzialmente espressi in suini di diverse razze sottoposti oppure no a trattamenti stressanti pre macellazione per identificare le basi genetiche della resistenza e suscettibilità allo stress nel suino nella fase premacellazione e vengono analizzati gli effetti dello stress sulla qualità della carne nei soggetti stressati e non stressati. I risultati indicano interessanti differenze nella risposta allo stress tra le razze Large White Italiana, Duroc Italiana e Pietrain. e diverse categorie di geni sovraregolati nel confronto tra soggetti stressati e non stressati

Methods for interpreting lists of affected genes obstained in a DNA microarray experiment

Background - The aim of this paper was to describe and compare the methods used and the results obtained by the participants in a joint EADGENE (European Animal Disease Genomic Network of Excellence) and SABRE (Cutting Edge Genomics for Sustainable Animal Breeding) workshop focusing on post analysis of microarray data. The participating groups were provided with identical lists of microarray probes, including test statistics for three different contrasts, and the normalised log-ratios for each array, to be used as the starting point for interpreting the affected probes. The data originated from a microarray experiment conducted to study the host reactions in broilers occurring shortly after a secondary challenge with either a homologous or heterologous species of Eimeria. Results - Several conceptually different analytical approaches, using both commercial and public available software, were applied by the participating groups. The following tools were used: Ingenuity Pathway Analysis, MAPPFinder, LIMMA, GOstats, GOEAST, GOTM, Globaltest, TopGO, ArrayUnlock, Pathway Studio, GIST and AnnotationDbi. The main focus of the approaches was to utilise the relation between probes/genes and their gene ontology and pathways to interpret the affected probes/genes. The lack of a well-annotated chicken genome did though limit the possibilities to fully explore the tools. The main results from these analyses showed that the biological interpretation is highly dependent on the statistical method used but that some common biological conclusions could be reached. Conclusion - It is highly recommended to test different analytical methods on the same data set and compare the results to obtain a reliable biological interpretation of the affected genes in a DNA microarray experimen

Analyses of non-coding somatic drivers in 2,658 cancer whole genomes.

The discovery of drivers of cancer has traditionally focused on protein-coding genes1-4. Here we present analyses of driver point mutations and structural variants in non-coding regions across 2,658 genomes from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium5 of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). For point mutations, we developed a statistically rigorous strategy for combining significance levels from multiple methods of driver discovery that overcomes the limitations of individual methods. For structural variants, we present two methods of driver discovery, and identify regions that are significantly affected by recurrent breakpoints and recurrent somatic juxtapositions. Our analyses confirm previously reported drivers6,7, raise doubts about others and identify novel candidates, including point mutations in the 5' region of TP53, in the 3' untranslated regions of NFKBIZ and TOB1, focal deletions in BRD4 and rearrangements in the loci of AKR1C genes. We show that although point mutations and structural variants that drive cancer are less frequent in non-coding genes and regulatory sequences than in protein-coding genes, additional examples of these drivers will be found as more cancer genomes become available

Elucidating halo structure by beta decay: beta gamma from the Li-11 decay

New values for the gamma ray intensities following the beta decay of Li-11 are presented. Special emphasis is put on the determination of the Gamow-Teller transition Li-11 --> Be-11 (1/2(-), 320 keV) to the only bound excited state in Be-11. We show that a shell-model calculation can simultaneously reproduce the half-life of Li-11 and the newly measured branching ratio to the 1/2(-) state provided the Li-11 ground state wave function contains about 50% of s-wave neutron components

Elucidating halo structure by beta decay: beta gamma from the Li-11 decay

New values for the gamma ray intensities following the beta decay of Li-11 are presented. Special emphasis is put on the determination of the Gamow-Teller transition Li-11 --> Be-11 (1/2(-), 320 keV) to the only bound excited state in Be-11. We show that a shell-model calculation can simultaneously reproduce the half-life of Li-11 and the newly measured branching ratio to the 1/2(-) state provided the Li-11 ground state wave function contains about 50% of s-wave neutron components

Probing the 11Li halo structure through ß-decay into the 11Be*(18 MeV) state

An experimental study of r-delayed charged particles (H, He, Be) from llLi shows a r-feeding to an excited state at 18.15(15) MeV in llBe with a large Gamow-Teller strength, BeT ~> 1.6. Branching ratios and reduced widths of 2-, 3- and 5- particle decay channels of this state are extracted. A strong suppression of the neutron branch from the 18 MeV state to the l°Beg.s, is observed. We suggest that the measured partial width may be sensitive to the (pu2) 2 component in the HLi halo. A rough estimate indicates that the (Pl/2) 2 component is not the dominant one in the halo wave-function