Effects of dietary deoxynivalenol or ochratoxin A on performance and selected health indices in Atlantic salmon (Salmo salar)

Post-smolt Atlantic salmon (Salmo salar) were fed with standard feed added one of five concentrations of either pure deoxynivalenol (DON; 0.5–6 mg/kg) or pure ochratoxin A (OTA; 0.2–2.4 mg/kg), or no added toxins for up to 8 weeks. Performance effects (feed intake, feed efficiency, gain, length and condition factor), various clinical biochemical parameters, packed cell volume and vaccination response against Aeromonas salmonicidae were all inversely correlated with DON dose, whereas relative liver weight increased with DON dose. In fish fed OTA, however, the effects at the doses tested were rather small. We observed no effects of OTA exposure on performance parameters, but some clinical biochemical parameters tended to increase with OTA dose primarily at 3 weeks, and compared with controls OTA exposure caused increased mRNA expression of two immune markers in the spleen. No liver histopathological effects were found from DON or OTA exposure. For DON, we derived a BMDL20 of 0.3 mg/kg feed for reduced total protein in plasma, a BMDL5 of 0.5 mg/kg feed for reduced condition factor, and a NOAEL of 1 mg/kg feed for DON. For OTA, a BMDL or NOAEL could not be derived (>2.4 mg/kg).publishedVersio

Art in Victoria : 1960-1986

The authors describe the arts in Victoria since 1945, focusing on the role of art galleries and art schools and on the work of individual artists. Includes 75 artists' statements and biographical notes

Genome-wide association study identifies 30 obsessive-compulsive disorder associated loci

Obsessive-compulsive disorder (OCD) affects ~1% of the population and exhibits a high SNP-heritability, yet previous genome-wide association studies (GWAS) have provided limited information on the genetic etiology and underlying biological mechanisms of the disorder. We conducted a GWAS meta-analysis combining 53,660 OCD cases and 2,044,417 controls from 28 European-ancestry cohorts revealing 30 independent genome-wide significant SNPs and a SNP-based heritability of 6.7%. Separate GWAS for clinical, biobank, comorbid, and self-report sub-groups found no evidence of sample ascertainment impacting our results. Functional and positional QTL gene-based approaches identified 249 significant candidate risk genes for OCD, of which 25 were identified as putatively causal, highlighting WDR6, DALRD3, CTNND1 and genes in the MHC region. Tissue and single-cell enrichment analyses highlighted hippocampal and cortical excitatory neurons, along with D1- and D2-type dopamine receptor-containing medium spiny neurons, as playing a role in OCD risk. OCD displayed significant genetic correlations with 65 out of 112 examined phenotypes. Notably, it showed positive genetic correlations with all included psychiatric phenotypes, in particular anxiety, depression, anorexia nervosa, and Tourette syndrome, and negative correlations with a subset of the included autoimmune disorders, educational attainment, and body mass index. This study marks a significant step toward unraveling its genetic landscape and advances understanding of OCD genetics, providing a foundation for future interventions to address this debilitating disorder