Biodensity is a major factor affecting the production and welfare of farmed fishes. Arctic charr (Salvelinus alpinus) (average mass 176.9?±?3.9?g) were held at biodensities of 30, 60, 90, 120, and 150?kg/m3 (4 replicates per treatment) during a 91?day study which examined key growth, stress physiology, and welfare parameters. During experimentation fish were fed to near satiety, and a random subsample of 20 fish (5 per replicate tank) were collected from each treatment every 21?days. Biodensity was found to have no significant effect on mortality rates or physical fin damage. Growth rates were lower in charr reared at the highest biodensities (120, and 150?kg/m3), while feed efficiency was negatively affected at both the highest (120, and 150?kg/m3) and lowest (30?kg/m3) biodensities. Plasma cortisol indicated that Arctic charr are more stressed at lower biodensities, but was not correlated with growth or feed efficiency measures. The results support an optimal biodensity range for charr culture between 60 and 90?kg/m3 to optimize production and welfare.
To identify the genetic defect in a Hutterite population from northern Alberta with Usher syndrome type I.
Complete ophthalmic examinations were conducted on two boys and two girls from two related Hutterite families diagnosed with Usher syndrome type I. DNA from patients and their parents was first evaluated for a mutation in exon 10 of the protocadherin-related 15 (PCDH15) gene (c.1471delG), previously reported in southern Alberta Hutterite patients with Usher syndrome (USH1F). Single nucleotide polymorphic linkage analysis was then used to confirm another locus, and DNA was analyzed with the Usher Chip v4.0 platform.
Severe hearing impairment, unintelligible speech, and retinitis pigmentosa with varying degrees of visual acuity and visual field loss established a clinical diagnosis of Usher syndrome type I. The patients did not carry the exon 10 mutation in the PCDH15 gene; however, with microarray analysis, a previously reported mutation (c.52C>T; p.Q18X) in the myosin VIIA (MYO7A) gene was found in the homozygous state in the affected siblings.
The finding of a MYO7A mutation in two related Hutterite families from northern Alberta provides evidence of genetic heterogeneity in Hutterites affected by Usher syndrome type I.
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