1. A field study was conducted to investigate the deterioration of eggshell quality at the end of lay and examine the potential to extend the production cycle. A total of 1200 eggs were assessed originating from commercial farms in Belgium: eggs were random sampled at the collection belt at 57-65 weeks of age and at the end of the production cycle (74-92 weeks). 2. Based on a linear mixed model, egg quality was estimated for an average flock at 60 weeks of age and changes in quality traits were predicted until the end of the laying cycle. 3. Egg weight increased by 0.07 g every week from 60 weeks of age onwards and shape index decreased by 0.04 unit weekly (P < 0.001). Haugh unit values decreased weekly by 0.38 units whereas relative yolk weight was unaffected after 60 weeks of age. Relative albumen weight showed a weekly increase of 0.02% and relative shell decreased by 0.02% weekly until the end of lay. 4. Shell quality traits were also influenced by age: shell index decreased by 0.013 g weekly, shell thickness was calculated to be 0.23 µm thinner every week, deformation increased by 0.06 µm weekly from 60 weeks to the end of the laying cycle. Variability of the deformation of eggs indicated more heterogeneous shell quality at the end of the production cycle. Dynamic stiffness increased from 60 weeks of age on. 5. Laying hens were depopulated on average at 80 weeks of age (varying from 74-92 weeks). Although ageing had a significant effect on most of the egg quality traits, egg quality was still acceptable at the end of lay, indicating the potential to extend the laying cycle.
Fabry's disease is an X-linked lysosomal storage disorder. alpha-Galactosidase deficiency leads to accumulation of globotriaosylceramide mainly in endothelial and smooth muscle cells. Cerebrovascular symptoms with predominant affection of the vertebrobasilar circulation are one of the major sources of morbidity in Fabry's disease. We present a Hungarian family with Fabry's disease caused by a new mutation in the alpha-galactosidase A gene (GLA), and describe a variant expression of the disease. Megadolichobasilar anomaly was diagnosed in two male patients in the family who died of thrombosis. In another female patient who had suffered from disturbance of the vertebrobasilar circulation, a strongly dilated basilar artery without thrombosis was found at autopsy. Another three family members had basilar strokes and large and elongated basilar arteries on MRI. Genetic analysis disclosed a c.47T-->C missense mutation resulting in L16P in the amino acid sequence of the alpha-galactosidase protein. This report suggests that megadolichobasilar anomaly is potentially life-threatening, and that L16P is a disease-causing mutation in patients with Fabry's disease. Early enzyme replacement therapy may prevent the development of these irreversible cerebrovascular complications.
This article explores how theories of radicalisation have placed an emphasis on the development of an indicators-based approach to identify individuals who might engage in politically motivated violence. We trace how policing agencies have juxtaposed the search for indicators as a defence against criticisms of racial profiling. However, through an analysis of Canadian counter-terrorism training programmes, we demonstrate that the search for radicalisation indicators reaffirms pre-emptive and discriminatory security practices. We insist that despite efforts to theorise radicalisation outside of the practices of the "war on terror", current trends risk rationalising prejudicial policing that affirms social exclusion and injustice.
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