Impact injuries and probability of survival in a large semiurban endemic pigeon in New Zealand, Hemiphaga novaeseelandiae.

The New Zealand Pigeon or kereru (Hemiphaga novaeseelandiae) frequently collides with windows and vehicles. In this study of 146 kereru collected from 1996 to 2009, we used 118 radiographs and 91 necropsies to determine skeletal and soft tissue injuries. Vehicle collisions resulted in more damage to the extremities (wing and femur), whereas collisions with windows resulted in trauma to the head, fractures/dislocations of the coracoids and clavicles, and ruptured internal organs.

The parathyroid hormone-responsive B1 gene is interrupted by a t(1;7)(q42;p15) breakpoint associated with Wilms' tumour.

Wilms' tumour (WT) has a diverse and complex molecular aetiology, with several different loci identified by cytogenetic and molecular analyses. One such locus is on chromosome 7p, where cytogenetic abnormalities and loss of heterozygosity (LOH) indicate the presence of a Wilms' tumour suppressor gene. In order to isolate a candidate gene for this locus, we have characterized the breakpoint regions at a novel constitutional chromosome translocation (t(1;7)(q42;p15)), found in a child with WT and skeletal abnormalities.

Loss of heterozygosity at 7p in Wilms' tumour development.

Chromosome 7p alterations have been implicated in the development of Wilms' tumour (WT) by previous studies of tumour cytogenetics, and by our analysis of a constitutional translocation (t(1;7)(q42;p15)) in a child with WT and radial aplasia. We therefore used polymorphic microsatellite markers on 7p for a loss of heterozygosity (LOH) study, and found LOH in seven out of 77 informative WTs (9%). The common region of LOH was 7p15-7p22, which contains the region disrupted by the t(1;7) breakpoint.

Transactivation of the WT1 antisense promoter is unique to the WT1[+/-] isoform.

The Wilms' tumour suppressor gene, WT1, encodes a zinc finger transcription factor that has been shown to repress a variety of cellular promoters via binding to cognate DNA elements. Our earlier work identified an antisense WT1 promoter that contains WT1 consensus sites, but is transcriptionally activated by WT1. In this study, we demonstrate that, unlike previous reports of transcriptional regulation by WT1, transactivation of the antisense promoter is unique to a single isoform of WT1.

Localization of a novel t(1;7) translocation associated with Wilms' tumor predisposition and skeletal abnormalities.

Cytogenetic analysis of predisposition syndromes has played a critical role in the elucidation of the genetics of Wilms' tumor (WT). Therefore, we became interested in a patient who presented with a WT and a nephrogenic rest in the contralateral kidney (suggestive of a predisposition) and a de novo t(1;7)(q42;p15) constitutional translocation as the only visible cytogenetic abnormality. He also had bilateral radial aplasia and other skeletal abnormalities, but there was no manifestation of any syndrome previously associated with WT.