The toxicity of Castanospermum australe seeds for cattle

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.     

Radiation belts of jupiter

Predictions of Jupiter's electron and proton radiation belts are based mainly on decimeter observations of 1966 and 1968. Extensive calculations modeling radial diffusion of particles inward from the solar wind and electron synchrotron radiation are used to relate the predictions and observations.     

Melting of (Mg,Fe)2SiO4 at the Core-Mantle Boundary of the Earth

The lower mantle of the Earth is believed to be largely composed of (Mg,Fe)O (magnesiowustite) and (Mg,Fe)SiO3 (perovskite). Radiative temperatures of single-crystal olivine [(Mg0.9,Fe0.1)2SiO4] decreased abruptly from 7040 +/- 315 to 4300 +/- 270 kelvin upon shock compression above 80 gigapascals. The data indicate that an upper bound to the solidus of the magnesiowustite and perovskite assemblage at 4300 +/- 270 kelvin is 130 +/- 3 gigapascals. These conditions correspond to those for partial melting at the base of the mantle, as has been suggested occurs within the ultralow-velocity zone beneath the central Pacific.     

Progressive ataxia associated with degenerative thoracic myelopathy in Merino sheep

A neurological disorder in Merino sheep, characterised clinically by progressive posterior ataxia and microscopically by Wallerian degeneration in thoracic segments of the spinal cord, is described. Animals of both sexes were affected, with the earliest onset of disease being at 5 months of age. Most affected animals died before 2 years of age. The clinical, pathological and epidemiological features suggest that this degenerative thoracic myelopathy is a previously unrecognised entity differing from other reported causes of ataxia in sheep in Australia.     

Finding the mutation responsible for inherited rickets in Corriedale sheep

Inherited rickets of Corriedale sheep is of simple autosomal recessive inheritance. The gross and histological lesions include segmental thickening of physes, persistence of hypertrophic chondrocytes at sites of endochondral ossification, excessive osteoclastic resorption, microfractures and wide unmineralised osteoid seams lining trabeculae and filling secondary osteons. Initial testing revealed concentrations of 25-hydroxyvitamin D₃ were normal, but those of 1,25-dihydroxyvitamin D₃ were increased in serum of affected sheep, suggesting a defect in the vitamin D receptor. However, in vitro studies on cultured skin fibroblasts revealed normal binding and function of the vitamin D receptor.

A genome-wide association study was conducted using the Illumina OvineSNP50 BeadChip. A homozygous region of 199 consecutive single-nucleotide polymorphism loci was identified in affected sheep, covering a region of 10 megabase pairs on ovine chromosome 6. Of the 91 candidate genes in this region, dentin matrix protein 1 gene (dmp1) was considered the most likely as it is known to play critical roles in osteocyte maturation and mineral metabolism. Sequencing of DNA from carriers showed a nonsense mutation 253T/C in dmp1. This T/C transition introduced a stop codon (R145X) that could truncate C-terminal amino acids. Using PCR restriction fragment length polymorphism for this mutation, genotyping showed that all affected sheep were “TT” genotypes, and phenotypically normal sheep were either “CT” or “CC”. These findings suggest that a mutation in dmp1 is responsible for inherited rickets of Corriedale sheep. A simple diagnostic test is currently being designed to identify carriers with the defective “T” alleles.     

Extreme neutrophilic leucocytosis and intrathoracic mass in a Fox Terrier

Extract

An 8-year-old female Fox Terrier was presented for acute anorexia and depression. A haemogram revealed extreme neutrophilic leucocytosis (136×10⁹/L neutrophils). By Day 4, the neutrophilia was more marked (214×10⁹/L segmented; 23×10⁹/L band). Imaging revealed a cranial mediastinal mass, pleural effusion and small pneumothorax. Needle aspiration of the mass showed cells resembling malignant histiocytes against a background of mature neutrophils. On Day 7, the mass was surgically removed. Histologically, it revealed a malignancy suggestive of histiocytic sarcoma intensely infiltrated with neutrophils. Immunocyto-chemical investigations are pending. Post-operatively, the dog's appetite and demeanour improved but breathing was laboured, and neutrophilia persisted (300×10⁹/L on Day 14). The dog was humanely killed on Day 14; post mortem examination revealed no distant metastases. This dog's illness is strongly reminiscent of a rare human condition, inflammatory malignant fibrous his-tiocytoma with leukaemoid reaction (IMFH-LR). In IMFH-LR, neoplastic cells produce cytokines that attract neutrophils to the tumour. Other cytokines stimulate the bone marrow to produce extreme neutrophilia. Although paraneoplastic neutrophilia has previously been described in dogs, this is an extreme example and the condition has not previously been associated with histiocytic or intrathoracic malignancies.     

Inherited chondrodysplasia in Texel sheep

CASE HISTORY: A skeletal disease characterised by dwarfism, limb deformity and sometimes sudden death occurred over a period of 5 years in lambs born on a commercial sheep farm in Southland. The disease showed variable expression and occurred in crossbred sheep. A genetic aetiology was supported by the birth of affected lambs over two seasons in a flock of putative carrier and affected sheep transported to Massey University.

CLINICAL FINDINGS: Affected lambs appeared normal at birth but showed evidence of dwarfism, wide-based stance and exercise intolerance as early as 1 week of age. Most died within the first 3 months of life, often after developing bilateral varus deformity of the forelimbs. Some severely-affected lambs died suddenly of respiratory embarrassment, probably due to tracheal collapse. Mildly-affected individuals had a short, blocky stature and some survived to breeding age.

PATHOLOGICAL FINDINGS: Gross and microscopic lesions of variable severity were present in the tracheal, articular, epiphyseal and physeal cartilages. In severe cases, articular cartilage in major joints was eroded from weight-bearing surfaces. The trachea was flaccid, abnormally kinked, and had thickened cartilaginous rings and a narrow lumen. Affected sheep that survived to breeding age eventually developed severe degenerative joint disease. Histologically, chondrocytes were disorganised, surrounded by concentric rings of abnormal fibrillar material, and the matrix often contained focal to coalescing areas of chondrolysis.

DIAGNOSIS: Inherited chondrodysplasia of Texel sheep.

CLINICAL RELEVANCE AND CONCLUSIONS: This chondrodysplasia differs from those previously described in sheep and is considered to be a newly-recognised, recessively-inherited genetic disease of the Texel breed. A defect in the synthesis of glycosaminoglycans in cartilage matrix is suspected. This disease of sheep may provide a suitable model for studying various forms of therapy for human chondrodysplasias.