Moxidectin as an Endectocide in Reindeer

During the winter 1991–92, 42 reindeer hinds of the Kaamanen Experimental Reindeer Herd in Finnish Lapland, naturally infected with various parasites, were allocated to 3 groups. One group was an untreated control group and the other 2 groups received either moxidectin or ivermectin at a dose of 200 µg kg−1 subcutaneously. The efficacy of treatment was followed with monthly faecal examinations for nematode eggs and counting of warbles, Hypoderma tarandi larvae, and throat bots, Cephenemyia trompe larvae, from live animals in spring. The efficacy of moxidectin against warbles (92.8%) and throat bots (70.8%) did not match that of ivermectin, which was 100% against both species. Both moxidectin and ivermectin were effective against gastrointestinal trichostrongylid egg production over the December to May trial period indicating good efficacy against adult and inhibited trichostrongylids. Only non-significant differences were seen in weight development and calf birth weights between the groups. Because of its only moderate insecticidal efficacy, moxidectin cannot be recommended as an endectocide in reindeer.     

Visual Features Underlying Perceived Brightness as Revealed by Classification Images

Along with physical luminance, the perceived brightness is known to depend on the spatial structure of the stimulus. Often it is assumed that neural computation of the brightness is based on the analysis of luminance borders of the stimulus. However, this has not been tested directly. We introduce a new variant of the psychophysical reverse-correlation or classification image method to estimate and localize the physical features of the stimuli which correlate with the perceived brightness, using a brightness-matching task. We derive classification images for the illusory Craik-O''Brien-Cornsweet stimulus and a “real” uniform step stimulus. For both stimuli, classification images reveal a positive peak at the stimulus border, along with a negative peak at the background, but are flat at the center of the stimulus, suggesting that brightness is determined solely by the border information. Features in the perceptually completed area in the Craik-O''Brien-Cornsweet do not contribute to its brightness, nor could we see low-frequency boosting, which has been offered as an explanation for the illusion. Tuning of the classification image profiles changes remarkably little with stimulus size. This supports the idea that only certain spatial scales are used for computing the brightness of a surface.     

Identification of a common risk haplotype for canine idiopathic epilepsy in the ADAM23 gene

Background

Idiopathic epilepsy is a common neurological disease in human and domestic dogs but relatively few risk genes have been identified to date. The seizure characteristics, including focal and generalised seizures, are similar between the two species, with gene discovery facilitated by the reduced genetic heterogeneity of purebred dogs. We have recently identified a risk locus for idiopathic epilepsy in the Belgian Shepherd breed on a 4.4 megabase region on CFA37.

Results

We have expanded a previous study replicating the association with a combined analysis of 157 cases and 179 controls in three additional breeds: Schipperke, Finnish Spitz and Beagle (p_c = 2.9e–07, p_GWAS = 1.74E-02). A targeted resequencing of the 4.4 megabase region in twelve Belgian Shepherd cases and twelve controls with opposite haplotypes identified 37 case-specific variants within the ADAM23 gene. Twenty-seven variants were validated in 285 cases and 355 controls from four breeds, resulting in a strong replication of the ADAM23 locus (p_raw = 2.76e–15) and the identification of a common 28 kb-risk haplotype in all four breeds. Risk haplotype was present in frequencies of 0.49–0.7 in the breeds, suggesting that ADAM23 is a low penetrance risk gene for canine epilepsy.

Conclusions

These results implicate ADAM23 in common canine idiopathic epilepsy, although the causative variant remains yet to be identified. ADAM23 plays a role in synaptic transmission and interacts with known epilepsy genes, LGI1 and LGI2, and should be considered as a candidate gene for human epilepsies.

Electronic supplementary material

The online version of this article (doi:10.1186/s12864-015-1651-9) contains supplementary material, which is available to authorized users.     

Impaired 3H-testosterone uptake and metabolism in the accessory sex glands of diabetic castrated male rats.

The uptake and retention of 1,2-3H-testosterone in accessory sex glands, muscle and liver of streptozotocin diabetic castrated male rats, insulin-treated diabetic castrated rats and non-diabetic castrated control rats were studied at various time intervals after an intravenous injection. Diabetes reduced the retention of 3H-testosterone in the prostate, the preputial gland and the epididymis. Exogenous insulin slightly increased the retention of 3H-testosterone in these tissues of diabetic rats. No significant differences in the radioactivity in the rectus abdominis muscle, the coagulating glands and the seminal vesicles were found between the various experimental groups. Ventral prostate homogenates obtained from diabetic and control rats were incubated with 3H-testosterone in vitro. The steroids were extracted and thin-layer chromatographs were scanned for radioactivity. In prostatic homogenates taken from diabetic rats, testosterone transformation to dihydrotestosterone was reduced. The results indicate that the impaired function and androgen retention of the accessory sex glands of diabetic male rats is at least partly due to the reduced formation of dihydrotestosterone from testosterone.     

Testicular lesions of streptozotocin diabetic rats.

Diabetes was induced in adult male albino rats by a single intravenous injection of streptozotocin (75 mg/kg body weight). The diabetes was allowed to stabilize for at least 15 days, whereafter the testicular and seminal vesicle histology was studied at various time intervals. Reduction in testis weights and tubule diameters was significant after 2 weeks of diabetes. The changes in seminiferous tubules ranged from premature sloughing of epithelium to total cessation of spermatogenesis. The testicular histology of diabetic animals frequently greatly simulated the situation described following hypophysectomy. By subjective visual assessment the number of Leydig cells was found to be normal or reduced in all of the diabetic animals. Diabetes was also demonstrated to induce seminal vesicle atrophy, which did not show any correlation with the degree of testicular lesions. The possible etiology of testicular damage in diabetic animals is discussed.