BackgroundDiagnostic imaging is essential to assess the lame patient; lesions of the elbow joint have traditionally been evaluated radiographically, however computed tomography (CT) has been suggested as a useful technique to diagnose various elbow pathologies. The primary objective of this study was to determine the sensitivity and specificity of CT to assess medial coronoid disease (MCD), using arthroscopy as gold standard. The secondary objective was to ascertain the radiographic sensitivity and specificity for MCD compared with CT.MethodsFor this study 180 elbow joints were assessed, of which 141 had been examined with radiography, CT and arthroscopy; and 39 joints, had radiographic and CT assessment. Sensitivity and specificity were calculated for CT and radiographic findings using available statistical software.ResultsSensitivity and specificity of CT using arthroscopy as gold standard resulted in high values for sensitivity (100 %) and specificity (93 %) for the assessment of MCD. For the radiographic evaluation, a sensitivity of 98 % and specificity of 64 - 69 % using CT as the technique of reference, were found.DiscussionThese results suggest that in case of doubt during radiographic assessment, CT could be used as a non-invasive technique to assess the presence of MCD.ConclusionBased on the high sensitivity and specificity obtained in this study it has been considered that CT, rather than arthroscopy, is the preferred noninvasive technique to assess MCD lesions of the canine elbow joint.

Host-parasite co-evolution history is lacking when parasites switch to novel hosts. This was the case for Western honey bees ( Apis mellifera ) when the ectoparasitic mite, Varroa destructor , switched hosts from Eastern honey bees ( Apis cerana ). This mite has since become the most severe biological threat to A. mellifera worldwide. However, some A. mellifera populations are known to survive infestations, largely by suppressing mite population growth. One known mechanism is suppressed mite reproduction (SMR), but the underlying genetics are poorly understood. Here, we take advantage of haploid drones, originating from one queen from the Netherlands that developed Varroa -resistance, whole exome sequencing and elastic-net regression to identify genetic variants associated with SMR in resistant honeybees. An eight variants model predicted 88% of the phenotypes correctly and identified six risk and two protective variants. Reproducing and non-reproducing mites could not be distinguished using DNA microsatellites, which is in agreement with the hypothesis that it is not the parasite but the host that adapted itself. Our results suggest that the brood pheromone-dependent mite oogenesis is disrupted in resistant hosts. The identified genetic markers have a considerable potential to contribute to a sustainable global apiculture.

No abstract

Background: The intranasal (IN) route for rapid drug administration in patients with brain disorders, including status epilepticus, has been investigated. Status epilepticus is an emergency, and the IN route offers a valuable alternative to other routes, especially when these fail.Objectives: To compare IN versus IV midazolam (MDZ) at the same dosage (0.2 mg/kg) for controlling status epilepticus in dogs.Abbreviations: BBB, blood-brain barrier; IN, intranasal; MAD, mucosal atomization device; MDZ, midazolam.

By limiting sequencing to those sequences transcribed as mRNA, whole exome sequencing is a cost-efficient technique often used in disease-association studies. We developed two target enrichment designs based on the recently released annotation of the canine genome: the exome-plus design and the exome-CDS design. The exome-plus design combines the exons of the CanFam 3.1 Ensembl annotation, more recently discovered protein-coding exons and a variety of non-coding RNA regions (microRNAs, long non-coding RNAs and antisense transcripts), leading to a total size of ≈152 Mb. The exome-CDS was designed as a subset of the exome-plus by omitting all 3’ and 5’ untranslated regions. This reduced the size of the exome-CDS to ≈71 Mb. To test the capturing performance, four exome-plus captures were sequenced on a NextSeq 500 with each capture containing four pre-capture pooled, barcoded samples. At an average sequencing depth of 68.3x, 80% of the regions and well over 90% of the targeted base pairs were completely covered at least 5 times with high reproducibility. Based on the performance of the exome-plus, we estimated the performance of the exome-CDS. Overall, these designs provide flexible solutions for a variety of research questions and are likely to be reliable tools in disease studies.

Whole exome sequencing is a technique that aims to selectively sequence all exons of protein-coding genes. A canine whole exome sequencing enrichment kit was designed based on the latest canine reference genome (build 3.1.72). Its performance was tested by sequencing 2 exome captures, each consisting of 4 pre-capture pooled, barcoded Illumina libraries on an Illumina HiSeq 2500. At an average sequencing depth of 102x, 83 to 86% of the target regions were completely sequenced with a minimum coverage of five and 90% of the reads mapped on the target regions. Additionally, it is shown that the reproducibility within and between captures is high and that pooling four samples per capture is a valid option. Overall, we have demonstrated the strong performance of this WES enrichment kit and are confident it will be a valuable tool in future disease association studies.

(1) Feline dystrophin-deficient muscular dystrophy (ddMD) is a fatal disease characterized by progressive weakness and degeneration of skeletal muscles and is caused by variants in the DMD gene. To date, only two feline causal variants have been identified. This study reports two cases of male Maine coon siblings that presented with muscular hypertrophy, growth retardation, weight loss, and vomiting. (2) Both cats were clinically examined and histopathology and immunofluorescent staining of the affected muscle was performed. DMD mRNA was sequenced to identify putative causal variants. (3) Both cats showed a significant increase in serum creatine kinase activity. Electromyography and histopathological examination of the muscle samples revealed abnormalities consistent with a dystrophic phenotype. Immunohistochemical testing revealed the absence of dystrophin, confirming the diagnosis of dystrophin-deficient muscular dystrophy. mRNA sequencing revealed a nonsense variant in exon 11 of the feline DMD gene, NC_058386.1 (XM_045050794.1): c.1180C>T (p.(Arg394*)), which results in the loss of the majority of the dystrophin protein. Perfect X-linked segregation of the variant was established in the pedigree. (4) ddMD was described for the first time in the Maine coon and the c.1180C>T variant was confirmed as the causal variant.

Please follow the link below to see and read the publisher's version for free (downloading and printing is not possible): https://rdcu.be/bFA7F. A feline orthologue of the human MYH7 c.5647G>A (p.(Glu1883Lys)) variant causes hypertrophic cardiomyopathy in a Domestic Shorthair cat The MYH7 c.5647G>A variant causes feline HCM