Prophylactic use of a lyophilized platelet product for rhinoscopic diagnosis and treatment of sinonasal aspergillosis in a dog with a P2Y12 platelet receptor mutation.

OBJECTIVE: To describe the periprocedural use of a lyophilized platelet product during rhinoscopic diagnosis and treatment of sinonasal aspergillosis in a Greater Swiss Mountain Dog with a P2Y12 platelet receptor disorder. CASE SUMMARY: After the development of severe epistaxis, a Greater Swiss Mountain Dog was diagnosed with thrombopathia secondary to a P2Y12 receptor gene mutation. Concurrent primary nasal disease was also suspected due to persistent mucopurulent nasal discharge. One month after the initial presentation for epistaxis, the dog was readmitted for workup of nasal disease. Computed tomography of the head showed turbinate lysis and regional lymphadenopathy. Because of concern for a high risk of bleeding in a thrombopathic patient subjected to rhinoscopy and nasal biopsies, a lyophilized platelet product was administered prior to the procedure. Rhinoscopic exam revealed fungal plaques consistent with Aspergillus spp. that were later confirmed on fungal culture to be Aspergillus fumigatus. Rhinoscopic biopsies were performed as well as debridement of the fungal plaques, followed by topical administration of clotrimazole solution. Bleeding was minimal during and after the procedure, and the dog recovered uneventfully. NEW OR UNIQUE INFORMATION PROVIDED: This is the first report of the prophylactic use of lyophilized platelets in a thrombopathic patient undergoing an invasive procedure with potential for significant hemorrhage. Minimal bleeding occurred during the procedure, suggesting that lyophilized platelets could be used for the prevention of bleeding in thrombopathic patients undergoing invasive procedures.

An initial genome-wide investigation of protein-losing enteropathy in Gordon setters: Exploratory observations.

The objective of this preliminary study was to identify genomic regions that may predispose Gordon setters from the United Kingdom to familial protein-losing enteropathy (PLE) at a young age. A total of 106 related Gordon setters was used, including 6 affected dogs from an affected litter, 6 case controls from the same litter, 10 related/affected dogs, and 84 related/unaffected dogs. Genomic DNA was collected from each Gordon setter and extracted from buccal mucosal swabs. Genotyping of affected and unaffected dogs was carried out using the Canine Illumina HD SNP array and data generated were analyzed with PLINK software, using fixation index (Fst) and runs of homozygosity (ROH) methods. Pairwise Fst analyses between the affected and unaffected Gordon setter dogs identified various regions of differentiation on chromosomes 10, 18, 21, and 23 that contained several important genes. These regions revealed 5 candidate genes, including RARB, TTC7A, SOCS5, PIGF, and RHOD, that are associated with human inflammatory bowel disease (IBD) and could potentially be associated with PLE in Gordon setters. Run of homozygosity (ROH) analyses revealed additional unique regions on chromosomes 15 and 17. These regions contained genes SYT1, UCN, and FNDC that could also be potential candidates for PLE in Gordon setters. The biological functions of the identified genes provided initial insights into the pathophysiology of PLE. Further large-scale studies are warranted to investigate the possible causality of these genomic regions and any possible genetic markers that could be used in predicting susceptibility to PLE syndrome.

L'objectif de cette étude préliminaire était d'identifier les régions génomiques susceptibles de prédisposer les chiens Gordon setter du Royaume-Uni à l'entéropathie familiale de perte de protéines (PLE) à un jeune âge. Un total de 106 Gordon setter apparentés a été utilisé, dont six chiens affectés d'une portée affectée, six cas témoins de la même portée, 10 chiens apparentés/affectés et 84 chiens apparentés/non affectés. L'ADN génomique a été obtenu à partir de chaque Gordon setter et extrait des écouvillons de la muqueuse buccale. Le génotypage des chiens affectés et non affectés a été effectué à l'aide de la matrice SNP Canine Illumina HD et les données générées ont été analysées avec le logiciel PLINK, en utilisant des méthodes d'indice de fixation (Fst) et d'homozygotie (ROH). Des analyses Fst par paires entre les chiens Gordon setter affectés et non affectés ont identifié diverses régions de différenciation sur les chromosomes 10, 18, 21 et 23 qui contenaient plusieurs gènes importants. Ces régions ont révélé cinq gènes candidats, dont RARB, TTC7A, SOCS5, PIGF et RHOD, qui sont associés à la maladie inflammatoire de l'intestin (IBD) humaine et pourraient potentiellement être associés à la PLE chez les Gordon setter. Les analyses d'homozygotie (ROH) ont révélé des régions uniques supplémentaires sur les chromosomes 15 et 17. Ces régions contenaient les gènes SYT1, UCN et FNDC qui pourraient également être des candidats potentiels pour la PLE chez les Gordon setter. Les fonctions biologiques des gènes identifiés ont fourni un aperçu initial de la physiopathologie de la PLE. D'autres études à grande échelle sont nécessaires pour étudier la causalité possible de ces régions génomiques et tous les marqueurs génétiques possibles qui pourraient être utilisés pour prédire la sensibilité au syndrome PLE.(Traduit par Docteur Serge Messier).

Adipose-Derived Stromal Vascular Fraction and Cultured Stromal Cells as Trophic Mediators for Tendon Healing.

Adipose-derived stromal vascular fraction (SVF) is a heterogeneous population of cells that yields a homogeneous population of plastic-adherent adipose tissue-derived stromal cells (ASC) when culture-expanded. SVF and ASC have been used clinically to improve tendon healing, yet their mechanism of action is not fully elucidated. The objective of this study was to investigate the potential for ASC to act as trophic mediators for tendon healing. Flexor digitorum superficialis tendons and adipose tissue were harvested from adult horses to obtain SVF, ASC, and tenocytes. Growth factor gene expression was quantified in SVF and ASC in serial passages and growth factors were quantified in ASC-conditioned medium (CM). Microchemotaxis assays were performed using ASC-CM. Tenocytes were grown in co-culture with autologous ASC or allogeneic SVF. Gene expression for insulin-like growth factor 1 (IGF-1), stromal cell-derived factor-1α (SDF-1α), transforming growth factor-ß1 (TGF-ß1) and TGF-ß3 was significantly higher in SVF compared to ASC. Concentrations were significantly increased in ASC-CM compared to controls for IGF-1 (4-fold) and SDF-1α (6-fold). Medium conditioned by ASC induced significant cell migration in a dose-dependent manner. Gene expression for collagen types I and III, decorin, and cartilage oligomeric matrix protein was modestly, but significantly increased following co-culture of tenocytes with autologous ASC. Our findings support the ability of SVF and ASC to act as trophic mediators in tendon healing, particularly through chemotaxis, which stands to critically impact the intrinsic healing response. In vivo studies to further delineate the potential for SVF and/or ASC to improve tendon healing are warranted. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:1429-1439, 2019.