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Post-mortem examination of 74 racing greyhounds with sudden, unexpected death was undertaken at the Veterinary School, University of Nottingham, UK, from 2015 to 2019. These investigations revealed severe, acute haemoabdomen with extensive retroperitoneal haemorrhage and an underlying severe, unilateral iliopsoas tear in four cases (5.4%). In all four cases, unilateral trauma and haemorrhage affecting the right iliopsoas muscle was common near the caudal insertion. Despite the acute clinical event, three cases demonstrated histological evidence of previous muscle damage with muscular regeneration, fibrosis and evidence of chronic haemorrhage. To our knowledge, this is the first detailed description of exercise-induced trauma to the iliopsoas muscle leading to extensive haemoretroperitoneum and haemoabdomen with subsequent hypovolaemic shock and death in racing greyhounds. Acute haemoretroperitoneum and haemoabdomen secondary to unilateral iliopsoas trauma and haemorrhage was identified in four racing greyhounds with sudden death immediately after racing (exercise-associated death). Image 1 [ABSTRACT FROM AUTHOR]

Canine urothelial carcinoma (UC) is the most common type of cancer of the lower urinary tract and tends to affect elderly neutered female dogs, with a high predisposition for Scottish terriers. Tumour stroma, inflammation and necrosis are poorly characterized in canine UC and their role as prognostic factors is unknown. The aims of this study were to (1) assess histologically 381 canine UCs, with emphasis on myxoid tumour stroma, inflammation and necrosis and (2) assess possible associations between these features and the available epidemiological data as well as bladder wall muscle invasion. In 103 of 381 (27%) cases, the stroma was mixed collagenous and myxoid (fibromyxoid), which was strongly associated with invasive growth of muscle (P <0.0001). Peritumoural and intratumoural inflammation was present in 308 of 345 (89%) and 287 of 381 (75%) cases, respectively, and was mostly mild and lymphoplasmacytic. One hundred and fifteen of the 381 (30%) cases showed a variable eosinophilic inflammation and 58 of 381 (15%) presented with formations of one or several lymphoid follicles. Twenty-four percent (91 of 381) of cases had tumour necrosis, which was typically mild. In 83 of 91 (91%) cases, the necrosis was comedo-like. Moderate to severe tumour necrosis was associated with the presence of moderate to predominant fibromyxoid tumour stroma (P <0.02). The results of this study indicate that fibromyxoid stroma is common in canine UC and is a strong indicator for invasive growth of muscle, which is consistent with a poor prognosis. Based on histomorphology, tumour necrosis in canine UC is best described as comedonecrosis. [ABSTRACT FROM AUTHOR]

Summary A 9-year-old neutered male crossbred dog with a 4-week history of progressive vestibulocerebellar signs was presented for necropsy examination. Gross examination revealed neoplastic growth in the lungs, thoracic lymph nodes, left kidney and cerebellum. Microscopically, the tumour consisted of an infiltrative, densely cellular, basaloid epithelial neoplastic growth with extensive areas of abrupt keratinization. Immunohistochemically, neoplastic cells expressed p63 and partially expressed cytokeratins 5/6. Based on these findings, the tumour was diagnosed as a primary pulmonary basaloid squamous cell carcinoma (BSSC) with metastasis to regional lymph nodes, kidney and brain. As far as the authors are aware, this is the first description of BSCC in an animal species. [ABSTRACT FROM AUTHOR]

Summary Feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) is a recently described inflammatory condition of domestic cats with unknown aetiology. A proportion of cases of FGESF are associated with bacteria, but antibiotic treatment is ineffective. It has been hypothesized that genetically predisposed cats may develop FGESF in response to the introduction of bacteria or other antigens into the intestinal wall. A 9-month-old male Persian cat presented with a history of marked acute haematemesis. A mass (10 cm diameter) was detected within the pylorus and proximal duodenum and this was not surgically accessible. On necropsy examination the duodenal wall was seen to be markedly thickened with extensive mucosal ulceration. Microscopically, there were haphazardly oriented trabecular bands of dense eosinophilic collagen, separated by wide, clear areas containing variable numbers of fibroblasts, eosinophils, mast cells, neutrophils, macrophages, lymphocytes and plasma cells. Numerous pleomorphic, non-parallel walled, sparsely septate hyphae, characteristic of phycomycetes, were present within the collagen matrix. Colonies of gram-positive and gram-negative rods were also present within the lesion. This is the first description of FGESF with intralesional fungi. [ABSTRACT FROM AUTHOR]

Summary: Necrotizing lymphadenitis is observed in approximately 2% of pigs affected by post-weaning multisystemic wasting syndrome (PMWS). The pathogenesis of the lesion has been linked to apoptosis induced by porcine circovirus type 2 (PCV2). The aim of the present study was to gain further insights into PCV2-associated lymphoid necrosis in pigs with PMWS. Three groups of animals were studied: (1) PMWS-affected pigs with necrotizing lymphadenitis (n =5), (2) PMWS-affected pigs without necrotizing lymphadenitis (n =5) and (3) healthy pigs with no PMWS-related lesions (n =5). Investigations performed included immunohistochemical evaluation of the expression of cleaved caspase-3 and von Willebrand factor, Mallory’s staining for fibrin and in-situ hybridization for detection of the PCV2 genome. The results of the study suggested that lymphoid necrosis in PMWS-affected pigs may be related to hypertrophy and hyperplasia of high endothelial venules (HEVs). The mechanism underlying these changes in HEVs was not clearly defined, but necrotizing lymphadenitis in pigs with PMWS may develop following vascular damage with thrombosis and subsequent follicular necrosis. Apoptosis was not found to be involved in lymphocyte depletion in PMWS or in PMWS-associated necrotizing lymphadenitis. [ABSTRACT FROM AUTHOR]

Rationnel: Les espèces réactives de l’oxygène (ROS) et le NADPH exercent des effets opposés sur l’état d’oxydation des thiols, un facteur probable de couplage métabolique peu étudié dans les cellules bêta-pancréatiques. Nous avons utilisé la sonde fluorescente ratiométrique roGFP2 fusionnée avec la glutaredoxine pour mesurer les effets aigus des nutriments sur l’oxydation du glutathion cytosolique (GRX1-roGFP2) et mitochondrial (mt-GRX1-roGFP2) dans les cellules bêta. Matériels et méthodes: Un jour après infection adénovirale, le ratio de fluorescence de la sonde a été mesuré dans des amas de>10 cellules d’îlots de rat périfusés avec une solution de Krebs contenant divers nutriments et substances tests. Les ratios de fluorescence (moyenne±SE pour 8–11 amas de 3 préparations) sont exprimés en pourcentage de la différence des ratios mesurés en fin d’expérience en présence de 10 mm dithiothréitol (0 %) puis 1 mm H2O2 (100 %). Statistiques : ANOVA à une voie + test de Newman-Keuls. Résultats: Le ratio de fluorescence de GRX1-roGFP2 était très faible (<5 % de la différence dithiothréitol-H2O2) et insensible au glucose entre 0 et 30mm (G0–G30). En comparaison, le ratio de fluorescence de mt-GRX1-roGFP2 était plus élevé et significativement diminué de façon réversible par le glucose : 39±0,5 % en absence de glucose, 36±0,7 % en G2, 27±0,6 % en G5, 21±0,1 % en G10 et 15±0,1 % en G30. Ce ratio diminuait aussi après ajout à G5 de substrats mitochondriaux insulinosécrétagogues, mais n’était pas affecté par des variations importantes de pH ou d’influx calcique (G10+diazoxide, G5+tolbutamide) ; il était rapidement diminué par la roténone, et augmenté par le FCCP. Conclusion: La stimulation de cellules d’îlots de rat par les nutriments réduit rapidement l’état d’oxydation des thiols (e.a. le glutathion) dans la matrice mitochondriale, mais n’a pas d’effet détectable dans le cytosol. Ceci pourrait contribuer au couplage stimulation-sécrétion dans les cellules bêta-pancréatiques et, à plus long terme, aux modifications de leur masse fonctionnelle. [ABSTRACT FROM AUTHOR]

Introduction: La survie d’îlots de rat en culture est optimale en présence de 10mM de glucose, alors que la culture prolongée en présence de 5 ou 30mM de glucose entraîne une augmentation de l’apoptose des cellules selon un profil en V asymétrique. Cet effet est précédé de changements parallèles de l’expression de l’ARNm de gènes de réponse au stress oxydatif comme la métallothionéine 1a (Mt1a). Dans cette étude, nous avons testé l’effet du ZnCl2, un inducteur connu des métallothionéines, sur la stimulation de l’apoptose des cellules par les concentrations extrêmes de glucose. Matériels et méthodes: Des îlots de rat Wistar mâles ont été cultivés de 18 h à 1 semaine dans du milieu RPMI contenant 5, 10 ou 30mM de glucose (G5, G10, G30) +/- 100μm ZnCl2. L’expression des ARNm a été mesurée par RT-qPCR. L’apoptose a été quantifiée par ELISA en mesurant les fragments d’ADN cytosoliques et par TUNEL. Comme marqueur du stress oxydatif, l’équilibre « thiols/disulfides » mitochondrial a été mesuré à l’aide de la sonde « redox sensitive GFP1 » dans des clusters de cellules d’îlots de rat cultivés 18–24h en présence de G5, G10 ou G30 +/- 50μm ZnCl2. Résultats: L’ajout de ZnCl2 au milieu stimule fortement l’expression de Mt1a et réduit significativement de &tilde;50% l’apoptose mesurée après 3 jours ou 1 semaine de culture en présence de G5 et de &tilde;75% l’apoptose induite par 1 semaine de culture en présence de G30. Le ZnCl2 protège également du stress oxydatif mitochondrial induit par 18–24h de culture en présence de concentrations extrêmes de glucose (réduction de 40% en G5 et de 27% en G30). Conclusion: Le ZnCl2 (100μm) protège les cellules de l’apoptose et du stress oxydatif mitochondrial induits par la culture en présence de concentrations extrêmes de glucose. [Copyright &y& Elsevier]