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Abstract A 14-year-old spayed female Miniature Pinscher presented with tongue curling, dysphagia, hypersalivation, and sublingual gland swelling. Comprehensive evaluation, including neurologic and musculoskeletal examinations, blood work, and urinalysis, revealed no abnormalities other than tongue-related signs. Magnetic resonance imaging (MRI) revealed a multilobed cystic structure in the occipito-atlanto-axial joint, compressing the right hypoglossal canal. The lesion appeared cerebrospinal fluid (CSF)-like on T1-weighted and T2-weighted images, and hyperintense compared with CSF on fluid-attenuated inversion recovery T2-weighted images. The scans suggested mucinous content with enhanced peripheral areas on contrast-enhanced images. Surgical removal and drainage of this cyst were performed, and clinical signs improved markedly. The dorsal cyst was tentatively diagnosed as a ganglion cyst based on histopathologic and imaging findings. Ganglion cysts should be considered in the differential diagnosis for dogs with similar MRI findings and neurologic signs.

A red ruffed lemur (Varecia rubra) from a zoo in Louisiana, USA, was euthanized for worsening paresis. Brain and spinal cord histology identified eosinophilic meningoencephalomyelitis with intralesional adult Angiostrongylus sp. nematodes. PCR and sequencing confirmed A. cantonensis infection, indicating this parasite constitutes an emerging zoonosis in the southeastern United States.

Canine melanocytic neoplasms have a highly variable biological behavior ranging from benign cutaneous melanocytomas to malignant oral melanomas that readily metastasize to lymph nodes and internal organs. This review focuses on the diagnosis and prognosis of canine melanocytic neoplasms. While pigmented melanocytic neoplasms can be diagnosed with fine-needle aspirates, an accurate prognosis requires surgical biopsy. However, differentiating amelanotic spindloid melanomas from soft tissue sarcomas is challenging and often requires immunohistochemical labeling with a diagnostic cocktail that contains antibodies against Melan-A, PNL-2, TRP-1, and TRP-2 as the current gold standard. For questionable cases, RNA expression analysis for TYR, CD34, and CALD can further differentiate these two entities. The diagnosis of amelanotic melanomas will be aided by submitting overlying and/or lateral flanking epithelium to identify junctional activity. Wide excision of lateral flanking epithelium is essential, as lentiginous spread is common for malignant mucosal melanomas. Combining histologic features (nuclear atypia, mitotic count, degree of pigmentation, level of infiltration, vascular invasion; tumor thickness and ulceration) with the Ki67 index provides the most detailed prognostic assessment. Sentinel lymph nodes should be evaluated in cases of suspected malignant melanomas using serial sectioning of the node combined with immunohistochemical labeling for Melan-A and PNL-2.

The prognostic significance of internal tandem duplication (ITD) mutations in exons 8 and 11 of c-kit has been well-described for canine cutaneous mast cell tumors (MCTs), but c-kit mutations have rarely been reported in subcutaneous MCTs. The objective of this study was to identify the prevalence of ITD mutations in exons 8 and 11 of c-kit in canine subcutaneous MCTs and to investigate its association with histologic grade, KIT pattern, and proliferation markers. ITD mutations in exons 8 and 11 of c-kit, mitotic count, Ki67 index, AgNOR number, Ki67xAgNOR score, KIT pattern, and histologic grade (two-tier system) were retrospectively recorded for 216 dogs with subcutaneous MCTs. ITD mutations in exons 8 and 11 of c-kit were detected in 23 (10.6%) and 12 (5.56%) subcutaneous MCTs, respectively. Exon 11 mutations were significantly associated with Kiupel high grade (p < 0.001) and increased mitotic count (p < 0.001) compared to subcutaneous MCTs with no mutations in exons 8 or 11 (p = 0.002) or subcutaneous MCTs with a mutation in exon 8 (p = 0.001). There was no significant association of either c-kit mutation with KIT patterns or proliferation activity. This study identified a higher prevalence of ITD mutations in exons 8 and 11 of c-kit in subcutaneous MCTs than previously reported. Like their cutaneous counterpart, subcutaneous MCTs with exon 11 mutations were more likely to be histologically high grade and have a higher mitotic count, whereas such associations were not observed in subcutaneous MCTs with exon 8 mutations.

Prevention and treatment options for hepatocellular carcinoma (HCC) are presently limited, underscoring the necessity for further elucidating molecular mechanisms underlying HCC development and identifying new prevention and therapeutic targets. Here, we demonstrate a unique protumorigenic niche in the livers of Ncoa5+/− mouse model of HCC, which is characterized by altered expression of a subset of genes including p21WAF1/CIP1 and proinflammatory cytokine genes, increased putative hepatic progenitors, and expansions of activated and tissue-resident memory (TRM) CD8+ T lymphocytes, myeloid-derived suppressor cells (MDSCs), and alternatively activated M2 macrophages. Importantly, prophylactic metformin treatment reversed these characteristics including aberrant p21WAF1/CIP1 expression and subsequently reduced HCC incidence in Ncoa5+/− male mice. Heterozygous deletion of the p21WAF1/CIP1 gene alleviated the key features associated with the protumorigenic niche in the livers of Ncoa5+/− male mice. Moreover, transcriptomic analysis reveals that preneoplastic livers of Ncoa5+/− mice are similar to the livers of nonalcoholic steatohepatitis patients as well as the adjacent noncancerous liver tissues of a subset of HCC patients with a relatively poor prognosis. Together, our results suggest that p21WAF1/CIP1 overexpression is essential in the development of protumorigenic microenvironment induced by NCOA5 deficiency and metformin prevents HCC development via alleviating p21WAF1/CIP1 overexpression and protumorigenic microenvironment.

During the 2019 Eastern equine encephalitis virus (EEEV) outbreak in Michigan, two 2-month old Mexican wolf pups experienced neurologic signs, lymphohistiocytic neutrophilic meningoencephalitis with neuronal necrosis and neuronophagia, and acute death. We identified EEEV by reverse transcription real-time PCR and in situ hybridization. Vector mosquitoes were trapped at the zoo.

Background Gastrointestinal stromal tumors (GISTs) are common mesenchymal neoplasms in the gastrointestinal tract of humans and dogs. Little is known about the pathogenesis of these tumors. This study evaluated the role of c-KIT in canine GISTs; specifically, we investigated activating mutations in exons 8, 9, 11, 13, and 17 of c-KIT and exons 12, 14, and 18 of platelet-derived growth factor receptor, alpha polypeptide ( PDGFRA ), all of which have been implicated in human GISTs. Methods Seventeen canine GISTs all confirmed to be positive for KIT immunostaining were studied. Exons 8, 9, 11, 13 and 17 of c-KIT and exons 12, 14, and 18 of PDGFRA , were amplified from DNA isolated from formalin-fixed paraffin-embedded samples. Results Of these seventeen cases, six amplicons of exon 11 of c-KIT showed aberrant bands on gel electrophoresis. Sequencing of these amplicons revealed heterozygous in-frame deletions in six cases. The mutations include two different but overlapping six base pair deletions. Exons 8, 9, 13, and 17 of c-KIT and exons 12, 14, and 18 of PDGFRA had no abnormalities detected by electrophoresis and sequencing did not reveal any mutations, other than synonymous single nucleotide polymorphisms (SNPs) found in exon 11 of c-KIT and exons 12 and 14 of PDGFRA . Conclusions The deletion mutations detected in canine GISTs are similar to those previously found in the juxtamembrane domain of c-KIT in canine cutaneous mast cell tumors in our laboratory as well as to those reported in human GISTs. Interestingly, none of the other c-KIT or PDGFRA exons showed any abnormalities in our cases. This finding underlines the critical importance of c-KIT in the pathophysiology of canine GISTs. The expression of KIT and the identification of these activating mutations in c-KIT implicate KIT in the pathogenesis of these tumors. Our results indicate that mutations in c-KIT may be of prognostic significance and that targeting KIT may be a rational approach to treatment of these malignant tumors. This study further demonstrates that spontaneously occurring canine GISTs share molecular features with human GISTs and are an appropriate model for human GISTs.

This study is the first documentation of the isolation and extensive characterization of mesenchymal stem cells from canine adipose tissue. Methods previously used by our group to isolate and differentiate human adipose-derived mesenchymal stem cells (hAD-MSCs) have been modified and optimized for derivation of similar cells from canine adipose tissues. The canine adipose tissue-derived mesenchymal stem cells (cAD-MSCs) showed lower proliferation ability and were refractory to osteogenic and adipogenic differentiation under conditions employed to differentiate hAD-MSCs. The differentiation of cAD-MSCs into osteoblasts and adipocytes was effectively achieved under modified conditions, by using laminin-coated plates and peroxisome proliferative activated receptor, gamma (PPARγ) ligands, respectively. The formation of micromass was sufficient to induce chondrogenesis, unlike hAD-MSCs, which require transforming growth factor beta (TGF-β). These cells displayed anchorage-independent growth in soft agar, and their colony-forming efficiency in plastic was comparable with human counterparts. The cAD-MSCs expressed genes associated with pluripotency, while their differentiated progeny expressed appropriate lineage-specific genes. The optimization of growth and differentiation of cAD-MSCs should facilitate future stem cell-based reparative and regenerative studies in dogs. The dog is a promising biomedical model that is suitable for evaluation of novel therapies such as those employing stem cells in experimental and in spontaneous disease settings.

Abstract Background Listeriosis is a rare disease in cats with naturally occurring cases usually being identified in individual animals. Listerial mesenteric lymphadenitis has not been described previously in cats. Objectives To describe the clinical and histological features of listerial mesenteric lymphadenitis in cats as well as treatment outcome. Animals Listerial mesenteric lymphadenitis was confirmed in 3 cats by histology, immunohistochemistry, and bacterial culture. Results The affected cats were young to middle aged and were examined for various clinical signs. On both palpation and abdominal ultrasound examination, all cats had marked mesenteric lymphadenomegaly. Survival was prolonged in all 3 cases. Two of the 3 cats were fed a raw meat-based diet before they developed clinical illness. Conclusions and Clinical Importance Lymphadenitis caused by listeriosis has a protracted time course and should be a differential diagnosis for abdominal lymphadenopathy in young to middle-aged cats. Feeding of a raw meat-based diet may be a contributing factor for development of listeriosis in cats.

Gastric plasmacytoma is rare in dogs, with only four previous reports providing limited descriptions of abdominal ultrasound (AUS) and computed tomography (CT) findings. This study presents the AUS and CT imaging features of two histopathologically suspected gastric plasmacytomas. Combining the four previous and two new cases, these tumors predominantly occurred in the greater curvature and pyloric antrum as solitary round masses connected to the submucosal or transmural layers. Pre- and post-contrast tissue attenuation (Hounsfield unit; HU) differences exceeded 40, with variable AUS echogenicity and echotexture. Imaging features may resemble those of spindle cell tumors, requiring histological and immunohistochemical examinations for definitive diagnosis.