Canine mammary carcinomas represent an important pathology in small animal clinic, and benign mixed type carcinomas (MC-BMT) are one of the most diagnosed worldwide. The use of chemotherapeutic carboplatin has been one of the new protocols for the treatment of BMT. In this respect, three-dimensional cell culture (3D) represents an alternative in the evaluation of drugs by simulating what occurs in vivo. The present study aimed to verify the effect of carboplatin on 3D culture of cells derived from TMB, in addition to possible changes in cell viability, ballpoint size, apoptosis and Bcl-2/Bax ratio. For this, tumours samples were collected during mastectomy surgery procedure in private veterinary clinics, which were submitted to in vitro culture and part to histopathological analysis. After 28 days of 3D culture, spheroids were documented in both groups (treated and control) and sizes and morphology were compared. The carboplatin interfered in the cell viability by affecting their division and promoting apoptotic events. In the treated group, a higher transcription of Bax and caspase 3 was observed, in addition to low levels of caspases 2, 8 and 9, which was not observed in the control group. We thus suggest that mitochondrial dysfunction plays a critical role in cancer progression and that targeting mitochondrial alterations and mitochondrial retrograde signalling might be a promising strategy for the development of selective anticancer therapy. Thus, it was possible to demonstrate that the results achieved may contribute to the establishment of a new chemotherapy therapy in female dogs with MC-BMT.
Emerging coronavirus infections are a major threat to global public health. In this respect, a novel recombination of canine coronavirus (CCoV) and feline coronavirus (FCoV) was described among human biological samples, giving rise to a potential zoonosis. Despite all efforts, the host‒virus immune response related to CCoV is missing. In this study, pantropic CCoV infection of canine macrophages derived from peripheral blood monocytes was performed. After infection, macrophages were first polarized to the M1 and/or M2 phenotype. Moreover, infection kinetics, cell viability, apoptosis, mitochondrial dysfunction associated with reactive oxygen species and oxide nitric production were measured. Our results demonstrated that virus infection mainly polarized host macrophages to the classically activated (M1) phenotype, as demonstrated by amoeboid morphology with numerous fibrillary cytoplasmic processes followed by classical phenotypes. Viral infection released new particles at 18 h post-infection associated with a decrease in viable cells. Furthermore, upon CCoV infection, M1 cells exhibited reduced phagocytosis properties, as evidenced by a neutral red uptake assay. This in vitro method open an avenue for further studies on host-virus interaction.
A peritonite infecciosa felina (PIF) é uma doença infectocontagiosa, sistêmica e progressiva, ocasionada por um coronavírus identificado como vírus da peritonite infecciosa felina (VPIF), representando uma das principais causas de óbito de origem infecciosa em gatos domésticos. Além disso, é considerada uma das doenças mais comuns do Sistema Nervoso Central (SNC) de felinos, com envolvimento deste em aproximadamente 38% dos casos de PIF não efusiva. Neste sentido, o presente estudo teve por objetivo descrever as manifestações neurológicas de 17 felinos que vieram a óbito com diagnóstico clínico sugestivo de PIF baseado no histórico fornecido por clínicas veterinárias particulares da cidade de Araçatuba – SP, além de comparar os resultados dos exames laboratoriais e dados referentes à idade, raça e sexo com os descritos na literatura. O mesmo foi feito para o grupo controle, composto por três felinos que vieram a óbito por causas naturais. Os animais foram avaliados clinicamente e os sinais neurológicos mais observados foram hiperatividade (5,8%), vocalização (17,6%) e ataxia (76,4%), sem indícios de efusão em cavidade. Alterações em hemograma e perfil bioquímico são comuns em gatos com PIF, embora não sejam patognomônicas. Na análise hematológica, foi verificada a presença de anemia e linfopenia com valores significativamente alterados em comparação ao grupo controle; na análise bioquímica observou-se aumento de proteínas totais, de enzimas hepáticas e azotemia. O curso clínico da doença até a morte dos gatos variou de uma a quatro semanas. Diante do exposto, demonstra-se a relevância de estudos acerca da PIF, devendo ser um diferencial importante quando há envolvimento neurológico na espécie felina.
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