Chia seed and flax seed oils are rich in polyunsaturated fatty acids, but are susceptible to oxidative deterioration. The aim of this study was to determine the oxidative stability of chia seed and flax seed oils and enhance the stability using rosemary or garlic extracts. During accelerated storage at 65 °C for 14 days, the antioxidant abilities of rosemary or garlic extracts were evaluated and compared with those of butylated hydroxy toluene, ascorbyl palmitate, and α-tocopherol using peroxide value, conjugated dienoic acids, free fatty acid, thiobarbituric acid value analysis. The profile of volatiles, fatty acid composition, and the tocopherol contents in the treated and/or untreated oils were also determined. Active ingredients of rosemary and garlic extracts were also determined. Rosemary extract was found to provide higher oxidative stability than garlic extract after 14 days in most assays (e.g., the CDA values of 4.8% for rosemary extract and 5.2% for garlic extract in chia seed oil). The contents of γ-tocopherol, linoleic acid, and α-linolenic acid were well retained in the functional oils treated with the two extracts. After accelerated storage, the content of the major odor-active volatiles varied based on the type of oil. Our findings show the potential of natural aromatic plant extracts with respect to improving the oxidative stability of functional oils.

Transitional cell carcinoma (TCC) is the most common malignant tumor of the canine urinary tract and tends to have a poor prognosis due to its invasive potential. Recent studies have reported that up to 80% of canine urothelial carcinoma has the BRAF V595E mutation, which is homologous to the human V600E mutation. Activating the BRAF mutation is an actionable target for developing effective therapeutic agents inhibiting the BRAF/mitogen-activated protein kinase (MAPK) pathway in canine cancer as well as human cancer. We established novel canine TCC cell lines from two tumor tissues and one metastatic lymph node of canine TCC patients harboring the BRAF V595E mutation. Tumor tissues highly expressed the BRAF mutant and phosphorylated extracellular signal-related kinases (ERK)1/2 proteins. The derived cell lines demonstrated activated MAPK pathways. We also evaluated the cell lines for sensitivity to BRAF inhibitors. Sorafenib, a multiple kinase inhibitor targeting RAF/vascular endothelial growth factor receptor (VEGFR), successfully inhibited the BRAF/MAPK pathway and induced apoptosis. The established canine TCC cell lines responded with greater sensitivity to sorafenib than to vemurafenib, which is known as a specific BRAF inhibitor in human cancer. Our results demonstrated that canine TCC cells showed different responses compared to human cancer with the BRAF V600E mutation. These cell lines would be valuable research materials to develop therapeutic strategies for canine TCC patients.

Background Recently, fusion variants of the breast cancer anti-oestrogen-resistance 4 (BCAR4) gene were recurrently discovered in lung adenocarcinoma from the genome-wide studies. However, the functional characterisation of BCAR4 fusion has not been investigated. Methods Based on the analysis of RNA-sequencing data, we identified a fusion transcript of CD63–BCAR4 in a Korean patient with lung adenocarcinoma who did not harbour any known activating mutations in EGFR and KRAS genes. To investigate the oncogenic effect of CD63–BCAR4, in vitro and in vivo animal experiments were performed. Results In vitro experiments showed strongly enhanced cell migration and proliferation by the exogenous expression of CD63–BCAR4 protein in bronchial epithelial cells. Cell migration was notably reduced after knockdown of BCAR4 fusion by small-interfering RNA. The tumorigenic and metastatic capability of the CD63–BCAR4 fusion was confirmed by using the mouse xenograft model. Fusion-overexpressed cells result in metastasis to the liver and lung as well as the primary tumours after subcutaneous injection into mice. Cyclin D1, MMP1, Slug and mesenchymal markers were significantly increased after CD63–BCAR4 overexpression in the in vitro and in vivo experiments. Conclusions Taken together, our results suggest a newly identified fusion gene, CD63–BCAR4 as a potential novel oncogene in lung adenocarcinoma.