The present experiment was conducted to evaluate the effect of dietary inclusion of quinoa seeds extract (QSE) as a natural antioxidant on broiler chicken performance, economical efficiency, meat quality and oxidative parameters of chickens' meat under refrigerated storage conditions. The extract was prepared and subjected to different analysis prior to use in broiler diets. A total number of 135 one-day old chickens of Ross strain were randomly allotted to three dietary treatments and each treatment contained 45 birds of 3 replicates each. The control group was fed a basal diet without supplementation while QSE was supplemented at a rate of 10 and 30 g/100 Kg diet to compose the other two experimental diets (T1 and T2), respectively. The results showed that QSE contains several phytochemical compounds with potential antioxidant activity. Those results were further confirmed by determining the total antioxidant capacity, total phenolic content and the radical scavenging activity of the extract. The dietary inclusion of QSE in broilers' diet showed that group T2 had significantly (p<0.05) higher body weight, weight gain and feed intake compared to T1 and control group. The proximate analysis results of chickens' meat showed that breast and thigh meat of the chickens in treatment T2 recorded significantly (p<0.05) higher protein content as compared to the other two groups. Regarding the antioxidant properties, the addition of quinoa seeds extract in broilers' diet resulted in a significant (p<0.05) improvement of the antioxidative properties of chicken meat. The oxidative stability of chicken meat under refrigerated storage conditions was evaluated at different storage days (1, 4 and 7) and it was shown that the dietary addition of QSE into broilers' diet succeeded in delaying the lipid oxidation of broilers' meat up to 7 days of refrigerated storage. The chicken meat of groups T1 and T2 showed no significant (p>0.05) reduction in their free radical scavenging activities at day 7 of storage compared to control group. From the present study, it can be concluded that the dietary inclusion of quinoa seeds extract in broilers' diet as a natural antioxidant have a positive effect on broilers performance, meat quality and also improved the chicken meat oxidative stability during refrigerated storage up to 7 days.

Oncolytic virus (OV) therapy is widely considered as a major breakthrough in anti-cancer treatments. In our previous study, the efficacy and safety of using C-REV for anti-cancer therapy in patients during stage I clinical trial was reported. The stimulator of interferon genes (STING)–TBK1–IRF3–IFN pathway is known to act as the central cellular host defense against viral infection. Recent reports have linked low expression levels of cGAS and STING in cancer cells to poor prognosis among patients. Moreover, downregulation of cGAS and STING has been linked to higher susceptibility to OV infection among several cancer cell lines. In this paper, we show that there is little correlation between levels of cGAS/STING expression and susceptibility to C-REV among human pancreatic cancer cell lines. Despite having a responsive STING pathway, BxPC-3 cells are highly susceptible to C-REV infection. Upon pre-activation of the STING pathway, BxPc-3 cells exhibited resistance to C-REV infection. However, without pre-activation, C-REV completely suppressed the STING pathway in BxPC-3 cells. Additionally, despite harboring defects in the STING pathway, other high-grade cancer cell lines, such as Capan-2, PANC-1 and MiaPaCa-2, still exhibited low susceptibility to C-REV infection. Furthermore, overexpression of STING in MiaPaCa-2 cells altered susceptibility to a limited extent. Taken together, our data suggest that the cGAS–STING pathway plays a minor role in the susceptibility of pancreatic cancer cell lines to C-REV infection.

Oncolytic viruses (OVs) remodel the tumor microenvironment by switching a “cold” tumor into a “hot” tumor with high CD8+ T‐cell infiltration. CD8+ T‐cell activity plays an essential role in the antitumor efficacy of OVs. However, the activity of T cells is impaired by the programmed cell death protein‐1/programmed cell death‐ligand 1 (PD‐1/PD‐L1) interaction. To date, it remains unclear why OVs alone have a significant antitumor activity even when PD‐L1 expression persists on tumor or immune cells. In this study, we found that canerpaturev (C‐REV) treatment significantly suppressed tumor growth, even though it induced a significant increase in PD‐L1 expression in tumors in vivo as well as persistence of high PD‐L1 expression on antigen‐presenting cells (macrophage and dendritic cells [DCs]). Surprisingly, we observed that C‐REV treatment increased the abundance of activated CD8+PD‐1− tumor‐infiltrating lymphocytes (TILs) in the tumor on both the injected and contralateral sides, although infiltration of CD8+PD‐1high TILs into the tumor was observed in the control group. Moreover, the difference in PD‐1 expression was observed only in tumors after treatment with C‐REV, whereas most CD8+ T cells in the spleen, tumor‐draining lymph nodes and blood were PD‐1‐negative, and this did not change after C‐REV treatment. In addition, changes in expression of T‐cell immunoglobulin and mucin‐domain containing‐3 and T‐cell immune‐receptor with Ig and ITIM domains were not observed on CD8+ TILs after C‐REV treatment. Taken together, our findings may reveal mechanisms that allow OVs to trigger an antitumor immune response, irrespective of a PD‐L1‐enriched tumor microenvironment, by recruitment of CD8+PD‐1− TILs.

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