Aim:Genotype VII Newcastle disease virus (NDV) is the most predominant NDV strains that circulating in Malaysia; thus, this study was aimed to determine the susceptibility of Japanese quails toward genotype VII NDV. Clinical signs, gross pathological lesions of organs, positive detection of virus in organs and cloacal swabs, as well as the expression of the antibody titer, were used as parameters to assess the susceptibility of Japanese quails following infection of genotype VII NDV.Materials and Methods:About 20 quails were divided into three groups (n=8 for Groups A and B; n=4 for the control group). The quails in the Groups A and B were infected via intraocular route with 0.03 ml of 103.5 ELD50 and 107.0 ELD50 of NDV strain IBS 002, respectively, while the control group received 1× phosphate-buffered saline. Cloacal swabs and necropsy were taken on day 7 post-infection for all quails were subjected to one-step reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) for detection of virus and examination for gross pathological lesion, respectively. Blood serums of infected quails were taken on day 10, 14, and 21 post-day infections and were subjected for hemagglutination inhibition (HI) assay.Results:Depression and ruffled feathers, trachea rales, leg paralysis, and torticollis were shown in some of the quails in both infected groups. Based on statistical analysis, there was no significant difference (p>0.05) in clinical signs between the infected groups. The results for RT-qPCR were found to be negative for all groups, and no gross pathological lesions of organs observed for quails in both infected groups. Trachea, proventriculus, and cecal tonsil were taken for the detection of NDV by RT-qPCR, and some of the organ samples showed positive detection of virus in both infected groups. HI assay showed an increase in mean titers of antibody across time and between infected groups.Conclusion:In summary, Japanese quails are susceptible to genotype VII NDV based on parameters assessed.

Background: Complement C5a is a potent in ammatory chemoattractant and might be a bene cial therapeutic target for the induction of an effective anti-tumour response. C5a agonist and antagonist modulation have demonstrated to have either promotes or inhibits tumour development, EMT6 murine mammary cancer cells through both in vitro and in vivo studies.Methods: For the in-vitro studies, Alamar Blue cell viability assay was used for cell viability determination and immuno uorescence assay was used to determine the location of C5aR expression on EMT6 cell line. For the in-vivo experiment, female Balb/c mice were subcutaneously injected with EMT6 tumour cells and subsequently treated with both C5aR agonist and antagonist peptides. At the end of in-vivo study period of 14 days, liver and tumour samples were obtained for an ELISA assay to quantify the levels of TNF-α, caspase-3, C5a and VEGF-A signals following the treatment with both C5aR agonist and antagonist. One-way ANOVA test was performed to evaluate the differences between the mean of treatments given in a group and that of the negative control Results: The in-vitro experiment revealed an expression of C5aR was found on the cell membrane of the EMT6 cells and treatment with EP54; which is the C5aR agonist has shown low cell viability after 48 hours post-treatment. For the in-vivo experiment, the ELISA assay outcome have shown that EP54 signi cantly promote high numbers of circling of signaling proteins except for VEGF-A, suggesting that the C5aR agonist modulation might inhibits tumour development and also trigger the induction of apoptosis. Conclusion:C5aR modulation through the in uence of EP54 agonism may have bene cial effects in terms of reduction of the tumour size and attenuation of its development.

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Background: Complement C5a is a potent inflammatory chemoattractant and might be a beneficial therapeutic target for the induction of an effective anti-tumour response. C5a agonist and antagonist modulation have demonstrated to have either promotes or inhibits tumour development, EMT6 murine mammary cancer cells through both in vitro and in vivo studies. Methods: For the in-vitro studies, Alamar Blue cell viability assay was used for cell viability determination and immunofluorescence assay was used to determine the location of C5aR expression on EMT6 cell line. For the in-vivo experiment, female Balb/c mice were subcutaneously injected with EMT6 tumour cells and subsequently treated with both C5aR agonist and antagonist peptides. At the end of in-vivo study period of 14 days, liver and tumour samples were obtained for an ELISA assay to quantify the levels of TNF-α, caspase-3, C5a and VEGF-A signals following the treatment with both C5aR agonist and antagonist. One-way ANOVA test was performed to evaluate the differences between the mean of treatments given in a group and that of the negative controlResults: The in-vitro experiment revealed an expression of C5aR was found on the cell membrane of the EMT6 cells and treatment with EP54; which is the C5aR agonist has shown low cell viability after 48 hours post-treatment. For the in-vivo experiment, the ELISA assay outcome have shown that EP54 significantly promote high numbers of circling of signaling proteins except for VEGF-A, suggesting that the C5aR agonist modulation might inhibits tumour development and also trigger the induction of apoptosis. Conclusion: C5aR modulation through the influence of EP54 agonism may have beneficial effects in terms of reduction of the tumour size and attenuation of its development.