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Macrobrachium acanthurus is a freshwater prawn with aquaculture potential. However, little is known about its nutrient requirements, particularly regarding protein and lipid-carbohydrate ratio interactions in the diet. To assess the effect of these macronutrients in growth performance and the activity of digestive and antioxidant enzymes, a 2 × 3 factorial design experiment was conducted using two different levels of protein (P35 and P40) and three lipid-carbohydrate ratios (L:C ratio): 2:1 (20 % L and 10 % C), 1:2 (10 % L and 20 %) and 1:6 (5 % L and 30 % C). Each diet was fed to triplicate groups of juveniles with an initial mean weight of 0.075 ± 0.015 g for 60 days. No significant differences in growth performance were found. Although treatment P35 LC 1:2 showed the highest values of weight gain and specific growth performance, survival rate in this diet was lowest among treatments. Interaction between protein and L:C ratio influenced trypsin, chymotrypsin, leucine aminopeptidase and amylase activities, but protein content alone affected the alkaline proteases. Lipase did not differ among treatments. Catalase, glutathione peroxidase, total antioxidant capacity, phenoloxidase and prophenoloxidase activities were also influenced by protein and lipid-carbohydrate interaction; however, super oxide dismutase activity was only affected by dietary protein level. The highest activities of phenoloxidase and prophenoloxidase were observed in prawns fed diet P40 and L:C ratio 1:6 which suggests oxidative stress. These results suggest that 35 % dietary protein and 10 % lipids and 20 % carbohydrates (L:C ratio 1:2) are optimal for growth performance and activity of digestive and antioxidant enzymes. However, measures should be taken to avoid cannibalism and increase the survival rate.

Summary: Inappropriate CD4+ T helper (Th) differentiation can compromise host immunity or promote autoimmune disease. To identify disease-relevant regulators of T cell fate, we examined mutations that modify risk for multiple sclerosis (MS), a canonical organ-specific autoimmune disease. This analysis identified a role for Zinc finger E-box-binding homeobox (ZEB1). Deletion of ZEB1 protects against experimental autoimmune encephalitis (EAE), a mouse model of multiple sclerosis (MS). Mechanistically, ZEB1 in CD4+ T cells is required for pathogenic Th1 and Th17 differentiation. Genomic analyses of paired human and mouse expression data elucidated an unexpected role for ZEB1 in JAK-STAT signaling. ZEB1 inhibits miR-101-3p that represses JAK2 expression, STAT3/STAT4 phosphorylation, and subsequent expression of interleukin-17 (IL-17) and interferon gamma (IFN-γ). Underscoring its clinical relevance, ZEB1 and JAK2 downregulation decreases pathogenic cytokines expression in T cells from MS patients. Moreover, a Food and Drug Administration (FDA)-approved JAK2 inhibitor is effective in EAE. Collectively, these findings identify a conserved, potentially targetable mechanism regulating disease-relevant inflammation.