Experiments were conducted to evaluate the effect of free-range raising systems on growth performance, carcass yield, and meat quality of slow-growing chickens. Slow-growing female chickens, Gushi chickens, were selected as the experimental birds. Two hundred 1-d-old female chicks were raised in a pen for 35 d. On d 36, ninety healthy birds, with similar BW (353.7+/-32.1g), were selected and randomly assigned to 2 treatments (indoor treatment and free-range treatment, P>0.05). Each treatment was represented by 3 groups containing 15 birds (45 birds per treatment). During the indoor treatment, the chickens were raised in floor pens in a conventional poultry research house (7 birds/m2). In the free-range treatment, the chickens were housed in a similar indoor house (7 birds/m2); in addition, they also had a free-range grass paddock (1 bird/m2). All birds were provided with the same starter and finisher diets and were raised for 112 d. Results showed that the BW and weight gain of the chickens in the free-range treatment were much lower than that of the chickens in the indoor floor treatments (P<0.05). There was no effect of the free-range raising system on eviscerated carcass, breast, thigh, and wing yield (P>0.05). However, the abdominal fat yield and tibia strength (P<0.05) significantly declined. The nutrient composition (water, protein, and fat), water-holding capacity, shear force, and pH of the muscle were largely unaffected (P>0.05) by the free-range raising system. The data indicated that the free-range raising system could significantly reduce growth performance, abdominal fat, and tibia strength, but with no effect on carcass traits and meat quality in slow-growing chickens.

Increasing evidence suggests that liver regeneration is suppressed in patients with chronic HCV infection; however, the underlying mechanisms remain unclear. Previously, we demonstrated that injection of the synthetic double-stranded RNA (dsRNA) poly I:C to mimic viral infection suppresses liver regeneration in the partial hepatectomy (PHx) model, whereby IFN-␥ contributes to the inhibition. In this study, we examined the role of the IFN-␥-activated downstream signal ( T he liver has the unique ability to regenerate after injury or loss of tissue. Liver regeneration is controlled by a wide array of signaling factors and plays a key role in recovery after acute and chronic liver injury 1-5 ; however, emerging evidence suggests that liver regeneration is suppressed in patients with acute and chronic hepatitis C virus (HCV) infection 6-12 or liver cirrhosis. 13,14 Moreover, infection with murine hepatitis virus 15,16 or cytomegalovirus (MCMV) 17 has been shown to suppress liver regeneration in mice. At present, the cellular and molecular mechanisms impairing liver regeneration after viral infection remain obscure. Previously, we showed that injection of the synthetic double-stranded RNA (dsRNA) polyinosinic-polycytidylic acid (poly I:C) that mimics viral effects, inhibits liver regeneration in the murine partial hepatectomy (PHx) model. 17 Further studies also suggest that poly I:C activates natural killer (NK) cells to produce interferon-␥ (IFN-␥), leading to inhibition of liver regeneration. 17 However, the downstream signals and genes activated by IFN-␥ in poly I:C negative regulation of liver regeneration are still unclear.Signaling mediated by IFN-␥ is initiated upon its binding to the corresponding receptors IFNGR1 and IF-NGR2, followed by activation of IFNGR-associated tyrosine kinases (JAK1 and JAK2) and subsequent activation of the cytoplasmic protein, signal transducer

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