Dominant mutations in superoxide dismutase cause amyotrophic lateral sclerosis (ALS), an adultonset neurodegenerative disease characterized by loss of motor neurons. Using mice carrying a deletable mutant gene, diminished mutant expression in astrocytes did not affect onset, but delayed microglial activation and sharply slowed later disease progression. These findings demonstrate that mutant astrocytes are viable targets for therapies to slow progression of non-cellautonomous killing of motor neurons in ALS.

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To elucidate the hemolytic suppression roles of taurine and the necessity of dietary taurine supplementation in yellowtail Seriola quinqueradiata fed a diet without fishmeal, juvenile fish with an initial body weight of 250 g were fed for 40 weeks in floating net cages on soybean protein diets supplemented with 0, 3.0, 4.5 and 6.0% taurine. Taurine concentration of the experimental diets were 0.03, 33.9, 52.8 and 71.6 mg/g, respectively. On the 21st week, fish fed the taurine unsupplemented diet had inferior growth and feed performances, higher death, and there were incidences of green liver and hemolytic anemia. In this group, hepatic and plasma taurine concentrations, serum osmolality and osmotic tolerance of erythrocytes (EC50 value) were significantly lower, and plasma hydroperoxide concentration was markedly higher than in the taurine supplemented groups. These conditions markedly improved corresponding with the increase of dietary taurine concentration. These results indicate that taurine plays a role in hemolytic suppression through osmoregulation and biomembrane stabilization in fish. In addition, it is suggested that yellowtail requires dietary taurine as an essential nutrition for maintaining physiological condition normally.

This study was performed to evaluate the efficacy of taurine supplementation for preventing green liver syndrome and improving growth performance in red sea bream Pagrus major fed a low-fishmeal (FM) diet. Yearling red sea bream were fed for 34 weeks on low-FM diets either supplemented with taurine, or without taurine, and the tissue taurine and bile pigment concentrations were measured. Compared to the fish fed the FM diet, fish fed the low-FM diet without taurine supplementation resulted in inferior feed performances and higher incidence of green liver related to the morphological transformation of the erythrocytes. In these fish, the hepatopancreatic taurine concentration was significantly lower and hepatopancreatic biliverdin concentration was high compared to the fish fed the FM diet. These parameters were markedly improved by taurine supplementation of the low-FM diet and were similar in levels to the fish fed the FM diet. These results indicate that green liver appearance and inferior feed performances of red sea bream fed the low-FM diet without taurine supplementation were caused by dietary taurine deficiency, and indicate the requirement of taurine supplementation to low-FM diets for red sea bream.KEY WORDS: alternative protein, bile pigment, green liver syndrome, low-fishmeal diet, red sea bream, taurine.

ABSTRACT-The efficacy of inactivated betanodavirus as a vaccine against viral nervous necrosis (VNN) was evaluated using juvenile sevenband grouper Epinephelus septemfasciatus.Fish were intraperitoneally injected once with formalin-inactivated redspotted grouper nervous necrosis virus (RGNNV). Virus-neutralizing antibodies were detected in the vaccinated fish from Day 10 to the end of the experimental period (Day 160), showing 1: 2,000 or higher mean antibody titers from Day 21 to Day 77. The vaccinated and unvaccinated control fish were challenged by intramuscular injection with the homologous virus at 14, 35 and 74 days post-vaccination.The vaccinated fish showed significantly lower mortalities at any challenges than the control fish, with the RPS (relative percent survival) values 67 or higher. A field trial, in which fish were exposed to natural infection in net pens, also resulted in higher survival rates in the vaccinated fish (RPS = 85) during the experi mental period of 9 weeks. This high induction of neutralizing antibodies and protection indicates the potential of the inactivated virus vaccine against VNN.