In addition, we did not see any abnormal development or behaviour in three live transgenic sheep up to at least six months of age. These results suggested that MSTNknockdown may not affect development of cloned embryo and lamb. Transgenic sheep M17, with largest reduction in MSTN expression levels, showed a tendency to faster increase in body weight.than control sheep. Myofiber mean diameter of M17 was bigger than that of the non-transgenic controls, suggesting that MSTN-knockdown possibly caused hypertrophy of M17 myofiber. However, owing to our morphometric analysis of only one muscle biopsy from M17, further research is required to clarify whether MSTN-knockdown in sheep causes myofiber hyperplasia or hypertrophy and the effect on fiber types. The increased muscle mass in MSTN null mice and transgenic mice expressing high levels of the propeptide, follistatin, or a dominant negative form of activin receptor type IIB resulted from both hyperplasia and hypertrophy. In contrast, missense mutant MSTN caused hyperplasia but not hypertrophy in mouse muscles, whereas dominant negative MSTN produced muscle hypertrophy without hyperplasia. These results indicated that this hypertrophic response and lack of hyperplasia may be due to the incomplete inhibition of MSTN gene expression. We acknowledge that the present study only contained analysis of three transgenic sheep and growth performance of transgenic sheep need to be further observed. Work is currently underway to generate more MSTN-knockdown sheep by reclone transgenic sheep M17. In addition, application of transgenic animals for meat production is forbidden in some countries and meat from cloned animals must be carefully assessed before entering the food chain. In summary, we successfully generated MSTN-knockdown transgenic sheep by RNAi and SCNT. Our findings demonstrate a promising approach to promoting muscle growth in livestock production. Spontaneous bacterial peritonitis is a common and severe infection in patients with cirrhosis. Short-term prognosis has improved in recent decades due to prompt diagnosis during routine paracentesis, standardization of diagnostic criteria based on ascitic fluid analyses,, and use of non-nephrotoxic third generation cephalosporins. However, a significant number of patients with SBP still develop complications such as infections, systemic hemodynamic dysAbMole L-701324 function and progressive renal failure, that lead to death,. Fifty percent of SBP patients who develop renal failure die during hospitalisation compared to only 6% of patients without this complication. The administration of albumin to these patients has demonstrated a reduction in the incidence of renal dysfunction and improvement in short-term survival,. Episodes of SBP are associated with a marked release of proinflammatory cytokines such as tumour necrosis factor alpha and effector molecules like nitric oxide metabolites that keep a close relationship with SBP-induced morbidity and mortality,. Patients with SBP show a long-lasting marked increase in serum NOx that may contribute to maintaining splanchnic vasodilatation and thus worsen the hemodynamic hyperkinetic state,. Besides, nitrite and nitrate levels in serum and ascitic fluid at diagnosis of infection are significantly higher in SBP patients who develop renal impairment as a consequence of the ascitic fluid infection than in patients who maintain a stable renal function.