Abstract: Disclosed is an expression vector system for variants of coagulation Factor VIII (FVIII) and von Willebrand Factor (vWF). In detail, mutant vWF the size of which is significantly reduced by deleting exons but which has remarkably increased FVIII stabilizing and activating efficiency, and an expression vector system useful for the treatment of hemophilia which is capable of expressing the same along with FVIII are disclosed. Use of the mutant vWF with a reduced size enables effective expression of FVIII in a viral vector and significantly enhanced FVIII activity. Further, the viral vector may be effectively used to treat hemophilia through gene therapy.

Abstract: Disclosed is an expression vector system for variants of coagulation Factor VIII (FVIII) and von Willebrand Factor (vWF). In detail, mutant vWF the size of which is significantly reduced by deleting exons but which has remarkably increased FVIII stabilizing and activating efficiency, and an expression vector system useful for the treatment of hemophilia which is capable of expressing the same along with FVIII are disclosed. Use of the mutant vWF with a reduced size enables effective expression of FVIII in a viral vector and significantly enhanced FVIII activity. Further, the viral vector may be effectively used to treat hemophilia through gene therapy.

Abstract: The present invention relates to a new use of TRIM72 as a target for muscle enhancer and heart enhancer, more particularly to a composition for enhancing muscle or heart comprising an expression or action inhibitor of TRIM72 protein. The present invention further relates to a new TRIM mutant protein inducing muscle differentiation and hypertrophy and its gene. The inventors of the present invention have identified that TRIM72 overexpression inhibits myogenesis whereas TRIM72 knockdown enhances myogenesis, and first elucidated that TRIM72 is a negative regulator of skeletal muscle differentiation. Accordingly, the inhibition of TRIM72 acts exclusively on skeletal muscle and heart muscle, but does not affect IGF-I signaling pathway in other tissues.

Abstract: An art therapy computer system and a computer-readable storage medium having recorded a program for art therapy are disclosed. An aspect of the present invention provides a computer system that includes a drawing module, which presents a plurality of patterns and in which the drawing module selects a certain pattern, composes and colors a picture according to the working of a person tested for art therapy, an analysis module, which analyzes one or more factors from the colored picture, and a parsing module, which parses the psychological state, symptoms or disorders of the person tested for art therapy from the analyzed factors.

Abstract: The present invention relates to a new use of TRIM72 as a target for muscle enhancer and heart enhancer, more particularly to a composition for enhancing muscle or heart comprising an expression or action inhibitor of TRIM72 protein. The present invention further relates to a new TRIM mutant protein inducing muscle differentiation and hypertrophy and its gene. The inventors of the present invention have identified that TRIM72 overexpression inhibits myogenesis whereas TRIM72 knockdown enhances myogenesis, and first elucidated that TRIM72 is a negative regulator of skeletal muscle differentiation. Accordingly, the inhibition of TRIM72 acts exclusively on skeletal muscle and heart muscle, but does not affect IGF-I signaling pathway in other tissues.