Abstract: The present invention relates to TNFR2-IL21R fusion protein acting as a double-antagonist to TNF-alpha (?) and IL-21. The composition containing the double antagonist to TNF-? and Il-21 (TNFR2-IL21R fusion protein), known as major causes of autoimmune rheumatoid arthritis, one of autoimmune diseases, can reduce the secretion of inflammatory cytokine, increase the secretion of anti-inflammatory cytokine, and suppress the differentiation of osteoclasts better than single proteins such as TNFR2-Fc and IL21R-Fc. The TNFR2-IL21R fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells. Therefore, the TNFR2-IL21R fusion protein of the present invention can be effectively used as an active ingredient for the composition for the prevention and treatment of autoimmune disease.

Abstract: The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-? and TWEAK, known as major causes of autoimmune arthritis which is one of autoimmune diseases. When the composition comprising TNFR2-TWEAKR fusion protein was treated to Th17 cells, the secretion of the inflammatory cytokine IL-17 was reduced but the secretion of the anti-inflammatory cytokine IL-10 generated in Treg cells was increased. Such effect of TNFR2-TWEAKR fusion protein was far greater than that of a single protein such as TNFR2-Fc or TWEAK-Fc. The TNFR2-TWEAKR fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells.

Abstract: A method of producing a building material using environment-friendly loess, comprising: preparing an environment-friendly composition by mixing 70˜90 percent by weight of at least one selected from among loess, kaolin, and clay, 3˜23 percent by weight of a resin coating agent, 0.1˜5 percent by weight of an inorganic pigment, and 1˜5 percent by weight of water; and molding the environment-friendly composition at 10 second˜20 minute intervals by introducing it into a molding machine having a temperature of 80˜140° C. and an internal pressure of 1˜20 kg/cm2.

Abstract: An oviduct specific expression promoter and a recombinant expression vector including the same. A promoter of an AGR2 gene is expressed specifically in the chicken oviduct, and a recombinant expression vector includes the promoter and a desired gene for encoding a desired protein. The oviduct specific promoter and the recombinant expression vector including the promoter can induce the expression of a protein specifically in the oviduct, i.e., an organ that secrets proteins so as to accumulate with a large amount in the egg. Accordingly, the oviduct specific promoter and the recombinant expression vector of the present invention can be advantageously used to produce transformed chickens, which can massively yield useful elements of high added value, produce functional eggs, and improve the economic traits of the poultry.

Abstract: The present invention relates to TNFR2-IL21R fusion protein acting as a double-antagonist to TNF-alpha (?) and IL-21. The composition containing the double antagonist to TNF-? and Il-21 (TNFR2-IL21R fusion protein), known as major causes of autoimmune rheumatoid arthritis, one of autoimmune diseases, can reduce the secretion of inflammatory cytokine, increase the secretion of anti-inflammatory cytokine, and suppress the differentiation of osteoclasts better than single proteins such as TNFR2-Fc and IL21R-Fc. The TNFR2-IL21R fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells. Therefore, the TNFR2-IL21R fusion protein of the present invention can be effectively used as an active ingredient for the composition for the prevention and treatment of autoimmune disease.

Abstract: The present invention relates to TNFR2-TWEAKR fusion protein, more precisely to TNFR2-TWEAKR fusion protein acting as a double-antagonist to TNF-? and TWEAK, known as major causes of autoimmune arthritis which is one of autoimmune diseases. When the composition comprising TNFR2-TWEAKR fusion protein was treated to Th17 cells, the secretion of the inflammatory cytokine IL-17 was reduced but the secretion of the anti-inflammatory cytokine IL-10 generated in Treg cells was increased. Such effect of TNFR2-TWEAKR fusion protein was far greater than that of a single protein such as TNFR2-Fc or TWEAK-Fc. The TNFR2-TWEAKR fusion protein of the present invention has not only excellent treatment effect on arthritis in CIA mouse model not also excellent treatment effect on autoimmune rheumatoid arthritis by increasing the expression of Treg, the immune suppressive cells.

Abstract: The present invention relates to compositions for preventing or treating angiogenesis-mediated diseases or allergic diseases which contain, as an active ingredient, an EC-SOD protein or a vector having a polynucleotide encoding thereof. The EC-SOD protein or the vector having a polynucleotide encoding the EC-SOD protein has the effect on inhibiting angiogenesis by inhibiting the expression of VEGF and MMP-9 which induce angiogenesis. Therefore, the EC-SOD protein or the vector may be useful for preventing or treating angiogenesis-mediated diseases. And the EC-SOD protein or the vector having a polynucleotide encoding said EC-SOD protein also has the effect on inhibiting over-differentiation of Th2 cells which cause allergic diseases, inhibiting transcription factor (NF-? B), and reducing degranulation of human mast cells. Accordingly, the EC-SOD protein or the vector may be useful for preventing or treating allergy diseases.

Abstract: A novel mutation in the SCN5A gene is associated with loss of cardiac sodium channel function. Analysis of the novel mutation provides an early diagnosis of subjects with cardiac diseases or disorders caused by loss of cardiac sodium channel function, particularly Brugada syndrome. Diagnostic methods include analyzing the sequences of the SCN5A gene or protein of an individual to be tested and comparing them with the sequences of the native, nonvariant SCN5A gene or protein. Pre-symptomatic diagnosis of these syndromes will enable practitioners to treat these disorders using existing medical therapy, e.g., using sodium channel blockers or through electrical stimulation.