Abstract: Provided a method of treating ocular surface damage caused by an eye disease or eye injury like dry eye disease, chemical or physical injury, infection, neurosensory abnormalities and unspecified etiologies in a subject, comprising administering to said subject a pharmaceutical composition comprising a therapeutically effective amount of microRNA-328 antagonist.

Abstract: Disclosed are a composition for preventing and treating atherosclerosis which includes chalcone compound. In particular, the chalcone compound bound with 2-hydroxyl in ring A and 4?-methyoxy in ring B has versatile therapeutic potentials on anti-atherosclerosis by acting as PPAR? inducer, p44/42 MAPK inhibitor and cell cycle blocker and does not show toxicity to human aortic smooth muscle cells (HASMCs). In addition, the chalcone compound exhibits synergistic effect with the PPAR? ligand (rosiglitazone) to inhibit cell proliferation and the upregulation of cyclin D1, cyclin D3, interleukin-1? (IL-1?) and interleukin-6 (IL-6) induced by oxidized low density lipoprotein (Ox-LDL).

Abstract: The present disclosure provides a method for treating and/or preventing myopia, including: administering an RNA interference (RNAi) to a subject, wherein the RNA interference is capable of counteracting another RNA interference, and the other RNA interference is an RNA interference capable of inhibiting an expression of PAX-6 gene, and the RNA interference capable of inhibiting an expression of PAX-6 gene comprises microRNA-328.

Abstract: The invention discloses a method of therapy of endothelial dysfunction, by administering microRNA let-7g to a subject in need, wherein the microRNA let-7g inhibits SMAD2 transcription factor from activation and translocation into nucleus, thereby decreasing monocyte cell adhesion, inflammation and thrombosis and increasing angiogenesis.

Abstract: The present disclosure provides a method for treating and/or preventing myopia, including: administering an RNA interference (RNAi) to a subject, wherein the RNA interference is capable of counteracting another RNA interference, and the other RNA interference is an RNA interference capable of inhibiting an expression of PAX-6 gene, and the RNA interference capable of inhibiting an expression of PAX-6 gene comprises microRNA-328.

Abstract: The invention discloses a method of therapy of endothelial dysfunction, by administering microRNA let-7g to a subject in need, wherein the microRNA let-7g inhibits SMAD2 transcription factor from activation and translocation into nucleus, thereby decreasing monocyte cell adhesion, inflammation and thrombosis and increasing angiogenesis.

Abstract: Disclosed are a composition for preventing and treating atherosclerosis which includes chalcone compound. In particular, the chalcone compound bound with 2-hydroxyl in ring A and 4?-methyoxy in ring B has versatile therapeutic potentials on anti-atherosclerosis by acting as PPAR? inducer, p44/42 MAPK inhibitor and cell cycle blocker and does not show toxicity to human aortic smooth muscle cells (HASMCs). In addition, the chalcone compound exhibits synergistic effect with the PPAR? ligand (rosiglitazone) to inhibit cell proliferation and the upregulation of cyclin D1, cyclin D3, interleukin-1? (IL-1?) and interleukin-6 (IL-6) induced by oxidized low density lipoprotein (Ox-LDL).

Abstract: There is provided a method of therapy of atherosclerosis, by providing microRNA let-7g, an analogue thereof or modified let-7g to organisms to inhibit the expression of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), and the binding of LOX-1 and oxidized low-density lipoprotein (oxLDL), so as to block the pathogenesis of atherosclerosis. Also, a method of diagnosis of atherosclerosis comprises determining the levels of microRNA let-7g in serum or plasma samples of organisms, in which the levels of microRNA let-7g is estimated in individuals with atherosclerosis as compared to individuals without atherosclerosis.

Abstract: There is provided a method of therapy of atherosclerosis, by providing microRNA let-7g, an analogue thereof or modified let-7g to organisms to inhibit the expression of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), and the binding of LOX-1 and oxidized low-density lipoprotein (oxLDL), so as to block the pathogenesis of atherosclerosis. Also, a method of diagnosis of atherosclerosis comprises determining the levels of microRNA let-7g in serum or plasma samples of organisms, in which the levels of microRNA let-7g is estimated in individuals with atherosclerosis as compared to individuals without atherosclerosis.

Abstract: Disclosed are a composition for preventing and treating atherosclerosis which includes chalcone compound. In particular, the chalcone compound bound with 2-hydroxyl in ring A and 4?-methyoxy in ring B has versatile therapeutic potentials on anti-atherosclerosis by acting as PPAR? inducer, p44/42 MAPK inhibitor and cell cycle blocker and does not show toxicity to human aortic smooth muscle cells (HASMCs). In addition, the chalcone compound exhibits synergistic effect with the PPAR? ligand (rosiglitazone) to inhibit cell proliferation and the upregulation of cyclin D1, cyclin D3, interleukin-1? (IL-1?) and interleukin-6 (IL-6) induced by oxidized low density lipoprotein (Ox-LDL).

Abstract: There is provided a method of therapy of atherosclerosis, by providing microRNA let-7g, an analogue thereof or modified let-7g to organisms to inhibit the expression of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), and the binding of LOX-1 and oxidized low-density lipoprotein (oxLDL), so as to block the pathogenesis of atherosclerosis. Also, a method of diagnosis of atherosclerosis comprises determining the levels of microRNA let-7g in serum or plasma samples of organisms, in which the levels of microRNA let-7g is estimated in individuals with atherosclerosis as compared to individuals without atherosclerosis.

Abstract: The invention provides a method for determining a risk, for a subject, of suffering from atopic dermatitis, including: obtaining a biosample of the subject; detecting the presence of the single-nucleotide polymorphism rs12313273 (C/T) at position 30881 of the ORAI1 gene (SEQ ID No.: 1) in the biosample; and determining the risk, for the subject, of suffering from atopic dermatitis, wherein the presence of a C allele or genotype CC of the single-nucleotide polymorphism rs12313273 (C/T) indicates that the subject is at increased risk for suffering from atopic dermatitis.