Abstract: The inventive concept provides a substrate treating method. The substrate treating method includes supplying a liquid to a substrate; and heating the substrate after the supplying the liquid, and wherein the supplying the liquid includes: supplying a first liquid to the substrate; and supplying a second liquid which is different from the first liquid to a substrate to which the first liquid is supplied, and wherein the second liquid is supplied as a test to the substrate and a contact angle between the second liquid which is supplied and the substrate is measured to determine a degree of hydrophilization of the substrate, and a supply mechanism of the second liquid supplied to the substrate is determined based on the degree of hydrophilization of the substrate which is determined, before the supplying the second liquid is performed.

Abstract: Disclosed are a spinning dope for an aramid and carbon-nanotube composite fiber and a method of manufacturing an aramid and carbon-nanotube composite fiber using the same.

Abstract: The inventive concept provides a substrate treating method. The substrate treating method includes pre-treating a substrate by cleaning the substrate; etching the substrate by supplying an etchant and heating a substrate supplied with the etchant; and post-treating the substrate after the etching the substrate, and wherein the pre-treating the substrate, the etching the substrate, and the post-treating the substrate are each performed in different chambers, a substrate on which the pre-treating the substrate is completed is transferred in a dry state to a chamber at which the etching the substrate is performed, and a substrate on which the etching the substrate is completed is transferred in a wetted state with a liquid to a chamber at which the post-treating the substrate is performed.

Abstract: The present invention relates to use of miR-18b for prevention, treatment, or diagnosis of muscle diseases or neuromuscular diseases, and specifically it was confirmed that, in a muscle disease by gene mutations model, gene mutations reduce miR-18b expression, cause dysregulation of miR-18b signaling pathways, and thus induce calcium signaling, cell differentiation inhibition, and apoptosis. Therefore, miR-18b of the present invention may be used as a target factor for diagnosing and treating muscle diseases caused by gene mutations such as ALS and DMD.

Abstract: A gene and cell therapy using a cell fusion technology is proposed. Cells overexpressing hemagglutinin neuraminidase (HN) and fusion (F) proteins have effects of enhancing cell fusion with other cells, restoring cell damage through the cell fusion with damaged cells, and transferring a normal gene. Therefore, when a vector including genes encoding the HN and F proteins of the present invention or a cell transformed with the vector is clinically applied to neurodegenerative diseases, muscular diseases, and the like, an effect of reducing the damage of damaged cells through cell fusion can be expected.

Abstract: The present invention relates to use of miR-18b for prevention, treatment, or diagnosis of muscle diseases or neuromuscular diseases, and specifically it was confirmed that, in a muscle disease by gene mutations model, gene mutations reduce miR-18b expression, cause dysregulation of miR-18b signaling pathways, and thus induce calcium signaling, cell differentiation inhibition, and apoptosis. Therefore, miR-18b of the present invention may be used as a target factor for diagnosing and treating muscle diseases caused by gene mutations such as ALS and DMD.

Abstract: The present invention relates to use of miR-18b for prevention, treatment, or diagnosis of muscle diseases or neuromuscular diseases, and specifically it was confirmed that, in a muscle disease by gene mutations model, gene mutations reduce miR-18b expression, cause dysregulation of miR-18b signaling pathways, and thus induce calcium signaling, cell differentiation inhibition, and apoptosis. Therefore, miR-18b of the present invention may be used as a target factor for diagnosing and treating muscle diseases caused by gene mutations such as ALS and DMD.

Abstract: The present invention relates to gene and cell therapy using a cell fusion technology and more particularly, cells overexpressing hemagglutinin neuraminidase (HN) and fusion (F) proteins have effects of enhancing cell fusion with other cells, restoring cell damage through the cell fusion with damaged cells, and transferring a normal gene. Therefore, when a vector including genes encoding the HN and F proteins of the present invention or a cell transformed with the vector is clinically applied to neurodegenerative diseases, muscular diseases, and the like, an effect of reducing the damage of damaged cells through cell fusion can be expected.

Abstract: The present invention relates to gene and cell therapy using a cell fusion technology and more particularly, cells overexpressing hemagglutinin neuraminidase (HN) and fusion (F) proteins have effects of enhancing cell fusion with other cells, restoring cell damage through the cell fusion with damaged cells, and transferring a normal gene. Therefore, when a vector including genes encoding the HN and F proteins of the present invention or a cell transformed with the vector is clinically applied to neurodegenerative diseases, muscular diseases, and the like, an effect of reducing the damage of damaged cells through cell fusion can be expected.

Abstract: A gene and cell therapy using a cell fusion technology is proposed. Cells overexpressing hemagglutinin neuraminidase (HN) and fusion (F) proteins have effects of enhancing cell fusion with other cells, restoring cell damage through the cell fusion with damaged cells, and transferring a normal gene. Therefore, when a vector including genes encoding the HN and F proteins of the present invention or a cell transformed with the vector is clinically applied to neurodegenerative diseases, muscular diseases, and the like, an effect of reducing the damage of damaged cells through cell fusion can be expected.

Abstract: The present invention relates to use of miR-18b for prevention, treatment, or diagnosis of muscle diseases or neuromuscular diseases, and specifically it was confirmed that, in a muscle disease by gene mutations model, gene mutations reduce miR-18b expression, cause dysregulation of miR-18b signaling pathways, and thus induce calcium signaling, cell differentiation inhibition, and apoptosis. Therefore, miR-18b of the present invention may be used as a target factor for diagnosing and treating muscle diseases caused by gene mutations such as ALS and DMD.

Abstract: The present invention relates to gene and cell therapy using a cell fusion technology and more particularly, cells overexpressing hemagglutinin neuraminidase (HN) and fusion (F) proteins have effects of enhancing cell fusion with other cells, restoring cell damage through the cell fusion with damaged cells, and transferring a normal gene. Therefore, when a vector including genes encoding the HN and F proteins of the present invention or a cell transformed with the vector is clinically applied to neurodegenerative diseases, muscular diseases, and the like, an effect of reducing the damage of damaged cells through cell fusion can be expected.

Abstract: Provided is an antiviral agent against animal viruses. The antiviral agent contains a protein or a nucleic acid sequence encoding the protein, as an active ingredient, the protein having binding ability and degrading ability to foreign nucleic acid chains invaded in an animal cell and that has no cytotoxicity to the animal cell itself. Also provided is an antiviral animal cell containing the protein according to the present invention, or the nucleic acid sequence encoding the protein. The antiviral agent and antiviral animal cell exhibit advantageous effects in that they selectively degrade foreign nucleic acid chains invaded in an animal cell and have no cytotoxicity to the animal cell, thus causing no death of the animal cell.

Abstract: Disclosed herein is an antiviral agent against animal viruses. The antiviral agent contains a protein or a nucleic acid sequence encoding the protein, as an active ingredient, the protein having binding ability and degrading ability to foreign nucleic acid chains invaded in an animal cell and that has no cytotoxicity to the animal cell itself. Disclosed herein is further an antiviral animal cell containing the protein according to the present invention, or the nucleic acid sequence encoding the protein. The antiviral agent and antiviral animal cell exhibit advantageous effects in that they selectively degrade foreign nucleic acid chains invaded in an animal cell and have no cytotoxicity to the animal cell, thus causing no death of the animal cell.

Abstract: A method of correcting a position of a prober, the method including obtaining a first image of a pad, the pad having a predetermined reference contact position, contacting the prober to the pad after obtaining the first image of the pad, obtaining a second image of the pad after contacting the prober to the pad, determining an actual contact position of an actual contact mark on the pad, the actual contact mark being produced by the contacting of the prober to the pad, comparing the second image to the first image to obtain an offset data, the offset data relating the actual contact position to the reference contact position, and correcting the position of the prober by aligning the actual contact position with the reference contact position based on the offset data.

Abstract: The present invention relates to a novel 2,6-substituted-3-nitropyridine derivative compound, a method for preparing same, a pharmaceutical composition for prevention and treatment of osteoporosis including same, applications of same for preparing the therapeutic agent of osteoporosis prevention and treatment, and a method for prevention and treatment of osteoporosis using same. The 2,6-substituted-3-nitropyridine derivative compound of the present invention effectively increases osteoblast activity and also inhibits the formation of osteoclasts, so that it may be usefully used for the prevention and treatment of osteoporosis.

Abstract: The present invention relates to a novel 2,6-substituted-3-nitropyridine derivative compound, a method for preparing the same, and a pharmaceutical composition including the same for prevention and treatment of osteoporosis. The 2,6-substituted-3-nitropyridine derivative compound of the present invention increases osteoblast activity and effectively inhibits the differentiation of osteoclasts, and thus can be usefully used for the prevention and treatment of osteoporosis.

Abstract: Disclosed herein is an antiviral agent against animal viruses. The antiviral agent contains a protein or a nucleic acid sequence encoding the protein, as an active ingredient, the protein having binding ability and degrading ability to foreign nucleic acid chains invaded in an animal cell and that has no cytotoxicity to the animal cell itself. Disclosed herein is further an antiviral animal cell containing the protein according to the present invention, or the nucleic acid sequence encoding the protein. The antiviral agent and antiviral animal cell exhibit advantageous effects in that they selectively degrade foreign nucleic acid chains invaded in an animal cell and have no cytotoxicity to the animal cell, thus causing no death of the animal cell.

Abstract: The present invention relates to novel benzamidine derivatives, a process for the preparation thereof and a pharmaceutical composition for preventing or treating osteoporosis comprising the same. The benzamidine derivatives of the present invention effectively inhibit osteoclast differentiation at an extremely low concentration, and thus can be advantageously used for the prevention and treatment of osteoporosis.

Abstract: A method of correcting a position of a prober, the method including obtaining a first image of a pad, the pad having a predetermined reference contact position, contacting the prober to the pad after obtaining the first image of the pad, obtaining a second image of the pad after contacting the prober to the pad, determining an actual contact position of an actual contact mark on the pad, the actual contact mark being produced by the contacting of the prober to the pad, comparing the second image to the first image to obtain an offset data, the offset data relating the actual contact position to the reference contact position, and correcting the position of the prober by aligning the actual contact position with the reference contact position based on the offset data.