Abstract: An air conditioning device for a vehicle includes: a housing having an inside divided into an inflow space, a heat exchange space, and an outflow space, which are straightly arranged, and having a plurality of discharge ports, which communicates with an interior, at the inflow space; a blowing unit disposed at the inflow space of the housing and configured to blow air; a heat exchange unit disposed at the heat exchange space of the housing and configured to adjust a temperature of conditioned air by exchanging heat with air; and an opening-closing door disposed at the outflow space of the housing and configured to open and close the plurality of discharge ports such that conditioned air at an adjusted temperature selectively flows to the plurality of discharge ports. The air conditioning device adjusts the temperature of conditioned air for respective modes and reduces a flow resistance of air.

Abstract: Disclosed are a wound treatment patch using static electricity, and a method for fabricating the wound treatment patch using static electricity. The patch includes a substrate made of a sticky polymer; a first electrode disposed in a first partial region of one face of the substrate and exposed to an outside; and a second electrode disposed in a second partial region other than the first partial region, and spaced apart from the first electrode, and encapsulated within the substrate, wherein each of the first electrode and the second electrode is made of hydrogel having electrical conductivity or a soft polymer having electrical conductivity.

Abstract: The present invention relates to a human Lefty A protein variant with improved productivity and stability, a fusion protein comprising the protein variant, and a composition for preventing and/or treating neuromuscular disease comprising the protein variant or the fusion protein. According to the present invention, a human Lefty A protein variant and a fusion protein comprising the variant are constructed, which have better stability than naturally occurring human Lefty A protein, and thus are expressed at high levels and produced in high yield in animal cells. In addition, administration of the constructed human Lefty A protein variant or fusion protein can restore the nerve and motor functions of nerve disease model animals. Accordingly, the use of the human Lefty A protein variant or fusion protein can effectively prevent or treat various nerve diseases and muscle diseases.

Abstract: Disclosed are a wound treatment patch using static electricity, and a method for fabricating the wound treatment patch using static electricity. The patch includes a substrate made of a sticky polymer; a first electrode disposed in a first partial region of one face of the substrate and exposed to an outside; and a second electrode disposed in a second partial region other than the first partial region, and spaced apart from the first electrode, and encapsulated within the substrate, wherein each of the first electrode and the second electrode is made of hydrogel having electrical conductivity or a soft polymer having electrical conductivity.

Abstract: Disclosed is a fine dust collecting device using a human body based electrostatic energy harvesting element. The fine dust collecting filter device includes an electrostatic energy harvesting element for collecting and generating current; a charging filter connected to the electrostatic energy harvesting element such that the charging filter is electrically charged to have a first polarity and thus electrically charges fine dust particles; a collecting filter connected to the electrostatic energy harvesting element such that the collecting filter is electrically charged to have a second polarity opposite to the first polarity; and a rectifier disposed between and connected to the electrostatic energy harvesting element, and the charging filter and the collecting filter.

Abstract: The technology described herein is directed to devices, systems, methods, and assays comprising electrode arrays for electroconductive cells. In particular, the technology generally relates to a microelectrode array (MEA) device comprising both field potential (FP) electrodes and impedance electrodes (IE) that are spatially separated for the functional analysis of the electrical connectivity between at least two cell populations, for example a plurality of neuronal cells and a plurality of contractile cells.

Abstract: The present invention relates to an artificially manipulated SC function-controlling factor for SC function control and/or the treatment or alleviation of a disease due to an SC function disorder, and to a use thereof. More specifically, the present invention relates to a system capable of performing artificial SC function control and/or treating or alleviating a disease due to an SC function disorder, the system comprising: an artificially manipulated SC function-controlling factor for SC function control and/or the treatment or alleviation of a disease due to an SC function disorder; and/or a composition for treating or alleviating a disease due to an SC function disorder. In a specific aspect, the present invention relates to an SC function-controlling system by an SC function-controlling factor, such as artificially manipulated PMP22, and/or an expression product thereof.

Abstract: An siRNA for specifically targeting a PMP22 mutant gene and a pharmaceutical composition for preventing or treating Charcot Marie Tooth disease, which includes the same, are provided. According to the present invention, it is confirmed that selective suppression of a PMP22 mutant allele by a non-viral delivery system of siRNA may improve demyelinating neuropathic symptoms of CMT in vivo, enhance a motor ability and increase a volume of muscle. Therefore, the siRNA may be used in a useful method for treating various dominantly inherited peripheral neuropathies including CMT.

Abstract: An siRNA for specifically targeting a PMP22 mutant gene and a pharmaceutical composition for preventing or treating Charcot Marie Tooth disease, which includes the same, are provided. According to the present invention, it is confirmed that selective suppression of a PMP22 mutant allele by a non-viral delivery system of siRNA may improve demyelinating neuropathic symptoms of CMT in vivo, enhance a motor ability and increase a volume of muscle. Therefore, the siRNA may be used in a useful method for treating various dominantly inherited peripheral neuropathies including CMT.

Abstract: The present invention relates to a HSP27 mutation (S135F) mediated Charcot-Marie-Tooth disease (CMT) animal model. Particularly, the vector expressing mutant HSP27 protein wherein the 135th serine is substituted with phenylalanine has been injected in the mouse zygote and then the mouse harboring the expression vector was selected. The selected mouse was confirmed to display Charcot-Marie-Tooth disease phenotype, so that the animal model was expected to be efficiently used for the evaluation of the effect of Charcot-Marie-Tooth disease treating material candidates.

Abstract: The present invention relates to a HSP27 mutation (S135F) mediated Charcot-Marie-Tooth disease (CMT) animal model. Particularly, the vector expressing mutant HSP27 protein wherein the 135th serine is substituted with phenylalanine has been injected in the mouse zygote and then the mouse harboring the expression vector was selected. The selected mouse was confirmed to display Charcot-Marie-Tooth disease phenotype, so that the animal model was expected to be efficiently used for the evaluation of the effect of Charcot-Marie-Tooth disease treating material candidates.

Abstract: The present invention relates to a method for the screening of a therapeutic agent for Charcot-Marie-Tooth disease (CMT) using induced pluripotent stem cells and motor neurons differentiated therefrom. Particularly, the present inventors prepared induced pluripotent stem cells from the human fibroblasts originated from CMT patient. When the motor neurons differentiated from the said induced pluripotent stem cells are used for the screening of a therapeutic agent for Charcot-Marie-Tooth disease, the pharmaceutical effect of the therapeutic agent candidates can be easily evaluated during the screening. In addition, by the method to prepare the induced pluripotent stem cells, autologous motor neurons which are usable for the screening of a patient-specific therapeutic agent and the patient-specific treatment can be prepared.

Abstract: The present invention newly identified a missense mutation in the MYH14 gene as a cause responsible for a complex phenotype of peripheral neuropathy, myopathy, hearing loss, and hoarseness. Further, the present invention provides a method for diagnosing inherited neuromuscular disorders showing a complex phenotype of peripheral neuropathy, myopathy, hearing loss, and hoarseness via detection of the mutated MYH14 gene or the protein encoded thereby, and a diagnostic kit therefor. According to the present invention, simple examination of the gene allows early diagnosis of inherited neuromuscular disorders showing the complex phenotype of peripheral neuropathy, myopathy, hearing loss, and hoarseness, which shows high inheritance and is caused by a single gene defect, and accurate diagnosis of the disease makes it possible to tailor therapy.

Abstract: Disclosed is a method for diagnosing Charcot-Marie-Tooth (CMT) disease. More specifically, disclosed is a method for diagnosing a subtype of Charcot-Marie-Tooth disease type 1, (i.e., CMT1A) and a subtype of the disease type 2 (i.e., CMT2A) by evaluating fatty infiltration behaviors in respective compartments of proximal lower extremity muscles via comparison and analysis of MRI on the proximal lower extremities. Further disclosed is a method for diagnosing CMT1A and CMT2A, by analyzing fatty infiltration levels between respective compartments by MRI examination on distal lower extremity muscles.

Abstract: Disclosed herein are a method and kit for diagnosing hereditary diseases CMT1A and HNPP, caused by duplication and deletion in the chromosome 17p11.2-p12 region. In accordance with the present invention, there is provided a method for diagnosing an inherited neuropathy, comprising, running the PCR amplification using microsatellites present in a chromosome 17p11.2-p12 region as markers and DNA typing the resulting PCR amplification products to determine the presence of duplication and deletion in the corresponding chromosomal region, wherein Multiplex PCR amplification is carried out using 6 loci of D17S921, D17S9B, D17S9A, D17S918, D17S2230 and D17S4A as markers, and DNA-typing of the resulting PCR amplification products is carried out to determine duplication and deletion in the corresponding chromosomal region. In accordance with the method of the present invention, the diagnosis accuracy of detecting duplication and deletion in the chromosome 17p11.2-p12 region is greater than 99.9%.

Abstract: Disclosed herein are a method and kit for diagnosing hereditary diseases CMT1A and HNPP, caused by duplication and deletion in the chromosome 17p11.2-p12 region. In accordance with the present invention, there is provided a method for diagnosing an inherited neuropathy, comprising, running the PCR amplification using microsatellites present in a chromosome 17p11.2-p12 region as markers and DNA typing the resulting PCR amplification products to determine the presence of duplication and deletion in the corresponding chromosomal region, wherein Multiplex PCR amplification is carried out using 6 loci of D17S921, D17S9B, D17S9A, D17S918, D17S2230 and D17S4A as markers, and DNA-typing of the resulting PCR amplification products is carried out to determine duplication and deletion in the corresponding chromosomal region. In accordance with the method of the present invention, the diagnosis accuracy of detecting duplication and deletion in the chromosome 17p11.2-p12 region is greater than 99.9%.