Abstract: Provided is a drug that allows highly-efficient skipping of exon 51 in the human dystrophin gene. The present invention provides an antisense oligomer which enables exon 51 in the human dystrophin gene to be skipped.

Abstract: Provided are a complex that comprises a nucleic acid-containing nanoparticle and a hollow particle of a non-enveloped virus, a method for producing the complex, and a pharmaceutical composition comprising the complex.

Abstract: An object of the present invention is to develop and provide a method for conveniently introducing a nucleic acid, a peptide, and/or a low-molecular-weight compound into an empty capsid with viral early infection activities kept. The present invention provides a method for producing a drug delivery particle, comprising the steps of: mixing an empty capsid or an empty particle with a drug including a nucleic acid, a peptide, and/or a low-molecular-weight compound in a solution comprising 0.1 to 20% of a surfactant; and keeping the obtained mixed solution at ?5 to 50° C. to introduce the drug into the empty capsid or the empty particle.

Abstract: Provided is a drug that allows highly-efficient skipping of exon. The present invention provides an antisense oligomer wherein two or more unit oligomers targeting sequences that are neither consecutive nor overlap with each other in the same exon are connected.

Abstract: An object of the present invention is to develop and provide a method for conveniently introducing a nucleic acid, a peptide, and/or a low-molecular-weight compound into an empty capsid with viral early infection activities kept. The present invention provides a method for producing a drug delivery particle, comprising the steps of: mixing an empty capsid or an empty particle with a drug including a nucleic acid, a peptide, and/or a low-molecular-weight compound in a solution comprising 0.1 to 20% of a surfactant; and keeping the obtained mixed solution at ?5 to 50° C. to introduce the drug into the empty capsid or the empty particle.

Abstract: Provided is a drug that allows highly-efficient skipping of exon. The present invention provides an antisense oligomer wherein two or more unit oligomers targeting sequences that are neither consecutive nor overlap with each other in the same exon are connected.

Abstract: The present invention provides a novel therapeutic agent for mental illness. The therapeutic agent for mental illness comprises an IL-6 inhibitor as an active ingredient.

Abstract: The present invention provides an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene. Also provided is a pharmaceutical composition which causes skipping of the 53rd exon in the human dystrophin gene with a high efficiency.

Abstract: The present invention provides an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene. Also provided is a pharmaceutical composition which causes skipping of the 53rd exon in the human dystrophin gene with a high efficiency.

Abstract: The present invention provides: a mutant of adeno-associated virus (AAV) capsid protein, which contains at least one amino acid substitution in PLA2 domain when compared with the amino acid sequence for wild-type AAV capsid protein; a nucleic acid encoding the mutant; a cell containing the nucleic acid; a method for producing a recombinant AAV particle, comprising a step of culturing the cell to produce the recombinant AAV particle; a recombinant AAV particle containing the mutant; a composition containing the recombinant AAV particle; and a method for transferring a gene into a target cell, comprising a step of bringing the recombinant AAV particle into contact with the target cell.

Abstract: The present invention provides a pharmaceutical agent which causes skipping of the 55th, 45th, 50th or 44th exon in the human dystrophin gene with a high efficiency. The present invention provides an oligomer which efficiently enables to cause skipping of the 55th, 45th, 50th or 44th exon in the human dystrophin gene.

Abstract: A reduced attention state estimation system includes an eyeball movement and eyelid activity measurement unit that measures an eyeball movement and an eyelid activity of a subject to obtain eyeball movement and eyelid activity data, a section determination unit that determines an eye opening section, an eye closing section, an eye-blinking section and a cluster section based on the eyeball movement and eyelid activity data, an eyeball movement and eyelid activity-related information calculation unit that calculates a sharpness of microsaccade or the like for each eye opening section based on the eyeball movement and eyelid activity data, and an attention assessment unit that determines an attention assessment or the like for an eye opening/cluster section, which is an eye opening section and cluster section, based on the sharpness of microsaccade or the like.

Abstract: Provided is a drug that allows highly-efficient skipping of exon 51 in the human dystrophin gene. The present invention provides an antisense oligomer which enables exon 51 in the human dystrophin gene to be skipped.

Abstract: The present invention provides an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene. Also provided is a pharmaceutical composition which causes skipping of the 53rd exon in the human dystrophin gene with a high efficiency.

Abstract: The present invention provides an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene. Also provided is a pharmaceutical composition which causes skipping of the 53rd exon in the human dystrophin gene with a high efficiency.

Abstract: The present invention provides an oligomer which efficiently enables to cause skipping of the 53rd exon in the human dystrophin gene. Also provided is a pharmaceutical composition which causes skipping of the 53rd exon in the human dystrophin gene with a high efficiency.

Abstract: The present invention provides: a mutant of adeno-associated virus (AAV) capsid protein, which contains at least one amino acid substitution in PLA2 domain when compared with the amino acid sequence for wild-type AAV capsid protein; a nucleic acid encoding the mutant; a cell containing the nucleic acid; a method for producing a recombinant AAV particle, comprising a step of culturing the cell to produce the recombinant AAV particle; a recombinant AAV particle containing the mutant; a composition containing the recombinant AAV particle; and a method for transferring a gene into a target cell, comprising a step of bringing the recombinant AAV particle into contact with the target cell.

Abstract: The present invention provides an oligomer which allows exon 45 skipping in the human dystrophin gene.

Abstract: An object of the present invention is to provide a vector capable of oligodendrocyte-specifically suppressing expression of the PLP1 gene for treating PMD caused by abnormality of the PLP1 gene, and a promoter and miRNA therefor, and a pharmaceutical composition comprising the vector. The oligodendrocyte-specific promoter of the present invention comprises a nucleic acid having a sequence identity of at least 90% to a nucleotide sequence set forth in SEQ ID NO: 1. The miRNA of the present invention specific to the PLP1 gene comprises a pair of nucleotide sequences consisting of a specific antisense sequence and sense sequence.

Abstract: Provided is an agent developed to be capable of alleviating and suppressing muscle atrophy or muscle mass decrease, even for the elderly and even without requiring exercise, by inducing muscle differentiation. Provided is a composition for treating or preventing disorders or diseases associated with muscle atrophy, or for promoting muscle regeneration, the composition comprising, as an active ingredient, an inducer of muscle differentiation consisting of miR-199 or DNA that contains miR-199 gene encoding the miR-199.