Disclosed are a composite nanomaterial based on a metal-organic framework (MOF) material loaded with horseradish peroxidase (HRP) and a preparation method and use thereof. The composite nanomaterial based on the MOF material loaded with HRP includes a hafnium-based MOF material and HRP loaded thereon, where the hafnium-based MOF material is formed by self-assembly of 2′-amino-1,1′:4,1″-terphenyl-4,4″-dicarboxylic acid and hafnium ions through a coordination bond.

Disclosed are a composite nanomaterial based on a metal-organic framework (MOF) material loaded with horseradish peroxidase (HRP) and a preparation method and use thereof. The composite nanomaterial based on the MOF material loaded with HRP includes a hafnium-based MOF material and HRP loaded thereon, where the hafnium-based MOF material is formed by self-assembly of 2′-amino-1,1′:4,1″-terphenyl-4,4″-dicarboxylic acid and hafnium ions through a coordination bond.

The present invention provides, among other things, methods and compositions for making and using recombinant heme oxygenase for treating sickle cell disease. In some embodiments, recombinant heme oxygenase proteins are truncation variants, or Fc fusion proteins with increased half-life and/or reduced aggregation.

The present invention provides, among other things, methods and compositions for making and using recombinant heme oxygenase for treating sickle cell disease. In some embodiments, recombinant heme oxygenase proteins are truncation variants, or Fc fusion proteins with increased half-life and/or reduced aggregation.

The present disclosure relates to microneedle devices and methods for treating a disease (for example, diabetes) using a degradable cross-linked gel for self-regulated delivery of a therapeutic agent (for example, insulin).

The present disclosure relates to microneedle devices and methods for treating a disease (for example, diabetes) using a degradable cross-linked gel for self-regulated delivery of a therapeutic agent (for example, insulin).

A method is provided for treating a recipient with a biological product obtained from at least one donor that may be the same as, or different from, the recipient. The method includes identifying a targeted level of gene expression of a first gene in a biological product to be transferred from at least one donor to a recipient; treating the at least one donor to achieve the targeted level of gene expression of the first gene in the biological product; and transferring the biological product from the at least one donor to the recipient.

The disclosure provides variants of nicotine oxidoreductase and methods to select such variants that are unexpectedly active in the catabolic destruction of nicotine by oxidation using oxygen as electron acceptor, and catabolically active fragments thereof. Also disclosed are compositions comprising the CycN cytochrome c protein and at least one of the variant nicotine oxidoreductase holoenzymes, the fragments thereof, or a naturally occurring nicotine oxidoreductase, as well as fusion proteins comprising catalytically active nicotine oxidoreductase fragments or holoenzymes and CycN cytochrome c fragments or holoenzymes. Additionally, variants of L-6-hydroxynicotine oxidase, or catalytically active fragments thereof, are provided. Further disclosed are polynucleotides encoding such proteins, vectors comprising such polynucleotides, and host cells comprising such polynucleotides or vectors. Also provided are methods of using any of the disclosed compositions or formulations to treat nicotine dependence or reduce the risk of relapse to nicotine dependence.

The disclosure provides variants of nicotine oxidoreductase and methods to select such variants that are unexpectedly active in the catabolic destruction of nicotine by oxidation using oxygen as electron acceptor, and catabolically active fragments thereof. Also disclosed are compositions comprising the CycN cytochrome c protein and at least one of the variant nicotine oxidoreductase holoenzymes, the fragments thereof, or a naturally occurring nicotine oxidoreductase, as well as fusion proteins comprising catalytically active nicotine oxidoreductase fragments or holoenzymes and CycN cytochrome c fragments or holoenzymes. Additionally, variants of L-6-hydroxynicotine oxidase, or catalytically active fragments thereof, are provided. Further disclosed are polynucleotides encoding such proteins, vectors comprising such polynucleotides, and host cells comprising such polynucleotides or vectors. Also provided are methods of using any of the disclosed compositions or formulations to treat nicotine dependence or reduce the risk of relapse to nicotine dependence.

The present disclosure pertains to a composition for treatment of glutaric aciduria and an administration method therefor and, specifically, to a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treatment of glutaric aciduria and a method for treating glutaric aciduria, the method comprising a step of administering the pharmaceutical composition. Provided according to an aspect of the present disclosure are a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treating glutaric aciduria and a novel method for treating glutaric aciduria through in vivo administration of the pharmaceutical composition (intravenously and subcutaneously; i.v. and s. c.), whereby an excellent effect is brought about through in vivo administration remarkably easier than intraventricular administration, with the expectation of more effectively regulating and treating glutaric aciduria.