A composition includes two exogenous enzymes from animals for consumption by human beings to prevent, treat and/or alleviate veisalgia and/or symptoms associated therewith arising from or caused by consumption or spontaneous production of alcohol through a dual-enzyme based breakdown of the alcohol, wherein a first enzyme of the two exogenous enzymes is capable of converting alcohol into a first metabolite while a second enzyme thereof is capable of converting the first metabolite into a second metabolite which is excretable to systemic circulation after an oxidation reaction of the alcohol in the presence of the two exogenous enzymes and NAD.sup.+/NADH, and wherein the first enzyme to the second enzyme is in a molar ratio of 1:3-51 in the composition in order to avoid an elevation in the level of the first metabolite in the human being.

Methods of and compositions for producing and using plant-based materials are provided. The methods include using biopolymers or their synthetic equivalents combined with a stable source of reactive oxygen species that when applied to or combined with a separate source of oxido-reducing enzyme or catalyst will cause the formation of an activated biopolymer with increased protein binding affinity and microbial control activities.

Methods of and compositions for producing and using plant-based materials are provided. The methods include using biopolymers or their synthetic equivalents combined with a stable source of reactive oxygen species that when applied to or combined with a separate source of oxido-reducing enzyme or catalyst will cause the formation of an activated biopolymer with increased protein binding affinity and microbial control activities.

Maple syrup urine disease (MSUD) is a rare autosomal recessive disease with an incidence that is caused by a defective activity of the branched-chain 2-keto acid dehydrogenase (BCKD) leading to accumulation of branched-chain amino acids (BCAA) leucine, isoleucine, valine and their corresponding alpha-ketoacids (BCKA) in tissues and body fluids. The inventors herein characterized the Bckdha.sup.−/− mouse and Bckdhb.sup.−/− mouse recapitulating the classical forms of MSUD. As a proof of concept, they developed a (liver-directed) AAV gene therapy based on the transfer of human BCKDHA (hBCKDHA) or BCKDHB (hBCKDHB) mediated by AAV8 during immediate neonatal period in Bckdha−/− or Bckdhb.sup.−/− mice. The inventors demonstrated that hBCKDHA gene transfer completely rescued the lethal early-onset phenotype of Bckdha−/− mice allowing long-term survival to age 12 months, at which they were systematically sacrificed, without overt phenotypic abnormalities. They also demonstrated that hBCKDHB gene transfer exhibited similar survival and a normal growth without overt phenotypic abnormalities at age 3 months, with a dramatic improvement of the biochemical phenotype. The present invention relates to a method of treating MSUD by gene therapy.

Maple syrup urine disease (MSUD) is a rare autosomal recessive disease with an incidence that is caused by a defective activity of the branched-chain 2-keto acid dehydrogenase (BCKD) leading to accumulation of branched-chain amino acids (BCAA) leucine, isoleucine, valine and their corresponding alpha-ketoacids (BCKA) in tissues and body fluids. The inventors herein characterized the Bckdha.sup.−/− mouse and Bckdhb.sup.−/− mouse recapitulating the classical forms of MSUD. As a proof of concept, they developed a (liver-directed) AAV gene therapy based on the transfer of human BCKDHA (hBCKDHA) or BCKDHB (hBCKDHB) mediated by AAV8 during immediate neonatal period in Bckdha−/− or Bckdhb.sup.−/− mice. The inventors demonstrated that hBCKDHA gene transfer completely rescued the lethal early-onset phenotype of Bckdha−/− mice allowing long-term survival to age 12 months, at which they were systematically sacrificed, without overt phenotypic abnormalities. They also demonstrated that hBCKDHB gene transfer exhibited similar survival and a normal growth without overt phenotypic abnormalities at age 3 months, with a dramatic improvement of the biochemical phenotype. The present invention relates to a method of treating MSUD by gene therapy.

This invention relates to formulations of uric acid lowering agent(s) (UALA) designed to inhibit xanthine oxidase and/or decrease serum or tissue uric acid concentration for the treatment and prevention of morbidities and mortality during viral infection. For example, acute kidney injury due to coronavirus infection by administering a therapeutically effective amount of an agent capable of inhibiting xanthine oxidase and/or decreasing uric acid levels in a patient in need of such treatment. Additionally, the scope of the invention includes a method of treating and preventing acute kidney injury and health consequences due to coronavirus infection.

This invention relates to formulations of uric acid lowering agent(s) (UALA) designed to inhibit xanthine oxidase and/or decrease serum or tissue uric acid concentration for the treatment and prevention of morbidities and mortality during viral infection. For example, acute kidney injury due to coronavirus infection by administering a therapeutically effective amount of an agent capable of inhibiting xanthine oxidase and/or decreasing uric acid levels in a patient in need of such treatment. Additionally, the scope of the invention includes a method of treating and preventing acute kidney injury and health consequences due to coronavirus infection.

This invention relates to formulations of uric acid lowering agent(s) (UALA) designed to inhibit xanthine oxidase and/or decrease serum or tissue uric acid concentration for the treatment and prevention of morbidities and mortality during viral infection. For example, acute kidney injury due to coronavirus infection by administering a therapeutically effective amount of an agent capable of inhibiting xanthine oxidase and/or decreasing uric acid levels in a patient in need of such treatment. Additionally, the scope of the invention includes a method of treating and preventing acute kidney injury and health consequences due to coronavirus infection.

The present invention discloses anti-cancer compositions, and associated methods, including an anti-cancer composition comprising: a cellular energy inhibitor having the structure according to formula I ##STR00001## wherein X is selected from the group consisting of: a nitro, an imidazole, a halide, sulfonate, a carboxylate, an alkoxide, and amine oxide; and R is selected from the group consisting of: OR′, N(R″).sub.2, C(O)R′″, C1-C6 alkyl, C6-C12 aryl, C1-C6 heteroalkyl, a C6-C12 heteroaryl, H, and an alkali metal; where R′ represents H, alkali metal, C1-C6 alkyl, C6-C12 aryl or C(O)R′″, R″ represents H, C1-C6 alkyl, or C6-C12 aryl, and R′″ represents H, C1-C20 alkyl or C6-C12 aryl. The anti-cancer composition can additionally comprise at least one sugar, which stabilizes the cellular energy inhibitor by substantially preventing the inhibitor from hydrolyzing. Also, the anti-cancer composition can comprise a hexokinase inhibitor. Further, the anti-cancer composition can comprise a biological buffer that is present in an amount sufficient to at least partially deacidify the cellular energy inhibitor and neutralize metabolic by-products of the cellular energy inhibitor.

The present invention discloses anti-cancer compositions, and associated methods, including an anti-cancer composition comprising: a cellular energy inhibitor having the structure according to formula I ##STR00001## wherein X is selected from the group consisting of: a nitro, an imidazole, a halide, sulfonate, a carboxylate, an alkoxide, and amine oxide; and R is selected from the group consisting of: OR′, N(R″).sub.2, C(O)R′″, C1-C6 alkyl, C6-C12 aryl, C1-C6 heteroalkyl, a C6-C12 heteroaryl, H, and an alkali metal; where R′ represents H, alkali metal, C1-C6 alkyl, C6-C12 aryl or C(O)R′″, R″ represents H, C1-C6 alkyl, or C6-C12 aryl, and R′″ represents H, C1-C20 alkyl or C6-C12 aryl. The anti-cancer composition can additionally comprise at least one sugar, which stabilizes the cellular energy inhibitor by substantially preventing the inhibitor from hydrolyzing. Also, the anti-cancer composition can comprise a hexokinase inhibitor. Further, the anti-cancer composition can comprise a biological buffer that is present in an amount sufficient to at least partially deacidify the cellular energy inhibitor and neutralize metabolic by-products of the cellular energy inhibitor.