The present invention relates to a carbohydrate-based peritoneal dialysis fluid, containing a compound selected from the group consisting of glutamine, preferably L-glutamine; a dipeptide capable of releasing glutamine, L-glutamine in free form, preferably selected from the group consisting of glutaminyl-glycine, glycinyl-glutamine, glutaminyl-alanine, alanyl-glutamine; an oligopeptide consisting of two to seven glutamine, preferably L-glutamine residues; and mixtures thereof. The peritoneal dialysis fluids of the present invention are useful for inhibition of technical failure in a person undergoing peritoneal dialysis treatment.

The present invention relates to a carbohydrate-based peritoneal dialysis fluid, containing a compound selected from the group consisting of glutamine, preferably L-glutamine; a dipeptide capable of releasing glutamine, L-glutamine in free form, preferably selected from the group consisting of glutaminyl-glycine, glycinyl-glutamine, glutaminyl-alanine, alanyl-glutamine; an oligopeptide consisting of two to seven glutamine, preferably L-glutamine residues; and mixtures thereof. The peritoneal dialysis fluids of the present invention are useful for inhibition of technical failure in a person undergoing peritoneal dialysis treatment.

A topical composition comprising ginger, curcumin, one or more of glutathione, MSM, Vitamin C, hyaluronic acid, sodium lauryl sulfate, Vitamin D and Vitamin E, and a carrier, wherein each of the glutathione, MSM, Vitamin C, hyaluronic acid, sodium lauryl sulfate, Vitamin D, and Vitamin E. When applied to human skin or animal skin, the composition can improve the appearance of skin and speed up wound healing.

A method is provided for treating a subject for a viral infection. The method includes diagnosing the subject as having a viral infection, and administering a pharmaceutically effective amount of a pharmaceutical composition to the subject. The pharmaceutical composition includes a poly-N-substituted glycine compound of a formula AX-Y-Z.sub.n—B, wherein A is a terminal N-alkyl substituted glycine residue; n is an integer; B is selected from the group consisting of NH.sub.2, one and two N-substituted glycine residues, and wherein said one and two N-substituted glycine residues have N-substituents which are independently selected from natural α-amino acid side chain moieties, isomers and carbon homologs thereof; X, Y and Z are independently selected from the group consisting of N-substituted glycine residues, wherein said N-substituents are independently selected from the group consisting of natural α-amino acid side chain moieties, isomers and carbon homologs thereof, and proline residues. In some embodiments, at least one of A, B, X, Y and Z contains a halogen-bearing moiety.

A method is provided for treating a subject for a viral infection. The method includes diagnosing the subject as having a viral infection, and administering a pharmaceutically effective amount of a pharmaceutical composition to the subject. The pharmaceutical composition includes a poly-N-substituted glycine compound of a formula AX-Y-Z.sub.n—B, wherein A is a terminal N-alkyl substituted glycine residue; n is an integer; B is selected from the group consisting of NH.sub.2, one and two N-substituted glycine residues, and wherein said one and two N-substituted glycine residues have N-substituents which are independently selected from natural α-amino acid side chain moieties, isomers and carbon homologs thereof; X, Y and Z are independently selected from the group consisting of N-substituted glycine residues, wherein said N-substituents are independently selected from the group consisting of natural α-amino acid side chain moieties, isomers and carbon homologs thereof, and proline residues. In some embodiments, at least one of A, B, X, Y and Z contains a halogen-bearing moiety.

The present invention relates to peptides for the treatment or prevention of nonalcoholic fatty liver disease (NAFLD), non-alcoholic fatty liver (NAFL), non-alcoholic steatohepatitis (NASH), hepatic steatosis (fatty liver), liver inflammation, cirrhosis, hepatocellular carcinoma or fibrosis, especially liver fibrosis.

The present invention relates to a composition for inhibiting the toxicity with respect to nanoparticles and particulate matters generated from the environment. Since it has been confirmed that a decrease in intracellular ATP, a decrease in cell viability, inflammation-induced morphological changes in cells and cell activation, which are induced by nanoparticles or environmentally-derived particulate matters, are inhibited by means of the composition of the present invention, the composition may be utilized as a reducing substance for the toxicity of nanoparticles and particulate matters.

The present invention relates to a composition for inhibiting the toxicity with respect to nanoparticles and particulate matters generated from the environment. Since it has been confirmed that a decrease in intracellular ATP, a decrease in cell viability, inflammation-induced morphological changes in cells and cell activation, which are induced by nanoparticles or environmentally-derived particulate matters, are inhibited by means of the composition of the present invention, the composition may be utilized as a reducing substance for the toxicity of nanoparticles and particulate matters.

Pharmaceutical compositions of the invention include substituted riluzole prodrugs useful for the treatment of cancers including melanoma, breast cancer, brain cancer, and prostate cancer through the release of riluzole. Prodrugs of riluzole have enhanced stability to hepatic metabolism and are delivered into systemic circulation by oral administration, and then cleaved to release riluzole in the plasma via either an enzymatic or general biophysical release process.

The present disclosure relates to, inter alia, a method of treating cancer in a human patient in need thereof, comprising administering a therapeutically effective amount of a substrate of AKR1B1, AKR1B10, or both to said patient, wherein said patient has, or is suspected to have, cancer cells with elevated levels of AKR1B1, AKR1B10, or both, wherein said substrate is not 2-deoxy-D-glucose.