The present invention is a method and composition for the treatment of skin conditions where the epidermal barrier has decreased function such as when the patient is suffering from eczema, in particular, Atopic Dermatitis. Epidermal barrier function can be significantly improved and the extraction of epidermal lipids can be reduced by using formulations containing high Krafft temperature surfactants, preferably, anionic surfactants.

The present invention is a method and composition for the treatment of skin conditions where the epidermal barrier has decreased function such as when the patient is suffering from eczema, in particular, Atopic Dermatitis. Epidermal barrier function can be significantly improved and the extraction of epidermal lipids can be reduced by using formulations containing high Krafft temperature surfactants, preferably, anionic surfactants.

A method for increasing susceptibility of microorganisms to antibiotics includes providing a microorganism; administering an antibiotic including a nitro-containing amphenicol compound to the microorganism; and administering any of an uronic, aldonic, ulosonic, and aldaric feedstock to the microorganism. The feedstock is adapted to promote cell metabolism, and inhibit antibiotic inactivation pathways in the microorganism causing increased sensitivity of the microorganism to the nitro-containing amphenicol.

A method for increasing susceptibility of microorganisms to antibiotics includes providing a microorganism; administering an antibiotic including a nitro-containing amphenicol compound to the microorganism; and administering any of an uronic, aldonic, ulosonic, and aldaric feedstock to the microorganism. The feedstock is adapted to promote cell metabolism, and inhibit antibiotic inactivation pathways in the microorganism causing increased sensitivity of the microorganism to the nitro-containing amphenicol.

The present application provides methods of functionalizing an organ or tissue of a mammal by administering a nutrient (e.g., peracetylated N-azido galactosamine Ac4GalNAz) to the mammal or by culturing an organ or tissue in a bioreactor containing such nutrient. The present application also provides methods of selectively functionalizing extracellular matrix (ECM) of an organ or tissue of a mammal by administering a nutrient (e.g., peracetylated N-azido galactosamine Ac4GalNAz) to the mammal. In some aspects, the present application provides a decellularized scaffold of a mammalian organ or tissue comprising an extracellular matrix, wherein the extracellular matrix of the decellularized scaffold is functionalized with a chemical group that is reactive in a bioorthogonal chemical reaction, such as an azide chemical group. The present application also provides biological prosthetic mesh and mammalian organs and tissues for transplantation prepared according to the methods of the application.

The present application provides methods of functionalizing an organ or tissue of a mammal by administering a nutrient (e.g., peracetylated N-azido galactosamine Ac4GalNAz) to the mammal or by culturing an organ or tissue in a bioreactor containing such nutrient. The present application also provides methods of selectively functionalizing extracellular matrix (ECM) of an organ or tissue of a mammal by administering a nutrient (e.g., peracetylated N-azido galactosamine Ac4GalNAz) to the mammal. In some aspects, the present application provides a decellularized scaffold of a mammalian organ or tissue comprising an extracellular matrix, wherein the extracellular matrix of the decellularized scaffold is functionalized with a chemical group that is reactive in a bioorthogonal chemical reaction, such as an azide chemical group. The present application also provides biological prosthetic mesh and mammalian organs and tissues for transplantation prepared according to the methods of the application.

Disclosed are improved compositions and methods for decreasing blood glucagon levels. As disclosed herein, L-glutamine is a selective stimulator of α-cell proliferation generated when glucagon signaling is interrupted. Therefore, disclosed is a method for treating a subject with hyperglucagonemia, e.g., a subject with diabetes, that involves administering to the subject a composition comprising an L-glutamine inhibitor in an amount effective to decrease blood glucagon levels.

Disclosed are improved compositions and methods for decreasing blood glucagon levels. As disclosed herein, L-glutamine is a selective stimulator of α-cell proliferation generated when glucagon signaling is interrupted. Therefore, disclosed is a method for treating a subject with hyperglucagonemia, e.g., a subject with diabetes, that involves administering to the subject a composition comprising an L-glutamine inhibitor in an amount effective to decrease blood glucagon levels.

A method for inducing a sustained immune response in humans or animal patient suffering from human immunodeficiency virus (HIV) acquired immune deficiency syndrome (AIDS, autoimmune disease, cancer, inflammation, and neurodegenerative diseases comprises daily administration to such patients a single oral tablet, rapidly dissolving film, capsule, liquid or cream dose of an Immediate release naltrexone composition comprising between about 0.01 to about 10 mg of naltrexone. In order to provide a benefit the naltrexone must be an Immediate release composition comprising between about 0.01 and about 10 mg of naltrexone.

The present disclosure describes a method to treat conditions, including bacterial infections and cancer, using a photosensitive compound that, upon exposure to white light, can be activated. The photosensitive compound can also interact synergistically with antibiotics used concomitantly to kill drug-resistant bacteria. The photosensitive compounds can also be used to inhibit the proliferation of cancer cells.