Abstract: The invention provides a method for treating or ameliorating the clinical manifestations of congenital erythropoietic porphyria in an animal (e.g. a human) by administering a retinoid to the animal.

Abstract: Provided herein are compositions methods for the treatment and/or prevention of liver injury. In particular, carbamoyl phosphate synthetase-1 (CPS-I) peptides and polypeptides (e.g., enzymatically active or inactive CPS-I peptides and polypeptides), and methods of use thereof for the treatment and/or prevention of liver injury are provided.

Abstract: Provided herein are compositions methods for the treatment and/or prevention of tissue or internal organ injury. In particular, carbamoyl phosphate synthatase-1 (CPS-1) peptides and polypeptides (e.g., enzymatically active or inactive CPS-1 peptides and polypeptides), and methods of use thereof for the treatment and/or prevention of disease that results in tissue injury are provided.

Abstract: Provided herein are biomarkers of acute liver injury (ALI), which includes acute liver failure, and methods of diagnosing ALI and/or monitoring treatment and prognosis therewith. In particular, serum levels of carbamoyl phosphate synthatase-1 (CPS1) are detected to diagnose and/or monitor treatment and prognosis of ALI.

Abstract: Provided herein are biomarkers of acute liver injury (ALI), which includes acute liver failure, and methods of diagnosing ALI and/or monitoring treatment and prognosis therewith. In particular, serum levels of carbamoyl phosphate synthatase-1 (CPS1) are detected to diagnose and/or monitor treatment and prognosis of ALI.

Abstract: Keratin 8 and 18 (K8/K18) mutations are shown to be associated with a predisposition to liver or biliary tract disease, particularly noncryptogenic hepatobiliary disease. Unique K8/K18 mutations are shown in patients with diseases including but without limitation to viral hepatitis, biliary atresia, alcoholic cirrhosis and other acute or chronic toxic liver injury, cryptogenic cirrhosis, acute fulminant hepatitis, autoimmune liver disease, cystic fibrosis, primary biliary cirrhosis, primary sclerosing cholangitis, diseases that are linked with cryptogenic cirrhosis, such as nonalcoholic steatohepatitis, and the like. Livers with keratin mutations had increased incidence of cytoplasmic filamentous deposits. Therefore, K8/K18 are susceptibility genes for developing cryptogenic and noncryptogenic forms of liver disease. Mutant alleles are associated with disease susceptibility, and their detection is used in the diagnosis of a predisposition to these conditions.

Abstract: Keratin 8 and 18 (K8/K18) mutations are shown to be associated with a predisposition to liver or biliary tract disease, particularly noncryptogenic hepatobiliary disease. Unique K8/K18 mutations are shown in patients with diseases including but without limitation to viral hepatitis, biliary atresia, alcoholic cirrhosis and other acute or chronic toxic liver injury, cryptogenic cirrhosis, acute fulminant hepatitis, autoimmune liver disease, cystic fibrosis, primary biliary cirrhosis, primary sclerosing cholangitis, diseases that are linked with cryptogenic cirrhosis, such as nonalcoholic steatohepatitis, and the like. Livers with keratin mutations had increased incidence of cytoplasmic filamentous deposits. Therefore, K8/K18 are susceptibility genes for developing cryptogenic and noncryptogenic forms of liver disease. Mutant alleles are associated with disease susceptibility, and their detection is used in the diagnosis of a predisposition to these conditions.

Abstract: Keratin 8 and 18 (K8/K18) mutations are shown to be associated with a predisposition to liver or biliary tract disease, particularly noncryptogenic hepatobiliary disease. Unique K8/K18 mutations are shown in patients with diseases including but without limitation to viral hepatitis, biliary atresia, alcoholic cirrhosis and other acute or chronic toxic liver injury, cryptogenic cirrhosis, acute fulminant hepatitis, autoimmune liver disease, cystic fibrosis, primary biliary cirrhosis, primary sclerosing cholangitis, diseases that are linked with cryptogenic cirrhosis, such as nonalcoholic steatohepatitis, and the like. Livers with keratin mutations had increased incidence of cytoplasmic filamentous deposits. Therefore, K8/K18 are susceptibility genes for developing cryptogenic and noncryptogenic forms of liver disease. Mutant alleles are associated with disease susceptibility, and their detection is used in the diagnosis of a predisposition to these conditions.

Abstract: The present invention provides a method of treating pancreatitis comprising administering to a human in need thereof an effective amount of hemin. The administration of hemin is preferably parenteral. In another aspect, the present invention provides a method of pancreatitis prophylaxis comprising administering to a human in need thereof an effective amount of hemin. In a still further aspect, the present invention contemplates a method of inducing an HO gene comprising administering to a human in need thereof an HO-inducing effective amount of hemin. Preferably, the HO gene is the HO-1 gene. In a still further aspect, the present invention contemplates a method of inducing an HO gene in leukocytes for recruitment to the pancreas to treat pancreatitis comprising administering to a human in need thereof an HO-inducing effective amount of hemin.

Abstract: The present invention provides a method of treating pancreatitis comprising administering to a human in need thereof an effective amount of hemin. The administration of hemin is preferably parenteral. In another aspect, the present invention provides a method of pancreatitis prophylaxis comprising administering to a human in need thereof an effective amount of hemin. In a still further aspect, the present invention contemplates a method of inducing an HO gene comprising administering to a human in need thereof an HO-inducing effective amount of hemin. Preferably, the HO gene is the HO-1 gene. In a still further aspect, the present invention contemplates a method of inducing an HO gene in leukocytes for recruitment to the pancreas to treat pancreatitis comprising administering to a human in need thereof an HO-inducing effective amount of hemin.

Abstract: Monoclonal antibodies are produced for a glycoprotein which is selectively expressed on the surface of human proliferating and immature hematopoietic cells but which is absent from normal peripheral blood cells. Mice are inoculated with human hematopoietic cells or fragments thereof, and spleen cells obtained from the mice are fused with mice myeloma cells to product hybridomas. The hybridomas are cultured as clones, and antibodies obtained from the individual clones are tested for their specificity for hematopoietic cells. Clones which produce antibodies specific for proliferating and immature hematopoietic cells are selected for further culturing to produce the antibody, and the antibody is obtained from the culture growth medium or from ascitic fluid of mice bearing the hybridoma tumor.