Abstract: This invention provides methods for preventing, treating or ameliorating one or more symptoms of a malignant tumor in a mammal in need thereof, by administering to the mammal a therapeutically effective amount of a composition comprising RNAi molecules, where the RNAi molecules can be active in reducing expression of Hsp47.

Abstract: This invention provides methods and compositions for preventing, treating or ameliorating one or more symptoms of a malignant tumor associated with KRAS mutation in a mammal in need thereof, by identifying a tumor cell in the mammal, the tumor cell comprising at least one of: (i) a mutation of the KRAS gene, and (ii) an aberrant expression level of KRAS protein; and administering to the mammal a therapeutically effective amount of a composition comprising one or more RNAi molecules that are active in reducing expression of GST-?.

Abstract: This invention provides methods and compositions for preventing, treating or ameliorating one or more symptoms of a malignant tumor associated with KRAS mutation in a mammal in need thereof, by identifying a tumor cell in the mammal, the tumor cell comprising at least one of: (i) a mutation of the KRAS gene, and (ii) an aberrant expression level of KRAS protein; and administering to the mammal a therapeutically effective amount of a composition comprising one or more RNAi molecules that are active in reducing expression of GST-?.

Abstract: The present invention relates to a wet start-up method for hydrogenation unit, an energy-saving hydrogenation process, and a hydrogenation apparatus. The method involves heating a start-up activating oil to a specific temperature and flowing the heated oil through a bed of hydrogenation catalyst bed, so that the temperature at the catalyst bed layer is increased to 180±10° C. or above by means of heat exchange and the reaction heat generated from activation in the start-up method.

Abstract: Compounds having activity as PKM2 activators are disclosed. The compounds have the following structure (I): including stereoisomers, tautomers, pharmaceutically acceptable salts and prodrugs thereof, wherein R1, R2, R3, R4, R5 and R6 are as defined herein. Methods associated with preparation and use of such compounds, as well as pharmaceutical compositions comprising such compounds, are also disclosed.

Abstract: This invention provides compositions and methods for preventing or treating a malignant tumor in a mammal in need thereof, by administering to the mammal a therapeutically effective amount of a composition comprising RNAi molecules, which RNAi molecules can be active in reducing expression of Hsp47, or a combination of RNAi molecules active for Hsp47 and p21.

Abstract: Compounds having activity as PKM2 activators are disclosed. The compounds have the following structure (I): including stereoisomers, tautomers, pharmaceutically acceptable salts and prodrugs thereof, wherein R1, R2, R3, R4, R5 and R6 are as defined herein. Methods associated with preparation and use of such compounds, as well as pharmaceutical compositions comprising such compounds, are also disclosed.

Abstract: This invention provides methods and compositions for preventing, treating or ameliorating one or more symptoms of a malignant tumor associated with KRAS mutation in a mammal in need thereof, by identifying a tumor cell in the mammal, the tumor cell comprising at least one of: (i) a mutation of the KRAS gene, and (ii) an aberrant expression level of KRAS protein; and administering to the mammal a therapeutically effective amount of a composition comprising one or more RNAi molecules that are active in reducing expression of GST-?.

Abstract: This invention provides compositions for use in distributing active agents for treating a malignant tumor in a subject. The compositions contain RNAi molecules targeted to a human GST-?, along with RNAi molecules targeted to a human p21, and a pharmaceutically acceptable carrier. The carrier can include nanoparticles composed of an ionizable lipid, a structural lipid, one or more stabilizer lipids, and a lipid for reducing immunogenicity of the nanoparticles. This invention further provides methods for preventing or treating a malignant tumor by administering a therapeutically effective amount of an RNAi composition.

Abstract: Compounds having activity as PKM2 activators are disclosed. The compounds have the following structure (I): including stereoisomers, tautomers, pharmaceutically acceptable salts and prodrugs thereof, wherein R1, R2, R3, R4, R5 and R6 are as defined herein. Methods associated with preparation and use of such compounds, as well as pharmaceutical compositions comprising such compounds, are also disclosed.

Abstract: Polymer conjugates characterized in that the backbone of the polymer is an anionic polymer and hydrophobic moieties are covalently attached to the polymer backbone are useful for preparing drug encapsulated polymer hydrotropes and compositions. Such materials are useful in methods for delivering the drug into cells, and for the treatment and alleviation of diseases and disorders such as cancer.

Abstract: The present invention relates to a wet start-up method for hydrogenation unit, an energy-saving hydrogenation process, and a hydrogenation apparatus. The method involves heating a start-up activating oil to a specific temperature and flowing the heated oil through a bed of hydrogenation catalyst bed, so that the temperature at the catalyst bed layer is increased to 180±10° C. or above by means of heat exchange and the reaction heat generated from activation in the start-up method.

Abstract: Disclosed are methods and compositions relating to the use of PKC-? activators in the treatment of disease.

Abstract: Phospholipid scramblase 3 (PLS3) is a newly recognized member of a family of proteins responsible for phospholipid translocation between two lipid compartments. A novel isoform of PLS3 is identified and characterized herein. The function of PLS3 in mitochondria was disrupted, yielding an inactive mutant PLS3(F258V). Cells transfected with PLS3(F258V) exhibited reduced proliferative capacity that was unaffected by the presence of Na3N. PLS3(F258V)-expressing cells exhibit abnormal mitochondrial metabolism and structure and were associated with decreased sensitivity to UV- and tBid-induced apoptosis, and diminished translocation of cardiolipin to the outer mitochondrial membrane. Cells transfected with wild-type PLS3 displayed increased sensitivity to apoptosis and enhanced cardiolipin translocation. These studies identify PLS3 as a regulator of mitochondrial structure and respiration, and cardiolipin transport in apoptosis.