Abstract: The present invention relates to methods for identifying susceptibility of impaired hepatic wound healing in a patient, most particularly by identifying modifications of the of PPAR-? and TGF?1 genes. It further relates to stratifying populations of patients to determine susceptibility to impaired hepatic wound healing and direct appropriate healthcare resources. More specifically methods can be used to stratify liver disease patient populations to identify those most likely to progress to cirrhosis, or to identify the likelihood that a patient with liver disease will progress to having cirrhosis.

Abstract: The present invention relates to the discovery of an epigenetic relay pathway that controls hepatic stellate cell activation and the wound-healing response in fibrogenesis, including fibrogenesis of the injured liver. Methods of inhibiting fibrogenesis, including liver fibrogenesis and secondary disease states and conditions thereof, and in treating liver damage, including cirrhosis of the liver (which may be caused by viruses or chemicals, including alcohol), are aspects of the present invention. The methods utilize certain nucleoside compounds and/or antibodies which are optionally conjugated. Pharmaceutical compositions represent additional aspects of the invention.

Abstract: The present invention relates to methods for identifying susceptibility of impaired hepatic wound healing in a patient, most particularly by identifying modifications of the of PPAR-? and TGF?1 genes. It further relates to stratifying populations of patients to determine susceptibility to impaired hepatic wound healing and direct appropriate healthcare resources. More specifically methods can be used to stratify liver disease patient populations to identify those most likely to progress to cirrhosis, or to identify the likelihood that a patient with liver disease will progress to having cirrhosis.

Abstract: The present invention relates to the discovery of an epigenetic relay pathway that controls hepatic stellate cell activation and the wound-healing response in fibrogenesis, including fibrogenesis of the injured liver. Methods of inhibiting fibrogenesis, including liver fibrogenesis and secondary disease states and conditions thereof, and in treating liver damage, including cirrhosis of the liver (which may be caused by viruses or chemicals, including alcohol), are aspects of the present invention. The methods utilize certain nucleoside compounds and/or antibodies which are optionally conjugated. Pharmaceutical compositions represent additional aspects of the invention.

Abstract: Use of a compound of formula (I), or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for use as a Nuclear Factor-kB (NF-kB) inhibitor wherein: A has the following structure; Z is —COOH, —P(O)(OH)2 or —SO2OH; each R1 is the same or different and is halogen, hydroxy, C1-6 alkyl, C2-6 alkenyl, C2-6 alkynyl, C1-6 alkoxy, C1-6 alkylthio, thio, amino, mono(C1-6 alkyl)amino, di(C1-6 alkyl)amino, nitro, cyano or —CO2R?, wherein R? represents hydrogen or C1-6 alkyl; n is 0, 1, 2 or 3; R2 is hydrogen, C1-6 alkyl, C2-6 alkenyl or C2-6 alkynyl; Y is a linking group; and X is C1-6 alkyl, C2-6 alkenyl, C2-6 alkynyl, aryl, heteroaryl, carbocyclyl, heterocyclyl, -M-aryl, -M-heteroaryl, -M-carbocyclyl or -M-heterocyclyl, wherein M is C1-6 alkylene, C2-6 alkenylene, C2-6 alkynylene, -Q-Het-Q?- or -Q-Het- wherein Q and Q? are the same or different and are C1-6 alkylene, C2-6 alkenylene or C2-6 alkynylene and Het is selected from —NR?—, —O—, —S—, —SO2—, —SO—, —C(O)—O—, —OC(O), —CO—, —

Abstract: The present invention relates to an electronic game, including a housing, electronic circuitry positioned within the housing, and a display unit positioned within the housing and electrically coupled to the circuitry. A first sensor is electrically coupled to the circuitry and when activated initiates a first response from the circuitry. A second sensor electrically coupled to the circuitry and when activated prior to activating the first sensor initiates a second response from the circuitry.

Abstract: The present invention is based on the finding that the artificial induction of hepatic stellate cell (HSC) apoptosis in vivo can promote the resolution of liver fibrosis. Thus, the present invention provides methods for treating liver disease in a subject involving administration of an inducer of apoptosis which is capable of selectively inducing hepatic stellate cell apoptosis in the liver of the subject or of an agent which is capable of giving rise to such an inducer in the subject. In addition, the invention provides methods for treating liver fibrosis in a subject comprising the selective delivery of an inducer of apoptosis specifically to the hepatic stellate cells of the subject or of an agent which is capable of giving rise to an inducer of hepatic stellate cell apoptosis.

Abstract: Apparatus for the oral administration of capsules to animals, particularly ruminants such as sheep, comprises a tubular member adapted to be inserted into the animal's mouth so that the tip of the tubular member is near the root of the animal's tongue, means for introducing a capsule into the tubular member and for propelling the capsule to its tip, in which the tip of the tubular member consists of two tip portions extending from the mouth of the tubular member and laterally spaced from one another so as to define a cavity in which a capsule is deposited at the root of the animal's tongue. The top of the tubular member has a convexly curved upper surface adapted to engage the animal's soft palate to encourage a swallowing reaction, and a lower surface shaped to engage and restrain movement of the dorsum and the front part of the animal's tongue.