Abstract: Provided are isolated expanded human hepatocytes and methods of producing isolated expanded human hepatocytes. In certain embodiments, the methods comprise introducing human hepatocytes into the liver of a non-human in vivo bioreactor, expanding the human hepatocytes in the liver of the non-human in vivo bioreactor, and collecting hepatocytes from the liver of the non-human in vivo bioreactor. The collected hepatocytes comprise a xenomixture of expanded human hepatocytes and non-human in vivo bioreactor cells, including hepatocytes endogenous to the in vivo bioreactor. Such methods may further comprise subjecting the xenomixture to centrifugal elutriation under conditions sufficient to produce an elutriation fraction enriched for the expanded human hepatocytes, and/or removing non-human in vivo bioreactor cells from the elutriation fraction via a negative selection process. Also provided are isolated expanded human hepatocytes produced according to such methods.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV. The reagents are artificial miRNA (shmiRNA) used alone or in combination with additional shmiRNA or shRNA.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV. The reagents are artificial miRNA (shmiRNA) used alone or in combination with additional shmiRNA or shRNA.

Abstract: This disclosure relates to RNA interference (RNAi) reagents for treatment of hepatitis B virus (HBV) infection, compositions comprising same, and use thereof to treat individuals infected with HBV.

Abstract: This invention is directed to an RNA interference (RNAi) agent and the use of that RNAi agent to treat Age-related Macular Degeneration, as well as pharmaceutical compositions containing the RNAi agents of the invention. The RNAi agent is a DNA-directed RNA interference (ddRNAi) agent (being an RNA molecule), together with an expression cassette or construct to express that agent in a cell (including in vivo), for inhibiting, preventing or reducing expression of an AMD associated gene. Preferably that AMD associated gene is one that is associated with wet AMD.

Abstract: This invention is directed to an RNA interference (RNAi) agent and the use of that RNAi agent to treat Age-related Macular Degeneration, as well as pharmaceutical compositions containing the RNAi agents of the invention. The RNAi agent is a DNA-directed RNA interference (ddRNAi) agent (being an RNA molecule), together with an expression cassette or construct to express that agent in a cell (including in vivo), for inhibiting, preventing or reducing expression of an AMD associated gene. Preferably that AMD associated gene is one that is associated with wet AMD.

Abstract: This invention is directed to an RNA interference (RNAi) agent and the use of that RNAi agent to treat Age-related Macular Degeneration, as well as pharmaceutical compositions containing the RNAi agents of the invention. The RNAi agent is a DNA-directed RNA interference (ddRNAi) agent (being an RNA molecule), together with an expression cassette or construct to express that agent in a cell (including in vivo), for inhibiting, preventing or reducing expression of an AMD associated gene. Preferably that AMD associated gene is one that is associated with wet AMD.

Abstract: The ability of miR-181a to support active signaling between Notch and pre-TCR pathways by coordinately dampening negative regulators of these pathways allows the use of miR-181a as a therapeutic target for T-ALL.

Abstract: The ability of miR-181a to support active signaling between Notch and pre-TCR pathways by coordinately dampening negative regulators of these pathways allows the use of miR-181a as a therapeutic target for T-ALL.