The present disclosure relates to RNAi agents, e.g., double stranded RNAi agents, able to inhibit 17P-hydroxy steroid dehydrogenase type 13 (HSD17B13 or 17β-H8013) gene expression. Also disclosed are pharmaceutical compositions that include HSD17B13 RNAi agents and methods of use thereof. The HSD17B13 RNAi agents disclosed herein may be conjugated to targeting ligands to facilitate the delivery′ to cells, including to hepatocytes. Delivery 7 of the HSD17B13 RNAi agents in vivo provides for inhibition of HSD17B13 gene expression. The RNAi agents can be used in methods of treatment of HSD17B13-related diseases and disorders, including non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hepatic fibrosis, and alcoholic or non-alcoholic liver diseases, including cirrhosis.

The present invention relates to methods and compositions for reducing the risk and severity of vancomycin-resistant Enterococci infection or colonization. It is based, at least in part, on the discovery that a restricted fraction of the gut microbiota, including the bacteria Clostridium scindens and/or the bacteria Blautia producta contribute substantially to resistance against vancomycin-resistant Enterococci infection or colonization. Without being bound by any particular theory, it is believed that this is achieved through the biosynthesis of secondary bile acids in the case of Clostridium scindens.

The present disclosure relates to the use of an amino acid dehydrogenase in combination with a cofactor regenerating system comprising a ketoreductase. In particular embodiments, the process can be used to prepare L-tert-leucine using a leucine dehydrogenase.

Methods, compounds, and compositions useful for inhibiting HSD17B13 expression are provided. Such compounds, compositions, and methods are useful for treating, preventing, or ameliorating a disease associated with HSD 17B 13.

The present invention relates to an NADP(H) nanosensor comprising i) a nucleic acid sequence to which a regulator is capable of binding, wherein the oxidation state of the regulator depends on the NADP(H) availability; ii) a promoter sequence following the nucleic acid sequence i), to which an RNA polymerase is capable of binding, wherein the affinity of the RNA polymerase for the promoter sequence is influenced by the oxidation state of the regulator; iii) a nucleic acid sequence which is under the control of the promoter sequence ii) and which codes for an autofluorescent protein.

The present invention also relates to a cell, a method for isolating genes which code for NADP(H)-dependent enzymes, and the use of an NADP(H) nanosensor.

The present invention relates to RNAi constructs for reducing expression of the HSD17B13 gene. Methods of using such RNAi constructs to treat or prevent liver disease, nonalcoholic fatty liver disease (NAFLD) are also described.

Methods, compounds, and compositions useful for inhibiting HSD expression are provided. Such compounds, compositions, and methods are useful for treating, preventing, or ameliorating a disease associated with HSD 17B 13.

The present invention relates to methods and compositions for reducing the risk and severity of vancomycin-resistant Enterococci infection or colonization. It is based, at least in part, on the discovery that a restricted fraction of the gut microbiota, including the bacteria Clostridium scindens and/or the bacteria Blautia producta contribute substantially to resistance against vancomycin-resistant Enterococci infection or colonization. Without being bound by any particular theory, it is believed that this is achieved through the biosynthesis of secondary bile acids in the case of Clostridium scindens.

The present disclosure relates to non-naturally occurring polypeptides useful for preparing Ezetimibe, polynucleotides encoding the polypeptides, and methods of using the polypeptides.

Compositions of peritoneal dialysis solutions and metabolizing enzymes, and their uses to treat disorders associated with elevated levels of metabolites are disclosed. Animal models of hyperoxalemia are also disclosed.