Gut microbes with the genes determine TMAO production from L-carnitine intake and serve as a biomarker for precision nutrition.

Gut microbial metabolism of L-carnitine, which leads to the production of detrimental trimethylamine N-oxide (TMAO), offers a plausible link between red meat consumption and cardiovascular risks. Several microbial genes, including , the operon, and the recently identified gene cluster, have been implicated in the conversion of dietary L-carnitine into TMA(O). However, the key microbial genes and associated gut microbes involved in this pathway have not been fully explored.

Optimally Miscible Polymer Bulk-Heterojunction-Particles for Nonsurfactant Photocatalytic Hydrogen Evolution.

Mini-emulsion and nanoprecipitation techniques relied on large amounts of surfactants, and unresolved miscibility issues of heterojunction materials limited their efficiency and applicability in the past. Through our molecular design and developed surfactant-free precipitation method, we successfully fabricated the best miscible bulk-heterojunction-particles (BHJP) ever achieved, using donor () and acceptor () polymers. The structural similarity ensures optimal miscibility, as supported by the interaction parameter of the / blend is positioned very close to the binodal curve.

Preclinical development of lentiviral vector gene therapy for Diamond-Blackfan anemia syndrome.

Diamond-Blackfan anemia syndrome (DBAS) is an inherited bone marrow failure disorder caused by haploinsufficiency of ribosomal protein genes, most commonly RPS19. Limited access to patient hematopoietic stem/progenitor cells (HSPCs) is a major roadblock to developing novel therapies for DBAS. We developed a novel self-inactivating third-generation RPS19-encoding lentiviral vector (LV), termed "SJEFS-S19", for DBAS gene therapy.

Stattic suppresses p‑STAT3 and induces cell death in T‑cell acute lymphoblastic leukemia.

The present study investigated the therapeutic potential of Stattic, a selective inhibitor of STAT3, in treating T‑cell acute lymphoblastic leukemia (T‑ALL). The effects of Stattic on cell viability, STAT3 phosphorylation, apoptosis and autophagy in T‑ALL cell lines, and on tumor growth in a xenograft mouse model of T‑ALL, were assessed. Methods, including the Cell Counting Kit‑8 assay for cell viability, propidium iodide/Annexin V staining for apoptosis detection, western blotting for protein expression analysis, and a xenograft mouse model for evaluating tumor growth, were employed.