Pim1 is Critical in T-cell-independent B-cell Response and MAPK Activation in B Cells.

The Pim family consists of three members that encode a distinct class of highly conserved serine/threonine kinases. In this study, we generated and examined mice with hematopoiesis-specific deletion of Pim1 and bone marrow (BM) chimeric mice with B-cell-specific targeted deletion of Pim1. Pim1 was expressed at all stages of B-cell development and hematopoietic-specific deletion of Pim1 altered B-cell development in BM, spleen and peritoneal.

Madecassoside alleviates acute kidney injury by regulating JNK-mediated oxidative stress and programmed cell death.

Background: Acute kidney injury (AKI) has high morbidity and mortality, which is manifested by inflammation and apoptosis. Effective treatment methods for AKI are currently lacking.

Objective: This study demonstrated the protecting effects of Madecassoside (MA) in the cisplatin- and hypoxia-reoxygenation-induced renal tubular epithelial cells in vitro and AKI mice in vivo.

Immune regulatory effects of microRNA9-3.

MicroRNAs are known to regulate cell proliferation, differentiation, and apoptosis. However, the immunological mechanism and role of microRNA9-3 (miR9-3) are unknown. This study used CRISPR/cas9 technology to knock out miR9-3 to modulate its expression level.

Potential implication of N-acetylcysteine detoxification on adhesive endodontics.

Methacrylate resin-based dentin adhesives and root canal sealers used for bonding of filling materials inside the root canal system are cytotoxic and result in reduction in cell proliferation to a variable extent. An in vitro study to examine the detoxifying effects of N-acetylcysteine (NAC) on four commercial adhesive systems on adhesive-induced cytotoxicity and cell survival was conducted so that the use of methacrylate resin-based materials for filling root canals could be optimized. The finding that NAC co-treatment protected the cells from adhesive-induced toxicity by increasing cellular proliferation, attenuating cell cycle arrest, and reducing cell death suggests the null hypothesis that NAC has no effect on dentin adhesive-induced cell death and cell cycle arrest should be rejected.