Unveiling heterointerface activation effects with different titanium dioxide crystal phases for electrocatalytic nitrate-to-ammonia reduction.

Nitrate pollution poses severe risks to aquatic ecosystems and human health. The electrocatalytic nitrate reduction reaction (NITRR) offers a promising environmental and economic solution for nitrate pollution treatment and nitrogen source recovery; however, it continues to experience limited efficiency in neutral electrolytes. This study explores the heterointerface activation effects of TiO/CuO heterogeneous catalysts with rutile (R-TiO) and anatase (A-TiO) phases and reveals that R-TiO is an active crystal phase with high nitrate reduction performance.

2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione protects against MPP-induced neurotoxicity by ameliorating oxidative stress, apoptosis and autophagy in SH-SY5Y cells.

2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD) is a cyclohexanedione compound extracted from the roots of Averrhoa carambola L. Several studies have documented its beneficial effects on diabetes, Alzheimer's disease, and cancer. However, its potential neuroprotective effects on Parkinson's disease (PD) have not yet been explored.

Acute effects of tissue flossing on boxers with chronic knee pain.

Objectives: To explore the acute intervention effects of tissue flossing on chronic knee pain (CKP) in boxers.

Methods: Eighteen boxers with CKP (12 male/6 female) were randomly divided into an experimental group (EG) with tissue flossing (n = 9) and a control group (CG) (n = 9). The visual analog scale (VAS), Lysholm knee function score, flexion range of motion (ROM), maximal isometric extensor muscle strength, and stability of the knee were measured pre- and post-intervention (EG: 3-minute tissue flossing, CG: rest).

Increasing cellular NAD protects hepatocytes against palmitate-induced lipotoxicity by preventing PARP-1 inhibition and the mTORC1-p300 pathway activation.

Hepatic lipotoxicity, resulting from excessive lipid accumulation in hepatocytes, plays a central role in the pathogenesis of various metabolic liver diseases. Despite recent progress, the precise mechanisms remain incompletely understood. Employing excessive exposure to palmitate in hepatocytes as our primary experimental model and mice studies, we aimed to uncover the mechanisms behind hepatic lipotoxicity, thereby developing potential treatments.