Ambient PM orchestrates M1 polarization of alveolar macrophages via activating glutaminase 1-mediated glutaminolysis in acute lung injury.

The temporary explosive growth events of atmospheric fine particulate matter (PM) pollution during late autumn and winter seasons still frequently occur in China. High-concentration exposure to PM aggravates lung inflammation, leading to acute lung injury (ALI). Alveolar macrophages (AMs) participate in PM-induced pulmonary inflammation and injury.

Macrophage-derived exosomal TNF-α promotes pulmonary surfactant protein expression in PM-induced acute lung injury.

Short-term high-concentration exposure to airborne fine particulate matter (PM) is strongly associated with the risk of acute lung injury (ALI). It has been recently reported that exosomes (Exos) involve in the progression of respiratory diseases. However, the molecular mechanisms by which exosome-mediated intercellular signaling exacerbate PM-induced ALI remains largely unaddressed.

Functional study of C-terminal domain of the thermoacidophilic raw starch-hydrolyzing α-amylase Gt-amy.

Since the thermoacidophilic raw-starch hydrolyzing -amylase Gt-amy can effectively hydrolyze corn starch under starch liquefaction conditions, it has potential for many industrial applications. To identify the raw starch-binding domain of Gt-amy, a C-terminal domain (CTD)-truncated mutant (Gt-amy-T) was constructed, and its enzymatic properties were compared with Gt-amy. In comparison to CTD of Gt-amy, which could effectively bind corn starch, the Gt-amy-T could not bind to and hydrolyze corn starch under similar conditions.