Fifty-year habitat subdivision enhances soil microbial biomass and diversity across subtropical land-bridge islands.

Although habitat loss and subdivision are considered main causes of sharp declines in biodiversity, there is still great uncertainty concerning the response of soil microbial biomass, diversity, and assemblage to habitat subdivision at the regional scale. Here, we selected 61 subtropical land-bridge islands (with small, medium, and large land areas) with a 50-year history of habitat subdivision and 9 adjacent mainland sites to investigate how habitat subdivision-induced unequal-sized patches and isolation affects biomass, diversity, and assemblages of soil bacteria and fungi. We found that the soil bacterial and fungal biomass on all unequal-sized islands were higher than that on mainland, while soil bacterial and fungal richness on the medium-sized islands were higher than that on mainland and other-sized islands.

Erratum: Tongxinluo inhibits neointimal formation by regulating the expression and post-translational modification of KLF5 in macrophages.

[This corrects the article on p. 4778 in vol. 8, PMID: 27904679.

Tongxinluo inhibits neointimal formation by regulating the expression and post-translational modification of KLF5 in macrophages.

Neointimal hyperplasia is a common pathological characteristic in diverse vascular remodeling diseases. The inflammatory response that follows vascular injury plays an important role in intimal hyperplasia. Tongxinluo (TXL), a traditional Chinese medicine, can ameliorate neointimal formation via suppressing vascular inflammatory response induced by vascular injury.

TMEM16A and myocardin form a positive feedback loop that is disrupted by KLF5 during Ang II-induced vascular remodeling.

The TMEM16A protein is an important component of Ca(2+)-dependent Cl(-) channels (CaCCs) in vascular smooth muscle cells. A recent study showed that TMEM16A inhibits angiotensin II-induced proliferation in rat basilar smooth muscle cells. However, whether and how TMEM16A is involved in vascular remodeling characterized by vascular smooth muscle cell proliferation remains largely unclear.