A 'hermit' shell-dwelling lifestyle in a Cambrian priapulan worm.

The Cambrian 'explosion', about 530 million years ago, marks a rapid diversification of the major animal lineages1. A concomitant increase in the complexity of ecosystems is believed to have accelerated this evolutionary radiation2, but direct evidence of the ecological modes of Cambrian taxa is nevertheless scarce - even in exceptional Burgess Shale-type deposits3. Here, we present new fossil material from the Cambrian (Stage 4) Guanshan biota in southern China that reveals the consistent occurrence of the priapulan worm ?Eximipriapulus4 within the conical shells of hyoliths. This represents the first direct evidence of a 'hermiting' life strategy - the adoption of a different organism's exoskeleton - in the priapulans and within the Palaeozoic era. It highlights the intense degree of convergent evolution during the Cambrian radiation. Hermiting behaviour has previously been linked with the escalation of predation pressure during the Mesozoic marine revolution5; such intensity of predation may also have characterised early Cambrian oceans.

Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway.

The aim of the current study was to investigate the effect and mechanism of schisandrin B (Sch B) on myocardial hypertrophy induced by pressure overload in mice. Male C57BL/6J mice were randomly divided into three groups: i) Sham (n=12); ii) transverse aortic constriction (TAC) (n=12); and iii) Sch B-treated (n=12; 80 mg·kg-1·d-1 per gavage). The model of myocardial hypertrophy was established by constricting the descending branch of the aortic arch. Following a 4-week treatment period, cardiac remodeling was evaluated using echocardiography and pathological and molecular analysis. Sch B improved cardiac function in the Sch B-treated group compared with the TAC group. Moreover, the Sch B-treated group had a smaller myocardial cell cross-sectional area and less fibrosis compared with the TAC group. The protein expression levels of cardiac hypertrophy and fibrosis markers in the TAC group were significantly higher compared with those in the sham group. The same markers in the Sch B-treated group were significantly lower compared with those in the TAC group. Additionally, the phosphorylation levels of the mitogen-activated protein kinase (MAPK) signaling pathway-associated proteins extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase 1/2 and P38 mitogen-activated protein kinase were significantly lower in the Sch B-treated group compared with the TAC group. Further in vitro investigation demonstrated that Sch B prevented the adverse effects of angiotensin II-induced hypertrophy and fibrosis by inhibiting the MAPK signaling pathway in H9c2 cells. In conclusion, Sch B may improve pathological myocardial remodeling and cardiac function induced by pressure overload, and its underlying mechanism may be associated with inhibition of the MAPK signaling pathway.