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Rhenium diselenide (ReSe2) has gathered much attention due to its low symmetry of lattice structure, which makes it possess in-plane anisotropic optical, electrical as well as excitonic properties and further enables ReSe2 have an important application in optoelectronic devices. Here, we report the thickness-dependent exciton relaxation dynamics of mechanically exfoliated few-layer ReSe2 flakes by using time-resolved pump–probe transient transmission spectroscopies. The results reveal two thickness-dependent relaxation processes of the excitons. The fast one correlates with the exciton formation (i.e., the conversion of hot carriers to excitons), while the slow one is attributed to the exciton recombination dominated by defect-assisted exciton trapping besides photon emission channel. The decrease of scattering probability caused by defects leads to the increase of fast lifetime with thickness, and the increase of slow lifetime with thickness is related to the trap-mediated exciton depopulation induced by surface defects. Polarization dependent transient spectroscopy indicates the isotropic exciton dynamics in the 2D plane. These results are insightful for better understanding of excitonic dynamics of ReSe2 materials and its application in future optoelectronic and electronic devices.

Atherosclerosis is a chronic inflammatory cardiovascular disease with high mortality worldwide. Tofacitinib (CP-690,550), an oral small-molecule Janus kinase inhibitor, has been shown to be effective in the treatment of rheumatoid arthritis, autoimmune encephalomyelitis and ulcerative colitis. However, its protective effect against atherosclerosis remains poorly understood. The aim of the present study was to evaluate the effects of Tofacitinib on atherogenic diet (ATD)-induced atherosclerosis using apolipoprotein E deficient (apoE−/−) mice. Atherosclerosis-prone apoE−/− mice were fed with ATD and treated with or without Tofacitinib through intragastrical administration (10 mg kg−1 day−1) for 8 weeks. Our results showed that Tofacitinib did not change plasma lipids, while significantly reduced the levels of plasma pro-inflammatory cytokines IL-6 and TNF-α. It also significantly attenuated atherosclerotic plaque lesion in the aortic root and macrophages contained in plaque as shown with Mac2 immuno-staining. Peritoneal macrophages (PMC) were separated from apoE−/− mice fed with 8-week ATD, and then subjected to inflammation tests. Flow cytometry analysis of F4/80 and CD206 and mRNA levels of M1 and M2 macrophages markers showed that M1 macrophages decreased while M2 macrophages increased in Tofacitinib treated group. Expressions of other inflammatory genes also indicated an anti-inflammatory status in mice treated with Tofacitinib. Ox-LDL was used to induce foam cell formation from PMC in wild type mice, and the results displayed a reduced formation of foam cells and decreased inflammation in mice with Tofacitinib administration (1 μM). The mRNA and protein levels of ATP binding cassette subfamily A member 1 (ABCA1), a key gene involved in cholesterol efflux, remarkably increased, while it was absence of alterations in scavenger receptors expression. Therefore, we demonstrated that Tofacitinib could attenuate atherosclerosis and foam cells formation by inhibiting inflammation and upregulating ABCA1 expression.