Lead halide perovskites always emerge complex interactions among different elemental ions,w hichl ead to multiple intrinsic imperfections.E lemental defects,s uch as amine,P b, and Iv acancies at A-, B-, and X-sites,a re main issues to deteriorate perovskite solar cells (PSCs). Unfortunately,m ost previous passivators can only temporarily fix partial inactive vacancies as sacrificial agents.H erein, we propose ar ecovery agent, ferrocene (Fc), which can form aone-dimensional perovskite with adequate steric cavities and suitable dissociation energy to recover all elemental defects backt oa ctive light-harvesting perovskites,a nd regenerate Fc itself meanwhile.Based on this perpetual chain-reaction cycle, corresponding PSCs maintain > 10 000-hour lifetime in inert condition and > 1000-hour durabilities under various extreme environments,i ncluding continuous 85 8 8Ch eating, 50 %r elative humidity wetting,and 1-sun light soaking.

No abstract

Notch controls skeletogenesis, but its role in the remodeling of adult bone remains conflicting. In mature mice, the skeleton can become osteopenic or osteosclerotic depending on the time point at which Notch is activated or inactivated. Using adult EGFP reporter mice, we find that Notch expression is localized to osteocytes embedded within bone matrix. Conditional activation of Notch signaling in osteocytes triggers profound bone formation, mainly due to increased mineralization, which rescues both age-associated and ovariectomy-induced bone loss and promotes bone healing following osteotomy. In parallel, mice rendered haploinsufficient in γ-secretase presenilin-1 (Psen1), which inhibits downstream Notch activation, display almost-absent terminal osteoblast differentiation. Consistent with this finding, pharmacologic or genetic disruption of Notch or its ligand Jagged1 inhibits mineralization. We suggest that stimulation of Notch signaling in osteocytes initiates a profound, therapeutically relevant, anabolic response.

No abstract

No abstract

No abstract

A growing body of evidence suggests that long-chain non-coding RNA (lncRNA) plays an important role in the malignant biological behavior and drug resistance of glioblastoma (GBM) cells. In this study, we analyzed the role and potential mechanism of lncRNA TMEM161B-AS1 in the malignant biological behavior of GBM cells and temozolomide (TMZ) resistance. Studies have found that FANCD2 and CD44 are significantly related to the occurrence of GBM, TMZ resistance and the survival of GBM patients. Knockdown of TMEM161B-AS1 down-regulated the expression of FANCD2 and CD44 by sponging hsa-miR-27a-3p, inhibited the proliferation, migration, invasion and promoted apoptosis, ferroptosis of U87 cells and U251 cells. Down-regulation of lncRNA TMEM161B-AS1 and/or over-expression of hsa-miR-27a-3p down-regulated the expression of FANCD2 and CD44, and inhibited the tumor growth in nude mice. These results demonstrated that the lncRNA TMEM161B-AS1-hsa-miR-27a-3p-FANCD2/CD44 signal axis regulated the malignant biological behavior of GBM and TMZ resistance. These findings were expected to provide promising therapeutic targets for the treatment of glioma.

No abstract