Tin‐based halide perovskites attract incremental attention due to the favorable optoelectronic properties and ideal bandgaps. However, the poor crystalline quality is still the biggest challenge for further progress in tin‐based perovskite solar cells (PVSCs) due to the unfavorable defects and uncontrollable crystallization kinetics. Here, acetic acid (HAc) is first introduced to reduce the supersaturated concentration of the precursor solution to preferentially form pre‐nucleation clusters, thus inducing rapid nucleation for effective regulation of crystallization kinetics. In particular, the hydrogen ion and acetate ion contained in HAc can effectively inhibit the oxidation of Sn2+, and the hydrogen bonding interaction between HAc and iodide ion (I‐) greatly reduces the loss of I‐, which guarantees the I‐/Sn2+ stoichiometric ratio of the corresponding perovskite film close to theoretical value, thus effectively reducing the defect density and maintaining the perfect crystal lattice. Consequently, the HAc‐assisted tin‐based PVSCs achieve a champion power conversion efficiency of 12.26% with superior open‐circuit voltage up to 0.75 V. Moreover, the unencapsulated device maintains nearly 90% of the initial PCE even after 3000 h storage in nitrogen atmosphere. This demonstrated strategy enables to prepare high‐quality tin‐based perovskite film with lower defect density and lattice distortion.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Recent years, circular RNA (circRNA) have been shown to exert vital functions in the pathological progressions of many diseases. A growing number of evidences have identified the representative function of exosomal circRNAs in the physiological state of donor cells, which further induces cellular responses after captured by recipient cells. However, the contributions of circRNAs to HCC remain largely unknown. In vitro and in vivo regulatory roles of circRNA Cdr1as in proliferative and migratory abilities of HCC were evaluated by CCK8, EdU, Transwell and tumourigenicity assays, respectively. Results showed circRNA Cdr1as was highly expressed in HCC cell lines and tissues. Overexpression of circRNA Cdr1as greatly accelerated HCC cells to proliferate and migrate. Mechanistically, we found that Cdr1as could promote the expression of AFP, a well-known biomarker for HCC, by sponging miR-1270. Further studies showed exosomes extracted from HCC cells overexpressing circRNA Cdr1as accelerated the proliferative and migratory abilities of surrounding normal cells. In all, circRNA Cdr1as serves as a ceRNA to promote the progression of HCC. Meanwhile, it is directly transferred from HCC cells to surrounding normal cells via exosomes to further mediate the biological functions of surrounding cells.

and modifying the charge transporting layers (CTLs), yet the interfacial mismatch between perovskite and CTLs is a non-negligible issue that dominates the efficiency and stability of corresponding devices. [7][8][9][10][11] Nickel oxide (NiO x ) nanocrystals as a promising stable hole transporting layer (HTL) in inverted p-i-n PVSCs are less prone to hysteresis and work well with flexible or tandem architectures. [12] Nevertheless, the PCE of NiO x -based inverted devices are usual inferior to the organic regular counterparts owing to the several interfacial issues: i) abundant surface traps and mismatch energy level restrict the charge carrier extraction, causing large energy offset; [13] ii) the redox reaction between Ni 3+ and A-site cation salts form a PbI 2 -rich hole extraction barrier, leading to severe interfacial destruction; [14] iii) inconsistent thermal expansion of lattice units in NiO x and perovskite results in tensile strain, prejudicing the microstructure and accelerating the degradation of perovskite. [15][16][17] Therefore, it is urge to solve these issues for performance enhancement and commercialization application of NiO x -based PVSCs.Recently, a great deal of molecular interlayers have been applied to passivate or adjust the energy level of NiO x /perovskite interface for strengthen the efficiency and stability in p-i-n devices, such as inorganic salts, [18][19][20] acids, [21] fullerene derivatives [22] and polymers buffer layer. [23][24][25] Nevertheless, most of the buffer layers are nonconductive and accompanied with the uncontrollable thickness and uniformity, which undoubtedly affect the optimization of charge transfer and perovskite crystal growth. Relatively speaking, the self-assembled small-molecule (SASM) can form thermodynamically favored ordered self-assembled layer that has been extensively proved as effective modifier to modulate the energy level and surface chemical state, as well as enhance the affinities of the deposition layer and substrate. [26] For instance, Fang et al. has reported that a polar chlorine-terminated SASM can modulate the energy-level alignment by forming a dipole moment at the interface. [27] Chen et al. has regulated the crystalline process and optimized the morphology of perovskite film by using 3-aminopropanioc acid SASM modified titanium oxide. [28] Other SASMs with different chemical terminations (such as amines, [29] carboxylates, [30] thiols, [31] and phosphonic acid [32] ) are also demonstrated to dramatically modify the electron Interfacial lattice mismatch and adverse reaction are the key issues hindering the development of nickel oxide (NiO x )-based inverted perovskite solar cells (PVSCs). Herein, a p-chlorobenzenesulfonic acid (CBSA) self-assembled small-molecule (SASM) is adopted to anchor NiO x and perovskite crystals to endow dual-passivation. The chlorine terminal of SASMs can provide growth sites for perovskite, leading to interfacial strain release. Meanwhile, the sulfonic acid group from SASMs can passivate surface defects of NiO x ,...

Research over the past decade suggested critical roles for circular RNAs in the natural growth and disease progression. However, it remains poorly defined whether the circular RNAs participate in Hirschsprung disease (HSCR). Here, we reported that the cir-ZNF609 was down-regulated in HSCR compared with normal bowel tissues. Furthermore, suppression of cir-ZNF609 inhibited the proliferation and migration of cells. We screened out several putative cir-ZNF609 ceRNAs of which the AKT3 transcript was selected. Finally, RNA immunoprecipitation and luciferase reporter assays demonstrated that cir-ZNF609 may act as a sponge for miR-150-5p to modulate the expression of AKT3. In conclusion, these findings illustrated that cir-ZNF609 took part in the onset of HSCR through the crosstalk with AKT3 by competing for shared miR-150-5p.