Search

Lewis acid–base passivation is a significant technique to achieve structural stability of perovskite solar cells (PSCs) by overcoming the issues of wide grain boundaries, crystal defects, and the instability of PSCs. In this work, the combined effects of thiophene with phthalocyanine (Pc) as isomers (S2 and S3) on the photovoltaic performance of PSCs were studied for the first time. Through density functional theory calculations, we confirmed that the position of the S atom in the structure affects Lewis acid–base interactions with under-coordinated Pb2+ sites. The morphology of methylammonium lead iodide (MAPbI3) for passivated devices was improved and thin dense layers with compact surface and large grain size were observed, leading to improvement of the charge extraction ability and reduction of non-radiative recombination and the trap density. A highest power conversion efficiency of 18% was achieved for the Pc S3 passivated device, which was 6.69% more than that of the controlled device. Furthermore, the Pcs passivated devices demonstrated remarkable stability under high-moisture and high-temperature conditions.

Novel hierarchical CuO@WO3 nanocomposites with various CuO contents (0–10 wt%) were synthesized by anchoring discrete CuO nanoparticles (CuO NPs) on WO3 nanoplates under a hydrothermal condition for low-temperature detection of H2S gas. In the CuO@WO3 nanocomposite, CuO NPs are uniformly distributed on WO3 nanoplates, forming a p-n CuO/WO3 heterojunction. The CuO@WO3 nanocomposites show highly sensitive to H2S gas at a low operating-temperature range (25–100 °C). The 5 wt%CuO@WO3 sensor shows a high response of 830 when exposed to a 10 ppm H2S gas at 100 °C. At even lower temperatures (e.g., 50 °C and 25 °C), the 5 wt%CuO@WO3 sensor shows an obvious response to 1 ppm H2S, and their response time is less than 3 min. In addition, the CuO@WO3 sensor exhibits a highly selective response to H2S, compared with SO2, CO, CH4, H2, and organic vapors, operating at 25–100 °C. The improvement of the CuO@WO3 sensor in H2S detection at a low operating temperature is ascribed to the unique hierarchical p-n heterojunctions formed between the CuO NPs and WO3 nanoplates.

Performance modulation of formaldehyde (HCHO) sensing active nanomaterials is of great significance in environmental monitoring and disease diagnosis. This paper reports a simple but robust solvothermal process to synthesize SnO2@rGO nanocomposites for HCHO sensors with rGO mass fractions of 0–2%. The phases, chemical compositions, microstructures and surface states of the as-obtained SnO2@rGO nanocomposites are well characterized. The results indicate that the addition of GO overcomes the agglomeration of SnO2 nanocrystals (3–5 nm) and highly enhances the specific surface area (SSA) of the SnO2@rGO nanocomposites, leading to higher response and lower operating temperature in the HCHO-sensing application. The SSA of SnO2@rGO is 133.1 m2/g, much larger than that (58.3 m2/g) of pure SnO2 nanocrystals. The SnO2@rGO nanocomposites exhibit highly selective and sensitive to HCHO vapors at a relatively low operating temperature range of 100–200 °C. The amount of GO added has a key effect on the HCHO-sensing performance, and the sample of SnO2@rGO-0.5% exhibits the highest response at 100 160 °C. Their recovery/response times are shorter than 20 s to HCHO vapors (less than 25 ppm). The enhanced HCHO-sensing performance is attributed to the formation of porous SnO2@rGO nanostructures with high SSAs and suitable electron transfer channels.

Pirfenidone has been widely used in the treatment of idiopathic pulmonary fibrosis (IPF). However, the role of pirfenidone in LPS-induced acute lung injury (ALI) remains unclear. This study aims to investigate the protective effects of pirfenidone in ALI and to explore its underlying mechanism. Pirfenidone clearly reduces LPS-triggered ALI as indicated by significant pathological alterations, reduced oxidative stress and inflammatory responses in vivo. Furthermore, pirfenidone also blocks apoptosis of LPS-induced alveolar epithelial type II (ATII) cells through inhibition of endoplasmic reticulum (ER) stress and mitochondrial injury in vivo and in vitro. A lower expression level of BAP31, an ER transmembrane protein, was found to be associated with ALI followed LPS challenge. The reintroduction of BAP31 blunted LPS induced ER stress and mitochondrial damage and therefore alleviated ATII cell apoptosis, which correlated with pirfenidone treatment. Knockdown of BAP31 expression in pirfenidone treated ATII cells re-activated ER stress, mitochondrial damage and followed cellular apoptosis. In summary, this study confirms the beneficial effect of pirfenidone on ER stress and mitochondrial dysfunction mediated apoptosis via upregulation of BAP31. Our results demonstrated that pirfenidone may be considered as a potential agent for the treatment of ALI in the future.

The aim of this study was to explore the population structure of multidrug-resistant (MDR) tuberculosis strains and distribution of resistance-associated nucleotide alteration among the different genotype MDR strains in China.The genotypes of 376 MDR strain were analyzed by 15-loci MIRU-VNTR and RD105 deletion-targeted multiplex PCR (DTM-PCR) method. In addition, all the MDR isolates were sequenced for genetic mutations conferring rifampicin (rpoB) and isonizid resistance (katG, inhA and oxyR-ahpC).Among the 376 MDR isolates, 261 (69.4%) belonged to Beijing genotype, including 177 modern Beijing strains (67.8%) and 84 ancient Beijing (32.2%) strains. The percentages of streptomycin-resistant, kanamycin-resistant, pre-XDR and XDR TB in modern Beijing genotype were significantly lower than ancient genotype (P0.05). The Beijing MDR strains had significantly higher proportions of ofloxacin-resistant and pre-XDR isolates than non-Beijing strains (P0.01). In addition, the clustering rate of modern Beijing strains was significantly higher than that of ancient Beijing strains (46.3% vs. 11.9%, P0.01). 94.7% and 79.3% of MDR isolates harbored genetic mutations conferring rifampicin and isonizid resistance, respectively, and the most prevalent mutation was located in codon rpoB531 and katG315. In addition, the rpoB531 and katG mutation were more frequently observed among Beijing genotype strains than non-Beijing strains, while non-Beijing genotype showed stronger association with isolates lacking mutation in rifampicin resistance determination region (P0.05).Our findings demonstrated that ancient Beijing MDR strains were associated with drug resistance, while modern Beijing MDR strains were more likely to be clustered.