A Review on Additives for Halide Perovskite Solar Cells

Additives are widely adopted for efficient, stable, and hysteresis‐free perovskite solar cells and play an important role in various breakthroughs of perovskite solar cells (PSCs). Herein the various additives adopted for PSCs are reviewed and their functioning mechanism and influence on device performance is described. The main roles of additives, modulating morphology of perovskite films, stabilizing phase of formamidinium (FA) and cesium (Cs)‐based perovskites, adjusting energy level alignment in PSCs, suppressing nonradiative recombination in perovskites, eliminating hysteresis, enhancing operational stability of PSCs, are summarized.     

Ultra‐high α‐linolenic acid accumulating developmental defective embryo was rescued by lysophosphatidic acid acyltransferase 2

For decades, genetic engineering approaches to produce unusual fatty acids (UFAs) in crops has reached a bottleneck, including reduced seed oil production and seed vigor. Currently, plant models in the field of research are primarily used to investigate defects in oil production and seedling development, while the role of UFAs in embryonic developmental defects remains unknown. In this study, we developed a transgenic Arabidopsis plant model, in which the embryo exhibits severely wrinkled appearance owing to α‐linolenic acid (ALA) accumulation. RNA‐sequencing analysis in the defective embryo suggested that brassinosteroid synthesis, FA synthesis and photosynthesis were inhibited, while FA degradation, endoplasmic reticulum stress and oxidative stress were activated. Lipidomics analysis showed that ultra‐accumulated ALA is released from phosphatidylcholine as a free FA in cells, inducing severe endoplasmic reticulum and oxidative stress. Furthermore, we identified that overexpression of lysophosphatidic acid acyltransferase 2 rescued the defective phenotype. In the rescue line, the pool capacity of the Kennedy pathway was increased, and the esterification of ALA indirectly to triacylglycerol was enhanced to avoid stress. This study provides a plant model that aids in understanding the molecular mechanism of embryonic developmental defects and generates strategies to produce higher levels of UFAs.     

金莲花液雾化吸入对慢性鼻窦炎功能性内窥镜术后患者鼻通气功能、生活质量和血清炎性因子的影响

目的:探讨金莲花液雾化吸入对慢性鼻窦炎(CRS)功能性内窥镜术后患者鼻通气功能、生活质量和血清炎性因子的影响。方法:选取2017年10月~2019年8月期间我院收治的CRS功能性内窥镜术后患者160例,采用随机数字表法将患者分为对照组(n=80)和研究组(n=80),对照组术后在常规治疗的基础上予以鼻腔生理盐水雾化吸入治疗,研究组在常规治疗的基础上予以金莲花液雾化吸入治疗,比较两组患者鼻通气功能[鼻腔最小截面积(NMCSA)、鼻腔容积(NV)]、生活质量和血清炎性因子[白介素-5(IL-5)、肿瘤坏死因子-α(TNF-α)、降钙素原(PCT)]及预后相关指标。结果:两组患者治疗10 d后NMCSA、NV均升高,且研究组高于对照组(P<0.05)。两组治疗10 d后情感职能、躯体疼痛、社会功能、生理功能、精神健康、活力、生理职能、总体健康的维度评分均升高,且研究组高于对照组(P<0.05)。两组治疗10 d后血清IL-5、TNF-α、PCT水平均较治疗前下降,且研究组低于对照组(P<0.05)。研究组术腔清洁时间、上皮化时间均短于对照组(P<0.05);研究组鼻黏液纤毛传输速度高于对照组(P<0.05)。结论:金莲花液雾化吸入治疗CRS功能性内窥镜术后患者,可有效改善其鼻通气功能及生活质量,抑制炎性反应,促进患者恢复。     

经鼻高流量氧疗对慢性阻塞性肺疾病急性加重期患者血气指标、膈肌功能及炎性反应的影响

摘要 目的：探讨经鼻高流量氧疗对慢性阻塞性肺疾病急性加重期（AECOPD）患者血气指标、膈肌功能及炎性反应的影响。方法：回顾性分析2018年2月~2020年8月我院收治的119例AECOPD患者的临床资料。根据不同氧疗方法分为传统组59例和研究组60例,传统组给予传统氧疗,研究组给予经鼻高流量氧疗。对比两组治疗前后血气指标、膈肌功能及炎性反应的变化情况,观察两组不良反应发生率、治疗后再插管率、喘急胸闷和咳痰困难消失率。结果：研究组治疗后动脉血二氧化碳分压（PaCO₂） 较传统组低,血氧饱和度（SaO₂）、动脉血氧分压（PaO₂）高于传统组（均P<0.05）。研究组治疗后膈肌浅快呼吸指数（D-RSBI）、平静呼吸膈肌移动度（DEq）低于传统组（均P<0.05）。研究组治疗后血清白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α 低于传统组（均P<0.05）。研究组治疗后再插管率低于传统组,喘急胸闷消失率、咳痰困难消失率高于传统组（均P<0.05）。两组的不良反应总发生率组间对比无统计学差异（P>0.05）。结论：与传统氧疗相比,经鼻高流量氧疗应用于AECOPD患者可有效改善血气指标、膈肌功能,减轻炎性反应,改善患者的临床症状。     

Decreased mitochondrial OGG1 expression is linked to mitochondrial defects and delayed hepatoma cell growth

Many solid tumor cells exhibit mitochondrial respiratory impairment; however, the mechanisms of such impairment in cancer development remain unclear. Here, we demonstrate that SNU human hepatoma cells with declined mitochondrial respiratory activity showed decreased expression of mitochondrial 8-oxoguanine DNA glycosylase/lyase (mtOGG1), a mitochondrial DNA repair enzyme; similar results were obtained with human hepatocellular carcinoma tissues. Among several OGG1-2 variants with a mitochondrial-targeting sequence (OGG1-2a, -2b, -2c, -2d, and -2e), OGG1-2a was the major mitochondrial isoform in all examined hepatoma cells. Interestingly, hepatoma cells with low mtOGG1 levels showed delayed cell growth and increased intracellular reactive oxygen species (ROS) levels. Knockdown of OGG1-2 isoforms in Chang-L cells, which have active mitochondrial respiration with high mtOGG1 levels, significantly decreased cellular respiration and cell growth, and increased intracellular ROS. Overexpression of OGG1-2a in SNU423 cells, which have low mtOGG1 levels, effectively recovered cellular respiration and cell growth activities, and decreased intracellular ROS. Taken together, our results suggest that mtOGG1 plays an important role in maintaining mitochondrial respiration, thereby contributing to cell growth of hepatoma cells.