Bu zhong Yiqi Decoction ameliorates mild cognitive impairment by improving mitochondrial oxidative stress damage via the SIRT3/MnSOD/OGG1 pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Bu-Zhong-Yi-Qi Decoction(BZYQD) is a traditional formula commonly used in China, known for its effects in tonifying Qi and raising Yang. It can relieve symptoms of cognitive impairment such as forgetfulness and lack of concentration caused by qi deficiency, which is common in aging and debilitating. However, much of the current research on BZYQD has been focused on its impact on the digestive system, leaving its molecular mechanisms in improving cognitive function largely unexplored. AIM OF THE STUDY: Cognitive decline in the aging central nervous system is intrinsically linked to oxidative damage. This study aims to investigate the therapeutic mechanism of BZYQD in treating mild cognitive impairment caused by qi deficiency, particularly through repair of mitochondrial oxidative damage. MATERIALS AND METHODS: A rat model of mild cognitive impairment (MCI) was established by administering reserpine subcutaneously for two weeks, followed by a two-week treatment with BZYQD/GBE. In vitro experiments were conducted to assess the effects of BZYQD on neuronal cells using a H2O2-induced oxidative damage model in PC12 cells. The open field test and the Morris water maze test evaluated the cognitive and learning memory abilities of the rats. HE staining and TEM were employed to observe morphological changes in the hippocampus and its mitochondria. Mitochondrial activity, ATP levels, and cellular viability were measured using assay kits. Protein expression in the SIRT3/MnSOD/OGG1 pathway was analyzed in tissues and cells through western blotting. Levels of 8-OH-dG in mitochondria extracted from tissues and cells were quantified using ELISA. Mitochondrial morphology in PC12 cells was visualized using Mito Red, and mitochondrial membrane potential was assessed using the JC-1 kit. RESULTS: BZYQD treatment significantly improved cognitive decline caused by reserpine in rats, as well as enhanced mitochondrial morphology and function in the hippocampus. Our findings indicate that BZYQD mitigates mtDNA oxidative damage in rats by modulating the SIRT3/MnSOD/OGG1 pathway. In PC12 cells, BZYQD reduced oxidative damage to mitochondria and mtDNA in H2O2-induced conditions and was associated with changes in the SIRT3/MnSOD/OGG1 pathway. CONCLUSION: BZYQD effectively counteracts reserpine-induced mild cognitive impairment and ameliorates mitochondrial oxidative stress damage through the SIRT3/MnSOD/OGG1 pathway.

PEA-m6A: an ensemble learning framework for accurately predicting N6-methyladenosine modifications in plants.

N 6-methyladenosine (m6A), which is the mostly prevalent modification in eukaryotic mRNAs, is involved in gene expression regulation and many RNA metabolism processes. Accurate prediction of m6A modification is important for understanding its molecular mechanisms in different biological contexts. However, most existing models have limited range of application and are species-centric. Here we present PEA-m6A, a unified, modularized and parameterized framework that can streamline m6A-Seq data analysis for predicting m6A-modified regions in plant genomes. The PEA-m6A framework builds ensemble learning-based m6A prediction models with statistic-based and deep learning-driven features, achieving superior performance with an improvement of 6.7% to 23.3% in the area under precision-recall curve compared with state-of-the-art regional-scale m6A predictor WeakRM in 12 plant species. Especially, PEA-m6A is capable of leveraging knowledge from pretrained models via transfer learning, representing an innovation in that it can improve prediction accuracy of m6A modifications under small-sample training tasks. PEA-m6A also has a strong capability for generalization, making it suitable for application in within- and cross-species m6A prediction. Overall, this study presents a promising m6A prediction tool, PEA-m6A, with outstanding performance in terms of its accuracy, flexibility, transferability, and generalization ability. PEA-m6A has been packaged using Galaxy and Docker technologies for ease of use and is publicly available at https://github.com/cma2015/PEA-m6A.

Charge injection engineering at organic/inorganic heterointerfaces for high-efficiency and fast-response perovskite light-emitting diodes.

The development of advanced perovskite emitters has considerably improved the performance of perovskite light-emitting diodes (LEDs). However, the further development of perovskite LEDs requires ideal device electrical properties, which strongly depend on its interfaces. In perovskite LEDs with conventional p-i-n structures, hole injection is generally less efficient than electron injection, causing charge imbalance. Furthermore, the popular hole injection structure of NiOx/poly(9-vinylcarbazole) suffers from several issues, such as weak interfacial adhesion, high interfacial trap density and mismatched energy levels. In this work, we insert a self-assembled monolayer of [2-(9H-carbazol-9-yl)ethyl]phosphonic acid between the NiOx and poly(9-vinylcarbazole) layers to overcome these challenges at the organic/inorganic heterointerfaces by establishing a robust interface, passivating interfacial trap states and aligning the energy levels. We successfully demonstrate blue (emission at 493 nm) and green (emission at 515 nm) devices with external quantum efficiencies of 14.5% and 26.0%, respectively. More importantly, the self-assembled monolayer also gives rise to devices with much faster response speeds by reducing interfacial capacitance and resistance. Our results pave the way for developing more efficient and brighter perovskite LEDs with quick response, widening their potential application scope.

Changes in m6A RNA methylation are associated with male sterility in wolfberry.

BACKGROUND: N6-methyladenosine (m6A) modification is the most abundant type of RNA modification in eukaryotic cells, playing pivotal roles in multiple plant growth and development processes. Yet the potential role of m6A in conferring the trait of male sterility in plants remains unknown. RESULTS: In this study, we performed RNA-sequencing (RNA-Seq) and m6A-sequencing (m6A-Seq) of RNAs obtained from the anther tissue of two wolfberry lines: 'Ningqi No.1' (LB1) and its natural male sterile mutant 'Ningqi No.5' (LB5). Based on the newly assembled transcriptome, we established transcriptome-wide m6A maps for LB1 and LB5 at the single nucleus pollen stage. We found that the gene XLOC_021201, a homolog of m6A eraser-related gene ALKBH10 in Arabidopsis thaliana, was significantly differentially expressed between LB1 and LB5. We also identified 1642 and 563 m6A-modified genes with hypermethylated and hypomethylated patterns, respectively, in LB1 compared with LB5. We found the hypermethylated genes significantly enriched in biological processes related to energy metabolism and lipid metabolism, while hypomethylation genes were mainly linked to cell cycle process, gametophyte development, and reproductive process. Among these 2205 differentially m6A methylated genes, 13.74% (303 of 2205) were differentially expressed in LB1 vis-à-vis LB5. CONCLUSIONS: This study constructs the first m6A transcriptome map of wolfberry and establishes an association between m6A and the trait of male sterility in wolfberry.

Novel Components of the Stress Assembly Sec Body Identified by Proximity Labeling.

Sec bodies are membraneless stress-induced assemblies that form by the coalescence of endoplasmic reticulum exit sites (ERES). Through APEX2 tagging of Sec24AB, we biotinylated and identified the full complement of Sec body proteins. In the presence of biotin-phenol and H2O2 (APEX on), APEX2 facilitates the transfer of a biotin moiety to nearby interactors of chimeric Sec24AB. Using this unbiased approach comparing APEX on and off (-H2O2) conditions, we identified 52 proteins specifically enriched in Sec bodies. These include a large proportion of ER and Golgi proteins, packaged without defined stoichiometry, which we could selectively verify by imaging. Interestingly, Sec body components are neither transcriptionally nor translationally regulated under the conditions that induce Sec body formation, suggesting that incorporation of these proteins into granules may be driven instead by the aggregation of nucleating proteins with a high content of intrinsically disordered regions. This reinforces the notion that Sec bodies may act as storage for ERES, ER and Golgi components during stress.

Importance of Electric-Field-Independent Mobilities in Thick-Film Organic Solar Cells.

In organic solar cells (OSCs), a thick active layer usually yields a higher photocurrent with broader optical absorption than a thin active layer. In fact, a ∼300 nm thick active layer is more compatible with large-area processing methods and theoretically should be a better spot for efficiency optimization. However, the bottleneck of developing high-efficiency thick-film OSCs is the loss in fill factor (FF). The origin of the FF loss is not clearly understood, and there a direct method to identify photoactive materials for high-efficiency thick-film OSCs is lacking. Here, we demonstrate that the mobility field-dependent coefficient is an important parameter directly determining the FF loss in thick-film OSCs. Simulation results based on the drift-diffusion model reveal that a mobility field-dependent coefficient smaller than 10-3 (V/cm)-1/2 is required to maintain a good FF in thick-film devices. To confirm our simulation results, we studied the performance of two ternary bulk heterojunction (BHJ) blends, PTQ10:N3:PC71BM and PM6:N3:PC71BM. We found that the PTQ10 blend film has weaker field-dependent mobilities, giving rise to a more balanced electron-hole transport at low fields. While both the PM6 blend and PTQ10 blend yield good performance in thin-film devices (∼100 nm), only the PTQ10 blend can retain a FF = 74% with an active layer thickness of up to 300 nm. Combining the benefits of a higher JSC in thick-film devices, we achieved a PCE of 16.8% in a 300 nm thick PTQ10:N3:PC71BM OSC. Such a high FF in the thick-film PTQ10 blend is also consistent with the observation of lower charge recombination from light-intensity-dependent measurements and lower energetic disorder observed in photothermal deflection spectroscopy.

Multidecadal, continent-level analysis indicates agricultural practices impact wheat aphid loads more than climate change.

Temperature has a large influence on insect abundances, thus under climate change, identifying major drivers affecting pest insect populations is critical to world food security and agricultural ecosystem health. Here, we conducted a meta-analysis with data obtained from 120 studies across China and Europe from 1970 to 2017 to reveal how climate and agricultural practices affect populations of wheat aphids. Here we showed that aphid loads on wheat had distinct patterns between these two regions, with a significant increase in China but a decrease in Europe over this time period. Although temperature increased over this period in both regions, we found no evidence showing climate warming affected aphid loads. Rather, differences in pesticide use, fertilization, land use, and natural enemies between China and Europe may be key factors accounting for differences in aphid pest populations. These long-term data suggest that agricultural practices impact wheat aphid loads more than climate warming.

Panax notoginseng Saponins Protect Brain Microvascular Endothelial Cells against Oxygen-Glucose Deprivation/Resupply-Induced Necroptosis via Suppression of RIP1-RIP3-MLKL Signaling Pathway.

Recently, necroptosis has emerged as one of the important mechanisms of ischemia stroke. Necroptosis can be rapidly activated in endothelial cells to cause vascular damage and neuroinflammation. Panax notoginseng saponins (PNS), an ingredient extracted from the root of Panax notoginseng (Burk.) F.H. Chen, was commonly used for ischemic stroke, while its molecular mechanism and targets have not been fully clarified. Our study aimed to clarify the anti-necroptosis effect of PNS by regulating RIP1-RIP3-MLKL signaling pathway in brain microvascular endothelial cells (BMECs) subjected to transient oxygen-glucose deprivation (OGD/resupply [R]). In vitro, the necroptosis model of rat BMECs was established by testing the effect of OGD/R in the presence of the pan-caspase inhibitor z-VAD-FMK. After administration of PNS and Nec-1, cell viability, cell death modality, the expression of RIP1-RIP3-MLKL pathway and mitochondrial membrane potential (Δψm) level were investigated in BMECs upon OGD/R injury. The results showed that PNS significantly enhanced cell viability of BMECs determined by CCK-8 analysis, and protected BMECs from necroptosis by Flow cytometry and TEM. In addition, PNS inhibited the phosphorylation of RIP1, RIP3, MLKL and the downstream expression of PGAM5 and Drp1, while similar results were observed in Nec-1 intervention. We further investigated whether PNS prevented the Δψm depolarization. Our current findings showed that PNS effectively reduced the occurrence of necroptosis in BMECs exposed to OGD/R by inhibition of the RIP1-RIP3-MLK signaling pathway and mitigation of mitochondrial damage. This study provided a novel insight of PNS application in clinics.

The RIG-I Signal Pathway Mediated Panax notoginseng Saponin Anti-Inflammatory Effect in Ischemia Stroke.

Panax notoginseng saponins (PNS), the main bioactive constituents of a traditional Chinese herb Panax notoginseng, were commonly used for ischemic stroke in China. However, the associated cellular and molecular mechanisms of PNS have not been well examined. This study aimed to decipher the underlying molecular target of PNS in the treatment of cerebral ischemia. The oxygen-glucose-deprived (OGD) model of rat brain microvascular endothelial cells (BMECs) was used in this study. The alteration of gene expression in rat BMECs after PNS treatment was measured by microarray and indicated that there were 38 signaling pathways regulated by PNS. Among them, RIG-I receptor and related signaling molecules TNF receptor-associated factor 2 (Traf2) and nuclear factor-kappa B (NF-κB) were significantly suppressed by PNS, which was verified again in OGD-induced BMECs measured by FQ-PCR and western blotting and in middle cerebral artery occlusion (MCAO) rats measured by immunohistochemistry. The levels of TNF-α, IL-8, and the downstream cytokines regulated by RIG-I receptor pathway were also decreased by PNS. Meanwhile, the neurological evaluation, hematoxylin and eosin (HE) staining, and Evans blue staining were conducted to evaluate the effect of PNS in MCAO rats. Results showed PNS significantly improved functional outcome and cerebral vascular leakage. Flow cytometry showed the number of the inflammatory cells infiltrated in brain tissue was decreased in PNS treatment. Our results identified that RIG-I signaling pathway mediated anti-inflammatory properties of PNS in cerebral ischemia, which provided the novel insights of PNS application in clinics.

Activation of IRE1, PERK and salt-inducible kinases leads to Sec body formation in Drosophila S2 cells.

The phase separation of the non-membrane bound Sec bodies occurs in Drosophila S2 cells by coalescence of components of the endoplasmic reticulum (ER) exit sites under the stress of amino acid starvation. Here, we address which signaling pathways cause Sec body formation and find that two pathways are critical. The first is the activation of the salt-inducible kinases (SIKs; SIK2 and SIK3) by Na+ stress, which, when it is strong, is sufficient. The second is activation of IRE1 and PERK (also known as PEK in flies) downstream of ER stress induced by the absence of amino acids, which needs to be combined with moderate salt stress to induce Sec body formation. SIK, and IRE1 and PERK activation appear to potentiate each other through the stimulation of the unfolded protein response, a key parameter in Sec body formation. This work shows the role of SIKs in phase transition and re-enforces the role of IRE1 and PERK as a metabolic sensor for the level of circulating amino acids and salt. This article has an associated First Person interview with the first author of the paper.

The Associations Between Sleep Architecture and Metabolic Parameters in Patients With Obstructive Sleep Apnea: A Hospital-Based Cohort Study.

Background and Objectives: The associations between objective sleep architecture and metabolic parameters have been rarely studied in patients with obstructive sleep apnea (OSA). Here, we evaluated the associations between objective sleep measures derived via polysomnography (PSG) and metabolic parameters. Methods: A total of 2,308 subjects with suspected OSA were included. We measured common metabolic parameters such as body mass index (BMI) and glucose, insulin, blood pressure, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels. All subjects underwent full-night PSG. PSG sleep parameters included total sleep time (TST), time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep, sleep efficiency, and the microarousal index (MAI). Results: The TST correlated with the BMI, glucose level, and systolic blood pressure. The SWS/TST ratio correlated with BMI and glucose, TC, and TG levels. The REM/TST ratio correlated with BMI, glucose, insulin, and TG levels, and diastolic blood pressure. We found significant relationships between sleep efficiency and BMI, glucose levels, and TG levels. The MAI was significantly correlated with all metabolic parameters. After adjustment for age, gender, smoking status, alcohol use, apnea hypopnea index, and oxygen desaturation index (ODI), multiple linear regression analysis showed that the MAI was independently associated with glucose level, TC, HDL, and LDL. REM/TST ratio was positively associated with diastolic blood pressure but negatively associated with glucose metabolism. Conclusions: Though some independent correlation between sleep and metabolic parameters was confirmed, only weak associations were observed, suggesting a clinically negligible influence of sleep structure. Further prospective studies are warranted to confirm our findings.

Efficacy of melatonin for sleep disturbance in middle-aged primary insomnia: a double-blind, randomised clinical trial.

BACKGROUND: The aim of this study was to determine the efficacy of exogenous melatonin supplementation for sleep disturbances in patients with middle-aged primary insomnia. METHODS: This is a randomized double-blind, placebo-controlled parallel study. Participants were recruited from Tianlin community, Xuhui district, Shanghai. Ninety-seven consecutive middle-aged patients with primary insomnia were randomized to receive 3 mg fast-release melatonin (n = 51) or placebo (n = 46) for four-weeks. Objective sleep parameters tested by overnight polysomnography, subjective sleep performance and daytime somnolence obtained from the Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI) and Epworth Sleepiness Scale (ESS) were obtained at baseline and after treatment. Treatment was taken daily 1 h before bedtime. Serious adverse events and side-effects were monitored. RESULTS: Melatonin supplementation significantly decreased early wake time [-30.63min (95% CI, -53.92 to -7.34); P = 0.001] and percentage of N2 sleep [-7.07% (95% CI, -13.47% to -0.68%); P = 0.031]. However, melatonin had no significant effect on other objective sleep parameters including sleep latency, sleep efficiency, wake during the sleep and percent of N1, N3 and REM sleep. Melatonin had no effect on insomnia symptoms and severity on the PSQI [1.53(95% CI, -0.55 to 3.61); p = 0.504]; ISI [0.81 (95% CI, -2.27 to 3.88); p = 0.165] and ESS [-0.83 (95% CI, -3.53 to 1.88); p = 0.147]. No serious adverse events were reported. CONCLUSIONS: Melatonin supplementation over a four-week period is effective and safe in improving some aspects of objective sleep quality such as total sleep time, percentage of rapid eye movement and early morning wake time in middle-aged patients with insomnia. TRIAL REGISTRATION: Identifier: ChiCTR-TRC-13003997; Prospectively registered on 2 December 2013.

Gan Shen Fu Fang ameliorates liver fibrosis in vitro and in vivo by inhibiting the inflammatory response and extracellular signal-regulated kinase phosphorylation.

BACKGROUND: Liver fibrosis is a common health problem worldwide and there is still a lack of effective medicines. The Chinese herbal medicine, Gan Shen Fu Fang (GSFF) is composed of salvianolic acid B and diammonium glycyrrhizinate. In this study, we observed the effects of GSFF on liver fibrosis in vivo and in vitro in an attempt to provide some hope for the treatment. AIM: To observe the effects of GSFF on liver fibrosis in vivo and in vitro and investigate the mechanism from the perspective of the inflammatory response and extracellular signal-regulated kinase (ERK) phosphorylation. METHODS: Common bile duct-ligated rats were used for in vivo experiments. Hepatic stellate cells-T6 (HSC-T6) cells were used for in vitro experiments. Hematoxylin and eosin staining and Masson staining, biochemical assays, hydroxyproline (Hyp) assays, enzyme-linked immunoasorbent assay and western blotting were performed to evaluate the degree of liver fibrosis, liver function, the inflammatory response and ERK phosphorylation. The CCK8 assay, immunofluorescence and western blotting were applied to test the effect of GSFF on HSC-T6 cell activation and determine whether GSFF had an effect on ERK phosphorylation in HSC-T6 cells. RESULTS: GSFF improved liver function and inhibited liver fibrosis in common bile duct-ligated rats after 3 wk of treatment, as demonstrated by histological changes, hydroxyproline assays and collagen I concentrations. GSFF alleviated inflammatory cell infiltration and reduced the synthesis of pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α) and interlukin-1ß] and NF-κB. In addition, GSFF decreased ERK phosphorylation. In vitro, GSFF inhibited the viability of HSC-T6 cells with and without transforming growth factor ß1 (TGF-ß1) stimulation and decreased the synthesis of collagen I. GSFF had the greatest effect at a concentration of 0.5 µmol/L. GSFF inhibited the expression of α-smooth muscle actin (α-SMA), a marker of HSC activation, in HSC-T6 cells. Consistent with the in vivo results, GSFF also inhibited the phosphorylation of ERK and downregulated the expression of NF-κB. CONCLUSION: GSFF inhibited liver fibrosis progression in vivo and HSC-T6 cell activation in vitro. These effects may be related to an alleviated inflammatory response and downregulated ERK phosphorylation.

Dependence of sperm structural and functional integrity on testicular calcineurin isoform PPP3R2 expression.

After leaving the testis, mammalian sperm undergo a sequential maturation process in the epididymis followed by capacitation during their movement through the female reproductive tract. These phenotypic changes are associated with modification of protein phosphorylation and membrane remodeling, which is requisite for sperm to acquire forward motility and induce fertilization. However, the molecular mechanisms underlying sperm maturation and capacitation are still not fully understood. Herein, we show that PPP3R2, a testis-specific regulatory subunit of protein phosphatase 3 (an isoform of calcineurin in the testis), is essential for sperm maturation and capacitation. Knockout of Ppp3r2 in mice leads to male sterility due to sperm motility impairment and morphological defects. One very noteworthy change includes increases in sperm membrane stiffness. Moreover, PPP3R2 regulates sperm maturation and capacitation via (i) modulation of membrane diffusion barrier function at the annulus and (ii) facilitation of cholesterol efflux during sperm capacitation. Taken together, PPP3R2 plays a critical role in modulating cholesterol efflux and mediating the dynamic control of membrane remodeling during sperm maturation and capacitation.

Highly Crystalline Near-Infrared Acceptor Enabling Simultaneous Efficiency and Photostability Boosting in High-Performance Ternary Organic Solar Cells.

The near-infrared (NIR) absorbing fused-ring electron acceptor, COi8DFIC, has demonstrated very good photovoltaic performance when combined with PTB7-Th as a donor in binary organic solar cells (OSCs). In this work, the NIR acceptor was added to state-of-the-art PBDBT-2F:IT4F-based solar cells as a third component, leading to (i) an efficiency increase of the ternary devices compared to the binary solar cells in the presence of the highly crystalline COi8DFIC acceptor and (ii) much-improved photostability under 1-sun illumination. The electron transport properties were investigated and revealed the origin of the enhanced device performance. Compared to the binary cells, the optimized ternary PBDBT-2F:COi8DFIC:IT4F blends exhibit improved electron transport properties in the presence of 10% COi8DFIC, which is attributed to improved COi8DFIC molecular packing. Furthermore, transient absorption spectroscopy revealed a slow recombination of charge carriers in the ternary blend. The improved electron transport properties were preserved in the ternary OSC upon aging, while in the binary devices they seriously deteriorated after simulated 1-sun illumination of 240 h. Our work demonstrates a simple approach to enhance both OSC efficiency and photostability.

Membrane-Bound Meet Membraneless in Health and Disease.

Membraneless organelles (MLOs) are defined as cellular structures that are not sealed by a lipidic membrane and are shown to form by phase separation. They exist in both the nucleus and the cytoplasm that is also heavily populated by numerous membrane-bound organelles. Even though the name membraneless suggests that MLOs are free of membrane, both membrane and factors regulating membrane trafficking steps are emerging as important components of MLO formation and function. As a result, we name them biocondensates. In this review, we examine the relationships between biocondensates and membrane. First, inhibition of membrane trafficking in the early secretory pathway leads to the formation of biocondensates (P-bodies and Sec bodies). In the same vein, stress granules have a complex relationship with the cyto-nuclear transport machinery. Second, membrane contributes to the regulated formation of phase separation in the cells and we will present examples including clustering at the plasma membrane and at the synapse. Finally, the whole cell appears to transit from an interphase phase-separated state to a mitotic diffuse state in a DYRK3 dependent manner. This firmly establishes a crosstalk between the two types of cell organization that will need to be further explored.

Fused Benzothiadiazole: A Building Block for n-Type Organic Acceptor to Achieve High-Performance Organic Solar Cells.

Narrow bandgap n-type organic semiconductors (n-OS) have attracted great attention in recent years as acceptors in organic solar cells (OSCs), due to their easily tuned absorption and electronic energy levels in comparison with fullerene acceptors. Herein, a new n-OS acceptor, Y5, with an electron-deficient-core-based fused structure is designed and synthesized, which exhibits a strong absorption in the 600-900 nm region with an extinction coefficient of 1.24 × 105 cm-1 , and an electron mobility of 2.11 × 10-4 cm2 V-1 s-1 . By blending Y5 with three types of common medium-bandgap polymers (J61, PBDB-T, and TTFQx-T1) as donors, all devices exhibit high short-circuit current densities over 20 mA cm-2 . As a result, the power conversion efficiency of the Y5-based OSCs with J61, TTFQx-T1, and PBDB-T reaches 11.0%, 13.1%, and 14.1%, respectively. This indicates that Y5 is a universal and highly efficient n-OS acceptor for applications in organic solar cells.

Silane-Capped ZnO Nanoparticles for Use as the Electron Transport Layer in Inverted Organic Solar Cells.

Zinc oxide (ZnO) nanoparticles are widely used as electron- transport layer (ETL) materials in organic solar cells and are considered to be the candidate with the most potential for ETLs in roll-to-roll (R2R)-printed photovoltaics. However, the tendency of the nanoparticles to aggregate reduces the stability of the metal oxide inks and creates many surface defects, which is a major barrier to its printing application. With the aim of improving the stability of metal oxide nanoparticle dispersions and suppressing the formation of surface defects, we prepared 3-aminopropyltrimethoxysilane (APTMS)-capped ZnO (ZnO@APTMS) nanoparticles through surface ligand exchange. The ZnO@APTMS nanoparticles exhibited excellent dispersibility in ethanol, an environmentally friendly solvent, and remained stable in air for at least one year without any aggregation. The capping of the ZnO nanoparticles with APTMS also reduced the number of surface-adsorbed oxygen defects, improved the charge transfer efficiency, and suppressed the light-soaking effect. The thickness of the ZnO@APTMS ETL could reach 100 nm without an obvious decrease in the performance. Large-area APTMS-modified ZnO films were successfully fabricated through roll-to-roll microgravure printing and exhibited good performance in flexible organic solar cells. This work demonstrated the distinct advantages of this ZnO@APTMS ETL as a potential buffer layer for printed organic electronics.