Effects of Iodine Doping on Carrier Behavior at the Interface of Perovskite Crystals: Efficiency and Stability

The interface related to the polycrystalline hybrid perovskite thin film plays an essential role in the resulting device performance. Iodine was employed as an additive to modify the interface between perovskite and spiro-OMeTAD hole transport layer. The oxidation ability of iodine significantly improved the efficiency of charge extraction for perovskite solar cells. It reveals that the Open Circuit Voltage (Voc) and Fill Factor (FF) of perovskite solar cells were improved substantially due to the dopant, which is mainly attributed to the interfacial improvement. It was found that the best efficiency of the devices was achieved when the dopant of iodine was in equivalent mole concentration with that of spiro-OMeTAD. Moreover, the long-term stability of the corresponding device was investigated

SChLAP1 contributes to non-small cell lung cancer cell progression and immune evasion through regulating the AUF1/PD-L1 axis

SChLAP1 is recently reported as a key oncogenic long non-coding RNA in human cancer. However, whether SChLAP1 functions in non-small cell lung cancer (NSCLC) and its specific potential regulatory mechanism remain unexplored. In this study, we found that depletion of SChLAP1 significantly inhibited NSCLC cell proliferation, migration and invasion in vitro, and retarded tumour growth and lung metastasis in vivo. SChLAP1 facilitated NSCLC cell immune evasion against CD8+ T cells through PD-1/PD-L1 immune checkpoint. In detail, SChLAP1 was able to directly interact with AUF1, antagonizing the binding between AUF1 and PDL1 mRNA 3′-UTR, resulting in increasing PDL1 mRNA stability and expression, thereby repressing CD8+ T cell function. Consistently, anti-PD-1/PD-L1 treatment evidently blocked the enhanced cell proliferation and invasion caused by SChLAP1 overexpression. Importantly, SChLAP1 was significantly upregulated in NSCLC cell lines, serum and tissues, which was identified as an excellent indicator for the diagnosis and prognosis of NSCLC. In conclusion, our data for the first time uncover that SChLAP1 functions an oncogene in NSCLC by promoting cancer cell immune evasion via regulating the AUF1/PDL1 axis, targeting of SChLAP1 may be a potential approach to improve the efficacy of immunotherapy in NSCLC patients

Balancing Energy-Level Difference for Efficient n-i-p Perovskite Solar Cells with Cu Electrode

Developing low cost and stable metal electrode is crucial for mass production of perovskite solar cells (PSCs). As an earth-abundant element, Cu becomes an alternative candidate to replace noble metal electrodes such as Au and Ag, due to its comparable physiochemical properties with simultaneously good stability and low cost. However, the undesirable band alignment associated with the device architecture impedes the exploration of efficient Cu-based n-i-p PSCs. Here, we demonstrated the ability of tuning the Fermi level (EF) of hole transport layer (HTL) to reduce the energy level difference (Schottky barrier) between HTLs and Cu. Further, we identified that the balance of energy level difference between HTL and adjacent layers (including perovskite and Cu) is crucial to efficient carrier transportation and photovoltaic performance improvement in the PSCs. Under the optimized condition, we achieve a device power conversion efficiency (PCE) of 20.10%, which is the highest on the planar n-i-p PSCs with Cu electrode. Meanwhile, the Cu-based PSCs can maintain 92% of their initial efficiency after 1000 h storage, which is comparable with Au-based devices. The present work not only extends the understanding on the band alignment of neighboring semiconductor functional layer in the device architecture to improve the resulting performance but also suggests great potential of Cu electrode for application in PSCs community

Variants in Exon 11 of MEF2A Gene and Coronary Artery Disease: Evidence from a Case-Control Study, Systematic Review, and Meta-Analysis

Background: Coronary artery disease (CAD) is the most common heart disease worldwide. Association of CAD with variants in the myocyte enhancer factor 2A (MEF2A) gene, the first identified CAD-causing gene, has attracted special attention but the results are controversial. We aimed to evaluate this genetic association via a case-control study and meta-analysis. Methodology/Principal Findings: We performed a case-control association study to investigate the relationship between variations in exon 11 of MEF2A gene and CAD in 1045 sporadic patients and 1008 controls enrolled angiographically among southern Chinese population, and then the data from this study were compared and discussed in a systematic review and meta-analysis with all available published studies on MEF2A gene and CAD. In total, eight variants were identified (21-bp deletion, CAG repeats, CCG repeats, a CCA deletion and four SNPs). No significant link was observed between the common (CAG) n polymorphism and CAD, whereas the rare 21-bp deletion was detected only in five affected individuals. The metaanalysis of (CAG)n polymorphism and CAD risk, including nine studies with 3801 CAD patients and 4020 controls, also provided no convincing evidence for the genetic association, even upon stratification by race (mainly Whites and Chinese). However, the 21-bp deletion was regarded as a potentially logical, albeit undetermined, candidate for CAD in the following systematic review. Conclusions/Significance: Our findings failed to demonstrate a correlation between (CAG)n polymorphism with CAD

Interactive association of five candidate polymorphisms in Apelin/APJ pathway with coronary artery disease among Chinese hypertensive patients.

BACKGROUND: Via sequencing the genes of apelin/angiotensin receptor-like 1 (apelin/APJ) pathway, we have recently identified and validated four common polymorphisms (rs3761581, rs56204867, rs7119375, and rs10501367) implicated in the development of hypertension. Extending these findings, we, in Chinese hypertensive patients, sought to investigate the association of these four polymorphisms and one additional promising candidate (rs9943582) from this pathway with the risk of developing coronary artery disease (CAD). METHODOLOGY/PRINCIPAL FINDINGS: Genotypes were obtained from 994 sporadic CAD patients and 708 age- and sex-matched controls. All participants were hypertensives and angiographically-confirmed. Data were analyzed by Haplo.Stats and multifactor dimensionality reduction (MDR) softwares. Genotype distributions of five examined polymorphisms satisfied Hardy-Weinberg equilibrium in controls of both genders. Single-locus analyses exhibited no significant differences in the genotype/allele frequencies of examined polymorphisms between CAD patients and controls (P>0.05), even after controlling traditional cardiovascular confounders. In haplotype analyses, low-penetrance haplotype G-A (in order of rs56204867 and rs3761581 from apelin gene) was significantly overrepresented in controls (1.73%) relative to in CAD patients (0.4%) in males (P = 0.047). Further interaction analyses suggested an overall best MDR model including rs3761581 in males (P = 0.0408) and including rs7119375 and rs9943582 in females (P<0.0001), which were further substantiated in the classical logistical regression model. CONCLUSIONS: Our findings demonstrated a contributive role of low-penetrance haplotype in apelin gene on CAD in males, and more importantly, interactive effects of genetic defects in apelin/APJ pathway might confer a potential risk in Chinese hypertensive patients

A Novel Complementation Assay for Quick and Specific Screen of Genes Encoding Glycerol-3-Phosphate Acyltransferases

The initial step in glycerolipid biosynthesis, especially in diverse allopolyploid crop species, is poorly understood, mainly due to the lack of an effective and convenient method for functional characterization of genes encoding glycerol-3-phosphate acyltransferases (GPATs) catalyzing this reaction. Here we present a novel complementation assay for quick and specific characterization of GPAT-encoding genes. Its key design involves rational construction of yeast conditional lethal gat1Δgat2Δ double mutant bearing the heterologous Arabidopsis AtGPAT1 gene whose leaky expression under repressed conditions does not support any non-specific growth, thereby circumventing the false positive problem encountered with the system based on the gat1Δgat2Δ mutant harboring the native episomal GAT1 gene whose leaky expression appears to be sufficient for generating enough GPAT activities for the non-specific restoration of the mutant growth. A complementation assay developed based on this novel mutant enables quick phenotypic screen of GPAT sequences. A high degree of specificity of our assay was exemplified by its ability to differentiate effectively GPAT-encoding genes from those of other fatty acyltransferases and lipid-related sequences. Using this assay, we show that Arabidopsis AtGPAT1, AtGPAT5, and AtGPAT7 can complement the phosphatidate biosynthetic defect in the double mutants. Collectively, our assay provides a powerful tool for rapid screening, validation and optimization of GPAT sequences, aiding future engineering of the initial step of the triacylglycerol biosynthesis in oilseeds

Genotype/allele frequencies of five polymorphisms in apelin/APJ system between CAD patients and controls.

*<p>Because the gene encoding apelin is mapped on the X chromosome, genotype data are unavailable.</p

MDR analysis summary.

*<p>The overall best MDR model.</p

Genomic organization of human apelin (upper panel) and APJ (lower panel) genes, and localization of examined polymorphisms.

<p>Each exon is represented by a black box. Lengths of exons and introns are on the proportional scale. The vertical line marks the position of each polymorphism.</p

The anthropometric index and clinical biomarkers of the study population between CAD patients and controls according to gender.

<p><i>Abbreviations</i>: BMI, body mass index; SBP, systolic blood pressure, DBP, diastolic blood pressure; TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; Apo A, Apolipoprotein A; Apo B, Apolipoprotein B; Lp(a), Lipoprotein(a); BUN, blood urea nitrogen; Cr, Creatinine; UA, uric acid; hsCRP, high sensitivity C-reactive protein. Continuous variables with skewed distributions were transformed in square for age; in log(10) for SBP, DBP, triglycerides, hsCRP; in square root for BMI, LDL-C, and comparison between CAD patients and controls was conducted using the unpaired t-test. The nonparametric Mann-Whitney U test was used for TC, HDL-C, Apo A, Apo B, Lp(a), glucose, BUN, Cr, and UA. Data are expressed as mean (standard deviation or SD). * For patients, age referred to the onset age of CAD, and for controls, age was recorded at enrollment.</p