Exceptional Hole-Selective Properties of Ta2O5 Films via Sn4+ Doping for High Performance Silicon Heterojunction Solar Cells.

Carrier-selective passivating contacts using transition metal oxides (TMOs) have attracted great attention for crystalline silicon (c-Si) heterojunction solar cells recently. Among them, tantalum oxide (Ta2O5) exhibits outstanding advantages, such as a wide bandgap, good surface passivation, and a small conduction band offset with c-Si, which is typically used as an electron-selective contact layer. Interestingly, it is first demonstrated that solution-processed Ta2O5 films exhibit a high hole selectivity, which blocks electrons and promotes hole transport simultaneously. Through the ozone pre-treatment of Ta2O5/p-Si interface and optimization of the film thickness (≈9 nm), the interfacial recombination is suppressed and the contact resistivity is reduced from 178.0 to 29.3 mΩ cm2. Moreover, the Sn4+ doping increases both the work function and oxygen vacancies of the film, contributing to the improved hole-selective contact performance. As a result, the photoelectric conversion efficiencies of Ta2O5/p-Si heterojunction solar cells are significantly improved from 14.84% to 18.47%, with a high thermal stability up to 300 °C. The work has provided a feasible strategy to explore new features of TMOs for carrier-selective contact applications, that is, bipolar carrier transport properties.

Strain Regulation and Defect Passivation of FA-Based Perovskite Materials for Highly Efficient Solar Cells.

Formamidine lead triiodide (FAPbI3 ) perovskites have attracted increasing interest for photovoltaics attributed to the optimal bandgap, high thermal stability, and the record power conversion efficiency (PCE). However, the materials still face several key challenges, such as phase transition, lattice defects, and ion migration. Therefore, external ions (e.g., cesium ions (Cs+ )) are usually introduced to promote the crystallization and enhance the phase stability. Nevertheless, the doping of Cs+ into the A-site easily leads to lattice compressive strain and the formation of pinholes. Herein, trioctylphosphine oxide (TOPO) is introduced into the precursor to provide tensile strain outside the perovskite lattice through intermolecular forces. The special strain compensation strategy further improves the crystallization of perovskite and inhibits the ion migration. Moreover, the TOPO molecule significantly passivates grain boundaries and undercoordinated Pb2+ defects via the forming of P═O─Pb bond. As a result, the target solar cell devices with the synergistic effect of Cs+ and TOPO additives have achieved a significantly improved PCE of 22.71% and a high open-circuit voltage of 1.16 V (voltage deficit of 0.36 V), with superior stability under light exposure, heat, or humidity conditions.

Hypermethylation of the CTRP9 promoter region promotes Hcy induced VSMC lipid deposition and foam cell formation via negatively regulating ER stress.

To provide a theoretical basis for the prevention and treatment of atherosclerosis (As), the current study aimed to investigate the mechanism underlying the effect of homocysteine (Hcy) on inducing the lipid deposition and foam cell formation of the vascular smooth muscle cell (VSMC) via C1q/Tumor necrosis factor-related protein9 (CTRP9) promoter region Hypermethylation negative regulating endoplasmic reticulum stress (ERs). Therefore, apolipoprotein E deficient (ApoE-/-) mice were randomly divided into the control [ApoE-/- + normal diet (NC)] and high methionine [ApoE-/- + (normal diet supplemented with 1.7% methionine (HMD)] groups (n = 6 mice/group). Following feeding for 15 weeks, the serum levels of Homocysteine (Hcy), total cholesterol (TC), and triglyceride (TG) were measured using an automatic biochemical analyzer. HE and oil red O staining were performed on the aorta roots to observe the pathological changes. Additionally, immunofluorescence staining was performed to detect the protein expression levels of CTRP9, glucose-regulated protein 78 kD (GRP78), phosphorylated protein kinase RNA-like ER kinase (p-PERK), activating transcription factor 6a (ATF6a), phosphorylated inositol-requiring enzyme-1α (p-IRE1α), sterol regulatory element binding proteins-1c (SREBP1c) and sterol regulatory element binding proteins-2 (SREBP2) in VSMC derived from murine aortic roots. In vitro, VSMC was stimulated with 100 µmol/l Hcy. After transfection of plasmids with overexpression and interference of CTRP9, ERs agonist (TM) and inhibitor (4-PBA) were given to stimulate VSMC cells. HE staining and oil red O staining were used to observe the effect of Hcy stimulation on lipid deposition in VSMC. Additionally, The mRNA and protein expression levels of CTRP9, GRP78, PERK, ATF6a, IRE1α, SREBP1c, and SREBP2 in VSMC were detected by RT-qPCR and western blot analysis, respectively. Finally, The methylation modification of the CTRP9 promoter region has been studied. The NCBI database was used to search the promoter region of the CTRP9 gene, and CpG Island was used to predict the methylation site. After Hcy stimulation of VSMC, overexpression of DNMT1, and intervention with 5-Azc, assess the methylation level of the CTRP9 promoter through bisulfite sequencing PCR (BSP). The results showed that the serum levels of Hcy, TC, and TG in the ApoE-/- + HMD group were significantly increased compared with the ApoE-/- + NC group. In addition, HE staining and oil red O staining showed obvious AS plaque formation in the vessel wall, and a large amount of fat deposition in VSMC, thus indicating that the hyperhomocysteinemia As an animal model was successfully established. Furthermore, CTRP9 were downregulated, while GRP78, p-PERK, ATF6a, p-IRE1α, SREBP1c, SREBP2 was upregulated in aortic VSMC in the ApoE-/- + HMD group. Consistent with the in vivo results, Hcy can inhibit the expression of CTRP9 in VSMC and induce ERs and lipid deposition in VSMC. Meanwhile, the increased expression of CTRP9 can reduce ERs and protect the lipid deposition in Hcy induced VSMC. Furthermore, ERs can promote Hcy induced VSMC lipid deposition, inhibition of ERs can reduce Hcy induced VSMC lipid deposition, and CTRP9 may play a protective role in Hcy induced VSMC lipid deposition and foam cell transformation through negative regulation of ERs. In addition, The CTRP9 promoter in the Hcy group showed hypermethylation. At the same time as Hcy intervention, overexpression of DNMT1 increases the methylation level of the CTRP9 promoter, while 5-Azc can reduce the methylation level of the CTRP9 promoter. Finally, Hcy can up-regulate the expression of DNMT1 and down-regulate the expression of CTRP9. After overexpression of DNMT1, the expression of CTRP9 is further decreased. After 5-Azc inhibition of DNMT1, the expression of DNMT1 decreases, while the expression of CTRP9 increases. It is suggested that the molecular mechanism of Hcy inhibiting the expression of CTRP9 is related to the hypermethylation of the CTRP9 promoter induced by Hcy and regulated by DNMT1. 5-Azc can inhibit the expression of DNMT1 and reverse the regulatory effect of DNMT1 on CTRP9. Overall, the results of the present study suggested that Hcy induces DNA hypermethylation in the CTRP9 promoter region by up-regulating DNMT1 expression, and negatively regulates ERs mediated VSMC lipid deposition and foam cell formation. CTRP9 may potentially be a therapeutic target in the treatment of hyperhomocysteinemia and As.

CuCl2-modified SnO2electron transport layer for high efficiency perovskite solar cells.

SnO2film is one of the most widely used electron transport layers (ETL) in perovskite solar cells (PSCs). However, the inherent surface defect states in SnO2film and mismatch of the energy level alignment with perovskite limit the photovoltaic performance of PSCs. It is of great interesting to modify SnO2ETL with additive, aiming to decrease the surface defect states and obtain well aligned energy level with perovskite. In this paper, anhydrous copper chloride (CuCl2) was employed to modify the SnO2ETL. It is found that the adding of a small amount of CuCl2into the SnO2ETL can improve the proportion of Sn4+in SnO2, passivate oxygen vacancies at the surface of SnO2nanocrystals, improve the hydrophobicity and conductivity of ETL, and obtain a good energy level alignment with perovskite. As a result, both the photoelectric conversion efficiency (PCE) and stability of the PSCs based on SnO2ETLs modified with CuCl2(SnO2-CuCl2) is improved in comparison with that of the PSCs on pristine SnO2ETLs. The optimal PSC based on SnO2-CuCl2ETL exhibits a much higher PCE of 20.31% as compared to the control device (18.15%). The unencapsulated PSCs with CuCl2modification maintain 89.3% of their initial PCE after exposing for 16 d under ambient conditions with a relative humidity of 35%. Cu(NO3)2was also employed to modify the SnO2ETL and achieved a similar effect as that of CuCl2, indicating that the cation Cu2+plays the main role in SnO2ETL modification.

Identification and Validation of Immune-Related Genes Diagnostic for Progression of Atherosclerosis and Diabetes.

Background: Atherosclerosis and type 2 diabetes mellitus contribute to a large part of cardiovascular events, but the underlying mechanism remains unclear. In this study, we focused on identifying the linking genes of the diagnostic biomarkers and effective therapeutic targets associated with these two diseases. Methods: The transcriptomic datasets of atherosclerosis and type 2 diabetes mellitus were obtained from the GEO database. Differentially expressed genes analysis was performed by R studio software, and differential analysis including functional enrichment, therapeutic small molecular agents prediction, and protein-protein interaction analysis were applied to the common shared differentially expressed genes. Hub genes were identified and further validated using an independent dataset and clinical samples. Furthermore, we measured the expression correlations, immune cell infiltration, and diagnostic capability of the three key genes. Results: We screened out 28 up-regulated and six down-regulated common shared differentially expressed genes. Functional enrichment analysis showed that cytokines and immune activation were involved in the development of these two diseases. Six small molecules with the highest absolute enrichment value were identified. Three critical genes (CD4, PLEK, and THY1) were further validated both in validation sets and clinical samples. The gene correlation analysis showed that CD4 was strongly positively correlated with PLEK, and ROC curves confirmed the good discriminatory capacity of CD4 and PLEK in two diseases.We have established the co-expression network between atherosclerosis lesions progressions and type 2 diabetes mellitus, and identified CD4 and PLEK as key genes in the two diseases, which may facilitate both development of diagnosis and therapeutic strategies.

Developing a Novel Immune-Related Seven-Gene Signature and Immune Infiltration Pattern in Patients with COVID-19 and Cardiovascular Disease.

BACKGROUND: patients with pre-existence of cardiovascular disease (CVD) are vulnerable to coronavirus disease 2019 (COVID-19), and COVID-19 will cause long-term burden of CVD. However, the common pathogenic mechanisms are not fully elucidated. More detailed knowledge of linking biological molecules and the role of immune signature would allow more valuable and specific clinical management. METHODS: the gene expression profiles of CVD and COVID-19 were retrieved from the GEO database. Common differentially expressed genes (DEGs) were screened with the Limma R package and the WGCNA algorithm, and then functional enrichment analysis, protein-protein interaction network, hub genes, and small therapeutic molecules analyses were performed. The hub immune-related genes (HIRGs) were intersected, and their associations with immune cells, expressional correlation, evaluated performance, and potential signal pathways were further investigated. RESULTS: In total, 57 common DEGs were identified as a shared transcriptional signature between CVD and COVID-19, and 12 hub genes were screened using five topological algorithms. There are common altered immune responses in the response of these two diseases, and seven HIRGs, including C5AR1, MMP9, CYBB, FPR2, CSF1R, TLR2, and TLR4, were identified, with positive correlation to altered macrophages and neutrophils. Nine small molecular agents (SMAs) were detected as promising therapeutic drugs. These seven HIRGs mainly participated in the inflammatory immune response through activation of Il2 stat5 signaling and Tnfa signaling via nfκb pathways, and ROC curves confirmed their good discriminatory capacity in the two diseases. CONCLUSIONS: this study established the co-expression network and identified a new immune-related seven-gene signature as therapeutic targets, which may provide new insights into pathogenic mechanisms and novel clinical management strategies.

Extracellular-superoxide dismutase DNA methylation promotes oxidative stress in homocysteine-induced atherosclerosis.

In the present study, we investigate the effect of homocysteine (Hcy) on extracellular-superoxide dismutase (EC-SOD) DNA methylation in the aorta of mice, and explore the underlying mechanism in macrophages, trying to identify the key targets of Hcy-induced EC-SOD methylation changes. ApoE -/- mice are fed different diets for 15 weeks, EC-SOD and DNA methyltransferase 1 (DNMT1) expression levels are detected by RT-PCR and western blot analysis. EC-SOD methylation levels are assessed by ntMS-PCR. After EC-SOD overexpression or knockdown in macrophages, following the transfection of macrophages with pEGFP-N1-DNMT1, the methylation levels of EC-SOD are detected. Our data show that the concentrations of Hcy and the area of atherogenic lesions are significantly increased in ApoE -/- mice fed with a high-methionine diet, and have a positive correlation with the levels of superoxide anions, which indicates that Hcy-activated superoxide anions enhance the development of atherogenic lesions. EC-SOD expression is suppressed by Hcy, and the content of superoxide anion is increased when EC-SOD is silenced by RNAi in macrophages, suggesting that EC-SOD plays a major part in oxidative stress induced by Hcy. Furthermore, the promoter activity of EC-SOD is increased following transfection with the -1/-1100 fragment, and EC-SOD methylation level is significantly suppressed by Hcy, and more significantly decreased upon DNMT1 overexpression. In conclusion, Hcy may alter the DNA methylation status and DNMT1 acts as the essential enzyme in the methyl transfer process to disturb the status of EC-SOD DNA methylation, leading to decreased expression of EC-SOD and increased oxidative stress and atherosclerosis.

Optimized photoelectric characteristics of MAPbCl3and MAPbBr3composite perovskite single crystal heterojunction photodetector.

MAPbBr3single crystal (SC) thin layer was successfully grown on MAPbCl3SC substrate to form perovskite SC heterojunction. Planar structure electrodes are deposited by thermal evaporation on the surfaces of MAPbCl3, MAPbBr3, and SCs heterojunction, respectively to evaluate their photoelectric performance. The SC heterojunction device exhibits excellent unidirectional conductivity in the voltage-current curves. Meanwhile, the current-time curves prove that SC heterojunction devices can effectively utilize the advantages of MAPbCl3and MAPbBr3, possessing relatively low dark current (∼300 nA), which is comparable to the dark current of MAPbCl3, but very high photocurrent (∼3500 nA), which is equivalent to the photocurrent of MAPbBr3. Rather than the photocurrent overshot and decay occurring at the exposure of light illumination in the MAPbBr3device, the photocurrent is extremely stable without overshot and decay in the SC heterojunction device. The light-to-dark ratio of the SC heterojunction device is twice that of MAPbCl3device and three times that of MAPbBr3device. Furthermore, the detectivity of the heterojunction device reaches as high as∼7×1011 Jones, an order of magnitude higher than MAPbCl3and MAPbBr3. The excellent characteristics of SC heterojunction further expand the practical application prospect of perovskite materials.

Ischemic Postconditioning Protects against Aged Myocardial Ischemia/Reperfusion Injury by Transcriptional and Epigenetic Regulation of miR-181a-2-3p.

Ischemic postconditioning (IPostC) has been proposed as a strategy to mitigate the risk of ischemia/reperfusion (I/R) injury, and autophagy is involved in I/R-induced aged myocardial injury, while the underlying mechanism of IPostC-regulated autophagy is unknown. Here, we implemented miRNA sequencing analysis in aged cardiomyocytes to identify a novel miR-181a-2-3p after HPostC, which inhibits autophagy by targeting AMBRA1 in aged myocardium to protect I/R-induced aged myocardial injury. Mechanistically, we identified that IPostC can induce DNA hypomethylation and H3K14 hyperacetylation of miR-181a-2-3p promoter due to the decreased binding of DNMT3b and HDAC2 at its promoter, which contributes to enhancing the expression of miR-181a-2-3p. More importantly, cooperation of DNMT3b and HDAC2 inhibits the binding of c-Myc at the miR-181a-2-3p promoter in aged cardiomyocytes. In summary, IPostC attenuates I/R-induced aged myocardial injury through upregulating miR-181a-2-3p expression, which is an attribute to transcriptional and epigenetic regulation of its promoter. Our data indicate that miR-181a-2-3p may be a potential therapeutic target against I/R injury in aged myocardium.

FABP4 activates the JAK2/STAT2 pathway via Rap1a in the homocysteine-induced macrophage inflammatory response in ApoE-/- mice atherosclerosis.

Atherosclerosis is a chronic inflammatory vascular disease, and inflammation plays a critical role in its formation and progression. Elevated serum homocysteine (Hcy) is an independent risk factor for atherosclerosis. Previous studies have shown that fatty acid binding protein 4 (FABP4) plays an important role in macrophage inflammation and lipid metabolism in atherosclerosis induced by Hcy. However, the underlying molecular mechanism of FABP4 in Hcy-induced macrophage inflammation remains unknown. In this study, we found that FABP4 activated the Janus kinase 2/signal transducer and activator of transcription 2 (JAK2/STAT2) pathway in macrophage inflammation induced by Hcy. Of note, we further observed that ras-related protein Rap-1a (Rap1a) induced the Tyr416 phosphorylation and membrane translocation of non-receptor tyrosine kinase (c-Src) to activate the JAK2/STAT2 pathway. In addition, the suppressor of cytokine signaling 1 (SOCS1)-a transcriptional target of signal transducer and activator of transcription (STATs) inhibited the JAK2/STAT2 pathway and Rap1a expression via a negative feedback loop. In summary, these results demonstrated that FABP4 promotes c-Src phosphorylation and membrane translocation via Rap1a to activate the JAK2/STAT2 pathway, contributing to Hcy-accelerated macrophage inflammation in ApoE-/- mice.

TGFB3-AS1 promotes Hcy-induced inflammationof macrophages via inhibiting the maturityof miR-144 and upregulating Rap1a.

It has been demonstrated that homocysteine (Hcy) can cause inflammatory diseases. Long noncoding RNAs (lncRNA) and microRNAs (miRNAs) are involved in this biological process, but the mechanism underlying Hcy-induced inflammation remains poorly understood. Here, we found that lncRNA TGFB3-AS1 was highly expressed in macrophages treated with Hcy and the peripheral blood monocytes from cystathionine beta-synthase heterozygous knockout (CBS +/-) mice with a high-methionine diet using lncRNA microarray. In vivo and in vitro experiments further confirmed that TGFB3-AS1 accelerated Hcy-induced inflammation of macrophages through the Rap1a/wnt signaling pathway. Meanwhile, TGFB3-AS1 interacted with Rap1a and reduced degradation of Rap1a through inhibiting its ubiquitination in macrophages treated with Hcy. Rap1a mediated inflammation induced by Hcy and serves as a direct target of miR-144. Moreover, TGFB3-AS1 regulated miR-144 by binding to pri-miR-144 and inhibiting its maturation, which further regulated Rap1a expression. More importantly, we found that high expression of TGFB3-AS1 was positively correlated with the levels of Hcy and proinflammatory cytokines in serum of healthy individuals and patients with HHcy. Our study revealed a novel mechanism by which TGFB3-AS1 promoted inflammation of macrophages through inhibiting miR-144 maturation to stay miR-144 regulated inhibition of functional Rap1a expression.

Interaction between PSMD10 and GRP78 accelerates endoplasmic reticulum stress-mediated hepatic apoptosis induced by homocysteine.

BACKGROUND: The liver plays an important role in production and metabolism of homocysteine (Hcy), which has been reported to be involved in liver injury. In our previous work, we confirm that Hcy can induce liver injury by activating endoplasmic reticulum (ER) stress. However, the underlying mechanisms remain largely unknown. RESULTS: In present study, we established the Hcy-induced liver injury model by feeding cbs+/- mice with high methionine diet, and found that a considerable mass of disordered arrangement of hepatocytes and enlarged space between hepatocytes were frequently occurred in the liver of cbs+/- mice, accompanied with elevated expression levels of apoptosis-related proteins. In addition, Hcy could activate ER stress both in cbs+/- mice and hepatocytes. Mechanistically, Hcy promoted the expression levels of proteasome 26S subunit non-ATPase 10 (PSMD10) in hepatocytes; and the expression of ER stress indicators and apoptosis-associated proteins were significantly suppressed when PSMD10 was silenced in hepatocytes under Hcy treatment. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that PSMD10 was a target gene of miR-212-5p. Consistently, miR-212-5p overexpression could inhibit ER stress-mediated apoptosis of hepatocytes under Hcy treatment. With the help of co-immunoprecipitation assay, we identified that the interaction between PSMD10 and GRP78 accelerated ER stress-mediated hepatic apoptosis induced by Hcy. CONCLUSIONS: Our findings indicate that miR-212-5p directly targets PSMD10 and subsequently activates ER stress to promote Hcy-induced apoptosis of hepatocytes. We propose that endogenous PSMD10 physically interacts with GRP78 to regulate ER stress. Our study may provide the therapeutic target for the liver injury induced by Hcy.

miR-195-3p alleviates homocysteine-mediated atherosclerosis by targeting IL-31 through its epigenetics modifications.

Atherosclerosis is a serious age-related disease, which has a tremendous impact on health care globally. Macrophage inflammation is crucial for the initiation and progression of atherosclerosis, and microRNAs (miRNAs) recently have emerged as potent modulators of inflammation, while the underlying mechanisms of its involvement in homocysteine (Hcy)-mediated macrophage inflammation of atherosclerosis remain largely unknown. Here, we demonstrated that elevated Hcy inhibits the expression of miR-195-3p, which in turn enhances IL-31 expression and thereby causes the secretion of macrophages pro-inflammatory factors IL-1ß, IL-6 and TNF-α and accelerate atherosclerosis. Furthermore, we identified that Hcy can induce DNA hypermethylation and H3K9 deacetylation of miR-195-3p promoter due to the increased the binding of DNMT3a and HDAC11 at its promoter. More importantly, Sp1 interacts with DNMT3a suppressed the binding of HDAC11 at miR-195-3p promoter and promoted its transcription. In summary, our results revealed a novel mechanism that transcriptional and epigenetic regulation of miR-195-3p inhibits macrophage inflammation through targeting IL-31, which provides a candidate diagnostic marker and novel therapeutic target in cardiovascular diseases induced by Hcy.

Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.

Chronic kidney disease (CKD) is a common and complex disease in kidneys which has been associated with an increased risk of renal cell carcinoma. Elevated homocysteine (Hcy) levels are known to influence the development and progression of CKD by regulating podocyte injury and apoptosis. To investigate the molecular mechanisms triggered in podocytes by Hcy, we used cbs+/- mice and observed that higher Hcy levels increased the apoptosis rate of podocytes with accompanying glomerular damage. Hcy-induced podocyte injury and apoptosis in cbs+/- mice was regulated by inhibition of microRNA (miR)-1929-5p expression. Overexpression of miR-1929-5p in podocytes inhibited apoptosis by upregulating Bcl-2. Furthermore, the expression of miR-1929-5p was regulated by epigenetic modifications of its promoter. Hcy upregulated DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, resulting in increased DNA methylation and H3K27me3 levels on the miR-1929-5p promoter. Additionally, we observed that c-Myc recruited DNMT1 and EZH2 to the miR-1929-5p promoter and suppressed the expression of miR-1929-5p. In summary, we demonstrated that Hcy promotes podocyte apoptosis through the regulation of the epigenetic modifiers DNMT1 and EZH2, which are recruited by c-Myc to the promoter of miR-1929-5p to silence miR-1929-5p expression.

Variational hysteresis and photoresponse behavior of MAPbX3(X= I, Br, Cl) perovskite single crystals.

High-quality MAPbX3(X= I, Br, Cl) single crystals with a desirable size were grown through an inverse temperature crystallization method. Systematically measurements of current-voltage (I-V) hysteresis show that the hysteresis is strongly dependent on the measuring protocol, including scan rate and light illumination condition, which reveals the competition of three main factors that influence the charge dynamics in different regimes, defect trap, MA+dipoles rotation, and ion migration. In the dark, defect trapping is the dominant charge transport dynamics at low bias in the MAPbI3, while the MA+dipole rotation is significant in MAPbBr3, and ion migration occurs in MAPbCl3. However, as bias increases, MA+dipole rotation plays a crucial role in the conductivity either in the dark or under light illumination. The time-dependent photoresponse exhibits different tendencies under various biases. The slow rising dynamics of photoresponse in MAPbX3is attributed to the slow rotation of MA+dipoles, while an immediate overshoot followed by a decay suggests significant ion migration contribution at high external bias. The results serve as comprehensive experimental support to understand the hysteresis behaviors and slow photoresponse in MAPbX3, particularly in MAPbCl3, and provide a guide for future work in MAPbX3based optoelectronic devices.

H3K14 hyperacetylation­mediated c­Myc binding to the miR­30a­5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury.

Our previous study reported that microRNA (miR)­30a­5p upregulation under hypoxia postconditioning (HPostC) exert a protective effect on aged H9C2 cells against hypoxia/reoxygenation injury via DNA methyltransferase 3B­induced DNA hypomethylation at the miR­30a­5p gene promoter. This suggests that miR­30a­5p may be a potential preventative and therapeutic target for ischemic heart disease in aged myocardium. The present study aimed to investigate the underlying mechanisms of miR­30a­5p transcription in aged myocardium in ischemic heart disease. Cardiomyocytes were treated with 8 mg/ml D­galactose for 9 days, and then exposed to hypoxic conditions. Cell viability was determined using a cell viability assay. Expression levels of histone deacetylase 2 (HDAC2), LC3B­II/I, beclin­1 and p62 were detected via reverse transcription­quantitative PCR and western blotting. Chromatin immunoprecipitation­PCR and luciferase reporter assays were performed to evaluate the effect of c­Myc binding and activity on the miR­30a­5p promoter in senescent cardiomyocytes following HPostC. It was found that HPostC enhanced the acetylation levels of H3K14 at the miR­30a­5p gene promoter in senescent cardiomyocytes, which attributed to the decreased expression of HDAC2. In addition, c­Myc could positively regulate miR­30a­5p transcription to inhibit senescent cardiomyocyte autophagy. Mechanically, it was observed that increased H3K14 acetylation level exposed to romidepsin facilitated c­Myc binding to the miR­30a­5p gene promoter region, which led to the increased transcription of miR­30a­5p. Taken together, these results demonstrated that HDAC2­mediated H3K14 hyperacetylation promoted c­Myc binding to the miR­30a­5p gene promoter, which contributed to HPostC senescent cardioprotection.

[Long non-coding RNA growth arrest specific transcript 5 (lncGAS5) promotes autophagy of hepatocytes induced by homocysteine].

Objective To study the role of long non-coding RNA growth arrest specific transcript 5 (lncGAS5) in the autophagy of hepatocytes induced by homocysteine (Hcy). Methods HL7702 human hepatocyte cells were cultured in vitro and divided into control group and Hcy group. Western blotting was used to detect the expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and P62. The cells were transfected with mRFP-GFP-LC3 adenovirus to observe the autophagy flow with laser scanning confocal microscope. Real-time quantitative PCR was performed to detect the expression level of lncGAS5. lncGAS5 small interfering RNA (si-lncGAS5) and negative control small interfering RNA (si-NC) were transfected into the cells. After the transfected cells were treated with Hcy, the changes of LC3B, P62 and autophagy flow were analyzed with the above methods. Results Compared with the control group, the LC3BII/LC3BI ratio increased and the expression of P62 protein decreased in the Hcy group. When the lever of Hcy lifted, the number of autophagosomes and autolysosomes and the expression of lncGAS5 increased in the cells. After knock-down of lncGAS5, the ratio of LC3BII/LC3BI decreased and the expression of P62 increased. Moreover, the number of autophagosomes and autolysosomes were reduced in the cells. Conclusion lncGAS5 can promote the autophagy of hepatocytes induced by Hcy.

Antisolvent engineering on low-temperature processed CsPbI3 inorganic perovskites for improved performances of solar cells.

CsPbI3 inorganic perovskites with ideal bandgap and much enhanced thermal stability compared with organic-inorganic hybrid perovskites, have attracted much interest in the field of solar cells. The performances of solar cells highly depend on the quality of perovskite films, yet the research on fabrication methods of inorganic perovskites is far below that of organic-inorganic hybrid counterparts. Antisolvent engineering is a widely used method in controlling the morphology and crystallinity of organic-inorganic hybrid perovskites. Its effect varies with parameters such as the physicochemical properties of antisolvents and the compositions of perovskite precursors. Specially, there lacks a comprehensive study comparing different antisolvents used in low-temperature processed CsPbI3 from dimethylammonium-based precursors. In this work, we used three different antisolvents to control the growth of CsPbI3 films in a low-temperature (<200 °C) processed procedure and systematically compared the properties of resultant films. The green antisolvent ethyl acetate (EA) engineered CsPbI3 films exhibit improved morphology and crystallinity as well as reduced defects, compared with the counterparts processed without antisolvent or those with widely employed toxic antisolvents toluene and chlorobenzene. The EA antisolvent engineering results in efficient CsPbI3 perovskite solar cells with a champion power conversion efficiency of 8.8%. Our work thus provides a green and viable way to prepare high quality CsPbI3 perovskite films for optoelectronic applications.

Identification of potential biomarkers and their clinical significance in gastric cancer using bioinformatics analysis methods.

BACKGROUND: Alternative splicing (AS) is an important mechanism for regulating gene expression and proteome diversity. Tumor-alternative splicing can reveal a large class of new splicing-associated potential new antigens that may affect the immune response and can be used for immunotherapy. METHODS: The RNA-seq transcriptome data and clinical information of stomach adenocarcinoma (STAD) cohort were downloaded from The Cancer Genome Atlas (TCGA) database data portal, and data of splicing events were obtained from the SpliceSeq database. Predicting genes were validated by Asian cancer research group (ACRG) cohort and Oncomine database. RT-qPCR was used to analysis the expression of ECT2 in STAD. RESULTS: A total of 32,166 AS events were identified, among which 2,042 AS events were significantly associated with patients survival. Biological pathway analysis indicated that these genes play an important role in regulating gastric cancer-related processes such as GTPase activity and PI3K-Akt signaling pathway. Next, we derived a risk signature, using alternate acceptor, that is an independent prognostic marker. Moreover, high ECT2 expression was associated with poorer prognosis in STAD. Multivariate survival analysis demonstrated that high ECT2 expression was an independent risk factor for overall survival. Gene set enrichment analysis revealed that high ECT2 expression was enriched for hallmarks of malignant tumors. The ACRG cohort and Oncomine also showed that high ECT2 expression was associated with poorer prognosis in gastric cancer patients. Finally, RT-qPCR showed ECT2 expression was higher in STAD compared to the normal tissues. CONCLUSION: This study excavated the alternative splicing events in gastric cancer, and found ECT2 might be a biomarkers for diagnosis and prognosis.

In-situ growth of high-density ultrafine Ag3PO4 nanoparticles on 3D TiO2 hierarchical spheres for enhanced photocatalytic degradation of organic pollutants.

Silver phosphate (Ag3PO4, APO) has attracted intense attention as a visible-light-driven photocatalyst, but its large-scale application is limited by severe charge recombination and inevitable photo-corrosion. Various rational APO-based heterostructures composed of APO nanoparticles (NPs) and band-matched semiconductor support are designed to address the above issues. Nevertheless, the size, density, stability, and dispersion of APO NPs are critical challenges for the photocatalytic performance of APO-based photocatalysts. Here, three-dimensional (3D) self-assembled TiO2 hierarchical spheres (THS) prepared by a simple one-step hydrothermal method are employed as innovative support, and ultrafine high-density APO NPs with an average size of about 3 nm are successfully deposited and uniformly dispersed throughout THS to form hierarchical THS/APO composites. The novel THS/APO microstructure provides abundant reactive sites for photocatalytic reactions and promotes the photogenerated charge separation and transfer due to the ultrafine size of APO NPs and the TiO2/APO Type-II heterojunction. As a result, the THS/APO composites show significant improvement in photocatalytic activity and stability in methylene blue (MB) degradation. The reaction constant of THS/APO composites far exceeds that of either THS or APO, roughly 16 and 7 times higher than that of THS and APO under full-spectrum light, and 41 and 4 times higher under visible light. Our results strongly suggest new insights into the low-cost, large-scale application of high-efficiency APO-based photocatalyst.