Nuclear KRT19 is a transcriptional corepressor promoting histone deacetylation and liver tumorigenesis.

BACKGROUND AND AIMS: Epigenetic reprogramming and escape from terminal differentiation are poorly understood enabling characteristics of liver cancer. Keratin 19 (KRT19), classically known to form the intermediate filament cytoskeleton, is a marker of stemness and worse prognosis in liver cancer. This study aimed to address the functional roles of KRT19 in liver tumorigenesis and to elucidate the underlying mechanisms. APPROACH AND RESULTS: Using multiplexed genome editing of hepatocytes in vivo, we demonstrated that KRT19 promoted liver tumorigenesis in mice. Cell fractionation revealed a previously unrecognized nuclear fraction of KRT19. Tandem affinity purification identified histone deacetylase 1 and REST corepressor 1, components of the corepressor of RE-1 silencing transcription factor (CoREST) complex as KRT19-interacting proteins. KRT19 knockout markedly enhanced histone acetylation levels. Mechanistically, KRT19 promotes CoREST complex formation by enhancing histone deacetylase 1 and REST corepressor 1 interaction, thus increasing the deacetylase activity. ChIP-seq revealed hepatocyte-specific genes, such as hepatocyte nuclear factor 4 alpha ( HNF4A ), as direct targets of KRT19-CoREST. In addition, we identified forkhead box P4 as a direct activator of aberrant KRT19 expression in liver cancer. Furthermore, treatment of primary liver tumors and patient-derived xenografts in mice suggest that KRT19 expression has the potential to predict response to histone deacetylase 1 inhibitors especially in combination with lenvatinib. CONCLUSIONS: Our data show that nuclear KRT19 acts as a transcriptional corepressor through promoting the deacetylase activity of the CoREST complex, resulting in dedifferentiation of liver cancer. These findings reveal a previously unrecognized function of KRT19 in directly shaping the epigenetic landscape in cancer.

Gut flora disequilibrium promotes the initiation of liver cancer by modulating tryptophan metabolism and up-regulating SREBP2.

The gut microbiota and liver cancer have a complex interaction. However, the role of gut microbiome in liver tumor initiation remains unknown. Herein, liver cancer was induced using hydrodynamic transfection of oncogenes to explore liver tumorigenesis in mice. Gut microbiota depletion promoted liver tumorigenesis but not progression. Elevated sterol regulatory element-binding protein 2 (SREBP2) was observed in mice with gut flora disequilibrium. Pharmacological inhibition of SREBP2 or Srebf2 RNA interference attenuated mouse liver cancer initiation under gut flora disequilibrium. Furthermore, gut microbiota depletion impaired gut tryptophan metabolism to activate aryl hydrocarbon receptor (AhR). AhR agonist Ficz inhibited SREBP2 posttranslationally and reversed the tumorigenesis in mice. And, AhR knockout mice recapitulated the accelerated liver tumorigenesis. Supplementation with Lactobacillus reuteri, which produces tryptophan metabolites, inhibited SREBP2 expression and tumorigenesis in mice with gut flora disequilibrium. Thus, gut flora disequilibrium promotes liver cancer initiation by modulating tryptophan metabolism and up-regulating SREBP2.

The Impact of Hydrogen Sulfide in the Paraventricular Nucleus on the MAPK Pathway in High Salt-Induced Hypertension.

ABSTRACT: The hypothalamic paraventricular nucleus (PVN) plays a central role in regulating cardiovascular activity and blood pressure. We administered hydroxylamine hydrochloride (HA), a cystathionine-ß-synthase inhibitor, into the PVN to suppress endogenous hydrogen sulfide and investigate its effects on the mitogen-activated protein kinase (MAPK) pathway in high salt (HS)-induced hypertension. We randomly divided 40 male Dahl salt-sensitive rats into 4 groups: the normal salt (NS) + PVN vehicle group, the NS + PVN HA group, the HS + PVN vehicle group, and the HS + PVN HA group, with 10 rats in each group. The rats in the NS groups were fed a NS diet containing 0.3% NaCl, while the HS groups were fed a HS diet containing 8% NaCl. The mean arterial pressure was calculated after noninvasive measurement using an automatic sphygmomanometer to occlude the tail cuff once a week. HA or vehicle was infused into the bilateral PVN using Alzet osmotic mini pumps for 6 weeks after the hypertension model was successfully established. We measured the levels of H 2 S in the PVN and plasma norepinephrine using enzyme linked immunosorbent assay. In addition, we assessed the parameters of the MAPK pathway, inflammation, and oxidative stress through western blotting, immunohistochemical analysis, or real-time polymerase chain reaction. In this study, we discovered that decreased levels of endogenous hydrogen sulfide in the PVN contributed to the onset of HS-induced hypertension. This was linked to the activation of the MAPK signaling pathway, proinflammatory cytokines, and oxidative stress in the PVN, as well as the activation of the sympathetic nervous system.

Two new sesquiterpenoid glycoside compounds from the calyces of Physalis alkekengi L. var. franchetii (Mast.) Makino.

Two new sesquiterpenoid glycosides, 8α (H)-eudesmane-1,3,11 (13)-triene-2-one -12-O-ß-D-glucopyranoside (1) and dmetelisproside B (2), together with ten known compounds (3-12) were isolated from calyces of Physalis alkekengi L. var. franchetii (Mast.) Makino (PAF). Their structures were unambiguously elucidated through HR-ESI-MS, UV, IR, and NMR spectral data. Compounds 1, 10, and 12 exhibited DPPH scavenging ability with IC50 values of 33.69 ± 6.65, 6.29 ± 0.06, and 25.66 ± 3.06 µM, respectively. Additionally, 10 and 12 demonstrated weak α-glucosidase inhibition activity with IC50 values of 250.9 ± 6.60 and 347.6 ± 2.48 µM, respectively.

A protein-based prognostic model for pancreatic ductal adenocarcinoma: Construction and validation.

BACKGROUND: Probing relevant proteomic biomarkers may facilitate effective pancreatic adenocarcinoma (PDAC) diagnosis, treatment and prevention. Here, we developed a protein-based prognostic model for PDAC by using relevant proteomic biomarkers data from The Cancer Genome Atlas (TCGA). METHODS: We obtained PDAC's proteomic and clinical data from TCGA and used various analytical tools to identify differentially expressed proteins between normal and cancer tissues. We constructed our protein-based prognostic model and confirmed its accuracy using receiver operating characteristic curve and Kaplan-Meier survival analyses. We elucidated clinical factor-signature protein correlations by clinical correlation assessments and protein coexpression networks. We also used immunohistochemistry (protein expression assessment), Gene Set Enrichment Analysis (protein role identification) and CIBERSORT (infiltrating immune cell distribution assessment). RESULTS: CIITA, BRAF_pS445, AR, YTHDF2, IGFBP2 and CDK1_pT14 were identified as PDAC-associated prognostic proteins. All risk scores calculated using our model provided 1-, 3-, 5-year survival probability at 70 % accuracy. The reliability of our model was validated by the GEO as well. In high- and low-risk groups, age, sex, T- and N- stage disparities were significant, and prognostic and coexpressed proteins correlated. PDAC tissues demonstrated significant CDK1_pT14 overexpression but significant BRAF_pS445, YTHDF2, and IGFBP2 underexpression. Downstream proteins of BRAF were validated by IHC. Low-risk tissues demonstrated more naïve B cells, eosinophils, activated NK cells and regulatory T cells, whereas high-risk tissues demonstrated more activated memory T cells, monocytes, neutrophils, dendritic cells and resting NK cells. CONCLUSIONS: Our protein-based prognostic model for PDAC, along with six signature proteins, might aid in predicting PDAC prognosis and therapeutic targets.

Retrieving Spectra of Pure Components from the DOSY-NMR Experiment via a Comprehensive Approach Involving the 2D Asynchronous Spectrum, 2D Quotient Spectrum, and Genetic Algorithm Refinement.

When diffusion coefficients of different components in a mixture are similar, NMR spectra of pure individual components are difficult to be obtained via a diffusion-ordered spectroscopy (DOSY) experiment. Two-dimensional correlation spectroscopy (2D-COS) is used to analyze the data from the DOSY experiment. Through the properties of the systematic absence of cross-peak (SACP) in the 2D asynchronous spectra, spectra of pure components can be obtained even if their diffusion coefficients are similar. However, fluctuations in peak-position and peak-width are often unavoidable in NMR spectra, which makes SACPs unrecognizable. To address the problem, a 2D quotient spectrum is used to identify the masked SACPs. However, undesirable interference peaks due to the fluctuations in peak-position and peak-width are still present when we extract a spectrum of a component by slicing the 2D asynchronous spectrum across the SACP. A genetic algorithm (GA) is used to select a suitable subset of spectra where the diversities of peak-position and peak-width are significantly reduced. Then, we used the selected spectra to construct a refined 2D asynchronous spectrum so that the spectra of pure components with significant attenuated interference can be obtained. The above approach has been proven to be effective on a model system and a real-world example, demonstrating that 2D-COS possesses a bright perspective in the analysis of the bilinear data from DOSY experiments.

Ball-Milled Silicon with Amorphous Al2O3/C Hybrid Coating Embedded in Graphene/Graphite Nanosheets with a Boosted Lithium Storage Capability.

Electrochemical active silicon has attracted great attention as anodes for lithium-ion batteries owing to a high theoretical capacity of 4200 mA h g-1. In this work, ball-milled silicon particles with submicron size were strategically modified with a hybrid coating of amorphous alumina and carbon, which simultaneously embedded in a porous framework of in situ exfoliated graphene/graphite nanosheets (GGN). The composite exhibits an enhanced electrochemical performance, including high cycling stability and superior rate capability. An initial discharge capacity of 1294 mA h g-1 and a reversible charge capacity of 1044 mA h g-1 at 0.2 A g-1 can be achieved with a high initial Coulombic efficiency of up to ca. 81%. Additionally, the composite can remain 902 mA h g-1 after 100 discharge/charge cycles, accounting for a high retention of about 86%. This silicon composite is a promising anode material for high performance lithium-ion batteries with a high energy density, and the facile one-pot fabrication route is low cost and scalable, with a great prospect for practical application.

Tetrandrine Attenuates Cartilage Degeneration, Osteoclast Proliferation, and Macrophage Transformation through Inhibiting P65 Phosphorylation in Ovariectomy-induced Osteoporosis.

BACKGROUND: Osteoporosis is a common metabolic bone disease with high prevalence. Tetrandrine (TET) suppressed osteoclastogenesis, while the roles of TET in osteoporosis regulation remained unclear. Thus, the study aimed to investigate the effect of TET on osteoporosis and the underlying mechanism. METHODS: The osteoporosis rabbit model was established through anterior cruciate ligament transection (ACLT) and bilateral ovariectomy (OVX). The degeneration of articular cartilage was assessed using HE staining and Alcian blue staining. The liver and kidney tissue injury was determined using HE staining. The activity of osteoclasts was evaluated using Tartrate-resistant acid phosphatase (TRAP) staining. The changes in bone structural parameters were determined through measuring the BMD, BV/TV, Tb.Th, Tb.N, and Tb.Sp, and the serum levels of calcium and phosphorus. Macrophage polarization was determined using Flow cytometry. RESULTS: The bone structural parameters including BMD, BV/TV, Tb.N, Tb.Th and Tb.Sp were changed in osteoporosis rabbit, which was reversed by TET. Besides, TET suppressed the increased serum levels of calcium and phosphorus in osteoporosis rabbit. Furthermore, TET inhibited the degeneration of articular cartilage and the activity of osteoclasts induced by osteoporosis. Moreover, TET inhibited the levels of MMP-9, PPAR-γ, RANKL, ß-CTX and TRACP-5b, and increased the levels of OPG, ALP and osteocalcin (OC) in osteoporosis. Additionally, TET promoted macrophage transformation from M1 to M2 in osteoporotic and inhibited the production of IL-1ß, TNF-α, and IL-6. TET also inhibited the p65 phosphorylation in osteoporosis. Besides, TET reversed RANKL-induced osteoclasts proliferation, p65 phosphorylation, and the expression changes of RANKL, Ki67, PPAR-γ, ALP, OPG. CONCLUSION: TET attenuated bone structural parameters including BMD, BV/TV, Tb.N, Tb.Th and Tb.Sp, inhibited articular cartilage degeneration, promoted bone formation, inhibited the inflammatory response, and promoted macrophage transformation from M1 to M2 via NF-κB inactivation in osteoporosis. TET may be a promising drug for osteoporosis therapy. ABBREVIATION: TET: Tetrandrine; ACLT: anterior cruciate ligament transection; OVX: ovariectomy; TRAP: Tartrate-resistant acid phosphatase; BMD: bone mineral density; BV/TV: Bone volume/total volume; Tb.Th: trabecular thickness; Tb.N: trabecular number; Tb.Sp: trabecular separation; MMP-9: Matrix metallopeptidase 9; PPAR-γ: Peroxisome proliferator-activated receptor gamma; RANKL: Receptor activator of nuclear factor kappa-B ligand; OPG: Osteoprotegerin; ALP: alkaline phosphatase; OC: osteocalcin; ß-CTX: ß isomer of C-terminal telopeptide of type I collagen; TRACP-5b: Tartrate-resistant acid phosphatase 5b; TNF-α: tumor necrosis factor-α; IL-1ß: interleukin-1ß; IL-6: interleukin 6; NF-κB: Nuclear factor kappa B; PKC-α: Protein kinase C alpha; qRT-PCR: Quantitative real-time polymerase chain reaction.

An adaptive tracking illumination system for optogenetic control of single bacterial cells.

Single-cell behaviors are essential during early-stage biofilm formation. In this study, we aimed to evaluate whether single-cell behaviors could be precisely and continuously manipulated by optogenetics. We thus established adaptive tracking illumination (ATI), a novel illumination method to precisely manipulate the gene expression and bacterial behavior of Pseudomonas aeruginosa on the surface at the single-cell level by using the combination of a high-throughput bacterial tracking algorithm, optogenetic manipulation, and adaptive microscopy. ATI enables precise gene expression control by manipulating the optogenetic module gene expression and type IV pili (TFP)-mediated motility and microcolony formation during biofilm formation through bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP) level modifications in single cells. Moreover, we showed that the spatial organization of single cells in mature biofilms could be controlled using ATI. Therefore, this novel method we established might markedly answer various questions or resolve problems in microbiology. KEY POINTS: • High-resolution spatial and continuous optogenetic control of individual bacteria. • Phenotype-specific optogenetic control of individual bacteria. • Capacity to control biologically relevant processes in engineered single cells.

Design, Synthesis and Molecular Docking of Novel Quinazolinone Hydrazide Derivatives as EGFR Inhibitors.

A series of novel quinazolinone hydrazide derivatives were designed and synthesized as EGFR inhibitors. The results indicated that most of the aimed compounds had potential anti-tumor cell proliferation and EGFR inhibitory activities. In the comprehensive analysis of all the tested compounds, the target compound 9c showed the best anti-tumor cell proliferation activity, (IC50 =1.31 µM for MCF-7, IC50 =1.89 µM for HepG2, IC50 =2.10 µM for SGC), and IC50 =0.59 µM for the EGFR inhibitory activity. Docking results showed that compound 9c could ideally insert the active site and interact with the critical amino acid residues (Val702, Lys721, Met769, Asp831) in the active site.

lncRNA-POIR promotes epithelial-mesenchymal transition and suppresses sorafenib sensitivity simultaneously in hepatocellular carcinoma by sponging miR-182-5p.

Sorafenib (SOR) resistance remains a major obstacle in the effective treatment of hepatocellular carcinoma (HCC). A number of long noncoding RNAs (lncRNAs) are responsible for this chemoresistance. This study aimed to reveal the essential function of a recently defined lncRNA, lncRNA-POIR, in the epithelial-mesenchymal transition (EMT) and SOR sensitivity of HCC cells. SOR-induced cytotoxicity was analyzed via cell counting kit-8 and ethynyl-2'-deoxyuridine incorporation assays, whereas immunoblotting and confocal immunofluorescence were used to determine the expression levels of EMT markers. Furthermore, loss- or gain-of-function approaches were used to demonstrate the role of lncRNA-POIR/miR-182-5p on EMT and SOR sensitivity in HCC. The direct interaction between lncRNA-POIR and miR-182-5p was verified using a luciferase reporter assay. We found that knockdown of lncRNA-POIR sensitized HCC cells to SOR and simultaneously reversed EMT. As expected, miR-182-5p was confirmed as the downstream target of lncRNA-POIR. Moreover, miR-182-5p overexpression clearly reversed EMT and promoted SOR-induced cytotoxicity in representative HCC cells, whereas miR-182-5p downregulation played a contrasting role; miR-182-5p knockdown abolished the modulatory effects of lncRNA-POIR siRNA on EMT and SOR sensitivity. Together, these pieces of data suggest that lncRNA-POIR promotes EMT progression and suppresses SOR sensitivity simultaneously by sponging miR-182-5p. Thus, we proposed a compelling rationale for the use of lncRNA-POIR as a promising predictor of SOR response and as a potential therapeutic target for HCC treatment in the future.

Early maternal deprivation impairs learning and memory and alters hippocampal gene expression in adult male rats.

Maternal deprivation (MD) in early life severely disrupts hippocampal development, leading to persistent cognitive and behavior deficits. The current study uncovered that early MD (P1-P21) impaired spatial learning and memory capacity detected by Morris water maze (MWM) tests from juvenile (P31) to adult (P81) rats compared to age-matched controls. And the protein expression in hippocampus were detected by two-dimensional gel electrophoresis (2-DE) before MWM, respectively. Protein changes in hippocampal were examined to identify the molecular pathways underlying MD-induced hippocampal dysfunction. There were 11 differentially expressed proteins analyzed between adult MD and control male rats, while the 8 proteins were then identified by UPLC-ESI-Q-TOF-MS. Gene Ontology (GO) annotations of the identified proteins were related to neuronal and glial cytoskeletal dynamics, membrane signaling, stress responses, biosynthesis, and metabolism. The different expression proteins spectrin alpha chain, non-erythrocytic 1 (Sptan1), ATP-citrate synthase (Acly), and heat shock protein 90-alpha (Hsp90aa1) have been verified by western blot analysis, and their expression levels showed consistent with 2-DE analysis. In addition, glial fibrillary acidic protein (GFAP) was also found reduced in adult hippocampus of MD rats. This study identifies candidate proteins encompassing a range of functional categories that may contribute to persistent learning and memory deficits due to early life MD.

The role of angiotensin-(1-7) on acquired platinum resistance-induced angiogenesis in non-small cell lung cancer in vitro and in vivo.

Renin-angiotensin system (RAS) signaling has been implicated in the development of cancer. The new RAS ACE2/Ang-(1-7)/Mas axis antagonizes the classical ACE/Ang II/AT1R axis. Ang-(1-7) has pleiotropic roles in lung cancer including suppressing proliferation, angiogenesis, and metastasis. This research was designed to investigate the effect of Ang-(1-7) on tumor-associated angiogenesis in DDP-resistant lung cancer cell lines. We first established acquired DDP-resistant cell lines A549 (A549-DDP) and LLC (LLC-DDP). We next performed RT-qPCR, western blot, ELISA, tube formation, microvessel density detection, immunohistochemistry, and tumor formation assays. The results showed that the mRNA and protein levels of RAS components and vascular endothelial growth factor A (VEGFa) were lessened in the A549/LLC-DDP+Ang-(1-7) group compared with the A549/LLC-DDP group. This effect could be blocked by the MAS receptor antagonist A779. The data revealed that Ang-(1-7) could perform its antiangiogenic function by PI3K/AKT and MAPK pathways. Furthermore, the impact of Ang-(1-7) on tumor-associated angiogenesis has been confirmed in lung cancer xenograft model with acquired DDP resistance. These results provide a theoretical basis for designing therapeutic strategies for targeting Ang-(1-7) in the treatment of NSCLC.

Applied organic-inorganic nanocomposite of PLA-TiO2 for preparing polysulfone membrane: structure, performance and UV-assisted cleaning strategy.

Blended organic copolymer (or homopolymer) and inorganic nanoparticles have been widely used (separately or simultaneously) for optimizing membrane pore structure and surface functionality. However, the prepared membranes suffer from degraded stability and insufficient integrity due to the high solubility or incompatibility of the blending additives. In this work, an organic-inorganic nanocomposite (i.e., PLA-TiO2) was designed, and employed for PSF membrane preparation. The Fourier transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS) analysis confirmed that bidentate chelating dominated the bonding mechanism between PLA and TiO2. The resultant PSF/PLA-TiO2 membranes possessed a highly porous surface with narrowed pore size distribution, demonstrating the strong pore forming ability of PLA-TiO2 for membrane preparations. Moreover, owing to the distinct inorganic-organic molecular conformation, the PLA-TiO2 exhibited enhanced stability and dispersibility within the PSF substance, which endowed the membrane with long-acting hydrophilicity and UV responsiveness. Given the UV responsiveness that is introduced by PLA-TiO2, UV-assisted strategies (UV-F and UV-C) were designed to further mitigate membrane fouling. The fouling analysis indicated that both reversible fouling and irreversible fouling were reduced in the UV-C process, signifying the synergistic effect between photocatalysis and hydraulics in membrane fouling mitigation. The enhanced membrane performance and the efficient preparation process highlight the potential of PLA-TiO2 in membrane modifications.

MicroRNA-145 suppresses gastric cancer progression by targeting Hu-antigen R.

Hu-antigen R (HuR) is involved in the carcinogenesis and progression of multiple types of cancer. However, its precise role in gastric cancer (GC) and the relevant molecular mechanism remain largely unclear. In the present study, we found that HuR expression level was higher in GC tissues and cell lines than in adjacent normal tissues and normal gastric epithelial cell lines, and this elevated expression was found to have a significant association with lymph node metastasis. Moreover, silencing HuR with RNA interference inhibited cell viability and induced cell apoptosis through the apoptosis-related regulators (Bcl-2 and Bax) in GC cells. In addition, bioinformatic analysis revealed that HuR expression was inversely correlated with miR-145 expression in GC tissue samples, and HuR was identified as a direct target of miR-145 with the dual-luciferase reporter. Enforced expression of miR-145 inhibited the HuR expression at both mRNA and protein levels and induced similar biologic effects of silencing HuR in GC cells. Additionally, we also found that restoration of HuR could eliminate the effects induced by miR-145 in GC cells. Taken together, these findings demonstrate the exact role of the miR-145-HuR axis in the progression of GC and indicate a potential target for GC therapy.

Patient-derived xenograft model engraftment predicts poor prognosis after surgery in patients with pancreatic cancer.

OBJECTIVES: To establish and evaluate a first generation patient-derived xenograft (PDX) model in nude mice using tumors resected from pancreatic cancer (PC) patients for the identification of key factors that influence xenograft success and prediction of patient prognosis. METHODS: Primary tumor samples harvested from PC patients who underwent curative resection between May 2016 and April 2018 at our hospital were xenografted into nude mice. Tumor size was evaluated for 2 months. Patients' baseline characteristics and follow-up data were analyzed. RESULTS: Tumor xenograft models were generated from 67 patients; 30 (44.8%) were successful and 37 (55.2%) failed. Xenograft models could recapitulate the pathology and genetic information of the primary tumors. Univariate analysis identified tumor engraftment, post-operation CA19-9, tumor size, lymph node status, and lymphovascular invasion as significant predictors (P=0.000, 0.023, 0.004, 0.035 and 0.005, respectively) of disease-free survival (DFS). Multivariate Cox regression analysis confirmed tumor engraftment, tumor size and lymphovascular invasion function as independent risk factors for DFS (P=0.000, 0.039 and 0.025, respectively). The hazard ratio of tumor engraftment for DFS was 0.239 (95% confidence interval, 0.109 to 0.524). Kaplan-Meier analysis of DFS indicated an unfavorable outcome in the engraftment group compared to that in the failed engraftment group (6.2 vs. 12.2 months, log rank P=0.000). CONCLUSION: The pathology and genetic information of primary PC tumors are recapitulated in the PDX tumor model in nude mice. Furthermore, engraftment success is an effective predictor of disease recurrence in patients after surgery.

Understanding the electrochemical properties of bulk phase and surface structures of Na3TMPO4CO3 (TM = Fe, Mn, Co, Ni) from first principles calculations.

First principles calculations were performed to investigate the electrochemical performance (voltage, cycling stability, electrical conductivity, mechanical properties and safety) of the bulk phase and surface structures of Na3TMPO4CO3 (TM = Fe, Mn, Co, Ni). Na3FePO4CO3 and Na3MnPO4CO3 are estimated to be promising candidates for the cathode materials of sodium ion batteries because of the moderate voltages, good stability and high safety during the cycling process of two sodium ions per formula unit. For the purpose of improving the rate performances, Na3MnPO4CO3 was chosen as an example to explore its surface performance. The surface energies, equilibrium morphology, redox potentials and electronic conductivities of surfaces are explored in detail. The results suggest that (010), (001), (111) and (110) orientations are the dominating surfaces in the Wulff shape, while the surfaces (010) and (001) possess high second surface redox potentials, corresponding to the unsatisfactory specific capacity and ionic conductivity. Moreover, low surface band gaps are discovered in all orientations, which gives a good explanation for the enhanced electronic conductivity as a consequence of decreasing particle size. In addition, the (110), (101) and (12-1) surfaces display significantly lower surface band gaps and comparatively lower second redox potentials, thus enlarging the relative surface areas of surfaces (110), (101) and (12-1) could be an efficient methodology to further improve the specific capacity and electronic conductivity of the Na3MnPO4CO3 material.

Electric field and uniaxial strain tunable electronic properties of the InSb/InSe heterostructure.

In this study, the InSb/InSe heterostructure is systematically examined in terms of its electronic properties through first-principles calculations. According to our findings, the InSb/InSe heterostructure is a kind of unique direct band gap semiconductor, which has inherent type-II band alignment, resulting in significant photogenerated electron-hole pair separation in space. When the external electric field is applied, the Stark effect is observed in the band gap. Interestingly, in the application of the -0.3 V Å-1 electric field, such a heterostructure is transformed into type-I from type-II. Simultaneously, the band gap is also effectively controlled by uniaxial strain. In particular, high carrier mobility is obtained at a compressive strain of 4% on the Y-axis. To sum up, based on the results in the present work, the InSb/InSe heterostructure can be potentially used in nanoelectronic and optoelectronic devices.

Type-II tunable SiC/InSe heterostructures under an electric field and biaxial strain.

In this study, first-principles calculations based on the density functional theory (DFT) are exploited to investigate the electronic capabilities of SiC/InSe heterostructures. According to our results, the SiC/InSe heterostructure possesses an inherent type-II band alignment, which displays a noticeable Stark effect on the band gap under a stable electric field. Besides, the heterostructure exhibits a low carrier effective mass and a narrower band gap when it is subject to tensile strain. More interestingly, the transition from an indirect to a direct band gap occurs when 8% of compressive strain is applied. Taken together, findings in this study indicate that the SiC/InSe heterostructure opens up a new avenue for its application in the fields of optoelectronics and microelectronics.

Band alignment control in a blue phosphorus/C2N van der Waals heterojunction using an electric field.

Well-controlled band engineering of a blue phosphorus/C2N van der Waals (vdW) heterojunction is investigated by density functional theory (DFT) calculations. The heterojunction has a natural type-II band alignment with a direct band gap value of 1.514 eV, which gives the enormous potential for solar cell applications. When the heterojunction is under solar illumination, the photogenerated electron-hole pairs can separate out on the disparate monolayers effectively. It induces the formation of spatially indirect excitons. Furthermore, it is found that the band gap of this heterojunction exhibits approximately linear variation with respect to the perpendicular external electric field. Very interestingly, a band alignment change from type-II to type-I occurs at an applied electric field of -0.2 V Å-1. This characteristic provides an attractive possibility to obtain novel multifunctional devices.