Novel Topological Motifs and Superconductivity in Li-Cs System.

In this work, we determined the phase diagram and electronic properties of the Li-Cs system by using an evolutionary crystal structure prediction algorithm coupled with first-principles calculations. We found that Li-rich compounds are more easily formed in a wide range of pressures, while the only predicted Cs-rich compound LiCs3 is thermodynamically stable at pressures above 359 GPa. A topological analysis of crystal structures concludes that both Li6Cs and Li14Cs have a unique topology that has not been reported in existing intermetallics. Of particular interest is the fact that four Li-rich compounds (Li14Cs, Li8Cs, Li7Cs, and Li6Cs) are found to be superconductors with a high critical temperature (∼54 K for Li8Cs at 380 GPa), due to their peculiar structural topologies and notable charge transfer from Li to Cs atoms. Our results not only extend an in-depth understanding of the high-pressure behavior of intermetallic compounds but also provide a new route to design new superconductors.

An EMT-related genes signature as a prognostic biomarker for patients with endometrial cancer.

BACKGROUND: The epithelial-mesenchymal transition (EMT) plays an indispensable role in the development and progression of Endometrial cancer (EC). Nevertheless, little evidence is reported to uncover the functionality and application of EMT-related molecules in the prognosis of EC. This study aims to develop novel molecular markers for prognosis prediction in patients with EC. METHODS: RNA sequencing profiles of EC patients obtained from The Cancer Genome Atlas (TCGA) database were used to screen differential expression genes (DEGs) between tumors and normal tissues. The Cox regression model with the LASSO method was utilized to identify survival-related DEGs and to establish a prognostic signature whose performance was evaluated by Kaplan-Meier curve, receiver operating characteristic (ROC) and calibration curve. Eventually, functional enrichment analysis and cellular experiments were performed to reveal the roles of prognosis-related genes in EC progression. RESULTS: A total of 540 EMT-related DEGs in EC were screened, and subsequently a four-gene risk signature comprising SIRT2, SIX1, CDKN2A and PGR was established to predict overall survival of EC. This risk signature could serve as a meaningfully independent indicator for EC prognosis via multivariate Cox regression (HR = 2.002, 95%CI = 1.433-2.798; P < 0.001). The nomogram integrating the risk signature and clinical characteristics exhibited robust validity and performance at predicting EC overall survival indicated by ROC and calibration curve. Functional enrichment analysis revealed that the EMT-related genes risk signature was associated with extracellular matrix organization, mesenchymal development and cellular component morphogenesis, suggesting its possible relevance to epithelial-mesenchymal transition and cancer progression. Functionally, we demonstrated that the silencing of SIX1, SIRT2 and CDKN2A expression could accelerate the migratory and invasive capacities of tumor cells, whereas the downregulation of PGR dramatically inhibited cancer cells migration and invasion. CONCLUSIONS: Altogether, a novel four-EMT-related genes signature was a potential biomarker for EC prognosis. These findings might help to ameliorate the individualized prognostication and therapeutic treatment of EC patients.

Bilirubin Induces A1-Like Reactivity of Astrocyte.

Astrocytes play an important role in the pathogenesis of bilirubin neurotoxicity, and activated astrocytes might be potential mediators of neuroinflammation processes contributing to neuronal cell death and tissue injury. Recent studies have reported that activated microglia induce two types of reactive astrocytes. A1 astrocytes could cause neuronal death and synaptic damage, as well as impaired phagocytosis. Therefore, the purpose of this study was to investigate whether unconjugated bilirubin (UCB)-induced A1-like astrocytes take on a neuroinflammation type and the underlying regulatory mechanisms. In this study, primary cortical astrocytes were treated with UCB in vitro. We detected the expression of complement component 3 (C3), S100 calcium binding protein A10 (S100A10), nuclear factor kappa B (NF-κB), NLR family pyrin domain containing 3 (NLRP3), activated caspase-1, gasdermin D N-terminal (GSDMD-N), PSD95, synaptophysin (SYP), the transcription levels of interleukin (IL)-1ß and IL-18, and the survival rate of astrocytes after UCB treatment. The results showed that an increase in C3 was accompanied by a decrease in S100A10, and that A1-like astrocytes were functionally expressed after UCB stimulation. Meanwhile, the NF-κB and caspase-1 pathways were activated after UCB stimulation. After adding the NF-κB-specific inhibitor trans-activator of transcriptional-NEMO-binding domain (TAT-NBD) and caspase-1 specific inhibitor VX-765, the survival rate of astrocytes and neurons increased, whereas the protein expression of C3, NF-κB, NLRP3, activated caspase-1, and GSDMD-N decreased, and the mRNA levels of IL-1ß and IL-18 reduced. Thus, we concluded that UCB stimulates the activation of A1-like astrocytes. Inhibition of NF-κB and caspase-1 alleviated A1-like astrocytes and exerted anti-inflammatory protective effects.

Lead activates neutrophil degranulation to induce early myocardial injury in mice.

Lead (Pb) is a pervasive toxic metal contaminant associated with a high risk of myocardial injury. However, the precise mechanism underlying Pb-induced myocardial injury has yet to be fully elucidated. In this study, a murine model of Pb exposure (0, 1, 5, and 10 mg/kg) was employed to investigate the involvement of neutrophil degranulation in the induction of myocardial injury. Notably, serum levels of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) increased significantly in Pb-exposed mice, whereas cTnI levels in cardiomyocytes decreased, suggesting that Pb exposure may cause early myocardial injury. Moreover, Pb exposure was found to promote neutrophil degranulation, as evidenced by elevated myeloperoxidase (MPO) and neutrophil elastase (NE) concentrations in both the serum of Pb-exposed workers and Pb-exposed mice, as well as the extracellular supernatant of neutrophils following exposure. However, we found that serum level of cTnI enhanced by Pb exposure is associated with increased NE levels in the serum, but not with MPO levels. Upon treatment with NE inhibitor (sivelestat), the serum level of cTnI markedly reduced in Pb-exposed mice, we found that early myocardial injury is associated with NE levels in the serum. At the molecular level, western blotting analysis revealed an upregulation of ERK1/2 expression in vitro following Pb exposure, suggesting that the activation of the ERK1/2 signaling pathway may underlie the participation of neutrophil degranulation in Pb-induced myocardial injury. In summary, our findings demonstrate that Pb exposure can initiate early myocardial injury by promoting the neutrophil degranulation process, thereby highlighting the potential role of this process in the pathogenesis of Pb-associated myocardial injury.

Investigation of genetic relationships within three Miscanthus species using SNP markers identified with SLAF-seq.

BACKGROUND: Miscanthus, which is a leading dedicated-energy grass in Europe and in parts of Asia, is expected to play a key role in the development of the future bioeconomy. However, due to its complex genetic background, it is difficult to investigate phylogenetic relationships in this genus. Here, we investigated 50 Miscanthus germplasms: 1 female parent (M. lutarioriparius), 30 candidate male parents (M. lutarioriparius, M. sinensis, and M. sacchariflorus), and 19 offspring. We used high-throughput Specific-Locus Amplified Fragment sequencing (SLAF-seq) to identify informative single nucleotide polymorphisms (SNPs) in all germplasms. RESULTS: We identified 257,889 SLAF tags, of which 87,162 were polymorphic. Each tag was 264-364 bp long. The obtained 724,773 population SNPs were used to investigate genetic relationships within three species of Miscanthus. We constructed a phylogenetic tree of the 50 germplasms using the obtained SNPs and grouped them into two clades: one clade comprised of M. sinensis alone and the other one included the offspring, M. lutarioriparius, and M. sacchariflorus. Genetic cluster analysis had revealed that M. lutarioriparius germplasm C3 was the most likely male parent of the offspring. CONCLUSIONS: As a high-throughput sequencing method, SLAF-seq can be used to identify informative SNPs in Miscanthus germplasms and to rapidly characterize genetic relationships within this genus. Our results will support the development of breeding programs with the focus on utilizing Miscanthus cultivars with elite biomass- or fiber-production potential for the developing bioeconomy.

The nesting preference of an invasive ant is associated with the cues produced by actinobacteria in soil.

Soil-dwelling animals are at risk of pathogen infection in soils. When choosing nesting sites, animals could reduce this risk by avoiding contact with pathogens, yet there is currently little evidence. We tested this hypothesis using Solenopsis invicta as a model system. Newly mated queens of S. invicta were found to nest preferentially in soil containing more actinobacteria of Streptomyces and Nocardiopsis and to be attracted to two volatiles produced by these bacteria, geosmin and 2-methylisoborneol. Actinobacteria-rich soil was favored by S. invicta and this soil contained fewer putative entomopathogenic fungi than adjacent areas. Queens in such soil benefited from a higher survival rate. In culture, isolated actinobacteria inhibited entomopathogenic fungi, suggested that their presence may reduce the risk of fungal infection. These results indicated a soil-dwelling ant may choose nest sites presenting relatively low pathogen risk by detecting the odors produced by bacteria with anti-fungal properties.

'Stress hyperglycemia ratio and in-hospital prognosis in non-surgical patients with heart failure and type 2 diabetes.

OBJECTIVE: To evaluate the impact of stress hyperglycemia on the in-hospital prognosis in non-surgical patients with heart failure and type 2 diabetes. RESEARCH DESIGN AND METHODS: We identified non-surgical hospitalized patients with heart failure and type 2 diabetes from a large electronic medical record-based database of diabetes in China (WECODe) from 2011 to 2019. We estimated stress hyperglycemia using the stress hyperglycemia ratio (SHR) and its equation, say admission blood glucose/[(28.7 × HbA1c)- 46.7]. The primary outcomes included the composite cardiac events (combination of death during hospitalization, requiring cardiopulmonary resuscitation, cardiogenic shock, and the new episode of acute heart failure during hospitalization), major acute kidney injury (AKI stage 2 or 3), and major systemic infection. RESULTS: Of 2875 eligible Chinese adults, SHR showed U-shaped associations with composite cardiac events, major AKI, and major systemic infection. People with SHR in the third tertile (vs those with SHR in the second tertile) presented higher risks of composite cardiac events ([odds ratio, 95% confidence interval] 1.89, 1.26 to 2.87) and major AKI (1.86, 1.01 to 3.54). In patients with impaired kidney function at baseline, both SHR in the first and third tertiles anticipated higher risks of major AKI and major systemic infection. CONCLUSIONS: Both high and low SHR indicates poor prognosis during hospitalization in non-surgical patients with heart failure and type 2 diabetes.

A female case with novel KDM5C heterozygous variation presenting with Claes-Jensen type-like phonotype.

BACKGROUND: Lysine(K)-specific demethylase 5C (KDM5C) dysfunction causes X-linked syndromic intellectual developmental disorder Claes-Jensen type in male patients. The clinical presentations of female individuals with heterozygous KDM5C variations vary widely and are only now beginning to be characterized in detail. CASE PRESENTATION: Herein, we identified a novel de novo heterozygous nonsense variation of KDM5C (c.3533C > A, p.S1178X) in a sporadic 4-year-old Chinese girl, who presented with Claes-Jensen type-like phenotypes, such as moderate developmental delay, serious expressive language delay, short stature, microcephaly, and typical facial particularities. Moreover, X-chromosome inactivation (XCI) analysis showed no significant skewed X-inactivation. CONCLUSION: The report expands the genotype of KDM5C variation in female patients, delineates the phenotype of affected females in this well-known X-linked disorder, and also reinforces the necessity to consider this X-linked gene, KDM5C, in sporadic female patients.

Occurrence and Transformation of Ephedrine/Pseudoephedrine and Methcathinone in Wastewater in China.

Previous wastewater-based epidemiology studies on methcathinone (MC), a controlled substance in many countries, attributed its occurrence in wastewater to its misuse. However, such attribution did not consider the possibility that MC may also come from the transformation of ephedrine (EPH) and pseudo-ephedrine (PEPH). In this work, EPH/PEPH and MC in wastewater of six major Chinese cities were systematically examined. EPH/PEPH concentrations in all the cities showed clear seasonal variations, with maximum and minimum concentrations observed in winter and summer, respectively. In contrast, MC concentrations were the lowest in winter, leading to minimum concentration ratios between MC and EPH/PEPH in winter. Lack of MC seizure in the cities suggests that MC abuse could not account for the ubiquitous detection of the substance in the wastewater of these cities. Batch experiments confirmed EPH/PEPH transformation into MC in wastewater. The significantly lower transformation rate at a lower temperature was consistent with low MC concentrations in winter. These results indicate that when monitoring MC through wastewater, EPH/PEPH concentrations must be determined simultaneously to avoid false identification of MC abuse. The observed ratios of MC to EPH/PEPH concentrations in this work may be used to determine MC abuse. Alternatively, other biomarkers (e.g., cathinone) may be considered to avoid interference from EPH/PEPH transformation.

Theoretical investigation of the role of hydrogenation-induced strain in single-layer h10-Si.

Although great efforts have been dedicated to exploring hydrogenated two-dimensional (2D) materials, there are few reports about the role of hydrogenation-induced equivalent strain effects in tuning the physical properties. Here, based on density functional theory, we systematically reveal the non-negligible role of the hydrogenation-induced strain and its effects on the electronic and optical properties in single-layer (SL) h10-Si. We demonstrate that hydrogenation can trigger an electronic transition from an indirect- to a direct-band-gap semiconductor mainly due to the energy level rearrangement of the partial p orbitals caused by the equivalent strain. The electronic transition in SL h10-Si occurs at a critical hydrogenation concentration of about 87.5%. Furthermore, it is found that hydrogenation can continuously shift the light absorption peak of SL h10-Si in the photon-energy range of 1.64-2.44 eV by changing the pz-pz dipole transition. Our findings provide an example of tuning the electronic properties of 2D materials via hydrogenation-induced strain, which is important for understanding the physical mechanism of the hydrogenation-tuned physical properties of such materials.

Novel pyrene-pyridine oligomer nanorods for super-sensitive fluorescent detection of Pd2.

Conjugated polymers (CPs) can be fabricated into conjugated polymer nanoparticles of various shapes, thus tuning the hydrophobicity and sensing performances of the parent polymers. Herein, two new hydrophobic oligomeric CPs containing pyrene-pyridyl moieties, P1 and P2, were directly prepared and conveniently converted into hydrophilic nanorods, i.e. P1NRs and P2NRs (about 4-21 and 6-20 nm in diameter), by a modified microemulsion method. Notably, separated P1NRs exhibit excellent stability while P2NRs tend to stack on each other perhaps due to their different rigidity of π-delocalized backbones, which may have a profound effect on their fluorescence properties. In addition, Pd2+ can coordinate with the pyridyl N atoms, thereby causing ultrasensitive fluorescence quenching of P1NRs and P2NRs owing to the aggregation of oligomeric CP nanorods. These two simple nanosensors can help to determine Pd2+ with detection limits as low as 1 and 70 nM, respectively. It is worth noting that biocompatible P1NRs with bright blue fluorescence can be employed for efficient imaging of trace level Pd2+ ions in live cells.

Pressure-Induced Structural Phase Transition and Superconductivity in NaSn5.

The structural and electronic properties of the tin-rich compound NaSn5 were investigated under pressures of up to 10 GPa on the basis of the evolutionary algorithm (EA) technique coupled with first-principles total energy calculations. Upon compression, the known metallic tetragonal P4̅21m phase transforms into a metallic hexagonal P6/mmm phase at 1.85 GPa accompanied by an unusual change in the existing form of Sn atoms. The P6/mmm phase can be interpreted as a quasi-layered sandwich structure with two Sn layers and one sodium layer. The presence of softening phonon modes and the existence of Fermi pockets together with the obvious Fermi surface nesting indicate a strong electron-phonon coupling (EPC) and thus potential superconductivity in the P6/mmm phase. The strong EPC in the P6/mmm phase is mainly attributed to the phonons from Sn1 atoms together with electrons from the Sn1 py and Sn1 pz states. The calculated superconducting critical temperature Tc of the P6/mmm phase is 5.91 K at 1.85 GPa. This study provides a new clue for designing intercalated compounds with superconductivity.

[Role of pyroptosis in bilirubin-induced microglial injury].

OBJECTIVE: To study whether pyroptosis is involved in the bilirubin-induced injury of primary cultured rat cortical microglial cells. METHODS: Primary cultured rat cortical microglial cells were randomly administered with 30 µmol/L bilirubin (bilirubin group), 30 µmol/L bilirubin following 30 µmol/L VX-765 pretreatment (VX-765+bilirubin group), or an equal volume of dimethyl sulfoxide (control group). Modified MTT assay was used to measure the viability of microglial cells. Western blot was used to measure the expression of the pyroptosis-related proteins Caspase-1 and gasdermin D (GSDMD). Lactate dehydrogenase (LDH)-release assay was used to evaluate the cytotoxicity of microglial cells. EtBr/EthD2 with different molecular weights (394 Da/1 293 Da) was used to measure the size of plasma membrane pores. ELISA was used to measure the level of the inflammatory factor interleukin-1ß (IL-1ß) in culture supernatant. RESULTS: After bilirubin stimulation, the viability of microglial cells decreased and LDH release increased, both in a time-dependent manner. Compared with the control group, the bilirubin group had a significantly higher positive rate of small-molecule EtBr passing through the cell membrane (P<0.001), while there was no significant difference in the pass rate of large-molecule EthD2 between groups (P>0.05). The expression of activated Caspase-1 significantly increased at 0.5 hour after bilirubin stimulation (P<0.05), and that of activated GSDMD significantly increased at 6 hours after bilirubin stimulation (P<0.05). The release of IL-1ß significantly increased at 6 hours after bilirubin stimulation and reached the peak at 24 hours (P<0.001). Compared with the bilirubin group, the VX-765+bilirubin group had a significant increase in cell viability (P<0.05) and significant reductions in the expression of activated GSDMD, the pass rate of EtBr, and the release of LDH and IL-1ß (P<0.05). CONCLUSIONS: Pyroptosis is involved in bilirubin-induced injury of primary cultured microglial cells.

Ranking near-native candidate protein structures via random forest classification.

BACKGROUND: In ab initio protein-structure predictions, a large set of structural decoys are often generated, with the requirement to select best five or three candidates from the decoys. The clustered central structures with the most number of neighbors are frequently regarded as the near-native protein structures with the lowest free energy; however, limitations in clustering methods and three-dimensional structural-distance assessments make identifying exact order of the best five or three near-native candidate structures difficult. RESULTS: To address this issue, we propose a method that re-ranks the candidate structures via random forest classification using intra- and inter-cluster features from the results of the clustering. Comparative analysis indicated that our method was better able to identify the order of the candidate structures as comparing with current methods SPICKR, Calibur, and Durandal. The results confirmed that the identification of the first model were closer to the native structure in 12 of 43 cases versus four for SPICKER, and the same as the native structure in up to 27 of 43 cases versus 14 for Calibur and up to eight of 43 cases versus two for Durandal. CONCLUSIONS: In this study, we presented an improved method based on random forest classification to transform the problem of re-ranking the candidate structures by an binary classification. Our results indicate that this method is a powerful method for the problem and the effect of this method is better than other methods.

Predicting RNA secondary structure via adaptive deep recurrent neural networks with energy-based filter.

BACKGROUND: RNA secondary structure prediction is an important issue in structural bioinformatics, and RNA pseudoknotted secondary structure prediction represents an NP-hard problem. Recently, many different machine-learning methods, Markov models, and neural networks have been employed for this problem, with encouraging results regarding their predictive accuracy; however, their performances are usually limited by the requirements of the learning model and over-fitting, which requires use of a fixed number of training features. Because most natural biological sequences have variable lengths, the sequences have to be truncated before the features are employed by the learning model, which not only leads to the loss of information but also destroys biological-sequence integrity. RESULTS: To address this problem, we propose an adaptive sequence length based on deep-learning model and integrate an energy-based filter to remove the over-fitting base pairs. CONCLUSIONS: Comparative experiments conducted on an authoritative dataset RNA STRAND (RNA secondary STRucture and statistical Analysis Database) revealed a 12% higher accuracy relative to three currently used methods.

Microbial Communities in Different Developmental Stages of the Oriental Fruit Fly, Bactrocera dorsalis, Are Associated with Differentially Expressed Peptidoglycan Recognition Protein-Encoding Genes.

The insect microbiota can change dramatically to enable adaptation of the host in different developmental stages and environments; however, little is known about how the host maintains its microbiota to achieve such adaptations. In this study, 16S rRNA sequencing revealed that the microorganisms in larvae and adults of the Oriental fruit fly, Bactrocera dorsalis, are primarily Gram-negative bacteria but that the major components in pupae are Gram-positive bacteria. Using suppression subtractive hybridization (SSH) and transcriptome analysis, we screened two specifically expressed genes encoding peptidoglycan recognition proteins (PGRP-LB and PGRP-SB1) and analyzed their relationship to B. dorsalis microbial communities. Knockdown of the PGRP-LB gene in larvae and adults led to increased ratios of Gram-positive bacteria; knockdown of the PGRP-SB1 gene in pupae led to increased ratios of Gram-negative bacteria. Our results suggest that maintenance of the microbiota in different developmental stages of B. dorsalis may be associated with the PGRP-LB and PGRP-SB1 genes.IMPORTANCE Microorganisms are ubiquitous in insects and have widespread impacts on multiple aspects of insect biology. However, the microorganisms present in insects can change dramatically in different developmental stages, and it is critical to maintain the appropriate microorganisms in specific host developmental stages. Therefore, analysis of the factors associated with the microbiota in specific development stages of the host is needed. In this study, we applied suppression subtractive hybridization (SSH) combined with transcriptome analysis to investigate whether the microbiota in development stages of the Oriental fruit fly, Bactrocera dorsalis, is associated with expression of PGRP genes. We found that two different PGRP genes were specifically expressed during development and that these genes may be associated with changes in microbial communities in different developmental stages of B. dorsalis.

Caspase-1 involves in bilirubin-induced injury of cultured rat cortical neurons.

BACKGROUND: Bilirubin encephalopathy, the most serious complication of hyperbilirubinemia during the neonatal period, with high mortality and morbidity, often causes irreversible neurological damage. Currently, caspase-1, a member of the cysteinyl aspartate-specific protease caspase family, is regarded as a key mediator of inflammatory processes, attracting widespread attention. The purpose of this study was to investigate whether caspase-1 is involved in bilirubin-induced neuronal injury. METHODS: VX-765, a highly potent and selective inhibitor of caspase-1, was used to investigate the effects of unconjugated bilirubin (UCB) on rat cortical neurons, including cell viability, morphological changes in the cell membrane, and nuclear factor-kappa B (NF-κB) activation. RESULTS: Neurons treated with UCB showed increased caspase-1 activity without the secretion of interleukin (IL)-1ß and IL-18, and caspase-1 was significantly inhibited by pretreatment with VX-765. The cell viability of the VX-765-pretreated neurons was improved, and cell membrane rupture was prevented, as detected by lactate dehydrogenase release and ethidium bromide uptake. Moreover, NF-κB activation by UCB exposure, was attenuated by VX-765 pretreatment. CONCLUSION: Bilirubin-induced neuronal injury involves the activation of caspase-1 and NF-κB, leading to membrane leakage, independently of IL-1ß and IL-18.

RASGRP1 mutation in autoimmune lymphoproliferative syndrome-like disease.

BACKGROUND: Autoimmune lymphoproliferative syndrome (ALPS) is a genetic disorder of lymphocyte homeostasis due to impaired apoptosis. It was initially regarded as a very rare disease, but recent studies show that it may be more common than previously thought. Defects in a couple of genes have been identified in a proportion of patients with ALPS, but around one-third of such patients remain undefined genetically. OBJECTIVE: We describe 2 siblings presenting with ALPS-like disease. This study aimed to identify the genetic cause responsible for this phenotype. METHODS: Whole-exome sequencing and molecular and functional analyses were used to identify and characterize the genetic defect. Clinical and immunological analysis was also performed and reported. RESULTS: The 2 patients presented with chronic lymphadenopathy, hepatosplenomegaly, autoimmune hemolytic anemia, immune thrombocytopenia, and the presence of antinuclear autoantibody and other autoantibodies, but normal double-negative T cells. They also suffered from recurrent infections. Novel compound heterozygous mutations of RASGRP1 encoding Ras guanyl nucleotide releasing protein 1 were identified in the 2 siblings. The mutations impaired T-cell receptor signaling, leading to defective T-cell activation and proliferation, as well as impaired activation-induced cell death of T cells. CONCLUSIONS: This study shows for the first time that RASGRP1 mutation should be considered in patients with ALPS-like disease. We also propose to investigate the intracellular proteins involved in the T-cell receptor signaling pathway in similar patients but with unknown genetic cause.

Structural diversity and electronic properties in potassium silicides.

Stable potassium silicides in the complete compositional landscape were systematically explored up to 30 GPa using the variable-composition evolutionary structure prediction method. The results show that K4Si, K3Si, K5Si2, K2Si, K3Si2, KSi, KSi2, KSi3, and K8Si46 have their stability fields in the phase diagram. The spatial dimensional diversity of polymerized silicon atoms (0D "isolated" anion, dimer, Si4 group, 1D zigzag chain, 2D layer, and 3D network) under the potassium sublattice was uncovered as silicon content increases. Especially, the 2D layered silicon presents interestingly a variety of shapes, such as the "4 + 6" ring, "4 + 8"ring, and 8-membered ring. K-Si bonding exhibits a mixed covalency and ionicity, while Si-Si bonding is always of covalent character. Semiconductivity or metallicity mainly depends on the form of sublattices and K:Si ratio, which allows us to find more semiconductors in the Si-rich side when closed-shell K cations are encompassed by polymerized Si. The semiconducting silicides present strong absorption in the infrared and visible light range. These findings open up the avenue for experimental synthesis of alkali metal-IVA compounds and potential applications as battery electrode materials or photoelectric materials.

TGF-ß1-miR-200a-PTEN induces epithelial-mesenchymal transition and fibrosis of pancreatic stellate cells.

Although the function of miR-200a has been discussed in many cancers and fibrotic diseases, its role in pancreatic fibrosis is still poorly understood. In this study, we for the first time confirm that miR-200a attenuates TGF-ß1-induced pancreatic stellate cells activation and extracellular matrix formation. First, we find that TGF-ß1 induces activation and extracellular matrix (ECM) formation in PSCs, and the effects are blocked by the inhibitor of PI3K (LY294002). Furthermore, we identify that miR-200a is down-regulated in TGF-ß1-activated PSCs, and up-regulation of miR-200a inhibits PSCs activation induced by TGF-ß1. Meanwhile, TGF-ß1 inhibits the expression of the epithelial marker E-cadherin, and increases the expression of mesenchymal markers vimentin, and the expression of ECM proteins a-SMA and collagen I, while miR-200a mimic reversed the above effects in PSCs, indicating that miR-200a inhibits TGF-ß1-induced activation and epithelial-mesenchymal transition (EMT). In addition, overexpression of miR-200a promotes the expression of PTEN and decreases the expression of matrix proteins and attenuates phosphorylation of Akt and mTOR. Taken together, our study uncovers a novel mechanism that miR-200a attenuates TGF-ß1-induced pancreatic stellate cells activation and ECM formation through inhibiting PTEN /Akt/mTOR pathway.