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The selective hydrogenation of the biomass platform molecule furfural (FAL) to produce furfuryl alcohol (FA) is of great significance to alleviate the energy crisis. Cu-based catalysts are the most commonly used catalysts, and their catalytic performance can be optimized by changing the preparation method. This paper emphasized the effect of calcination atmosphere on the performance of a Cu/Al2O3 catalyst for the selective hydrogenation of FAL. The precursor of the Cu/Al2O3 catalyst prepared by the ammonia evaporation method was treated with different calcination atmospheres (N2 and air). On the basis of the combined results from the characterizations using in situ XRD, TEM, N2O titration, H2-TPR and XPS, the Cu/Al2O3 catalyst calcined in the N2 atmosphere was more favorable for the dispersion and reduction of Cu species and the reduction process could produce more Cu+ and Cu0 species, which facilitated the selective hydrogenation of FAL to FA. The experimental results showed that the N2 calcination atmosphere improved the FAL conversion and FA selectivity, and the FAL conversion was further increased after reduction. Cu/Al2O3-N2-R exhibited the outstanding performance, with a high yield of 99.9% of FA after 2 h at 120 °C and an H2 pressure of 1 MPa. This work provides a simple, efficient and economic method to improve the C=O hydrogenation performance of Cu-based catalysts. [ABSTRACT FROM AUTHOR]

A switching‐angle‐based hybrid modulation method of full wind speed and low carrier wave ratio for direct‐drive permanent‐magnet wind power generation system is proposed here, which order to improve the control performance of wind turbines in the full wind speed range. The combination manner of the proposed method is based on the harmonic distortion rate of the stator current, a modulation mode with a higher carrier wave ratio is adopted within the maximum switching frequency allowed by the system, the switching angle from optimized synchronous modulation also is introduced. In order to solve the problem of current impact caused by switching different modulation modes, the switching strategy between different modulation modes is developed from the perspective of harmonic current. And the sectors are redivided for the problem of sudden change in carrier wave ratio during switching, which improve the control effect of permanent‐magnet synchronous wind generator when changing the modulations modes. Finally, the feasibility and correctness of the proposed method are verified by theoretical analysis and simulation. [ABSTRACT FROM AUTHOR]

Excessively activated microglia exhibit increased migration, resulting in tissue damage and chronic inflammation. Src was confirmed to play an important role in regulation of cell motility following lipopolysaccharide (LPS) treatment. SET8 plays an important part in multiple cellular signal pathways. In this study, we speculated that SET8 is involved in LPS-induced microglial migration via regulation of Src expression. Our study showed that LPS promoted cell migration via augmentation of Src expression in BV2 cells. Moreover, LPS treatment decreased SET8 expression and upregulated the expression of the transcription factor ETS proto-oncogene 1 (ETS1). Overexpression of both SET8 and small interfering ETS1 reversed LPS-induced Src expression and cell migration. The effects of short hairpin SET8 (shSET8) and ETS1 overexpression are the same as the effects of LPS treatment. Decrease of Src expression reversed the shSET8-induced and ETS1 overexpression-induced migration of BV2 cells. Furthermore, SET8 was observed to associate with ETS1. Chromatin immunoprecipitation assay indicated H4K20me1, a downstream target of SET8, in addition to ETS1, was enriched at the Src promoter region. Furthermore, shSET8 increased Src promoter activity and also increased the positive effect of ETS1 overexpression on Src promoter activity. This study shows that SET8 associates with ETS1 to regulate Src expression, which is involved in LPSinduced BV2 cell migration. Key words: lipopolysaccharide, BV2 cells, SET8, ETS proto-oncogene 1, cell migration. La microglie excessivement activee presente une augmentation de la migration entrainant des lesions tissulaires et de l'inflammation chronique. On a confirme que Src joue un role important dans la regulation de la motilite des cellules a la suite de l'administration de lipopolysaccharides (LPS). SET8 joue un role important dans de multiples voies de signalisation cellulaires. Dans cette etude, nous avons pose l'hypothese selon laquelle SET8 participe a la migration de la microglie provoquee par les LPS par l'intermediaire de la regulation de l'expression de Src. Notre etude a montre que les LPS favorisaient la migration des cellules par l'intermediaire de l'augmentation de l'expression de Src dans les cellules BV2. En outre, l'administration de LPS entrainait une diminution de l'expression de SET8 et une regulation a la hausse de l'expression du proto-oncogene 1 du facteur de transcription ETS (ETS1). La surexpression de SET8 comme de siETS1 permettait d'inverser l'expression de Src et la migration cellulaire engendrees par les LPS. Les effets de shSET8 et de la surexpression d'ETS1 sont les memes qu'avec l'administration de LPS. La diminution de l'expression de Src entrainait l'inversion de la migration des cellules BV2 engendree par shSET8 et et la surexpression d'ETS1. De plus, nous avons observe que SET8 est associe avec le facteur ETS1. A l'aide de l'epreuve de ChIP, nous avons montre que H4K20me1, une cible en aval de SET8, en plus du facteur ETS1, etait enrichi dans la region promotrice de Src. En outre, shSET8 entrainait une augmentation de l'activite promotrice de Src avec aussi un accroissement de l'effet positif de la surexpression d'ETS1 sur l'activite promotrice de Src. Cette etude expose que SET8 s'associe avec ETS1 dans la regulation de l'expression de Src, laquelle joue un role dans la migration des cellules BV2 provoquee par les LPS. [Traduit par la Redaction] Mots-cles: lipopolysaccharides, cellules BV2, SET8, ETS1, migration cellulaire., Introduction Microglia, macrophage-like immune cells, play a crucial role in maintaining homeostasis in the central nervous system. In response to pathological changes, microglia switch to an activated status, exhibiting wound [...]

This paper aims at the problems of the traditional modular model predictive control (MPC) of modular multilevel converter (MMC) with huge computational complexity and high equivalent switching frequency. In this paper, a model predictive control method based on fixed switch state set (FSS‐MPC) is proposed. In this method, two cost functions are used to control phase current and circulating current. Meanwhile, the number of the upper and lower on‐state sub‐modules (SM) is obtained by cost functions. In order to obtain the optimal switching sequence of SM, FSS‐MPC adopts a SM capacitive voltage balancing strategy which has low sorting frequency. Under the control of the FSS‐MPC, the amount of switch combination and sorting computation are greatly reduced. In addition, the switching frequency is extremely low. Finally, to verify the effectiveness and feasibility of the proposed control strategy, a simulation system of 11‐level MMC for offshore wind power has built on the MATLAB/Simulink platform. [ABSTRACT FROM AUTHOR]

Many effective methods extract and fuse different protein features to study the relationship between protein sequence, structure, and function, but different methods have preferences in solving the research of protein structure and function, which requires selecting valuable and contributing features to design more effective prediction methods. This work mainly focused on the feature selection methods in the study of protein structure and function, and systematically compared and analyzed the efficiency of different feature selection methods in the prediction of protein structures, protein disorders, protein molecular chaperones, and protein solubility. The results show that the feature selection method based on nonlinear SVM performs best in protein structure prediction, protein solubility prediction, protein molecular chaperone prediction, and protein solubility prediction. After selection, the accuracy of features is improved by 13.16% ~71%, especially the Kmer features and PSSM features of proteins. [ABSTRACT FROM AUTHOR]

Drug-disease correlations play an important role in revealing the mechanism of disease, finding new indications of available drugs, or drug repositioning. A variety of computational approaches were proposed to find drug-disease correlations and achieve good performances. However, these methods used a variety of network information, but integrated networks were rarely used. In addition, the role of known drug-disease association data has not been fully played. In this work, we designed a combination algorithm of random walk and supervised learning to find the drug-disease correlations. We used an integrated network to update the model and selected a gene set as the start of random walk based on the known drug-disease correlations data. The experimental results show that the proposed method can effectively find the correlation between drugs and diseases, and the prediction accuracy is 82.7%. We found that there are 8 pairs of drug-disease relationships that have not yet been reported, and 5 of them have pharmacodynamic effects on Parkinson's disease. We also found that a key linkage between Parkinson's disease and phenylhexol, a drug for the treatment of Parkinson's disease α-synuclein and tau protein, provides a useful exploration for the effectiveness of the treatment of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Bitterlings are carp‐like teleost fish (Cypriniformes: Acheilanathidae) known for their specialized brood parasitic lifestyle. Bitterling embryos, in fact, develop inside the gill chamber of their freshwater mussel hosts. However, little is known about how their parasitic lifestyle affects brain development in comparison to nonparasitic species. Here, we document the development of the brain of the rosy bitterling, Rhodeus ocellatus, at four embryonic stages of 165, 185, 210, 235 hours postfertilization (hpf) using micro‐computed tomography (microCT). Focusing on developmental regionalization and brain ventricular organization, we relate the development of the brain divisions to those described for zebrafish using the prosomeric model as a reference paradigm. Segmentation and three‐dimensional visualization of the ventricular system allowed us to identify changes in the longitudinal brain axis as a result of cephalic flexure during development. The results show that during early embryonic and larval development, histological differentiation, tissue boundaries, periventricular proliferation zones, and ventricular spaces are all detectable by microCT. The results of this study visualized with differential CT profiles are broadly consistent with comparable histological studies, and with the genoarchitecture of teleosts like the zebrafish. Compared to the zebrafish, our study identifies distinct developmental heterochronies in the rosy bitterling, such as a precocious development of the inferior lobe. [ABSTRACT FROM AUTHOR]

Human papillomavirus (HPV) can cause condyloma acuminatum and cervical cancer. Some mutations of these viruses are closely related to the persistent infection of cervical cancer and are ideal cancer vaccine targets. Several databases have been developed to collect HPV sequences, but no HPV mutation database has been published. This paper reports a Chinese HPV mutation database (HPVMD-C), which contains 149 HPV genotypes, 468 HPV mutations, 3409 protein sequences, 4727 domains and 236 epitopes. We analyzed the mutation distribution among HPV genotypes, domains and epitopes. We designed a visualization tool to display these mutations, domains and epitopes and provided more detailed information about the disease, region and related literature. We also proposed an HPV genotype prediction tool, which can predict HPV carcinogenic or non-carcinogenic risk genotypes. We expect that HPVMD-C will complement the existing database and provide valuable resources for HPV vaccine research and cervical cancer treatment. HPVMD-C is freely available at Database URL : http://bioinfo.zstu.edu.cn/hpv. [ABSTRACT FROM AUTHOR]

Background: Trimethylamine N-oxide, a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients, has been associated with a poor prognosis for patients with cardiovascular disease. However, the role and underlying mechanisms of trimethylamine N-oxide in the cardiac function of patients with heart failure with preserved ejection fraction (HFpEF) have not been elucidated.Methods and Results: C57BL/6 mice were fed a normal diet, high-choline (1.2%) diet, and/or 3-dimethyl-1-butanol diet 3 weeks before the operation (uninephrectomy followed by a continuous saline or aldosterone infusion). Mice were assessed for 4 weeks after the operation. Echocardiographic and hemodynamic measurements were performed. Blood samples were evaluated for choline, trimethylamine N-oxide, and inflammatory factor levels. Left ventricular tissues were collected to assess myocardial fibrosis and inflammation. Left ventricular hypertrophy, pulmonary congestion, and diastolic dysfunction were markedly exacerbated in HFpEF mice fed high-choline diets compared with mice fed the control diet. Myocardial fibrosis and inflammation were markedly increased in HFpEF mice fed high-choline diets compared with animals fed the control diet. Additionally, 3,3-dimethyl-1-butanol DMB markedly ameliorated cardiac diastolic dysfunction, myocardial fibrosis and inflammation in the choline-fed HFpEF mice.Conclusions: A high-choline diet exacerbates cardiac dysfunction, myocardial fibrosis, and inflammation in HFpEF mice, and 3,3-dimethyl-1-butanol ameliorates the high-choline diet-induced cardiac remodeling. [ABSTRACT FROM AUTHOR]

2,5-Distyryl-dithieno[2,3-b:2′,3′-d]thiophene (DEP-bt-DTT), an isomer of 2,5-distyryl-dithieno [2,3-b:3′,2′-d]thiophene (DEP-bb-DTT) and 2,5-distyryl-dithieno[3,2-b:2′,3′-d]thiophene (DEP-tt-DTT), was synthesized. Organic field-effect transistors (OFETs) based on these three isomers were fabricated. The structure cell parameters and the formation of intermolecular interactions in their single crystals show regular change when the positions of sulphur atoms vary from top–bottom–top in DEP-tt-DTT to bottom–bottom–top in DEP-bt-DTT, then to bottom–bottom–bottom in DEP-bb-DTT. Combining the results of theoretical calculations and OFET performances, it reveals that: (1) the positions of sulphur atoms determine the contribution extent of sulphur atoms to the molecular conjugation and the formation of intermolecular interactions; (2) the existence of the intermolecular interactions, especially for S–π, benefits for the charge transport; (3) the field-effect mobility (μ) increases with increasing of the sulphur atom contribution to the molecular conjugation. [ABSTRACT FROM AUTHOR]

The conformational conversion of the cellular prion protein (PrPC) into its β-sheet-rich scrapie isoform (PrPSc) causes fatal prion diseases, which are also called transmissible spongiform encephalopathies (TSEs). Recent studies suggest that the expression of PrPC by the PRNP gene is crucial for the development of TSEs. Therefore, the identification of the exogenous and endogenous stimulating factors that regulate PRNP expression would help to understand the pathogenesis of TSEs. Here, we demonstrate that forkhead box O3a (FOXO3a) negatively regulates PRNP expression by binding to the PRNP promoter, which is negatively regulated by insulin-like growth factor 1 (IGF-1). Our results show that the IGF-1-induced enhancement of PRNP mRNA and protein levels is due to the activation of the PI3K-Akt signaling pathway. The activation of Akt then induces the phosphorylation of FOXO3a, leading to its translocation from the nucleus to the cytoplasm and preventing its binding to the PRNP promoter. Treatment with the PI3K-Akt inhibitor LY294002 induces the nuclear retention of FOXO3a, which leads to a decrease in PRNP expression. We present a new IGF-1-PI3K-Akt-FOXO3a pathway, which influences PRNP expression. The results of this work are vital for understanding the function of PrPC and for future therapeutic approaches to human TSEs. [ABSTRACT FROM AUTHOR]

• The substitutional effects of shared mobility result in 371 thousand toe energy savings, and 518 thousand tons CO 2 emission reductions in year 2018. • The activity increase effects of shared mobility raise the energy consumption and emissions. • Shared mobility changes the travelling structure by increasing the rail trips and reducing public bus trips. • Though the share for vehicle kilometers travelled is limited, electric vehicles on the shared platform produce significant environmental benefits, and mutual promotion exists. The shared mobility, as an emerging shared economy business mode, has been changing the travelling style of Chinese citizens. This study draws the annual data in year 2018 from DiDi Chuxing, as well as other survey and statistical data, to evaluate the shared mobility influence on energy consumption, emission and transportation structure, in the comprehensive national level. The results indicate that the substitution effects of shared mobility are conducive to energy saving and emission reduction, by the number of 371 thousand toe for energy savings, as well as 518 thousand tons CO 2 emission reductions, respectively in year 2018. The shared mobility platform could prioritize the transportation structure, and promote the penetration of electric vehicles with better cost returns. The big data from the platform now is used for smart traffic light control, ending up with 47 toe energy savings in 8 applied cities, and other emission reduction benefits. [ABSTRACT FROM AUTHOR]

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell‐intrinsic mechanism governing astrocyte function during MS and EAE. Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE. Mice with astrocyte‐specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1‐deficient astrocytes were hyperactivated in response to IFN‐γ, a fingerprint cytokine of encephalitogenic T cells, and produced more proinflammatory cytokines and chemokines than control astrocytes. Mechanistically, OTUB1 inhibited IFN‐γ‐induced Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling by K48 deubiquitination and stabilization of the JAK2 inhibitor suppressor of cytokine signaling 1 (SOCS1). Thus, astrocyte‐specific OTUB1 is a critical inhibitor of neuroinflammation in CNS autoimmunity. Synopsis: The deubiquitinating enzyme OTUB1 regulates cell signaling by blocking ubiquitin transfer from E2 conjugating enzymes to E3 ligases or by cleavage of ubiquitin chains from target proteins, but the in vivo cell type‐specific function of OTUB1 is largely unknown. During CNS autoimmunity, human and murine astrocytes upregulate OTUB1, which limits CNS pathology by inhibiting IFN‐γ‐induced activation of the JAK2/STAT1 pathway and concomitant chemokine and cytokine production in astrocytes. OTUB1 expression of astrocytes is induced in the CNS of treatment‐naïve patients with multiple sclerosis and in mice with experimental autoimmune encephalomyelitis.OTUB1 inhibits IFN‐γ‐induced JAK2/STAT1 signaling by K48 deubiquitination and stabilization of the JAK2 inhibitor SOCS1.OTUB1‐dependent inhibition of the JAK2/STAT1 signaling limits IFN‐γ‐induced cytokine and chemokine production of astrocytes.OTUB1 expression in astrocytes ameliorates the clinical severity of murine experimental autoimmune encephalomyelitis by limiting astrocytic cytokine and chemokine production, recruitment of encephalitogenic T cells to the CNS, and demyelination. [ABSTRACT FROM AUTHOR]

The complete mitochondrial DNA (mtDNA) sequence ofRhodeus fangiis 16,733 bp in length. It consists of 13 protein-coding genes, 22 transfer RNA genes, 2 ribosome RNA genes and 2 non-coding regions. Base composition of the genome is A (28.54%), G (17.67%), C (27.03%) and T (26.76%) with an A + T-rich hallmark as that of other vertebrate mitochondrial genomes. The complete mitogenome of theR. fangican provide a basic data for phylogenetic relationship study and useful information for taxonomic identification of theR. smithiicomplex in genusRhodeus. [ABSTRACT FROM AUTHOR]

Abstract: Microbial enhanced oil recovery (MEOR) is a petroleum biotechnology for manipulating function and/or structure of microbial environments existing in oil reservoirs for prolonged exploitation of the largest source of energy. In this study, an Enterobacter cloacae which is capable of producing water-insoluble biopolymers at 37°C and a thermophilic Geobacillus strain were used to construct an engineered strain for exopolysaccharide production at higher temperature. The resultant transformants, GW3-3.0, could produce exopolysaccharide up to 8.83gl−1 in molasses medium at 54°C. This elevated temperature was within the same temperature range as that for many oil reservoirs. The transformants had stable genetic phenotype which was genetically fingerprinted by RAPD analysis. Core flooding experiments were carried out to ensure effective controlled profile for the simulation of oil recovery. The results have demonstrated that this approach has a promising application potential in MEOR. [Copyright &y& Elsevier]

Henoch-Schonlein purpura nephritis (HSPN) is a systemic vascular inflammatory disease. Huanglian Decoction (HLD) ameliorates renal injury in nephritis; however, the mechanism of action of HLD on HSPN has not been investigated. This study aimed to investigate the protective mechanism of HLD treatment in HSPN. The effects of HLD on HSPN biochemical indices, kidney injury and NF-κB/NLRP3 signaling pathway were analyzed by biochemical analysis, ELISA, HE and PAS staining, immunohistochemistry, immunofluorescence, and Western Blot. In addition, the effects of HLD on HSPN cells were analyzed. We found that HLD treatment significantly reduced renal tissue damage, decreased the levels of IL-17, IL-18, TNF-α, and IL-1β, and increased the levels of TP and ALB in HSPN mice. It also inhibited the deposition of IgA, IgG, and C3 in kidney tissues and significantly decreased the expression of IκBα, p-IκBα, NLRP3, caspase-1, and IL-1β in kidney tissues and cells. In addition, PMA treatment inhibited the above-mentioned effects of HLD. These results suggested that HLD attenuates renal injury, IgA deposition, and inflammation in HSPN mice and its mechanism of action may be related to the inhibition of the NF-κB/NLRP3 pathway.

Embryonic development is often considered shielded from the effects of natural selection, being selected primarily for reliable development. However, embryos sometimes represent virulent parasites, triggering a coevolutionary "arms race" with their host. We have examined embryonic adaptations to a parasitic lifestyle in the bitterling fish. Bitterlings are brood parasites that lay their eggs in the gill chamber of host mussels. Bitterling eggs and embryos have adaptations to resist being flushed out by the mussel. These include a pair of projections from the yolk sac that act as an anchor. Furthermore, bitterling eggs all adopt a head-down position in the mussel gills which further increases their chances of survival. To examine these adaptations in detail, we have studied development in the rosy bitterling ( Rhodeus ocellatus ) using molecular markers, X-ray tomography, and time-lapse imaging. We describe a suite of developmental adaptations to brood parasitism in this species. We show that the mechanism underlying these adaptions is a modified pattern of blastokinesis-a process unique, among fish, to bitterlings. Tissue movements during blastokinesis cause the embryo to do an extraordinary "front-flip" on the yolk. We suggest that this movement determines the spatial orientation of the other developmental adaptations to parasitism, ensuring that they are optimally positioned to help resist the ejection of the embryo from the mussel. Our study supports the notion that natural selection can drive the evolution of a suite of adaptations, both embryonic and extra-embryonic, via modifications in early development., Competing Interests: Competing interests statement:The authors declare no competing interest.

Context: Chronic myeloid leukemia (CML) is a malignant hematopoietic stem cell disease caused by excessive proliferation and abnormal differentiation of hematopoietic stem cells. Asperuloside (ASP) is considered to have good biological activity and may be a good anti-CML drug., Objective: This study aimed to explore the effects and possible mechanisms of ASP on the biological behavior of K562 cells based on RNA-seq., Materials and Methods: The IC 50 of ASP in K562 cells was calculated by the concentration-effect curve. Cell viability, apoptosis, and differentiation were detected by CCK8, flow cytometry, benzidine staining, and WB analysis, respectively. Further, RNA-seq was used to analyze the possible mechanism of ASP regulating K562 cells., Results: ASP significantly inhibited the proliferation, and promoted apoptosis and differentiation of K562 cells. A total of 117 differentially expressed genes were screened by RNA-seq, mainly involved in the RAS/MEK/ERK pathway. PD98059 was used to inhibit the RAS/MEK/ERK pathway in K562 cells, and results confirmed that PD98059 could not only inhibit the RAS/MEK/ERK pathway, but also inhibit the regulation of ASP on the proliferation and differentiation of K562 cells., Conclusion: ASP inhibited the proliferation, promoted apoptosis and differentiation of K562 cells by regulating the RAS/MEK/ERK pathway, and played a good anti-CML role., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Thiol-ene click reactions are important for the construction of carbon-sulfur bonds. The use of visible-light photoredox catalysis for the formation of C-S bonds has attracted much attention. In this work, two-dimensional metal-free graphitic carbon nitride (g-C 3 N 4 ) nanosheets are prepared through a simple thermal polymerization method and used to catalyze the thiol-ene click reaction under visible light-illumination. This green, atom-economic, and inexpensive approach for the hydrothiolation of alkenes is applicable for structurally different substrates and exhibits superior yields. In air or nitrogen atmosphere, the reaction yield decreases when a hole scavenging agent, CH 3 OH, is introduced, which indicates that photogenerated holes in the g-C 3 N 4 nanosheets play an important role in the formation of thiyl radicals. The g-C 3 N 4 nanosheets still show a good stability and favorable photocatalytic activity after five cycles of the reaction. Moreover, this approach can be scaled up to the gram-scale synthesis of benzyl(phenethyl)sulfane with a yield up to 93%. Our study suggests a good potential of semiconducting g-C 3 N 4 nanosheets as a metal-free, efficient photocatalyst for various thiol-ene click reactions and even for other organic reactions.

In this research, with the assistance of scanning tunneling microscopy (STM), we observed the two-dimensional (2D) self-assembly transition of a star-shaped oligofluorene derivative (StOF) from disordered structure to honeycomb network by adjusting StOF concentration in solution. By introducing guest molecules coronene (COR), we for the first time achieved novel triangle-shaped COR trimers on liquid/highly oriented pyrolytic graphite (HOPG) interface in both honeycomb network and the disordered structure. In thermal tests, the COR/StOF-disorder system underwent a structural conformation to form well-ordered ladder structures, while the COR/StOF-honeycomb system remained the perfect hexagonal network with COR trimers included in the cavities. Density functional theory (DFT) calculations have been employed to investigate the forming mechanism of the molecular nanoarrays. These studies are expected to enhance controlling on 2D self-assembly and provide a facial approach toward constructing on-surface molecular clusters.

Background: Ginsenoside Rg1, the major effective component of ginseng, possesses a variety of pharmacologic activities. The objective of this study was to investigate the effects of Rg1 on liver ischemia-reperfusion (IR) injury and explore its potential mechanisms., Materials and Methods: Liver warm IR injury was achieved by occluding the portal vein and hepatic artery for 1 h followed by 6-h reperfusion. Eighteen mice were equally randomized into three groups: sham group, IR group, and IR plus Rg1 group (n = 6 mice per group). Mice received an intravenous dose of 20 mg/kg Rg1 or an equivalent volume of saline before ischemic insult. Liver samples and serum were collected for analyses. Serum aminotransferase, histopathology, and apoptosis were determined. Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylation of nuclear factor kappa B (NF-κB) p65 was assessed by Western blotting. In addition, the effect of Rg1 in a simulated IR model in vitro was also investigated. Rg1 (100 ug/mL and 500 ug/mL) was administered 1 h before hypoxia insult, and then apoptosis was measured after 12-h reperfusion., Results: Liver IR injury led to a dramatic increase in aminopherase activity, apoptosis and necrosis of hepatocytes, and production of proinflammatory cytokines. Pretreatment with Rg1 protected mice from IR-induced liver injury. Treatment with a high-dose Rg1 (500 ug/mL) significantly suppressed apoptosis compared with a lower dose or control (both P < 0.001). Phosphorylation of NF-κB p65 was increased significantly in IR group, and administration with Rg1 suppressed the level of phosphorylation., Conclusions: Pretreatment of mice with Rg1 reduced hepatocellular apoptosis and inhibited inflammatory response, which was in part through the NF-κB signaling pathway. Rg1 may provide a novel therapeutic strategy for the treatment of IR-induced liver injury., (Copyright © 2014 Elsevier Inc. All rights reserved.)

The conformational conversion of the cellular prion protein (PrP(C)) into its β-sheet-rich scrapie isoform (PrP(Sc)) causes fatal prion diseases, which are also called transmissible spongiform encephalopathies (TSEs). Recent studies suggest that the expression of PrP(C) by the PRNP gene is crucial for the development of TSEs. Therefore, the identification of the exogenous and endogenous stimulating factors that regulate PRNP expression would help to understand the pathogenesis of TSEs. Here, we demonstrate that forkhead box O3a (FOXO3a) negatively regulates PRNP expression by binding to the PRNP promoter, which is negatively regulated by insulin-like growth factor 1 (IGF-1). Our results show that the IGF-1-induced enhancement of PRNP mRNA and protein levels is due to the activation of the PI3K-Akt signaling pathway. The activation of Akt then induces the phosphorylation of FOXO3a, leading to its translocation from the nucleus to the cytoplasm and preventing its binding to the PRNP promoter. Treatment with the PI3K-Akt inhibitor LY294002 induces the nuclear retention of FOXO3a, which leads to a decrease in PRNP expression. We present a new IGF-1-PI3K-Akt-FOXO3a pathway, which influences PRNP expression. The results of this work are vital for understanding the function of PrP(C) and for future therapeutic approaches to human TSEs.