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[Display omitted] The performance of perovskite solar cells (PSCs) can be improved by optimizing the perovskite film quality and electron transfer layers (ETLs). In this study, high-efficient PSCs with multi-cation hybrid electron transport layer (SnO 2 @Na:Cs ETL) were fabricated using continuous spin-coating. Compared to the pristine SnO 2 , the power conversion efficiency (PCE) of device based on SnO 2 @Na:Cs ETL have reached 22.06% (with an open circuit voltage of 1.13 V), up approximately 21%. The photovoltaic performance of the device is enhanced due to the increase in the transmission rate, electrical conductivity, electron mobility and surface state owing to the multi-cation hybrid. In addition, because SnO 2 @Na:Cs ETL can significantly improve interface contact with the perovskite film and improve its crystallinity, the transport defect state and carrier transport efficiency are significantly improved at the ETL/Perovskite interface. Therefore, the open circuit voltage (V oc) and fill factor (FF) of PSCs was significantly increased. The application of SnO 2 @Na:Cs ETL provides a simple and efficient method to obtain highly-efficient PSCs. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H 2 S) as an endogenous gaseous signaling molecule had been proved to play a vital role in gametes physiology, covering meiosis, maturation and aging. However, little is known about H 2 S involvement in embryonic development. The present study explored the positive effect of H 2 S on human early embryonic development. Results validated that the two H 2 S producing enzymes, CBS and CSE mRNA and proteins were identified in donated human cleavage and blastocyst-stage embryos. The l -cysteine incubation produced endogenous H 2 S in human blastocysts. NaHS positively affected in vitro blastulation. Single-cell RNA-seq analysis identified 228 differentially expressed genes (DEGs) after NaHS treatment versus the control. The Gene Ontology (GO) enrichment analysis of DEGs showed that genes for protein modification and metabolism were significantly enriched in the NaHS treatment group. For the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, 2-oxocarboxylic acid metabolism, glycosaminoglycan biosynthesis-keratan sulfate, steroid biosynthesis, carbon metabolism, and biosynthesis of amino acids were significantly enriched. Six DEGs, including Neural EGFL like 1 (NELL1) , aconitase 1 (ACO1) , phosphoglycerate mutase 1 (PGAM1) , TP53 induced glycolysis regulatory phosphatase (TIGAR) , UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 (B3GNT2) , and c arbohydrate Sulfotransferase 4 (CHST4) were validate by real-time RT-PCR. These findings suggest that H 2 S is a positive regulator of early embryonic development and may alter the transcription of embryonic genes for protein modification and metabolism in human embryos. • Human embryos endogenously synthesize hydrogen sulfide. • Hydrogen sulfide regulates human embryonic development. • Hydrogen sulfide changes metabolism-related gene expression. [ABSTRACT FROM AUTHOR]

• NJC41 inhibited C. cassiicola mycelial growth and spore germination. • NJC41 showed high colonization ability in soybean pods. • NJC41 secreted antifungal phenethyl alcohol and competed for nutrients and space. • NJC41 reduced target spot symptoms in vivo. • The first method for the biocontrol of C. cassiicola in soybean is reported. Corynespora cassiicola is a hazardous fungal pathogen that causes target spot disease in soybean. Numerous resistant C. cassiicola strains have emerged during recent years, leading to uncontrolled spreads and enormous economic losses in several soybean production areas. For these reasons, new methods for the control of this pathogen are urgently needed. In this study, a new Meyerozyma caribbica strain, NJC41, was isolated from C. cassiicola -infected soybean plants in China and identified by ITS and LSU sequencing. NJC41 inhibited C. cassiicola mycelial growth, and showed high colonization ability in soybean pods, maintaining its population for one week. NJC41 produced antifungal phenethyl alcohol, which was detected at 44.6 μg/mL in NJC41 secretions, and competed for space and nutrients with C. cassiicola. Curative application of 1 × 109 cells/mL NJC41 reduced C. cassiicola symptoms by 47.1%, providing higher curative efficacy than commercial fungicide carbendazim (29.8% lesion length inhibition). This study reveals the first biocontrol method for the management of target spot disease in soybean. [ABSTRACT FROM AUTHOR]

Transforming growth factor-β-activating kinase 1 (TAK1) is triggered by foreign pathogenic infection and involves in proinflammatory response through the activation of nuclear factor-κB (NF-κB), which is specifically regulated by TAK1-binding protein 1 (TAB1). However, the expression and regulatory characterizations of TAK1 and TAB1 in fish immune response remain largely unknown. In the present study, the cDNA sequences of TAK1 ( Lc TAK1) and TAB1 ( Lc TAB1) were identified from large yellow croaker, Larimichthys crocea . The open reading frame (ORF) of Lc TAK1 was 1725 bp in length, encoding 574 amino acids. The putative Lc TAK1 protein contained a protein kinase domain and a C-terminal coiled-coil region. The ORF of Lc TAB1 was 1518 bp encoding 505 amino acids. And a typical PP2Cc domain and a conserved sequence motif (PYVDFSQFYLLWGSDH) at C-terminal were identified in the predicted Lc TAB1 protein. Multiple alignments showed that Lc TAK1 shared 74.0–97.9% and Lc TAB1 shared 37.4–95.8% sequence identities with TAK1 and TAB1 proteins from other species, respectively. Quantitative PCR analysis indicated that both Lc TAK1 and Lc TAB1 were broadly expressed in all examined tissues, with the most predominant expression in brain and the weakest expression in muscle, respectively. Subcellular localization revealed that both Lc TAK1 and Lc TAB1 expressed in the cytoplasm. In addition, Lc TAK1 transcripts increased significantly in LCK cells after flagellin, LPS and poly I:C stimulation while Lc TAB1 enhanced greatly after LPS and poly I:C challenge. Furthermore, the roles of them in NF-κB activation were investigated by overexpression of Lc TAK1 and Lc TAB1 in HEK293T cells. Our results revealed that NF-κB luciferase promoter expression could not be induced by overexpression of Lc TAK1 or Lc TAB1 alone, however, it could be induced by co-expression of Lc TAK1 and Lc TAB1 together. Moreover, the roles of Lc TAK1 and Lc TAB1 in immune response analysis showed that NF-κB activation enhanced significantly in co-overexpressed HEK293T cells following LPS and poly I:C stimulation. However, the expression levels of tumor necrosis factor (TNF)-α, Interleukin-6 (IL-6) and IL-8 were induced only after LPS challenge ( p  < .05). These findings suggested that the TAK1-TAB1 complex of large yellow croaker might play an important role in pro-inflammatory cytokines and chemokine release after LPS stimulation via inducing NF-κB activation. [ABSTRACT FROM AUTHOR]

[Display omitted] • Four sections of subgenus Chamaecerasus plus six outgroup taxa were used to recover the main clades of Lonicera L. • Extensive cytonuclear discordance across sections of subgenus Chamaecerasus. • Results suggest merging L. korolkowii into section Coeloxylosteum , L. caerulea into section Nintooa and L. albiflora into subgenus Lonicera. • The genus Lonicera is estimated to have originated in the Early Oligocene (26.45 Ma). • Subgenus Chamaecerasus may have originated in Eastern Asia and Central Asia during the Late Miocene, with subsequent dispersal or vicariance across other areas. The genus Lonicera L. is widely distributed in the north temperate zone and is well-known for its high species richness and morphological diversity. Previous studies have suggested that many sections of Lonicera are not monophyletic and phylogenetic relationships within the genus are still poorly resolved. In this study, we sampled 37 accessions of Lonicera , covering four sections of subgenus Chamaecerasus plus six outgroup taxa, to recover the main clades of Lonicera based on sequences of nuclear loci generated by target enrichment and cpDNA from genome skimming. We found extensive cytonuclear discordance across the subgenus. Both nuclear and plastid phylogenetic analyses supported subgenus Chamaecerasus sister to subgenus Lonicera. Within subgenus Chamaecerasus , sections Isika and Nintooa were each polyphyletic. Based on the nuclear and chloroplast phylogenies, we propose to merge Lonicera korolkowii into section Coeloxylosteum and Lonicera caerulea into section Nintooa. In addition, Lonicera is estimated to have originated in the mid Oligocene (26.45 Ma). The stem age of section Nintooa was estimated to be 17.09 Ma (95% HPD: 13.30–24.45). The stem age of subgenus Lonicera was estimated to be 16.35 Ma (95% HPD: 14.12–23.66). Ancestral area reconstruction analyses indicate that subgenus Chamaecerasus originated in East Asia and Central Asia. In addition, sections Coeloxylosteum and Nintooa originated in East Asia, with subsequent dispersals into other areas. The aridification of the Asian interior likely promoted the rapid radiation of sections Coeloxylosteum and Nintooa within this region. Moreover, our biogeographic analysis fully supports the Bering and the North Atlantic Land Bridge hypotheses for the intercontinental migrations in the Northern Hemisphere. Overall, this study provides new insights into the taxonomically complex lineages of subgenus Chamaecerasus and the process of speciation. [ABSTRACT FROM AUTHOR]

In this study, the effects of microwave treatment on the microorganism mortality and PPO activity in whole-wheat flour (WWF) and storage stability of WWF fresh noodles were investigated, as well as the rheological properties of WWF, viscosity and gelatinization properties of starch component, and polymerization and conformational changes of protein. TPC and PPO activity were largely reduced in WWF treated for over 60s. Moreover, it was amazing that microwave treatment significantly increased ( P < 0.05) dough stability and the resistance to extension. Peak and final viscosity of starch were increased after microwave treatment, with no observable loss of birefringence; SDS-extractable proteins were limitedly decreased and protein aggregating occurred mainly on the large and medium glutenin polymers as shown by the SE–HPLC profiles. In addition, microbial growth and darkening rate of WWF fresh noodles were significantly inhibited, shelf-life of the samples was extended for 3 times after treating for 90 s. [ABSTRACT FROM AUTHOR]

Objective Estrogen receptor alpha 36 (ER-α36), a truncated variant of ER-α, is different from other nuclear receptors of the ER-α family. Previous findings indicate that ER-α36 might be involved in cell growth, proliferation, and differentiation in carcinomas and primarily mediates non-genomic estrogen signaling. However, studies on ER-α36 and cervical cancer are rare. This study aimed to detect the expression of ER-α36 in cervical cancer; the role of ER-α36 in 17-β-estradiol (E2)-induced invasion, migration and proliferation of cervical cancer; and their probable molecular mechanisms. Methods Immunohistochemistry and immunofluorescence were used to determine the location of ER-α36 in cervical cancer tissues and cervical cell lines. CaSki and HeLa cell lines were transfected with lentiviruses to establish stable cell lines with knockdown and overexpression of ER-α36. Wound healing assay, transwell invasion assay, and EdU incorporation proliferation assay were performed to evaluate the migration, invasion, and proliferation ability. The phosphorylation levels of mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling molecules were examined with western blot analysis. Results ER-α36 expression was detected in both cervical cell lines and cervical cancer tissues. Downregulation of ER-α36 significantly inhibited cell invasion, migration, and proliferation. Moreover, upregulation of ER-α36 increased the invasion, migration, and proliferation ability of CaSki and HeLa cell lines. ER-α36 mediates estrogen-stimulated MAPK/ERK activation. Conclusion ER-α36 is localized on the plasma membrane and cytoplasm in both cervical cancer tissues and cell lines. ER-α36 mediates estrogen-stimulated MAPK/ERK activation and regulates migration, invasion, proliferation in cervical cancer cells. [ABSTRACT FROM AUTHOR]

Peptidoglycan recognition proteins (PGRPs) are members of the innate immune system that interact with bacteria by binding to bacterial peptidoglycan. In this study, we examined the expression and function of a short type of PGRP, CsPGRP-SC2, from tongue sole ( Cynoglossus semilaevis ). CsPGRP-SC2 contains 164 amino acid residues and shares 54.5%–65.3% overall sequence identities with other teleost PGRPs. CsPGRP-SC2 possesses an amidase domain with a conserved zinc binding site. CsPGRP-SC2 expression occurred in multiple tissues and was upregulated by bacterial and viral infection. Purified recombinant CsPGRP-SC2 (rCsPGRP-SC2) was able to bind and agglutinate Gram-positive bacteria in a Zn 2+ -dependent manner. rCsPGRP-SC2 enhanced the uptake of the bound bacteria by host phagocytes and reduced bacterial dissemination and colonization in host tissues. These results indicate that CsPGRP-SC2 is an innate immune factor that participates in host defense against bacterial infection. [ABSTRACT FROM AUTHOR]

NAC proteins are plant-specific transcription factors that play essential roles in plant development and various abiotic stress responses. A comprehensive analysis of maize NAC genes was performed in this study. A total of 157 non-redundant maize NAC genes including seven membrane-bound members were identified and found to be unevenly distributed on 10 maize chromosomes. Motif composition analysis indicated that the maize NAC proteins share three relatively conserved motifs in the NAC domain within the N-terminal region. Phylogenetic analysis of 157 maize NAC proteins accompanied by 117 NAC proteins from Arabidopsis and 151 from rice were presented. The NAC proteins evaluated were divided into two large groups including 18 subgroups. Gene duplication analysis indicated that gene loss occurred during maize evolution. Seven NAC members that belong to the same clade of maize NAC domain genes were isolated, and overlapping expression patterns were observed under various abiotic stresses, including low temperature, high salinity and dehydration, and phytohormone abscisic acid treatments. This suggested that NAC members function as stress-responsive transcription factors in ABA-dependent signaling pathways. Relatively higher expression levels of these selected maize NAC genes were detected in roots. The stress responsive NAC genes may have applications in molecular breeding to improve crop stress tolerance. [ABSTRACT FROM AUTHOR]

Background: In our previous study, it was indicated that hyperbaric oxygen preconditioning (HOP) could induce a preconditioning against myocardial infarction and promote neovascularization. In this study, attempts were made to investigate whether a modified short-term pre-exposure protocol could also induce cardioprotection, and its potential mechanisms. Materials and methods: Adult male Sprague Dawley rats were divided into seven groups; group 1 was sham surgery (SHAM) and group 2 was pre-exposed to normal air (CTL), and the other groups to HOP 1, 6, 24, 48, and 72 h (H1, H6, H24, H48, H72 groups) before permanent ischemia. The infarct size was measured by triphenyltetrazolium chloride staining, and left ventricular function parameters were recorded. The extent of apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive staining. Caspase-3 activity, Bcl-2, and Bax expression were also measured. Results: Compared with CTL group, myocardial infarct size was significantly decreased as well as cardiac cell apoptosis in area at risk zones (AAR) in H48 group. Meanwhile, the activity of caspase 3 was reduced, the ratio of Bcl-2/Bax expression was up-regulated, and the heart function parameters, including left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVEDP), +(dP/dt)max, and –(dP/dt)max were also significantly improved after preconditioning in H48 group. Conclusion: The results indicate that short-term HOP could induce cardioprotection and may not last for more than 24 h. HOP prevents myocardium from permanent ischemia injury by suppression of apoptotic pathways. [Copyright &y& Elsevier]

Abstract: Mesoporous VO x –TiO2 with high surface areas were prepared using the procedure of evaporation-induced self-assembly combined with ammonia posttreatment. The samples were characterized by X-ray diffraction (XRD), laser Raman spectroscopy (LRS), transmission electron microscopy (TEM), N2 adsorption, temperature-programmed reduction (H2-TPR), microcalorimetry for the adsorption of NH3, and isopropanol probe reaction. Their catalytic activities were evaluated for the reaction of selective oxidation of methanol to dimethoxymethane (DMM). It was found that the VO x –TiO2 materials exhibited high surface areas with pore diameters of 4nm. The vanadia species were highly dispersed in the VO x –TiO2 within 30wt% VO x content, evidenced by the results of XRD and LRS. The VO x –TiO2 samples exhibited both surface acidic and redox properties. The surface acidity was further enhanced on the addition of . The catalyst exhibited good performance for the selective oxidation of methanol (57% conversion) to DMM (83% selectivity) at 423K. [Copyright &y& Elsevier]

Microglia and its interaction with Müller cells are responsible to retinal surveillance during retinal neurodegeneration, however, the role and mechanism of microglia-derived tumor necrosis factor (TNF)-α in the activation of retinal Müller cells have not been fully elucidated. In the present study, primary microglia and Müller cells were isolated from newborn Sprague-Dawley (SD) rats with purities of 88.2 ± 6.2% and 92.2 ± 2.2%, respectively. By performing immunofluorescence and Western blot analysis, we found that TNF receptor (TNFR)-1 and TNFR2 were expressed in Müller cells. After co-cultured with microglia-conditioned medium (MCM), the elevated mRNA levels of glial fibrillary acidic protein (GFAP), proinflammatory factors (TNF-α, IL-1β, CXCL-1, CSF-1, NOS2, COX2) and decreased CNTF mRNA levels were found in Müller cells. However, pretreatment with R-7050 (a TNF-α receptor inhibitor) or anti-TNFR1 significantly abrogated the changes. Simultaneously, pretreatment with anti-TNFR2 slightly inhibited the expression of GFAP in MCM-incubated Müller cells. Meanwhile, anti-TNFR1 treatment reversed the increased expression of CSF-1 and IL-1β induced by TNF-α. Compared to the control groups, the phosphorylation of NF-κB P65, MAPK P38 and ERK1/2 in TNF-α-treated Müller cells was significantly increased. Nevertheless, pretreatment with anti-TNFR1 inhibited the phosphorylation of NF-κB P65 and MAPK p38, especially NF-κB P65. Additionally, pretreatment with Bay117082 (an NF-κB inhibitor) also significantly inhibited NF-κB P65 phosphorylation and GFAP expression. Moreover, anti-TNFR1 and Bay117082 treatment reduced NF-κB P65 phosphorylation of Müller cells induced by MCM. These results suggested that microglia-derived TNF-α served as a vital role in regulating Müller cells activation during retinal neurodegeneration. • TNFR-1 and TNFR2 were expressed in retinal Müller cells. • MCM treatment obviously elevated proinflammatory factors mRNA levels and lowered CNTF mRNA levels in Müller cells. • Microglia-derived TNF-α acted on TNFR1 and TNFR2 on Müller cells (mainly TNFR1). • TNF-α/TNFR1 mediated Müller cell activation through the intracellular NF-κB signaling pathway.. [ABSTRACT FROM AUTHOR]

The complex interactions of contaminants with microplastics significantly affect ecological risk assessments. Studies of the sorption behavior of freely dissolved hydrophobic organic contaminants (HOCs) on microplastics are common. However, concentrations of HOCs in the actual aquatic environment sometimes exceed their water solubility. A possible explanation is that a microplastic-sol-water three-phase medium (TPM) is formed in the actual water environment. Both states HOCs (in solute and sol) have the potential to migrate to particles suspended in water. To confirm this view, four kinds of microplastics and eight halogenated polycyclic aromatic hydrocarbons (HPAHs) were selected to examine the partitioning of HPAHs between microplastics and water (sol and solute). Both monolayer and multilayer coverage of HPAHs onto microplastics occurred, and chemical sorption dominated the pseudo−sorption mechanism. The microplastic−water partition ratios of HPAHs (0.12–0.74) were approximately four to five orders of magnitude lower than their corresponding K OW values, suggesting that mechanisms other than sorption were involved. Apparently, the sol HPAHs contributed almost identically large increments to both microplastics and water, and closed the gap. For microplastic−supported HPAHs, the contribution of the sol fraction was more than triple that of the dissolved fraction; the key influencing factor was the water solubility of HPAHs. • A microplastic-sol-water three-phase medium is formed in oversaturated solutions. • The Freundlich model is suitable for describing this pseudo-sorption experiment. • Both monolayer and multilayer coverage of HPAHs onto microplastics occurred. • The microplastic-water partition ratios of HPAHs are about 1/100,000 of their KOWs. • Sol contributes over triple that of dissolved part to HPAHs AECP. [ABSTRACT FROM AUTHOR]

Abstract: Dimethoxymethane (DMM) is nontoxic and of high hydrogen content and may be used as a H2 storage material for small H2 sources. Steam reforming of DMM requires a bifunctional catalyst composed of an acidic component and a traditional copper catalyst, on which DMM is hydrolyzed on the acidic sites to methanol and formaldehyde, which are then further reformed to H2 and CO2 on metallic copper sites. In this work, samples of niobium phosphate with high surface areas were synthesized, characterized, and tested for the hydrolysis of DMM and used as acidic components for the reforming of DMM to produce H2. The structure and surface areas of these samples were characterized, and the activity for the hydrolysis of DMM was correlated with the surface acidities. It was found that all of the niobium phosphate samples exhibited high activity for the hydrolysis of DMM. The one with a high surface area (394 m2/g) was highly acidic with mainly Brønsted acid sites and thus was the most active for the hydrolysis of DMM among the niobium samples studied in this work. Mixing the niobium phosphate with CuZnO/Al2O3 did not affect the activity of CuZnO/Al2O3 for the reforming of methanol. The activity and selectivity to H2 were low for the steam reforming of DMM over traditional CuZnO/Al2O3 alone. Mechanically mixing niobium phosphate with CuZnO/Al2O3 greatly enhanced the conversion of DMM (e.g., 100% at 493 K) with high selectivity to H2. This indicates that niobium phosphate is an effective acidic component for the hydrolysis of DMM and can be used with CuZnO/Al2O3 for reforming DMM to produce H2. [Copyright &y& Elsevier]

Abstract: p21-activated kinase 1 (PAK1), a member of the evolutionarily conserved PAK family of serine/threonine kinases, is essential for a variety of cellular functions. Our previous studies showed that PAK1 participated in the apoptotic pathway mediated by p110C. To further investigate its functions, we used the yeast two-hybrid system to screen a human fetal brain cDNA library and identified dynein light chain 2 (DLC2)/myosin light chain (MLC) as an interacting partner of PAK1. The association of PAK1 with DLC2 was further confirmed by in vitro binding assay. With the stimulation of EGF, PAK1 interacted with HA-DLC2 in vivo and relocalized in cytoplasm near the perinuclear location in confocal microscope analysis. The deletion analysis showed that the interaction of DLC2 with PAK1 occurred within the residues 210–332 of PAK1. For that studies showed that DLC2 was a subunit of myosin complex, so it is possible that PAK1 binds to DLC2 and transports by myosin complex. [Copyright &y& Elsevier]

Magnetorheological (MR) materials show variations in their rheological properties when subjected to varying magnetic fields. They have quick time response, in the order of milliseconds, and thus are potentially applicable to structures and devices when a tunable system response is required. When incorporated into an adaptive structural system, they can yield higher variations in the dynamic response of the structure. This study presents a detailed analysis of dynamic characteristics of adaptive beam based on MR materials. The relationship between the magnetic field and the complex shear modulus of MR materials in the pre-yield regime is researched using oscillatory rheometry techniques. A structural dynamic modelling approach is discussed and vibration characteristics of MR adaptive structures are predicted for different magnetic field levels. In addition to the model predictions, actual MR adaptive beam is fabricated and tested. Both studies illustrate the vibration minimization capabilities of the MR adaptive beam at different magnetic field levels. [Copyright &y& Elsevier]

Streptococcus pneumoniae is a gram-positive bacterial pathogen causing invasive pneumonia, meningitis, otitis media, and bacteremia. Owing to the current pitfalls of polysaccharide and polysaccharide-conjugate vaccines, protein vaccines are considered promising candidates against pneumonia. Pneumococcal surface protein A (PspA) and pneumococcal surface adhesin A (PsaA) are virulence proteins showing good immunogenicity and protective effects against S. pneumoniae strains in mice. In this study, we expressed the fusion protein PsaA-PspA, which consists of PsaA and the N-terminal region of PspA family 1 and 2, in Escherichia coli. We describe a novel and effective method to purify PsaA-PspA using hydroxyapatite and two-step chromatography. After determining the optimal induction conditions and a series of purification steps, we obtained PsaA-PspA fusion protein with over 95% purity at a final yield of 22.44% from the starting cell lysate. The molecular weight of PsaA-PspA was approximately 83.6 kDa and its secondary structure was evaluated by circular dichroism. Immunization with the purified protein induced high levels of IgG antibodies in mice. Collectively, these results demonstrate that our purification method can effectively produce high-purity PsaA-PspA fusion protein with biological activity and chemical integrity, which can be widely applied to the purification of other PspA subclass proteins. • Protein vaccines are promising candidates against Streptococcus pneumoniae. • We constructed the fusion protein PspA-PsaA containing two virulence proteins. • We show a new purification method using hydroxyapatite and two-step chromatography. • With our novel method, we obtained PspA-PsaA fusion protein with 95.28% purity. • The purified PspA-PsaA fusion protein shows good immunogenicity in mice. [ABSTRACT FROM AUTHOR]

[Display omitted] Perovskite solar cells (PSCs) have become a promising photovoltaic (PV) technology. Meanwhile, developing an electron transport layer (ETL) has been an effective way to promote the power conversion efficiency (PCE) of PSCs. Here, a 4-morpholine ethane sulfonic acid sodium salt (MES Na+) doped SnO 2 ETL is utilized in planar heterojunction PSCs. The results show that the MES Na+ doped ETL can improve the crystallinity, and absorbance of perovskite films, and passivate interface defects between the perovskite film and SnO 2 ETL. The doping effect accounts for the enhancement of conductivity and the decreasing work function of SnO 2. When 10 mg mL−1 MES Na+ was added to the SnO 2 precursor solution, the device showed the best performance Jsc, Voc, and FF of the PSCs values, which were 23.88 mA cm−2, 1.12 V and 78.69%, respectively, and the PCE was increased from 17.43% to 21.05%. This doping ETL strategy provides an avenue for defect passivation to further increase the efficiency of perovskite solar cells. [ABSTRACT FROM AUTHOR]

To set up a rapid real-time nondestructive detection of moisture content, this paper reported the results of a combination of LF-NMR and BP-ANN to monitor the relationship between drying parameters and state of water under different microwave vacuum drying conditions. Three kinds of materials, carrot (fruit), banana (vegetable) and pleurotus eryngii (edible fungus), were tested in the experiment of applicability. The resulted showed that the information of A total and T 23 can be used to analyze the drying behavior and the information of A 20 , A 21 and A 22 can be used as the fingerprint characteristics of material discrimination. Three classic models (PLS, SVM and BP-ANN) were compared to study the prediction ability of moisture content with the inputs of A 20 , A 21 , A 22 , A 23 and A total. The performance of BP-ANN model was the best. Although the BP-ANN model of mixed species was not as good as the BP-ANN model of single fruit or vegetable, it still had excellent predictive performances with R2 0.9969 and RMSE 0.0184 to meet the needs of current industry and production. • A rapid real-time nondestructive detection method of combination of LF-NMR and BP-ANN was set up. • The information of A total and T 23 can be used to analyze the drying behavior. • The information of A 20 , A 21 and A 22 can be used as the fingerprint characteristics of material discrimination. • The BP-ANN model of mixed species had excellent predictive performances with R2 0.9969 and RMSE 0.0184. [ABSTRACT FROM AUTHOR]

LINC00525 is a new-researched long non-coding RNA (lncRNA) in a few cancers. This study aims at researching the function of LINC00525 in spinal chordoma and the underlying mechanism of action. LINC00525, microRNA-31–5p (miR-31–5p) and microRNA-125a-5p (miR-125a-5p) detection was performed by quantitative real-time polymerase chain reaction (qRT-PCR). We found the high expression of LINC00525 but the low levels of miR-31–5p and miR-125a-5p in spinal chordoma tissues. After LINC00525 was downregulated in spinal chordoma cells, there were inhibitory effects on cell proliferation, migration, invasion and EMT but a promoting effect on cell apoptosis. MiR-31–5p and miR-125a-5p were the downstream targets of LINC00525. The function of LINC00525 knockdown in spinal chordoma cells were achieved by upregulating miR-31–5p and miR-125a-5p. Tumorigenesis of spinal chordoma in vivo was also inhibited by knockdown of LINC00525 via the promotion of miR-31–5p and miR-125a-5p. All these results suggested that LINC00525 targeted miR-31–5p and miR-125a-5p to promote the tumorigenesis and progression of spinal chordoma. LINC00525 can be a novel molecular target in spinal chordoma. • LINC00525 knockdown inhibits cell proliferation and metastasis while enhances cell apoptosis in spinal chordoma cells. • LINC00525 targets miR-31–5p and miR-125a-5p. • LINC00525 contributes to tumor growth via negatively regulating miR-31–5p and miR-125a-5p in vivo. [ABSTRACT FROM AUTHOR]

ORR activity and selectivity on native oxide film-covered Ti were quantitatively studied by the reactive tip generation/substrate collection (RTG/SC) mode of scanning electrochemical microscopy (SECM) and further clarified by theoretical calculations. The ORR behavior on Ti is highly film characteristics-dependent. [Display omitted] • ORR activity and selectivity on spontaneous film-covered Ti were studied. • Effects of key factors were quantified by SECM and further clarified by theoretical calculations. • ORR is sensitive to film features, especially on the highly reduced Ti surface. • Hydrogen bonds and/or electrostatic effect improve 4e– selectivity while Cl– suppress reactivity. • This work provides theoretical support and possible guidance for ORR on oxide-covered metals. Unlike noble metals, the oxygen reduction reaction (ORR) behavior on Ti is more complicated due to its spontaneously formed oxide film. This film results in sluggish ORR kinetics and tends to be reduced within ORR potential region, causing the weak and multi-reaction coupled current. Though Ti is being used in chemical and biological fields, its ORR research is still underexplored. We innovatively employed the modified reactive tip generation-substrate collection (RTG/SC) mode of scanning electrochemical microscopy (SECM) with high efficiency of 97.2 % to quantitatively study the effects of film characteristics, solution environment (pH, anion, dissolved oxygen), and applied potential on the ORR activity and selectivity of Ti. Then, density functional theory (DFT) and molecular dynamics (MD) analyses were employed to elucidate its ORR behavior. On highly reduced Ti, film properties dominate ORR behavior with promoted 4e– selectivity. Rapid film regeneration in alkaline/O 2 -saturated conditions inhibits ORR activity. Besides, ORR is sensitive to anion species in neutral solutions while showing enhanced 4e– reduction in alkaline media. All the improved 4e– selectivities originate from the hydrogen bond/electrostatic stabilization effect, while the decayed ORR activity by Cl– arises from the suppressed O 2 adsorption. This work provides theoretical support and possible guidance for ORR research on oxide-covered metals. [ABSTRACT FROM AUTHOR]

Streptococcus pneumoniae is a major pathogen that causes life-threatening diseases, such as pneumonia, otitis media, bacteremia, and meningitis, worldwide and especially in young children and the elderly. Pneumococcal surface protein A (PspA) is a widely studied candidate protein vaccine that represents a promising replacement for current polysaccharide and polysaccharide-conjugate vaccines. In this study, we describe a simple method to produce PspA of clade 4 from an Escherichia coli expression system using hydroxylapatite and ion-exchange chromatography. Using this method, we successfully expressed soluble PspA4 in 10 L of autoinducing culture medium, with a wet-cell yield of 19 g/L and a final PspA4 concentration of 22.8 mg/L. Additionally, we improved PspA4 purity from 17% to 70% in a single step through the use of hydroxylapatite, resulting in acquisition of recombinant PspA4 (>95% purity) at a final yield of 43% from the starting cell-lysis solution. We subsequently verified the secondary structure molecular weight of recombinant PspA4 by circular dichroism and mass spectrometry, respectively. These results demonstrated a highly efficient method for mass producing PspA4 protein and that can also be applied for purification of PspA proteins from other clades. [ABSTRACT FROM AUTHOR]

Psoriasis is a chronic inflammatory disease characterized by increased keratinocyte proliferation and local inflammation. Long noncoding RNAs (lncRNAs) play important regulatory roles in many immune-mediated diseases, including psoriasis. In this study, we aimed to investigate the role and mechanism of lnc-SPRR2G-2 (SPRR2G) in M5-treated psoriatic keratinocytes. Fluorescence in situ hybridization and quantitative real-time polymerase chain reaction (qRT-PCR) showed that lnc-SPRR2G-2 was significantly upregulated in psoriasis tissues and psoriatic keratinocytes. In psoriatic keratinocytes, functional and molecular experiment analyses demonstrated that SPRR2G regulated proliferation, cell cycle and apoptosis, and induced the expression of S100 calcium binding protein A7 (S100A7), interleukin (IL)-1β, IL-8 and C-X-C motif chemokine ligand 10 (CXCL10). The function of SPRR2G in psoriasis is related to the STAT3 signaling pathway and can be inhibited by a STAT3 inhibitor. Moreover, KH-type splicing regulatory protein (KHSRP) was proved to be regulated by lnc-SPRR2G-2 and to control the mRNA decay of psoriasis-related cytokines (p < 0.05). In summary, we reported the functions of lnc-SPRR2G-2 and KHSRP in psoriasis. Our findings provide new insights for the further exploration of the pathogenesis and treatment of psoriasis. • lnc-SPRR2G-2 was highly expressed in psoriasis. • lnc-SPRR2G-2 promoted proliferation and inflammation of psoriatic keratinocytes. • lnc-SPRR2G-2 activated the STAT3 pathway. • lnc-SPRR2G-2 regulated KHSRP to stabilize cytokines mRNA. [ABSTRACT FROM AUTHOR]

[Display omitted] Based on their characteristics, transition metal layered double hydroxides have been of great scientific interest for their use in supercapacitors. Up until now, severe aggregation and low intrinsic conductivity have been the major hurdles for their application. In this work, nickel–iron sulfide nanosheets (NiFeSx) and carbon nanotubes (CNTs) were synthesized on diatomite using chemical vapor deposition and a two-step hydrothermal method to overcome these challenges. Synthesis of this composite successfully exploits the synergistic effect of multicomponent materials to improve the electrochemical performance. Diatomite is selected as a substrate to provide preferable surroundings for the uniform dispersion of nanomaterial on its surface, which enlarges the active sites that come in contact with the electrolytes, significantly improving the electrochemical properties. Combined with high conductivity and a synchronous sulfurization effect, the NiFeSx@CNTs@MnS@Diatomite electrode delivered a high specific capacitance of 552F g−1 at a current density of 1 A g−1, a good rate capability of 68.4% retention at 10 A g−1, and superior cycling stability of 89.8% capacitance retention after 5000 cycles at 5 A g−1. Furthermore, an asymmetric supercapacitor assembled via NiFeSx@CNTs@MnS@Diatomite and graphene delivered a maximum energy density of 28.9 Wh kg−1 and a maximum power density of 9375 W kg−1 at a potential of 1.5 V. This research lays the groundwork for ideal material preparation as well as a rational design for the electrode material, including property enhancement of diatomite-based material for use in supercapacitors. [ABSTRACT FROM AUTHOR]

Abstract: Survivin is a member of inhibitors of apoptosis proteins (IAPs), and also belongs to be a member of the chromosomal passenger complex (CPC) which has multiple functions including inhibition of apoptosis and regulation of cell division and SAC activity. Plk1 (polo-like kinase 1) associates with the spindle poles and also distributes to the kinetochores and is shown to involve in spindle organization, APC/C activation and cytokinesis in many models. Our recent work has shown that Survivin is a critical regulator of chromosome segregation and spindle assembly checkpoint (SAC) in meiosis. In the present study, we found that Plk1 co-localized with Survivin at metaphase I (MI) and telophase I (TI) stage after GVBD. Plk1 dispersed into the oocyte cytoplasm or accumulated near the chromosomes after the depletion of Survivin by morpholino (MO) injection. Our results showed that the localization of Plk1 to kinetochores required the involvement of Survivin. [Copyright &y& Elsevier]

During follicle growth, DNA methylation is gradually established, which is important for oocyte developmental competence. Due to the facts that oocytes from prepubertal individuals show reduced developmental outcomes when compared to those from sexually mature individuals, and the fact that oocytes derived from in vitro follicle culture have much lower developmental competence, it is worth exploring whether prepubertal superovulation and in vitro follicle culture will cause changes in DNA methylation imprinting status in oocytes. In this study, we found that the CpG island in maternally imprinted GNAS clusters was hypermethylated in the MII-stage oocytes from sexually mature mice, but was hypomethylated in oocytes from prepuberty individuals. The GNAS clusters in the MII-stage oocytes obtained by in vitro follicle culture showed heterogeneous methylation levels, indicating different qualities of oocytes, however, three other maternally imprinted genes, Peg1 , Lot1 and Impact , were all hypermethylated in the MII-stage oocytes derived from both prepubertal superovulation and in vitro follicle culture. Taken together, the findings suggest that the methylation status in GNAS clusters may potentially represent a novel epigenetic marker for oocyte quality detection. • The methylation of CpG island of GNAS clusters in MII-stage oocytes is established in an age-dependent manner. • The methylation levels in GNAS clusters obtained by in vitro follicle culture fluctuated, showing different qualities of oocytes. • The methylation of GNAS clusters may potentially represent a novel epigenetic marker for oocyte quality detection. [ABSTRACT FROM AUTHOR]

Oocyte meiotic maturation failure and unfaithful chromosome segregation are major causes for female infertility. Here, we showed that CENP-W, a relatively novel member of the kinetochore protein family, was expressed in mouse oocytes from the germinal vesicle (GV) to metaphase II (MII) stages. Confocal microscopy revealed that CENP-W was localized in the germinal vesicle in the GV stage, and then became concentrated on kinetochores during oocyte maturation. Knockdown of CENP-W by specific siRNA injection in vitro caused kinetochore-microtubule detachment, resulting in severely defective spindles and misaligned chromosomes, leading to metaphase I arrest and failure of first polar body (PB1) extrusion. Correspondingly, spindle assembly checkpoint (SAC) activation was observed in CENP-W knockdown oocytes even after 10h of culture. Our results suggest that CENP-W acts as a kinetochore protein, which takes part in kinetochore-microtubule attachment, thus mediating the progression of oocyte meiotic maturation. • CENP-W directs chromosome segregation. • CENP-W regulates meiotic cell cycle. • CENP-W mediates kinetochore-microtubules attachment. [ABSTRACT FROM AUTHOR]

Before fertilization, ovulated mammalian oocytes are arrested at the metaphase of second meiosis (MII), which is maintained by the so-called cytostatic factor (CSF). It is well known that the continuous synthesis and accumulation of cyclin B is critical for maintaining the CSF-mediated MII arrest. Recent studies by us and others have shown that Ccnb3 is required for the metaphase-to-anaphase transition during the first meiosis of mouse oocytes, but whether Ccnb3 plays a role in MII arrest and exit remains unknown. Here, we showed that the protein level of Ccnb3 gradually decreased during oocyte meiotic maturation, and exogenous expression of Ccnb3 led to release of MII arrest, degradation of securin, separation of sister chromatids, extrusion of the second polar body (PB2), and finally entry into interphase. These phenotypes could be rescued by inhibition of Wee1B or CDK2. Our results indicate that Ccnb3 plays a critical regulatory role in MII arrest and exit in mouse oocytes. • Ccnb3 protein levels gradually decreased during mouse oocyte meiotic maturation. • Exogenous expression of Ccnb3 leads to MII exit in mouse oocyte. • MII arrest disruption is associated with complete APC/C activation in oocytes with exogenously expressed Ccnb3. • Wee1B inhibitor and CDK2 inhibitor can antagonize the effects of exogenously expressed Ccnb3 on MII exit in mouse oocytes. • Our results indicate that Ccnb3 plays a critical regulatory role in MII arrest and exit in mouse oocytes. [ABSTRACT FROM AUTHOR]

Activation of P2X 7 R is linked to the occurrence and development of glaucoma. The present study concentrated on the activated P2X 7 R-NLRP3 pathway underlying the retinal microglia in retinal ganglion cells (RGCs) in chronic ocular hypertension (COH). Mouse COH model was set up to investigate the changes of P2X 7 R-NLRP3 inflammatory pathway in vivo. Primary microglia cells and primary RGCs were cultured and purified in vitro experiments. The expression of P2X 7 R, NLRP3, CASP-1, and ASC was detected and analyzed using Western blot, Quantitative polymerase chain reaction (qPCR) and immunofluorescence. Hoechst stains labeled nucleus to count microglia cells after experimental treatment. RGCs survival rate was examined utilizing LIVE/DEAD viability kit. The level of cytokines was measured by qPCR and enzyme-linked immunosorbent assay (ELISA). Consequently, the expression of P2X 7 R, NLRP3, CASP-1, and ASC was raised in COH mice retina. The number of microglia cells was increased after addition of BzATP, the agonist of P2X 7 R, to the culture medium of primary rat microglia cells. However, survival rates of RGCs decreased after addition of conditioned media to the RGC cultures. A438079 (100 μM), the inhibitor of P2X 7 R, and Mcc950 (1 μM), the inhibitor of NLRP3, blocked the effect of P2X 7 R activation in rat retinal microglia cells. Both inhibitors attenuated RGC death with the treatment of retina microglia cell conditioned medium (MCM). The production of some pro-inflammatory cytokines, such as TNF-α, CXCL-1, CSF-1, IL-6, IL-1β, and IL-18 was increased markedly with the activation of P2X 7 R in microglia. However, the effect suffered as a result of A438079 and partially inhibited by Mcc950. These data suggested a role of P2X 7 R -NLRP3 pathway in activated retinal microglia cell-mediated RGC damages in COH. • P2X 7 R-NLRP3 pathway is activated during chronic ocular hypertension (COH) process. • P2X 7 R-NLRP3 pathway activation triggers retinal microglia cells proliferation. • Retinal microglia cells mediates cytokine production through P2X 7 R-NLRP3 pathway. [ABSTRACT FROM AUTHOR]

Mitochondrial DNA (mtDNA) is important for oxidative phosphorylation; dysfunctions can play a role in many mitochondrial diseases and can also affect the aging of cells and individuals. DNA methylation is an important epigenetic modification that plays a critical role in regulating gene expression. While recent studies have revealed the existence of mtDNA methylation there are still controversies about mtDNA methylation due to the special structure of mtDNA. Mitochondria and DNA methylation are both essential for regulating oocyte maturation and early embryo development, but whether mtDNA methylation changes during this process is unknown. By employing bisulfite sequencing, we found that in the process of mouse oocyte maturation, postovulatory oocyte aging, and early embryo development, all analyzed mitochondrial genes, including 16S-CpGI , DCR , ND6 , 12S , and ATP8, lacked 5'mC. Thus, mtDNA methylation does not occur in the oocyte and early embryo. [ABSTRACT FROM AUTHOR]

Hypoxic-ischemic encephalopathy (HIE) is an important factor leading to permanent damage of central nervous system (CNS) and even neonatal death. Long non-coding RNAs (lncRNAs) has been shown to get involved in the pathogenesis of nervous system diseases. LINC00938 is an intergenic lncRNA which is reported to be involved in neurodegenerative disease. However, the potential role of LINC00938 in nerve injury of neonatal HIE is undetermined. Here, we found that the expression of LINC00938 in the whole blood of neonates with HIE was downregulated compared with the non-HIE group. Functional study revealed that the expression of LINC00938 was significantly decreased in oxygen-glucose deprivation (OGD)-induced SH-SY5Y. Knockdown of LINC00938 induced the neural cell apoptosis by increased the protein level of Bax, Cleaved-Caspase3 and decreased the expression of Bcl-2. In addition, overexpression of LINC00938 prevented the apoptosis of SH-SY5Y from OGD injury. RNA-seq analysis showed that MAPK signaling was involved in the anti-apoptosis function of LINC00938. LINC00938 knockdown induced the activation of c-Jun-N-terminal kinase (JNK), p38 mitogen-activated protein kinase, and inhibited the activation of ERK signaling. However, LINC00938 play neuroprotective role in OGD-induced SH-SY5Y by suppression the phosphorylation of JNK and p38 MAPK rather than regulation of ERK signaling pathway. Further analyses illustrated that the cell apoptosis of neuronal cell was dependent on the elevation of reactive oxygen species (ROS) and result in mitochondria dysfunction in LINC00938 knockdown SH-SY5Y. Pretreated with ROS inhibitor N -acetylcysteine amide (NACA) dramatically suppressed LINC00938 knockdown induced oxidative stress and mitochondria dysfunction which induced cell apoptosis. In addition, NACA treatment significantly reduced the expression of p-JNK and p-p38 in OGD-induced SH-SY5Y. Furthermore, overexpression of LINC00938 displayed a notably neuroprotective effect by suppress central nervous system cell apoptosis via alleviating oxidative stress in CoCl 2 -induced hypoxic HIE model of zebrafish. Taken together, these results suggested that LINC00938 can act as a neuroprotective factor to inhibit oxidative stress and apoptosis of CNS under HIE conditions. [Display omitted] • LINC00938 is highly expressed in neuronal cell and involved in the pathophysiology of HIE. • LINC00938, as a long noncoding RNA, participate in the neuronal survival both in vitro and in vivo. • LINC00938 plays an important role in the OGD induced neuronal cell survival through regulating cellular oxidative stress and MAPK signaling. [ABSTRACT FROM AUTHOR]

We investigate the dynamics of bright–bright solitons in one-dimensional two-component Bose–Einstein condensates with Raman-induced spin–orbit coupling, via the variational approximation and the numerical simulation of Gross–Pitaevskii equations. For the uniform system without trapping potential, we obtain two population balanced stationary solitons. By performing the linear stability analysis, we find a Goldstone eigenmode and an oscillation eigenmode around these stationary solitons. Moreover, we derive a general dynamical solution to describe the center-of-mass motion and spin evolution of the solitons under the action of spin–orbit coupling. The effects of a harmonic trap have also been discussed. [ABSTRACT FROM AUTHOR]

Competitive endogenous RNAs (ceRNAs) regulate RNA transcripts by competing for shared miRNAs and play critical roles in disease development. Psoriasis is a long-lasting, recurring chronic inflammatory skin disease characterized by hyperproliferation of keratinocytes. The keratinocyte response is triggered by the activation of inflammatory cytokines, like interleukin-22 (IL-22). We used lncRNA array analysis to detect differentially expressed lncRNAs in skin (HaCaT) cells treated with or without IL-22. We used hematoxylin and eosin (H&E) staining to determine the pathological changes in skin cells and immunohistochemistry to evaluate the expression of S100A7. We used qRT-PCR and Western blotting to detect the expression levels of MSX2P1 and S100A7. We down-regulated the expression of MSX2P1 by infecting with lentiviral-vector shRNA. We measured cell proliferation, cell cycle status, and apoptosis by the CCK-8 assay, flow cytometry, and Annexin Ⅴ-FITC/PI staining, respectively. In addition, we used the luciferase reporter gene assay to determine the relationships between MSX2P1 or miR-6731-5p and S100A7, respectively. LncRNA array analysis revealed that 103 lncRNAs were up-regulated and 51 were down-regulated. Furthermore, qRT-PCR showed that the mRNAs levels of MSX2P1 was significantly altered in HaCaT cells treated with IL-22, compared with control cells; and MSX2P1 was mainly in the cytoplasm. Based on the IL-22-stimulated lncRNA-associated ceRNA network, we selected MSX2P1-miR-6731-5p-S100A7 for further study. H&E staining exhibited characteristic features specific to psoriatic lesions. Immunohistochemistry demonstrated significantly increased expression levels of S100A7 in psoriatic lesions, compared with normal skin tissue. We observed a positive correlation between lncRNA-MSX2P1 expression and S100A7 expression. In addition, miR-6731-5p suppressed proliferation, accelerated apoptosis in IL-22-stimulated keratinocytes, and decreased the expressions of S100A7, IL-12β, IL-23, HLA-C, CCHCR1, TNF-α, and NF-κB proteins. Our data demonstrated that MSX2P1 facilitate the progression and growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7. We speculate that the biological network of MSX2P1-miR-6731-5p-S100A7 is a potential novel therapeutic target for the future treatment of psoriasis. [ABSTRACT FROM AUTHOR]

As a member of Ubiquitin-specific protease subfamily, ubiquitin specific protease 7 (USP7) has been reported to participate in a variety of cellular processes, including cell cycle, apoptosis, DNA damage response, and epigenetic modification. However, its function in preimplantation embryos is still obscure. To investigate the functions of USP7 during preimplantation embryo development, we used siRNA to degrade endogenous USP7 messenger RNA. We found that USP7 knockdown significantly decreased the development rate of mouse early embryos. Moreover, depletion of USP7 induced the accumulation of the DNA lesions and apoptotic blastomeres in early embryos. In addition, USP7 knockdown caused an abnormal H3K27me3 modification in 2-cell embryos. Overall, our results indicate that USP7 maintains genome stability perhaps via regulating H3K27me3 and DNA damage, consequently controlling the embryo quality. • Depletion of USP7 compromises the early embryo development. • USP7 knockdown increases DNA damage and apoptosis in mouse early embryos. • USP7 knockdown causes an abnormal H3K27me3 modification in mouse early embryos. [ABSTRACT FROM AUTHOR]

Several studies have implicated estrogen and the estrogen receptor (ER) in the pathogenesis of benign prostatic hyperplasia (BPH); however, the mechanism underlying this effect remains elusive. In the present study, we demonstrated that estrogen (17β-estradiol, or E2)-induced activation of the G protein-coupled receptor 30 (GPR30) triggered Ca 2+ release from the endoplasmic reticulum, increased the mitochondrial Ca 2+ concentration, and thus induced prostate epithelial cell (PEC) apoptosis. Both E2 and the GPR30-specific agonist G1 induced a transient intracellular Ca 2+ release in PECs via the phospholipase C (PLC)-inositol 1, 4, 5-triphosphate (IP 3 ) pathway, and this was abolished by treatment with the GPR30 antagonist G15. The release of cytochrome c and activation of caspase-3 in response to GPR30 activation were observed. Data generated from the analysis of animal models and human clinical samples indicate that treatment with the GPR30 agonist relieves testosterone propionate (TP)-induced prostatic epithelial hyperplasia, and that the abundance of GPR30 is negatively associated with prostate volume. On the basis of these results, we propose a novel regulatory mechanism whereby estrogen induces the apoptosis of PECs via GPR30 activation. Inhibition of this activation is predicted to lead to abnormal PEC accumulation, and to thereby contribute to BPH pathogenesis. [ABSTRACT FROM AUTHOR]

As crucial signaling transducer in Toll-like receptor (TLR) and interleukin (IL)-1 receptor (IL-1R) signaling pathway, IL-1R-associated kinase 4 (IRAK4) mediates downstream signaling cascades and plays important roles in innate and adaptive immune responses. In the present study, an IRAK4 orthologue was characterized from large yellow croaker ( Larimichthys crocea ), named Lc -IRAK4, with a conservative N -terminal death domain and a C -terminal protein kinase domain. The genome of Lc -IRAK4 is structured into eleven exons and ten introns. Expression analysis indicated that Lc -IRAK4 was widely expressed in tested tissues, with the highest level in liver and weakest in muscle. Additionally, in the spleen, liver tissues and blood, it could be induced by poly I:C and LPS stimulation, but not be induced by Vibrio parahemolyticus infection. Fluorescence microscopy assays revealed that Lc -IRAK4 localized in the cytoplasm in HEK 293T cells. It was also determined that Lc -IRAK4 could interact with MyD88, whereas MyD88-mediated NF-κB activation was significantly impaired when co-transfected the two in HEK 293T cells. These findings collectively indicated that although Lc -IRAK4 was evolutionarily conserved in vertebrates, the exact function especially the signaling transduction mediated by IRAK4 in fish immune response was different from that in mammals, which impaired MyD88-mediated NF-κB activation. [ABSTRACT FROM AUTHOR]

Gastric cancer is the most common digestive malignant tumor worldwide and the underlying mechanisms are not fully understood. The E3 ligase UBR5 (also known as EDD1) is essentially involved in diverse types of cancer. Here we aimed to study the functions of UBR5 in human gastric cancer. We first analyzed the mRNA and protein levels of UBR5 in human gastric cancer tissues and the results showed that UBR5 was markedly increased in gastric cancer tissues compared with normal gastric mucosa or matched non-cancer gastric tissues. The relationship between UBR5 and survival of gastric cancer patients was analyzed and we found that high UBR5 expression was associated with poor overall and disease-free survival. We further tried to investigate the effects of UBR5 on gastric cancer cell growth in vitro and in vivo . Therefore, we knocked down UBR5 with lentivirus-mediated shRNA and found that UBR5 knockdown repressed in vitro proliferation and colony formation of gastric cancer cells AGS, MG803 and MNK1. In vivo xenograft experiment also demonstrated that UBR5 knockdown inhibited AGS growth. Finally, we explored the mechanism by which UBR5 contributed to the growth of gastric cancer cells. We found that UBR5 bound the tumor suppressor gastrokine 1 (GKN1) and increased its ubiquitination to reduce the protein stability of GKN1. GKN1 knockdown with lentivirus-mediated shRNA increased the in vitro colony formation and in vivo growth of AGS cells, and UBR5 knockdown was unable to affect the colony formation and in vivo growth of AGS cells when GKN1 was knocked down, indicating that GKN1 contributed to the effects of UBR5 in human gastric cancer cells. Taken together, UBR5 plays an essential role in gastric cancer and may be a potential diagnosis and treatment target for gastric cancer. [ABSTRACT FROM AUTHOR]

Nek11 , a member of the never in mitosis gene A (NIMA) family, is activated in somatic cells associated with G1/S or G2/M arrest. However, its function in meiosis is unknown. In this research, the expression, localization and functions of NEK11 in the mouse oocyte meiotic maturation were examined. Western blotting indicated that NEK11S was the major NEK11 protein in mouse oocyte. MYC-tagged Nek11 mRNA microinjection and immunofluorescent staining showed that NEK11 was localized to the meiotic spindles at MI and MII stage. Knockdown of Nek11 by microinjection of siRNA did not affect germinal vesicle breakdown (GVBD) and the first polar body extrusion, but caused formation of 2-cell-like eggs. These results demonstrate that Nek11 regulates asymmetric cell division during oocyte meiotic maturation. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) are considered to be critical for regenerative medicine. However, long-term culturing of MSCs will induce aging of MSCs, and thereafter impair cellular function. Changes in proteomics have been reported to be involved in cell aging, and therefore investigations on cell aging of MSCs at levels of proteomics and post-translational protein modifications (PTM) are ultimately important. In the present study, human umbilical cord mesenchymal stem cells (hUMSCs) were exposed to different culture conditions for either 7 or 30 days. Proteins changes during cell culture were investigated using tandem mass tag (TMT) labeling quantitative approach, and N- glycosylation patterns were analyzed using multistage mass spectrometry. We identified 66 proteins (fold change >1.50) that were differentially expressed in long-term culture. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that aging exerts a side effect on hUMSCs by affecting various molecular functions and biological processes, such as lysosome, autophagy and post-translational protein modification. Glycosylation analysis indicates that cell N- glycan patterns are associated with aging of MSCs. Our results presented here should contribute to future studies on cell aging and cellular quality controls related to MSCs as regenerative medicine. [Display omitted] • Changes in proteomics and post-translational modifications were related to hUMSCs aging. • Proteins (fold change >1.50 and P < 0.05) were differentially expressed in long term culture hUMSCs. • These DEPS were mainly involved in lysosome organization and PTM. • Cell N-glycan patterns were associated with hUMSCs aging. [ABSTRACT FROM AUTHOR]

Tumor cell invasion and proliferation remain the overwhelming causes of death for malignant glioma patients. To establish effective therapeutic methods, new targets implied in these processes have to be identified. Tetraspanin 8 (Tspn8) forms complexes with a large variety of trans-membrane and/or cytosolic proteins to regulate several important cellular functions. In the current study, we found that Tspn8 was over-expressed in multiple clinical malignant glioma tissues, and its expression level correlated with the grade of tumors. Tspn8 expression in malignant glioma cells (U251MG and U87MG lines) is important for cell proliferation and migration. siRNA-mediated knockdown of Tspn8 markedly reduced in vitro proliferation and migration of U251MG and U87MG cells. Meanwhile, Tspn8 silencing also increased the sensitivity of temozolomide (TMZ), and significantly increased U251MG or U87MG cell death and apoptosis by TMZ were achieved with Tspn8 knockdown. We observed that Tspn8 formed a complex with activated focal adhesion kinase (FAK) in both human malignant glioma tissues and in above glioma cells. This complexation appeared required for FAK activation, since Tspn8 knockdown inhibited FAK activation in U251MG and U87MG cells. These results provide evidence that Tspn8 contributes to the pathogenesis of glioblastoma probably by promoting proliferation, migration and TMZ-resistance of glioma cells. Therefore, targeting Tspn8 may provide a potential therapeutic intervention for malignant glioma. [ABSTRACT FROM AUTHOR]

Microtubule plus-end tracking proteins (+TIPs) associate with growing microtubule plus ends and control microtubule dynamics and interactions with different cellular structures during cell division, cell migration and morphogenesis. Microtubule-associated RP/EB family member 2 (MAPRE2/EB2) is a highly conserved core component of +TIPs networks, but whether this molecule is required for mammalian meiotic progression is unknown. In this study, we investigated the expression and function of MAPRE2 during oocyte maturation. Our results showed that MAPRE2 was consistently expressed from germinal vesicle (GV) to metaphase II (MII) stages and that MAPRE2 was distributed in the cytoplasm of oocytes at GV stage and along the spindle at metaphase I (MI) and MII stages. Small interfering RNA-mediated knockdown of Mapre2 severely impaired microtubule stability, kinetochore-microtubule attachment, and chromosome alignment and subsequently caused spindle assembly checkpoint (SAC) activation and cyclin B1 nondegradation, leading to failure of chromosome segregation and first polar body extrusion. This study demonstrates for the first time that MAPRE2 plays an important role during mouse oocyte meiosis. [ABSTRACT FROM AUTHOR]

Abstract: Background: Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI. Hence, we designed the current study to explore the intestinal expression pattern of CD40 after TBI in rats. We hypothesized that CD40 could mediate inflammation and ultimately contribute to acute intestinal mucosal injury after TBI. Methods: We randomly divided rats into control and TBI groups at 3, 6, 12, 24, and 72 h, respectively. We assessed the expression of CD40 by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical study, and detected the levels of tumor necrosis factor-α (TNF-α), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by enzyme-linked immunosorbent assay. Results: The mRNA and protein levels of -CD40 increased by 3 and 6 h, peaked at 6 and 12 h, and remained elevated until 24 and 72 h post-injury, respectively. Levels of TNF-α, VCAM-1, and ICAM-1 also markedly increased in jejunum tissue after TBI. Interestingly, there was a positive relationship between the expression of CD40 and that of TNF-α, VCAM-1, and ICAM-1. Conclusions: CD40 could be markedly elevated in intestine after TBI in rats, and it might have an important role in the pathogenesis of acute intestinal mucosal injury mediated by inflammatory response. [Copyright &y& Elsevier]

Highlights: [•] Gambogic acid induces growth inhibition and apoptosis in cultured U87 glioma cells. [•] Gambogic acid inhibits Akt/mTORC1 signaling in cultured U87 glioma cells. [•] LRIG1 induction by gambogic acid promotes EGFR degradation. [•] AMPK activation mediates gambogic acid-induced LRIG1 upregulation and cytotoxicity. [ABSTRACT FROM AUTHOR]

Abstract: Prolonged residence of postovulatory oocyte in the oviduct or prolonged culture in vitro can lead to oocyte aging, which significantly affects pre- and post-implantation embryo development. In this study, we employed bisulfite sequencing and COBRA methods to investigate the DNA methylation status of differentially methylated regions (DMRs) of Snrpn and Peg1/Mest, two maternally imprinted genes, in postovulatory oocytes aged in vivo and in vitro. The results showed that Snrpn DMR was clearly demethylated in oocytes aged in vivo at 29h post-hCG and in denuded oocytes aged in vitro for the same time period. However, Peg1/Mest did not show any demethylation in all aged groups at 29h post-hCG. These data indicate that oocytes undergo time-dependent demethylation of Snrpn DMR during the process of postovulatory aging. [Copyright &y& Elsevier]

Abstract: Epigenetic modifications are closely associated with embryo developmental potential. One of the epigenetic modifications thought to be involved in genomic imprinting is DNA methylation. Here we show that the maternally imprinted genes Snrpn and Peg1/Mest were nearly unmethylated or heavily methylated, respectively, in their differentially methylated regions (DMRs) at the two-cell stage in parthenogenetic embryos. However, both genes were gradually de novo methylated, with almost complete methylation of all CpG sites by the morula stage in parthenogenetic embryos. Unexpectedly, another maternally imprinted gene, Peg3, showed distinct dynamics of methylation during preimplantation development of diploid parthenogenetic embryos. Peg3 showed seemingly normal methylation patterns at the two-cell and morula stages, but was also strongly de novo methylated in parthenogenetic blastocysts. In contrast, the paternally imprinted genes H19 and Rasgrf1 showed complete unmethylation of their DMRs at the morula stage in parthenogenetic embryos. These results indicate that diploid parthenogenetic embryos adopt a maternal-type methylation pattern on both sets of maternal chromosomes and that the aberrantly homogeneous status of methylation imprints may partially account for developmental failure. [Copyright &y& Elsevier]

Abstract: Polar body formation in oocytes is an extreme form of asymmetric cell division, but what regulates the asymmetric spindle positioning and cytokinesis is poorly understood. During mouse oocyte maturation, the metaphase I spindle forms at the center but then moves to the cortex prior to anaphase I and first polar body emission. We show here that treating denuded mouse oocytes with brefeldin A, an inhibitor of Golgi-based membrane fusion, abolished the asymmetric positioning of the metaphase I spindle and resulted in the formation of two half-size metaphase II eggs, instead of a full-sized egg and a polar body. The normal metaphase II spindle is similarly asymmetrically positioned in the mature egg, where the spindle lies with its axis parallel to the cortex but becomes perpendicular before anaphase II and emission of the second polar body. When ovulated eggs were activated with strontium in the presence of brefeldin A, the metaphase II spindle failed to assume perpendicular position, and the chromosomes separated without the extrusion of the second polar body. Remarkably, symmetric cytokinesis began following a 3 h delay, forming two half-size eggs each containing a pronucleus. BFA-sensitive intracellular vesicular transport is therefore required for spindle positioning in both MI and MII. [Copyright &y& Elsevier]

Abstract: Transportation of copper (II) ions from aqueous solutions to a fly ash and bentonite complex amorphous heterogeneous oxides (AHO: CaO–SiO2–Al2O3–MgO–FeO) system was studied. The particles of the fly ash and bentonite complex AHO system were highly porous and composed of platelike grains. They provide the physical basis for establishing a liquid–solid reaction model applicable to mesoporous solids. The main innovation of this model was in simplifying the powder granules to aggregates of close particles, while the particles act in accordance with the model better. The calculated curves from the models were well in line with the experimental results. [Copyright &y& Elsevier]

Abstract: Histone modifications are thought to play important roles in various cellular functions. In this article, the distribution patterns of acetylation on histone H4, methylation on histone H3 lysine 9, and phosphorylation on histone H3 serine 10 were examined in in vivo and in vitro fertilization (IVF) preimplantation mouse embryos by using indirect immunofluorescence and scanning confocal microscopy. We desired to know whether the IVF, which has been widely used as a routine assisted reproductive technology in animal and human, was safe at the epigenetic level. As results, we found that there was no difference in these histone modification patterns in in vivo and IVF mouse embryos from zygote to blastocyst stage. Moreover, these histone modifications had different distributions at all examined stages, but they were consistent with the mouse embryo developmental stages. [Copyright &y& Elsevier]

Abstract: Centrosomes, the main microtubule-organizing centers (MTOCs) in most animal cells, are important for many cellular activities such as assembly of the mitotic spindle, establishment of cell polarity, and cell movement. In nuclear transfer (NT), MTOCs that are located at the poles of the meiotic spindle are removed from the recipient oocyte, while the centrosome of the donor cell is introduced. We used mouse MII oocytes as recipients, mouse fibroblasts, rat fibroblasts, or pig granulosa cells as donor cells to construct intraspecies and interspecies nuclear transfer embryos in order to observe centrosome dynamics and functions. Three antibodies against centrin, γ-tubulin, and NuMA, respectively, were used to stain the centrosome. Centrin was not detected either at the poles of transient spindles or at the poles of first mitotic spindles. γ-tubulin translocated into the two poles of the transient spindles, while no accumulated γ-tubulin aggregates were detected in the area adjacent to the two pseudo-pronuclei. At first mitotic metaphase, γ-tubulin was translocated to the spindle poles. The distribution of γ-tubulin was similar in mouse intraspecies and rat–mouse interspecies embryos. The NuMA antibody that we used can recognize porcine but not murine NuMA protein, so it was used to trace the NuMA protein of donor cell in reconstructed embryos. In the pig–mouse interspecies reconstructed embryos, NuMA concentrated between the disarrayed chromosomes soon after activation and translocated to the transient spindle poles. NuMA then immigrated into pseudo-pronuclei. After pseudo-pronuclear envelope breakdown, NuMA was located between the chromosomes and then translocated to the spindle poles of first mitotic metaphase. γ-tubulin antibody microinjection resulted in spindle disorganization and retardation of the first cell division. NuMA antibody microinjection also resulted in spindle disorganization. Our findings indicate that (1) the donor cell centrosome, defined as pericentriolar material surrounding a pair of centrioles, is degraded in the 1-cell reconstituted embryos after activation; (2) components of donor cell centrosomes contribute to the formation of the transient spindle and normal functional mitotic spindle, although the contribution of centrosomal material stored in the recipient ooplasm is not excluded; and (3) components of donor cell centrosomes involved in spindle assembly may not be species-specific. [Copyright &y& Elsevier]

Abstract: Although communications between mammalian oocytes and their surrounding granulosa cells mediated by the Kit–Kit ligand (KL, or stem cell factor, SCF) system have been proven to be crucial for follicular development, Kit downstream signaling pathways in mammalian oocytes are largely unknown. In this study, by using ovaries and isolated oocytes from postnatal mice and rats, we demonstrated for the first time that components of the PI3 kinase pathway, the serine/threonine kinase Akt (PKB) which enhances cellular proliferation and survival, and an Akt substrate FKHRL1 which is a transcription factor that leads to apoptosis and cell cycle arrest, are expressed in mammalian oocytes. By using an in vitro oocytes culture system, we found that oocytes-derived Akt and FKHRL1 are regulated by SCF. Treatment of cultured oocytes with SCF cannot only rapidly phosphorylate and activate Akt, but also simultaneously phosphorylate and may therefore functionally suppress FKHRL1, through the action of PI3 kinase. Together with our in situ hybridization and immunohistochemistry data that Akt and FKHRL1 are mostly expressed in oocytes in primordial and primary ovaries and reports that FKHRL1 gene-deficient mice exhibited excessive activation from primordial to primary follicles as well as enlarged oocyte sizes, we suppose that in mammalian oocytes, actions of granulosa cell derived SCF on primordial to primary follicle transition and subsequent follicle development may involve activation of Akt and inhibition of FKHRL1 activities in oocytes. The role of oocyte''s Akt may be to enhance follicle development and the role of oocyte''s FKHRL1 may be to inhibit follicle development. We propose that the cascade from granulosa cell SCF to oocyte Kit-PI3 kinase-Akt-FKHRL1 may play an important role to regulate the growth rate of mammalian oocytes and hypothetically also the oocyte secretion of factors that may regulate the activation and early development of ovarian follicles. [Copyright &y& Elsevier]