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Myocardial infarction (MI) is defined as cardiomyocyte death in a clinical context consistent with ischemic insult. MI remains one of the leading causes of morbidity and mortality worldwide. Although there are a number of effective clinical methods for the diagnosis and treatment of MI, further investigation of novel biomarkers and molecular therapeutic targets is required. Circular RNAs (circRNAs), novel non-coding RNAs, have been reported to function mainly by acting as microRNA (miRNA) sponges or binding to RNA-binding proteins (RBPs). The circRNA-miRNA-mRNA (protein) regulatory pathway regulates gene expression and affects the pathological mechanisms of various diseases. Undoubtedly, a more comprehensive understanding of the relationship between MI and circRNA will lay the foundation for the development of circRNA-based diagnostic and therapeutic strategies for MI. Therefore, this review summarizes the pathophysiological process of MI and various approaches to measure circRNA levels in MI patients, tissues, and cells; highlights the significance of circRNAs in the regulation MI pathogenesis and development; and provides potential clinical insight for the diagnosis, prognosis, and treatment of MI., Graphical abstract, Myocardial infarction (MI) is an ischemic and life-threatening disease, and circular RNAs (circRNAs) could play important roles in the processes of MI. A comprehensive understanding of the emerging roles of circRNAs in the pathological process of MI is significant for circRNAs to serve as the diagnosis, prognosis, and therapeutic intervention of MI.

In order to improve radio over fiber (RoF) system performance and reduce system complexity, a novel RoF system scheme with continuously tunable optical carrier-to-sideband ratio (OCSR) was proposed. Using polarization multiplexing technology, the OCSR can be tuned from −36 dB to 26 dB by adjusting a polarization controller (PC). The effects of polarization angle of PC, modulation index and extinction ratio on OCSR were studied by theoretical analysis and experimental simulation, in which the results of theoretical calculation and experimental simulation are in good agreement. It is found that the receiver sensitivity can be improved 7.8 dB by tuning the OCSR from 10.41 dB to 0 dB. The power penalty is 0.07 dB for the 0 dB OCSR after 40 km transmission, which means the impact from the fiber link can be ignored.

Background: Tumor initiating cells (TICs) were confirmed to drive the therapeutic resistance of hepatocellular carcinoma (HCC), but the mechanism by which tumor microenvironment maintains the HCC stemness is not fully understood. This study aims to investigate the effect of regulatory T cells (Tregs) on the TICs characteristics of HCC. Methods: Immunocytochemistry, flow cytometry, real-time PCR, western blot, in vitro sphere-formation, and in vivo tumorigenesis assay were used to detect HCC TIC characteristics. Additionally, the association between FoxP3 expression, Wnt/β-catenin pathway activation, and HCC stemness were analyzed by forced expression or inhibition of FoxP3. Results: It was showed Tregs enhanced the stemness of HCC cells by upregulation of TIC-related markers CD133, Oct3/4, Sox2, c-Myc, Klf4, Nanog, CD13, EpCAM, and induction of epithelial to mesenchymal transition (EMT), increase of TICs ratio, as well as promotion of tumorigenic ability. Moreover, β-catenin and c-Myc were upregulated in HCC cells when co-cultured with Tregs. After Wnt/β-catenin pathway inhibition, HCC stemness was also inhibited. In addition, Tregs-derived exosomes played the same role as Tregs in enhancing HCC TIC properties, and exosome inhibition led to decreased TIC ratio as well as TIC markers expression. Furthermore, Tregs-derived exosomes down-regulate FoxP3 and GSK3β of HCC cells. Forced expression of FoxP3 resulted in increased GSK3β, decreased β-catenin and TIC ratio of HCC. In contrast, FoxP3 interference reduced GSK3β, increased β-catenin and TIC ratio. Conclusions: This study, for the first time, demonstrated Tregs enhanced HCC stemness through Wnt//β-catenin pathway by down-regulating FoxP3.

In this study, a rapid and sensitive method that combines ethidium bromide monoazide (EMA) staining with real-time loop-mediated isothermal amplification (Rti-LAMP) assay was tested in detecting and evaluating viable but non-culturable state (VBNC) Escherichia coli (E. coli) O157:H7 induced by low temperature. When 1.7 × 104 CFU/ml of E. coli O157:H7 was 3 cycles of freeze-thaw, the cells were all dead. However, E. coli O157:H7 in 1.7 × 106 CFU/ml and 1.7 × 108 CFU/ml gradually transferred into VBNC state reaching 6.8 × 102 CFU/ml (0.04%) and 4.1 × 105 CFU/ml (0.24%) after 6 cycles of freeze-thaw, respectively. Keeping E. coli O157:H7 (1.7 × 108 CFU/ml) at 4 °C and − 20 °C, the culturable cells persistently decreased in plate counting. Meanwhile, the VBNC cells increased from 0 to 1.1 × 106 CFU/ml and 5.5 × 106 CFU/ml detected by both EMA-Rti-LAMP and direct epifluorescence method (DEM) up to 258-day storage at 4 °C and − 20 °C, respectively. The EMA-Rti-LAMP had similar accuracy with DEM in detecting viable including VBNC cells, the former had specificity but not the later. Furthermore, the EMA-Rti-LAMP could detect as low as 25 CFU/g of VBNC E. coli O157:H7 derived from contaminated chicken combined with bentonite-coated activated carbon (BCAC) treatment to remove DNA amplification inhibitors, and the entire assay could be completed in 5 h. In addition, one same sample for E. coli O157:H7 positive was detected by both BCAC-EMA-Rti-LAMP and plate count method from 24 retail chicken samples, but four positive samples by BCAC-Rti-LAMP assay. The results obviously suggested that the BCAC-EMA-Rti-LAMP assay might be a rapid and sensitive method for detection of viable including VBNC E. coli O157:H7 cells in food without enrichment.

The biosynthesis of aromatic aldehydes and alcohols from renewable resources is currently receiving considerable attention because of an increase in demand, finite fossil resources, and growing environmental concerns. Here, a temperature-directed whole-cell catalyst was developed by using two novel enzymes from a thermophilic actinomycete. Ferulic acid, a model lignin derivative, was efficiently converted into vanillyl alcohol at a reaction temperature at 30 °C. However, when the temperature was increased to 50 °C, ferulic acid was mainly converted into vanillin with a productivity of 1.1 g L-1 h-1 . This is due to the fact that the redundant endogenous alcohol dehydrogenases (ADHs) are not active at this temperature while the functional enzymes from the thermophilic strain remain active. As the biocatalyst could convert many other renewable cinnamic acid derivatives into their corresponding aromatic aldehydes/alcohols, this novel strategy may be extended to generate a vast array of valuable aldehydes or alcohols.

In this study, a rapid and sensitive method of real-time loop-mediated isothermal amplification (Rti-LAMP) assays was developed for quantification and discrimination of viable and heat-killed E. coli O157:H7 cells treated with low concentration of ethidium bromide monoazide (EMA). Four micrograms per milliliter of EMA was chosen as the optimal concentration which did not inhibit DNA amplification derived from viable cells, but significantly increased the Tt values of dead cells in Rti-LAMP assays. When the DNA from 2.0 × 103 viable CFU of E. coli O157:H7 was subjected to EMA-Rti-LAMP, the resulting Tt value was 17.73 min. In contrast, the DNA from 2.0 × 103 CFU completely heat destroyed CFU of E. coli O157:H7 did not yield a positive amplification which Tt value was regarded as 60 min. When the DNA from viable plus heat-killed CFU at a ratio of 5:2995 was subjected to EMA-Rti-LAMP, the resulting Tt value was 23.06 min, which was statistically identical (P

The physiological roles of silent genes are still unsolved puzzles and their application potentials are unexplored. Herein, a silent glycerol catabolism pathway encoded by glp system was activated in a Klebsiella pneumoniae mutant, of which the acetoin degradation pathway was blocked. Surprisingly, the activation produced significant effects on cellular metabolism and over 90% of the carbon flux was redirected to acetoin biosynthesis, which was formerly a minor product in this mutant. Transcription analyses suggest that the genes involved in acetoin, 1,3-propanediol and adenosyl-cobalamin biosynthesis were differentially regulated upon the glp system activation, demonstrating the cross-talk between silent and active pathways. Through pathway, cofactor and bioprocess engineering, high-level acetoin production from glycerol (32.2gL-1, 90.8% of the theoretical value) was achieved. Our findings suggest that some silent genes represent unexplored switches of cellular metabolic status and activating them may be an easy strategy for reprogramming microorganisms into efficient cell factories.

Nephrolithiasis is one of the world’s major public health burdens with a high incidence and a risk of persistent renal dysfunction. Fu-Fang-Jin-Qian-Chao granules (FFJQC), a traditional Chinese herb formula, is commonly used in treatment of nephrolithiasis. However, the therapeutic mechanism of FFJQC on kidney stone has still been a mystery. The objective of the present study is to explore the therapeutic mechanism of FFJQC on kidney injury and identify unique metabolomics patterns using a mouse model of kidney stone induced by a calcium oxalate (CaOx) deposition. Von Kossa staining and immuno-histopathological staining of osteopontin (OPN), cluster of differentiation 44 (CD44) and calbindin-D28k were conducted on renal sections. Biochemical analysis was performed on serum, urine, and kidney tissues. A metabolomics approach based on ultra-HPLC coupled with quadrupole-TOF-MS (UHPLC-Q-TOF/MS) was used for serum metabolic profiling. The immunohistopathological and biochemical analysis showed the therapeutic benefits of FFJQC. The expression levels of OPN and CD44 were decreased while calbindin-D28k increased after the CaOx injured mice were treated with FFJQC. In addition, total of 81 serum metabolites were identified to be associated with protective effects of FFJQC on CaOx crystal injured mice. Most of these metabolites were involved in purine, amino acid, membrane lipid and energy metabolism. Potential metabolite biomarkers were found for CaOx crystal-induced renal damage. Potential metabolite biomarkers of CaOx crystal-induced renal damage were found. FFJQC shows therapeutic benefits on CaOx crystal injured mice via regulation of multiple metabolic pathways including amino acids, purine, pyrimidine, glycerolipid, arachidonic acid (AA), sphingolipid, glycerophospholipid, and fatty acid.

Removal of arsenic using the low-temperature vacuum carbothermal reduction method was investigated by taking dusts with high contents of arsenic and copper from furnaces for pyrometallurgical refining of Cu as raw materials. Based on TGA-DSC, differential thermal analysis was applied to the raw materials; by virtue of various methods including XRD, ICP, and SEM: the phases, chemical compositions and morphologies of dusts and evaporation residues were separately analysed; on the basis of thermodynamic analysis, the influences of the evaporating temperature, residual pressure, reductant dosage, and evaporation time on the removal rates of As and other valuable metals were explored. The results show that at an evaporating temperature of 350 °C, the residual pressure of 100 Pa, reductant dosage of 25%, and evaporation time for 50 min, the As removal rate can reach 93.48% while guaranteeing that the other metals are essentially not evaporated. This realises the selective separation of As from the other valuable metals. The evaporation products are higher-purity As2O3, which can be used as a primary As2O3 product. The valuable metals are concentrated in evaporation residues, being conducive to subsequent recovery by leaching with waste acids.

In order to get the entire data in the optical measurement, a multi-view three-dimensional (3D) measurement method based on turntable is proposed. In the method, a turntable is used to rotate the object and obtain multi-view point cloud data, and then multi-view point cloud data are registered and integrated into a 3D model. The measurement results are compared with that of the sticking marked point method. Experimental results show that the measurement process of the proposed method is simpler, and the scanning speed and accuracy are improved.

High rates of misdiagnosis and delayed intervention in neonatal PWS are leading to poor prognoses. To determine the clinical and image characteristics of newborns with Prader-Willi syndrome (PWS). A total of 102 cases of newborns definitively diagnosed with PWS at the Children's Hospital of Fudan University from 02/2014 to 12/2017 were retrospectively analyzed. We analyzed the modulated voxel-based morphology (VBM) of gray matter in PWS by T2 weighted imaging. Of 102 cases, 75 (73.5%) have paternal deletion of 15q11.2-q13, whereas 27 (26.5%) have maternal uniparental disomy (UPD). Of the 75 deletion cases, 75 (100%) week crying, 71 (94.7%) hypotonia, 70 (93.3%) poor feeding, 46 (61.3%) hypopigmentation, 43 (57.3%) male cryptorchidism, 10 (13.3%) female labia minora, 48 (64%) characteristic facial features. Of 27 UPD cases, 27 (100%) week crying and hypotonia, 25 (92.6%) hypophagia, 20 (74.1%) male cryptorchidism, 1 (3.7%) female labia minora, 19 (70.4%) characteristic facial features, 12 (44.4%) hypopigmentation. The modulated VBM analysis shows that the middle frontal gyrus, orbitofrontal cortex (middle), and inferior frontal gyrus are the most variable brain regions that determine the endo-phenotype difference between the two genotypes. Hypotonia, hypophagia, and maldevelopment of sexual organs are general characteristics of newborns with PWS in Chinese population. In UPD cases, the proportions of premature newborns, elderly parturient women and congenital malformations were higher than for paternal deletion cases. The differences in the gray matter volume of these three regions between the two genotypes may explain the differences in maladaptive behaviors and emotions.

Background: Xuebijing injection (XBJ), transforming from Xuefuzhuyu decoction, is the only Chinese medicine injection approved for sepsis. XBJ and ulinastatin (UTI) combination therapy is supposed to be beneficial for sepsis patients. To fill the gap between the lack of evidence for the efficacy of combination therapy and its increasing application among patients, an extensive meta-analysis was performed.Methods: Eight databases were searched to identify randomized controlled trials (RCTs) comparing XBJ plus UTI with UTI alone in treating sepsis from inception to February 5, 2018. Data extraction and methodological quality assessment of the included RCTs were implemented by two investigators independently. All data were synthesized and analyzed utilizing Review Manager 5.3.Results: Seventeen RCTs with a total of 1,247 participants corresponded with the inclusion criteria of our study. The findings reflected that in comparison to single UTI, XBJ and UTI combination therapy could significantly lower 28-day mortality (RR = 0.54, 95% CI [0.39, 0.73], P < 0.0001), shorten duration of mechanical ventilation (SMD = −1.13, 95% CI [−1.30, −0.95], P < 0.00001), reduce length of ICU stay (SMD = −0.84, 95% CI [−1.00, −0.67], P < 0.00001), and decrease APACHE II score (SMD = −1.09, 95% CI [−1.49, −0.69], P < 0.00001). Additionally, XBJ plus UTI had superiority over single UTI in lowering PCT levels (SMD = −1.61, 95% CI [−2.23, −0.98], P < 0.00001), and improving inflammatory cytokines—IL-6 and TNF-α levels (SMD = −1.45, 95% CI [−1.71, −1.19], P < 0.00001; SMD = −1.11, 95% CI [−1.42, −0.80], P < 0.00001). Moreover, CRP, hs-CRP, and LPS levels were remarkably reduced by XBJ plus UTI compared with UTI alone (SMD = −1.50, 95% CI [−2.00, −1.00], P < 0.00001; SMD = −1.31, 95% CI [−1.70, −0.93], P < 0.00001; SMD = −1.17, 95% CI [−1.42, −0.92], P < 0.00001). Three studies involving 14 patients reported the occurrences of adverse events.Conclusions: Comparing with UTI alone, XBJ and UTI combination therapy appeared to be more effective for sepsis. However, owing to the limitations of this meta-analysis, additional RCTs with higher-quality and more rigorous design are needed to confirm our findings.

Peroxisome proliferator-activated receptors (PPARs) play vital roles in cardiovascular pathophysiology, such as energy balance, cell proliferation/apoptosis, inflammatory response, and adipocyte differentiation. These vital roles make PPARs potential targets for therapeutic prevention of cardiovascular diseases (CVDs). Emerging evidence indicates that the crosstalk of microRNAs (miRNAs) and PPARs contributes greatly to CVD pathogenesis. PPARs are inhibited by miRNAs at posttranscriptional mechanisms in the progress of pulmonary hypertension and vascular dysfunction involving cell proliferation/apoptosis, communication, and normal function of endothelial cells and vascular smooth muscle cells. In the development of atherosclerosis and stroke, the activation of PPARs could change the transcripts of target miRNA through miRNA signalling. Furthermore, the mutual regulation of PPARs and miRNAs involves cell proliferation/apoptosis, cardiac remodeling, and dysfunction in heart diseases. In addition, obesity, an important cardiovascular risk, is modulated by the regulatory axis of PPARs/miRNAs, including adipogenesis, adipocyte dysfunction, insulin resistance, and macrophage polarization in adipose tissue. In this review, the crosstalk of PPARs and miRNAs and their emerging regulatory roles are summarized in the context of CVDs and risks. This provides an understanding of the underlying mechanism of the biological process related to CVD pathophysiology involving the interaction of PPARs and miRNAs and will lead to the development of PPARs/miRNAs as effective anti-CVD medications.

This paper discusses the technical pattern and management mode of cross-border convergence between Internet and network music industry nation-based entrepreneurship. It also involves the issue that information-based entrepreneurship promotes the diversified development of network music industry. This paper studies the affecting factors which promote the cross-border intergration of Internet+ and network music industry.

GFRP bars and PC strand composite pile is a new supporting piles, according to the engineering field test and analysis of experimental data prove that there is a significant effect on the control aspects of the horizontal displacement of supporting piles. Principle energy method can calculate the horizontal displacement of pile foundation pit in theory, by comparing the size of the horizontal displacement of the supporting piles of ordinary reinforcement, to demonstrate the feasibility of using GFRP bars and PC strand combination of techniques to reduce the horizontal displacement of excavation, provide reference for future engineering practice.

Concrete cover thinkness of GFRP to ensure the safety, applicability and durability of the structure is of great significance. Based on studies to 30 the drawing specimens of concrete ,get bond strength of same GFRP diameter,same concrete strength, different concrete cover thinkness. Through the analysis of test data,it is concluded the relationship of the bond strength and the concrete cover thinkness.And basis on the relationship,it is determine the suggestive values on concrete cover thinkness of GFRP.Experimental data and suggestion can provide reference and theoretical basis for the GFRP engineering application and the establishment of the relevant specification.

Epidemiologic studies suggest that increased concentrations of airborne spores of Aspergillus fumigatus closely relate to asthma aggravation. Chronic exposure to A. fumigatus aggravates airway inflammation, remodeling, and airway hyperresponsiveness in asthmatic rats. The effects of chronic exposure to A. fumigatus on epidermal growth factor receptor (EGFR) expression in the airway epithelial cells of asthmatic rats remain unclear. This study aimed to investigate the effects of chronic exposure to A. fumigatus on injury and shedding of airway epithelium, goblet cell metaplasia, and EGFR expression in the airway epithelial cells of asthmatic rats. A rat model of chronic asthma was established using ovalbumin (OVA) sensitization and challenge. Rats with chronic asthma were then exposed to long-term inhalation of spores of A. fumigatus, and the dynamic changes in injury and shedding of airway epithelium, goblet cell metaplasia, and EGFR expression were observed and analyzed. Chronic exposure to A. fumigatus could aggravate airway epithelial cell damage, upregulate the expression of EGFR and its ligands EGF and TGF-α, promote goblet cell metaplasia, and increase airway responsiveness in rats with asthma. Chronic exposure to A. fumigatus upregulates the expression of EGFR and its ligands in asthmatic rats. The EGFR pathway may play a role in asthma aggravation induced by exposure to A. fumigatus.

The using inductively coupled plasma etching techniques, the surface of fused silica was etched by CF4 as etching reaction gases. The results show that the fused silica surface scratches buried defects can be effectively removed with no replication effect, with the etching process proceeds, fused silica at 355nm laser light R: 1 under irradiated, the initial damage threshold of component surface is worth to an effective improved, damage resistance level of element surface more balanced, low damage threshold is worth to significantly improve.

The mechanism of thermostabilization of the thermostable exo-ß-D-glucosaminidase (Bglph) from Pyrococcus horikoshii was investigated. Conserved domains analysis and C-terminal truncated mutation showed that the C-terminal region was indispensable for the enzymes thermostability. Two site directed mutagenesis proteins (C103A and C103AandC550A) were as active as the native enzyme and showed no structural difference with the native enzyme. By comparison with two mesophilic exo-ß-D-glucosaminidases (CsxA and CsxT) from actinomycetes Amycolatopsis orientalis and fungi Trichoderma reesei respectively, it was shown that the amino acids composition of Bglph was consistent with its high thermostability, hydrophobic interactions, homodimerization and ion pairs could play key roles. These results presented the overall properties of the thermostability of Bglph from diverse aspects.

This study fitted the measured loading-settlement curve of half-screwed pilewith least square model solution of difference form of integrated exponential functional model, and predict ultimate bearing capacity of half-screwed pile according to the fitted curve of maximum curvature point. Combined with practical engineering research, the study explored the feasibility, rationality and limitations of predicting the half-screwed single pile ultimate bearing capacity with least square model solution of difference form of integrated exponential functional model, and provided the theoretical basis for the popularization and application of the half-screwed pile.

Half-screwed pile is cylinder type in the top, and screwed at the bottom. As a new type of pile with very high practical value, its development prospect is very broad. The pile process and technical performance are analyzed generally, and advantages in application are introduced.

Cytokine-induced killer (CIK) cells have been used as adoptive immunotherapy in cancer. The present study evaluated the effect of CIK cells on immune function in patients with lung cancer. Patients were divided into three groups, according to the treatment received prior to CIK cell treatment: CIK group (no prior treatment), Che-Sur group (prior chemotherapy and surgery) and Che-Rad group (prior chemotherapy and radiotherapy). Following treatment, the average percentage of cluster of differentiation (CD)3+CD4+, CD3+, natural killer (NK) and NKT cells in peripheral blood was significantly higher than that prior to CIK treatment in the Che-Sur and CIK groups, and the levels of interferon-γ in serum were significantly higher than those prior to CIK treatment in the Che-Sur and CIK groups. On the contrary, the levels of interleukin-10 had decreased in these groups following CIK treatment. Subsequently, patients were divided into three groups according to the percentage of CD3+CD56+ CIK cells that were administered to the patients. The number of NK and NKT cells increased with increasing number of CD3+CD56+ cells. The patients in the CIK and Che-Sur groups were the most benefited ones following CIK treatment, contrarily to those in the Che-Rad group, since the increase in the number of CD3+CD56+ CIK cells in the aforementioned patients enhanced the number of NK cells, which exhibit antitumor activity.

Proteasome inhibitors represent a novel class of anticancer agents that are used in the treatment of hematologic malignancies and various solid tumors. However, mechanisms underlying their anticancer actions were not fully understood. It has been reported that strong 14‐3‐3 protein expression is observed and associated with tumor genesis and progression of astrocytoma. In addition, global inhibition of 14‐3‐3 functions with a general 14‐3‐3 antagonist difopein induces apoptosis of human astrocytoma cells, validating 14‐3‐3 as a potential molecular target for anticancer therapeutic management. In the current study, for the first time we demonstrated that proteasome inhibitors downregulated 14‐3‐3ε and 14‐3‐3θ/τ in U87 and SF295 glioma cells. Overexpression of 14‐3‐3ε and 14‐3‐3θ/τ significantly suppressed apoptosis of human glioma cells induced by proteasome inhibitors. We also demonstrated that MG132 activated ASK1 and siASK1 compromised the MG132‐induced apoptosis of glioma cells. Furthermore, overexpression of 14‐3‐3ε and 14‐3‐3θ/τ markedly suppressed activation of ASK1. Collectively, the current study supported that proteasome inhibitors, at least in part, caused cytotoxicity of glioma cells via downregulation of 14‐3‐3ε and 14‐3‐3θ/τ and subsequent activation of ASK1. (Cancer Sci 2013; 104: 55–61)

Background Epidemiologists have recently investigated sunlight exposure as a risk factor for age-related macular degeneration (AMD), but there remains an ongoing dispute over this association due to insufficient evidence and unreliable data. Objectives To analyse comprehensively the epidemiological literature concerning the association between AMD and sunlight exposure. Methods We systematically reviewed the epidemiological literature concerning the association between AMD and sunlight exposure. An electronic search was performed of PubMed, Web of Science and CNKI, which was supplemented by hand searching. The selection of studies, data abstraction and quality assessment were performed independently by three reviewers. After these steps, we performed a random-effects meta-analysis, followed by subgroup analysis and sensitivity analysis, including a random-effects meta-regression for study-specific covariates. Results Fourteen studies were identified. Twelve studies identified an increasing risk of AMD with greater sunlight exposure, six of which reported significant risks. The pooled OR was 1.379 (95% CI 1.091 to 1.745). The subgroup of non-population-based studies revealed a significant risk (OR 2.018, 1.248 to 3.265, p=0.004). We identified the gross domestic product (GDP) per capita (p=0.048), but not the latitude (p=0.21), as a factor that led to heterogeneity according to the meta-regression. Conclusions The epidemiological literature published to date indicates that individuals with more sunlight exposure are at a significantly increased risk of AMD. The OR significantly decreased with increasing GDP per capita.

Formic acid and formate have been proven to be among the most promising fuels for direct liquid fuel cells. To take advantage of both formic acid and formate, the oxidation activity of a formic acid–formate blended solution was studied using cyclic voltammetry, Tafel polarization measurements, and chromoamperometry. With increased concentration of formate, the oxidation potential of formic acid shifted to the negative direction, and the peak current significantly increased, suggesting a greatly enhanced oxidation activity. The transition of formic acid from an indirect to a direct oxidation route was also observed. The enhanced oxidation activity indicated that a formic acid–formate blended solution is a promising fuel system for direct liquid fuel cells. Hence, a new concept of fuel cell, i.e., direct formic acid–formate blended fuel cell, was proposed.

Lipopolysaccharide (LPS) is an outer-membrane glycolipid component of Gram-negative bacteria known for its fervent ability to activate monocytic cells and for its potent proinflammatory capabilities. Bcl-2-associated athanogene 3 (BAG3) is a survival protein that has been shown to be stimulated during cell response to stressful conditions, such as exposure to high temperature, heavy metals, proteasome inhibition, and human immunodeficiency virus 1 (HIV-1) infection. In addition, BAG3 regulates replication of Varicella-Zoster Virus (VZV) and Herpes Simplex Virus (HSV) replication, suggesting that BAG3 could participate in the host response to infection. In the current study, we found that LPS increased the expression of BAG3 in a dose- and time-dependent manner. Actinomycin D completely blocked the LPS-induced BAG3 accumulation, as well as LPS activated the proximal promoter of BAG3 gene, supported that the induction by LPS occurred at the level of gene transcription. LPS-induced BAG3 expression was blocked by JNK or NF-κB inhibition, suggesting that JNK and NF-κB pathways participated in BAG3 induction by LPS. In addition, we also found that induction of BAG3 was implicated in monocytic cell adhesion to extracellular matrix induced by LPS. Overall, the data support that BAG3 is induced by LPS via JNK and NF-κB-dependent signals, and involved in monocytic cell-extracellular matrix interaction, suggesting that BAG3 may have a role in the host response to LPS stimulation.

A series of NaLa(WO4)2:Tb3+ green phosphors have been prepared by a facile combustion method. X-ray powder diffraction (XRD) and photoluminescence were used to characterize the structure and luminescence properties of as-synthesized phosphors, respectively. The XRD results confirm that the as-synthesized phosphors exhibit sheelite-type structure without any impurity phase. The excitation band of the phosphors covers a wide region of 200-300 nm. The as-obtained phosphors emit strong green light centered at 546 nm under ultraviolet light excitation (261 nm). The results show that the optimum temperature is 800°C and the optimum concentration of Tb3+-dopant is 50 at%.

Bundle-like ZnO nanostructure was rapidly synthesized by a sonochemical method at 70 °C, using zinc nitrate, citric acid, ammonia, and sodium hydroxide as reactants. The resulting materials were characterized by X-ray diffraction, scanning electron microscopy, and photoluminescence measurements. The bundle-like nanostructure was formed by the anisotropic growth of the ball-like nanostructure. The room-temperature PL spectrum of the bundle-like nanostructure exhibits a weak ultraviolet emission band and a strong visible emission.

Our previous data showed that reactive oxygen species generation might be ascribed to the cytotoxic response of thyroid cancer cells to proteasome inhibition and the ability of cancer cells to induce catalytic subunit for glutamate cysteine ligase (GCLC) and subsequent production of glutathione, thereby scavenging reactive oxygen species was partly ascribed to the cytotoxic responses of thyroid cancer cells to proteasome inhibition. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor responsible for transcriptional activation of various cytoprotective genes including GCLC.The purpose of this study was to determine the involvement of Nrf2 in GCLC induction and cytotoxicity of thyroid cancer cells mediated by proteasome inhibition.The effects of proteasome inhibition on the expression and distribution of Nrf2 were analyzed using immunocytochemistry and Western blot. To ascertain the effect of Nrf2 and p38 MAPK, cells were transfected with Nrf2 plasmid or small interfering RNA against Nrf2 or p38 MAPK. Apoptotic cells, production of glutathione, and induction of GCLC mediated by proteasome inhibition were investigated using flow cytometry, spectrophotometry, and real-time RT-PCR, respectively.Proteasome inhibition caused accumulation and nuclear translocation of Nrf2, which compromised the cytotoxic effects of proteasome inhibition, at least in part, via induction of GCLC. In addition, nuclear translocation of Nrf2 was p38 MAPK dependent, and p38 MAPK inhibition augmented the cytotoxic effects of proteasome, at least partly, via suppression of transactivation of Nrf2.These studies support the hypothesis that proteasome inhibitors activate an antiapoptotic survival program through p38 MAPK that involves transcriptional activity of Nrf2.

Proteasome inhibitors represent a novel class of antitumor agents with pre-clinical and clinical evidence of activity against hematologic malignancies and solid tumors. However, emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that the activation of survival signaling cascades might compromise their antitumoral effects. Peroxiredoxins (PRDXs) are a family of thiol-containing peroxidases identified primarily by their ability to remove cellular hydroperoxides. The function of PRDX1 in particular has been implicated in regulating cell proliferation, differentiation, and apoptosis. Another important finding is that aberrant upregulation of PRDX1 has been discovered in various cancers. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase and p38 MAPK, and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, one of which is through interaction with PRDX1. In this study, for the first time we report that upregulation of PRDX1 expression was found in thyroid cancer cells treated with proteasome inhibitors, and PRDX1 knockdown resulted in accelerated proteasome inhibitor-induced cell death. In addition, we demonstrated that ASK1 activity was implicated in the PRDX1-dependent response of thyroid cancer cells to proteasome inhibitor-mediated cell death.

A novel circularly polarized microstrip rectenna operating on C-band with low proflle is proposed. The input and output match networks of the rectifying circuit are realized by ‚=4 microstrip lines and open stubs with the harmonics being inhibited. The circularly polarized receiving antenna is a truncated-corner square patch fed by microstrip line with DGS (Defect Ground Structure) for suppressing high order harmonics further. The voltage of 4.34V on the load of 298› is measured and the overall RF-DC conversion e-ciency of 68.4% is obtained. This kind of rectenna can be extended to large arrays for wireless power transmission applications.

Background and purpose: Proteasome inhibitors represent a novel class of anti-tumour agents that have clinical efficacy against haematological and solid cancers. The anti-apoptotic protein BAG3 is a member of the Bcl-2-associated athanogene family. We have previously shown that BAG3 is up-regulated after exposure to proteasome inhibitors and that inhibition of BAG3 sensitized cells to apoptosis induced by proteasome inhibition. However, the mechanisms by which proteasome inhibition induced BAG3 expression remained unclear and the present experiments were designed to elucidate these mechanisms. Experimental approach: Effects of the proteasome inhibitor MG132 on activation of mitogenic signalling pathways were evaluated in kidney cancer cells (A498, Caki1, Caki2), with Western blotting. Specific inhibitors against individual mitogenic signalling pathways, real-time reverse transcription-polymerase chain reaction and luciferase reporter assays were used to investigate the roles of mitogenic signalling pathways in BAG3 induction after proteasome inhibition. Cell death was evaluated using Annexin V/propidium iodide staining and subsequent FACS. Key results: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities. Induction of BAG3 by MG132 was inhibited by blocking JNK, but not ERK1/2 and p38 MAPK signalling pathways. In addition, SP600125 and dominant-negative JNK1 suppressed BAG3 promoter-driven reporter gene expression. Furthermore, activation of the JNK pathway induced BAG in kidney cancer cells after treatment with MG132. Conclusions and implications: Our results suggested that the JNK pathway was associated with the protective response against proteasome inhibition, by mediating induction of BAG3.

BAG3 protein, a member of the BAG co-chaperones family, sustains cell survival in a variety of normal and neoplastic cell types, via its interaction with a variety of partners, such as the heat shock protein (HSP) 70, Bcl-2, Raf-1 and others. Expression of BAG3 is induced by some stressful stimuli, such as heat shock, heavy metal exposure. We have reported that proteasome inhibitors can also induce BAG3 expression at the transcriptional level and the induction of BAG3 compromises proteasome inhibitors-mediated apoptosis. However, the molecular mechanism of BAG3 upregulation has not been elucidated. In the current study, we provide evidence that heat shock transcription factor 1 (HSF1) is involved in BAG3 induction by proteasome inhibitor MG132. Using a series of varying lengths of 5'-flanking region of the BAG3 gene into luciferase reporter vectors, we found that MG132 stimulated the promoter activity via the -326/-233 and -825/-689 regions, which contains one putative heat shock-responsive element (HSE) for HSF1-binding, respectively. Site-directed deletion of the sites abrogated the enhanced reporter activity in response to MG132 treatment. Chromatin immunoprecipitation assay demonstrated that HSF1 directly bound to the MG132-responsive site on the BAG3 promoter. Activation of HSF1 occurred with MG132 along with BAG3 upregulation. Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.

Kruppel-like factor 4 is a transcription factor which plays an important role in development and progression of various carcinomas. Curcumin characterized by excellent anti-cancer properties is regarded as a serviceable natural compound used in carcinoma therapy. This study aimed at exploring the impact of KLF4 overexpression in cooperation with curcumin on the proliferation, apoptosis and invasion of human gastric carcinoma BGC- 823 cells. Flow cytometry analysis, CCK-8 assays, transwell assays and Western blot results showed that KLF4 overexpression combined with curcumin had significant anti-proliferation, pro-apoptosis and anti-invasion effects on BGC-823 cells. We also found that KLF4 had synergistic effects with curcumin, better promoting apoptosis and inhibiting proliferation and invasion of gastric carcinona cells. These results indicate that KLF4 could be used as a potential therapeutic target; curcumin could act as an auxiliary and provide a promising therapeutic strategy in stomach cancer.