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Find video protocols related to scientific articles indexed in Pubmed.
Trade-offs of the opto-electrical properties of a-Si:H solar cells based on MOCVD BZO films.
Phys Chem Chem Phys
PUBLISHED: 11-20-2014
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Boron-doped zinc oxide (BZO) films, deposited by metal-organic chemical vapor deposition (MOCVD), have been widely used as front electrodes in thin-film solar cells due to their native pyramidal surface structure, which results in efficient light trapping. This light trapping effect can enhance the short-circuit current density (Jsc) of solar cells. However, nanocracks or voids in the silicon active layer may form when the surface morphology of the BZO is too sharp; this usually leads to degraded electrical properties of the cells, such as open-circuit voltage (Voc) and the fill factor (FF), which in turn decreases efficiency (Eff) [Bailat et al., Photovoltaic Energy Conversion, Conference Record of the 2006 IEEE 4th World Conference on. IEEE, 2006, vol. 2, pp. 1533-1536]. In this paper, an etching and coating method was proposed to modify the sharp "pyramids" on the surface of the BZO films. As a result, an evident enhancement was achieved for these modified, BZO-based cells' Voc, FF, and Eff, although the Jsc exhibited a small decrease. In order to increase the Jsc and maintain the improved electrical properties (Voc, FF) of the cell, a thin BZO coating, deposited by MOCVD, was introduced to coat the sputtering-treated BZO film. Finally, we optimized the trade-off among the Voc, FF, and Jsc, that is, we identified a regime with an increase of the Jsc as well as a further improvement of the other electrical properties.
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Constructing a FRET-based molecular chemodosimeter for cysteine over homocysteine and glutathione by naphthalimide and phenazine derivatives.
Analyst
PUBLISHED: 11-20-2014
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A molecular chemodosimeter , with a naphthalimide fluorophore connected to a newly designed phenazine energy acceptor, for the selective detection of cysteine was effectively synthesized. featured efficient intramolecular fluorescence resonance energy transfer (FRET) based on spectral overlap between the emission of naphthalimide and the absorption of phenazine. A cystamine chain with a S-S bond was applied to play the role of recognition moiety and the linker part. The specific reaction between the biological thiols and gave rise to an obvious fluorescence intensity enhancement at 540 nm, which is induced by cleavage of the disulfide bond followed by elimination of the FRET effect. High sensitivity and selectivity for cysteine over homocysteine and glutathione were also achieved. In addition, upon excitation at 400 nm, a relatively weak NIR emission provided an internal standard making a promising ratiometric sensor for cellular detection of cysteine.
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Up-Regulation of miR-21 and miR-23a Contributes to As2 O3 -induced hERG Channel Deficiency.
Basic Clin. Pharmacol. Toxicol.
PUBLISHED: 11-15-2014
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Arsenic trioxide (As2 O3 ) is used to treat acute promyelocytic leukaemia. However, the cardiotoxicity of long QT syndrome restricts its clinical application. Previous studies showed that As2 O3 can damage the hERG current via disturbing its trafficking to cellular membrane. Consistent with these findings, in this study we reported that As2 O3 inhibited hERG channel at both protein and mRNA levels, damage hERG current but did not affect channel kinetics. Further, we demonstrated that As2 O3 up-regulated miR-21 and miR-23a expression in hERG-HEK293 cells and neonatal cardiomyocytes. In addition, knockdown of miR-21 by its specific antisense molecules AMO-21 was able to rescue Sp1 and hERG inhibition caused by As2 O3 . Consistently, phosphorylation of NF-?B, the upstream regulatory factor of miR-21, was significantly up-regulated by As2 O3 . This finding revealed that regulation of the NF-?B-miR-21-Sp1 signalling pathway is a novel mechanism for As2 O3 -induced hERG inhibition. Meanwhile, the expression of HSP90 and hERG was rescued by transfection with AMO-23a. And the hERG channel inhibition induced by As2 O3 was rescued after being transfected with AMO-23a, which may be a molecular mechanism for the role of As2 O3 in hERG trafficking deficiency. In brief, our study revealed that miR-21 and miR-23a are involved in As2 O3 -induced hERG deficiency at transcriptional and transportational levels. This discovery may provide a novel mechanism of As2 O3 -induced hERG channel deficiency and these miRNAs may serve as potential therapeutic targets for the handling of As2 O3 cardiotoxicity. This article is protected by copyright. All rights reserved.
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Matrix metalloproteinase 1, 3, and 9 polymorphisms and esophageal squamous cell carcinoma risk.
Med. Sci. Monit.
PUBLISHED: 11-14-2014
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Background Matrix metalloproteinases (MMPs) are multifunctional zinc-dependent proteinases that play a fundamental role in the pathogenesis of tumors. We have analyzed the association between 3 single-nucleotide polymorphisms (SNPs; MMP1 -1607 1G/2G, MMP3 -1612 5A/6A, and MMP9 -1562 C/T) and the risk of esophageal squamous cell carcinoma (ESCC). Material and Methods We investigated these 3 SNPs in 132 patients and 132 controls using polymerase chain reaction-restriction fragment length polymorphism methods. The MMP1 and MMP3 genes are located on the same chromosome. Haplotype analysis was performed to study the combined effect of the linked MMP polymorphisms on ESCC risk. Results The MMP1 and MMP9 promoter polymorphisms were not associated with ESCC risk, while the MMP3 -1612 5A/6A polymorphism was significantly associated with susceptibility to ESCC. Patients carrying the 5A allele had a significantly higher risk for developing ESCC compared with individuals carrying the 6A allele (OR=1.93; 95% CI 1.34-2.77; p<0.01). The 2G-5A and 1G-5A haplotypes were associated with a significantly increased risk of ESCC as compared with the 2G-6A haplotype (OR=2.04, 95% CI 1.37-3.04 and OR=3.65, 95% CI 1.26-10.55, respectively). Conclusions These findings implicate this MMP3 polymorphism as a contributor to ESCC susceptibility.
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Increased micronucleus, nucleoplasmic bridge, and nuclear bud frequencies in the peripheral blood lymphocytes of diesel engine exhaust-exposed workers.
Toxicol. Sci.
PUBLISHED: 11-06-2014
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The International Agency for Research on Cancer has recently reclassified diesel engine exhaust (DEE) as a Group 1 carcinogen. Micronucleus (MN), nucleoplasmic bridge (NPB), and nuclear bud (NBUD) frequencies in peripheral blood lymphocytes (PBLs) are associated with cancer risk. However, the impact of DEE exposure on MN frequency has not been thoroughly elucidated due to mixed exposure and its impact on NPB and NBUD frequencies has never been explored in humans. We recruited 117 diesel engine testing workers with exclusive exposure to DEE and 112 non-DEE-exposed workers, and then we measured urinary levels of four mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) using high performance liquid chromatography-mass spectrometry as well as MN, NPB, and NBUD frequencies in PBLs using cytokinesis-block micronucleus assay. The DEE-exposed workers exhibited significantly higher MN, NPB, and NBUD frequencies than the non-DEE-exposed workers (p<0.05). Among all study subjects, increasing levels of all four urinary OH-PAHs, on both quartile and continuous scales, were associated with increased MN, NPB, and NBUD frequencies (all p<0.05). When the associations were analyzed separately in DEE-exposed and non-DEE-exposed workers, we found that the association between increasing quartiles of urinary 9-hydroxyphenanthrene (9-OHPh) and MN frequencies persisted in DEE-exposed workers (p=0.001). The percent of MN frequencies increased, on average, by 23.99% (95% confidential interval, 9.64-39.93) per 1-unit increase in ln-transformed 9-OHPh. Our results clearly show that exposure to DEE can induce increases in MN, NPB, and NBUD frequencies in PBLs and suggest that DEE exposure level is associated with MN frequencies.
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Healthcare access among circular and undocumented Mexican migrants: results from a pilot survey on the Mexico-US border.
Int J Migr Bord Stud
PUBLISHED: 11-04-2014
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Temporary and unauthorized migrants may face unique obstacles to access health care services in the U.S.
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[Laser and vision measurement research on parameters of miniature quartz plate-sensitive glass part].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 11-01-2014
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High-precision, rapid and non-contact geometry parameter measurements of plate glass parts has become a main problem in the field of testing-related production and processing and also an important applied direction for laser spectroscopy. Accurately detect the geometric parameters of plate glass parts can not only improve the processing technology and the precision of assembly, but also bring about sub-file management according to the parameters. This paper presents a novel multi-parameter measurement method based on the laser and vision image processing technology, which can be used to measure parameters of miniature quartz plate-sensitive glass part accurately. The testing system consisting of self-adaption coaxial visual detection unit and laser vision thickness inspection unit was designed. A constant power drive control system was set up to ensure the laser diode (LD) can provide a stable light source for the testing system. A modified sub-pixel edge position algorithm of conic features was proposed to implement the sub-pixel image processing, and the parameters can be extracted. According to the data detected from curve edge points and a new-defined error function, which was minimized, the parameters of miniature quartz plate-sensitive glass part can be calculated. The experiments show that the average deviation of the measurement results is less than 2 ?m, and the method has good stability and high accuracy measurement, which can meet the precision requirement of parameter measurement for miniature plate glass part.
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Mesoporous Bi2S3 nanorods with graphene-assistance as low-cost counter-electrode materials in dye-sensitized solar cells.
Nanoscale
PUBLISHED: 10-24-2014
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In this work, we report the synthesis of mesoporous Bi2S3 nanorods under hydrothermal conditions without additives, and investigated their catalytic activities as the CE in DSCs by I-V curves and tested conversion efficiency. To further improve their power conversion efficiency, we added different amounts of reduced graphene by simple physical mixing. With the addition of 9 wt% reduced graphene (rGO), the short-circuit current density, open-circuit voltage and fill factor were Jsc = 15.33 mA cm(-2), Voc = 0.74 V and FF = 0.609. More importantly, the conversion efficiency reached 6.91%, which is slightly inferior to the commercial Pt counter electrode (7.44%). Compared to the conventional Pt counter electrodes of solar cells, this new material has the advantages of low-cost, facile synthesis and high efficiency with graphene assistance. To the best of our knowledge, this Bi2S3 + 9 wt% rGO system has the best performance ever recorded in all Bi2S3-based CEs in the DSCs system.
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Protective Effects of Epigallocatechin-3 Gallate on Atrial Electrical and Structural Remodeling in a Rabbit Rapid Atrial Pacing Model.
Cell Biochem. Biophys.
PUBLISHED: 10-15-2014
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Epigallocatechin-3 gallate (EGCG) is the major catechin in green tea. The aim of this study is to investigate the effects of EGCG on atrial electrical and structural remodeling in a rabbit rapid atrial pacing (RAP) model. New Zealand white rabbits were subjected to RAP with or without EGCG treatment. The atrial electrophysiology was studied. ELISA, Western blots, and RT-PCR were performed to determine the level of the inflammation markers, oxidative stress, and fibrogenic agents. Atrial tissue was stained with Masson's trichrome stain for fibrosis detection. RAP rabbits showed a significantly shorter atrial effective refractory period than control rabbits. Higher AF inducibility and longer AF duration were seen in the RAP group. AERP of rabbits received high dose EGCG were prolonged compared to RAP rabbits, and AF inducibility and duration of rabbits received high dose EGCG were lower. RAP rabbits have higher inflammation markers, higher oxidative stress, and more significant fibrosis within atrium, while high dose intervention of EGCG can lower the inflammation, oxidative stress, and fibrosis induced by RAP. Results showed that EGCG have protective effects on atrial electrical and structural remodeling in a rabbit RAP model in terms of attenuating of inflammation and oxidative stress.
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Interferon regulatory factor 7 protects against vascular smooth muscle cell proliferation and neointima formation.
J Am Heart Assoc
PUBLISHED: 10-12-2014
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Interferon regulatory factor 7 (IRF7), a member of the interferon regulatory factor family, plays important roles in innate immunity and immune cell differentiation. However, the role of IRF7 in neointima formation is currently unknown.
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Resolving Fine Structures of the Electric Double Layer of Electrochemical Interfaces in Ionic Liquids with an AFM Tip Modification Strategy.
J. Am. Chem. Soc.
PUBLISHED: 10-10-2014
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We report enhanced force detection selectivity based on Coulombic interactions through AFM tip modification for probing fine structures of the electric double layer (EDL) in ionic liquids. When AFM tips anchored with alkylthiol molecular layers having end groups with different charge states (e.g., -CH3, -COO(-), and -NH3(+)) are employed, Coulombic interactions between the tip and a specified layering structure are intensified or diminished depending on the polarities of the tip and the layering species. Systematic potential-dependent measurements of force curves with careful inspection of layered features and thickness analysis allows the fine structure of the EDL at the Au(111)-OMIPF6 interface to be resolved at the subionic level. The enhanced force detection selectivity provides a basis for thoroughly understanding the EDL in ionic liquids.
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[Inhibitory effect of taurine in hypoxia-induced rat pulmonary artery smooth muscle cell proliferation and signal transduction mechanism].
Zhongguo Zhong Yao Za Zhi
PUBLISHED: 10-07-2014
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To discuss the effect of taurine (Tau) on the proliferation of hypoxia-induced pulmonary artery smooth muscle cells (PASMCs), and study whether the extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathway participated in the Tau-inhibited PASMC proliferation process and the possible molecular mechanism.
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Flush-mounted probe diagnostics for argon glow discharge plasma.
Rev Sci Instrum
PUBLISHED: 10-03-2014
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A comparison is made between plasma parameters measured by a flush-mounted probe (FP) and a cylindrical probe (CP) in argon glow discharge plasma. Parameters compared include the space potential, the plasma density, and the effective electron temperature. It is found that the ion density determined by the FP agrees well with the electron density determined by the CP in the quasi-neutral plasma to better than 10%. Moreover, the space potential and effective electron temperature calculated from electron energy distribution function measured by the FP is consistent with that measured by the CP over the operated discharge current and pressure ranges. These results present the FP can be used as a reliable diagnostic tool in the stable laboratory plasma and also be anticipated to be applied in other complicated plasmas, such as tokamaks, the region of boundary-layer, and so on.
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Risk factors for bunyavirus-associated severe Fever with thrombocytopenia syndrome, china.
PLoS Negl Trop Dis
PUBLISHED: 10-01-2014
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Severe fever with thrombocytopenia syndrome (SFTS) is an emerging disease that is caused by a novel bunyavirus, referred to as SFTS virus. During January 2011 to December 2011 we conducted a case-control study in Henan, Hubei and Shandong Provinces of China to determine the risk factors for SFTS.
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The effect of clopidogrel on pharmacokinetics of ivabradine and its metabolite in rats.
Drug Dev Ind Pharm
PUBLISHED: 09-25-2014
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Abstract The present study aimed to investigate the effect of clopidogrel (CLO) on pharmacokinetics of ivabradine (IVA) and its metabolite in rats and develop a reliable method to determine IVA and its metabolite N-demethyl ivabradine in serum. Healthy male SD rats were randomized to be given 0.8?mg/kg IVA or IVA combined with 8?mg/kg CLO. Blood samples were collected at 0.083, 0.16, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24?h after administration. The serum concentrations of IVA and N-demethyl ivabradine were determined by ultra-performance liquid chromatography-mass spectrometry and pharmacokinetic parameters were calculated using DASver3.0 software. The parameters of AUC(0?-?t), AUC(0?-??), and Cmax for IVA in the group of IVA?+?CLO were significantly higher than those in the group of IVA (p?
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[Adsorption kinetic mechanism of ionic soluble dye mixture on fly ash].
Huan Jing Ke Xue
PUBLISHED: 09-24-2014
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The fly ash from coal combustion was used as adsorbent for the removal of binary mixtures of dyes from aqueous solution. The binary solution included reactive red 23 and one of reactive blue 4, reactive yellow 4, acid black 1 and acid blue 193. The experimental findings show the removal efficiency of reactive red 23 is about 60% -70% while the removal of acid dyes exceeds 90%. The removal value of reactive blue 4 is about 85%, while the value is only 50% for reactive yellow 4. The adsorption kinetic data are good fitted with the pseudo-second-order kinetic model. The external diffusion coefficient solution is in the order of 10(-4) cm x s(-1), while the intraparticle diffusion coefficient is in the order of 10(-8) cm2 x s(1). Because all B(N) numbers are smaller than 100, adsorption of dyes on fly ash is mainly controlled by the external diffusion mechanism.
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Interferon regulatory factor 9 is an essential mediator of heart dysfunction and cell death following myocardial ischemia/reperfusion injury.
Basic Res. Cardiol.
PUBLISHED: 08-24-2014
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This study aimed to investigate whether interferon regulatory factor 9 (IRF9) is involved in the pathogenesis of myocardial ischemia-reperfusion (I/R) injury and to explore the underlying molecular mechanisms of this process. Cell death plays a major role in myocardial I/R injury. We recently determined the importance of IRF9 in coordinating molecular events in response to hypertrophic stress in cardiomyocytes. However, the roles of IRF9 in lethal myocardial injury remain to be elucidated. The involvement of IRF9 was assessed via functional assays in a mouse myocardial I/R injury model by genetic knockout and cardiomyocyte-specific transgenic overexpression of IRF9, and its effects on cardiomyocyte apoptosis and inflammation were further studied in vivo and in vitro. IRF9 was upregulated in human ischemic heart tissue and mouse hearts after I/R injury. Ablation of IRF9 protected the heart against I/R-induced cardiomyocyte death, development of inflammation, and loss of heart function. In contrast, cardiomyocyte-specific transgenic overexpression of IRF9 aggravated myocardial reperfusion injury and inflammation. IRF9 negatively regulated the Sirt1-p53 axis under I/R conditions in vivo and in vitro. Downregulation of Sirt1 expression and its downstream apoptosis-related signaling cascade, which results from I/R, was ameliorated by loss of IRF9 and exacerbated by overexpression of IRF9. Cardiomyocyte-specific deletion of Sirt1 abolished the protective effect of IRF9 knockout against I/R injury, which further indicated that IRF9 mediated myocardial reperfusion injury by modulating the Sirt1-p53 axis. Thus, IRF9 may be a novel therapeutic target for the prevention of I/R injury resulting from revascularization therapy after acute myocardial infarction (MI).
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Interferon Regulatory Factor 9 is a Key Mediator of Hepatic Ischemia/Reperfusion Injury.
J. Hepatol.
PUBLISHED: 08-21-2014
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Hepatic ischemia/reperfusion (I/R) injury is characterised by anoxic cell injury and the generation of inflammatory mediators, leading to hepatic parenchymal cell death. The activation of interferon regulatory factors (IRFs) has been implicated in hepatic I/R injury, but the role of IRF9 in this progression is unclear.
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[Near infrared spectroscopy analysis method of maize hybrid seed purity discrimination].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 08-07-2014
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Near infrared spectroscopy analysis method of discrimination of maize hybrid seed purity was studied with the sample of Nong Hua 101 (NH101) from different origins and years. Spectral acquisition time lasted for 10 months. Using Fourier transform (FT) near infrared spectroscopy instruments, including 23 days in different seasons (divided into five time periods), a total of 920 near infrared diffuse reflectance spectra of single corn grain of those samples were collected. Moving window average, first derivative and vector normalization were used to pretreat all original spectra, principal component analysis (PCA) and linear discriminant analysis (LDA) were applied to reduce data dimensionality, and the discrimination model was established based on biomimetic pattern recognition (BPR) method. Spectral distortion was calibrated by spectra pretreatment, which makes characteristics spatial distribution range of sample spectra set contract. The relative distance between hybrid and female parent increased by nearly 70-fold, and the discrimination model achieved the identification of hybrid and female parent seeds. Through the choice of representative samples, the model's response capacity to the changes in spectral acquisition time, place and environment, etc. was improved. Besides, the model's response capacity to the changes in time and site of seed production was also improved, and the robustness of the model was enhanced. The average correct acceptance rate (CAR) of the test set reached more than 95% while the average correct rejection rate (CRR) of the test set also reached 85%.
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Storage of Gold Nanoclusters in Muscle Leads to their Biphasic in Vivo Clearance.
Small
PUBLISHED: 07-25-2014
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Ultrasmall gold nanoclusters (Au NCs) show great potential in biomedical applications. Long-term biodistribution, retention, toxicity, and pharmacokinetics profiles are pre-requisites in their potential clinical applications. Here, the biodistribution, clearance, and toxicity of one widely used Au NC species-glutathione-protected Au NCs or GSH-Au NCs-are systematically investigated over a relatively long period of 90 days in mice. Most of the Au NCs are cleared at 30 days post injection (p.i.) with a major accumulation in liver and kidney. However, it is surprising that an abnormal increase of the Au amount in the heart, liver, spleen, lung, and testis is observed at 60 and 90 days p.i., indicating that the injected Au NCs form a V-shaped time-dependent distribution profile in various organs. Further investigations reveal that Au NCs are steadily accumulating in the muscle in the first 30 days p.i., and the as-stored Au NCs gradually release into the blood in 30-90 days p.i., which induces a re-distribution and re-accumulation of Au NCs in all blood-rich organs. Further hematology and biochemistry studies show that the re-accumulation of Au NCs still causes some liver toxicity at 30 days p.i. The muscle storage and subsequent release may give rise to the potential accumulation and toxicity risk of functional nanomaterials over long periods of time.
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Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells.
Cell. Signal.
PUBLISHED: 07-21-2014
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Recent studies are indicative for strong carcinogenetic roles of Runt related transcription factor 2 (Runx2) and Yes associated protein (YAP) in several cancer types. However, whether and how the interaction between Runx2 and YAP plays a role in liver tumorigenesis still remain illusive. Here, we identified a close relationship between Runx2 and YAP in liver cancer cells. Runx2 had a positive role on YAP expression and vice versa. We also found that Rux2 and YAP were capable of inhibiting long non-coding RNA (lncRNA), Metallothionein 1D, Pseudogene (MT1DP) expression through direct promoter binding. Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effect, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression. Furthermore, we found that FoxA1 plays a positive role on YAP and Runx2 expression. Specially, opening the compacted chromatin by FoxA1 around CREB binding site within the YAP promoter facilitates CREB-mediated YAP transcription. Finally, MT1DP-inhibited in vivo liver cancer cell growth could be rescued by a combination of overexpression of FoxA1, Runx2 and YAP. Taken together, the close relationship between Rnux2 and YAP plays a pro-carcinogenetic role in liver cancer cells through inhibiting tumor suppressor lncRNA, MT1DP in a FoxA1 dependent manner.
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[Correlation research on the MRI quantity of lumbar modic changes and low back pain].
Zhongguo Gu Shang
PUBLISHED: 07-01-2014
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To analyzed the relationship between lumbar endplate Modic area changes rate and low back pain by measuring MRI T2 sagittal image of lumbar endplate Modic area changes rate.
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A recurrent deletion mutation in OPA1 causes autosomal dominant optic atrophy in a Chinese family.
Sci Rep
PUBLISHED: 06-16-2014
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Autosomal dominant optic atrophy (ADOA) is the most frequent form of hereditary optic neuropathy and occurs due to the degeneration of the retinal ganglion cells. To identify the genetic defect in a family with putative ADOA, we performed capture next generation sequencing (CNGS) to screen known retinal disease genes. However, six exons failed to be sequenced by CNGS in optic atrophy 1 gene (OPA1). Sequencing of those exons identified a 4?bp deletion mutation (c.2983-1_2985del) in OPA1. Furthermore, we sequenced the transcripts of OPA1 from the patient skin fibroblasts and found there is six-nucleotide deletion (c.2984-c.2989, AGAAAG). Quantitative-PCR and Western blotting showed that OPA1 mRNA and its protein expression have no obvious difference between patient skin fibroblast and control. The analysis of protein structure by molecular modeling suggests that the mutation may change the structure of OPA1 by formation of an alpha helix protruding into an existing pocket. Taken together, we identified an OPA1 mutation in a family with ADOA by filling the missing CNGS data. We also showed that this mutation affects the structural intactness of OPA1. It provides molecular insights for clinical genetic diagnosis and treatment of optic atrophy.
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Interferon regulatory factor 9 is critical for neointima formation following vascular injury.
Nat Commun
PUBLISHED: 06-02-2014
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Interferon regulatory factor 9 (IRF9) has various biological functions and regulates cell survival; however, its role in vascular biology has not been explored. Here we demonstrate a critical role for IRF9 in mediating neointima formation following vascular injury. Notably, in mice, IRF9 ablation inhibits the proliferation and migration of vascular smooth muscle cells (VSMCs) and attenuates intimal thickening in response to injury, whereas IRF9 gain-of-function promotes VSMC proliferation and migration, which aggravates arterial narrowing. Mechanistically, we show that the transcription of the neointima formation modulator SIRT1 is directly inhibited by IRF9. Importantly, genetic manipulation of SIRT1 in smooth muscle cells or pharmacological modulation of SIRT1 activity largely reverses the neointima-forming effect of IRF9. Together, our findings suggest that IRF9 is a vascular injury-response molecule that promotes VSMC proliferation and implicate a hitherto unrecognized 'IRF9-SIRT1 axis' in vasculoproliferative pathology modulation.
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Catalytic Oxidation of Biorefinery Lignin to Value-added Chemicals to Support Sustainable Biofuel Production.
ChemSusChem
PUBLISHED: 06-02-2014
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Transforming plant biomass to biofuel is one of the few solutions that can truly sustain mankind's long-term needs for liquid transportation fuel with minimized environmental impact. However, despite decades of effort, commercial development of biomass-to-biofuel conversion processes is still not an economically viable proposition. Identifying value-added co-products along with the production of biofuel provides a key solution to overcoming this economic barrier. Lignin is the second most abundant component next to cellulose in almost all plant biomass; the emerging biomass refinery industry will inevitably generate an enormous amount of lignin. Development of selective biorefinery lignin-to-bioproducts conversion processes will play a pivotal role in significantly improving the economic feasibility and sustainability of biofuel production from renewable biomass. The urgency and importance of this endeavor has been increasingly recognized in the last few years. This paper reviews state-of-the-art oxidative lignin depolymerization chemistries employed in the papermaking process and oxidative catalysts that can be applied to biorefinery lignin to produce platform chemicals including phenolic compounds, dicarboxylic acids, and quinones in high selectivity and yield. The potential synergies of integrating new catalysts with commercial delignification chemistries are discussed. We hope the information will build on the existing body of knowledge to provide new insights towards developing practical and commercially viable lignin conversion technologies, enabling sustainable biofuel production from lignocellulosic biomass to be competitive with fossil fuel.
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Genetic, cellular, and functional evidence for Ca2+ inflow through Cav1.2 and Cav1.3 channels in murine spiral ganglion neurons.
J. Neurosci.
PUBLISHED: 05-23-2014
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Spiral ganglion neurons (SGNs) of the eighth nerve serve as the bridge between hair cells and the cochlear nucleus. Hair cells use Cav1.3 as the primary channel for Ca(2+) inflow to mediate transmitter release. In contrast, SGNs are equipped with multiple Ca(2+) channels to mediate Ca(2+)-dependent functions. We examined directly the role of Cav1.3 channels in SGNs using Cav1.3-deficient mice (Cav1.3(-/-)). We revealed a surprising finding that SGNs functionally express the cardiac-specific Cav1.2, as well as neuronal Cav1.3 channels. We show that evoked action potentials recorded from SGNs show a significant decrease in the frequency of firing in Cav1.3(-/-) mice compared with wild-type (Cav1.3(+/+)) littermates. Although Cav1.3 is the designated L-type channel in neurons, whole-cell currents recorded in isolated SGNs from Cav1.3(-/-) mice showed a surprising remnant current with sensitivity toward the dihydropyridine (DHP) agonist and antagonist, and a depolarization shift in the voltage-dependent activation compared with that in the Cav1.3(+/+) mice. Indeed, direct measurement of the elementary properties of Ca(2+) channels, in Cav1.3(+/+) neurons, confirmed the existence of two DHP-sensitive single-channel currents, with distinct open probabilities and conductances. We demonstrate that the DHP-sensitive current in Cav1.3(-/-) mice is derived from Cav1.2 channel activity, providing for the first time, to our knowledge, functional data for the expression of Cav1.2 currents in neurons. Finally, using shRNA gene knockdown methodology, and histological analyses of SGNs from Cav1.2(+/-) and Cav1.3(+/-) mice, we were able to establish the differential roles of Cav1.2 and Cav1.3 in SGNs.
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Inhibitory effects of 3-bromopyruvate on human gastric cancer implant tumors in nude mice.
Asian Pac. J. Cancer Prev.
PUBLISHED: 05-13-2014
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Gastric cancer is a common malignant tumor. Our previous study demonstrated inhibitory effects of 3-bromopyruvate (3-BrPA) on pleural mesothelioma. Moreover, we found that 3-BrPA could inhibit human gastric cancer cell line SGC-7901 proliferation in vitro, but whether similar effects might be exerted in vivo have remained unclear.
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[Study on the polarized reflectance characteristics of single greenhouse tomato nutrient deficiency leaves].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 05-03-2014
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In order to improve accuracy of quantitative analysis model for the greenhouse tomato nitrogen, phosphorus and potassium nutrient stress, and explore the advantages of polarization non-destructive detection in single-leaf plants scale, polarized reflectance characteristics of greenhouse nutrient deficiency tomato leaves in different growing seasons and different deficiency extents were both examined via means of polarized reflectance spectroscopy system, which was self-developed by the research group. The main factors with effects on the polarized reflectance characteristics of tomato leaves were discussed, such as incident zenith angle, azimuth angle, detection zenith angle, light source polarizer degree, and detector polarizer degree. Experiments were carried out to verify the optimum level of above five parameters by means of range analysis of orthogonal experiments, through that way we can know the best angle combination of five parameters. Based on the above analysis, the angle combination and sorting of detecting tomato nutrients deficiency leaves via means of polarization spectroscopy system were obtained as follows: incident zenith angle 60 degrees, light source polarizer degree 0 degrees, detection zenith angle 45 degrees, detector polarizer degree 45 degrees and azimuth angle 180 degrees. At the same time, both the spectra of nitrogen, phosphorus and potassium deficiency leaves in different growth stages and different deficiency extent leaves were compared with each other. Results show that there is a positive correlation between the greenhouse nutrient deficiency tomato leaves growth cycle and tomato leaves polarized reflectance spectra. Nutrient excess or nutrient deficiency can both lead to polarized reflectance decline and polarized reflectance decline extent of greenhouse tomato leaves is more obvious during the fruiting and harvest period. This paper has a certain theoretical and practical significance in the research on nutrition rapid detection on the plant single leaf scale by means of polarized reflectance spectrum.
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Hepatitis B virus X protein accelerates the development of hepatoma.
Cancer Biol Med
PUBLISHED: 04-18-2014
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The chronic infection of hepatitis B virus (HBV) is closely related to the occurrence and development of hepatocellular carcinoma (HCC). Accumulated evidence has shown that HBV X protein (HBx protein) is a multifunctional regulator with a crucial role in hepatocarcinogenesis. However, information on the mechanism by which HBV induces HCC is lacking. This review focuses on the pathological functions of HBx in HBV-induced hepatocarcinogenesis. As a transactivator, HBx can modulate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) and transcription factor AP-2. Moreover, HBx can affect regulatory non-coding RNAs (ncRNAs) including microRNAs and long ncRNAs (lncRNAs), such as miRNA-205 and highly upregulated in liver cancer (HULC), respectively. HBx is also involved in epigenetic modification, including methylation and acetylation. HBx interacts with various signal-transduction pathways, such as protein kinase B/Akt, Wnt/?-catenin, signal transducer and activator of transcription, and NF-?B pathways. Moreover, HBx affects cellular fate by shifting the balance toward cell survival. HBx may lead to the loss of apoptotic functions or directly contributes to oncogenesis by achieving transforming functions, which induce hepatocarcinogenesis. Additionally, HBx can modulate apoptosis and immune response by direct or indirect interaction with host factors. We conclude that HBx hastens the development of hepatoma.
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Long-term follow-up of sigmoid bladder augmentation for low-compliance neurogenic bladder.
Urology
PUBLISHED: 04-17-2014
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To assess the clinical and urodynamic outcomes of patients with low-compliance neurogenic bladder who were treated with sigmoid bladder augmentation (SBA) over a long-term follow-up.
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Interferon regulatory factor 1 is required for cardiac remodeling in response to pressure overload.
Hypertension
PUBLISHED: 04-14-2014
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Interferon regulatory factor 1 (IRF1), a critical member of the IRF family, was previously shown to be associated with the immune system and to be involved in apoptosis and tumor suppression. However, the role of IRF1 in pressure overload-induced cardiac remodeling has remained unclear. Using genetic approaches, we established a central role for the IRF1 transcription factor in the regulation of cardiac remodeling both in vivo and in vitro, and we determined the mechanism underlying this process. The expression level of IRF1 was remarkably altered in both failing human hearts and hypertrophic murine hearts. Transgenic mice with cardiac-specific IRF1 overexpression exacerbated aortic banding-induced cardiac hypertrophy, ventricular dilation, fibrosis, and dysfunction, whereas IRF1-deficient (knockout) mice exhibited a significant reduction in the hypertrophic response. Similar results were observed in a global IRF1-knockout rat model. Mechanistically, the prohypertrophic effects elicited by IRF1 in response to pathological stimuli were associated with the direct activation of inducible nitric oxide synthase (iNOS). Furthermore, we identified 1 IRF1-binding site in the promoter region of the iNOS gene, which was essential for its transcription. To examine the IRF1-iNOS axis in vivo, we generated IRF1-transgenic/iNOS-knockout mice. IRF1 exerted profoundly detrimental effects in these mice; however, these effects were nullified by iNOS ablation. These data suggest the IRF1-iNOS axis as a crucial regulator of cardiac remodeling and that IRF1 could be a potent therapeutic target for cardiac remodeling.
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cDNA cloning and localization of Sp3111 (also called Ms4a14) in the rat testis.
Reproduction
PUBLISHED: 04-02-2014
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With tetraspanning topology, members of the membrane-spanning four-domain subfamily A (MS4A) may facilitate signaling or ion channel functions in many tissues. In this study, we report the cloning of a full-length cDNA from rat testis, designated Ms4a14 (Sp3111), which encodes the MS4A protein with 1139 amino acid residues. In situ hybridization and immunohistochemical analyses indicate that Ms4a14 is predominantly expressed from round spermatids to spermatozoa at specific stages in the rat testis at both the mRNA and protein level. Immunofluorescence analysis revealed that MS4A14 (SP3111) is located in the acrosome and the midpiece of the flagellum in mature sperm. Previously, we explored and reported the involvement of MS4A14 in reproductive functions, using antibody blockage during IVF and a transgenic RNA interference method in a mouse model. Our results suggested that MS4A14 is involved in fertilization and zygote division. As MS4A14 protein exists in mammals, such as humans, cows, dogs, and rodents, MS4A14 may play a ubiquitous role in mammalian reproduction.
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Bladder neck incision for female bladder neck obstruction: long-term outcomes.
Urology
PUBLISHED: 04-01-2014
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To evaluate the long-term outcomes of bladder neck incision (BNI) for primary bladder neck obstruction in women.
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UbcH10 overexpression increases carcinogenesis and blocks ALLN susceptibility in colorectal cancer.
Sci Rep
PUBLISHED: 03-28-2014
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Cyclins are essential for cell proliferation, the cell cycle and tumorigenesis in all eukaryotes. UbcH10 regulates the degradation of cyclins in a ubiquitin-dependent manner. Here, we report that UbcH10 is likely involved in tumorigenesis. We found that cancer cells exposed to n-acetyl-leu-leu-norleucinal (ALLN) treatment and UbcH10 depletion exhibit a synergistic therapeutic effect. Abundant expression of UbcH10 drives resistance to ALLN-induced cell death, while cells deficient in UbcH10 were susceptible to ALLN-induced cell death. The depletion of UbcH10 hindered tumorigenesis both in vitro and in vivo, as assessed by colony formation, growth curve, soft agar and xenograft assays. These phenotypes were efficiently rescued through the introduction of recombinant UbcH10. In the UbcH10-deficient cells, alterations in the expression of cyclins led to cell cycle changes and subsequently decreases in tumorigenesis. The tumorigenesis of xenograft tumors from UbcH10-deficient cells treated with ALLN was decreased relative to wild-type cells treated with ALLN in nude mice. On the molecular level, we observed that UbcH10 deficiency enhances the activation of caspase 8 and caspase 3 but not caspase 9 to impair cell viability upon ALLN treatment. Collectively, our results suggest that, as an oncogene, UbcH10 is a potential drug target for the treatment of colorectal cancer.
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MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3'UTR.
Acta Pharmacol. Sin.
PUBLISHED: 03-24-2014
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MiR-506 is a miRNA involved in carcinogenesis of several kinds of cancer. In this study, we explored whether miR-506 played a critical role in hepatocellular carcinoma (HCC).
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Down-regulated aquaporin 5 inhibits proliferation and migration of human epithelial ovarian cancer 3AO cells.
J Ovarian Res
PUBLISHED: 03-04-2014
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Recent studies suggested that aquaporins 5 (AQP5) was associated with many kinds of cancers and regulated many processes of various kinds of cancer cells. Our previous studies also demonstrated that AQP5 was highly expressed in epithelial ovarian cancer and contributed to the progress of ovarian cancer.
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Interferon regulatory factor 3 protects against adverse neo-intima formation.
Cardiovasc. Res.
PUBLISHED: 03-04-2014
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Vascular smooth muscle cell (VSMC) proliferation is central to the pathophysiology of neo-intima formation. Interferon regulatory factor 3 (IRF3) inhibits the growth of cancer cells and fibroblasts. However, the role of IRF3 in vascular neo-intima formation is unknown. We evaluated the protective role of IRF3 against neo-intima formation in mice and the underlying mechanisms.
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Air pollution exposure and lung function in highly exposed subjects in Beijing, China: a repeated-measure study.
Part Fibre Toxicol
PUBLISHED: 03-03-2014
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BackgroundExposure to ambient particulate matter (PM) has been associated with reduced lung function. Elemental components of PM have been suggested to have critical roles in PM toxicity, but their contribution to respiratory effects remains under-investigated. We evaluated the effects of traffic-related PM2.5 and its elemental components on lung function in two highly exposed groups of healthy adults in Beijing, China.MethodsThe Beijing Truck-Driver Air Pollution Study (BTDAS) included 60 truck drivers and 60 office workers evaluated in 2008. On two days separated by 1-2 weeks, we measured lung function at the end of the work day, personal PM2.5, and nine elemental components of PM2.5 during eight hours of work, i.e., elemental carbon (EC), potassium (K), sulfur (S), iron (Fe), silicon (Si), aluminum (Al), zinc (Zn), calcium (Ca), and titanium (Ti). We used covariate-adjusted mixed-effects models including PM2.5 as a covariate to estimate the percentage change in lung function associated with an inter-quartile range (IQR) exposure increase.ResultsThe two groups had high and overlapping exposure distributions with mean personal PM2.5 of 94.6 ¿g/m3 (IQR: 48.5-126.6) in office workers and 126.8 ¿g/m3 (IQR: 73.9-160.5) in truck drivers. The distributions of the nine elements showed group-specific profiles and generally higher levels in truck drivers. In all subjects combined, forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) did not significantly correlate with PM2.5. However, FEV1 showed negative association with concentrations of four elements: Si (-3.07%, 95%CI: -5.00; -1.11, IQR: 1.54), Al (-2.88%, 95%CI: -4.91; -0.81, IQR: 0.86), Ca (-1.86%, 95%CI: -2.95; -0.76, IQR: 1.33), and Ti (-2.58%, 95%CI: -4.44; -0.68, IQR: 0.03), and FVC showed negative association with concentrations of three elements: Si (-3.23%, 95%CI: -5.61; -0.79), Al (-3.26%, 95%CI: -5.73; -0.72), and Ca (-1.86%, 95%CI: -3.23; -0.47). In stratified analysis, Si, Al, Ca, and Ti showed associations with lung function only among truck drivers, and no significant association among office workersConclusionSelected elemental components of PM2.5 showed effects on lung function that were not found in analyses of particle levels alone.
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Nemo-like kinase (NLK) negatively regulates NF-kappa B activity through disrupting the interaction of TAK1 with IKK?.
Biochim. Biophys. Acta
PUBLISHED: 03-02-2014
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Stringent negative regulation of the transcription factor NF-?B is essential for maintaining cellular stress responses and homeostasis. However, the tight regulation mechanisms of IKK? are still not clear. Here, we reported that nemo-like kinase (NLK) is a suppressor of tumor necrosis factor (TNF?)-induced NF-?B signaling by inhibiting the phosphorylation of IKK?. Overexpression of NLK largely blocked TNF?-induced NF-?B activation, p65 nuclear localization and I?B? degradation; whereas genetic inactivation of NLK showed opposing results. Mechanistically, we identified that NLK interacted with I?B kinase (IKK)-associated complex, which in turn inhibited the assembly of the TAK1/IKK? and thereby, diminished the I?B kinase phosphorylation. Our results indicate that NLK functions as a pivotal negative regulator in TNF?-induced activation of NF-?B via disrupting the interaction of TAK1 with IKK?.
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Ultrasmall Au(10-12)(SG)(10-12) nanomolecules for high tumor specificity and cancer radiotherapy.
Adv. Mater. Weinheim
PUBLISHED: 02-24-2014
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Radiosensitizers can increase local treatment efficacy under a relatively low and safe radiation dose, thereby facilitating tumor eradication and minimizing side effects. Here, a new class of radiosensitizers is reported, which contain several gold (Au) atoms embedded inside a peptide shell (e.g., Au10-12 (SG)10-12 ) and can achieve ultrahigh tumor uptake (10.86 SUV at 24 h post injection) and targeting specificity, efficient renal clearance, and high radiotherapy enhancement.
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Interferon regulatory factor 8 protects against cerebral ischaemic-reperfusion injury.
J. Neurochem.
PUBLISHED: 02-07-2014
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Interferon regulatory factor 8 (IRF8), a transcriptional regulator in the IRF family, has been implicated in innate immunity, immune cell differentiation and tumour cell apoptosis. In the present study, we found that IRF8 is constitutively expressed in the brain and suppressed after cerebral ischaemia in a time-dependent manner. IRF8 knockout (IRF8-KO) mice, wild type (WT) mice, neuron-specific IRF8 transgenic (TG) mice and non-transgenic mice were used in a transient cerebral ischaemic model. The IRF8 knockout mice exhibited aggravated apoptosis, inflammation and oxidative injury in the ischaemic brain, eventually leading to poorer stroke outcomes, whereas neuron-specific IRF8 transgenic mice showed a marked inhibition of apoptosis and improved stroke outcomes. To model ischaemia/reperfusion conditions in vitro, primary cortical neurons were cultured and subjected to transient oxygen and glucose deprivation for 60 min. Similar to the in vivo study, IRF8 knockdown by Ad-shIRF8 resulted in increased apoptosis, whereas IRF8 over-expression by Ad-IRF8 significantly decreased neuronal apoptosis. These data indicate that IRF8 is strongly protective in ischaemic stroke by regulating neuronal apoptosis, the inflammatory response and oxidative stress. In the present study, we found that the transcriptional factor IRF8 plays a protective role in the cerebral ischaemic-reperfusion injury by attenuating neuronal apoptosis, oxidative stress and inflammation. Besides the known function of IRF8 in regulating the inflammatory gene expression, we first demonstrated that IRF8 can directly modulate apoptosis and oxidative stress by controlling the relative genes expression.
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Optimal rhythm-control strategy for recurrent atrial tachycardia after catheter ablation of persistent atrial fibrillation: a randomized clinical trial.
Eur. Heart J.
PUBLISHED: 02-03-2014
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Although catheter ablation (CA) has replaced antiarrhythmic drugs (AAD) as first-line treatment in selected patients with atrial fibrillation (AF), optimal treatment of recurrent atrial tachycardia (AT) after AF ablation remains unclear. This parallel randomized controlled study compared CA vs. AAD for recurrent AT after persistent AF ablation.
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Multimodality magnetic resonance imaging in hepatic encephalopathy: an update.
World J. Gastroenterol.
PUBLISHED: 01-29-2014
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Hepatic encephalopathy (HE) is a neuropsychiatric complication of cirrhosis or acute liver failure. Currently, HE is regarded as a continuous cognitive impairment ranging from the mildest stage, minimal HE to overt HE. Hyperammonaemia and neuroinflammation are two main underlying factors which contribute to the neurological alterations in HE. Both structural and functional impairments are found in the white mater and grey mater involved in HE. Although the investigations into HE pathophysiological mechanism are enormous, the exact pathophysiological causes underlying HE remain controversial. Multimodality magnetic resonance imaging (MRI) plays an important role in helping to understand the pathological process of HE. This paper reviews the up-to-date multimodality MRI methods and predominant findings in HE patients with a highlight of the increasingly important role of blood oxygen level dependent functional MRI.
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Ginsenoside Rb1 improves energy metabolism in the skeletal muscle of an animal model of postoperative fatigue syndrome.
J. Surg. Res.
PUBLISHED: 01-28-2014
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Postoperative fatigue syndrome (POFS) is a common clinical complication followed by almost every major abdominal surgery. Ginsenoside Rb1 (GRb1), a principle ginsenoside in ginseng, could exert a potent anti-fatigue effect on POFS. However, the mechanism is still unknown. Previous studies revealed that alterations in the energy metabolism in the skeletal muscle may play a vital role in the development and progression of fatigue. In the present study, we investigate the effect of GRb1 on energy metabolism in the skeletal muscle of a rat model of POFS induced by major small intestinal resection.
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IRF8 suppresses pathological cardiac remodelling by inhibiting calcineurin signalling.
Nat Commun
PUBLISHED: 01-23-2014
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Interferon regulatory factor 8 (IRF8) is known to affect the innate immune response, for example, by regulating the differentiation and function of immune cells. However, whether IRF8 can influence cardiac hypertrophy is unknown. Here we show that IRF8 levels are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts. Mice overexpressing Irf8 specifically in the heart are resistant to aortic banding (AB)-induced cardiac hypertrophy, whereas mice lacking IRF8 either globally or specifically in cardiomyocytes develop an aggravated phenotype induced by pressure overload. Mechanistically, we show that IRF8 directly interacts with NFATc1 to prevent NFATc1 translocation and thus inhibits the hypertrophic response. Inhibition of NFATc1 ameliorates the cardiac abnormalities in IRF8(-/-) mice after AB. In contrast, constitutive activation of NFATc1 nullifies the protective effects of IRF8 on cardiac hypertrophy in IRF8-overexpressing mice. Our results indicate that IRF8 is a potential therapeutic target in pathological cardiac hypertrophy.
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TRIM38 inhibits TNF?- and IL-1?-triggered NF-?B activation by mediating lysosome-dependent degradation of TAB2/3.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 01-13-2014
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TNF? and IL-1? are two proinflammatory cytokines that play critical roles in many diseases, including rheumatoid arthritis and infectious diseases. How TNF?- and IL-1?-mediated signaling is finely tuned is not fully elucidated. Here, we identify tripartite-motif protein 38 (TRIM38) as a critical negative regulator of TNF?- and IL-1?-triggered signaling. Overexpression of TRIM38 inhibited activation of NF-?B and induction of downstream cytokines following TNF? and IL-1? stimulation, whereas knockdown or knockout of TRIM38 had the opposite effects. TRIM38 constitutively interacted with critical components TGF-?-activated kinase 1 (TAK1)-binding protein 2/3 (TAB2/3) and promoted lysosome-dependent degradation of TAB2/3 independent of its E3 ubiquitin ligase activity. Consistently, deficiency of TRIM38 resulted in abolished translocation of TAB2 to the lysosome, increased level of TAB2 in cells, and enhanced activation of TAK1 after TNF? and IL-1? stimulation. We conclude that TRIM38 negatively regulates TNF?- and IL-1?-induced signaling by mediating lysosome-dependent degradation of TAB2/3, two critical components in TNF?- and IL-1?-induced signaling pathways. Our findings reveal a previously undiscovered mechanism by which cells keep the inflammatory response in check to avoid excessive harmful immune response triggered by TNF? and IL-1?.
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Dickkopf-3 attenuates pressure overload-induced cardiac remodelling.
Cardiovasc. Res.
PUBLISHED: 01-09-2014
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Dickkopf-3 (DKK3), a secreted protein in the Dickkopf family, is expressed in various tissues, including the heart, and has been shown to play an important role in tissue development. However, the biological function of DKK3 in the heart remains largely unexplored. This study aimed to examine the role of DKK3 in pathological cardiac hypertrophy.
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Interferon regulatory factor 7 functions as a novel negative regulator of pathological cardiac hypertrophy.
Hypertension
PUBLISHED: 01-06-2014
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Cardiac hypertrophy is a complex pathological process that involves multiple factors including inflammation and apoptosis. Interferon regulatory factor 7 (IRF7) is a multifunctional regulator that participates in immune regulation, cell differentiation, apoptosis, and oncogenesis. However, the role of IRF7 in cardiac hypertrophy remains unclear. We performed aortic banding in cardiac-specific IRF7 transgenic mice, IRF7 knockout mice, and the wild-type littermates of these mice. Our results demonstrated that IRF7 was downregulated in aortic banding-induced animal hearts and cardiomyocytes that had been treated with angiotensin II or phenylephrine for 48 hours. Accordingly, heart-specific overexpression of IRF7 significantly attenuated pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction, whereas loss of IRF7 led to opposite effects. Moreover, IRF7 protected against angiotensin II-induced cardiomyocyte hypertrophy in vitro. Mechanistically, we identified that IRF7-dependent cardioprotection was mediated through IRF7 binding to inhibitor of ?B kinase-?, and subsequent nuclear factor-?B inactivation. In fact, blocking nuclear factor-?B signaling with cardiac-specific inhibitors of ?B?(S32A/S36A) super-repressor transgene counteracted the adverse effect of IRF7 deficiency. Conversely, activation of nuclear factor-?B signaling via a cardiac-specific conditional inhibitor of ?B kinase-?(S177E/S181E) (constitutively active) transgene negated the antihypertrophic effect of IRF7 overexpression. Our data demonstrate that IRF7 acts as a novel negative regulator of pathological cardiac hypertrophy by inhibiting nuclear factor-?B signaling and may constitute a potential therapeutic target for pathological cardiac hypertrophy.
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Development and validation of the pre-hospital stroke symptoms coping test.
PLoS ONE
PUBLISHED: 01-01-2014
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Measures of specific knowledge of coping with pre-hospital stroke symptoms can help educate high-risk patients and family caregivers. This study aimed to develop and validate the Pre-hospital Stroke Symptoms Coping Test (PSSCT).
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Passing through the renal clearance barrier: toward ultrasmall sizes with stable ligands for potential clinical applications.
Int J Nanomedicine
PUBLISHED: 01-01-2014
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The use of nanoparticles holds promise for medical applications, such as X-ray imaging, photothermal therapy and radiotherapy. However, the in vivo toxicity of inorganic nanoparticles raises some concern regarding undesirable side effects which prevent their further medical application. Ultrasmall sub-5.5 nm particles can pass through the barrier for renal clearance, minimizing their toxicity. In this letter we address some recent interesting work regarding in vivo toxicity and renal clearance, and discuss the possible strategy of utilizing ultrasmall nanomaterials. We propose that small hydrodynamic sized nanoclusters can achieve both nontoxic and therapeutic clinical features.
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Toll-interacting protein (Tollip) negatively regulates pressure overload-induced ventricular hypertrophy in mice.
Cardiovasc. Res.
PUBLISHED: 11-26-2013
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Toll-interacting protein (Tollip) is a critical regulator of the Toll-like receptor-mediated signalling pathway. However, the role of Tollip in chronic pressure overload-induced cardiac hypertrophy remains unclear. This study aimed to determine the functional significance of Tollip in the regulation of aortic banding-induced cardiac remodelling and its underlying mechanisms.
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Critical roles of a small conductance Ca2+-activated K+ channel (SK3) in the repolarization process of atrial myocytes.
Cardiovasc. Res.
PUBLISHED: 11-26-2013
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Small conductance Ca(2+)-activated K(+) channels (KCa2 or SK channels) have been reported in excitable cells, where they aid in integrating changes in intracellular Ca(2+) () with membrane potentials. We have recently reported the functional expression of SK channels in human and mouse cardiac myocytes. Additionally, we have found that the channel is highly expressed in atria compared with the ventricular myocytes. We demonstrated that human cardiac myocytes expressed all three members of SK channels (SK1, 2, and 3); moreover, the different members are capable of forming heteromultimers. Here, we directly tested the contribution of SK3 to the overall repolarization of atrial action potentials.
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Interferon Regulatory Factor 8 Modulates Phenotypic Switching of Smooth Muscle Cells through Regulating the Activity of Myocardin.
Mol. Cell. Biol.
PUBLISHED: 11-18-2013
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Interferon regulatory factor 8 (IRF8), a member of IRF transcription factor family, was recently implicated in vascular diseases. In the present study, using the mouse left carotid artery wire injury model, we unexpectedly observed that the expression of IRF8 was greatly enhanced in SMCs by injury. Compared with wild-type controls, IRF8 global knockout mice exhibited reduced neointimal lesions and maintained SMC-marker gene expression. We further generated SMC-specific IRF8 transgenic mice using an SM22?-driven IRF8 plasmid construct. In contrast to the knockout mice, the SMCs-overexpressing IRF8 exhibited a synthetic phenotype and enhanced neointima formation in the mice. Mechanistically, IRF8 inhibited SMC-marker gene expression through regulating serum response factor (SRF) transactivation in a myocardin-dependent manner. Furthermore, co-immunoprecipitation assay indicated a direct interaction of IRF8 with myocardin, in which a specific region of myocardin was essential for recruiting acetyltransferase p300. Altogether, IRF8 is crucial in modulating SMC phenotype switching and neointima formation in response to vascular injury via direct interaction with SRF/myocardin complex.
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Interferon regulatory factor 9 protects against cardiac hypertrophy by targeting myocardin.
Hypertension
PUBLISHED: 10-21-2013
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Pathological cardiac hypertrophy is a major risk factor for heart failure. In this study, we identified interferon regulatory factor 9 (IRF9), a member of the IRF family, as a previously unidentified negative regulator of cardiac hypertrophy. The level of IRF9 expression was remarkably elevated in the hearts from animals with aortic banding-induced cardiac hypertrophy. IRF9-deficient mice exhibited pronounced cardiac hypertrophy after pressure overload, as demonstrated by increased cardiomyocyte size, extensive fibrosis, reduced cardiac function, and enhanced expression of hypertrophy markers, whereas transgenic mice with cardiac-specific overexpression of murine IRF9 exhibited a significant reduction in the hypertrophic response. Mechanistically, IRF9 competes with p300 for binding to the transcription activation domain of myocardin, a coactivator of serum response factor (SRF). This interaction markedly suppresses the transcriptional activity of myocardin because IRF9 overexpression strongly inhibits the ability of myocardin to activate CArG box-dependent reporters. These results provide compelling evidence that IRF9 inhibits the development of cardiac hypertrophy by suppressing the transcriptional activity of myocardin in the heart.
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Signal Regulatory Protein-? Protects Against Cardiac Hypertrophy Via the Disruption of Toll-Like Receptor 4 Signaling.
Hypertension
PUBLISHED: 10-07-2013
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Signal regulatory protein-? (SIRPA/SIRP?) is a transmembrane protein that is expressed in various tissues, including the heart. Previous studies have demonstrated that SIRPA is involved in multiple biological processes, including macrophage multinucleation, skeletal muscle differentiation, neuronal survival, protection against diabetes mellitus, and negative regulation of immune cells. However, the role of SIRPA in cardiac hypertrophy remains unknown. To examine the role of SIRPA in pathological cardiac hypertrophy, we used SIRPA knockout mice and transgenic mice that overexpressed mouse SIRPA in the heart. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. We observed downregulation of SIRPA expression in dilated cardiomyopathy human hearts and in animal hearts after aortic banding surgery. Accordingly, SIRPA(-/-) mice displayed augmented cardiac hypertrophy, which was accompanied by increased cardiac fibrosis and reduced contractile function, as compared with SIRPA(+/+) mice 4 weeks after aortic banding. In contrast, transgenic mice with the cardiac-specific SIRPA overexpression exhibited the opposite phenotype in response to pressure overload. Likewise, SIRPA protected against angiotensin II-induced cardiomyocyte hypertrophy in vitro. Mechanistically, we revealed that SIRPA-mediated protection during cardiac hypertrophy involved inhibition of the Toll-like receptor 4/nuclear factor-?B signaling axis. Furthermore, we demonstrated that the disruption of Toll-like receptor 4 rescued the adverse effects of SIRPA deficiency on pressure overload-triggered cardiac remodeling. Thus, our results identify that SIRPA plays a protective role in cardiac hypertrophy through negative regulation of the Toll-like receptor 4/nuclear factor-?B pathway.
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[Application of rational ant colony optimization to improve the reproducibility degree of laser three-dimensional copy].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 09-25-2013
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Three-dimensional (3D) copying of artificial ears and pistol printing are pushing laser three-dimensional copying technique to a new page. Laser three-dimensional scanning is a fresh field in laser application, and plays an irreplaceable part in three-dimensional copying. Its accuracy is the highest among all present copying techniques. Reproducibility degree marks the agreement of copied object with the original object on geometry, being the most important index property in laser three-dimensional copying technique. In the present paper, the error of laser three-dimensional copying was analyzed. The conclusion is that the data processing to the point cloud of laser scanning is the key technique to reduce the error and increase the reproducibility degree. The main innovation of this paper is as follows. On the basis of traditional ant colony optimization, rational ant colony optimization algorithm proposed by the author was applied to the laser three-dimensional copying as a new algorithm, and was put into practice. Compared with customary algorithm, rational ant colony optimization algorithm shows distinct advantages in data processing of laser three-dimensional copying, reducing the error and increasing the reproducibility degree of the copy.
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Expression and genomic imprinting of the porcine Rasgrf1 gene.
Gene
PUBLISHED: 08-28-2013
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Imprinted genes play important roles in mammalian growth, development and behavior. The Rasgrf1 (Ras protein-specific guanine nucleotide exchange factor 1) gene has been identified as an imprinted gene in mouse and rat. In the present study, we detected its sequence, imprinting status and expression pattern in the domestic pigs. A 228bp partial sequence located in exon 14 and a 193bp partial sequence located in exon 1 of the Rasgrf1 gene in domestic pigs were obtained. A G/A transition, was identified in Rasgrf1 exon 14, and then, the reciprocal Berkshire×Wannan black F1 hybrid model and the RT-PCR-RFLP method were used to detect the imprinting status of porcine Rasgrf1 gene at the developmental stage of 1-day-old. The expression profile results indicated that the porcine Rasgrf1 mRNA was highly expressed in brain, pituitary and pancreas, followed by kidney, stomach, lung, testis, small intestine, ovary, spleen and liver, and at low levels of expression in longissimus dorsi, heart, and backfat. The expression levels of Rasgrf1 gene in brain, pituitary and pancreas tissues were significantly different between the two reciprocal F1 hybrids. Imprinting analysis showed that porcine Rasgrf1 gene was maternally expressed in the liver, small intestine, paternally expressed in the lung, but biallelically expressed in brain, heart, spleen, kidney, stomach, pancreas, backfat, testis, ovary, longissimus dorsi and pituitary tissues.
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Slc26a6 functions as an electrogenic Cl-/HCO3- exchanger in cardiac myocytes.
Cardiovasc. Res.
PUBLISHED: 08-09-2013
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Alterations in cardiac acid-base balance can produce profound impact on excitation-contraction coupling and precipitate cardiac dysfunction and arrhythmias. A member of the solute carrier (SLC) family, Slc26a6, has been shown to be a chloride-hydroxyl exchanger and the predominant chloride-bicarbonate exchanger in the mouse heart. However, the exact isoforms and functional characteristics of cardiac Slc26a6 remain unknown. The objective of the present study is to determine the molecular identity of cardiac Slc26a6 isoforms, to examine their cellular expressions in the heart, and to test the function of Slc26a6 in cardiomyocytes.
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Risk effects of GST gene polymorphisms in patients with acute myeloid leukemia: a prospective study.
Asian Pac. J. Cancer Prev.
PUBLISHED: 07-27-2013
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Glutathione S-transferase (GST) enzyme levels are associated with risk of many cancers, including hematologic tumours. We here aimed to investigate the relationships between GSTM1, GSTT1 and GSTP1 polymorphisms and the risk of AML. Genotyping of GSTs was based upon duplex polymerase-chain-reactions with the confronting- two-pair primer (PCR-CTPP) method in 163 cases and 204 controls. Individuals carrying null GSTT1 genotype had a 1.64 fold risk of acute leukemia relative to a non-null genotype (P<0.05). A heavy risk was observed in those carrying combination of null genotypes of GSTM1 and GSTT1 and GSTP1 Val allele genotypes when compared with those carrying wild genotypes, with an OR (95% CI) of 3.39 (1.26-9.26) (P<0.05). These findings indicate that genetic variants of GST and especially the GSTT1 gene have a critical function in the development of AML. Our study offers important insights into the molecular etiology of AML.
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ALLN hinders HCT116 tumor growth through Bax-dependent apoptosis.
Biochem. Biophys. Res. Commun.
PUBLISHED: 06-20-2013
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Continual high expression of cysteine proteases calpain I and II have been implicated in tumorigenicity; conversely, N-acetyl-leu-leunorleucinal (ALLN), which inhibits calpain I and II, should also influence tumor growth and carcinogenesis. To explore the role of ALLN against colon cancer and in promoting apoptosis, we used colon cancer HCT116 cell lines, p53 or Bax-deficient HCT116 cell lines. Cell viability and tumor growth decreased in a concentration-dependent manner when treated with 0-26?M ALLN. Treatment with ALLN induced apoptosis in HCT116 cell; however, flow cytometry showed that apoptosis significantly decreased in Bax-deficient HCT116 cell lines, but not in p53-deficient HCT116 cell lines. In addition, the ALLN-induced apoptosis response was through Bax translocation from cytosol to mitochondria. In this study we showed intraperitoneally injected ALLN to inhibit colon tumor formation in nude mice, and found ALLN to inhibit tumor growth in colon cancer cells, mainly through apoptosis that depends on translocation of Bax to a mitochondrial endogenous pathway; this implies a molecular mechanism for ALLN against human colon cancer. These results suggest that ALLN could become a novel agent for prevention of colon cancer.
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[Expression and role of vascular endothelial growth inhibitor in sporadic clear cell renal cell carcinoma].
Zhonghua Yi Xue Za Zhi
PUBLISHED: 06-13-2013
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To evaluate the expression of vascular endothelial growth inhibitor (VEGI) in sporadic clear cell renal cell carcinoma (CCRCC) and explore its relationships between VEGI expression, pathologic grade and tumor staging.
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Growth/differentiation factor 1 alleviates pressure overload-induced cardiac hypertrophy and dysfunction.
Biochim. Biophys. Acta
PUBLISHED: 06-12-2013
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Pathological cardiac hypertrophy is a major risk factor for developing heart failure, the leading cause of death in the world. Growth/differentiation factor 1 (GDF1), a transforming growth factor-? family member, is a regulator of cell growth and differentiation in both embryonic and adult tissues. Evidence from human and animal studies suggests that GDF1 may play an important role in cardiac physiology and pathology. However, a critical role for GDF1 in cardiac remodelling has not been investigated. Here, we performed gain-of-function and loss-of-function studies using cardiac-specific GDF1 knockout mice and transgenic mice to determine the role of GDF1 in pathological cardiac hypertrophy, which was induced by aortic banding (AB). The extent of cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. Our results demonstrated that cardiac specific GDF1 overexpression in the heart markedly attenuated cardiac hypertrophy, fibrosis, and cardiac dysfunction, whereas loss of GDF1 in cardiomyocytes exaggerated the pathological cardiac hypertrophy and dysfunction in response to pressure overload. Mechanistically, we revealed that the cardioprotective effect of GDF1 on cardiac remodeling was associated with the inhibition of the MEK-ERK1/2 and Smad signaling cascades. Collectively, our data suggest that GDF1 plays a protective role in cardiac remodeling via the negative regulation of the MEK-ERK1/2 and Smad signaling pathways.
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Comparison of catheter ablation and surgical ablation in patients with long-standing persistent atrial fibrillation and rheumatic heart disease: a four-year follow-up study.
Int. J. Cardiol.
PUBLISHED: 06-11-2013
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In our previous prospective and randomized study, we have demonstrated that the concomitant surgical ablation using saline-irrigated cooled tip radiofrequency ablation (SICTRA) system is more effective than subsequent circumferential pulmonary vein isolation (CPVI) combined with substrate modification in treating patients with long-standing persistent atrial fibrillation (LS-AF) and rheumatic heart disease (RHD) undergoing cardiac surgery during middle-term follow-up. Whether this strategy also decreases longer-term arrhythmia recurrence is unknown. This study describes the 4-year efficacy of SICTRA for these patients. Furthermore, we seek to compare the electrophysiological characteristics for recurrent atrial tachyarrhythmia (ATa) at the session of catheter ablation between two groups.
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Study on incompatibility of traditional chinese medicine: evidence from formula network, chemical space, and metabolism room.
Evid Based Complement Alternat Med
PUBLISHED: 06-07-2013
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A traditional Chinese medicine (TCM) formula network including 362 TCM formulas was built by using complex network methodologies. The properties of this network were analyzed including network diameter, average distance, clustering coefficient, and average degree. Meanwhile, we built a TCM chemical space and a TCM metabolism room under the theory of chemical space. The properties of chemical space and metabolism room were calculated and analyzed. The properties of the medicine pairs in "eighteen antagonisms and nineteen mutual inhibitors," an ancient rule for TCM incompatibility, were studied based on the TCM formula network, chemical space, and metabolism room. The results showed that the properties of these incompatible medicine pairs are different from those of the other TCM based on the analysis of the TCM formula network, chemical space, and metabolism room. The lines of evidence derived from our work demonstrated that the ancient rule of TCM incompatibility, "eighteen antagonisms and nineteen mutual inhibitors," is probably scientifically based.
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[Research on lettuce leaves moisture prediction based on hyperspectral images].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 05-24-2013
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In order to conduct rational management of watering lettuce, the model of detecting lettuce leaves moisture was built. First of all, the hyperspectral images of lettuce leaves were acquired and simultaneously the moisture proportions of leaves were measured. Meanwhile, hyperspectral images were analyzed and the characteristic bands of lettuce leaves moisture were found. Then the images in characteristic bands were processed and the image features of lettuce leaves moisture were computed. The image features highly relevant to moisture were obtained through correlation analysis. Furthermore, due to the possible correlation among image features, the principal components of the images were extracted by principal components analysis and were used as BP neural networks inputs to establish PCA-ANN model. At the same time, other models were constructed by using BP neural network and traditional MLR (multiple liner regression) method respectively. Prediction examinations of the three models were made based on the same sample data. The experimental results show that the average prediction error of PCA-ANN prediction model of tillering stage reaches 9.323% which is improved compared with BP-ANN and MLR prediction models.
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Interferon regulatory factor 7 deficiency prevents diet-induced obesity and insulin resistance.
Am. J. Physiol. Endocrinol. Metab.
PUBLISHED: 05-21-2013
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Obesity-related inflammation has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. In this study, we addressed the potential role of interferon regulatory factor 7 (IRF7), a master regulator of type I interferon-dependent immune responses, in the regulation of energy metabolism. The expression levels of IRF7 were increased in white adipose tissue, liver tissue, and gastrocnemius muscle of both diet-induced obese mice and ob/ob mice compared with their lean counterparts. After feeding a high-fat diet (HFD) for 24 wk, IRF7 knockout (KO) mice showed less weight gain and adiposity than wild-type controls. KO of IRF7 improved glucose and lipid homeostasis and insulin sensitivity. Additionally, KO of IRF7 ameliorated diet-induced hepatic steatosis. Next, we assessed the inflammatory state of the IRF7 KO mice on the HFD. These mice showed less macrophage infiltration into multiple organs and were protected from local and systemic inflammation. This study demonstrates a role for IRF7 in diet-induced alterations in energy metabolism and insulin sensitivity. Our results also suggest that IRF7 is involved in the etiology of metabolic abnormalities, which suggests a new strategy for treating obesity and type 2 diabetes.
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Effects of Bailing capsules for renal transplant recipients: a retrospective clinical study.
Chin. Med. J.
PUBLISHED: 05-16-2013
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The administration of immunosuppressive agents is always an important factor affecting the long-term survival of organ transplantation recipients. The best therapeutic regimen which either decreases the side effects of immune inhibitors or enhances the immunosuppressive efficacy is the goal of transplantation surgeons continue to search. This study investigated the effects of Bailing (Cordyceps sinensis) capsules on renal function and other systems of the body after renal transplantation.
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Enhanced Tumor Accumulation of Sub-2 nm Gold Nanoclusters for Cancer Radiation Therapy.
Adv Healthc Mater
PUBLISHED: 05-15-2013
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A new type of metabolizable and efficient radiosensitizers for cancer radiotherapy is presented by combining ultrasmall Au nanoclusters (NCs, <2 nm) with biocompatible coating ligands (glutathione, GSH). The new nanoconstruct (GSH-coated Au25 NCs) inherits attractive features of both the Au core (strong radiosensitizing effect) and GSH shell (good biocompatibility). It can preferentially accumulate in tumor via the improved EPR effect, which leads to strong enhancement for cancer radiotherapy. After the treatment, the small-sized GSH-Au25 NCs can be efficiently cleared by the kidney, minimizing any potential side effects due to the accumulation of Au25 NCs in the body.
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Subchronic safety evaluation of EPO-018B, a pegylated peptidic erythropoiesis stimulating agent, after 5-week subcutaneous injection in Cynomolgus monkeys and Sprague-Dawley rats.
Food Chem. Toxicol.
PUBLISHED: 05-07-2013
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EPO-018B, a synthetic peptide-based erythropoiesis stimulating agent (ESA), is coupled to polyethylene glycol (PEG) and designed to specifically bind and activate the erythropoietin (EPO) receptor to result in production of red blood cells. This study was designed to evaluate the potential subchronic toxicity of EPO-018B for Cynomolgus monkeys and Sprague-Dawley rats both at 0, 0.5, 5 and 50 mg/kg every week for 5 weeks, followed by 6-week recovery for rats and 12-week recovery for monkeys. The No Observed Adverse Effect Level (NOAEL) for rats and monkeys were both considered to be at least 0.5 mg/kg/day, the minimum toxic dose to be 5.0 mg/kg/day and the severe toxic dose to be more than 50.0 mg/kg/day. The toxicological effects included the exaggerated pharmacology and secondary sequelae that resulted from an erythropoiesis-stimulating agent treatment to healthy animals. Most treatment induced effects were reversible or showed ongoing recovery upon discontinuation of treatment. The anticipated patient population for EPO-018B treatment is targeted to be the anemia patients caused by chronic renal failure or chemotherapy against to cancer and is expected to have an ideal clinical application prospect.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.