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Background: Paclitaxel plays a pivotal role in the chemotherapy of breast cancer, but resistance to this drug is an important obstacle in the treatment. It is reported that microRNA-152-3p (miR-152-3p) is involved in tamoxifen resistance in breast cancer, but whether it is involved in paclitaxel resistance in breast cancer remains unknown. Materials and methods: We examined the expression of miR-152-3p in breast cancer tissues and cells by qRT-PCR. After transfecting paclitaxel-resistant MCF-7/TAX cells with miR-152-3p mimics, we analyzed the function of miR-152-3p in these cells by MTT assay and flow cytometry. We screened the target gene, endothelial PAS domain-containing protein 1 (EPAS1), using bioinformatics analysis and verified it with the dual luciferase reporter gene experiment. The relationship between EPAS1 and miR-152-3p and their roles in paclitaxel resistance of breast cancer were further investigated using RNA interference and transfection techniques. Results: The expression of miR-152-3p in normal breast tissues and cells was markedly higher than that in breast cancer. Overexpression of miR-152-3p decreased the survival rate and increased the apoptosis rate and sensitivity of MCF-7/TAX cells to paclitaxel. We confirmed that EPAS1 is the target of miR-152-3p and is negatively regulated by this miRNA. Moreover, transfection with EPAS1 siRNA enhanced the susceptibility and apoptosis rate of MCF-7/TAX cells to paclitaxel. Co-transfection of miR-152-3p mimics and EPAS1 increased paclitaxel sensitivity and apoptosis induced by the drug. Conclusion: miR-152-3p inhibits the survival of MCF-7/TAX cells and promotes their apoptosis by targeting the expression of EPAS1, thereby, enhancing the sensitivity of these breast cancer cells to paclitaxel.

Background Cardiovascular disease is the leading cause of death worldwide. Tissue repair after pathological injury in the heart remains a major challenge due to the limited regenerative ability of cardiomyocytes in adults. Stem cell-derived cardiomyocytes provide a promising source for the cell transplantation-based treatment of injured hearts. Aim To explore the function and mechanisms of miR-301a in regulating cardiomyocyte differentiation of mouse embryonic stem (mES) cells, and provide experimental evidence for applying miR-301a to the cardiomyocyte differentiation induction from stem cells. Methods mES cells with or without overexpression of miR-301a were applied for all functional assays. The hanging drop technique was applied to form embryoid bodies from mES cells. Cardiac markers including GATA-4, TBX5, MEF2C, and α-actinin were used to determine cardiomyocyte differentiation from mES cells. Results High expression of miR-301a was detected in the heart from late embryonic to neonatal mice. Overexpression of miR-301a in mES cells significantly induced the expression of cardiac transcription factors, thereby promoting cardiomyocyte differentiation and beating cardiomyocyte clone formation. PTEN is a target gene of miR-301a in cardiomyocytes. PTEN-regulated PI3K-AKT-mTOR-Stat3 signaling showed involvement in regulating miR-301a-promoted cardiomyocyte differentiation from mES cells. Conclusion MiR-301a is capable of promoting embryonic stem cell differentiation to cardiomyocytes.

Background Colorectal cancer (CRC) is one of the most common malignancies worldwide. Studies have demonstrated that epigenetic modifications play essential roles in the development of CRC. ADHFE1 is a differentially expressed gene that has been reported to be hypermethylated in CRC. However, the role and mechanism of ADHFE1 in the proliferation of CRC remain unclear. Materials and methods ADHFE1 expression was analyzed in CRC tissues by IHC and qRT-PCR, and the relationship between ADHFE1 expression and the clinicopathological parameters was analyzed. Cell proliferation were assessed by the in vitro and in vivo experimental models. GSEA assay was performed to explore the mechanism of ADHFE1 in the proliferation of CRC. Flow cytometry and Western blot were used to detect the activation of the cell cycle signaling. Bisulfite genomic sequence (BSP) assay was used to test the methylation degree of ADHFE1 gene promoter in CRC tissues. Results Here, we verified that ADHFE1 was down-regulated and hypermethylated in CRC tissues. The down-regulation of ADHFE1 was correlated with poor differentiation and advanced TNM stage of CRC patients. And ADHFE1 expression restored when the CRC cell line SW620 was treated with the demethylating agent 5-Aza-CdR. Overexpression of ADHFE1 inhibited the proliferation of CRC, while ADHFE1 knockdown promoted the proliferation of CRC cells in vitro and in vivo. Moreover, ADHFE1 overexpression could induce a significant G1-S cell cycle arrest in CRC cells and vice versa. Conclusion Hypermethylation of ADHFE1 might promote cell proliferation by modulating cell cycle progression in CRC, potentially providing a new therapeutic target for CRC patients.

Background: The incidence and mortality of colorectal cancer (CRC) are rising worldwide. Long-noncoding RNAs (lncRNAs) are known to play key roles in the development of human cancers, including CRC. However, the function and underlying mechanism of long intergenic noncoding RNA 00707 (LINC00707) in the development of CRC are unknown. Materials and methods: The expression of LINC00707 and miR-206 in tissue samples or cell lines was measured by quantitative reverse transcription PCR (qRT-PCR). The protein expression of neurogenic locus notch homolog protein 3 (NOTCH3) and transmembrane 4 L6 family member 1 (TM4SF1) was assessed by Western blotting. Cell proliferation, migration, and invasion were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Luciferase reporter assay and biotin-coupled miRNA capture assay were used to explore the relationship between LINC00707 and miR-206 expression. Results: The expression of LINC00707 was significantly upregulated in CRC tissues as compared with the adjacent non-CRC tissues. LINC00707 expression was significantly correlated with tumor size, lymphatic metastasis, and distant metastasis, but not significantly correlated with age and gender. Knockdown of LINC00707 expression significantly inhibited LoVo and HCT116 cell proliferation, migration, and invasion. LINC00707 acted as a molecular sponge by competing for miR-206 and indirectly modulating the expression of its targets, NOTCH3 and TM4SF1. Conclusion: LINC00707 promotes CRC cell proliferation and metastasis by sponging miR-206, suggestive of its potential application for CRC treatment.

The premise of analyzing and researching robot technology is to establish a proper mathematical model and then to solve it with kinematics. In this study, a self-developed humanoid hydraulically driven dual-arm robot is taken as the research object, and the DH (Denavit–Hartenberg) parameter method and the rotational exponential formula (POE) are used to solve the kinematics of the robot. The calculation results are verified by simulation. The advantages and disadvantages of the two methods are analyzed. The differences between the two methods are compared. It lays a foundation for other scholars to choose mathematical models when analyzing the mechanism in the future.

Hepatocellular carcinoma (HCC) is a leading cause of tumour-associated mortality worldwide, but no significant improvement in treating HCC has been reported with currently available systemic therapies. Immunotherapy represents a new frontier in tumour therapy. Therefore, the immunobiology of hepatocarcinoma has been under intensive investigation. Decoy receptor 3 (DcR3), a member of the tumour necrosis factor receptor (TNFR) superfamily, is an immune suppressor associated with tumourigenesis and cancer metastasis. However, little is known about the role of DcR3 in the immunobiology of hepatocarcinoma. In this study, we found that overexpression of DcR3 in HCC is mediated by the TGFβ3-Smad-Sp1 signalling pathway, which directly targets DcR3 promoter regions. Moreover, overexpression of DcR3 in HCC tissues is associated with tumour invasion and metastasis and significantly promotes the differentiation and secretion of Th2 and Treg cells while inhibiting the differentiation and secretion of Th1 cells. Conversely, knockdown of DcR3 expression in HCC significantly restored the immunity of CD4+ T cells. Inhibition of DcR3 expression may provide a novel immunotherapeutic approach to restoring immunity in HCC patients.

Background Colorectal cancer (CRC) is one of the most common malignancies worldwide. Studies have demonstrated that epigenetic modifications play essential roles in the development of CRC. ADHFE1 is a differentially expressed gene that has been reported to be hypermethylated in CRC. However, the role and mechanism of ADHFE1 in the proliferation of CRC remain unclear. Materials and methods ADHFE1 expression was analyzed in CRC tissues by IHC and qRT-PCR, and the relationship between ADHFE1 expression and the clinicopathological parameters was analyzed. Cell proliferation were assessed by the in vitro and in vivo experimental models. GSEA assay was performed to explore the mechanism of ADHFE1 in the proliferation of CRC. Flow cytometry and Western blot were used to detect the activation of the cell cycle signaling. Bisulfite genomic sequence (BSP) assay was used to test the methylation degree of ADHFE1 gene promoter in CRC tissues. Results Here, we verified that ADHFE1 was down-regulated and hypermethylated in CRC tissues. The down-regulation of ADHFE1 was correlated with poor differentiation and advanced TNM stage of CRC patients. And ADHFE1 expression restored when the CRC cell line SW620 was treated with the demethylating agent 5-Aza-CdR. Overexpression of ADHFE1 inhibited the proliferation of CRC, while ADHFE1 knockdown promoted the proliferation of CRC cells in vitro and in vivo. Moreover, ADHFE1 overexpression could induce a significant G1-S cell cycle arrest in CRC cells and vice versa. Conclusion Hypermethylation of ADHFE1 might promote cell proliferation by modulating cell cycle progression in CRC, potentially providing a new therapeutic target for CRC patients.

Sepsis‐induced cardiac dysfunction represents a main cause of death in intensive care units. Previous studies have indicated that GSK‐3β is involved in the modulation of sepsis. However, the signalling details of GSK‐3β regulation in endotoxin lipopolysaccharide (LPS)‐induced septic myocardial dysfunction are still unclear. Here, based on the rat septic myocardial injury model, we found that LPS could induce GSK‐3β phosphorylation at its active site (Y216) and up‐regulate FOXO3A level in primary cardiomyocytes. The FOXO3A expression was significantly reduced by GSK‐3β inhibitors and further reversed through β‐catenin knock‐down. This pharmacological inhibition of GSK‐3β attenuated the LPS‐induced cell injury via mediating β‐catenin signalling, which could be abolished by FOXO3A activation. In vivo, GSK‐3β suppression consistently improved cardiac function and relieved heart injury induced by LPS. In addition, the increase in inflammatory cytokines in LPS‐induced model was also blocked by inhibition of GSK‐3β, which curbed both ERK and NF‐κB pathways, and suppressed cardiomyocyte apoptosis via activating the AMP‐activated protein kinase (AMPK). Our results demonstrate that GSK‐3β inhibition attenuates myocardial injury induced by endotoxin that mediates the activation of FOXO3A, which suggests a potential target for the therapy of septic cardiac dysfunction.

Aims To explore the biological function and mechanism of Syntaxin2 (STX2) in Colorectal cancer (CRC) proliferation. Main methods A series of gain- and loss-of-function analysis were conducted the to explore the biological function of STX2 in CRC proliferation in vivo and in vitro. Western blot, Co-immunoprecipitation (Co-IP) and the functional analyses were taken to analyze the regulative role of STX2 on Exosome Complex 4 (EXOSC4) in CRC proliferation; Immunohistochemistry (IHC) and Real-time quantitative polymerase chain reaction (qPCR) were used to further verify the relationship between the expression of STX2 and EXOSC4 in human CRC samples. Key findings Our study revealed that the over-expression of STX2 promoted CRC proliferation, while knockdown of STX2 repressed CRC proliferation; STX2 promoted CRC proliferation via increasing EXOSC4 protein; There was a positive correlation between STX2 and EXOSC4 expression. Significance The current data verify that STX2 drives the proliferation of CRC via increasing the expression of EXOSC4.

// Yan-Ping Liu 1, 2, 3, * , Hui-Fang Zhu 1, 2, 3, * , Ding-li Liu 4, * , Zhi-Yan Hu 1, 2, 3 , Sheng-Nan Li 1, 2, 3 , He-Ping Kan 5 , Xiao-Yan Wang 1, 2, 3 , Zu-Guo Li 1, 2, 3 1 Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China 2 Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou, China 3 Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China 4 State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China 5 Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China * These authors have contributed equally to this work Correspondence to: Xiao-Yan Wang, email: wangxiaoyan639@163.com Zu-Guo Li, email: Lizg@smu.edu.cn Keywords: decoy receptor 3, colorectal cancer, TGF-β3/SMAD signaling, metastasis, epithelial-mesenchymal transition Received: May 30, 2016 Accepted: September 28, 2016 Published: October 13, 2016 ABSTRACT Decoy receptor 3 (DcR3), a novel member of the tumor necrosis factor receptor (TNFR) family, was recently reported to be associated with tumorigenesis and metastasis. However, the role of DcR3 in human colorectal cancer (CRC) has not been fully elucidated. In this study, we found that DcR3 expression was significantly higher in human colorectal cancer tissues than in paired normal tissues, and that DcR3 expression was strongly correlated with tumor invasion, lymph node metastases and poor prognoses. Moreover, DcR3 overexpression significantly enhanced CRC cell proliferation and migration in vitro and tumorigenesis in vivo . Conversely, DcR3 knockdown significantly repressed CRC cell proliferation and migration in vitro , and DcR3 deficiency also attenuated CRC tumorigenesis and metastasis in vivo . Functionally, DcR3 was essential for TGF-β3/SMAD-mediated epithelial-mesenchymal transition (EMT) of CRC cells. Importantly, cooperation between DcR3 and TGF-β3/SMAD-EMT signaling-related protein expression was correlated with survival and survival time in CRC patients. In conclusion, our results demonstrate that DcR3 may be a prognostic biomarker for CRC and that this receptor facilitates CRC development and metastasis by participating in TGF-β3/SMAD-mediated EMT of CRC cells.

Background Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. Methods The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC. Results MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3. Conclusion Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3. Electronic supplementary material The online version of this article (10.1186/s12935-018-0628-6) contains supplementary material, which is available to authorized users.

Heart diseases (HDs) represent a common group of diseases that involve the heart, a number of which are characterized by high morbidity and lethality. Recently, increasing evidence demonstrates diverse non-coding RNAs (ncRNAs) play critical roles in HDs. However, currently there lacks a systematic investigation of the association between HDs and ncRNAs. Here, we developed a Heart Disease-related Non-coding RNAs Database (HDncRNA), to curate the HDs-ncRNA associations from 3 different sources including 1904 published articles, 3 existing databases [the Human microRNA Disease Database (HMDD), miR2disease and lncRNAdisease] and 5 RNA-seq datasets. The HDs-ncRNA associations with experimental validations curated from these articles, HMDD, miR2disease and part of data from lncRNAdisease were ‘direct evidence’. Relationships got from high-through data in lncRNAdisease and annotated differential expressed lncRNAs from RNA-seq data were defined as ‘high-throughput associations’. Novel lncRNAs identified from RNA-seq data in HDs had least credibility and were defined as ‘predicted associations’. Currently, the database contains 2304 HDs-ncRNA associations for 133 HDs in 6 species including human, mouse, rat, pig, calf and dog. The database also has the following features: (i) A user-friendly web interface for browsing and searching the data; (ii) a visualization tool to plot miRNA and lncRNA locations in the human and mouse genomes; (iii) information about neighboring genes of lncRNAs and (iv) links to some mainstream databases including miRbase, Ensemble and Fantom Cat for the annotated lncRNAs and miRNAs. In summary, HDncRNA provides an excellent platform for exploring HDs related ncRNAs. Database URL: http://hdncrna.cardiacdev.com

It is major, simple structure and wide scope of use on Gravity abutment of plain concrete, But most of the wall of abutment appears irregular cracks, affect the economy and durability of the abutment and bridge seriously. The paper is based on a bridge of Jiang Xi Rui Xun high-speed engineering, analysis the crack mechanism of abutment by using large-scale finite element software ANSYS to establish reinforcement simulation model of top and bottom ring beam. The stress and vertical deflection of the abutment are meet the requirements, it is meaningful for gravity abutment of plain concrete Strengthening in the future.

Response gene to complement 32 (RGC32) is a transcription factor that regulates the expression of multiple genes involved in cell growth, viability and tissue-specific differentiation. However, the role of RGC32 in tumorigenesis and tumor progression in colorectal cancer (CRC) has not been fully elucidated. Here, we showed that the expression of RGC32 was significantly up-regulated in human CRC tissues versus adjacent normal tissues. RGC32 expression was significantly correlated with invasive and aggressive characteristics of tumor cells, as well as poor survival of CRC patients. We also demonstrated that RGC32 overexpression promoted proliferation, migration and tumorigenic growth of human CRC cells in vitro and in vivo. Functionally, RGC32 facilitated epithelial-mesenchymal transition (EMT) in CRC via the Smad/Sip1 signaling pathway, as shown by decreasing E-cadherin expression and increasing vimentin expression. In conclusion, our findings suggested that overexpression of RGC32 facilitates EMT of CRC cells by activating Smad/Sip1 signaling.

The glioma accounts for half of the central nervous tumors, among which the glioblastoma multiforme (GBM) is one of the most aggressive and lethal brain tumors. The difficulties in glioma therapy indicate the need of appropriate animal models for preclinical studies. Benefiting from the development of molecular biology, genetics, and transgenic technology, variable animal models of glioma have been established. These animal models of human glioma are reviewed in this paper.

The analysis and modeling of road network capacity provides a useful measure for urban planning and traffic management. Therefore, the primary purpose of this research is to construct a novel approach of modeling the capacity of road network, based on the theory of space and time consumption. Based on the analysis of model parameters, a bi-level model is proposed to determine and optimize the capacity of road network Meanwhile, this paper elaborates on solution algorithm for its upper and lower level model. Taking the area of Ming Dynasty City Wall in Xi’an, China into account as a case study, the effectiveness of this proposed model is verified. The results presents that the model’s validity is verified. The results show that the main road network capacity in city wall of Ming Dynasty is 721883 pcu/d.

The effects of annealing on the optical properties of InAs/GaAs quantum dots (QDs) grown under different conditions by metalorganic chemical vapor deposition (MOCVD) are studied. A lower QD growth rate leads to an earlier and faster decrease of QD photoluminescence (PL) intensity with increasing annealing temperature. which is proposed to be related to the increased QD two-dimensional (2D)-three-dimensional (3D) transition critical layer thickness at low QD growth rate. High-quality GaAs cap layers grown at high temperature and a low deposition rate are shown to decrease the blueshift of the QDs' emission wavelength significantly during in-situ I h annealing experiments, which is important for the fabrication of long-wavelength InAs/GaAs QD lasers by MOCVD technique. (C) 2009 Elsevier B.V. All rights reserved.

We have grown InAs self-assembled islands on vicinal GaAs( 001) substrates. Atomic force microscopy and photoluminescence studies show that the islands have a clear bimodal size distribution. While most of the small islands whose growth is limited by the width of one multi-atomic step have compact symmetric shapes, a large fraction of the large islands limited by the width of one step plus one terrace have asymmetric shapes which are elongated along the multi-atomic step lines. These results can be attributed to the shape-related energy of the islands at different states of their growth. (C) 2008 Elsevier B. V. All rights reserved.

Three novel coordination polymers [Cd3( L )2(μ-Br)(μ-Cl)Br3Cl] (1), [Cd3( L )2(μ-Cl)2Cl4] (2) and [Cd( L )Cl]2[CdCl4]·H2O (3) were obtained by reactions of an imidazole-containing tripodal ligand N1-(2-aminoethyl)-N1-(2-imidazolethyl)-ethane-1,2-diamine (L) with Cd(II) salts. Their structures were determined by X-ray crystallography. Crystal data for 1, monoclinic system, P21/c, a=7.752(4) A, b=31.70(2) A, c=14.012(7) A, β=109.439(7)°, V=3247(3) A3, Z=4. 2, monoclinic system, P21/c, a=7.6564(15) A, b=31.433(6) A, c=13.925(3) A, β=109.89(3)°, V=3151.1(11) A3, Z=4. 3, orthorhombic system, Pbcn, a=22.950(2) A, b=8.435(7) A, c=17.360(2) A, V=3360.3(51) A3, Z=4. Complexes 1 and 2 have similar one-dimensional (1D) branched-chain structure while complex 3 features a 1D zigzag cationic chain with [CdCl4]2− serving as counter anion. The photoluminescent measurements reveal that all the complexes exhibit blue fluorescence at room temperature in the solid state.

// Zhi-Yan Hu 1, 2, 3, * , Xiao-Yan Wang 1, 2, 3, * , Wen-bin Guo 4, 5, 6, * , Lin-Ying Xie 1, 2, 3 , Yu-qi Huang 4 , Yan-Ping Liu 1, 2, 3 , Li-Wei Xiao 1, 2, 3 , Sheng-Nan Li 1, 2, 3 , Hui-Fang Zhu 1, 2, 3 , Zu-Guo Li 1, 2, 3 , Heping Kan 4 1 Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China 2 Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China 3 Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Southern Medical University, Guangzhou, China 4 Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China 5 Department of Urology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 6 Department of Urology, The Third Affiliated Hospital of Southern Medical University, Southern Medical University, Guangzhou, China * These authors contributed equally to this work Correspondence to: Heping Kan, e-mail: khp5513@126.com Zu-Guo Li, e-mail: Lizg@smu.edu.cn Keywords: long non-coding RNA, MALAT-1, AKAP-9, SRSF1, colorectal cancer Received: September 24, 2015 Accepted: January 23, 2016 Published: February 13, 2016 ABSTRACT Our earlier findings indicate that the long non-coding RNA MALAT1 promotes colorectal cancer (CRC) cell proliferation, invasion and metastasis in vitro and in vivo by increasing expression of AKAP-9. In the present study, we investigated the molecular mechanism by which MALAT1 enhances AKAP9 expression in CRC SW480 cells. We found that MALAT1 interacts with both SRPK1 and SRSF1. MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation. Following MALAT1 knockdown, overexpression of SRPK1 was sufficient to restore SRSF1 phosphorylation and AKAP-9 expression to a level that promoted cell proliferation, invasion and migration in vitro . Conversely, SRPK1 knockdown after overexpression of MALAT1 in SW480 cells diminished SRSF1 phosphorylation and AKAP-9 expression and suppressed cell proliferation, invasion and migration in vitro . These findings suggest MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in CRC cells. These results reveal a novel molecular mechanism by which MALAT1 regulates AKAP-9 expression in CRC cells.

An imidazole-containing tripodal polyamine ligand N 1 -(2-aminoethyl)- N 1 -(2-imidazol-1-ylethyl)-ethane-1,2-diamine (L) was prepared and its dinuclear zinc(II) complex [Zn(L)(H 2 O)] 2 (ClO 4 ) 4 · 4 H 2 O ( 1 ) was obtained and examined as a catalyst for the hydrolysis of 4-nitrophenyl acetate (NA). X-ray crystal structure analysis of the complex revealed that the complex features a dinuclear cation unit with a Zn ⋯ Zn distance of 8.34 A and both Zn(II) centers adopt distorted trigonal-bipyramid geometry. The solution complexation investigation performed at 25 °C by means of potentiometric titration revealed that the mononuclear species [ZnL] 2+ is predominating in the pH rage of 7.0–9.7 in the solution and the p K a1 for the Zn-bound water is 8.50 ± 0.01. Complex 1 promoted hydrolysis of NA showed a second-order rate constant of 0.046 ± 0.004 M −1 s −1 at pH 9.0 in 10% (v/v) CH 3 CN aqueous solution at 25 °C. The pH-rate profile for the second-order rate constant of NA hydrolysis with complex 1 gave a sigmoidal curve. And the results show that in the hydrolysis process the two Zn(II) centers of the dinuclear deprotonated species do not cooperate with each other and the Zn-bound hydroxide servers as reactive nucleophile toward the ester.

A pseudo-rotaxane, [(H2C6N3)(CB[6])](NO3)2·H2O (1), and three polyrotaxanes, [Ag(H2C6N3)(CB[6])](NO3)3·8H2O (2), [Ag(H2BDMN3)(CB[6])](NO3)3·10H2O (3), and [Ag(H2BDMN3)(CB[6])(H2O)][Ag(H2BDMN3)(CB[6...

Three novel metal-organic architectures, [Ag3(bta)].1.5H2O (1), [Cd3(bta)2(H2O)7].5H2O (2), and [Cu11(bta)6(Hbta)2(H2O)10].29H2O (3), were obtained by reactions of the corresponding metal salts with a flexible tripodal ligand, benzene-1,3,5-triacetic acid (H3bta), and their structures were determined by single-crystal X-ray diffraction studies. The results revealed that, in complexes 1 and 2, the carboxylate groups of the bta3- ligand adopted varied coordination modes to link metal atoms and further to form three-dimensional structures with open channels occupied by water molecules, while in complex 3, for the first time, the flexible H3bta acted as a secondary building unit to generate a novel nanometer-sized metallocage, which is composed of a Cu(II) paddle wheel (square secondary building units) and bta3-/Hbta2- organic links (triangular secondary building units). The photoluminescence properties of complexes 1 and 2 were investigated, and the results showed that 2 exhibited photoluminescence in the solid state at room temperature.

The reaction of benzene-1,3,5-triacetic acid (H3bta) with [Mn(salen)]ClO4·2H2O yields [Mn(salen)H2bta]·0.5H2O (1) [H2salen = N,N′-bis(salicylideneaminato)ethylene]. Complex 1 was characterized by X-ray crystal structure determination, elemental analysis, FT-IR and ES-MS spectroscopic methods. The X-ray crystallographic study reveals that the complex has a one-dimensional chain structure, and self-organizes to a three-dimensional network by O–H···O hydrogen bonds between the oxygen atom of carboxyl groups without deprotonation and the carbonyl oxygen atom of the bta ligand, and by C–H···O hydrogen bonds between the carbon atom of the salen group and the carboxyl oxygen atom of the bta ligand as well as the salen unit. In addition, 1 was studied by cyclic voltammetry.

Three coordination polymers [Co(L) 2 (SCN) 2 ] ( 1 ), [Mn(L) 2 (SCN) 2 ] ( 2 ) and [Cd(H 4 L) 2 Cl 2 ] ( 3 ), were obtained by the reaction of Co II , Mn II , Cd II salts with di-Schiff base ligand N , N ′-bis(3-pyridylmethyl)-4,4′-biphenylenedimethyleneimine (L) and its reduced form (H 4 L), respectively and their structures were determined by X-ray crystallography. In the solid state, complexes 1 and 2 feature 1D hinged chains, while complex 3 has a 2D network structure. Complex 2 was found to show optical limiting property with a 3 ns pulsed laser at 532 nm in DMF solution.

Two novel series of coordination frameworks [Ln(bta)(H2O)2]·nH2O·mEtOH (Ln = La 1a, n = 4.5, m = 0; Ln = Ce 1b, n = 4, m = 0; Ln = Pr 1c, n = 2.88, m = 0.35) and [Ln2(bta)2(H2O)3]·nH2O (Ln = La 2a, n = 2.14; Ln = Ce 2b, Pr 2c, n = 2) were synthesized by the reaction of 1,3,5-benzenetriacetic acid (H3bta) with the corresponding lanthanide salts using different methods. X-ray diffraction analyses reveal that all six complexes have 3D channel structures, but in the first series of complexes, each bta3- ligand adopts a cis, trans, trans conformation and acts as a μ5-bridge linking five lanthanide atoms, while in the second series, the bta3- ligands adopt cis, trans, trans and cis, cis, cis conformations and act as μ6- and μ5-bridges, respectively. Thus two series of complexes have the same metal atoms and ligands but different structures. The results show that the flexible triacid ligand is versatile and can adopt different conformations according to different reaction conditions. The variable-temperature mag...

Two new coordination polymers [Ca3(bta)2(H2O)8]·3H2O (1) and Ba3(bta)2(H2O)8 (2) were obtained by self-assembly of the corresponding metal carbonate with a flexible tripodal ligand, benzene-1,3,5-triacetic acid (H3bta), and their structures were determined by single-crystal X-ray diffraction studies. The results revealed that complex 1 crystallizes in the triclinic space group P1 with a = 8.3045(10) A, b = 10.4883(10) A, c = 11.0184(16) A, α = 102.703(3)°, β = 100.001(4)°, γ = 108.842(7)°, V = 854.36(18) A3, and Z = 1; compound 2 is in the monoclinic space group C2/c with a = 23.4363(8) A, b = 6.9782(3) A, c = 21.7150(8) A, β = 111.4480(10)°, V = 3305.4(2) A3, and Z = 4. Complexes 1 and 2 have two-dimensional network structures, and each bta3- ligand coordinates to Ca(II) or Ba(II) atoms using two of three carboxylate groups adopting different coordination modes: μ3-η2:η2-bridging and μ2-η2:η1-bridging coordination modes in 1 or μ3-η2:η2-bridging and μ3-η2:η1-bridging coordination modes in 2. The noncoo...

Six novel complexes, [Zn(IIMB)4(H2O)2](NO3)2·5H2O 1, {[Ag2(IIMB)2][2,6-C10H6(COO)2]·6H2O}n 2, {[Cu(IIMB)2]Br2·0.5H2O}n 3, {[Co(IIMB)2(SCN)2]}n 4, {[Cu(IIMB)2(SO4)]·8.5H2O}n 5, and {[Co(IIMB)2(H2O)(SO4)]4·29H2O}n 6, were obtained by reactions of 1-(1-imidazolyl)-4-(imidazol-1-ylmethyl)benzene (IIMB) with the corresponding metal salts. X-ray diffraction analyses reveal that 1 is monomeric, in which IIMB acts as monodentate ligand, while the IIMB ligand in complexes 2−6 acts as bidentate ligand. Complex 2 has a single chain structure, while complexes 3 and 4 are double stranded chains. Complexes 5 and 6 display similar 2-D polycatenated architectures formed by the inclined interpenetration of 1-D double stranded chains. This kind of 1-D → 2-D inclined interpenetration has rarely been reported until now. In addition, the photoluminescence properties of the synthesized compounds were investigated in the solid state at room temperature.

Five novel coordination polymers, [Co(bpb)2Cl2] (1), [Co(bpb)2(SCN)2] (2), [Cd(H4bpb)0.5(dmf)(NO3)2] (3), [Cd2(H4bpb)Br4] (4), and [Hg2(H4bpb)I4] (5) [bpb=N,N′-bis(3-pyridylmethyl)-1,4-benzenedimethyleneimine, H4bpb=N,N′-bis(3-pyridylmethyl)-1,4-benzenedimethylamine], were synthesized and their structures were determined by X-ray crystallography. In the solid state, complex 1 is a 1D hinged chain, while 2 has 2D network structure with the ligand bpb serving as a bridging ligand using its two pyridyl N atoms. The imine N atoms keep free of coordination and bpb acts as a bidentate ligand in both 1 and 2. Complexes 3, 4, and 5 with reduced bpb ligand, i.e. H4bpb, show similar 2D network structure, in which ligand H4bpb serves as a tetradentate ligand. Thermogravimetric analyses for complexes 1–5 were carried out and found that they have high thermal stability. The magnetic susceptibilities of compounds 1, 2 were measured over a temperature range of 75–300 K.

Reactions of a new asymmetric ligand, 1-(1-imidazolyl)-4-(imidazol-1-ylmethyl)benzene (IIMB), with various metal [Cd(II), Mn(II), Zn(II)] salts led to the formation of molecular, one- (1D) and two-dimensional (2D) architectures [Cd(IIMB)2(H2O)(SO4)]·7.5H2O 1, [Cd(IIMB)2Cl2]·H2O 2, [Cd(IIMB)4(H2O)2](NO3)2·5H2O 3, [Cd(IIMB)(OAc)2]·H2O 4, [Mn(IIMB)2(SO4)(H2O)]·8.2H2O 5, [Mn(IIMB)4(H2O)2]Cl2·5H2O 6 and [Zn(IIMB)2]4(NO3)8·13.5H2O 7. All the structures were established by single-crystal X-ray diffraction analysis. Both compounds 1 and 5 with sulfate anion are 2D polycatenanes formed by the interlocking of 1D double-stranded chains, while 2 and 4 with chloride and acetate anions are 1D chains. The results provide nice examples of topologies of metal-organic frameworks controlled by the counter anions. Interestingly, 3 and 6 are discrete molecular complexes with monometallic cores and form 2D networks through strong intermolecular hydrogen bonds. Complex 7, obtained under the same conditions as 3, is a 1D tubular chain. The structural difference between 3 and 7 suggests the metal ions also have a significant effect on the construction of supramolecular architectures. Furthermore, the photoluminescence properties of these compounds were investigated in the solid state at room temperature.

Complex [Ag(tpba)N 3 ] (1) was obtained by reaction of novel tripodal ligand N,N',N"-tris(pyrid-3-yl-methyl)-1,3,5-benzenetricarboxamide (TPBA) with [Ag(NH 3 ) 2 ]N 3 . While the reactions between 1,3,5-tris(imidazol-1-ylmethyl)-2,4,6-trimethylbenzene (TITMB) and silver(I) salts with different anions and solvent systems give six complexes: [Ag 3 (titmb) 2 ](N 3 ) 3 .CH 3 O-H.4H 2 O (2), [Ag 3 (titmb) 2 ](CF 3 SO 3 ) 2 -(OH).5H 2 O (3), [Ag 3 (titmb) 2 ][Ag-(NO 3 ) 3 ]NO 3 .H 2 O (4), [Ag 3 (titmb) 2 -(py)](NO 3 ) 3 .H 2 O (py=pyridine) (5), [Ag 3 (titmb) 2 (py)](ClO 4 ) 3 (6), and [Ag 3 -(titmb) 2 ](ClO 4 ) 3 .CHCl 3 (7). The structures of these complexes were determined by X-ray crystallography. The results of structural analysis of complexes 1 and 2, with the same azide anion but different ligands, revealed that 1 is a twofold interpenetrated 3D framework with interlocked cage-like moieties, while 2 is a M 3 L 2 type cage-like complex with a methanol molecule inside the cage. Entirely different structure and topology between 1 and 2 indicates that the nature of organic ligands affected the structures of assemblies greatly. While in the cases of complexes 2-7 with flexible tripodal ligand TITMB, they are all discrete M 3 L 2 type cages. The results indicate that the framework of these complexes is predominated by the nature of the organic ligand and geometric need of the metal ions, but not influenced greatly by the anions and solvents. It is interesting that there is a divalent anion [Ag(NO 3 ) 3 ] 2 - inside the cage 4 and an anion of ClO 4 - or NO 3 -spontaneously encapsulated within the cage of complexes 5, 6 and 7.

Two supramolecular complexes, [Cd(bimb)2Cl2] (1) and [Cd(bimb)(DMF)Cl2]·DMF (2) [bimb=4,4′-bis(imidazol-1-ylmethyl)biphenyl], were synthesized by reactions of CdCl2·2.5H2O with bimb ligand in ethanol and N,N′-dimethylformamide (DMF), respectively, and their structures were determined by X-ray crystallography. Complex 1 is an infinite 2D grid network bridged by bimb ligands, and the 2D sheets were further linked by C–H Cl hydrogen bonds to form a polycatenated 3D framework. Complex 2 has dicadmium(II) di-μ-chloride units which are connected by bimb bridging ligands to form an infinite non-interpenetrating 2D network. The results provide a nice example of the solvent system exerting a great effect on the construction of supramolecular frameworks.

Four novel coordination complexes, [Ag(bpb)]NO3·2H2O (1), [Cu2(CH3COO)4(bpb)] (2), [ZnCl2(bpb)2] (3) and [MnCl2(bpb)2] (4) [bpb = N,N′-bis(3-pyridylmethyl)-1,4-benzenedimethyleneimine], with one-dimensional chain structures were synthesized and their structures were determined by X-ray crystallography. A structure analysis revealed that the bpb acts as a bridging ligand using two pyridyl N atoms to link two metal atoms, while the two imine N atoms do not participate in the coordination with the metal atoms. The photoluminescence properties of the title complexes were also studied. Although Cu(II) (2) and Zn(II) (3) complexes show intense violet-blue photoluminescence, no clear photoluminescence was observed for the Ag(I) (1) and Mn(II) (4) complexes.

Transition metal complexes [M(Hbta)(H 2 O) 4 ] [M=Co(II) ( 1 ), Ni(II) ( 2 ), H 3 bta=1,3,5-benzenetriacetic acid] have been prepared by reaction of H 3 bta with the M(OH) 2 in water by hydrothermal method. The complexes were characterized by X-ray crystallography and electrospray mass spectrometry. The coordination geometries around Co(II) and Ni(II) atoms are both distorted octahedral with O 6 donor set. And the conformation of flexible triacid is cis , trans , trans in the title complexes.

Two novel metal-organic frameworks (MOFs) [Zn(TITMB)(OAc)](OH).8.5H(2)O (1) and [Ag(TITMB)N(3)].H(2)O (2) [TITMB = 1,3,5-tris(imidazol-1-ylmethyl)-2,4,6-trimethylbenzene, OAc = acetate anion] were synthesized and their structures were determined by X-ray crystallography. Complex 1 crystallizes in tetragonal space group P(-)4 with a = 23.2664(7) and c = 11.9890(3) A and Z = 8. 1 has a one-dimensional tubelike structure with large inner pore size of approximately 17 A. Complex 2 crystallizes in monoclinic space group C2 with a = 20.7193(10), b = 11.5677(8), and c = 12.2944(6) A, beta = 125.5770(10) degrees, and Z = 4. 2 consists of two-dimensional honeycomb networks that interpenetrate each other to generate a polycatenated structure. In these two complexes, both zinc(II) and silver(I) atoms are four-coordinated with the same tetrahedral coordination geometry. The topologies of 1 and 2 are predominated by the conformations of TITMB, which are cis, trans, trans in 1 and cis, cis, cis in 2, respectively.

To investigate the mechanism that the formulas for activating blood and resolving stasis can regulate hemopoietic stem cell to produce new blood.Rats were established animal model of acute cerebral infarction by referencing Olivette' method. They were randomly divided into model group, the group of the high, middle, low dose of the formulas for activating blood and resolving stasis. Each group and then wasrandomly divided into subgroups by 1, 3, 7, 14, 28 d. Xuesaitong capsule was formulated into 20, 40, 60 g x L(-1) with normal saline. The rats were given gavage drugs once a day until the experient ended, and the model group was administrated by intragastrical perfusion of normal saline. ELISA was used to detect the expression of SCF in peripheral blood and bone marrow among different groups at different time points. Flow cytometry was used to observe the changes of CD117 in blood and bone marrow.The CD117+ HSC and SCF concentration in peripheral blood and bone marrow of model group were increasing during 1-14 d,there was a peak on the 14th day, then the expression was reducing. CD117+ HSC and SCF concentration rising trend in the group of the high, middle dose of the formulas for activating blood and resolving stasis was preceded model group (P0.05).Activating blood and resolving stasis can regulate hemopoietic stem cell to produce new blood, and it is through the regulation of CD117+ HSC number to achieve the purpose.

The glioma accounts for half of the central nervous tumors, among which the glioblastoma multiforme (GBM) is one of the most aggressive and lethal brain tumors. The difficulties in glioma therapy indicate the need of appropriate animal models for preclinical studies. Benefiting from the development of molecular biology, genetics, and transgenic technology, variable animal models of glioma have been established. These animal models of human glioma are reviewed in this paper.

A novel snake-like zinc(II) coordination polymer with blue photoluminescence, {[Zn(bimb)(OAc)2]·6H2O}∞ [bimb = 4,4′-bis(imidazol-1-ylmethyl)biphenyl, OAc = acetate anion], was obtained by reaction of Zn(OAc)2·2H2O with the ligand bimb. The X-ray crystal structural analysis indicates that two independent single-stranded helical chains are interwoven like two entwined snakes and held together through hydrogen bonds and π-π interactions.

To investigate the clinical effects of treatment for superior tibial fracture complicating with crotch injury of distal popliteal artery by an alternative micro-surgical operation.During Feb. 2002 to Oct. 2007, there were 19 patients with superior tibial fracture complicating with crotch injury of distal popliteal artery included 15 males and 4 females aged from 21 to 48 years (means 35 years). There were 6 cases complicating with fracture of tibial plateau, 3 cases complicating with nerve injury. The tibial fracture were fixed with external fixator and the anterior tibial artery and vein and posterior tibial artery and vein were treated by transplantable great saphenous vein (Y-shape) combined with windowing for interosseous membrane by the posterior and anterolateral incision. Evaluations of clinical effect were performed according to Rasmussen functional score system.All patients survived after operation. All fracture achieved bony union, the union time was from 3 to 14 months (means 5.5 months). All patients were followed-up for from 8 to 23 months (means 13 months). The mean Rasmussen functional score was (27.0 + 2.9). The results were excellent in 11 cases, good in 7, and fair in 1.The surgical exploration should be done as soon as possible when diagnosis of injuries of large arteries is definite or highly suspected. Simultaneous reconstruction of both posterior tibial artery and anterior tibial artery associated with vein can reduce the rate of disability and recover function of limb.

To detect the genotoxicity of dental machinable ZrO(2)/LaPO(4) diphase ceramics on human peripheral blood lymphocytes in vitro.The evaluation of DNA damage on human lymphocytes was performed by comet assay for three groups of ZrO(2)/LaPO(4) diphase ceramics with 30wt% of LaPO(4) (with 3wt% and 5wt% of Y(2)O(3)) and 40wt% of LaPO(4) (with 5wt% of Y(2)O(3)). The results were analyzed with SPSS16.0 software package for one-factor ANOVA and LSD.Three experimental groups with different concentration of LaPO(4) of ZrO(2)/LaPO(4) diphase ceramics, the negative control of IPS Empress II ceramics and the blank behaved little migration of the DNA strands respectively after six-day test, and there was no significant difference in all the groups except the positive control (P0.05).The study indicates little effect of DNA damage of ZrO(2)/LaPO(4) diphase ceramics.

To investigate the effect of calmodulin antagonist O-(4-ethoxyl-butyl)-berbamine (EBB) on proliferation of human breast cancer cell MCF-7 and its possible mechanism.MTT assay was used to analyze the effect of EBB on tumor cells growth. Flow cytometry was used to detect its impact on the cell cycle of MCF-7 cells. Immunofluoresce labeling technique and laser scanning confocal microscope were used to reveal the changes of the microtubule, microfilament, mitochondrion, and endoplasmic reticulum in the cells.The IC50 value of EBB in MCF-7 cells was (13.0 +/- 3.7) micromol/L. MCF-7 cells were arrested at S phase after EBB treatment. Meanwhile, depolymerization of the microtubule and microfilament, impairment of the mitochondrion and swelling of endoplasmic reticulum were observed.EBB arrests MCF-7 cells at S phase by inhibiting the growth of MCF-7 cells, which may be related to the changes of structures and functions of the microtubule, microfilament, mitochondrion, and endoplasmic reticulum.

To compare the effect between mini-traumatic bone-grafting and non-bone-grafting in percutaneous K-wire fixation for treating the calcaneal fractures.From 2002 to 2006, 112 patients with the type II (Paley type) fractures of calcaneus were studied. There were 56 cases in bone-grafting group involving 36 males and 20 famales,aged from 21 to 65, averaged (42.0 +/- 2.3) years; 11 cases were in type II a and 45 were in type II b; the course was from 3 to 14 days, averaged (6.0 +/- 1.2) days. And there were 56 cases in non-bone-grafting group involving 38 males and 18 famales,aged from 22 to 67, averaged (43.0 +/- 2.5)years; 13 cases were in type II a and 43 were in type II b; the course was from 2 to 15 days, averaged (5.0-2.1) days. All the cases were treated by closed reduction and percutaneous K-wire fixation, and bone-grafting group(56 cases) were treated by mini-traumatic bone-grafting, but the other group (56 cases) were not. The collapsing rate and fineness rate were compared.All the cases were followed up from 5 to 52 months. There were no collapsing cases in the bone-grafting group after operation, but 3 cases occurrenced re-collapsing in the non-bone-grafting group. According to the Zhang Tie-liang's evaluation criterion, in the bone-grafting group,the results were excellent in 43 cases, good in 12, fair in 1, the fineness rate was 98.2%. In the non-bone-grafting group,the results were excellent in 37 cases, good in 16, fair in 2, poor in 1, the fineness rate was 94.7%.Treatment of the type II fracture of calcaneus with closed reduction, percutaneous K-wire fixation and mini-traumatic bone-grafting can prevent the posterior talar articular surface of caltaneus from collapsing again after operation, enhance the union of fracture, elevate the curative effect, thus it should be taken with the standard therapeutic regimen.

To characterize the immune responses including local and systemic immunity induced by infection with H pylori, especially with CagA+ H pylori strains and the underlying immunopathogenesis.A total of 711 patients with different gastric lesions were recruited to determine the presence of H pylori infection and cytotoxin associated protein A (CagA), the presence of T helper (Th) cells and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMCs), expression of plasma cytokines, and RNA and protein expression of IFN-gamma and IL-4 in gastric biopsies and PBMCs were determined by rapid urease test, urea [(14)C] breath test, immunoblotting test, flow cytometry , real time RT-PCR and immunohistochemistry.Of the patients, 629 (88.47%) were infected with H pylori; 506 (71.16%) with CagA+ and 123 (17.30%) with CagA- strains. Among patients infected with CagA+ H pylori strains, Th1-mediated cellular immunity was associated with earlier stages of gastric carcinogenesis, while Th2-mediated humoral immunity dominated the advanced stages and was negatively associated with an abundance of Treg cells. However, there was no such tendency in Th1/Th2 polarization in patients infected with CagA- H pylori strains and those without H pylori infection.Polarization of Th cell immune responses occurs in patients with CagA+ H pylori infection, which is associated with the stage and severity of gastric pathology during the progression of gastric carcinogenesis. This finding provides further evidence for a causal role of CagA+ H pylori infection in the immunopathogenesis of gastric cancer.