Biomedical subjects

Jing Yuan

Publications and source records attributed to Jing Yuan.

At least 37 records · Page 2Linked to original sources

PubMed2006

Mammalian Pol III promoter H1 can transcribe shRNA inducing RNAi in chicken cells.

Double-stranded RNA-mediated interference (RNAi) has recently emerged as a powerful reverse genetic tool to silence gene expression in multiple organisms. RNAi based on DNA vector is not sufficiently established in chicken species. The present study was performed to evaluate RNAi induced by shRNA transcribed from mammalian Pol III promoter H1 in the chicken cells by using a dual fluorescence reporter assay, a plasmid encoding GFP and a plasmid encoding RFP. The evaluation of RNAi efficiency was performed in two kinds of chicken cell type: primary CEF cells and chicken DT-40 cells by lipofection. GFP- and RFP-expressing cells were observed under fluorescent microscopy, and their mRNAs content were analyzed by quantitative RT-PCR. The intensity of the green fluorescence generated by GFP was greatly suppressed by human H1 promoter transcribed GFP-shRNA. Quantitative RT-PCR analysis showed that normalized GFP mRNA expression was reduced to 37 and 32 in primary CEF and DT-40 cells, respectively. In contrast to GFP, the intensity of the red fluorescence generated by RFP protein and the RFP mRNA levels remained unchanged. Consequently, it was concluded that the RNAi induced by shRNA transcribed from mammalian Pol III promoter H1 is applicable to suppress the gene expression specifically and efficiently in chicken cells.

Animals↗

PubMed2006

Analysis of IgG subclass antibodies and expression of T-Cell receptor signaling molecules in anti-CD4 monoclonal antibody treated mice with autoimmune cardiomyopathy.

T-cell immune abnormality in patients of dilated cardiomyopathy has been intensively studied over the past 10 years. In this study, we aim to focus on the molecular mechanism of T-cells in autoimmune cardiomyopathy mouse model by detecting the expression of three T-cell signaling molecules. Balb/C mice (n = 12) were immunized with the peptides derived from human ADP/ATP carrier on the 1st, 14th, 28th, 49th and 79th days, and half of them were also injected with anti-L3T4 McAb on the - 1st, 0 and 1st days. The sham-immunized mice were taken as the controls (n = 6). The main result shows that the antibody response of IgG subclasses such as IgG1, IgG2b and IgG3 were definitely blocked except IgG2a in CD4+ cell-depleted Balb/C mice. In addition, the average mRNA expression of p56lck, p59fyn and zap-70 were all found to be dramatically higher in the mice immunized with only ADP/ATP carrier peptides than in the control-group. At meantime, reduced levels of the protein kinases p56lck, p59fyn and zap-70 were clearly observed in anti-CD4 McAb immunized group compared with DCM group. We propose that the proliferation of T-cells was significantly inhibited in anti-CD4 treated mice and CD4+ T-cells may play a critical role in ADP/ATP carrier caused mouse DCM.

Animals↗

PubMed2006

Orthogonal adaptation for multichannel feedforward control.

In active noise control, it is desired to generate destructive interference by model-independent control. This is possible for single-channel systems to which a recently proposed method, called orthogonal adaptation, is applicable. In this study, the new method is extended to multichannel systems. An important issue is how to optimize a feedforward controller in the minimum H2 norm sense. In practice, secondary paths of some multichannel systems may be nonminimum phase. It is a difficult problem to design H2 feedforward controllers for multichannel systems with nonminimum phase secondary paths. The problem is solved analytically here with the best achievable, a practical and an economical solution. A recursive least squares algorithm is presented for online identification of multiple paths without persistent excitations. These solutions make it possible to implement noninvasive mode-independent controllers for multichannel systems. Experiment results are presented to verify the analytical results.

Journal Article↗

PubMed2006

Virus and cell RNAs expressed during Epstein-Barr virus replication.

Changes in Epstein-Barr virus (EBV) and cell RNA levels were assayed following immunoglobulin G (IgG) cross-linking-induced replication in latency 1-infected Akata Burkitt B lymphoblasts. EBV replication as assayed by membrane gp350 expression was approximately 5% before IgG cross-linking and increased to more than 50% 48 h after induction. Seventy-two hours after IgG cross-linking, gp350-positive cells excluded propidium iodide as well as gp350-negative cells. EBV RNA levels changed temporally in parallel with previously defined sensitivity to inhibitors of protein or viral DNA synthesis. BZLF1 immediate-early RNA levels doubled by 2 h and reached a peak at 4 h, whereas BMLF1 doubled by 4 h with a peak at 8 h, and BRLF1 doubled by 8 h with peak at 12 h. Early RNAs peaked at 8 to 12 h, and late RNAs peaked at 24 h. Hybridization to intergenic sequences resulted in evidence for new EBV RNAs. Surprisingly, latency III (LTIII) RNAs for LMP1, LMP2, EBNALP, EBNA2, EBNA3A, EBNA3C, and BARTs were detected at 8 to 12 h and reached maxima at 24 to 48 h. EBNA2 and LMP1 were at full LTIII levels by 48 h and localized to gp350-positive cells. Thus, LTIII expression is a characteristic of late EBV replication in both B lymphoblasts and epithelial cells in immune-comprised people (J. Webster-Cyriaque, J. Middeldorp, and N. Raab-Traub, J. Virol. 74:7610-7618, 2000). EBV replication significantly altered levels of 401 Akata cell RNAs, of which 122 RNAs changed twofold or more relative to uninfected Akata cells. Mitogen-activated protein kinase levels were significantly affected. Late expression of LTIII was associated with induction of NF-kappaB responsive genes including IkappaBalpha and A20. The exclusion of propidium, expression of EBV LTIII RNAs and proteins, and up-regulation of specific cell RNAs are indicative of vital cell function late in EBV replication.

Blotting, Western↗

PubMed2006

Concerted functions of Gab1 and Shp2 in liver regeneration and hepatoprotection.

Liver regeneration is a rapid and concerted response to injury, in which growth factor-generated intracellular signals result in activation of transcription factors, DNA synthesis, and hepatocyte proliferation. However, the link between cytoplasmic signals resulting in proliferative response to liver injury remains to be elucidated. We show here that association of Gab1 adaptor protein and Shp2 tyrosine phosphatase is a critical event at the early phase of liver regeneration. Partial hepatectomy (PH) rapidly and transiently induced assembly of a complex comprising Shp2 and tyrosine-phosphorylated Gab1 in wild-type hepatocytes. Consistently, liver-specific Shp2 knockout (LSKO) and liver-specific Gab1 knockout (LGKO) mice displayed very similar phenotypes of defective liver regeneration triggered by PH, including blunted extracellular signal-regulated kinase 1/2 (Erk1/2) activation, decreased expression of immediate-early genes, and reduced levels of cyclins A, E, and B1, as well as suppression of hepatocyte proliferation. In contrast, the Akt and interleukin-6/Stat3 pathways were up-regulated posthepatectomy in LSKO and LGKO mice, accompanied by improved hepatoprotection. Collectively, this study establishes the physiological significance of the Gab1/Shp2 link in promoting mitogenic signaling through the Erk pathway in mammalian liver regeneration.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Polymorphisms in the two helicases ERCC2/XPD and ERCC3/XPB of the transcription factor IIH complex and risk of lung cancer: a case-control analysis in a Chinese population.

The transcription factor IIH (TFIIH) helicases ERCC2/XPD and ERCC3/XPB are responsible for opening the DNA strand around the lesion site during nucleotide excision repair process. Genetic variants in these two genes may be markers for interindividual variability in DNA repair capacity and thus predisposition to cancer risk. In this case-control study of 1,010 incident lung cancer cases and 1,011 age and sex frequency-matched cancer-free controls in a Chinese population, we genotyped eight tagging polymorphisms of ERCC2 and ERCC3 using the high-throughput Taqman platform to determine their associations with risk of lung cancer. Although none of the eight polymorphisms was individually associated with lung cancer risk, we found that genetic variants in ERCC2 and ERCC3 jointly contributed to lung cancer risk in a dose-response manner. Compared with those with 0 to 1 "at-risk" locus, subjects carrying >1 at-risk loci were at increased risk for lung cancer [adjusted odds ratio (OR), 1.29; 95% confidence interval (95% CI), 0.98-1.70 for 2 at-risk loci; adjusted OR, 1.38; 95% CI, 1.02-1.85 for 3 at-risk loci; and adjusted OR, 1.51; 95% CI, 1.09-2.10 for > or =4 at-risk loci, respectively; P(trend) = 0.015]. This combined effect was slightly more evident in young subjects (<60 years), males, current smokers, and those with family history of cancer, particularly for histologic type of adenocarcinomas. No evidence for interaction was found. These findings indicate that these tagSNPs of the ERCC2 and ERCC3 along with their surrounding regions may serve as biomarkers of susceptibility to lung cancer, which warrant further validation by other population-based and phenotypic studies to determine the biological relevance of these tagSNPs.

Adenocarcinoma↗

PubMed2006

Association of polymorphisms in AhR, CYP1A1, GSTM1, and GSTT1 genes with levels of DNA damage in peripheral blood lymphocytes among coke-oven workers.

Accumulating evidence has shown that both DNA damage caused by the metabolites of polycyclic aromatic hydrocarbons (PAH) and genetic polymorphisms in PAH-metabolic genes contribute to individual susceptibility to PAH-induced carcinogenesis. However, the functional relevance of genetic polymorphisms in PAH-metabolic genes in exposed individuals is still unclear. In this study of 240 coke-oven workers (the exposed group) and 123 non-coke-oven workers (the control group), we genotyped for polymorphisms in the AhR, CYP1A1, GSTM1, and GSTT1 genes by PCR methods, and determined the levels of DNA damage in peripheral blood lymphocytes using the alkaline comet assay. We found that the ln-transformed Olive tail moment (Olive TM) values in the exposed group were significantly higher than those in the control group (P < 0.001). Furthermore, in the exposed group, the Olive TM values in subjects with the AhR Lys(554) variant genotype were higher than those with the AhR Arg(554)/Arg(554) genotype (P = 0.021). Similarly, the Olive TM values in the non-coke-oven workers with the CYP1A1 MspI CC + CT genotype were lower than the values of those with the CYP1A1 MspI TT genotype (P = 0.005). However, these differences were not evident for GSTM1 and GSTT1. These results suggested that the polymorphism of AhR might modulate the effects of PAHs in the exposed group; however, the underlying molecular mechanisms by which this polymorphism may have affected the levels of PAH-induced DNA damage warrant further investigation.

Adult↗

PubMed2006

Elevated levels of urinary 8-hydroxy-2 -deoxyguanosine, lymphocytic micronuclei, and serum glutathione S-transferase in workers exposed to coke oven emissions.

To investigate associations among occupational exposure to coke oven emissions (COEs), oxidative stress, cytogenotoxic effects, change in the metabolizing enzyme glutathione S-transferase (GST), and internal levels of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers, we recruited 47 male coke oven workers and 31 male control subjects from a coke oven plant in northern China. We measured the levels of 1-hydroxypyrene (1-OHP) and 8-hydroxy-2 -deoxyguanosine (8-OHdG) in urine, micronucleated binucleated cells (BNMNs) in peripheral blood lymphocyte, and GST in serum. Our results showed that the group exposed to COEs had significantly increased levels of 1-OHP [median 5.7; interquartile range (IQR), 1.4-12.0 micromol/mol creatinine] compared with the control group (3; 0.5-6.4 micromol/mol creatinine). In addition, the median levels (IQR) of 8-OHdG, BNMNs, and GST were markedly increased in the exposed [1.9 (1.4-15.4) micromol/mol creatinine; 6 (2-8) per thousand ; 22.1 (14.9-31.2) U/L, respectively] compared with controls [1.3 (1.0-4.0) micromol/mol creatinine, 2 (0-4) per thousand; and 13.1 (9.5-16.7) U/L, respectively]. These results appeared to be modified by smoking. However, multivariate logistic regression analysis revealed that exposure to COEs had the highest odds ratio among variables analyzed and that smoking was not a significant confounder of the levels of studied biomarkers. Overall, the present findings suggest that COE exposure led to increased internal PAH burden, genetic damage, oxidative stress, and GST activity. The consequences of the changes in these biomarkers, such as risk of cancer, warrant further investigations.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2006

Overexpressed heat shock protein 70 protects cells against DNA damage caused by ultraviolet C in a dose-dependent manner.

Heat shock protein 70 (Hsp70) comprises proteins that have been reported to protect cells, tissues, and organisms against damage from a wide variety of stressful stimuli; however, little is known about whether Hsp70 protects against DNA damage. In this study, we investigated the relationship between Hsp70 expression and the levels of ultraviolet C (UVC)-induced DNA damage in A549 cells with normal, inhibited, and overexpressed Hsp70 levels. Hsp70 expression was inhibited by treatment with quercetin or overexpressed by transfection of plasmids harboring the hsp70 gene. The level of DNA damage was assessed by the comet assay. The results showed that the levels of DNA damage (shown as the percentage of comet cells) in A549 cells increased in all cells after exposure to an incident dose of 0, 10, 20, 40, and 80 J/m2 whether Hsp70 was inhibited or overexpressed. This response was dose dependent: a protection against UVC-induced DNA damage in cells with overexpressed Hsp70 was observed at UVC dose 20 J/m2 with a maximum at 40 J/m2 when compared with cells with normal Hsp70 levels and in quercetin-treated cells. This differential protection disappeared at 80 J/m2. These results suggest that overexpressed Hsp70 might play a role in protecting A549 cells from DNA damage caused by UVC irradiation, with a threshold of protection from at UVC irradiation-induced DNA damage by Hsp70. The detailed mechanism how Hsp70 is involved in DNA damage and possible DNA repair warrants further investigation.

Cell Line, Tumor↗

PubMed2006

[Relationship between Shenzhen HBV genotype and precore/core promoter mutation and antiviral effects].

BACKGROUND: To study the relationship between hepatitis B virus genotyping Shenzhen isolates and HBV precore/core promoter mutation and antiviral effects. METHODS: The HBV genotyping of 165 patients with HBV was carried out with mAbs ELISA. HBV precore/core promoter mutation was detected with gene chip technology in 24 patients with CHB. The relationship between HBV genotyping and interferon, lamivudine effects was analyzed. RESULTS: (1) Out of 165 cases, 106 (64.2%) of type B but 48 (29.1%) of type C were found. Type B accounted for 95.4% in group ASC, and type C for 64.7%in group LC (P<0.05). (2) Precore/core promoter mutation was found in 16 cases (10 of type B, and 6 of type C) out of 24 cases. Out of 16 cases, precore/core promoter mutation (nt1896, 1862) was found in 10 cases (9 cases of type B and 1 case of type C), while basal core promoter mutation (BCP mutation, nt1762,1764) was found in 6 cases (1 case of type B and 5 of type C). (3) Among 27 patients with CHB HBAg (+) treated with interferon, 11 cases of type B but 1 case of type C were tested to be fully responsive to interferon. Among 29 patients with CHB HBAg (+) treated with lamivudine, 15 cases of type B but 3 cases of type C were tested to be continuously responsive to lamivudine. CONCLUSION: (1) HBV genotype popularity in Shenzhen area was classified as type B the first and type C the second. (2) Type C seems more apt to develop BCP mutation and cirrhosis, and to be less responsive to interferon or lamivudine.

Adolescent↗

PubMed2006

[Role of reactive oxygen species in sodium selenite induced DNA damage in HepG2 cells].

OBJECTIVE: To investigate the mechanisms of sodium selenite induced DNA damage in HepG2 cells. METHODS: HepG2 cells were treated with the designed concentrations of sodium selenite and the selenite (10 micromol/L) added simultaneously with GSH (10 mmol) and NAC (5 mmol). Then the cell viability was detected by MTT, and the flurescent intensity of reactive oxygen species (ROS) was determined by flow cytometry, and DNA damage was detected by commet assay. RESULTS: The level of ROS was increased after HepG2 was treated with 5, 10, 20 micromol/L sodium selenite for one hour, and the cell viability was decreased after 12 hours, and the DNA damage was enhanced. Compared with the control group, the difference was statistically significant (P < 0.05) . GSH and NAC effectively inhibited the ROS increased and cell viability decreased and DNA damage weakened. CONCLUSION: ROS may be the important reason that sodium selenite induced HepG2 cells DNA damage.

DNA Damage↗

PubMed2006

[Stress proteins of Bifidobacterium longum NCC2705].

Stress proteins of Bifidobacterium longum strain NCC2705 were identified and characterized during stationary phase. According to the proteomic map of L. lactics IL1403 and theoretical Mr/pl of stress proteins in B. longum NCC2705 genome annotation, spots of stress proteins in gels were localized, and proteins were identified by matrix-assisted laser desorption/ionization time of flight (MALDI-TOF) and/or ESI-MS/MS mass spectrometry. For protein identification by peptide mass fingerprinting, peptide masses were searched against database of B. longum NCC2705 by Mascot licensed in-house. 44 spots representing 8 protein entries have been identified, these proteins were hydrophilic proteins and predicted acid proteins. Spot and protein analysis revealed that post-translational modifications might be common in these proteins. Except for DnaJ, the stress proteins were encoded by genes with CAI value above 0.5, and represented a large proportion of the most abundant proteins. Moreover, the results of scavenging effects on free radicals in vitro showed that B. longum NCC2705 can inhibit fatty acid oxidation and scavenge DPPH, but they scavenge weakly active oxygen free radicals. We identified a key protein that can reverse oxidative damage to proteins and lipids: alkyl hydroperoxide reductase (ahpC, BL0615)synthesized under our experimental conditions.

Bacterial Proteins↗

PubMed2006

[Protective effects of Denghuang injection on cerebral infarction in animal].

OBJECTIVE: To observe the protective effects of Denghuang injection on cerebral infarction in animal. METHOD: The study evaluated the protective effects of Denghuang injection on cerebral infarction through 3 experiments: 1. ligating the arteria cerebri media of dog; 2. blocking the internal carotid artery of rat; 3. ligating the common carotiol artery of gerbil. RESULT: The results showed Denghuang injection could reduce the cerebral infarction area after the dog's arteria cerebri media was ligated, and also could restrain the AKP&CK increase. The injection could reduce the cerebral infarction area of rat after the internal carotid artery was bloked by thrombus, and the mark of behavior and nerve symptom was better than that in the control group. Denghuang injection could obviously reduce the water content in pallium of gerbil after the common carotiol artery was ligated, and also could increase the amount of living pyramidal neuron in hippocampus, and reduce the MDA&LDH increase in pallium slurry. CONCLUSION: Denghuang injection can obviously protect animal on cerebral infarction.

Alkaline Phosphatase↗

PubMed2005

[Effects of immunotherapy with anti-L3T4 monoclonal antibody on autoimmune cardiomyopathy: experiment with mice].

OBJECTIVE: To evaluate the effects of immunotherapy with anti-L3T4 monoclonal antibody (McAb) on autoimmune cardiomyopathy. METHODS: 24 male Balb/c mice were immunized with mitochondria ADP/ATP carrier peptides so as to establish a model of autoimmune cardiomyopathy, and then randomly divided into 4 equal groups: cardiomyopathy control group, early-treated group injected with anti-L3T4 McAb on the day before immunization, the very day of immunization, and 1 day after the immunization, mid-term-treated group, administrated with anti-L3T4 McAb on the 89th, 90th and 91st days after immunization, and sham-immunization control group, injected with solution without anti-L3T4 McAb. Six months after blood samples were collected. The serum antibodies against ADP/ATP carrier were examined with ELISA, and the expression of IFN-gamma and IL-4, T cell cytokines, in T cells were detected by 3-color flow cytometry. The myocardium underwent pathological examination by using light and electron microscopes. The bulk percentages of cardiac collagen fiber were calculated with computer. RESULTS: Antibodies against ADP/ATP carrier were negative in the early-treated group and the sham-immunization control group and positive in the mid-term-treated and cardiomyopathy groups with a transient decline in the mid-term-treated group. By the end of 6 month, there were no cardiac morphological and histopathological changes like those in dilated cardiomyopathy (DCM) in the early-treated group and sham-immunization group, while they were found in the mid-term-treated and cardiomyopathy groups with severer myocardial impairments in the cardiomyopathy group. The percentage of IFN-gamma/IL-4 of the early-treated group was 6.56% +/- 0.21%/2.54% +/- 0.20%, not significantly different from that of the control group (5.87% +/- 0.19%/2.16% +/- 0.10%), however, the values of these 2 groups were significantly higher than those of the mid-term-treated group (8.91% +/- 0.33%/5.15% +/- 0.13%, both P < 0.01) and the cardiomyopathy group (7.85% +/- 1.42%/9.45% +/- 1.70%, both P < 0.01). CONCLUSION: Anti-L3T4 McAb administration is effective on protection from autoimmune cardiomyopathy induced by mitochondria ADP/ATP carrier peptides, especially being used at the initial phase of this disease.

Animals↗

PubMed2005

The heteromeric Nanoarchaeum equitans splicing endonuclease cleaves noncanonical bulge-helix-bulge motifs of joined tRNA halves.

Among the tRNA population of the archaeal parasite Nanoarchaeum equitans are five species assembled from separate 5' and 3' tRNA halves and four species derived from tRNA precursors containing introns. In both groups an intervening sequence element must be removed during tRNA maturation. A bulge-helix-bulge (BHB) motif is the hallmark structure required by the archaeal splicing endonuclease for recognition and excision of all introns. BHB motifs are recognizable at the joining sites of all five noncontinuous tRNA species, although deviations from the canonical BHB motif are clearly present in at least two of them. Here, we show that the N. equitans splicing endonuclease cleaves tRNA precursors containing normal introns, as well as all five noncontinuous precursor tRNAs, at the predicted splice sites, indicating the enzyme's dual role in the removal of tRNA introns and processing of tRNA halves to be joined in trans. The cleavage activity on a set of synthetic canonical and noncanonical BHB constructs showed that the N. equitans splicing endonuclease accepts a broader range of substrates than the homodimeric Archaeoglobus fulgidus enzyme. In contrast to the A. fulgidus endonuclease, the N. equitans splicing enzyme possesses two different subunits. This heteromeric endonuclease type, found in N. equitans, in all Crenarchaeota, and in Methanopyrus kandleri, is able to act on the noncanonical tRNA introns present only in these organisms, which suggests coevolution of enzyme and substrate.

Base Pairing↗

PubMed2005

Chlorinated river and lake water extract caused oxidative damage, DNA migration and cytotoxicity in human cells.

Consumption of chlorinated drinking water is suspected to be associated with adverse health effects, including mutations and cancer. In the present study, the genotoxic potential of water from Donghu lake, Yangtze river and Hanjiang river in Wuhan, an 8-million metropolis in China, was investigated using HepG2 cells and the alkaline version of the comet assay. It could be shown that all water extracts caused dose-dependent DNA migration in concentrations corresponding to dried extracts of 0.167-167 ml chlorinated drinking water per ml medium. To explore whether the intracellular redox status is regulated by chlorinated drinking water, we determined lipid peroxidation (LPO) and depletion of reduced glutathione (GSH). The malondialdehyde (thiobarbituric acid (TBA)-reactive aldehydes) concentration increased after chlorinated drinking water treatment of HepG2 cells in a dose-dependent manner, the GSH content decreased. The activity of lactate dehydrogenase (LDH) increased in chlorinated drinking water treated HepG2 cells indicating cytotoxicity. In accordance with former studies which dealt with in vivo and in vitro micronucleus induction the present study shows that chlorinated drinking water from polluted raw water may entail genetic risks.

China↗

PubMed2005

The RhoGAP protein DLC-1 functions as a metastasis suppressor in breast cancer cells.

The identification of molecular signatures characteristic of tumor cells that are capable of metastatic spread is required for the development of therapeutic interventions to abrogate this lethal process. To facilitate this, we have previously characterized an experimental system in which the role of candidate metastasis-related genes can be screened and tested. Monoclonal cell lines M4A4 and NM2C5 are spontaneously occurring sublines of the MDA-MB-435 cell breast tumor cell line that exhibit phenotypic differences in growth, invasion, and metastatic efficiency in athymic mice. In this study, transcriptional profiles of these cell lines were created using oligonucleotide microarrays representing over 12,000 genes. Intensity modeling and hierarchical clustering analysis identified a 171-gene expression signature that correlated with metastatic phenotype and highlighted several GTPase signaling components. Restoration of one of these GTPases, deleted in liver cancer-1 (DLC-1), in metastatic M4A4 cells to levels observed in the nonmetastatic NM2C5 cell line resulted in the inhibition of migration and invasion in vitro and a significant reduction in the ability of these cells to form pulmonary metastases in athymic mice. These studies show the utility of expression profiling, in an appropriate experimental system, to identify genetic determinants of metastatic sufficiency. The finding that DLC-1 can act as a metastasis-suppressor gene supports an influential role for GTPase signaling in tumor progression.

Animals↗

PubMed2005

Supramolecular assemblies of a series of 2-arylbenzimidazoles at the air/water interface: in situ coordination, surface architecture and supramolecular chirality.

The spreading behavior and supramolecular assemblies of some arylbenzimidazoles with 2-substituted aromatic groups such as phenyl, naphthyl, anthryl and pyrenyl on water surface and the subphase containing AgNO3 were investigated. It was observed that although these compounds lack long alkyl chains, they showed surface activity when spread from chloroform solution on water surface and formed the supramolecular assemblies. When AgNO3 was present in the subphase, a coordination between the imidazole group of the compounds and Ag(I) occurred in situ in the spreading film, which was verified by the surface pressure/area (pi-A) isotherms and UV/Vis absorption spectra. Both the spreading films from water and the aqueous AgNO3 subphase were transferred onto solid substrates and their surface morphologies as well as properties were characterized by AFM, UV/Vis absorption and CD spectra. Various surface morphologies such as nanoparticles, block domains and nanoutensils were observed depending on the substituted aromatic groups. Interestingly, although all of these compounds were achiral, supramolecular chirality was obtained for some of the arylbenzimidazole films assembled from either the water surface or the subphase containing AgNO3. It was revealed that chiral assemblies could be obtained from water surface for the benzimidazoles which have pyrenyl or alpha-naphthyl groups. For benzimidazole derivative with anthryl group, chiral assemblies could be obtained when spreading on the aqueous AgNO3 subphase. For the benzimidazoles with phenyl or beta-naphthyl groups, no chirality was obtained. It was suggested that both the overcrowded stacking of the aromatic groups and the cooperative arrangement of the molecules on water surface or aqueous AgNO3 subphase play a crucial role in forming the chiral supramolecular assemblies.

Journal Article↗