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We demonstrate the regulation of metal-support interactions (MSI) by impregnating Co(NO3)2 as a precursor of cobalt over the silica coated with different amounts of amorphous carbon via carbonizing the glucose as a precursor in the inert atmosphere of an Ar. The materials were characterized by XRD, H2-TPR, H2-TPD, XPS, O2 titration, and N2 adsorption-desorption at low temperatures. In comparison with the parent 10 wt% Co/SiO2, the Co-supported carbon-coated SiO2 (10 wt% Co/xC-SiO2) showed obviously higher dispersion of the metallic cobalt (Co0) and smaller Co0 particle size. Moreover, the Co0 dispersion was increased and the Co0 particle size was decreased with increasing the carbon content over the catalysts. The weakened MSI between Co0 and the xC-SiO2, the extent of which is dependent on the carbon content, was clearly revealed from the characterization results. This was further supported by the reaction results of Fischer-Tropsch synthesis (FT), and the highest CO conversion was obtained over 10 wt% Co/1C-SiO2. The simple procedure and the cheap glucose make it important for developing a more efficient FT catalyst.

The present study investigated the role of echinocystic acid (EA) on the expression of nuclear factor (NF)-κB and cytochrome P450 1A1 (CYP1A1), and aortic morphology, in a rat model of hyperhomocysteinemia (Hhcy). A total of 50 Sprague Dawley rats were randomly divided into five groups as follows: Normal control (NC), model control (MC), vitamin control (VC; folic acid 1 mg/kg + vitamin B2 2 mg/kg + vitamin B12 10u g/kg), EA1 (20 mg/kg EA) and EA2 (40 mg/kg EA). Plasma homocysteine (Hcy) levels were determined via high performance liquid chromatography, and the morphology of the aorta was investigated using hematoxylin and eosin staining. Furthermore, aortic mRNA and protein levels of NF-κB and CYP1A1 were measured using reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. Plasma Hcy levels, and aortic mRNA and protein levels of NF-κB and CYP1A1, were significantly lower in the EA-treated group compared with the MC group (all P

To clarify the effects of lung function following exposure to diesel engine exhaust (DEE), we recruited 137 diesel engine testing workers exposed to DEE and 127 non-DEE-exposed workers as study subjects. We performed lung function tests and measured cytokinesis-block micronucleus (CBMN) cytome index and levels of urinary polycyclic aromatic hydrocarbons (PAHs) metabolites. There was a significant decrease of forced expiratory volume in 1 second (FEV1), ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1/ FVC), maximal mid expiratory flow curve (MMF), forced expiratory flow at 50% of FVC (FEF50%), and forced expiratory flow at 75% of FVC (FEF75%) in the DEE-exposed workers than non-DEE-exposed workers (all p

// Chengcao Sun 1, * , Chuanfeng Huang 1, 2, * , Shujun Li 1, 3 , Cuili Yang 1 , Yongyong Xi 1 , Liang Wang 1 , Feng Zhang 1 , Yunfeng Fu 4 , Dejia Li 1 1 Department of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, P.R.China 2 Department of Pharmacology, Basic Medical School, Nanyang Medical College, 473003 Nanyang, P.R.China 3 Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, 430071 Wuhan, P.R.China 4 The Third Xiang-Ya Hospital, Central South University, 410013 Changsha, P.R.China * These authors contributed equally to this work Correspondence to: Dejia Li, e-mail: lodjlwhu@sina.com Yunfeng Fu, e-mail: fuyfeng427@163.com Keywords: Hsa-miRNA-326 (miR-326), cyclin D1, non-small cell lung cancer (NSCLC), proliferation, apoptosis Received: August 18, 2015 Accepted: January 13, 2016 Published: January 29, 2016 ABSTRACT Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1 .

Chronic hepatitis B virus (HBV) infection, which can lead to hepatic disease, has become a critical national healthcare problem, and many people die each year as a result of HBV infection and its complications. Although microRNA-33a (miR-33a) is a novel modulator of lipid and cholesterol metabolism, the role of miR-33a in the hepatic fibrogenesis is still unknown. Here, we aimed to explore the roles and mechanisms of miR-33a in liver fibrosis. miR-33a expression in whole liver and serum samples was measured from chronic hepatitis B (CHB) patients by quantitative real-time PCR (qRT-PCR). In addition, different murine hepatic fibrosis models were produced to consolidate the results in human tissue. Human and murine primary liver fibrosis-associated cells were isolated and treated with transforming growth factor-β1 (TGF-β1). miR-33a expression levels in liver tissue significantly increased with a fibrosis progression manner in the human liver. Furthermore, serum miR-33a levels associated positively with progressing process of hepatic fibrosis. miR-33a was in particular increased in hepatic stellate cells (HSC) than other liver fibrosis-associated cells. Stimulation of HSCs with TGF-β1 leads to a critical increase of miR-33a. Increasing miR-33a levels increased (whereas inhibiting miR-33a weakened) the activation role of TGF-β1 in LX-2 cells, which might be a potential mechanism through moderating Smad7 expression. miR-33a may be a novel marker for HSC activation and hepatic fibrosis progress, suggesting a new therapeutic target in liver fibrosis.

To investigate the roles and mechanisms of miR-33a in liver fibrosis, miR-33a expression in whole liver and serum samples was measured from chronic hepatitis B (CHB) patients by quantitative real-time PCR (qRT-PCR). In addition, Human and murine primary liver fibrosis-associated cells were isolated and treated with transforming growth factor-β1 (TGF-β1). We found that miR-33a expression levels in liver tissue significantly increased with a fibrosis progression manner in the human liver. Furthermore, serum miR-33a levels associated positively with progressing process of hepatic fibrosis. miR-33a was in particular increased in hepatic stellate cells (HSC) than other liver fibrosis-associated cells. Stimulation of HSCs with TGF-β1 leads to a critical increase of miR- 33a. Increasing miR-33a levels increased (whereas inhibiting miR-33a weakened) the activation role of TGF-β1 in LX-2 cells, which might be a potential mechanism through moderating Smad7 expression. Altogether, data suggest that miR-33a may be a novel marker for HSC activation and hepatic fibrosis progress, suggesting a new therapeutic target in liver fibrosis.

To elucidate the mechanism of carcinogenesis induced by coke oven emissions by investigating the cell genetic damage index and the methylation of O⁶-methylguanine-DNA methyltransferase (MGMT).The human bronchial epithelial cell 16HBE was treated by 1 µmol/L B(a)P for 48 h, and then was exposed continuously to either 1‰ dimethyl sulfoxide (DMSO) or organic extracts of coke oven emission (OE-COE) for five days at the concentrations of 0, 2.5, 5.0, 10.0 and 20.0 µg/ml. The methylation-specific PCR (MSP-PCR), RT-PCR and immunoblotting were applied to detect the methylation status, changes of mRNA and protein of MGMT, respectively. Single cell gel electrophoresis was used to detect DNA damage induced by OE-COE.Compared with the control group (DMSO), there was a significant hypermethylation in all study groups, along with the suppression of mRNA and protein in a dose-dependent manner, and the gradation ratio of them was 1.0, 0.96, 0.96, 0.85, 0.32 and 1.0, 1.0, 1.1, 0.41, 0.52, separately. There was a significant DNA damage with a dose-effect relationship in all study groups (F = 41.22, P0.05), and the comet Olive tail moment was (2.98 ± 1.43), (4.76 ± 1.79), (10.09 ± 1.75), (11.38 ± 1.77), (11.67 ± 1.88). The further study found that the index of DNA damage was negatively correlated to the expression of MGMT mRNA and its protein.The DNA damage induced by COE might be associated with the suppression of MGMT caused by its hypermethylation.

Under the presupposition of competition level keeping unchangeable, we construct a random evolution model of Incomplete Competitive System to explore its structure, nature and evolution behavior based on the random choice mechanism to competitors by mathematical analysis and numerical simulation. In this model, the death probability of node keeps a logarithm correlation with its original competence. System size may present three kinds of states: monotonic increase, stable, monotonic decrease, and it depends on the quitting threshold of system node and system competitive coefficient. The competence of node will decrease with an exponential or power speed, and in a long time, the competence distribution appears stable which is overlapped by a power law with -1 and original competence distribution. There is a power law or logarithmic correlation between node’s life and its original competence. The number of one node’s competitor will be monotonic increasing logarithmically before its death, and will be proportional to the logarithm of its age. System’s degree distribution obeys an exponential distribution approximately, and it doesn’t depend on the original node competence distribution.

To investigate the associations of polymorphisms of metabolic enzyme genes with urinary 1-hydroxypyrene levels in coke oven workers.One hundred and forty-eight workers from a coke oven plant and 69 controls without occupational PAHs exposure were selected in this study. Urinary 1-hydroxypyrene was detected by high performance liquid chromatography with florescence detector. The genotypes at I462V site in exon 7 of CYP1A1 gene, GSTM1, GSTT1, I105V site in GSTP1gene, Pst1 and Dra1 sites in CYP2E1 gene, P187S site in NQO1 gene, Kpn1, BamH1 and Taq1 sites in NAT2 gene, and H113Y, R139H sites in mEH gene were determined by PCR-based methods. Personal information including occupational exposure history, age, sex, smoking and drinking status was collected by the questionnaire.The level of urinary 1-hydroxypyrene in coke oven workers [(5.61 +/- 1.04) mol/mol Cr] was higher than that in control [(0.74 +/- 0.32) micro mol/mol Cr]. After adjusting external occupational exposure category and smoking, coke oven workers with variant homozygotes at H113Y site of mEH gene had significantly higher urinary 1-hydroxypyrene concentrations than those with heterozygotes, and wild homozygotes (6.41 +/- 1.09 vs. 6.24 +/- 1.08, and 4.62 +/- 0.95 micro mol/mol Cr, P0.05), and gene-gene interaction was found between CYP1A1 and mEH.Genetic polymorphism of mEH gene could be a susceptible biomarker in coke oven workers which was involved in the individual susceptibility on metabolism of PAHs.