• Transactions of the Korean Society of Automotive Engineers
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• v.14 no.3
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• pp.178-185
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• 2006

This paper investigates the steady-state combustion characteristics of the Homogeneous charge compression ignition(HCCI) engine with variable valve timing(VVT) and dimethyl ether(DME) direct injection, to find out its benefits in exhaust gas emissions. HCCI combustion is an attractive way to lower carbon dioxide($CO_2$), nitrogen oxides(NOx) emission and to allow higher fuel conversion efficiency. However, HCCI engine has inherent problem of narrow operating range at high load due to high in-cylinder peak pressure and consequent noise. To overcome this problem, the control of combustion start and heat release rate is required. It is difficult to control the start of combustion because HCCI combustion phase is closely linked to chemical reaction during a compression stroke. The combination of VVT and DME direct injection was chosen as the most promising strategy to control the HCCI combustion phase in this study. Regular gasoline was injected at intake port as main fuel, while small amount of DME was also injected directly into the cylinder as an ignition promoter for the control of ignition timing. Different intake valve timings were tested for combustion phase control. Regular gasoline was tested for HCCI operation and emission characteristics with various engine conditions. With HCCI operation, ignition delay and rapid burning angle were successfully controlled by the amount of internal EGR that was determined with VVT. For best IMEP and low HC emission, DME should be injected during early compression stroke. IMEP was mainly affected by the DME injection timing, and quantities of fuel DME and gasoline. HC emission was mainly affected by both the amount of gasoline and the DME injection timing. NOx emission was lower than conventional SI engine at gasoline lean region. However, NOx emission was similar to that in the conventional SI engine at gasoline rich region. CO emission was affected by the amount of gasoline and DME.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1171-1176
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• 2014

Objective: The tumor suppressor gene, Ras-association domain family (RASSF)2A, is inactivated by promoter hypermethylation in many cancers. The current study was performed to evaluate the methylation status of RASSF2A in epithelial ovarian cancer (EOC) tissues and plasma, and correlations with gene expression and clinicopathologic characteristics. Method: We detected methylation of the RASSF2A gene in tissues and corresponding plasma samples from 47 EOC patients and 14 patients with benign ovarian tumors and 10 with normal ovarian tissues. The methylation status was determined by methylation-specific PCR while gene expression of mRNA was examined by RT-PCR. The EOC cell line, SKOV3, was treated with 5-aza-2'-deoxycytidine (5-azadC). Results: RASSF2A mRNA expression was significantly low in EOC tissues. The frequency of aberrant methylation of RASSF2A was 51.1% in EOC tissues and 36.2% in corresponding plasma samples, whereas such hypermethylation was not detected in the benign ovarial tumors and normal ovarian samples. The expression of RASSF2A mRNA was significantly down-regulated or lost in the methylated group compared to the unmethylated group (p<0.05). After treatment with 5-aza-dC, RASSF2A mRNA expression was significantly restored in the Skov3 cell line. Conclusion: Epigenetic inactivation of RASSF2A through aberrant promoter methylation may play an important role in the pathogenesis of EOC. Methylation of the RASSF2A gene in plasma may be a valuable molecular marker for the early detection of EOC.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.11
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• pp.4945-4949
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• 2016

Background: Breast cancer is the commonest cancer in Egyptian females. Nrf2 is involved in oxidative stress while P73 functions in response to DNA damage. This study aimed to assess the role of Nrf2 promoter and P73 G4C14 to A4T14 SNPs in breast cancer in Egypt. Patients: Eighty-five female patients with breast tumours (41 malignant, 44 benign) were included. Nrf2 (rs6721961) and p73 (G4A) SNPs were determined by PCR- CTPP assay. Results: Genotype frequencies of the Nrf2 promoter SNP were 34.2% and 37.9% for AA in benign and malignant groups respectively, and 43.9% and 40.5% for CC and, 21.9 % and 21.6% for CA. Genotype frequencies for the P73 G4A SNP were 52.9% and 44.7% for GA in benign and malignant groups respectively, and 47.1% and 55.3% for GG. Discussion: Nrf2 genotypes in pre - and post-menopausal patients, showed significantly different distributions in the 2 patient groups, the AA genotype being significantly more common in pre-menopausal patients. The P73 G4A SNP showed no relation to age of disease onset. Conclusion: The Nrf2 (rs6721961) AA genotype might be related to early breast cancer onset. In contrast the P73 G4A polymorphism showed no relation to either disease risk or age at presentation.

• Microbiology and Biotechnology Letters
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• v.20 no.5
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• pp.511-518
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• 1992

We subcloned a 58 KD chitinase gene of Serratia marcescens into Escherichia coli and investigated the expression and secretion of the chitinase. Chitinase was produced in E. coli by using its own promoter but the levels of enzyme were very low, less than 5 mU/m$\ell$. However, by the combined action of the chitinase and lac promoters, the chitinase activity increased up to about 80 mU/m$\ell$. The most of the chitinase produced in E. coli was localized in periplasm and the small amounts were observed in cytosol and culture medium. Intracellular chitinase activities increased in proportion to the growth of E. coli up to the early stationary phase but rapidly decreased thereafter, which was assumed to be degradation of the chitinase by E. coli proteolytic enzymes.

• BMB Reports
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• v.45 no.12
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• pp.730-735
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• 2012

p13 gene was first described in Leucania separata multinuclear polyhedrosis virus (Ls-p13) several years ago, but the function of P13 protein has not been experimentally investigated to date. In this article, we indicated that the expression of p13 from Heliothis armigera single nucleocapsid nucleopolyhedrovirus (Ha-p13) was regulated by both early and late promoter. Luciferase assay demonstrated that the activity of Ha-p13 promoter with hr4 enhancer was more than 100 times in heterologous Sf9 cells than that in nature host Hz-AM1 cells. Both Ls-P13 and Ha-P13 are transmembrane proteins. Confocal microscopic analysis showed that both mainly located in the cytoplasm membrane at 48 h. Results of RNA interference indicated that Ha-p13 was a killing-associated gene for host insects H. armigera. The AcMNPV acquired the mentioned killing activity and markedly accelerate the killing rate when expressing Ls-p13. In conclusion, p13 is a killing associated gene in both homologous and heterologous nucleopolyhedrovirus.

• ALGAE
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• v.17 no.1
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• pp.59-68
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• 2002

A phylogenetic affinity between charophytes and embryophytes (land plants) has been explained by a few chloroplast genomic characters including gene and intron (Manhart and Palmer 1990; Baldauf et al. 1990; Lew and Manhart 1993). Here we show that a charophyte, Spirogyra maxima, has the largest operon of angiosperm chloroplast genomes, rpl23 operon (trnⅠ-rpl23-rpl2-rps19-rpl22-rps3-rpl16-rpl14-rps8-infA-rpl36-rps11-rpoA) containing both embryophyte introns, rpl16.i and rpl2.i. The rpl23 gene cluster of Spirogyra contains a distinct eubacterial promoter sequence upstream of rpl23, which is the first gene of the green algal rpl23 gene cluster. This sequence is completely absent in angiosperms but is present in non-flowering plants. The results imply that, in the rpl23 gene cluster, early charophytes had at least two promoters, one upstream of trnⅠ and and another upstream of rpl23, which partially or completely lost its function in land plants. A comparison of gene clusters of prokaryotes, algal chloroplast DNAs and land plant cpDNAs indicated a loss of numerous genes in chlorophyll a+b eukaryotes. A phylogenetic analysis using presence/absence of genes and introns as characters produced trees with a strongly supported clade containing chlorophyll a+b eukaryotes. Spirogyra and embryophytes formed a clade characterized by the loss of rpl5 and rps9 and the gain of trnⅠ (CAU) and introns in rpl2 and rpl16. The analyses support the hypothesis that the rpl23 gene cluster and the rpl2 and rpl16 introns of land plants originated from a common ancestor of Spirogyra and land plants.

• Development and Reproduction
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• v.18 no.1
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• pp.1-11
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• 2014

Early growth response 1 (Egr1) is a zinc-finger transcription factor to direct second-wave gene expression leading to cell growth, differentiation and/or apoptosis. While it is well-known that Egr1 controls transcription of an array of targets in various cell types, downstream target gene(s) whose transcription is regulated by Egr1 in the uterus has not been identified yet. Thus, we have tried to identify a list of potential target genes of Egr1 in the uterus by performing multi-step in silico promoter analyses. Analyses of mRNA microarray data provided a cohort of genes (102 genes) which were differentially expressed (DEGs) in the uterus between Egr1(+/+) and Egr1(-/-) mice. In mice, the frequency of putative EGR1 binding sites (EBS) in the promoter of DEGs is significantly higher than that of randomly selected non-DEGs, although it is not correlated with expression levels of DEGs. Furthermore, EBS are considerably enriched within -500 bp of DEG's promoters. Comparative analyses for EBS of DEGs with the promoters of other species provided power to distinguish DEGs with higher probability as EGR1 direct target genes. Eleven EBS in the promoters of 9 genes among analyzed DEGs are conserved between various species including human. In conclusion, this study provides evidence that analyses of mRNA expression profiles followed by two-step in silico analyses could provide a list of putative Egr1 direct target genes in the uterus where any known direct target genes are yet reported for further functional studies.

• BMB Reports
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• v.54 no.10
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• pp.497-504
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• 2021

EGR1 (early growth response 1) is dysregulated in many cancers and exhibits both tumor suppressor and promoter activities, making it an appealing target for cancer therapy. Here, we used a systematic multi-omics analysis to review the expression of EGR1 and its role in regulating clinical outcomes in breast cancer (BC). EGR1 expression, its promoter methylation, and protein expression pattern were assessed using various publicly available tools. COSMIC-based somatic mutations and cBioPortal-based copy number alterations were analyzed, and the prognostic roles of EGR1 in BC were determined using Prognoscan and Kaplan-Meier Plotter. We also used bc-GenEx-Miner to investigate the EGR1 co-expression profile. EGR1 was more often downregulated in BC tissues than in normal breast tissue, and its knockdown was positively correlated with poor survival. Low EGR1 expression levels were also associated with increased risk of ER+, PR+, and HER2- BCs. High positive correlations were observed among EGR1, DUSP1, FOS, FOSB, CYR61, and JUN mRNA expression in BC tissue. This systematic review suggested that EGR1 expression may serve as a prognostic marker for BC patients and that clinicopathological parameters influence its prognostic utility. In addition to EGR1, DUSP1, FOS, FOSB, CYR61, and JUN can jointly be considered prognostic indicators for BC.

• Journal of Animal Science and Technology
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• v.63 no.6
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• pp.1286-1300
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• 2021

The objective of this study was to evaluate in vitro antimicrobial and anti-biofilm activity of sodium long chain polyphosphate (SLCPP) and effect of dietary supplementation of SLCPP on growth performance, organ characteristics, blood metabolites, and intestinal microflora of broilers. Antimicrobial activities of SLCPP were observed against Escherichia coli O157:H7, Listeria monocytogenes, Salmonella enterica ser. Pullorum, Shigella sonnei, Klebsiella pneumonia, Pseudomonas aeruginosa in agar well diffusion assay. In addition, SLCPP demonstrated good anti-biofilm activity against K. pneumonia and P. aeruginosa. Furthermore, to investigate the dietary effect of SLCPP, a total of 480 1-day-old male Ross 308 broiler chicks were randomly allotted to three dietary treatment groups (4 replicates per group, 40 birds in each replicate): an antibiotic-free corn-soybean meal basal diet (NC); basal diet + enramycin 0.01% (PC); and basal diet + 0.1% SLCPP (SPP). The experiment lasted for 35 days. Results showed that birds fed with SLCPP had higher body weight (BW) and average daily gain (ADG), and lower feed conversion ratio (FCR) during the grower phase (days 7 to 21) (p < 0.05). Except for blood urea nitrogen, all other blood biochemical parameters remained unaffected by the dietary supplementation of SLCPP. Compared to the control group, lengths of the duodenum and ileum in the SPP group were significantly shorter (p < 0.05). Moreover, counts of lactic acid bacteria (LAB), total aerobes, and Streptococcus spp. in jejunum as well as LAB in cecum were increased in the SPP group than in the PC group (p < 0.05). These results suggest that dietary supplementation of SLCPP might promote the growth of broilers in their early growth phase.

• BMB Reports
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• v.53 no.12
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• pp.628-633
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• 2020

WNT11 is a member of the non-canonical Wnt family and plays a crucial role in tumor progression. However, the regulatory mechanisms underlying WNT11 expression are unclear. Tumor necrosis factor-alpha (TNFα) is a major inflammatory cytokine produced in the tumor microenvironment and contributes to processes associated with tumor progression, such as tumor invasion and metastasis. By using site-directed mutagenesis and introducing a serial deletion in the 5'-regulatory region of WNT11, we observed that TNFα activates the early growth response 1 (EGR1)-binding sequence (EBS) in the proximal region of WNT11 and that the transcription factor EGR1 is necessary for the TNFα-induced transcription of WNT11. EGR1 bound directly to the EBSs within the proximal 5'-regulatory region of WNT11 and ectopic expression of EGR1 stimulated WNT11 promoter activity, whereas the knockdown of EGR1 expression by RNA interference reduced TNFα-induced WNT11 expression in T47D breast cancer cells. We also observed that mitogen-activated protein kinases (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 kinase mediated TNFα-induced transcription of WNT11 via EGR1. Our results suggest that EGR1 directly targets WNT11 in response to TNFα stimulation in breast cancer cells.