Improvement of Biomineralization of Sporosarcina pasteurii as Biocementing Material for Concrete Repair by Atmospheric and Room Temperature Plasma Mutagenesis and Response Surface Methodology

( Pei-pei Han ),( Wen-ji Geng ),( Meng-nan Li ),( Shi-ru Jia ),( Ji-long Yin ),( Run-ze Xue ) 한국미생물 · 생명공학회 2021 Journal of microbiology and biotechnology Vol.31 No.9

Microbially induced calcium carbonate precipitation (MICP) has recently become an intelligent and environmentally friendly method for repairing cracks in concrete. To improve on this ability of microbial materials concrete repair, we applied random mutagenesis and optimization of mineralization conditions to improve the quantity and crystal form of microbially precipitated calcium carbonate. Sporosarcina pasteurii ATCC 11859 was used as the starting strain to obtain the mutant with high urease activity by atmospheric and room temperature plasma (ARTP) mutagenesis. Next, we investigated the optimal biomineralization conditions and precipitation crystal form using Plackett-Burman experimental design and response surface methodology (RSM). Biomineralization with 0.73 mol/l calcium chloride, 45 g/l urea, reaction temperature of 45°C, and reaction time of 22 h, significantly increased the amount of precipitated calcium carbonate, which was deposited in the form of calcite crystals. Finally, the repair of concrete using the optimized biomineralization process was evaluated. A comparison of water absorption and adhesion of concrete specimens before and after repairs showed that concrete cracks and surface defects could be efficiently repaired. This study provides a new method to engineer biocementing material for concrete repair.

시멘트의 분말도가 모르터의 물리적 특성에 미치는 영향

문학룡,배정렬,한천구 청주대학교 산업과학연구소 2003 産業科學硏究 Vol.21 No.1

This study discusses the influence of fineness of cement on the properties of cement mortar. According to the results, compressive strength shows a higher value in order of high early cement with 8000㎠/g of fineness(C), 4600㎠/g of fineness(B), 3000㎠/g of fineness(A) and ordinary cement(OPC) at mixture proportion of 1:3, and it does in order of C, B, OPC and A at mixture proportion of 1:1. Compressive strength shows a higher value in order of exposure at outside, standard and air curing with variation of curing condition. Flexural strength shows the similar tendency with compressive strength, and is about 1/7∼1/6 in comparison with compressive strength. And, its correlativity is above 0.93, so it is very favorable. Length change by drying shrinkage is higher in order of C, B, OPC and A at mixture proportion of 1:1 and 1:3.

콘크리트의 블리딩에 미치는 골재 조립률의 영향

文學龍,裵正烈,황인성,한천구 대한건축학회 2003 대한건축학회 학술발표대회 논문집 - 계획계/구조계 Vol.23 No.1(구조계)

This study is to investigate the influence of W/C and fineness modulus of aggregate on the bleeding of concrete. According to the result, the lower W/C is, the less bleeding occurs. As for the properties of bleeding with the variation of fineness modulus, the amount of bleeding is small with the continuous grading in the middle of the standard grading range in the case of coarse aggregate, and it grows smaller with a decrease of fineness modulus in the case of fine aggregate. Therefore, it proves that using coarse aggregate with the continuous grading in the middle of the standard grading range and fine aggregate with smaller fineness modulus in the standard grading range is the effective method for reducing bleeding at the same W/C.

Deficiency or activation of peroxisome proliferator-activated receptor ⍺ reduces the tissue concentrations of endogenously synthesized docosahexaenoic acid in C57BL/6J mice

Wen-Ting Hsiao,Hui-Min Su,Kuan-Pin Su,Szu-Han Chen,Hai-Ping Wu,Yi-Ling You,Ru-Huei Fu,Pei-Min Chao 한국영양학회 2019 Nutrition Research and Practice Vol.13 No.4

BACKGROUND/OBJECTIVES: Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the in vivo conversion of α-linolenic acid. Many enzymes participating in LCPUFA synthesis are regulated by peroxisome proliferator-activated receptor alpha (PPARα). Therefore, it was hypothesized that the tissue accretion of endogenously synthesized DHA could be modified by PPARα. MATERIALS/METHODS: The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among PPARα homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate (PPARα agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. RESULTS: PPARα ablation reduced the hepatic Acox, Fads1, and Fads2 mRNA levels, as well as the DHA concentration in the liver, but not in the brain cortex. In contrast, PPARα activation increased hepatic Acox, Fads1, Fads2, and Elovl5 mRNA levels, but reduced the DHA concentrations in the liver, retina, and phospholipid of brain cortex, and decreased mRNA and protein levels of the brain-derived neurotrophic factor in brain cortex. CONCLUSIONS: LCPUFA enzyme expression was altered by PPARα. Either PPARα deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance.

The effect of diabetes and prediabetes on the prevalence, complications and mortality in nonalcoholic fatty liver disease

Cheng Han Ng,Kai En Chan,Yip Han Chin,Rebecca Wenling Zeng,Pei Chen Tsai,Wen Hui Lim,Darren Jun Hao Tan,Chin Meng Khoo,Lay Hoon Goh,Zheng Jye Ling,Anand Kulkarni,Lung-Yi Loey Mak,Daniel Q Huang,Mark C 대한간학회 2022 Clinical and Molecular Hepatology(대한간학회지) Vol.28 No.3

Background/Aims: Nonalcoholic fatty liver disease (NAFLD) is closely associated with diabetes. The cumulative impact of both diseases synergistically increases risk of adverse events. However, present population analysis is predominantly conducted with reference to non-NAFLD individuals and has not yet examined the impact of prediabetes. Hence, we sought to conduct a retrospective analysis on the impact of diabetic status in NAFLD patients, referencing non-diabetic NAFLD individuals. Methods: Data from the National Health and Nutrition Examination Survey 1999–2018 was used. Hepatic steatosis was defined with United States Fatty Liver Index (US-FLI) and FLI at a cut-off of 30 and 60 respectively, in absence of substantial alcohol use. A multivariate generalized linear model was used for risk ratios of binary outcomes while survival analysis was conducted with Cox regression and Fine Gray model for competing risk. Results: Of 32,234 patients, 28.92% were identified to have NAFLD. 36.04%, 38.32% and 25.63% were non-diabetic, prediabetic and diabetic respectively. Diabetic NAFLD significantly increased risk of cardiovascular disease (CVD), stroke, chronic kidney disease, all-cause and CVD mortality compared to non-diabetic NAFLD. However, prediabetic NAFLD only significantly increased the risk of CVD and did not result in a higher risk of mortality. Conclusions: Given the increased risk of adverse outcomes, this study highlights the importance of regular diabetes screening in NAFLD and adoption of prompt lifestyle modifications to reduce disease progression. Facing high cardiovascular burden, prediabetic and diabetic NAFLD individuals can benefit from early cardiovascular referrals to reduce risk of CVD events and mortality.

Deficiency or activation of peroxisome proliferator-activated receptor α reduces the tissue concentrations of endogenously synthesized docosahexaenoic acid in C57BL/6J mice

Hsiao, Wen-Ting,Su, Hui-Min,Su, Kuan-Pin,Chen, Szu-Han,Wu, Hai-Ping,You, Yi-Ling,Fu, Ru-Huei,Chao, Pei-Min The Korean Nutrition Society 2019 Nutrition Research and Practice Vol.13 No.4

BACKGROUND/OBJECTIVES: Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the in vivo conversion of ${\alpha}$-linolenic acid. Many enzymes participating in LCPUFA synthesis are regulated by peroxisome proliferator-activated receptor alpha ($PPAR{\alpha}$). Therefore, it was hypothesized that the tissue accretion of endogenously synthesized DHA could be modified by $PPAR{\alpha}$. MATERIALS/METHODS: The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among $PPAR{\alpha}$ homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate ($PPAR{\alpha}$ agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. RESULTS: $PPAR{\alpha}$ ablation reduced the hepatic Acox, Fads1, and Fads2 mRNA levels, as well as the DHA concentration in the liver, but not in the brain cortex. In contrast, $PPAR{\alpha}$ activation increased hepatic Acox, Fads1, Fads2, and Elovl5 mRNA levels, but reduced the DHA concentrations in the liver, retina, and phospholipid of brain cortex, and decreased mRNA and protein levels of the brain-derived neurotrophic factor in brain cortex. CONCLUSIONS: LCPUFA enzyme expression was altered by $PPAR{\alpha}$. Either $PPAR{\alpha}$ deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance.

Turbulence-tolerant Manchester On-off Keying Transmission for Free-space Optical Communication

Qian-Wen Jing,Pei-Zheng Yu,Han-Lin Lv,Yanqing Hong 한국광학회 2023 Current Optics and Photonics Vol.7 No.4

We propose a turbulence-tolerant Manchester on-off keying (M-OOK) transmission for free-space optical (FSO) communication. At the transmitter end, a M-OOK signal featuring a spectrum with lowfrequency components absent is modulated and transmitted into a turbulent channel. At the receiver end, a low-pass filter (LPF) -based adaptive-threshold decision (ATD) with LPF-extracted channelstate information (CSI) and a high-pass filter (HPF)-based fixed-threshold decision (FTD) are employed to compensate for the effects of turbulence, owing to the low-frequency spectral characteristics of the turbulent channel. The performance of LPF-based ATD and HPF-based FTD are evaluated for various cutoff frequencies for the LPF and HPF. Besides, the proposed M-OOK transmission is compared to conventional non-return-to-zero OOK (NRZ-OOK) for different data rates. The proposed technique is verified in simulation. The simulation results show that the proposed M-OOK detection with optimized cutoff frequencies of LPF and HPF has better bit-error-rate (BER) performance compared to NRZOOK, and it is close to the theoretical ATD with the knowledge of precise CSI under various degrees of turbulence effects.

Abstract : Arsenic sequestration in iron plaque and its effect on As uptake by rice plants grown in paddy soils with high contents of As, iron oxides, and organic matter

( Chien Hui Syu ),( Pei Yu Jiang ),( Hsuan Han Huang ),( Wen Ting Chen ),( Tzu Huei Lin ),( Dar Yuan Lee ) 한국환경농학회 2012 한국환경농학회 워크샵자료 Vol.2012 No.2

The iron plaque formed on rice root has been confirmed to be a barrier on the uptake of arsenic in many hydroponic experiments. However, few studies provide the information about the relationship between soil characteristics, iron plaque formation and As uptake by rice in Ascontaminated soils. Therefore, the aim of this study is to investigate the effect of the rice root`s iron plaques on the As uptake by rice plants grown in geologically As-contaminated soils with high contents of iron oxides and organic matter from the Guandu Plain of northern Taiwan. A soil flooding incubation study was performed and a pot experiment was conducted. The rice seedling was pre-cultivated in solution cultures and then transplanted in three level As-contaminated soils for growing 39 days. The amounts of iron plaque on rice root were determined by extraction using dithionite-citrate-bicarbonate (DCB). The As species on iron plaque and the concentrations of As and Fe in iron plaque, root, root base and shoot of rice plants were determined. The results of the soil incubation study showed that both As and Fe concentrations in the soil solutions increased with flooding time due to reductive dissolution of iron oxides induced by high contents of organic matter in soils. High amounts of iron plaque were deposited on rice roots and large amounts of As were sequestrated in these iron plaques. Results of the As K-edge X-ray absorption nearedge spectroscopy (XANES) indicated that arsenate was the main species of arsenic sorbed on iron plaque of rice roots. About 74.0 to 93.2 % of total As released from soils were distributed in the iron plaques and only small proportion was distributed in the rice plants. This study provides evidence that the iron plaques of the rice roots was the main controlling factor in limiting the uptake and accumulation of As into the rice plants grown in paddy soils with high contents of iron oxides and organic matter, meanwhile, it suggests that enhancement of iron plaque formation could be the approach used for reducing the uptake of As by paddy rice grown in As-contaminated soils.

Up-Regulation of MiR-1915 Inhibits Proliferation, Invasion, and Migration of Helicobacter pylori-Infected Gastric Cancer Cells via Targeting RAGE

Xin-cai Xu,Wen-bin Zhang,Chun-xing Li,Hua Gao,Qi Pei,Bo-wei Cao,Tie-han He 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.1

Purpose: Helicobacter pylori (HP)-infected gastric cancer (GC) is known to be a fatal malignant tumor, but the molecular mechanismsunderlying its proliferation, invasion, and migration remain far from being completely understood. Our aim in this studywas to explore miR-1915 expression and its molecular mechanisms in regulating proliferation, invasion, and migration of HP-infectedGC cells. Materials and Methods: Quantitative real-time PCR and western blot analysis were performed to determine miR-1915 and receptorfor advanced glycation end product (RAGE) expression in HP-infected GC tissues and gastritis tissues, as well as humangastric mucosal cell line GES-1 and human GC cell lines SGC-7901 and MKN45. CCK8 assay and transwell assay were performedto detect the proliferation, invasion, and migration capabilities. MiR-1915 mimics and miR-1915 inhibitor were transfected intoGC cells to determine the target relationship between miR-1915 and RAGE. Results: MiR-1915 was under-expressed, while RAGE was over-expressed in HP-infected GC tissues and GC cells. Over-expressedmiR-1915 could attenuate cellular proliferation, invasion, and migration capacities. RAGE was confirmed to be the target gene ofmiR-1915 by bioinformatics analysis and luciferase reporter assay. Moreover, HP-infected GC cellular proliferation, invasion, andmigration were inhibited after treatment with pcDNA-RAGE. Conclusion: MiR-1915 exerted tumor-suppressive effects on cellular proliferation, invasion, and migration of HP-infected GCcells via targeting RAGE, which provided an innovative target candidate for treatment of HP-infected GC.

The tyrosine kinase inhibitor nintedanib activates SHP-1 and induces apoptosis in triple-negative breast cancer cells

Chun-Yu Liu,Tzu-Ting Huang,Pei-Yi Chu,Chun-Teng Huang,Chia-Han Lee,Wan-Lun Wang,Ka-Yi Lau,Wen-Chun Tsai,Tzu-I Chao,Jung-Chen Su,Ming-Huang Chen,Chung-Wai Shiau,Ling-Ming Tseng,Kuen-Feng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.