Review : Lessons We have Learnt from the Fright Against Tuberculosis During the Past 100 Years

( Tadao Shimao ) 대한결핵 및 호흡기학회 1982 Tuberculosis and Respiratory Diseases Vol.29 No.2

What we have learet from the fight against TB during past 100 years

( Tadao Shimao ) 대한결핵 및 호흡기학회 1982 춘계학술대회 초록집 Vol.54 No.-

Parthenolide inhibits transforming growth factor β1induced epithelial-mesenchymal transition in colorectal cancer cells

zhu shimao,Yong Ran Park,서승영,In Hee Kim,Soo Teik Lee,Sang Wook Kim 대한장연구학회 2019 Intestinal Research Vol.17 No.4

Background/Aims: Transforming growth factor-β1 (TGF-β1) induction of epithelial-mesenchymal transition (EMT) is one of the mechanisms by which colorectal cancer (CRC) cells acquire migratory and invasive capacities, and subsequently metastasize. Parthenolide (PT) expresses multiple anti-cancer and anti-inflammatory activities that inhibit nuclear factor κB by targeting the IκB kinase complex. In the present study, we aimed to investigate whether PT can inhibit TGF-β1-induced EMT in CRC cell lines. Methods: HT-29 and SW480 cell lines were used in the experiment. Cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and sub-G1 analysis was measured by flow cytometry. The induction of EMT by TGF-β1 and inhibition of the process by PT was analyzed by phase contrast microscopy, wounding healing, cellular migration and invasion assays, and Western blotting. Results: TGF-β1 inhibits HT-29 cell proliferation, but has no effect on SW480 cell proliferation; different concentrations of TGF-β1 did not induce apoptosis in HT-29 and SW480 cells. PT attenuates TGF-β1-induced elongated, fibroblast-like shape changing in cells. PT inhibits TGF-β1-induced cell migration and cell invasion. In addition, other EMT markers such as β-catenin, Vimentin, Snail, and Slug were suppressed by PT, while E-cadherin was increased by PT. Conclusions: Our findings show that PT inhibits TGF-β1-induced EMT by suppressing the expression of the mesenchymal protein and increasing expression of the epithelial protein. These findings suggest a novel approach for CRC treatment by suppression of TGF-β1-induced EMT.

Sintering and Mechanical Properties of Chromium Boride-chromium Carbide Composites

Matsushita Jun-Ichi,Shimao Kenji,Machida Yoshiyuki,Takao Takumi,Iizumi Kiyokata,Sawada Yutaka,Shim Kwang-Bo 한국분말야금학회 2006 한국분말야금학회 학술대회논문집 Vol.2006 No.1

Several boride sintered bodies such as , , and were previously reported. In the present study, the sinterability and physical properties of chromium boride containing chromium carbide sintered bodies were investigated in order to determine its new advanced material. The samples were sintered at desired temperature for 1 hour in vacuum under a pressure by hot pressing. The relative density of sintered bodies was measured by Archimedes' method. The relative densities of addition of 0, 5, 10, 15 and 20 mass% composites were 92 to 95%. The Vickers hardness of the with 10 and 15 mass% composites were about 14 and 15 GPa at room temperature, respectively. The Vickers hardness at high temperature of the addition of 10 mass% composite decreased with increasing measurement temperature. The Vickers hardness at 1273 K of the sample was 6 GPa. The Vickers hardness of addition of composites was higher than monolithic sintered body. The powder X-ray diffraction analysis detected CrB and phases in containing composites.

Study on chitosan/carbon nanotubes modified materials used to enhance the performance of dental binder

Tingyu Tian,Yuping Cai,Shimao Yang,Yanwei Guo,Wei Zhou 한국탄소학회 2023 Carbon Letters Vol.33 No.6

In this study, we successfully grafted chitosan (CS) onto multi-walled carbon nanotubes (MWCNTs) to enhance their properties and potential applications in the biomedical field. FTIR spectroscopy confirmed the successful covalent bonding of CS onto MWCNTs, indicated by the new absorption peak of the amide bond (–CONH–). Thermal analysis showed that the modified MWCNTs (MWCNT-CS) had significant weight loss around 260 °C, suggesting the decomposition of hydroxypropyl chitosan, and confirming its presence in the nanocomposite. SEM images revealed that CS grafting improved the dispersibility of MWCNTs, a property crucial for their use as nanofillers in polymers. Moreover, the micro-tensile bond strength of dentin surface increased with increasing MWCNT-CS concentrations, indicating the potential of MWCNT-CS as a pretreatment for dentin bonding. After simulated aging, the bond strength remained significantly higher for MWCNT-CS groups compared to those without pretreatment. In biocompatibility assessment using the MTT assay, MWCNT-CS showed higher cell viability than MWCNT, suggesting improved biocompatibility after CS modification. The results of this study suggest that CS-modified MWCNTs could be promising materials for applications in dentin bonding, dentin mineralization, bone scaffolding, implants, and drug delivery systems.

연제발표 : 보건소 등록치료 환자의 사회의학적 배경과 환자관리 개선에 관한 연구

김성진,진병원,( T. Shimao ),( T. Mori ) 대한결핵 및 호흡기학회 1982 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.55 No.-

Structural Characterization and Antioxidant and Immunomodulation Activities of Polysaccharides from the Spent Rice Substrate of Cordyceps militaris

Yan Zeng,Ying Zhang,Lijiao Zhang,Shimao Cui,Yuanxia Sun 한국식품과학회 2015 Food Science and Biotechnology Vol.24 No.5

P20, P40, P60, and P80 polysaccharide fractions were isolated from the spent rice substrate of Cordyceps militaris and structure and antioxidant and immunomodulation activities were studied. P20 contained mainly starch from rice. Purified P40 was an α-1, 4-glucan with some α-1, 4, 6 l ink ed branches. P60 containing t-Galp and 1, 2-Manp had the highest FRAP value of 78.4 μmol Fe2+/g. P80 containing t-Galp, 1,6-Galp, and 1, 2-Manp had the highest TEAC and ORACFL values and the lowest IC50 value of 0.32 mg/mL against DPPH radicals. All polysaccharides showed good biosafety in an MTT assay. P40, P60, and P80 stimulated NO production in a dose-dependent manner. Polysaccharides from the spent substrate of C. militaris can be used as safe antioxidants and immunomodulators and can be used for new applications in the food industry.

Treatment with 3-Bromo-4,5-Dihydroxybenzaldehyde Improves Cardiac Function by Inhibiting Macrophage Infiltration in Mice

Ningning Ji,Honghong Lou,Xinyan Gong,Ting Fu,Shimao Ni 대한심장학회 2018 Korean Circulation Journal Vol.48 No.10

Background and Objectives Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. Methods Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-κB was determined by western blot. Results BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68+ macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-κB in the infarcted hearts. Conclusions These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.

MicroRNA-148a Can Regulate Runt-Related Transcription Factor 3 Gene Expression via Modulation of DNA Methyltransferase 1 in Gastric Cancer

Junbo Zuo,Hong Zhou,Jiazeng Xia,Feng Ju,Jiang Yan,Akao Zhu,Shimao Jin,Ting Shan 한국분자세포생물학회 2013 Molecules and cells Vol.35 No.4

Underexpression of the gene runt-related transcription fac-tor 3 (RUNX3), an important tumor suppressor, is known to contribute to gastric cancer progression. However, the mechanism underlying aberrant RUNX3 expression has not been fully elucidated. We investigated the role of microRNA-148a (miR-148a) and DNA methyltransferases (DNMTs) in RUNX3 promoter methylation and gene expression. RUNX3 mRNA, RUNX3 protein, and methylation levels were assayed in human gastric cancer tissues and matched normal tissues, and AGS and BGC-823 cells by real-time reverse transcription PCR, Western blot, and methylation-specific PCR, respectively. A correlation between RUNX3 mRNA levels and that of miR-148a was also investigated in gastric cancer tissues. We found that RUNX3 mRNA levels were significantly downregulated in gastric cancer tissues compared with their matched normal tissues, and were closely associated with miR-148a expression. After treatment of human gastric cancer AGS and BGC-823 cells with the DNA methylation inhibitor 5-aza-2’-deoxycytidine, a significant increase in RUNX3 mRNA, RUNX3 protein, and the non-methylated form of the RUNX3 promoter were observed relative to untreated cells. Enforced expression of miR-148a, which can modulate DNMT1 and DNMT3B, also increased the expression of RUNX3 in gastric cancer cells. Knockdown of DNMT1 was associated with increased levels of RUNX3 mRNA and RUNX3 protein, while knockdown of DNMT3B did not have any effect on these in BGC-823 cells. Our results show that miR-148a may regulate RUNX3 expression through modulation of DNMT1-dependent DNA methylation in gastric cancer and highlight a miRNA-epigenetics regulation mechanism of gene expression.