• 제목/요약/키워드: B13

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韓國産 捕食線蟲(Mononchida: Nematoda)의 4 新種 기재 (Descriptions of Four New Species of Predatory Nematodes (Mononchida) From Korea)

  • 최영연;;이성민
    • 한국토양동물학회지
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    • 제4권2호
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    • pp.89-100
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    • 1999
  • 捕食線蟲目 (Mononchida)의 4신종을 기재하였다; Iotonchus obtusus sp. n.는 체장이 2.8 mm, a=33, b=4.2, c=61, V=68, 口腔은 61${\times}$45 ${\mu}$m이고, 背部齒는 基部에 있고, 陰門突起가 있으며, 꼬리는 짧고 반원형이며 末端部의 표피는 두꺼운 것이 특징이다. Miconchus valvapapillatum sp. n.는 體長이 2.7-3.6 mm, a=29-36, b=4.1-4.5, c=18.4-21, V=65-69, 口腔은 53-61${\times}$29-33 ${\mu}$m, 交接刺는 132-137 ${\mu}$m, 復中央補助突起는 28-31개이며, 陰門 前後方에 5-8개의 연속적인 돌기를 가지며, 3쌍의 陰門腺이 있다. Clarkus koreanus sp. n.는 體長이 1.1-1.3 mm, a=27.5-28.8, b=3.5-3.9, c=12-14.5, V=60-64, 口腔은 24-28${\times}$13.5-15 ${\mu}$m이고, 口脣部는 잘 區劃졌고, 雙器는 背部齒에 대해서 후방에 있으며, 陰脣을 가진다. Coomansus ulsani sp. n.는 體長이 1.2-1.5 mm이고, a=23.5-26, b=3.4-3.8, c=13.6-14.8, V=65-68, 口腔은 36-39${\times}$21-23 ${\mu}$m이고, 口脣部는 잘 區劃졌고 口腔壁은 1줄의 가는 세로 隆起部가 있다.

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국내지형환경에서의 IMT-2000주파수 대 경로손실 측정 및 고찰 (The Measurement and Consideration of Path Loss in Domestic Terrain Environments for IMT-2000)

  • 이상수;이동진;최학근;김준철;박원진
    • 대한전자공학회논문지TC
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    • 제39권12호
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    • pp.547-552
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    • 2002
  • 본 논문에서는 국내지형환경에서 차세대 이동통신인 IMT-2000을 위한 경로손실을 측정 및 고찰하였다. 이를 위해 국내지형환경을 분류하였으며, 주파수 1.9201GHz에서 비가시(non line of sight) 경로로 수신전력을 측정하였다. 또한 이를 토대로 안테나 복사패턴을 고려하여 경로손실을 계산하였다. 국내지형환경에서 경로손실을 고찰하기 위해 각 지형환경에 대해 계산된 경로손실 데이터를 비교기준모델인 COST-231 HATA Urban Model 기울기로 fitting하고 비교하였다. 결과를 살펴볼 때 국내지형환경의 경우, 비교기준 모델인 COST-231 HATA Urban Model에 비해 도심환경의 경우 약 5dB, 한산한 도심환경의 경우 약 8dB, 밀집한 부심환경의 경우 약 12dB, 부심환경의 경우 약 13dB, 한산한 부심환경의 경우 약 19dB, 도로환경의 경우 약 29dB가 적게 나타남을 확인할 수 있었다.

Intragenic DNA Methylation Concomitant with Repression of ATP4B and ATP4A Gene Expression in Gastric Cancer is a Potential Serum Biomarker

  • Raja, Uthandaraman Mahalinga;Gopal, Gopisetty;Rajkumar, Thangarajan
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권11호
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    • pp.5563-5568
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    • 2012
  • Based on our previous report on gastric cancer which documented ATP4A and ATP4B mRNA down-regulation in gastric tumors relative to normal gastric tissues, we hypothesized that epigenetic mechanisms could be responsible. ATP4A and ATP4B mRNA expression in gastric cancer cell lines AGS, SNU638 and NUGC-3 was examined using reverse transcriptase PCR (RT-PCR). AGS cells were treated with TSA or 5'-AzaDC and methylation specific PCR (MSP) and bisulfite sequencing PCR (BSP) analysis were performed. MSP analysis was on DNA from paraffin embedded tissues sections and plasma. Expression analysis revealed downregulation of ATP4A and ATP4B genes in gastric cancer cell lines relative to normal gastric tissue, while treatment with 5'-AzaDC re-activated expression of both. Search for CpG islands in their putative promoter regions did not indicate CpG islands (CGI) but only further downstream in the bodies of the genes. Methylation specific PCR (MSP) in the exon1 of the ATP4B gene and exon7 in ATP4A indicated methylation in all the gastric cancer cell lines tested. MSP analysis in tumor tissue samples revealed methylation in the majority of tumor samples, 15/19, for ATP4B and 8/8 for ATP4A. There was concordance between ATP4B and ATP4A down-regulation and methylation status in the tumour samples tested. ATP4B methylation was detectable in cell free DNA from gastric cancer patient's plasma samples. Thus ATP4A and ATP4B down-regulation involves DNA methylation and methylated ATP4B DNA in plasma is a potential biomarker for gastric cancer.

Lack of Increased P15INK4B Protein Expression in Basal Cell Carcinomas

  • Moad, Ahmed Ismail Hassan;Tan, Mei Lan;Kaur, Gurjeet;Mabruk, Mohamed
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권12호
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    • pp.6239-6244
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    • 2012
  • Background: The basal cell carcinoma (BCC) is the most common non-melanoma skin cancer (NMSK). BCC might develop because of the faulty cell cycle arrest. $p15^{INK4b}$ is a tumor suppressor gene, involved in cell cycle arrest and inactivated in most human cancers. The role of $p15^{INK4b}$ protein expression in the genesis of BCC is as yet unknown. In a previous study we showed the absence of $p15^{INK4b}$ expression in the majority of tissue microarray cores of cutaneous squamous cell carcinoma (SCCs), another type of non-melanoma skin cancer, indicating that $p15^{INK4b}$ could possibly be involved in the pathogenesis of cutaneous SCC. The aim of this study was to investigate $p15^{INK4b}$ protein expression in BCCs. Materials and Method: Protein expression of $p15^{INK4b}$ in 35 cases of BCC tissue arrays and 19 cases of normal human skin tissue was studied using an immunohistochemical approach. Results: The expression of $p15^{INK4b}$ was not significantly different in the BCC cases as compared with normal human skin (p=0.356; p>0.05). In addition, there were no significant relationship between clinicopathologic variables of patients (age and sex) and $p15^{INK4b}$ protein expression. Conclusions: Our finding may indicate that $p15^{INK4b}$ protein expression does not play a role in the genesis of BCC.

Knockdown of Cdc25B in Renal Cell Carcinoma is Associated with Decreased Malignant Features

  • Yu, Xiu-Yue;Zhang, Zhe;Zhang, Guo-Jun;Guo, Kun-Feng;Kong, Chui-Ze
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권3호
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    • pp.931-935
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    • 2012
  • Cdc25 phosphatases are important regulators of the cell cycle. Their abnormal expression detected in a number of tumors implies that their dysregulation is involved in malignant transformation. However, the role of Cdc25B in renal cell carcinomas remains unknown. To shed light on influence on renal cell carcinogenesis and subsequent progression, Cdc25B expression was examined by real-time RT-PCR and western blotting in renal cell carcinoma and normal tissues. 65 kDa Cdc25B expression was higher in carcinomas than in the adjacent normal tissues (P<0.05), positive correlations being noted with clinical stage and histopathologic grade (P<0.05). To additionally investigate the role of Cdc25B alteration in the development of renal cell carcinoma, Cdc25B siRNA was used to knockdown the expression of Cdc25B. Down-regulation resulted in slower growth, more G2/M cells, weaker capacity for migration and invasion, and induction of apoptosis in 769-P transfectants. Reduction of 14-3-3 protein expression appeared related to Cdc25B knockdown. These findings suggest an important role of Cdc25B in renal cell carcinoma development and provide a rationale for investigation of Cdc2B-based gene therapy.

Clinical Significance of SH2B1 Adaptor Protein Expression in Non-small Cell Lung Cancer

  • Zhang, Hang;Duan, Chao-Jun;Chen, Wei;Wang, Shao-Qiang;Zhang, Sheng-Kang;Dong, Shuo;Cheng, Yuan-Da;Zhang, Chun-Fang
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권5호
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    • pp.2355-2362
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    • 2012
  • The SH2B1 adaptor protein is recruited to multiple ligand-activated receptor tyrosine kinases that play important role in the physiologic and pathologic features of many cancers. The purpose of this study was to assess SH2B1 expression and to explore its contribution to the non-small cell lung cancer (NSCLC). Methods: SH2B1 expression in 114 primary NSCLC tissue specimens was analyzed by immunohistochemistry and correlated with clinicopathological parameters and patients' outcome. Additionally, 15 paired NSCLC background tissues, 5 NSCLC cell lines and a normal HBE cell line were evaluated for SH2B1 expression by RT-PCR and immunoblotting, immunofluorescence being applied for the cell lines. Results: SH2B1 was found to be overexpressed in NSCLC tissues and NSCLC cell lines. More importantly, high SH2B1 expression was significantly associated with tumor grade, tumor size, clinical stage, lymph node metastasis, and recurrence respectively. Survival analysis demonstrated that patients with high SH2B1 expression had both poorer disease-free survival and overall survival than other patients. Multivariate Cox regression analysis revealed that SH2B1 overexpression was an independent prognostic factor for patients with NSCLC. Conclusions: Our findings suggest that the SH2B1 protein may contribute to the malignant progression of NSCLC and could offer a novel prognostic indicator for patients with NSCLC.

Effects of neutron irradiation on superconducting critical temperatures of in situ processed MgB2 superconductors

  • Kim, C.J.;Park, S.D.;Jun, B.H.;Kim, B.G.;Choo, K.N.;Ri, H.C.
    • 한국초전도ㆍ저온공학회논문지
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    • 제16권1호
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    • pp.9-13
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    • 2014
  • Effects of neutron irradiation on the superconducting properties of the undoped $MgB_2$ and the carbon(C)-doped $MgB_2$ bulk superconductors, prepared by an in situ reaction process using Mg and B powder, were investigated. The prepared $MgB_2$ samples were neutron-irradiated at the neutron fluence of $10^{16}-10^{18}n/cm^2$ in a Hanaro nuclear reactor of KAERI involving both fast and thermal neutron. The magnetic moment-temperature (M-T) and magnetization-magnetic field (M-H) curves before/after irradiation were obtained using magnetic property measurement system (MPMS). The superconducting critical temperature ($T_c$) and transition width were estimated from the M-T curves and critical current density ($J_c$) was estimated from the M-H curves using a Bean's critical model. The $T_cs$ of the undoped $MgB_2$ and C-doped $MgB_2$ before irradiation were 36.9-37.0 K and 36.6-36.8 K, respectively. The $T_cs$ decreased to 33.2 K and 31.6 K, respectively after irradiation at neutron fluence of $7.16{\times}10^{17}n/cm^2$, and decreased to 22.6 K and 24.0 K, respectively, at $3.13{\times}10^{18}n/cm^2$. The $J_c$ cross-over was observed at the high magnetic field of 5.2 T for the undoped $MgB_2$ irradiated at $7.16{\times}10^{17}n/cm^2$. The $T_c$ and $J_c$ variation after the neutron irradiation at various neutron fluences were explained in terms of the defect formation in the superconducting matrix by neutron irradiation.

삼백초 에탄올 추출물의 위출혈성 스트레스 위염 억제 효과 (Inhibitory Activities of Ethanol Extracts from Saururus chinensis L. against Stress-Induced Hemorrhagic Gastritis)

  • 박소영;조영제
    • 한국식품영양과학회지
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    • 제44권6호
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    • pp.800-808
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    • 2015
  • 천연 생리활성 물질 탐색 연구의 일환으로 삼백초로부터 위염 억제 물질을 추출하여 효능을 검정하였다. 삼백초 추출물 0.25~2 g/kg B.W.를 마우스에 경구 투여한 결과 1.5 g/kg B.W. 미만 투여량의 급성독성 실험에서 안정성을 나타내었으며 $LD_{50}$은 1.81 g/kg B.W.였다. 삼백초 추출물 0.5 g/kg B.W.를 마우스에 경구 투여한 만성독성 실험에서는 13주간의 투여기간 동안 독성이 없는 것으로 나타났다. 위염을 유발시키기 전에 삼백초 추출물을 250 및 500 mg/kg B.W. 농도로 미리 섭취시킨 결과 위출혈 및 위부종과 세포손상이 농도 의존적으로 감소하였다. 또한 사이토카인의 발현도 억제되었다. 따라서 삼백초 추출물은 스트레스성 위염에 의한 출혈 및 세포손상을 농도 의존적으로 억제하는 효과가 있으며, 그 mechanism은 염증성 사이토카인의 발현 억제에 의한 것이라 생각되었다.

Ginsenoside Rh2 reduces m6A RNA methylation in cancer via the KIF26B-SRF positive feedback loop

  • Hu, Chunmei;Yang, Linhan;Wang, Yi;Zhou, Shijie;Luo, Jing;Gu, Yi
    • Journal of Ginseng Research
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    • 제45권6호
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    • pp.734-743
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    • 2021
  • Background: The underlying mechanisms of the potential tumor-suppressive effects of ginsenoside Rh2 are complex. N6-methyladenosine (m6A) RNA methylation is usually dysregulated in cancer. This study explored the regulatory effect of ginsenoside Rh2 on m6A RNA methylation in cancer. Methods: m6A RNA quantification and gene-specific m6A RIP-qPCR assays were applied to assess total and gene-specific m6A RNA levels. Co-immunoprecipitation, fractionation western blotting, and immunofluorescence staining were performed to detect protein interactions and distribution. QRT-PCR, dual-luciferase, and ChIP-qPCR assays were conducted to check the transcriptional regulation. Results: Ginsenoside Rh2 reduces m6A RNA methylation and KIF26B expression in a dose-dependent manner in some cancers. KIF26B interacts with ZC3H13 and CBLL1 in the cytoplasm of cancer cells and enhances their nuclear distribution. KIF26B inhibition reduces m6A RNA methylation level in cancer cells. SRF bound to the KIF26B promoter and activated its transcription. SRF mRNA m6A abundance significantly decreased upon KIF26B silencing. SRF knockdown suppressed cancer cell proliferation and growth both in vitro and in vivo, the effect of which was partly rescued by KIF26B overexpression. Conclusion: ginsenoside Rh2 reduces m6A RNA methylation via downregulating KIF26B expression in some cancer cells. KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.