WordNet

make famous forever; "This melody immortalized its composer" (同)immortalise, eternize, eternise, eternalize, eternalise

PrepTutorEJDIC

〈詩・詩人などが〉〈人・その勇気など〉‘を'不滅にする,永久に伝える

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1. ヒトパピローマウイルス（HPV）感染のウイルス学および癌との関連 virology of human papillomavirus infections and the link to cancer
2. 肝細胞移植 hepatocyte transplantation

English Journal

miR-31 is up-regulated in oral premalignant epithelium and contributes to the immortalization of normal oral keratinocytes.

Hung PS, Tu HF, Kao SY, Yang CC, Liu CJ, Huang TY, Chang KW, Lin SC.Author information Department of Surgery, National Yang-Ming University Hospital, Yi-Lan, Taiwan.AbstractOral squamous cell carcinoma (OSCC) is a prevalent malignancy worldwide. MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression and are crucial for tumorigenesis. Previously, we have identified that miR-31 is frequently up-regulated in OSCC and that this miR-31 increase, together downstream effector modulation, enhances oral carcinogenesis. We have identified higher levels of miR-31 expression in oral potential malignant disorder (OPMD) tissues compared to normal oral mucosa. Exogenous miR-31 and human telomerase reverse transcriptase (hTERT) expression were introduced into cultured normal oral keratinocytes (NOKs), which led to the immortalization; these lines were designated M31OK1 and M31OK3. These immortalized lines maintained the capability to undergo squamous differentiation. In addition, migration by both cell lines was attenuated by hTERT and miR-31 knockdown. M31OK1 carries a p53 gene mutation at codon 273. A serum-tolerant subclone, M31OK1-D, exhibits potent anchorage-independent growth that is attenuated by knock-down of both hTERT and miR-31. miR-31 targeted factors inhibiting HIF (FIH), which up-regulated VEGF was found crucial for oral tumorigenesis. The proliferation, migration and epithelial-mesenchymal transition of M31OK1-D are associated with down-regulation of FIH and up-regulation of VEGF, which require miR-31 expression. High miR-31 expression is correlated with higher VEGF expression and lower E-cadherin expression in OPMD tissue. It can be concluded that miR-31 collaborates with hTERT to immortalize NOKs and that this may contribute to early stage oral carcinogenesis. The targeting of downstream factors by miR-31 may further advance the neoplastic progression of immortalized NOKs, allowing them to become malignant.
Carcinogenesis.Carcinogenesis.2014 Jan 30. [Epub ahead of print]
Oral squamous cell carcinoma (OSCC) is a prevalent malignancy worldwide. MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression and are crucial for tumorigenesis. Previously, we have identified that miR-31 is frequently up-regulated in OSCC and that this miR-31 increase, together
PMID 24480806

The nuclear export signal (NES) within CALM is necessary for CALM-AF10-induced leukemia.

Suzuki M, Yamagata K, Shino M, Aikawa Y, Akashi K, Watanabe T, Kitabayashi I.Author information Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan.AbstractThe CALM-AF10 fusion gene, which results from a t(10;11) translocation, is found in a variety of hematopoietic malignancies. Certain HOXA cluster genes and MEIS1 genes are upregulated in patients and mouse models that express CALM-AF10. Wild-type CALM primarily localizes in a diffuse pattern within the cytoplasm, whereas AF10 localizes in the nucleus; however, it is not clear where CALM-AF10 acts to induce leukemia. To investigate the influence of localization on leukemogenesis involving CALM-AF10, we determined the nuclear export signal (NES) within CALM that is necessary and sufficient for cytoplasmic localization of CALM-AF10. Mutations in the NES eliminated the capacity of CALM-AF10 to immortalize murine bone-marrow cells in vitro and to promote development of acute myeloid leukemia in mouse models. Furthermore, a fusion of AF10 with the minimal NES could immortalize bone-marrow cells and induce leukemia in mice. These results suggest that during leukemogenesis, CALM-AF10 plays its critical roles in the cytoplasm. This article is protected by copyright. All rights reserved.
Cancer science.Cancer Sci.2014 Jan 8. doi: 10.1111/cas.12347. [Epub ahead of print]
The CALM-AF10 fusion gene, which results from a t(10;11) translocation, is found in a variety of hematopoietic malignancies. Certain HOXA cluster genes and MEIS1 genes are upregulated in patients and mouse models that express CALM-AF10. Wild-type CALM primarily localizes in a diffuse pattern within
PMID 24397609

Genetic manipulation of B cells for the isolation of rare therapeutic antibodies from the human repertoire.

Kwakkenbos MJ1, Bakker AQ2, van Helden PM3, Wagner K4, Yasuda E5, Spits H6, Beaumont T7.Author information 1AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: mjkwakkenbos@aimmtherapeutics.com.2AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: aqbakker@aimmtherapeutics.com.3AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: pmvanhelden@aimmtherapeutics.com.4AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: kwagner@aimmtherapeutics.com.5AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: eyasuda@aimmtherapeutics.com.6AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: hspits@aimmtherapeutics.com.7AIMM Therapeutics, Academic Medical Center, Meibergdreef 59, 1105 BA Amsterdam, The Netherlands. Electronic address: tbeaumont@aimmtherapeutics.com.AbstractAntibody based therapies are increasingly applied to prevent and treat human disease. While the majority of antibodies currently on the market are chimeric or humanized antibodies from rodents, the focus has now shifted to the isolation and development of fully human antibodies. By retroviral transduction of B cell lymphoma-6 (BCL-6), which prevents terminal differentiation of B cells and, the anti-apoptotic gene B-cell lymphoma-extra large (Bcl-xL) into primary human B cells we efficiently immortalize antibody-producing B cells allowing the isolation of therapeutic antibodies. Selection of antigen-specific B cell clones was greatly facilitated because the transduced B cells retain surface immunoglobulin expression and secrete immunoglobulin into the culture supernatant. Surface immunoglobulin expression can be utilized to stain and isolate antigen specific B cell clones with labeled antigen. Immunoglobulins secreted in culture supernatant can directly be tested in functional assays to identify unique B cell clones. Here we describe the key features of our Bcl-6/Bcl-xL culture platform (AIMSelect).
Methods (San Diego, Calif.).Methods.2014 Jan 1;65(1):38-43. doi: 10.1016/j.ymeth.2013.07.002. Epub 2013 Jul 15.
Antibody based therapies are increasingly applied to prevent and treat human disease. While the majority of antibodies currently on the market are chimeric or humanized antibodies from rodents, the focus has now shifted to the isolation and development of fully human antibodies. By retroviral transd
PMID 23867338

Japanese Journal

震災体験を永遠に伝える(第2回)関東大震災時のがれき処理について

溝入茂
月刊廃棄物 = Monthly the waste 39(4), 34-38, 2013-04
NAID 40019664277

Beyond Life and Death:An Essay on Meta-thanatology

森一郎
哲学 (61), 35-52_L4, 2010
… Political life and metaphysics were among the main ways for mortals to immortalize themselves. …
NAID 130004553919

ヒトパピローマウイルスによる発がんの分子機構

温川恭至,清野透
ウイルス 58(2), 141-154, 2008
　今から25年前Harald zur Hausen博士らによって子宮頸がんから16型ならびに18型ヒトパピローマウイルス(human papillomavirus: HPV)のDNAが発見され，その因果関係が初めて示唆された．その後の疫学的・分子生物学的研究から，子宮頸がんはHPV感染によって発症することに疑いの余地はなくなり，HPVは子宮頸がんの原因ウイルスとして確定している．90%以上の子宮頸 …
NAID 130004470914