WordNet
- be a contributing factor; "make things factor into a companys profitability"
- any of the numbers (or symbols) that form a product when multiplied together
- an independent variable in statistics
- anything that contributes causally to a result; "a number of factors determined the outcome"
- consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
- resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
- an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
- a concept whose truth can be proved; "scientific hypotheses are not facts"
- a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
- a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
- anything that belongs to a set or class; "snakes are members of the class Reptilia"; "members of the opposite sex"
- one of the persons who compose a social group (especially individuals who have joined and participate in a group organization); "only members will be admitted"; "a member of the faculty"; "she was introduced to all the members of his family" (同)fellow member
- an organization that is a member of another organization (especially a state that belongs to a group of nations); "the library was a member of the interlibrary loan association"; "Canada is a member of the United Nations"
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- the localized death of living cells (as from infection or the interruption of blood supply) (同)mortification, gangrene, sphacelus
PrepTutorEJDIC
- (…の)『要因』,(…を生み出す)要素《+『in』+『名』(do『ing』)》 / 囲数,約数 / 代理人,《おもに英》仲買人 / =factorize
- 〈C〉『事実』,実際にある(あった)事 / 〈U〉真相,真実(truth) / 《the~》(法律用語で)犯行
- (集団の)『一員』,会員,メンバー《+『of』+『名』》 / 《またM-》国会議員 / (数式の)項,辺 / 《文》身体の一部;(特に)手,足 / 《遠回しに》男根
- =sense organ / 受信装置
- 壊疽(えそ)
UpToDate Contents
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- 1. 腫瘍壊死因子受容体-1関連周期性発熱症候群（TRAPS） tumor necrosis factor receptor 1 associated periodic syndrome traps
- 2. 複合免疫不全 combined immunodeficiencies
- 3. 周期性発熱症候群およびその他の自己炎症性疾患：概要 periodic fever syndromes and other autoinflammatory diseases an overview
- 4. 分類不能型低ガンマグロブリン血症の病因 pathogenesis of common variable immunodeficiency
- 5. 進行黒色腫に対する免疫チェックポイント分子阻害による免疫療法 immunotherapy of advanced melanoma with immune checkpoint inhibition
English Journal
- Mechanisms underlying differential response to estrogen-induced apoptosis in long-term estrogen-deprived breast cancer cells.
- Sweeney EE, Fan P, Jordan VC.Author information Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.AbstractModels of long-term estrogen-deprived breast cancer cells are utilized in the laboratory to mimic clinical aromatase inhibitor-resistant breast cancer and serve as a tool to discover new therapeutic strategies. The MCF-7:5C and MCF-7:2A subclones were generated through long-term estrogen deprivation of estrogen receptor (ER)-positive MCF-7 cells, and represent anti-hormone‑resistant breast cancer. MCF-7:5C cells paradoxically undergo estrogen-induced apoptosis within seven days of estrogen (estradiol, E2) treatment; MCF-7:2A cells also experience E2-induced apoptosis but evade dramatic cell death until approximately 14 days of treatment. To discover and define the mechanisms by which MCF-7:2A cells survive two weeks of E2 treatment, systematic experiments were performed in this study. The data suggest that MCF-7:2A cells employ stronger antioxidant defense mechanisms than do MCF-7:5C cells, and that oxidative stress is ultimately required for MCF-7:2A cells to die in response to E2 treatment. Tumor necrosis factor (TNF) family member activation is also essential for E2-induced apoptosis to occur in MCF-7:2A cells; upregulation of TNFα occurs simultaneously with oxidative stress activation. Although the unfolded protein response (UPR) signaling pattern is similar to that in MCF-7:5C cells, it is not sufficient to cause cell death in MCF-7:2A cells. Additionally, increased insulin-like growth factor receptor β (IGF-1Rβ) confers a mechanism of growth and anti-apoptotic advantage in MCF-7:2A cells.
- International journal of oncology.Int J Oncol.2014 May;44(5):1529-38. doi: 10.3892/ijo.2014.2329. Epub 2014 Mar 6.
- Models of long-term estrogen-deprived breast cancer cells are utilized in the laboratory to mimic clinical aromatase inhibitor-resistant breast cancer and serve as a tool to discover new therapeutic strategies. The MCF-7:5C and MCF-7:2A subclones were generated through long-term estrogen deprivation
- PMID 24604139
- Analysis of changes in transcription start site distribution by a classification approach.
- Liang KC1, Suzuki Y2, Kumagai Y3, Nakai K4.Author information 1Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.2Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa-shi, Chiba-ken 227-8561, Japan.3Laboratory of Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.4Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa-shi, Chiba-ken 227-8561, Japan. Electronic address: knakai@ims.u-tokyo.ac.jp.AbstractChange in transcription start site (TSS) usage is an important mechanism for the control of transcription process, and has a significant effect on the isoforms being transcribed. One of the goals in the study of TSS is the understanding of how and why their usage differs in different tissues or under different conditions. In light of recent efforts in the mapping of transcription start site landscape using high-throughput sequencing approaches, a quantitative and automated method is needed to process all the data that are being produced. In this work we propose a statistical approach that will classify changes in TSS distribution between different samples into several categories of changes that may have biological significance. Genes selected by the classifiers can then be analyzed together with additional supporting data to determine their biological significance. We use a set of time-course TSS data from mouse dendritic cells stimulated with lipopolysaccharide (LPS) to demonstrate the usefulness of our method.
- Gene.Gene.2014 Mar 1;537(1):29-40. doi: 10.1016/j.gene.2013.12.038. Epub 2013 Dec 31.
- Change in transcription start site (TSS) usage is an important mechanism for the control of transcription process, and has a significant effect on the isoforms being transcribed. One of the goals in the study of TSS is the understanding of how and why their usage differs in different tissues or unde
- PMID 24389500
- Excess LIGHT contributes to placental impairment, increased secretion of vasoactive factors, hypertension, and proteinuria in preeclampsia.
- Wang W1, Parchim NF, Iriyama T, Luo R, Zhao C, Liu C, Irani RA, Zhang W, Ning C, Zhang Y, Blackwell SC, Chen L, Tao L, Hicks MJ, Kellems RE, Xia Y.Author information 1Department of Biochemistry and Molecular Biology, University of Texas Medical School at Houston, TX 77030. yang.xia@uth.tmc.edu.AbstractPreeclampsia, a prevalent hypertensive disorder of pregnancy, is believed to be secondary to uteroplacental ischemia. Accumulating evidence indicates that hypoxia-independent mediators, including inflammatory cytokines and growth factors, are associated with preeclampsia, but it is unclear whether these signals directly contribute to placental damage and disease development in vivo. We report that LIGHT, a novel tumor necrosis factor superfamily member, is significantly elevated in the circulation and placentas of preeclamptic women compared with normotensive pregnant women. Injection of LIGHT into pregnant mice induced placental apoptosis, small fetuses, and key features of preeclampsia, hypertension and proteinuria. Mechanistically, using neutralizing antibodies specific for LIGHT receptors, we found that LIGHT receptors herpes virus entry mediator and lymphotoxin β receptor are required for LIGHT-induced placental impairment, small fetuses, and preeclampsia features in pregnant mice. Accordingly, we further revealed that LIGHT functions through these 2 receptors to induce secretion of soluble fms-like tyrosine kinase-1 and endothelin-1, 2 well-accepted pathogenic factors in preeclampsia, and thereby plays an important role in hypertension and proteinuria in pregnant mice. Lastly, we extended our animal findings to human studies and demonstrated that activation of LIGHT receptors resulted in increased apoptosis and elevation of soluble fms-like tyrosine kinase-1 secretion in human placental villous explants. Overall, our human and mouse studies show that LIGHT signaling is a previously unrecognized pathway responsible for placental apoptosis, elevated secretion of vasoactive factors, and subsequent maternal features of preeclampsia, and reveal new therapeutic opportunities for the management of the disease.
- Hypertension.Hypertension.2014 Mar;63(3):595-606. doi: 10.1161/HYPERTENSIONAHA.113.02458. Epub 2013 Dec 9.
- Preeclampsia, a prevalent hypertensive disorder of pregnancy, is believed to be secondary to uteroplacental ischemia. Accumulating evidence indicates that hypoxia-independent mediators, including inflammatory cytokines and growth factors, are associated with preeclampsia, but it is unclear whether t
- PMID 24324043
Related Links
- CD40-like protein, herpes virus entry mediator A, tumor necrosis factor receptor superfamily member 14, tumor necrosis factor receptor superfamily, member 14 (herpesvirus entry mediator), tumor necrosis factor receptor-like gene2 ...
- Gene ID: 51330, updated on 13-Jan-2015 Summary Other designations FGF-inducible 14, fibroblast growth factor-inducible immediate-early response protein 14, tumor necrosis factor receptor superfamily member 12A, tweak-receptor ...
Related Pictures
★リンクテーブル★
| リンク元 | 「腫瘍壊死因子受容体メンバー14」 |
| 関連記事 | 「fact」「factor」「tumor」「member」 |
「腫瘍壊死因子受容体メンバー14」
「fact」
- n.
「factor」
- n.
「tumor」
- n.
「member」