WordNet

(genetics) the process of expressing a gene
the feelings expressed on a persons face; "a sad expression"; "a look of triumph"; "an angry face" (同)look, aspect, facial_expression, face
the act of forcing something out by squeezing or pressing; "the expression of milk from her breast"
expression without words; "tears are an expression of grief"; "the pulse is a reflection of the hearts condition" (同)manifestation, reflection, reflexion
the communication (in speech or writing) of your beliefs or opinions; "expressions of good will"; "he helped me find verbal expression for my ideas"; "the idea was immediate but the verbalism took hours" (同)verbal expression, verbalism
form a pattern; "These sentences pattern like the ones we studied before"
a model considered worthy of imitation; "the American constitution has provided a pattern for many republics"
make light, rapid and repeated sounds; "gently pattering rain" (同)pitter-patter
a quick succession of light rapid sounds; "the patter of mice"; "the patter of tiny feet"

PrepTutorEJDIC

〈U〉〈C〉(思想・意見・考えなどを)『言葉で表すこと』,(…の)『表現』《+『of』+『名』》 / 〈C〉(考え・気持ちなどの)『現れ』,印《+『of』+『名』》 / 〈C〉(考え・気持ちなどを表す)『顔つき』,表情《+『of』+『名』》 / 〈U〉(考え・気持ちなどを表す)声の調子 / 〈C〉語句,言い回し,表現法 / 〈C〉(数量・運算などを示す)式
《所有・所属》…『の』,…のものである,…に属する・《材料・要素》…『でできた』,から成る・《部分》…『の』[『中の』] ・《数量・単位・種類を表す名詞に付いて》…の・《原因・動機》…『で』,のために(because of) ・《主格関係》…『の』,による,によって・《目的格関係》…『を』,の・《同格関係》…『という』・《関係・関連》…『についての』[『の』],の点で・《抽象名詞などと共に》…の[性質をもつ] ・《『It is』+『形』+『of』+『名』+『to』 doの形で,ofの後の名詞を意味上の主語として》・《分離》…『から』・《起原・出所》…『から』[『の』](out of) ・《『名』+『of』+『a』(『an』)+『名』の形で》…のような・《『名』+『of』+『mine』(『yours, his』など独立所有格)の形で》…の…・《時》(1)《副詞句を作って》…に《形容詞句を作って》…の・《時刻》《米》…前(to,《米》before)
(壁紙・織物などの)『模様』,柄,デザイン / 『模範』,手本 / 『原型』,ひな型 / (行動・性資の)『型』,様式パターン / (…の型)・手本に従って)…‘を'型どる,作る,まねる《+『名』+『upon』(『on, after』)+『名』》 / …‘を'模様をつける
〈雨などが〉パラパラ降る / 〈子供・動物などが〉パタパタ走る / (…の)パラパラ(パタパタ)イウ音《+『of』+『名』》
《時にa~》早口ぺらぺらしゃべること…早口のせりふ / おしゃべり,むだ話 / (ある職業・階級の)仲間言葉,符ちょう / 早口に話す,ぺらぺらしゃべる / 〈祈り・詩など〉‘を'早口に唱える

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. ALK陽性未分化大細胞型リンパ腫の臨床症状、病理学的特徴、および診断 clinical manifestations pathologic features and diagnosis of anaplastic large cell lymphoma alk positive
2. バーキットリンパ腫の疫学、臨床症状、病理学的特徴、および診断 epidemiology clinical manifestations pathologic features and diagnosis of burkitt lymphoma
3. 濾胞性リンパ腫の病理生物学 pathobiology of follicular lymphoma
4. 子宮体癌：病理組織学および病因 endometrial carcinoma histopathology and pathogenesis
5. 甲状腺ホルモンの作用 thyroid hormone action

English Journal

The use of Fusarium secondary metabolite biosynthetic genes in chemotypic and phylogenetic studies.

Stępień L.Author information Institute of Plant Genetics, Polish Academy of Sciences , Poznań , Poland.AbstractAbstract Fusarium genus contains a large number of species which occur in all climate zones and are pathogenic to agriculturally important crops. The majority of the species produce secondary metabolites, many of which are toxic to plants, animals and humans. The core biosynthetic genes display conserved organization (gene clusters), and a common expression pattern due to synchronized regulation. Although broadly specified enzymatic activities are present in different metabolic paths, the reactions catalyzed by those are limited to a specific step and no compensation effect is observed when the essential gene from one of the clusters is disrupted. Still, inter- and intraspecific diversity of the core biosynthetic genes is consistently higher than that of housekeeping genes, even though the biochemical specificity is maintained. Thus, the core biosynthetic genes of known sequence and structure emerge as good targets for designing tools aimed at the discrimination of closely related (and economically important) Fusarium species. The review covers the present and potential use of sequence analysis and biosynthetic gene-derived molecular markers as applied to taxonomic and chemotype studies, utilizing both toxic (fumonisins, trichothecenes, zearalenone, fusaric acid, fusarins, enniatins and beauvericin) and nontoxic (bikaverin) metabolites produced by Fusarium fungi.
Critical reviews in microbiology.Crit Rev Microbiol.2014 May;40(2):176-85. doi: 10.3109/1040841X.2013.770387. Epub 2013 Mar 7.
Abstract Fusarium genus contains a large number of species which occur in all climate zones and are pathogenic to agriculturally important crops. The majority of the species produce secondary metabolites, many of which are toxic to plants, animals and humans. The core biosynthetic genes display cons
PMID 23465044

Obesity induced a leptin-Notch signaling axis in breast cancer.

Battle M, Gillespie C, Quarshie A, Lanier V, Harmon T, Wilson K, Torroella-Kouri M, Gonzalez-Perez RR.Author information Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA.AbstractTo investigate whether obesity induces a leptin-Notch signaling axis in breast cancer (BC), leptin-induced Notch was determined in human MCF-7 and MDA-MB231 and mouse E0771 cells and in E0771-BC hosted by syngeneic lean and diet-induced obesity (DIO) C57BL/6J female mice. Lean and DIO mice were treated for 3 weeks with leptin inhibitor (PEG-LPrA2) 1 week after the inoculation of E0771 cells. Leptin induced Notch1, 3 and 4 in BC cells, but Notch2 expression showed opposite pattern in MCF-7 compared to MDA-MB231 cells. Notch loss-of-function (DAPT and dominant negative [R218H] RBP-Jk [CSL/CBF1]) showed that a functional leptin-Notch signaling axis was involved in the proliferation and migration of E0771 cells. E0771-BC onset was affected by obesity (lean mice7/10 [70%] vs. DIO mice: 11/12 [92%]; Pearson χ(2) : p = 0.06]). PEG-LPrA2 significantly reduced BC growth (untreated: 19/42; [45%] vs. treated: 8/42 [19%]; Pearson χ(2) : p = 0.008). PEG-LPrA2 did not influence the caloric intake of mice but increased carcass and/or body weights of lean and DIO mice inoculated with E0771 cells, which could be related to the improvement of health conditions (less aggressive disease). Importantly, BC from obese mice had higher levels of Notch3, JAG1 and survivin than lean mice. Inhibition of leptin signaling reduced protein levels of Notch (NICD1, NICD4, Notch3, JAG1 and survivin) and significantly decreased mRNA expression of Notch receptors, ligands and targets. PEG-LPrA's effects were more prominent in DIO mice. Present data suggest that leptin induces Notch, which could be involved in the reported higher incidence and aggressiveness and, poor prognosis of BC in obese patients.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 Apr 1;134(7):1605-16. doi: 10.1002/ijc.28496. Epub 2013 Oct 8.
To investigate whether obesity induces a leptin-Notch signaling axis in breast cancer (BC), leptin-induced Notch was determined in human MCF-7 and MDA-MB231 and mouse E0771 cells and in E0771-BC hosted by syngeneic lean and diet-induced obesity (DIO) C57BL/6J female mice. Lean and DIO mice were trea
PMID 24114531

High glucose driven expression of pro-inflammatory cytokine and chemokine genes in lymphocytes: Molecular mechanisms of IL-17 family gene expression.

Kumar P1, Natarajan K1, Shanmugam N2.Author information 1Department of Biomedical Science, Bharathidasan University, Tiruchirappalli 620 024, Tamilnadu, India.2Department of Biomedical Science, Bharathidasan University, Tiruchirappalli 620 024, Tamilnadu, India. Electronic address: nshanmugam@bdu.ac.in.AbstractHigh glucose is an independent risk factor that alters the expression pattern of cytokines/chemokine leading to leukocyte activation in diabetes. Fluctuation of cytokine milieu in lymphocytes may lead to differentiation into a particular subset. Our objectives were to profile high glucose induced inflammatory gene expression in lymphocytes, to examine in vivo relevance in diabetes and to identify the key transcription factors and signaling pathways involved. Cytokine gene arrays and T-helper (Th1/Th2/Th17) cytokine profiler RT(2)-PCR arrays used for cytokine expression profiling followed by validation using Real Time-qPCR and relative RT-PCR in Jurkat T-lymphocytes, peripheral blood lymphocytes (PBLCs) from normal and diabetes subjects. Luciferase reporter plasmid, pharmacological inhibitors and mutant plasmids were used for promoter activation and signaling pathway studies. High glucose induced gene profiling in Jurkat T-lymphocytes showed significantly increased expression of 64 proinflammatory genes including IL-6 and IL-17A and most of these genes were Nuclear Factor (NF)-κB and AP-1 regulated. RT(2)-PCR array results suggested the transcriptional activation of IL-17 and its downstream signaling in Jurkat T-lymphocytes upon high glucose treatment. Candidate genes like Interleukin (IL)-17A, IL-17E IL-17F and IL-6 were up-regulated in both Jurkat T-lymphocytes and PBLCs from normal and diabetes subjects. This high glucose induced cytokine expression was due to promoter activation. Pharmacology inhibitor studies showed the involvement of NF-κB, protein kinase-C, p38 Mitogen activated protein kinase; Janus activated kinase-signal transducer and activator of transcription and extracellular regulated kinase signaling pathways. Further, high glucose treatment increased the adhesion of lymphocytes to human umbilical vein endothelial cells. These results show that IL-17 cytokines are induced by high glucose via key signaling pathways leading to lymphocyte activation and relevant to the pathogenesis of diabetic complications like atherosclerosis.
Cellular signalling.Cell Signal.2014 Mar;26(3):528-39. doi: 10.1016/j.cellsig.2013.11.031. Epub 2013 Dec 2.
High glucose is an independent risk factor that alters the expression pattern of cytokines/chemokine leading to leukocyte activation in diabetes. Fluctuation of cytokine milieu in lymphocytes may lead to differentiation into a particular subset. Our objectives were to profile high glucose induced in
PMID 24308966