WordNet

to remain unmolested, undisturbed, or uninterrupted -- used only in infinitive form; "let her be"
work in a specific place, with a specific subject, or in a specific function; "He is a herpetologist"; "She is our resident philosopher" (同)follow
have life, be alive; "Our great leader is no more"; "My grandfather lived until the end of war" (同)live
be identical to; be someone or something; "The president of the company is John Smith"; "This is my house"
happen, occur, take place; "I lost my wallet; this was during the visit to my parents house"; "There were two hundred people at his funeral"; "There was a lot of noise in the kitchen"
have the quality of being; (copula, used with an adjective or a predicate noun); "John is rich"; "This is not a good answer"
occupy a certain position or area; be somewhere; "Where is my umbrella?" "The toolshed is in the back"; "What is behind this behavior?"
spend or use time; "I may be an hour"
stake on the outcome of an issue; "I bet $100 on that new horse"; "She played all her money on the dark horse" (同)wager, play
the act of gambling; "he did it on a bet" (同)wager
maintain with or as if with a bet; "I bet she will be there!" (同)wager
second in order of importance; "the candidate, considered a beta male, was perceived to be unable to lead his party to victory"
the 2nd letter of the Greek alphabet
preliminary or testing stage of a software or hardware product; "a beta version"; "beta software"
the 16th letter of the Roman alphabet (同)p

PrepTutorEJDIC

《連結語として補語を伴なって…『である』,…だ,…です / 《位置・場所を表す語句を伴って》(…に)『ある』,いる(occupy a place or situation) / 〈物事が〉『存在する』,ある(exist);〈生物が〉生存する,生きている(live) / 行われる,起こる,発生する(take place, occur) / 存続する,そのままでいる(remain as before) / 《『be to』 do》 / …する予定である,…することになっている / …すべきだ / 《受動態の不定詞を伴って》…できる / 《命令》…するのだ / 《条件節に》…する意図がある / 《『if…were to』 do》…するとしたなら / 《『be』 do『ing』》《進行形》 / 《進行中の動作》…している,しつつある / 《近い未来》…しようとしている,するつもり / 《動作の反復》(いつも)…している / 《『be』+『他動詞の過去分詞』》《受動態》…される,されている / 《『be』+『自動詞の過去分詞』》《完了形》…した[状態にある]
『かけ』・(…との)かけ《+『with』+『名』》 / かけた物(金) / かけの対象 / 〈金・物〉'を'『かける』 / (かけ事・ゲームなどで)〈人〉‘と'『かけをする』《+『名』〈人〉+『on』+『名』》 / (…に)『かける』《+『on』(『against』)+『名』(one's do『ing』)》
ベータ(ギリシア語アルファベットの第2文字;B,β;英語のB,b に遭当)
parking
phosphorusの化学記号

UpToDate Contents

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1. 慢性苔癬状粃糠疹 pityriasis lichenoides chronica
2. ペプチドホルモンのシグナル伝達および調節 peptide hormone signal transduction and regulation
3. 血小板生物学 platelet biology
4. 肥満細胞：表面受容体とシグナル伝達 mast cells surface receptors and signal transduction
5. 急性痘瘡状苔癬状粃糠疹（PLEVA） pityriasis lichenoides et varioliformis acuta pleva

English Journal

Inhibitory effects of mulberry fruit extract in combination with naringinase on the allergic response in IgE-activated RBL-2H3 cells.

Yoo JM1, Kim NY1, Seo JM2, Kim SJ2, Lee SY3, Kim SK3, Kim HD4, Lee SW4, Kim MR1.Author information 1Department of Food and Nutrition, Chungnam National University, Yuseong-gu, Daejeon 305-764, Republic of Korea.2Department of Bio-Environmental Chemistry, Chungnam National University, Yuseong-gu, Daejeon 305-764, Republic of Korea.3College of Pharmacy, Chungnam National University, Yuseong-gu, Daejeon 305-764, Republic of Korea.4Department of Herbal Crop Research, National Institute of Horticultural and Herbal Science (NIHHS), RDA, Eumseong 369-873, Republic of Korea.AbstractIn this study, we investigated the anti-allergic action of mulberry fruit extract (MFE) or MFE in combination with naringinase (MFEN) in IgE-activated RBL-2H3 cells, and investigated the mechanisms responsible for the anti-allergic effects of MFEN. β-hexosaminidase release assay was used to measure the amount of β-hexosaminidase released from the cells, and ELISA was used to measure the levels of tumor necrosis factor-α (TNF-α). We found that MFE significantly reduced the release of β-hexosaminidase (IC50, 10.59 mg/ml) and TNF-α (IC50, 4.87 mg/ml). Moreover, MFEN enhanced the inhibitory effects on the release of β-hexosaminidase (IC50, 123.10 µg/ml) and TNF-α (IC50, 65.01 µg/ml). Furthermore, MFEN had no cytotoxicity at the concentration range used to exert the anti-allergic effects. In addition, we evaluated the effects of MFEN on the formation of pro-inflammatory lipid mediators, such as prostaglandin D2 (PGD2), leukotriene C4 (LTC4) and leukotriene B4 (LTB4) using enzyme immunoassay (EIA) kits. MFEN markedly reduced the formation of PGD2 (IC50, 6.47 µg/ml) and LTC4 (IC50, 0.31 µg/ml), but not LTB4 (IC50, 25.75 µg/ml). In mechanistic analyses, we measured the phosphorylation of Syk, Lyn and Fyn by immunoblot analysis. MFEN significantly inhibited the phosphorylation of Syk, but not that of Lyn or Fyn. MFEN also suppressed the phosphorylation of phospholipase C (PLC)γ1/2, protein kinase C (PKC)δ, linker for activation of T cells (LAT), extracellular signal-regulated protein kinase (ERK)1/2, JNK, GRB2-associated binding protein 2 (Gab2), phosphoinositide-3-kinase (PI3K), Akt, cytosolic phospholipase A2 and 5-lipoxygenase, as well as the expression of cyclooxygenase-2. In conclusion, these results suggest that MFEN exerts potent inhibitory effects on allergic response through the suppression of the activation of the FcεRI signaling cascade. Our data demonstrating the anti-allergic effects of MFEN may provide further insight into the therapeutic application of MFEN or its use as a functional food.
International journal of molecular medicine.Int J Mol Med.2014 Feb;33(2):469-77. doi: 10.3892/ijmm.2013.1590. Epub 2013 Dec 13.
In this study, we investigated the anti-allergic action of mulberry fruit extract (MFE) or MFE in combination with naringinase (MFEN) in IgE-activated RBL-2H3 cells, and investigated the mechanisms responsible for the anti-allergic effects of MFEN. β-hexosaminidase release assay was used to measure
PMID 24336971

Metabolism and functions of copper in brain.

Scheiber IF1, Mercer JF2, Dringen R3.Author information 1Department of Parasitology, Faculty of Science, Charles University, Prague, Czech Republic.2Centre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood Campus, 221 Burwood Highway, Burwood, Victoria 3125, Australia.3Center for Biomolecular Interactions Bremen, University of Bremen, PO. Box 330440, D-28334 Bremen, Germany; Center for Environmental Research and Sustainable Technology, Leobener Strasse, D-28359 Bremen, Germany. Electronic address: ralf.dringen@uni-bremen.de.AbstractCopper is an important trace element that is required for essential enzymes. However, due to its redox activity, copper can also lead to the generation of toxic reactive oxygen species. Therefore, cellular uptake, storage as well as export of copper have to be tightly regulated in order to garantee sufficient copper supply for the synthesis of copper-containing enzymes but also to prevent copper-induced oxidative stress. In brain, copper is of importance for normal development. In addition, both copper deficiency as well as excess of copper can seriously affect brain functions. Therefore, this organ possesses ample mechanisms to regulate its copper metabolism. In brain, astrocytes are considered as important regulators of copper homeostasis. Impairments of homeostatic mechanisms in brain copper metabolism have been associated with neurodegeneration in human disorders such as Menkes disease, Wilson's disease and Alzheimer's disease. This review article will summarize the biological functions of copper in the brain and will describe the current knowledge on the mechanisms involved in copper transport, storage and export of brain cells. The role of copper in diseases that have been connected with disturbances in brain copper homeostasis will also be discussed.
Progress in neurobiology.Prog Neurobiol.2014 Jan 16. pii: S0301-0082(14)00012-4. doi: 10.1016/j.pneurobio.2014.01.002. [Epub ahead of print]
Copper is an important trace element that is required for essential enzymes. However, due to its redox activity, copper can also lead to the generation of toxic reactive oxygen species. Therefore, cellular uptake, storage as well as export of copper have to be tightly regulated in order to garantee
PMID 24440710

Chemical modulation of glycerolipid signaling and metabolic pathways.

Scott SA1, Mathews TP2, Ivanova PT1, Lindsley CW3, Brown HA4.Author information 1Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.2Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University Medical Center, Nashville, TN 37232, USA.3Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Department of Chemistry, Vanderbilt University, Nashville, TN 37235, USA; Vanderbilt Institute of Chemical Biology, Vanderbilt University, Nashville, TN 37235, USA.4Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Department of Biochemistry, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Institute of Chemical Biology, Vanderbilt University, Nashville, TN 37235, USA. Electronic address: alex.brown@vanderbilt.edu.AbstractThirty years ago, glycerolipids captured the attention of biochemical researchers as novel cellular signaling entities. We now recognize that these biomolecules occupy signaling nodes critical to a number of physiological and pathological processes. Thus, glycerolipid-metabolizing enzymes present attractive targets for new therapies. A number of fields-ranging from neuroscience and cancer to diabetes and obesity-have elucidated the signaling properties of glycerolipids. The biochemical literature teems with newly emerging small molecule inhibitors capable of manipulating glycerolipid metabolism and signaling. This ever-expanding pool of chemical modulators appears daunting to those interested in exploiting glycerolipid-signaling pathways in their model system of choice. This review distills the current body of literature surrounding glycerolipid metabolism into a more approachable format, facilitating the application of small molecule inhibitors to novel systems.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jan 15. pii: S1388-1981(14)00014-6. doi: 10.1016/j.bbalip.2014.01.009. [Epub ahead of print]
Thirty years ago, glycerolipids captured the attention of biochemical researchers as novel cellular signaling entities. We now recognize that these biomolecules occupy signaling nodes critical to a number of physiological and pathological processes. Thus, glycerolipid-metabolizing enzymes present at
PMID 24440821

Japanese Journal

Ca(v)2.1 in Cerebellar Purkinje Cells Regulates Competitive Excitatory Synaptic Wiring, Cell Survival, and Cerebellar Biochemical Compartmentalization

Miyazaki Taisuke,Yamasaki Miwako,Hashimoto Kouichi,Yamazaki Maya,Abe Manabu,Usui Hiroshi,Kano Masanobu,Sakimura Kenji,Watanabe Masahiko
JOURNAL OF NEUROSCIENCE 32(4), 1311-1328, 2012-01-25
… Furthermore, the mutually complementary expression of phospholipase C beta 3 (PLC beta 3) and PLC beta 4 was altered such that their normally sharp boundary was blurred in the PCs of PC-Cav2.1 KO mice. …
NAID 120005208889

Pleckstrin homology domain of PLC-beta2 confers G-βγ activation to catalytic core

WANG T.
J. Biol. Chem. 275, 7466-7469, 2000
NAID 30016330515

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