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1 polipoprotein E, protein phosphatase 2A, and prostaglandin D.
3 tamine, cysteinyl-leukotrienes (cys-LTs) and prostaglandin D(2) (PGD(2) ) was assessed as was express
5 hat mediates the pro-inflammatory effects of prostaglandin D(2) (PGD(2)) generated in allergic inflam
7 lt of increased levels of the lipid mediator prostaglandin D(2) (PGD(2)) in the respiratory tract wit
10 omologous molecule on Th2 cells (CRTH2) is a prostaglandin D(2) (PGD(2)) receptor, expressed by Th2 c
11 o mediate the metabolism of sex hormones and prostaglandin D(2) (PGD(2)), a lipid mediator that promo
12 pressed on TH2 cells (CRTH2), a receptor for prostaglandin D(2) (PGD(2)), is expressed by human ILC2s
13 nism, thought to be caused by the release of prostaglandin D(2) (PGD(2)), is not well understood.
15 e effect of inhaled PGE(2) on the release of prostaglandin D(2) (PGD(2)), preformed mast cell mediato
16 racerebroventricular (icv) administration of prostaglandin D(2) (PGD(2); 20 microg/5 microl) to consc
17 es, eosinophils and basophils in response to prostaglandin D(2) and may be involved in the pathogenes
19 thesis was developed for the production of a prostaglandin D(2) receptor antagonist for the treatment
20 for the production of the core structure of prostaglandin D(2) receptor antagonists for the treatmen
21 tment of bone marrow-derived mast cells with prostaglandin D(2) reduced their ability to generate leu
22 ed by CD34(+) cells, decreased apoptosis and prostaglandin D(2) release by cultured MCs, and higher p
23 cts of gene knock-out (KO) of lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at
26 J(2)) are naturally occurring derivatives of prostaglandin D(2) that have been suggested to exert ant
29 ew blockers of specific mediators, including prostaglandin D(2), IL-5, IL-9, and IL-13, are also in c
33 ry (LC-MS/MS) assay that accurately measures prostaglandins D(2) (PGD(2)) and E(2) (PGE(2)) in cell c
34 ts of PGD(2), prostaglandin J(2), as well as prostaglandin D receptor (DP) agonists and antagonists o
35 ing, chemokine ligand 5 (CCL5) hematopoietic prostaglandin D synthase (HPGDS) and neuropeptide S rece
36 PGD(2), which is generated by hematopoietic prostaglandin D synthase (HPGDS), acts on 3 G protein-co
38 n proinflammatory conditions, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons
39 e found to have elevated levels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and
40 is study, we define a new role for lipocalin prostaglandin D synthase (L-PGDS) in the control of meta
41 trated a twofold reduction in lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, aft
42 ed for the urinary biomarkers lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycop
43 of decorin and significantly lower levels of prostaglandin D synthase (PGDS) and keratan sulfate.
45 ression of prostaglandin synthase-1 (PGHS1), prostaglandin D synthase (PTGDS), human prostaglandin tr
47 cological blockade of cyclooxygenase-2 or of prostaglandin D synthase prevented the effects of increa
48 ient substrate for the hematopoietic type of prostaglandin D synthase resulting in formation of HKD(2
49 ilar to those of GSH-dependent hematopoietic prostaglandin D synthase, except for the two large loop
50 ssociated with allergic responses, including prostaglandin D synthase, histamine receptor type 1 (H1R
51 reater IL-5 and IL-13 than did hematopoietic prostaglandin D synthase-negative and CD161(-) cT(H)2 ce
52 H)2 cells-positive (CRTH2(+)), hematopoietic prostaglandin D synthase-positive CD161(hi) CD4 T cells.
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