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1  and osteoblastic metastases in vivo via the endothelin A receptor.
2 eases PKC activity via binding to endogenous endothelin(A) receptors.
3         Therefore, we assessed the effect of endothelin-A receptor antagonism in the response of pulm
4              Treatment with an orally active endothelin A receptor antagonist dramatically decreased
5 ety of zibotentan (ZD4054), an oral specific endothelin A receptor antagonist, has been investigated
6                      Atrasentan, a selective endothelin A receptor antagonist, has been shown to redu
7                                    BQ123, an endothelin A receptor antagonist, prevented thrombin's i
8 209,670, and the less potent, but selective, endothelin-A receptor antagonist BMS-182,874 in radiocon
9 -phenyl-4H-1-benzopyran-4-one (LY294002) and endothelin-A receptor antagonist cyclo(L-Leu-D-Trp-D-Asp
10  with a highly selective, well-characterized endothelin-A receptor antagonist partly protected GFR, a
11                                          The endothelin-A receptor antagonist, BQ-123, could attenuat
12   Half of the rings were pretreated with the endothelin-A receptor antagonist, BQ123 (10(-5) M or 10(
13                  Interest has grown in using Endothelin A receptor antagonists as adjuvant or combina
14 gations involving alpha-emitting radium-223, endothelin-A receptor antagonists atrasentan and ziboten
15 ishment of osteoblastic bone metastases, and endothelin A receptor blockade represents effective trea
16                                        Acute endothelin A receptor blockade with FR-139317 resulted i
17                                              Endothelin-A receptor blockade is an effective means of
18                                  In summary, endothelin-A receptor blockade with a highly selective,
19 riction, which was reversed partially by the endothelin A receptor blocker BQ123 and completely by fa
20  experiments, endothelin 1 (which stimulates endothelin A receptors) caused comparable contraction of
21 dothelin signaling via the activation of the endothelin-A receptor (EDNRA) by endothelin-1 may play a
22 helin-1 (Edn1)-induced signaling through the endothelin-A receptor (Ednra) is crucial for cranial NCC
23                                              Endothelin-A receptor (Ednra) signaling in crest cells i
24 cranial NCCs, some of which are regulated by endothelin-A receptor (Ednra) signaling.
25 tions mediated by two receptor subtypes, the endothelin A receptor (ET(A)R) and the endothelin B rece
26 amined the effect of atrasentan, a selective endothelin A receptor (ET(A)R) antagonist, on albuminuri
27 uring ischaemia through direct activation of endothelin A receptors (ET(A)Rs).
28 othelins stimulate leptin production via the endothelin-A receptor (ET(A)), as judged by a potency ra
29 can produce ET-1, undergo ET-1-dependent and endothelin-A receptor (ET(A))-dependent activation, and
30                                Activation of endothelin-A receptor (ET(A)R) by endothelin-1 (ET-1) dr
31 o three groups: placebo (RVD+PTRAS), chronic endothelin-A receptor (ET-A) blockade (RVD+PTRAS+ET-A),
32 ly identical to the defects seen in ET-1 and endothelin A receptor (ETA)-deficient embryos.
33 g-term treatment strategy with the selective endothelin-A receptor (ETA) antagonist, ambrisentan, des
34  angiotensin II type 1A receptor (AT1AR) and endothelin A receptor (ETAR), activation of ETARs result
35                             Mechanistically, endothelin A receptor (ETAR)-positive macrophages are hi
36 on of its cognate G protein-coupled receptor endothelin A receptor (ETAR).
37        In EOC, the endothelin-1 (ET-1, EDN1)-endothelin A receptor (ETAR, EDNRA) signaling axis regul
38                 Mice with a null mutation in endothelin A receptor gene (ET(A)) or in the gene of its
39 eviously showed that activation of the human endothelin A receptor (HETAR) by endothelin-1 (Et-1) sel
40 ion of similar magnitude (P </= 0.05) of the endothelin A receptor in the lung tissue.
41                   Selectively inhibiting the endothelin A receptors in dogs with CHF produced hemodyn
42 ults are consistent with the hypothesis that endothelin-A receptors mediate endothelin-induced change
43 sed in rejecting allotransplanted lungs, (3) endothelin-A receptors mediate the proliferative respons
44                   No change in expression of endothelin A receptor was observed 7 days after inductio
45                 This effect, mediated by the endothelin-A receptor, was associated with a shift in ML

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