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1 ncreasing beta(2)AR expression or minimizing tachyphylaxis.
2  desensitize at a faster rate and attenuated tachyphylaxis.
3  this partial agonist acted without inducing tachyphylaxis.
4  altered the kinetics of desensitization and tachyphylaxis.
5 as attenuated over time, suggesting possible tachyphylaxis.
6 ions in the TRPV1-ARD binding site eliminate tachyphylaxis.
7  plays an opposing role and is necessary for tachyphylaxis.
8  whether receptor trafficking contributes to tachyphylaxis.
9 a pivotal role in receptor sensitization vs. tachyphylaxis.
10  cell signaling that are limited by receptor tachyphylaxis.
11 s of CRF were reproducible, and there was no tachyphylaxis.
12 ardial application of bradykinin demonstrate tachyphylaxis.
13 injections of IL-12 do not induce a state of tachyphylaxis.
14 ng, contributing to receptor desensitization/tachyphylaxis.
15  in asthma is limited by desensitization and tachyphylaxis.
16 fects and induce receptor downregulation and tachyphylaxis.
17 cal use of certain MR agonists is limited by tachyphylaxis, a reduced responsiveness to repeated comp
18                 Importantly, interruption of tachyphylaxis and bradyphylaxis restores cancer cell cyt
19  aqueous humour can lead us to understanding tachyphylaxis and changes in intraocular immune mechanis
20 in most patients for up to 156 weeks without tachyphylaxis and had an acceptable safety profile.
21 t of bronchodilators that are not subject to tachyphylaxis and would thus avoid beta2-adrenoceptor ag
22                   Resistance reflects rapid (tachyphylaxis) and slow (bradyphylaxis) mechanisms of de
23 mpairment of normal inotropic and lusitropic tachyphylaxis, and exhibited accelerated development of
24 nate, which elicits channel desensitization, tachyphylaxis, and transient pain, GNE551 activates TRPA
25 vels may play a very minor role in mediating tachyphylaxis; and 4) alterations in adiponectin recepto
26 agonist-induced TRPV1 desensitization and/or tachyphylaxis are still incompletely understood.
27                                      Motilin tachyphylaxis both in the presence or absence of tetrodo
28 st UP is blocked by alpha-beta methylene ATP tachyphylaxis, by reactive blue 2, and by apamin.
29 ary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykini
30 d response during constant Cap exposure) and tachyphylaxis (diminished response to successive applica
31                     In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially rest
32 llular solutions resulted in nearly complete tachyphylaxis even with intracellular Ca2+ buffered to l
33 c tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rig
34  a bell-shaped dose-response relationship or tachyphylaxis in preclinical models.
35 P sorting cycle seemed to correlate with the tachyphylaxis-inducing properties of each compound, but
36                                              Tachyphylaxis is mediated by cGMP-dependent protein kina
37                                 One cause of tachyphylaxis is receptor desensitization, usually accom
38  response on repetitive drug exposure (i.e., tachyphylaxis) is a particular problem for the vasoconst
39                                Tolerance and tachyphylaxis may occur, particularly with longer-term i
40 ely, desensitization of sst on tumor tissue (tachyphylaxis) may occur occasionally in patients on chr
41                                      Neither tachyphylaxis nor apparent toxicity has been noted.
42                                Surprisingly, tachyphylaxis of increased local vascular permeability w
43 rmined if repeated challenges with BK led to tachyphylaxis of neurally mediated responses in subjects
44                Repeated BK challenges led to tachyphylaxis of sneezing and of neurally mediated serou
45 ll agonist, such as nicotine, produces rapid tachyphylaxis of the P20N40-measured sensory inhibition
46 does not result in the development of either tachyphylaxis or upregulation of sst as assessed by chan
47                         We did not observe a tachyphylaxis phenomenon.
48         The principal findings were that (1) tachyphylaxis rapidly developed to the BJR-mediated hemo
49 d that this reduction was not an artifact of tachyphylaxis resulting from repeated administration of
50 re-wiring is manifested by type I interferon tachyphylaxis selectively downstream of STING and a corr
51 eated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on sub
52                  These findings suggest that tachyphylaxis to 5-HT(3) receptor agonists may be due to
53 utamol (0.3 to 3.5 nmol.min-1) did not cause tachyphylaxis to an identical repeated infusion after a
54 r factor regulating inotropic and lusitropic tachyphylaxis to beta-adrenergic agonist, which likely c
55 markedly attenuated after the development of tachyphylaxis to PBG in saline- and in L-NAME-treated ra
56          However, the rate of development of tachyphylaxis to PBG was markedly faster in the L-NAME-t
57                  These findings suggest that tachyphylaxis to PBG was not due to the loss of central
58        Furthermore, the TREC did not display tachyphylaxis to prolonged agonist exposure (desensitiza
59                                          The tachyphylaxis to repeated coronary artery occlusions may
60 ificant and prolonged responses to 5-HT with tachyphylaxis to repeated injections.
61 dditional studies provided evidence that (1) tachyphylaxis to the 5-HT(3)R agonists was not due to im
62 progressive disease while on K may be due to tachyphylaxis to the adrenolytic properties of K.
63                               The pronounced tachyphylaxis to the Bezold-Jarisch reflex (BJR) respons
64 hyl-5-HT were not responsible for preventing tachyphylaxis to the BJR reflex responses elicited by 5-
65  inhibition of NOS alters the development of tachyphylaxis to the BJR responses elicited by PBG in co
66 HT(2)R agonist, alpha-methyl-5-HT, prevented tachyphylaxis to the BJR-mediated hemodynamic responses
67  NAC response developed a profound tolerance/tachyphylaxis to the drug-induced increase in extracellu
68 improves insulin resistance in DIO mice; 3) "tachyphylaxis" to the effect of chronic MTII treatment o
69  the first transmembrane domain that confers tachyphylaxis upon ASIC2a.
70                                              Tachyphylaxis was hypothesized to account for the reduce
71                                              Tachyphylaxis was not observed.
72  diminished over the following 72 hours, the tachyphylaxis was reversible.
73 in agonist-promoted TAS2R14 desensitization (tachyphylaxis), we generated fusion proteins of both the
74  that chronic exposure to octreotide induces tachyphylaxis, we hypothesized that chronic exposure of
75               Both acute desensitization and tachyphylaxis were greatly diminished by reductions in e
76 to repeated applications of capsaicin, i.e., tachyphylaxis, while calmodulin plays an opposing role a
77 .d. SLIGRL-NH(2) for 9 min, to partial (25%) tachyphylaxis with repeated injection.
78 own-regulation of TAS2R14 expression because tachyphylaxis would be an undesirable therapeutic charac