ライフサイエンスコーパス: stunning

1 llows brief periods of ischemia ("myocardial stunning").

2 ximately 50%) ("late preconditioning against stunning").

3 3 d later (late preconditioning [PC] against stunning).

4 urs later (late preconditioning [PC] against stunning).

5 ctive response (late preconditioning against stunning).

6 x microstructural patterns that are visually stunning.

7 annel blockers have been shown to ameliorate stunning.

8 lation to ischemic stress, which induced the stunning.

9 ed for hours or days because of postischemic stunning.

10 s diagnostic scan for any visual evidence of stunning.

11 n in a canine model of repetitive myocardial stunning.

12 oiodine ablation without concern for thyroid stunning.

13 ndicating the development of late PC against stunning.

14 use atherosclerotic disease or microvascular stunning.

15 ny delayed deleterious actions on myocardial stunning.

16 unknown whether it triggers late PC against stunning.

17 amine stress and a reduction in postischemic stunning.

18 his gene therapy protects against myocardial stunning.

19 ate (ISMN, 50 mg once daily) on postexercise stunning.

20 ndicating the development of late PC against stunning.

21 ther, suggesting the induction of myocardial stunning.

22 p IV, n = 6) failed to block late PC against stunning.

23 dicating a late PC effect against myocardial stunning.

24 m overload implicated in the pathogenesis of stunning.

25 the sixth reperfusion, indicating myocardial stunning.

26 utamine recovery, consistent with myocardial stunning.

27 myofilament proteolysis underlies myocardial stunning.

28 e of late preconditioning against myocardial stunning.

29 mined at baseline, during ischemia and after stunning.

30 of the first sequence, indicating myocardial stunning.

31 gineered human-transmissible H5N1 strain are stunning.

32 species, has been associated with myocardial stunning.

33 diagnostic (131)I, the phenomenon was called stunning.

34 -C during reperfusion may prolong myocardial stunning.

35 ion of blood flow, which is called metabolic stunning.

36 or swelling and failed to prevent myocardial stunning.

37 with no stunning, and group S, patients with stunning.

38 ared with postablation scans for evidence of stunning.

39 ion (group 3, n = 6), designed to produce no stunning.

40 th the protective effects of late PC against stunning.

41 olecular identification, and the results are stunning.

42 ardium but may not play a role in reversible stunning.

43 emic preconditioning (PC) against myocardial stunning.

44 ective effects of late PC against myocardial stunning.

45 SOD2) isoforms to protect against myocardial stunning.

46 xygen species (ROS) contribute to myocardial stunning.

47 and duration of postconversion left atrial "stunning."

48 confer marked protection against myocardial stunning 1-3 d later (late preconditioning [PC] against

49 e from the natural product itself that are a stunning 100-fold more active (IC50 values, 50-75 pM vs.

50 (group V, n = 5), the severity of myocardial stunning 24 h later was not modified.

51 id not exacerbate the severity of myocardial stunning 24 hours later; therefore, the absence of late

52 he heart relatively resistant to myocardial "stunning" 24 hours later (late preconditioning [PC] agai

53 of trehalases in desiccated cell reveals the stunning ability of cells to retain enzymatic activity w

54 In the basic science arena, there have been stunning advancements that illustrate novel biological a

55 ther molecules that mediate taste has led to stunning advances in our understanding of the basic mech

56 Despite stunning advances in our understanding of the genetics a

57 ical concentration and ameliorate myocardial stunning after ischemia-reperfusion.

58 0% for 90 minutes, and subsequent myocardial stunning after reperfusion in chronically instrumented c

59 echo contrast and frequently develop atrial stunning after restoration of sinus rhythm.

60 Left atrial appendage stunning also occurs in patients with atrial flutter, al

61 ons in preload after global ischemia-induced stunning also prevented TnI degradation.

62 pite such response dimorphism, we observed a stunning anatomical monomorphism of cortical penis and c

63 ts; p = 0.03) for patients predicted to have stunning and a marked decline in LVEF outside the infarc

64 , clinical exploitation of the powerful anti-stunning and anti-infarct actions of late PC has been el

65 ated TnI proteolysis can be dissociated from stunning and arises from elevations in preload rather th

66 similarly may be associated with myocardial stunning and cell necrosis associated with ischemia/repe

67 ardial infarction (MI) because of myocardial stunning and compensatory hyperkinesia in noninfarct-rel

68 mia in the setting of CD results in enhanced stunning and development of infarct.

69 hat relates to the time course of myocardial stunning and differs transmurally in relation to ischemi

70 This process is known as myocardial stunning and has important clinical ramifications.

71 ught to prospectively identify patients with stunning and hyperkinesia at hospital discharge on the b

72 AR and VR technologies allow for stunning and immersive experiences, offering untapped op

73 before ischemia would enhance the degree of stunning and induce a sustained decrease in glucose upta

74 ne receptor agonist, in models of myocardial stunning and infarction in chronically instrumented cons

75 tely ablated the late PC effect against both stunning and infarction.

76 e effects of late PC against both myocardial stunning and myocardial infarction, indicating that COX-

77 e effects of late PC against both myocardial stunning and myocardial infarction, indicating that NF-k

78 Closed-chest stunning and SEMI were produced by angioplasty balloon o

79 mibi SPECT and low-dose dobutamine in canine stunning and subendocardial infarction (SEMI).

80 mmalian models of both ischemia/reperfusion (stunning) and chronic pressure overload with hypertrophy

81 powerful protection against both reversible (stunning) and irreversible (infarction) injury during ac

82 tion 24 hours later against both reversible (stunning) and irreversible (infarction) ischemia/reperfu

83 result in reduced postoperative reversible (stunning) and irreversible myocardial injury, as assesse

84 rt failure, ischemia and reperfusion injury, stunning, and familial hypertrophic cardiac myopathies.

85 into two groups: group NS, patients with no stunning, and group S, patients with stunning.

86 ng residual viability, microvascular damage, stunning, and right ventricular infarction.

87 est remains normal, consistent with "chronic stunning," and contrasts with reduced flow and increased

88 lso prevented the contractile dysfunction of stunning; and (3) calpain I could similarly degrade TnI,

89 mia can have a negative effect on the heart: stunning; and on the other hand, they have a protective

90 We hypothesized that stunning arose from the early effects of the therapeutic

91 This research line continues to produce stunning arrays of enantioselective technologies either

92 nt cellular processes, leading to myocardial stunning, arrhythmias, and ultimately cell damage and de

93 S and MPT have been implicated in myocardial stunning associated with reperfusion in ischemic hearts,

94 ROS contribute to the genesis of myocardial stunning but, at the same time, trigger the development

95 the 6th CS, reflecting persistent myocardial stunning, but baseline CBF was not changed.

96 thout catalase fails to alleviate myocardial stunning, but extracellular SOD (Ec-SOD) may be more eff

97 implicated in the pathogenesis of myocardial stunning, but the precise mechanism by which OFRs foster

98 fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode o

99 oronary occlusions induces severe myocardial stunning, but when the same sequence is repeated 24 hour

100 st the hypothesis that persistent myocardial stunning can lead to hibernating myocardium, 13 pigs wer

101 Thyroid stunning can occur with 185 MBq of 131I in diagnostic im

102 Biological systems display stunning capacities to self-organize.

103 scope from the Sputnik era, they assembled a stunning collection of micrographs that illustrated how

104 Prior structural studies have revealed the stunning complexity of the purified rotor and C-ring ass

105 In phase I (studies of myocardial stunning), conscious rabbits underwent a sequence of six

106 id left ventricular pacing and that regional stunning contributes to persistent global left ventricul

107 schemic LV dysfunction at 1 and 7 days after stunning correlates with the degree of enhanced regional

108 Stunning could potentially reduce the therapeutic effica

109 Stunning decreases contractility at the level of the con

110 The former is often preferred to avoid "stunning"-defined as a reduction in uptake of the therap

111 their design, have allowed the creation of a stunning diversity of nucleic acid-based nanodevices.

112 rimary difficulties exist: Viruses exhibit a stunning diversity of strategies for evading the host im

113 Atrial mechanical stunning due to atrial fibrillation may persist after re

114 The stunning Early Cretaceous diversity of maniraptorans fro

115 dose of (131)I produces a visually apparent stunning effect 72 h before (131)I ablation therapy.

116 10 mCi) (131)I may be capable of producing a stunning effect on thyroid tissue that may interfere wit

117 APC and IPC exhibit anti-infarct and anti-stunning effects in the ovine heart, but these effects a

118 study, the anti-infarct effects and the anti-stunning effects of APC in contributing to enhanced post

119 ained depressed for 2 hours (ie, endothelial stunning [ES]).

120 These results indicate that persistent stunning, even in the absence of chronic ischemia, can r

121 this symbiosis has produced one of the most stunning examples of rapid adaptive radiation documented

122 One of the more stunning examples of the resourcefulness of human vision

123 obably with immune compromise following cold stunning (extended hypothermia), developed a disseminate

124 an immediate injurious role (as mediators of stunning) followed by a useful function (as mediators of

125 cted to a partial occlusion to produce acute stunning, followed by reperfusion through a critical ste

126 hough doxycycline did not improve myocardial stunning following coronary artery bypass graft surgery

127 The magnitude and time course of myocardial stunning from cardiac arrest is unknown.

128 usion, and the differentiation of myocardial stunning from myocardial necrosis.

129 echocardiography accurately differentiates 'stunning' from necrosis, delineates transmural extent of

130 duced late PC effect against both myocardial stunning (groups VII through X) and myocardial infarctio

131 Stunning has been observed in several clinical scenarios

132 tic (131)I were measured at 2 d, a time when stunning has been observed, and expressed as ratios of r

133 The mechanism of myocardial stunning has been studied extensively in rodents and is

134 Left atrial appendage stunning has recently been proposed as a key mechanistic

135 This transient "stunning" has potential implications for (3)H-FDG PET, e

136 Patients with stunning have late increases in LVEF; patients with hype

137 hemia-reperfusion-induced LV dysfunction or "stunning" have normal contractile function and normal [C

138 lisation microscopy, which have all produced stunning images of cellular structures.

139 with single particle averaging, has produced stunning images of the intact bacterial flagellum, revea

140 viduals synchronize their states, giving the stunning impression that the group behaves as one.

141 nt time after ischemia eliminates myocardial stunning in conscious pigs during augmented carbohydrate

142 the mechanism of late PC against myocardial stunning in conscious rabbits involves a PKC-mediated si

143 he development of late PC against myocardial stunning in conscious rabbits, indicating that NO genera

144 We studied the mechanism of stunning in isolated myocytes from chronically instrumen

145 Thus, mechanisms of stunning in the pig are radically different from the wid

146 olytic ATP in the recovery from postischemic stunning in vivo.

147 ing the genes up-regulated during myocardial stunning, including those not previously described in th

148 development of late preconditioning against stunning, indicating that the production of reactive oxy

149 th chronic animal window models has provided stunning insight into tumor pathophysiology, including g

150 m salvaged by reperfusion." The mechanism of stunning involves generation of oxygen radicals as well

151 Endothelial stunning is caused by oxidant processes inhibited by asc

152 Myocardial stunning is characterized by decreased myofilament Ca2+

153 ilament proteins in situ during ischemia and stunning is evaluated, and it is concluded that C-termin

154 Recovery from stunning is incompletely understood but may involve adap

155 is repeated 24 hours later, the severity of stunning is markedly reduced (approximately 50%) ("late

156 troponin I (cTnI) proteolysis in myocardial stunning is not fully understood.

157 ecovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental model of v

158 esis that the development of late PC against stunning is triggered by increased generation of NO duri

159 st infarction, their role in late PC against stunning is unknown.

160 h transient contractile dysfunction, termed "stunning." It is not clear whether this phenomenon is pr

161 After stunning, left ventricular ejection fraction (LVEF) incr

162 ible DNA alkylation reaction) and define the stunning magnitude of its effect.

163 Myocardial stunning may cause prolonged left ventricular dysfunctio

164 Possible poststress myocardial stunning may have caused gated Tl LVEFs to overestimate

165 eved, reversible myocardial dysfunction, or "stunning," may occur.

166 dramatic subunit rearrangements, providing a stunning molecular explanation for the allosteric regula

167 ion followed by reperfusion to create either stunning (n=12) or transmural myocardial infarction (n=1

168 hat TOR controls protein synthesis through a stunning number of downstream targets.

169 Stunning occurred more often with ISMN than amlodipine (

170 Although stunning occurs after brief total occlusions and prolong

171 If thyroid remnant stunning occurs due to 74 MBq (131)I used as a diagnosti

172 t to determine whether left atrial appendage stunning occurs in patients with atrial flutter and to c

173 sed NGF protects against postischemic neural stunning of sympathetic cardiac innervation.

174 Coronary occlusion produced stunning of the anterolateral left ventricle that resolv

175 This "mechanical stunning" of left atrial systolic function appears to be

176 These results support the hypothesis that "stunning" of thyroid tissues, often observable by 2 d, i

177 d by XO + P, mimic the effects of myocardial stunning on cardiac excitation-contraction coupling.

178 ecessary not only to trigger late PC against stunning on day 1 but also to mediate the protection on

179 idant therapy markedly attenuates myocardial stunning on day 1, indicating that ROS play an important

180 ntioxidant therapy in attenuating myocardial stunning on day 1, it has no effect on late precondition

181 a (group VI, n = 11) induced late PC against stunning on day 2 and the magnitude of this effect was e

182 r; therefore, the absence of late PC against stunning on day 2 in group II cannot be ascribed to a de

183 rmed on day 1 failed to precondition against stunning on day 2, but the same sequence performed on da

184 pletely prevented the late PC effect against stunning on day 2.

185 performed on day 2 did precondition against stunning on day 3.

186 However, data did not show any effect of stunning on the efficacy of 131I therapy for differentia

187 y compared the effects of porcine myocardial stunning on the uptake of [18F]-fluorodeoxyglucose (FDG)

188 the 10th reperfusion, indicating myocardial "stunning." On days 2 and 3, however, the recovery of WTh

189 ic myocardium in the presence of infarction, stunning or hibernation, alone or in combination.

190 nt the development of late PC against either stunning or infarction on day 2.

191 fter acute MI may be secondary to myocardial stunning or necrosis.

192 fter acute MI may be secondary to myocardial stunning or necrosis.

193 o limitation of infarct size, alleviation of stunning, or both.

194 tion in myocardial infarct size, severity of stunning, or incidence of cardiac arrhythmias.

195 d to produce different degrees of myocardial stunning; or (c) a single episode of 2 minutes of occlus

196 In the early postischemic stunning phase of reperfusion, the inotropic response to

197 The future challenge is how to minimize the stunning phenomenon and maximize the preconditioning phe

198 y flow velocity was unchanged, indicating LV stunning post balloon occlusion.

199 formed in this way, may be used for hunting/stunning prey and communication.

200 Despite the stunning progress in all disciplines of auxin research,

201 he role of the erbB2 gene in cancers and the stunning progress in developing targeted therapies for e

202 arch, we explore the gap between 25 years of stunning progress in fundamental neuroscience and the pe

203 In phase I (studies of myocardial stunning), rabbits were subjected to six 4-minute corona

204 he perfusion findings suggested that chronic stunning rather than hibernation is the principal cause

205 reduced L-type Ca2+ current contribute to a stunning reduction of intracellular Na+ concentration fo

206 felt to be sufficient to allow recovery from stunning, regional function was disproportionately low f

207 t the precise mechanism by which OFRs foster stunning remains unclear.

208 hus, late preconditioning against myocardial stunning requires > 6 hours to develop, lasts for at lea

209 Finally, evidence of both stunning (rest asynergy with normal flow) and hibernatio

210 ernation may represent persistent myocardial stunning resulting from repeated episodes of ischemia an

211 dase-4 inhibition mitigated the postischemic stunning seen in the control scan.

212 Myocardium subjected to repetitive stunning showed a prolonged yet reversible reduction in

213 Recent discoveries have uncovered stunning similarities among the molecular circuitries of

214 o decades of network science have discovered stunning similarities in the topological characteristics

215 The stunning simplicity of the motif and its surprisingly st

216 Although crystal structures provide stunning snap shots, biochemical approaches addressing t

217 future and pursue a path that builds on the stunning successes of the past.

218 ays and protects against both infarction and stunning, suggesting that it may have greater clinical r

219 development of late preconditioning against stunning supports a complex pathophysiological paradigm,

220 Stunning technical advances in the ability to image the

221 a unique metabolic adaptation in repetitive stunning that is different from that typically seen in c

222 urrent segmental ischemic injury (myocardial stunning) that drives cumulative cardiac damage.

223 protects against infarction but not against stunning, the late phase of PC lasts 3 to 4 days and pro

224 datory strains use karlotoxins as a means of stunning their prey, before ingesting it.

225 transition from a physiological phenotype of stunning to hibernation.

226 Late PC against stunning was also abrogated when LD-A was given before t

227 In contrast, in DCA pigs, myocardial stunning was ameliorated (P<0.05).

228 n and metabolism, suggesting that myocardial stunning was common.

229 Stunning was defined when the diagnostic scan showed act

230 Stunning was induced in 14 anesthetized swine by partial

231 Myocardial stunning was induced in conscious pigs by coronary steno

232 Stunning was induced in eight swine by partially occludi

233 ere chronically instrumented, and persistent stunning was induced regionally by 6 repetitive episodes

234 egional cardiac denervation (CD), myocardial stunning was intensified, ie, at 12 hours reperfusion wa

235 The severity of myocardial stunning was measured as the total deficit of LV wall th

236 rts subjected to 20-minute ischemia in which stunning was mitigated by 10-minute reperfusion with low

237 during dobutamine stress, and (3) myocardial stunning was observed during postdobutamine recovery.

238 In the absence of DCA, myocardial stunning was observed; ie, wall thickening was reduced b

239 easure of the overall severity of myocardial stunning) was reduced by 68% (control, 129 +/- 16 arbitr

240 mental stress echocardiography parameters of stunning were attenuated in patients while taking amlodi

241 The protective effects of IB-MECA against stunning were completely blocked by pretreatment with th

242 No cases of visually apparent thyroid stunning were observed on any of the postablation scans

243 le levels of ischemia, amlodipine attenuated stunning when compared with ISMN.

244 denosine blocker 8-PT enhanced the degree of stunning when given before ischemia but did not induce a

245 n = 10) abrogated the late PC effect against stunning, whereas a 10-fold lower dose (0.5 mg/kg; group

246 rfusion followed by ventricular dysfunction (stunning), which more closely resembles clinical conditi

247 ized that hibernation is preceded by chronic stunning with normal resting perfusion.

248 eatment to assess the degree of postexercise stunning with simultaneous sestamibi single-photon emiss

249 Significant myocardial stunning with subsequent improvement of ventricular func

250 th substantial protection against myocardial stunning without the need for concomitant administration