ライフサイエンスコーパス: postischemic

1 ing may have value in preventing or treating postischemic acute kidney injury after transplantation.

2 study compared the effectiveness of pre- and postischemic administration of the ET receptor antagonis

3 pathology and renal dysfunction during early postischemic AKI.

4 studied for the protective effects of RHP on postischemic and cytokine-induced cerebrovascular inflam

5 Finally, ferroptosis mediates postischemic and toxic renal necrosis, which may be ther

6 cted diabetes mellitus-induced impairment of postischemic angiogenesis and blood flow recovery.

7 an essential role for endogenous VEGF during postischemic angiogenesis and hindlimb perfusion.

8 resuscitation has attempted to mitigate the postischemic-anoxic encephalopathy.

9 Early postischemic APC application activates the cellular prot

10 These studies identify postischemic apoptosis by myocardial Bnip3 as a major de

11 chondrial cell-death pathways, and therefore postischemic ATP preservation is the result of tissue sp

12 oton in vivo imaging, we show that PS blocks postischemic BBB disruption in Tyro3(+/+), Axl(-/-), and

13 In contrast, aspirin did not increase postischemic blood flow or reduce infarction volume, but

14 ivo-engineered with anti-miR-15a/16 improved postischemic blood flow recovery and muscular arteriole

15 al adhesion molecule mRNAs, and also reduced postischemic blood--brain barrier permeability to endoge

16 treatment with hypertonic saline attenuated postischemic blood-brain barrier disruption at 48 hr in

17 eriphery are the major source of CD36 in the postischemic brain and contribute to stroke-induced brai

18 /6 mice with SS31 reduced CD36 expression in postischemic brain and mouse peritoneal macrophages (MPM

19 We investigated neoepitope expression in the postischemic brain and the role of natural Abs in recogn

20 r example, VEGFs are beneficial in promoting postischemic brain angiogenesis, but the newly formed ve

21 outcome and increases CD36 expression in the postischemic brain as well as in peripheral monocytes/ma

22 Our findings suggested that improved postischemic brain blood flow and ADO-induced hypothermi

23 in part, by an inhibitory environment in the postischemic brain, but factors preventing successful re

24 ay as a key mechanism explaining the complex postischemic brain-immune interactions.

25 plement activation, and in particular to the postischemic brain.

26 l mechanism influencing plastic responses in postischemic brain.

27 e therapeutic window for APC intervention in postischemic brain.

28 eam genes GRIA2, NFkappaB2, and GRIN1 in the postischemic brain.

29 regulating neurorestorative processes in the postischemic brain.

30 But when injected into postischemic brains, Sema3A increased cortical damage by

31 he late rise in intracellular free Zn(2+) in postischemic CA1 neurons and afforded partial protection

32 Strategies that modulate postischemic Ca2+ overload may have clinical promise for

33 ther hand, PostC did not significantly alter postischemic cardiac contractile function and coronary f

34 MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyt

35 nous tumor necrosis factor (TNF)-alpha or by postischemic cardiac lymph containing TNF-alpha.

36 Inflammatory cells orchestrate postischemic cardiac remodeling after MI.

37 open the door for using anakinra to prevent postischemic cardiac remodeling and heart failure.

38 suggested key roles for mast cells (MCs) in postischemic cardiac remodeling.

39 In addition, incidence of postischemic cardiomyocyte apoptosis was attenuated in t

40 he mechanisms regulating Akt activity in the postischemic cardiomyocyte are not known.

41 , impacts dramatically on the progression of postischemic cardiomyopathy in mice and prevents oxidati

42 Postischemic caspase-3 activation and cytochrome c relea

43 mmunocyte activation, insulin secretion, and postischemic cell death.

44 Protein S at 2 mg/kg improved postischemic cerebral blood flow by 21% to 26% and reduc

45 hat contributes over 50% of the variation in postischemic cerebral infarct volume observed between in

46 In a setting of postischemic cerebral injury in mice, MFGE8 deficiency w

47 Early leukoadhesive events in postischemic cerebral microvessels are mediated by upreg

48 Histological examination of postischemic cerebral microvessels revealed a strong upr

49 solCD39 reconstituted these mice, restoring postischemic cerebral perfusion and rescuing them from c

50 mmation represent important risk factors for postischemic chronic kidney disease development.

51 [10.2%]), glomerulopathies (n = 69 [7.7%]), postischemic CKD (n = 42 [4.7%]), and other CKD (n = 58

52 ralateral uninjured hemisphere and that this postischemic complication can be manipulated by hyperton

53 Despite similar postischemic concentrations of corticosterone, the major

54 nned myocardium, which represents "prolonged postischemic contractile dysfunction of myocardium salva

55 ndorff perfused hearts indicated exacerbated postischemic contractile function in Sestrin2 KO hearts

56 efore ischemia showed significantly improved postischemic contractile function relative to untreated

57 parative fibroblasts, iPS treatment restored postischemic contractile performance, ventricular wall t

58 ischemic insult, as demonstrated by impaired postischemic contractile recovery in a perfused whole-or

59 r adenosine has a regulatory function in the postischemic control of renal perfusion.

60 rotect donor kidney from complement-mediated postischemic damage and therefore increase the number of

61 meant that new methods are needed to prevent postischemic damage.

62 Importantly, on postischemic day 1, glomerular filtration rates were red

63 tantly, inhibition of GRK2 activity prevents postischemic defects in myocardial insulin signaling and

64 geting moiety may extend the time window for postischemic detection by targeting the early (P-selecti

65 Delayed postischemic DHA administration after 15 min or 3 h also

66 ion, reduced leukocyte infiltration, reduced postischemic disruption of the actin cytoskeleton, and r

67 Although postischemic dopamine treatment improved contractility,

68 Postischemic dopamine treatment of contractile dysfuncti

69 expression conferred striking resistance to postischemic dysfunction, with no measurable effects on

70 mice, hypertonic saline had no effect on the postischemic edema (hypertonic saline: 80.3% +/- 0.7%; 0

71 The persistence of postischemic edema allows T2-weighted CMR to delineate t

72 us, CD38 activation is an important cause of postischemic endothelial dysfunction and presents a nove

73 Thus, BH(4) depletion contributes to postischemic eNOS dysfunction, and BH(4) treatment is ef

74 In animals subjected to ischemia, acute postischemic estradiol further enhances activation and n

75 However, postischemic exposure to exogenous C1q increased both mi

76 rmore, estrogen replacement stimulated early postischemic expression of bcl-2 and bfl-1 and reduced d

77 ption of the actin cytoskeleton, and reduced postischemic expression of kidney injury molecule-1 (Kim

78 , Mpo(-/-) mice showed decreased ventricular postischemic fibrosis reflecting reduced accumulation of

79 The postischemic flow-mediated dilation of brachial artery d

80 Brachial artery reactivity, using postischemic flow-mediated dilation, was also measured.

81 as a proinflammatory effect; it also impairs postischemic flow-mediated vasodilation of the brachial

82 tudies have a limited role in discriminating postischemic from remote myocardium after dobutamine str

83 This would make it difficult to discriminate postischemic from remote myocardium with glucose tracers

84 ith either lithium or SB 216763 had improved postischemic function and reduced infarct size.

85 enol, NCX-KO hearts still exhibited improved postischemic function compared with wild-type hearts.

86 In FGF2 Tg hearts, an 88% recovery of postischemic function occurred (P<0.05).

87 bioenergetic recovery without improvement in postischemic function, compared with continuous global i

88 ardioplegia and perfusate solutions restored postischemic function.

89 d E2-treated hearts had significantly better postischemic functional recovery and decreased infarct s

90 nhibitors of arginase significantly improved postischemic functional recovery in rat hearts if admini

91 Postischemic functional recovery is more sensitive to a

92 ential (DeltaPsi(m)) is a key determinant of postischemic functional recovery of the heart.

93 r the treatment of type 2 diabetes, improves postischemic functional recovery.

94 on of bone marrow mesenchymal stromal cells, postischemic functional renal impairment was reduced, bu

95 paB, a transcription factor that coordinates postischemic gene expression, is attenuated in CD36-null

96 Significantly, the kidneys from postischemic Gpnmb mutant mice exhibited a 5-fold increa

97 eneous electrophysiological substrate of the postischemic heart and highlight the mitochondrial membr

98 changes associated with these agents in the postischemic heart are unclear.

99 approach to enhance late cardioprotection in postischemic heart disease.

100 0A1 levels in development and progression of postischemic heart failure (HF).

101 tial strategy to protect the heart from late postischemic heart failure.

102 c receptor stimulation and in a rat model of postischemic heart failure.

103 dly suppresses in vivo O2 consumption in the postischemic heart through modulation of mitochondrial r

104 Coronary vasodilation is impaired in the postischemic heart with a loss of endothelial nitric oxi

105 on of the eNOS substrate NADPH occurs in the postischemic heart with near total depletion from the en

106 In the postischemic heart, coronary vasodilation is impaired du

107 vivo regulation of oxygen consumption in the postischemic heart.

108 ile function and decreased infarction in the postischemic heart.

109 that trigger endothelial dysfunction in the postischemic heart.

110 s was significantly higher than in untreated postischemic hearts (32.5+/-9 versus 5.5+/-1.6/1000 nucl

111 reduction of ischemic brain damage and that postischemic helium at 75 vol% reduces ischemic brain da

112 s) at Schaffer collateral to CA1 synapses in postischemic hippocampus exhibit properties of Ca(2+)/Zn

113 ased flow-mediated dilatation in response to postischemic hyperemia as well as to heating, as shown b

114 ond hour of reperfusion only; (4) late-onset postischemic hypothermia (LPostH) cooled to 28 degrees C

115 s C during the 1-h ischemic period only; (3) postischemic hypothermia (PostH)-28 degrees C for the se

116 Postischemic hypothermia altered the distribution of Fos

117 Late-onset postischemic hypothermia did not reduce infarct volume.

118 Therefore, both intraischemic and postischemic hypothermia provided neuroprotection in the

119 Both intra- and postischemic hypothermia reduced the number of caspase-i

120 Postischemic hypothermia was not effective in reducing l

121 rm ischemic protection observed after 1 h of postischemic hypothermia was remarkable and distinct fro

122 a) or during the second hour of reperfusion (postischemic hypothermia).

123 Postischemic/hypoxic bryostatin-1 treatment effectively

124 d IGF-1 and further indicate that short-term postischemic IGF-1 therapy may be beneficial for stroke.

125 e, alpha-Syn knockdown significantly reduced postischemic induction of phospho-Drp1, 3-nitrotyrosine,

126 role in hemostasis, arterial thrombosis, and postischemic infarct progression remains to be determine

127 All of these parameters impact upon postischemic infarct size following stroke.

128 is [assessed by fibrin(ogen) deposition] and postischemic inflammation (phospho-nuclear factor-kappaB

129 alloproteinase-9 secretion by neutrophils in postischemic inflammation at the BBB after stroke.

130 ronal apoptosis from ischemia and subsequent postischemic inflammation if administered soon after a s

131 y, the role of mast cells in immunity and in postischemic inflammation is reviewed.

132 to MI released IL-1alpha in the plasma, and postischemic inflammation was attenuated in Il1a(-/-) mi

133 dministration, indicating that reductions in postischemic inflammation were not secondary to smaller

134 to abrogation of the deleterious effects of postischemic inflammation, a process contributing to the

135 , a probable cause of increased swelling and postischemic inflammation, in the peri-infarct area.

136 unity receptor involved in the initiation of postischemic inflammation, is a previously unrecognized

137 ach to counteract the deleterious effects of postischemic inflammation.

138 ding to nuclear factor-kappaB activation and postischemic inflammation.

139 ovel therapeutic opportunities to ameliorate postischemic inflammatory injury.

140 Evidence now suggests that postischemic inflammatory responses strongly contribute

141 s alphaMbeta2-integrin blockade reversed the postischemic, inflammatory phenotype of Cd39-/- mice, th

142 STZ injection, rosiglitazone also prevented postischemic injury and significantly improved functiona

143 ata, demonstrating that rosiglitazone limits postischemic injury in isolated hearts, suggest an impor

144 during ischemia is reported to contribute to postischemic injury.

145 or EPO administration are protected against postischemic injury.

146 f nu/nu mice with wild-type T cells restored postischemic injury.

147 Surprisingly, postischemic iNOS expression was enhanced in the endothe

148 prolonged functional recovery subsequent to postischemic, intracoronary pyruvate dehydrogenase kinas

149 to identify whether natural Abs bind to the postischemic kidney and contribute to complement activat

150 Neutrophils recruited to the postischemic kidney contribute to the pathogenesis of is

151 Infiltration of neutrophil and macrophage in postischemic kidney did not correlate with the protectio

152 rs and inflammatory cell infiltration in the postischemic kidney, which was reversed by blockade of v

153 of the maximally induced genes early in the postischemic kidney.

154 B cells infiltrated postischemic kidneys and subsequently activated and diff

155 light the dynamic regulation of autophagy in postischemic kidneys and suggest a role of mTOR in autop

156 The accumulation of autophagosomes in postischemic kidneys may be renoprotective, but whether

157 Neutrophil infiltration in postischemic kidneys of FucT-IV/FucT-VII-deficient mice

158 Postischemic kidneys of muMT mice expressed higher IL-10

159 In postischemic kidneys of wild-type mice, IRAK-M expressio

160 26 increased and B-1 B cells trafficked into postischemic kidneys with distinct kinetics.

161 mitotic cells are present in the tubules of postischemic kidneys, the origins of the proliferating c

162 capacity of MSC binding sites is expanded in postischemic kidneys.

163 are expressed in tubular epithelial cells of postischemic kidneys.

164 mmatory mediators, and adhesion molecules in postischemic kidneys.

165 The fate of postischemic lactate, which can be converted back to pyr

166 on of IL-18BP MSCs before ischemia increased postischemic left ventricular (LV) developed pressure to

167 Chronic hypoxia increased recovery of postischemic left ventricular developed pressure (LVDP).

168 Postischemic left ventricular dysfunction was created by

169 F20 before no-flow ischemia and reperfusion, postischemic left ventricular function improved commensu

170 ties in vitro and has been reported to limit postischemic lesion volume in vivo.

171 administered during reperfusion reduces the postischemic leukocyte activation and causes neuroprotec

172 BSF-208075 dose-dependently reduced postischemic leukocytes rolling (7.3+/-2.3 vs. 3.3+/-1.4

173 obally or in myeloid lineage cells, quenches postischemic leukosequestration and reduces stroke-induc

174 ttenuated the CD4+ T cell recruitment in the postischemic liver and reduced I/R injury as compared to

175 ugh the mechanisms of their migration in the postischemic liver remain unclear.

176 reduces miR-92a levels and infarct size and postischemic loss of function.

177 atment enhances the Th2 cytokine response in postischemic lungs during reperfusion, reduces lung edem

178 used therapeutically to improve function of postischemic lungs.

179 d by alpha-1 agonism, significantly improves postischemic LV dysfunction without worsening the overal

180 ic agents are frequently required to support postischemic LV dysfunction.

181 ocked the PC- and ISO-induced improvement in postischemic LVDP and infarct size.

182 toxin blocked the ISO-induced improvement in postischemic LVDP and infarct size.

183 On reperfusion after ischemia, recovery of postischemic LVDP and size of infarct were examined.

184 llutant-mixture group had better recovery of postischemic LVDP and smaller infarct size.

185 GSNO increased recovery of postischemic LVDP in GA-treated normoxic and hypoxic hea

186 a2-AR-/-) and found that PC had no effect on postischemic LVDP or infarct size in beta2-AR-/-.

187 very in WT hearts and abolishes the improved postischemic LVDP recovery in CYP2J2 Tr hearts.

188 0 minutes before ischemia results in reduced postischemic LVDP recovery in WT hearts and abolishes th

189 cts (29% reduction), and greater recovery of postischemic mechanical function (23%).

190 ts (27% reduction), and improved recovery of postischemic mechanical function (35%) as compared with

191 isolated perfused hearts in both healthy and postischemic metabolic states.

192 Postischemic Mn-SOD content and activity in the HSP72-tr

193 osDT knockdown significantly ameliorated the postischemic motor deficits and reduced the infarct volu

194 of NGAL mRNA and protein levels in the early postischemic mouse kidney was confirmed.

195 Here, we examined B cell trafficking into postischemic mouse kidneys and compared the repair respo

196 ncement was seen for MB(Ab) and MB(YSPSL) in postischemic muscle and was more stable over time for MB

197 Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfu

198 h a causative link between Trx nitration and postischemic myocardial apoptosis.

199 -regulating kinase-1 activation, and reduced postischemic myocardial apoptosis.

200 whether Omi/HtrA2 plays an important role in postischemic myocardial apoptosis.

201 e PI3-kinase-dependent mechanism and reduced postischemic myocardial apoptotic death.

202 TNF contributes to postischemic myocardial dysfunction and induces proinfla

203 l reperfusion, a period of low flow improves postischemic myocardial function and energetic recovery,

204 Interestingly, TNFR1 ablation improved postischemic myocardial function, decreased activation o

205 temporally assess the severity and extent of postischemic myocardial inflammation and could be used t

206 y and spatially characterize the severity of postischemic myocardial inflammation.

207 TNFR2 deficiency decreased postischemic myocardial recovery in both sexes but had a

208 operoxidase emerges as a crucial mediator of postischemic myocardial remodeling and may evolve as a n

209 Nitric oxide (NO) production is increased in postischemic myocardium, and NO can control mitochondria

210 ute effects of enhanced glucose oxidation on postischemic myocardium.

211 us, the binding of pathogenic natural IgM to postischemic neoepitopes initiates complement-dependent

212 Interestingly, enhanced postischemic neovascularization in CHOP-10(-/-) mice was

213 Two weeks later, the postischemic neovascularization was evaluated.

214 is increased in murine muscle tissue during postischemic neovascularization.

215 tion of CHOP-10 that substantially inhibited postischemic neovascularization.

216 t miR487b editing plays an intricate role in postischemic neovascularization.

217 le anesthetics have been shown to accelerate postischemic neurogenesis; this suggests that anesthetic

218 lls (Tregs) are key endogenous modulators of postischemic neuroinflammation.

219 the first treatment with proven efficacy for postischemic neurological injury.

220 ole in pathogen-evoked phagocyte activation, postischemic neuronal apoptosis, and glucose-evoked insu

221 and insulin secretion and is responsible for postischemic neuronal cell death.

222 The results demonstrate that the extent of postischemic neuronal damage correlates with plasma CT l

223 activated by upstream signaling pathways in postischemic neurons are not well delineated.

224 Postischemic neutrophil free radical production was atte

225 As anticipated, postischemic neutrophil infiltration in CD36(-/-) -->CD3

226 Our results indicate that postischemic NF-kappaB activation in renal tubular epith

227 vascular endothelia effectively prevented a postischemic no-reflow phenomenon.

228 Nicotinamide effectively attenuated postischemic nuclear factor-kappa]B activation and exhib

229 improved mitochondrial respiratory function (postischemic percent respiratory control index; NAD(+)-l

230 creased cerebral infarct volumes and reduced postischemic perfusion.

231 SCr level in the early postischemic period (24-72 hr) seems to be a valid indic

232 expression of CL-11 rapidly increases in the postischemic period and colocalizes with complement depo

233 ased number and activity of dendrites in the postischemic period.

234 Prior UO results in reduced postischemic phosphorylation of c-Jun N-terminal stress-

235 was increased by 63% and 46% in healthy and postischemic pigs, respectively.

236 myocardial oxygen consumption in healthy and postischemic pigs, respectively.

237 butable to a short-lived sensitive period of postischemic plasticity defined by unique genetic, molec

238 ing with respect to stroke onset; the unique postischemic plasticity milieu; and the extent of cortic

239 ue interaction between types of training and postischemic plasticity, and find ways to augment and pr

240 Postischemic platelet and fibrin deposition were decreas

241 Similarly, in the postischemic rat kidney, sigma1-receptor activation by f

242 he human brain, where it could contribute to postischemic recovery and represent a target for stroke

243 control, IPC and GSNO significantly improved postischemic recovery of left ventricular developed pres

244 ed with EPO exhibited significantly improved postischemic recovery of left ventricular developed pres

245 ts, prolongs ischemic contracture, increases postischemic recovery of LVDP, and reduces infarct size.

246 Postischemic recovery of mechanical function was greater

247 a inhibition also was associated with faster postischemic recovery of phosphocreatine, ATP, and pH as

248 Female WT mice had better postischemic recovery than did male WT mice, an effect t

249 Postischemic recovery was impaired in hypertrophied hear

250 ontrast, arginase inhibition did not improve postischemic recovery when administered with buffer solu

251 75 becomes an age-related limiting factor in postischemic recovery, it may be a potential gene target

252 with decreased/absent TNFR2/p75 signaling in postischemic recovery.

253 standing of the molecular pathways promoting postischemic reflow could provide new candidate targets

254 rdium may be a critical factor that triggers postischemic remodeling.

255 um creatinine (SCr) level as an indicator of postischemic renal dysfunction in mice.

256 2 hr) seems to be a valid indicator of early postischemic renal dysfunction, and that renal function

257 In mouse models of postischemic renal fibrosis and obstructive uropathy, tr

258 The protection is reflected by improved postischemic renal function, reduced leukocyte infiltrat

259 ovide novel insight into how preservation of postischemic renal perfusion by endothelial cell adenosi

260 ecognizes an abnormal pattern of L-fucose on postischemic renal tubule cells and activates a destruct

261 their potential to signal injury and afford postischemic renoprotection and repair remains obscure.

262 hat exocytosis of Weibel-Palade bodies links postischemic repair with inflammation and mobilization o

263 s impairs endothelial cell (EC) function and postischemic reparative neovascularization by molecular

264 Early after postischemic reperfusion and in the presence of severely

265 During low-flow ischemia and postischemic reperfusion in vitro, KD hearts failed to a

266 analyzed the role of MASP-2 in two models of postischemic reperfusion injury (IRI).

267 Fructose-1,6-diphosphate (FDP) reduces postischemic reperfusion injury and is used alone and in

268 d recovery of LV contractile function during postischemic reperfusion that was associated with a lowe

269 Impaired coronary flow during postischemic reperfusion was improved by BH(4) infusion.

270 acid metabolism during cardiac ischemia and postischemic reperfusion, stimulation of B cell insulin

271 imilar in CD4+ T-cell depleted and wild-type postischemic reperfusion.

272 < 0.05), 221% above control, after 5 min of postischemic reperfusion.

273 stress after ischemia-reperfusion, and that postischemic restoration of neuronal GSH levels can be n

274 or activation alters TNF-alpha levels in the postischemic retina.

275 schemia, which spatially correlated with the postischemic risk area.

276 ome inhibitor reversed the effects of IPC on postischemic Rpt5 carbonylation, cardiac function, morph

277 aled prolonged enhancement of Gd-ESMA in the postischemic scar compared with Gd-DTPA.

278 MSC adhesion was asymmetrical, with postischemic sections exhibiting more than twofold highe

279 amage, increases infarct volume, and induces postischemic seizures.

280 , we address both the biology of the brain's postischemic sensitive period and the difficult question

281 also increased infarct size and exacerbated postischemic sensorimotor behavioral deficits measured b

282 ctin (alpha-SMA), an indication of long term postischemic sequelae.

283 rombosis as well as cerebral infarction in a postischemic stroke model.

284 eptidyl peptidase-4 inhibition mitigated the postischemic stunning seen in the control scan.

285 during dobutamine stress and a reduction in postischemic stunning.

286 In neuron cultures, postischemic superoxide production and cell death were c

287 on injury, sigma1-receptor agonists improved postischemic survival and renal function via activation

288 ased blood-brain barrier permeability in the postischemic territory, and a 3- to 5-fold increase in i

289 This postischemic therapeutic approach is further shown to pr

290 examine the impact of platelet Galpha(i2) in postischemic thrombo-inflammatory infarct progression, G

291 ion triggered by ligand-CL-11 interaction in postischemic tissue is a potent source of acute kidney i

292 proach to reverse endothelial dysfunction in postischemic tissues.

293 oxidative stress were measured at 4 hr after postischemic treatment (5 min or 6 hr).

294 Here we report that late postischemic treatment of mice with 3K3A-APC stimulates

295 ht protect function by reducing apoptosis in postischemic tubules.

296 ry), IkappaBalpha production (Western blot), postischemic tumor necrosis factor-alpha (TNF-alpha) pro

297 mine the hypothesis that early IPC preserves postischemic UPS function thus facilitating prosurvival

298 reperfusion injury as evidenced by increased postischemic ventricular dysfunction, increased myocardi

299 MB(sLex) caused greater opacification in postischemic versus nonischemic myocardium at both time

300 in hemichannels is a significant mediator of postischemic white and gray matter dysfunction and injur