ライフサイエンスコーパス: postischemic

1 ive microvascular degeneration followed by a postischemic aberrant neovascularization.

2 ation of mononuclear phagocytes increased in postischemic Ackr2(-/-) kidneys.

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

4 Postischemic adaptation results in characteristic myocar

5 pathology and renal dysfunction during early postischemic AKI.

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

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

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

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

10 Sema3E/PlexinD1 signaling inhibits postischemic angiogenesis by regulating endothelial DLL4

11 Early postischemic APC application activates the cellular prot

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

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

14 his study highlights a potential "defect" in postischemic barrier formation that may underlie prolong

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

16 Postischemic bile duct slices were incubated in oxygenat

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

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

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

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

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

22 /6 mice with SS31 reduced CD36 expression in postischemic brain and mouse peritoneal macrophages (MPM

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

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

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

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

27 ce recovery after photobleaching analysis of postischemic brain endothelial cells and cells overexpre

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

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

30 l mechanism influencing plastic responses in postischemic brain.

31 e therapeutic window for APC intervention in postischemic brain.

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

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

34 regulating neurorestorative processes in the postischemic brain.

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

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

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

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

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

40 Inflammatory cells orchestrate postischemic cardiac remodeling after MI.

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

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

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

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

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

46 Postischemic caspase-3 activation and cytochrome c relea

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

48 15a/16-1 cluster is a negative regulator for postischemic cerebral angiogenesis and long-term neurolo

49 f the miR-15a/16-1 cluster in endothelium on postischemic cerebral angiogenesis is not known.

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

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

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

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

54 Histological examination of postischemic cerebral microvessels revealed a strong upr

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

56 data to identify regional heterogeneities in postischemic changes.

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

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

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

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

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

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

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

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

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

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

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

68 Although postischemic dopamine treatment improved contractility,

69 Postischemic dopamine treatment of contractile dysfuncti

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

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

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

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

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

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

76 However, postischemic exposure to exogenous C1q increased both mi

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

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

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

80 The postischemic flow-mediated dilation of brachial artery d

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

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

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

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

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

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

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

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

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 In the postischemic heart, this regulatory mechanism is critica

108 vivo regulation of oxygen consumption in the postischemic heart.

109 ile function and decreased infarction in the postischemic heart.

110 that trigger endothelial dysfunction in the postischemic heart.

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

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

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

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

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

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

117 Postischemic hypothermia altered the distribution of Fos

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

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

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

121 Postischemic hypothermia was not effective in reducing l

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

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

124 Postischemic/hypoxic bryostatin-1 treatment effectively

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

126 rovides novel therapeutic targets to prevent postischemic immunopathology and heart failure.

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

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

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

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

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

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

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

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

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

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

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

138 ach to counteract the deleterious effects of postischemic inflammation.

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

140 ss-priming DC contributes to exacerbation of postischemic inflammatory damage of the myocardium and c

141 ovel therapeutic opportunities to ameliorate postischemic inflammatory injury.

142 Evidence now suggests that postischemic inflammatory responses strongly contribute

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

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

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

146 during ischemia is reported to contribute to postischemic injury.

147 or EPO administration are protected against postischemic injury.

148 Surprisingly, postischemic iNOS expression was enhanced in the endothe

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

150 nificantly improved sensorimotor recovery in postischemic KI mice.

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

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

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

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

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

156 B cells infiltrated postischemic kidneys and subsequently activated and diff

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

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

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

160 Postischemic kidneys of muMT mice expressed higher IL-10

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

162 26 increased and B-1 B cells trafficked into postischemic kidneys with distinct kinetics.

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

164 mmatory mediators, and adhesion molecules in postischemic kidneys.

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

166 are expressed in tubular epithelial cells of postischemic kidneys.

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

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

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

170 Postischemic left ventricular dysfunction was created by

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

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

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

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

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

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

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

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

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

180 used therapeutically to improve function of postischemic lungs.

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

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

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

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

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

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

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

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

189 0 minutes before ischemia results in reduced postischemic LVDP recovery in WT hearts and abolishes th

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

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

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

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

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

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

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

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

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

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

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

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

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

203 TNF contributes to postischemic myocardial dysfunction and induces proinfla

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

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

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

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

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

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

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

211 ute effects of enhanced glucose oxidation on postischemic myocardium.

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

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

214 Two weeks later, the postischemic neovascularization was evaluated.

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

216 is increased in murine muscle tissue during postischemic neovascularization.

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

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

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

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

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

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

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

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

225 Postischemic neutrophil free radical production was atte

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

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

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

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

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

231 creased cerebral infarct volumes and reduced postischemic perfusion.

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

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

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

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

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

248 75 becomes an age-related limiting factor in postischemic recovery, it may be a potential gene target

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

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

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

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

253 2 hr) seems to be a valid indicator of early postischemic renal dysfunction, and that renal function

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

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

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

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

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

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

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

261 Early after postischemic reperfusion and in the presence of severely

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

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

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

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

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

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

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

269 < 0.05), 221% above control, after 5 min of postischemic reperfusion.

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

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

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

273 In vivo, postischemic ROS formation, infarct volume, and function

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

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

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

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

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

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

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

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

282 Results: Postischemic structural and functional adaptations in al

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

284 during dobutamine stress and a reduction in postischemic stunning.

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

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

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

288 This postischemic therapeutic approach is further shown to pr

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

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

291 proach to reverse endothelial dysfunction in postischemic tissues.

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

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

294 erience dependency of new spine fates in the postischemic turnover context.SIGNIFICANCE STATEMENT Mot

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

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

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

298 the CMR scar and 31.2% of the total abnormal postischemic VT substrate area.

299 demonstrated regional heterogeneities in the postischemic VT substrate not appreciated by any single

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