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1 s mitochondrial structure and function after reperfusion.
2 of 5 days +/- 1.9 (standard deviation) after reperfusion.
3 e conditions, as well as during ischemia and reperfusion.
4 rom reactive oxygen species generated during reperfusion.
5 ve in preclinical stroke models of ischaemia-reperfusion.
6 GPX4 and ACSL4) expression alteration during reperfusion.
7 ntation, hearts were evaluated at 3 hours of reperfusion.
8 naling, focusing on the dynamics early after reperfusion.
9 point of BBB opening following 1 h tMCAO and reperfusion.
10 cally relevant time frame and independent of reperfusion.
11 (SMA) for 45 minutes followed by 120 minutes reperfusion.
12 cerebral artery occlusion followed by 28-day reperfusion.
13 des modest protection only in the context of reperfusion.
14 ken before, and immediately after, allograft reperfusion.
15 pore channel inhibitor Ned-19 at the time of reperfusion.
16 eriostin during the repair phase of ischemia reperfusion.
17 ice, right through to cold preservation and reperfusion.
18 king period) or the full 45-minute period of reperfusion.
19 than when administered orally shortly after reperfusion.
20 selective reduction of the ILC2 subset after reperfusion.
21 ut not in miR-34a(-/-) mice following stroke reperfusion.
22 lammatory mediators were assessed 24 h after reperfusion.
23 liver grafts in response to cold storage and reperfusion.
24 apies, typically focused on pulmonary artery reperfusion.
25 rior descending artery (10 min), followed by reperfusion (2 min), and arrhythmia incidence quantified
26 irectly after 45 minutes of ischemia without reperfusion (45I-0R), after 30 minutes of reperfusion (4
27 erfusion (45I-30R), and after 120 minutes of reperfusion (45I-120R), as well as a control sample not
28 ut reperfusion (45I-0R), after 30 minutes of reperfusion (45I-30R), and after 120 minutes of reperfus
29 significantly higher ILC1 frequencies before reperfusion, accompanied by elevated ILC2 frequencies af
30 sis was observed frequently after 6 hours of reperfusion, accompanied by upregulation of Rubicon, att
31 ive, 30-minute flow reductions and 30-minute reperfusions achieving complete occlusion after four cyc
32 in Cerebral Infarction (mTICI) grade 2b to 3 reperfusion (adjusted OR per 30 minutes increase in time
33 1 signaling to sensory neurons from ischemia/reperfusion-affected muscle directly modulated nocicepti
34 infarct cortex were evaluated at 24 hours of reperfusion after a 90-minute unilateral middle cerebral
35 n a rat model with acute myocardial ischemia-reperfusion (AMI/R) injury and myocardial necrosis, as w
36 t is also overexpressed after renal ischemia-reperfusion, an event that induces kidney injury and fib
37 ce and QKI-7 is knocked-down in vivo in ECs, reperfusion and blood flow recovery are markedly promote
39 donor ILC subsets is altered after allograft reperfusion and is associated with PGD development, sugg
40 before and after cardiopulmonary bypass and reperfusion and left ventricular (LV) tissue from mice s
42 reter) were acquired 15 and 45 minutes after reperfusion and subsequently analyzed using specialized
49 s, chronic and acute kidney injury, ischemia/reperfusion, atherosclerosis, and inflammation, which ar
53 , probably less than 10% of patients require reperfusion by thrombolysis or interventional treatments
54 emic stroke has greatly advanced, with rapid reperfusion by use of intravenous thrombolysis and endov
58 by elevated ILC2 frequencies after allograft reperfusion.Conclusions: The composition of donor ILC su
62 ention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascu
64 hether they're still efficacious in the post-reperfusion era is currently debated in the light of rec
67 vein (PV) sample] and post-(liver flush; LF) reperfusion for their ability to activate a panel of PRR
72 e have previously demonstrated that ischemia/reperfusion (I/R) impairs endoplasmic reticulum (ER)-bas
73 In the present study, myocardial ischemia/reperfusion (I/R) induced autosis in CMs, as evidenced b
74 ave an impaired recovery from acute ischemia/reperfusion (I/R) injury ex vivo, the role of dysferlin
75 ng adverse outcomes associated with ischemia/reperfusion (I/R) injury in multiple disease models.
76 We used a glaucoma model of retinal ischemia-reperfusion (I/R) injury in rats and found that endothel
77 usceptibility of steatotic liver to ischemia-reperfusion (I/R) injury is due to impaired recruitment
78 ors of MMPs (TIMPs) plays a role in ischemia/reperfusion (I/R) injury post-myocardial infarction (MI)
82 erized by glycocalyx derangement is ischemia-reperfusion (I/R) of the whole body as well as during se
83 The latter trigger a version of ischemia/reperfusion (I/R) pathobiology that is singular in its o
84 Here, using a model of hind limb ischemia-reperfusion (I/R) remote lung injury, we present evidenc
85 e progression of TIF caused by UUO, ischemic/reperfusion (I/R), aristolochic acid, and repeated acute
89 ediate reperfusion (IR), LV unloading before reperfusion improves myocardial energy substrate use and
90 ular unloading limits ischemic injury before reperfusion, improves myocardial energy substrate use, a
91 oute that would aid faster tissue repair and reperfusion in "no-option" patients suffering from perip
94 udy testing whether LV unloading and delayed reperfusion in patients with STEMI without cardiogenic s
97 UDCA protects against ischaemia-induced and reperfusion-induced arrhythmias in the adult myocardium,
98 idence of mitochondrial injury, specifically reperfusion-induced reactive oxygen species generation a
99 linical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion for 60 minu
101 t also contributes significantly to ischemia reperfusion injury (IRI) associated with myocardial infa
103 ic aneurysm (AAA) repair results in ischemia-reperfusion injury (IRI) in local (i.e. kidney) and dist
109 lammatory responses associated with ischemia/reperfusion injury (IRI) play a central role in alloimmu
111 is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic events,
112 irected pharmacomodulation of renal ischemia-reperfusion injury (IRI) without the need for systemic d
113 released from cells damaged during ischemia-reperfusion injury (IRI), in heart attack or stroke sett
114 C57BL/6 mice challenged with renal ischemia reperfusion injury (IRI), treated before or after injury
121 e as pathogenically contributing to ischemia-reperfusion injury and delayed graft function (DGF) in h
122 ose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function, demonst
123 f exercise on metabolic parameters, ischemia-reperfusion injury and regeneration after hepatectomy.
125 nct donor macrophage populations in ischemia-reperfusion injury and rejection, including their intera
127 The patients in the low-PF group had severe reperfusion injury and were more frequently complicated
128 ted within a few hours of bilateral ischemia-reperfusion injury at these sites and new sites of proxi
129 ture and cardiomyocyte death during ischemia-reperfusion injury by inducing mitochondrial permeabilit
130 yocytes and partial protection from ischemia-reperfusion injury by reducing mitochondrial permeabilit
131 d2 ablation protected against renal ischemia-reperfusion injury by suppressing the expression of proi
134 renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congeneic renal t
139 mirococept (APT070) for preventing ischaemia-reperfusion injury in the kidney allograft (EMPIRIKAL) t
140 ied and compared renal responses to ischemia-reperfusion injury in the presence and absence of GDF15.
143 ule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased function i
145 und After acute myocardial infarction (AMI), reperfusion injury is associated with microvascular lesi
148 g periostin expression in the renal ischemia-reperfusion injury model, and primary cultures of isolat
149 a human-disease-relevant myocardial ischemia reperfusion injury mouse model after i.v. injection conf
153 g the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resid
154 were protected from fibrosis after ischemia-reperfusion injury or unilateral ureteral obstruction de
155 subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstruction.
156 se after brain death (BD) and posttransplant reperfusion injury play significant roles in the pathoge
157 ry blood flow after a heart attack can cause reperfusion injury potentially leading to impaired cardi
158 eutic trials aimed at prevention of ischemia/reperfusion injury to allografts based on animal data sh
159 kidney fibrosis induced via UUO or ischemia/reperfusion injury was ameliorated by systemic genetic k
162 'deactive transition' (relevant to ischemia-reperfusion injury) and their effects on the ubiquinone-
163 uromuscular diseases of childhood, ischaemia-reperfusion injury, and age-related neurodegenerative di
165 sis for cell therapy in mice after ischaemia-reperfusion injury, and find that-although heart functio
166 rmal kidney and following bilateral ischemia-reperfusion injury, and quantified and compared renal re
167 the patients in the high-PF group had milder reperfusion injury, but had lower intraoperative hepatic
168 d the effect of LV unloading on ischemia and reperfusion injury, cardiac metabolism, and mitochondria
169 or renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and
170 the pathophysiology of myocardial ischaemia-reperfusion injury, including the role of autophagy and
171 otective effects against myocardial ischemic/reperfusion injury, indicating their potential applicati
173 ic vascular complications, cardiac ischaemia-reperfusion injury, myocardial infarction, heart failure
175 that promotes recovery from anoxia, reduces reperfusion injury, prevents oedema, and metabolically s
176 Similarly, in a rat model of renal ischemia/reperfusion injury, SAR247799 preserved renal structure
177 en the central importance of mitochondria in reperfusion injury, we hypothesized that compared with i
178 endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation of endothelial
179 on of proregenerative factors after ischemia-reperfusion injury, whereas knockout mice exhibited the
180 ns have a higher risk of developing ischemia-reperfusion injury, which can lead to posttransplant com
206 ferences in responses to intestinal ischemia-reperfusion (IR) have been recognized in animal studies.
209 dependent mouse model of intestinal ischemia-reperfusion (IR) injury to investigate the underexplored
210 -17A play critical roles in hepatic ischemia reperfusion (IR) injury, we tested whether mice lacking
214 we hypothesized that compared with immediate reperfusion (IR), LV unloading before reperfusion improv
216 h the presence of CsA for the full 45-minute reperfusion is associated with impaired mitochondrial in
218 (LV) workload (LV unloading) before coronary reperfusion is emerging as a potential approach to reduc
221 ial infarction, following heart ischemia and reperfusion, is associated with profound changes in key
222 he loss of BBB integrity following ischaemic/reperfusion-like conditions was significantly worsened b
223 Portal blood immediately following allograft reperfusion (liver flush; LF) had increased total HMGB1,
228 so protective in renal and cerebral ischemia/reperfusion models, demonstrating its widespread utility
230 the clinically relevant unilateral ischemia-reperfusion murine model of AKI at days 1, 2, 4, 7, 11,
235 %]) demonstrated localized areas of apparent reperfusion of nonperfused retina, more commonly in the
236 number of participants with greater than 50% reperfusion of the previously occluded vascular territor
238 hanges in the percentage of ILC subsets with reperfusion or PGD (grade 3 within 72 h) were assessed.M
239 LT1E1 expression to bilateral renal ischemia-reperfusion or sham surgery, either in the absence or pr
243 intestinal flow changes during the occlusion-reperfusion phases were accompanied by parallel changes
244 nd acute stress conditions, such as ischemia-reperfusion, phosphorylations are lost, leading to maxim
246 nous thrombolysis with tenecteplase improves reperfusion prior to endovascular thrombectomy for ische
249 SL111, 80 mg/kg) delivered immediately after reperfusion reduced the systemic and cardiac inflammator
252 motor unit deactivation, and (2) blood flow reperfusion (REP) would result in muscle recovery and re
253 sed.Measurements and Main Results: Allograft reperfusion resulted in significantly decreased frequenc
255 g use and success of interventional coronary reperfusion strategies, morbidity and mortality from acu
257 orary role of an evidence-based fibrinolytic reperfusion strategy as part of a pharmacoinvasive appro
260 and safety of nerinetide in human ischaemia-reperfusion that occurs with rapid endovascular thrombec
261 +/- 109 000 ng/L, P=0.023) at 6 hours after reperfusion, the levels of NT-proBNP (N-terminal pro-B-t
262 ls (RCTs), where all patients had to receive reperfusion therapies, either intravenous thrombolysis a
263 iched clinical studies of patients receiving reperfusion therapies, might prove more effective than i
266 Myocardial infarction patients receiving reperfusion therapy show magnetic susceptibility changes
267 he safety, efficacy, and treatment window of reperfusion therapy with t-PA by limiting hemorrhagic tr
268 ermia were also assessed in combination with reperfusion therapy, but in RCTs that only included feas
271 facing the treatment of stroke in the era of reperfusion therapy: hemorrhagic transformation and the
272 tion was found between force and full finger reperfusion time (beta = -0.033 +/- 0.016; 95% CI, -0.06
273 temperature was associated with full finger reperfusion time (beta = -0.18 +/- 0.041; 95% CI, -0.26
275 a consistent difference between full finger reperfusion time and clinician capillary refill time (fu
276 Correlation coefficient between full finger reperfusion time and clinician capillary refill time was
277 10 measurements, including five full finger reperfusion time and five clinician capillary refill tim
278 aster activation is associated with improved reperfusion time and outcomes in the American Heart Asso
279 d focus on the clinical value of full finger reperfusion time as a monitoring device for hemodynamics
281 bility and validity of the novel full finger reperfusion time measurement using clinicians' visual ca
284 core volume with age and expected imaging-to-reperfusion time will improve assessment of prognosis an
285 class correlation coefficient of full finger reperfusion time within each patient was 0.76 (95% CI, 0
287 in door-out times (40 versus 68 minutes) and reperfusion times (98 versus 135 minutes) with 80.1% tre
289 rate experimental AKI triggered by ischaemia-reperfusion, toxic injury and systemic inflammation.
290 after stroke onset and might help to expand reperfusion treatment beyond the current time windows.
292 ferroptotic death in different durations of reperfusion was evaluated by assessing the iron content,
294 d as the time from symptom onset to coronary reperfusion, was a pre-specified subgroup of interest.
296 implanted allografts during early stages of reperfusion while patient is hemodynamically supported o
297 earts with return of intrinsic activity, and reperfusion with 155 mM [Na(+)](o) further depressed mec
299 cardiac mechanical function during ischemia-reperfusion with perfusates containing 145 or 155 mM Na(