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1 ioprotective capabilities against myocardial ischemic injury.
2 to allow sufficient tissue reperfusion after ischemic injury.
3 thways can be beneficial in the treatment of ischemic injury.
4 potential therapeutic for combating cardiac ischemic injury.
5 es that become activated under conditions of ischemic injury.
6 ffers a means to protect the myocardium from ischemic injury.
7 itioning, is not associated with ischemia or ischemic injury.
8 hancing AMPK activation and reducing cardiac ischemic injury.
9 long-term regional visual field loss due to ischemic injury.
10 ogical changes and cell death during cardiac ischemic injury.
11 e molecular pattern molecules released after ischemic injury.
12 this cardiac mitochondrial subpopulation on ischemic injury.
13 death signaling and neuroprotection against ischemic injury.
14 e remnant nephrons precondition them against ischemic injury.
15 kidneys have been subjected to warm or cold ischemic injury.
16 ac remodeling and function in the setting of ischemic injury.
17 nt of therapeutics to protect the brain from ischemic injury.
18 memory and in protection of neurons against ischemic injury.
19 kineticin 2 (PK2) as a mediator for cerebral ischemic injury.
20 of cardiac autophagy and displayed increased ischemic injury.
21 activation and proliferation in response to ischemic injury.
22 esearch by serving as a surrogate measure of ischemic injury.
23 disruption of blood supply which results in ischemic injury.
24 iac fibrosis, and in myocardial responses to ischemic injury.
25 t has therapeutic potential to prevent renal ischemic injury.
26 s of the lectin complement pathway, in brain ischemic injury.
27 miRNAs to therapeutically inhibit miR-15 on ischemic injury.
28 beneficial effects on outcome after hypoxic-ischemic injury.
29 ess and an endogenous repair mechanism after ischemic injury.
30 s rapidly and greatly following traumatic or ischemic injury.
31 lerated long-term in eyes with acute retinal ischemic injury.
32 arction, a model of acute inflammation after ischemic injury.
33 ole in protecting lean and fatty livers from ischemic injury.
34 epresent one of the brain's defenses against ischemic injury.
35 e neuroprotective strategy to treat cerebral ischemic injury.
36 EC, which promotes cardioprotection against ischemic injury.
37 d to the repair and recovery phase following ischemic injury.
38 ve responses in adult and neonatal models of ischemic injury.
39 he regenerative capacity even in spite of an ischemic injury.
40 a variety of diseases ranging from cancer to ischemic injury.
41 n the setting of a severe form of myocardial ischemic injury.
42 protein S (PS) protects neurons from hypoxic/ischemic injury.
43 st predictive when combined with presence of ischemic injury.
44 model play a role in vessel formation after ischemic injury.
45 ng HDAC activity can protect the retina from ischemic injury.
46 orrhages, and 35 (35%) had evidence of acute ischemic injury.
47 nduces tolerance against a subsequent lethal ischemic injury.
48 r and regenerate the damaged myocardium from ischemic injury.
49 ve, anti-inflammatory and protective against ischemic injury.
50 d poor survival after transplantation due to ischemic injury.
51 ogenesis, inflammation, atherosclerosis, and ischemic injury.
52 aggravates brain damage and cell death after ischemic injury.
53 cells, which may play a role in repair after ischemic injury.
54 [3, 4-d] pyramidine), against neonatal brain ischemic injury.
55 mation in the mouse brain following cerebral ischemic injury.
56 ffective strategy to protect the kidney from ischemic injury.
57 that developing WM axons are susceptible to ischemic injury.
58 metabolism, induce apoptosis, and exacerbate ischemic injury.
59 ity under pathological conditions, including ischemic injury.
60 neurons in these mice are protected against ischemic injury.
61 hat exhibits neuroprotection against hypoxic/ischemic injury.
62 Cs for restoration of cardiac function after ischemic injury.
63 ediates myocardial survival and repair after ischemic injury.
64 reparative neovascularization in response to ischemic injury.
65 ing-associated increase of susceptibility to ischemic injury.
66 in various neurological disorders, including ischemic injury.
67 ox9 blunted the cardiac fibrotic response on ischemic injury.
68 ammation and leukocyte recruitment following ischemic injury.
69 it is also a major pathomechanism underlying ischemic injury.
70 and meningeal IL-17(+) gammadelta T cells on ischemic injury.
71 to attenuate cell death and protect against ischemic injury.
72 ntioxidant and neuroprotective agent against ischemic injury.
73 ccompanied by increased infarct volume after ischemic injury.
74 supports tubular proliferation after sterile ischemic injury.
75 ction, and impairment of tissue repair after ischemic injury.
76 es in intracellular compartments after renal ischemic injury.
77 ion abolished the increase of 5hmC caused by ischemic injury.
78 ed the myocardial leukocyte population after ischemic injury.
79 PUFA is sufficient to protect the liver from ischemic injury.
80 tion to the intercalated discs against acute ischemic injury.
81 ule (PT) cells are critical targets of acute ischemic injury.
82 he receptor and ligand are upregulated after ischemic injury.
83 r impact and the impact of Candq1, alone, on ischemic injury.
84 candidate to limit neuronal apoptosis after ischemic injury.
85 n and prevention of fibrosis following acute ischemic injury.
86 survival and reparative proliferation after ischemic injury.
87 yocyte cell death following ischemic and non-ischemic injuries.
88 eneration associated with stroke and hypoxic-ischemic injuries.
89 p53 may facilitate muscle regeneration after ischemic injuries.
91 ) were hemorrhagic transformation of primary ischemic injuries (14 with neonatal cerebral sinovenous
92 protected from both transient and permanent ischemic injury; (2) Polyman2, the newly synthesized man
93 noid hemorrhage (4/80; 5%) or global hypoxic-ischemic injury (20/202, 10%) were more likely to achiev
101 o a novel treatment option that can decrease ischemic injury after traumatic brain injury without inc
103 ia protects the rodent brain from subsequent ischemic injury, although the protection wanes within da
106 ular protons produced during inflammation or ischemic injury and belong to the superfamily of degener
108 cells or mononuclear phagocytes, markers of ischemic injury and CML were significantly reduced, and
109 ; for example, miR-214 is upregulated during ischemic injury and heart failure, but its potential rol
111 lecular events that regulate the response to ischemic injury and identify new therapeutic targets tha
112 regulation of emergency hematopoiesis after ischemic injury and identify potential therapeutic targe
113 he one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial
115 (FSTL1) is a cardioprotective factor against ischemic injury and is induced in cardiomyocytes and ske
117 ment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effec
118 spects of the natural protective response to ischemic injury and may be novel therapeutic targets for
120 the human EPHX2 gene alter susceptibility to ischemic injury and neuronal survival in a manner linked
121 lecular pathways that regulate the extent of ischemic injury and post-myocardial infarction (MI) remo
122 of insulin signaling, which increases after ischemic injury and precedes heart failure development.
123 zation of cardiac vasculature that mitigated ischemic injury and predicted outcomes after myocardial
124 nt role for MBL in the pathogenesis of brain ischemic injury and provide a strong support to the conc
125 Remarkably, mAPC(PS/N329Q) limited cerebral ischemic injury and reduced brain lesion volume signific
126 ility of the immature fetal brain to hypoxic-ischemic injury and subsequent motor deficits in newborn
127 st, when genetic labeling was induced during ischemic injury and subsequent recovery, the number of l
128 rain during the recovery phase from an acute ischemic injury and that uPA binding to uPAR promotes ne
129 protection to minimize procedure-associated ischemic injury and to improve outcomes of revasculariza
132 eurogenesis has been observed in response to ischemic injury, and can be enhanced via infusion of app
133 xymethylated regions (DhMRs) associated with ischemic injury, and DhMRs were enriched among the genes
134 strate dendrimer uptake in cells involved in ischemic injury, and in ongoing inflammation, leading to
135 al hemorrhage, hemorrhagic transformation of ischemic injury, and presumed perinatal hemorrhagic stro
136 show that 5hmC abundance was increased after ischemic injury, and Tet2 was responsible for this incre
137 ammatory pathways to protect neurons against ischemic injury, and these beneficial effects of IF are
138 cells in the CNS) also express EPO following ischemic injury, and this response is known to ameliorat
139 is often taking medications that may affect ischemic injury; and (5) animal studies may not involve
140 ignals that activate the inflammasome during ischemic injury are not well characterized, we show that
141 t H(2)S provided profound protection against ischemic injury as evidenced by significant decreases in
142 ection of the brain from a subsequent severe ischemic injury, as induced by middle cerebral artery oc
144 ls, resulting in lower perfusion and greater ischemic injury at all time points over 21 days followin
146 ls versus brain resident cells contribute to ischemic injury, bone marrow chimeras were generated by
147 orm-specific inhibition of GSK-3 exacerbates ischemic injury but protects against I/R injury by modul
148 Antioxidant therapy can protect against ischemic injury, but the inability to selectively target
149 d during renal epithelial regeneration after ischemic injury, but the molecular signals that control
150 lts demonstrated that EA attenuated cerebral ischemic injury by inhibiting NAPDH oxidase-mediated oxi
151 ocker, capsaicin, suggesting that RIP blocks ischemic injury by modulating protein synthesis and nerv
152 Organotypic cortical brain slices exposed to ischemic injury by oxygen-glucose deprivation were treat
153 r animals (12 months) was not protected from ischemic injury by removal of extracellular Ca2+ or by b
154 important role in the pathogenesis of acute ischemic injury by signaling both MyD88-dependent and My
155 these results indicate miR-24 promotes renal ischemic injury by stimulating apoptosis in endothelial
159 these compounds were evaluated further in an ischemic injury cell survival assay and a reactive oxyge
163 whether DCD livers with steatotic and severe ischemic injury could be discriminated from 'transplanta
164 ed susceptibility of early maturing axons to ischemic injury described here may significantly contrib
166 y determination-of-death (DCD) donors suffer ischemic injury during a preextraction period of cardiac
167 suggests that female rats are vulnerable to ischemic injury during exposure and manipulation of the
170 nimals treated with morphine 24-hours before ischemic injury, ERG waveforms were preserved in a dose-
171 that brain tissue becomes more resistant to ischemic injury following a sublethal ischemic insult.
173 integrity can be reversible in traumatic and ischemic injuries, highlighting mitochondria as a potent
175 repair or regeneration of tissues suffering ischemic injury, however clinical translation is limited
176 stem cells (MSCs) is a promising therapy for ischemic injury; however, inadequate survival of implant
177 ly regulates adult muscle regeneration after ischemic injury, implying that it coordinates adult myog
178 icits tolerance to subsequent lethal hypoxic/ischemic injury in a natural process known as ischemic p
179 ession and increased heart susceptibility to ischemic injury in adult offspring, suggesting an in ute
181 n shown to improve myocardial function after ischemic injury in animal models and in early clinical e
182 in vivo, leading to an improved response to ischemic injury in animal models of hindlimb ischemia.
183 ffect of electroacupuncture (EA) on cerebral ischemic injury in diabetic mice, and explored the role
186 ter neuronal damage following focal cerebral ischemic injury in many experimental injury models, howe
191 a role as a therapeutic agent to counteract ischemic injury in neural, cardiac and endothelial cells
193 ter (WM) is intrinsically more vulnerable to ischemic injury in older animals and that the mechanisms
198 e of extracellular adenosine triphosphate in ischemic injury in specific organs, in order to provide
199 kt1 was proposed as a therapeutic target for ischemic injury in the context of myocardial infarction
200 e that HDAC inhibitors alter the response to ischemic injury in the heart and reduce infarct size, su
201 t role in cardiac myocyte protection against ischemic injury in the heart and supports the idea that
206 ver, the therapeutic role of gAD in cerebral ischemic injury in type 1 diabetes mellitus (T1DM) remai
209 This finding is physiologically relevant as ischemic injury in vivo provoked identical TLR4 response
210 1A, could lead to neuroprotection following ischemic injury in vivo The minimal syntaxin 1A-binding
213 ring chronic stroke, weeks after the initial ischemic injury, in male Sprague-Dawley rats via intrasp
214 suggested to improve cardiac function after ischemic injury, in particular by promoting neovasculari
218 of miR-592 in neurons decreases the level of ischemic injury-induced p75(NTR) and attenuates activati
220 ulation of local blood flow, protection from ischemic injury, inhibition of inflammation, the release
221 esence of MH at SW imaging-followed by acute ischemic injury, initial Glasgow Coma Scale score, and a
222 The observation that WM vulnerability to ischemic injury is age dependent has possible implicatio
224 demonstrate that induction of p75(NTR) after ischemic injury is independent of transcription but requ
228 ha mediates the cardioprotective response to ischemic injury, its upregulation may be an effective th
231 flammatory response also resulted in smaller ischemic injury, less swelling, and fewer foam cells at
232 arly, inflammatory phase of acute myocardial ischemic injury, Ly-6C(high) monocytes accrue in respons
233 ring the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have bee
234 ays after stroke and thus further exacerbate ischemic injury, manipulating its function presents a un
235 iRNA to p53 injected intravenously 4 h after ischemic injury maximally protected both PTCs and kidney
237 lphaKlotho upregulates autophagy, attenuates ischemic injury, mitigates renal fibrosis, and retards A
239 dialysis (HD) results in recurrent segmental ischemic injury (myocardial stunning) that drives cumula
240 gical conditions including myocardial aging, ischemic injury, myocardial fibrosis, and cardiomyocyte
242 cted to assess the protective effect against ischemic injury of a preservative solution supplemented
245 that miRNAs are dysregulated in response to ischemic injury of the heart and actively contribute to
246 important role in the pathogenesis of acute ischemic injury of the kidney, although possibly through
249 roblasts and ensuing fibrosis in response to ischemic injury or chronic neurohumoral stimulation.
250 s can be therapeutically useful for treating ischemic injury or for delivering anti-cancer agents to
253 delivery of EPCs protects the brain against ischemic injury, promotes neurovascular repair, and impr
254 vestigate whether HDAC inhibition can reduce ischemic injury, rats were treated with TSA (2.5 mg/kg i
258 chimera experiments determined that maximal ischemic injury required IRF-1 expression by both leukoc
259 ing via CD47, and its limiting role in acute ischemic injury responses is not shared by thrombospondi
261 ee distinct M-channel openers at 0-6 h after ischemic injury significantly decreased brain infarct si
262 or, cancer susceptibility, and recovery from ischemic injury, suggesting an epigenetic basis for risk
263 the proliferation of tubular cells following ischemic injury, suggesting that they may have a role in
265 ubjects myocardium to hypothermic reversible ischemic injury that can impair cardiac function which r
266 provide long-term durable protection against ischemic injury that is mild to moderate in severity.
267 xhibit infarct size and heart function after ischemic injury that is similar to that of control mice.
268 s early loss of axons results from a primary ischemic injury that triggers a wave of calcium signalin
269 ndogenous opioid receptor-activation reduces ischemic injury, the effects of the opioid antagonist na
270 ter the great success of therapies to reduce ischemic injury, the time has come to focus efforts on t
271 can confer acute protection against cardiac ischemic injury, their mechanism of action is unclear.
272 ility of the adult heart to regenerate after ischemic injury, there is a great opportunity to identif
273 hat makes cells and organs more resistant to ischemic injury, thereby extending the time they can tol
274 neuroprotection against subsequent cerebral ischemic injury through activation of its receptor, Toll
275 endogenous histones function as DAMPs after ischemic injury through the pattern recognition receptor
280 a major source of extracellular glutamate in ischemic injury to the cerebral white matter of the pret
287 tabilization in the first 6-24 h after renal ischemic injury was significantly reduced in mice lackin
288 increase in superoxide contributes to renal ischemic injury, we created the folate-antioxidant conju
289 ther investigating the role of the spleen in ischemic injury, we found that prior splenectomy (-7d) o
290 nd the contribution of neuronal PPARgamma to ischemic injury, we generated conditional neuron-specifi
291 of caveolins in the pathogenesis of cerebral ischemic injury, we next investigated the effects of cer
292 (-/-) and pifithrin-alpha-treated mice after ischemic injury were the anti-inflammatory M2 phenotype.
293 d are capable of being recruited to sites of ischemic injury where they contribute to neovascularizat
294 he systemic circulation and home to sites of ischemic injury where they promote neoangiogenesis.
295 hy in the newborn heart can exacerbate these ischemic injuries, which may partly be due to a decrease
296 usly evaluate multiple vascular responses to ischemic injury, which can be useful in improving our un
297 received limited success in the treatment of ischemic injury, which include therapeutics against exci
298 ular capillaries (PTCs), promoting secondary ischemic injury, which may be central to disease progres
299 blood (HUCB) cells protect the brain against ischemic injury, yet the mechanism of protection remains
300 Effective progenitor cell recruitment to the ischemic injury zone is a prerequisite for any potential
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