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1 hronic inflammation and ischemia-reperfusion injury.
2 cal for tissue protection during acute liver injury.
3 nd ischemia/reperfusion-induced acute kidney injury.
4 art still allows for marked vulnerability to injury.
5 synaptic plasticity, and regeneration after injury.
6 cognitive performance after traumatic brain injury.
7 improved survival independent of pancreatic injury.
8 lial restitution after intestinal epithelial injury.
9 rallel rodent and human studies of radiation injury.
10 nding correlating with AKI was acute tubular injury.
11 that RGC cell size is dynamic in response to injury.
12 utrophils relative to those with C5a-induced injury.
13 n patterns under homeostasis and after acute injury.
14 ury, but they are also involved in repair of injury.
15 otein are induced after ischemia-reperfusion injury.
16 rains are regions of high deformation during injury.
17 ate kidneys with AKI from those with chronic injury.
18 ple stresses, including radiation and tissue injury.
19 the contributions of these cells to hepatic injury.
20 of the vascular system and the repair after injury.
21 lation method carries a higher risk of brain injury.
22 rt as therapy for macrophage-dependent liver injury.
23 these RGC subtypes in response to disease or injury.
24 plays an important role in radiation-induced injury.
25 ents who are at risk of subsequent allograft injury.
26 of cognitive deficits after traumatic brain injury.
27 e potential to result in profound myocardial injury.
28 a respectively, mimicking events after brain injury.
29 on the frequency of different types of brain injury.
30 I, 32% had type 2 MI, and 13% had myocardial injury.
31 itial macrophages and dampening inflammatory injury.
32 re also actively repressed in the absence of injury.
33 own regarding the initial phase of astrocyte injury.
34 ally ill patients with oliguric acute kidney injury.
35 , steatosis, ER stress, apoptosis, and liver injury.
36 rain tissue deformation from traumatic brain injury.
37 iation-induced oxidative stress and cellular injury.
38 ALB/c strain) with an LPS-induced acute lung injury.
39 independent of active liver inflammation or injury.
40 le duct after cholestatic and hepatocellular injury.
41 platin-, and rhabdomyolysis-associated renal injury.
42 location of transfection are not affected by injury.
43 nd miR-548b that are known mediators of lung injury.
44 tion during recovery from neonatal hyperoxic injury.
45 extensor muscles after cervical spinal cord injury.
46 lination and myelin regeneration after nerve injury.
47 ata on how such anomalies affect deaths from injuries.
48 t and to recognize any conceivable repeating injuries.
49 cted manner during homeostasis or after mild injuries.
50 mtTBI subjects had moderate, and 17 had mild injuries.
51 etrogradely-labeled from muscle before nerve injuries.
52 whole-body computed tomography (WBCT) due to injuries.
53 ays a protective role in ZIKV-mediated brain injuries.
54 years, mortality was highest for myocardial injury (45.6%), followed by type 2 MI (34.2%) and type 1
55 1), carotid injuries versus vertebral artery injuries (49 of 420 [11.7%] vs 35 of 667 [5.2%]; P < .00
56 ions during admission included: acute kidney injury (63%), transaminitis (31%), shock (31%), acute re
57 -eIF4E activity in animals with spared nerve injury, a model of peripheral nerve injury (PNI)-induced
58 r evidence of ongoing neuronal or astrocytic injury/activation or induction of dementia-related brain
59 mortality in patients with both acute kidney injury (adjusted relative risk, 2.38; 95% CI, 1.75-2.98)
60 ntial to prevent and to treat the acute lung injury after SARS-CoV-2 infection, especially for those
63 tion is common in patients with acute kidney injury (AKI) and the risk of mortality is high, especial
64 Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis b
66 ts with ACLF diagnosed with HRS acute kidney injury (AKI) were randomized to albumin with infusion of
67 ss can result in recovery after acute kidney injury (AKI) with adaptive proliferation of tubular epit
69 ntral role in the pathogenesis of acute lung injury (ALI) during both the acute pneumonitis stage and
70 stroke, hemorrhagic stroke, traumatic brain injury, Alzheimer's disease, and multiple sclerosis, and
73 orthopaedic trauma patients with high-energy injuries and to investigate their impact on the incidenc
74 se the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly typ
79 ned mechanisms controlling myelination after injury and during axon regeneration in the central nervo
80 ulated autophagic response is triggered upon injury and during the early stages of the regeneration p
81 cs have an overall protective effect in lung injury and fibrosis and fit with a mechanism whereby lun
83 e immune responses that result in less organ injury and improved survival after polymicrobial sepsis.
84 tion, reduced myocardial damage, shock, lung injury and improved survival independent of pancreatic i
85 itioning with metformin lowers hepatobiliary injury and improves hepatobiliary function in an in situ
86 the roles of myeloid cell subsets in kidney injury and in the limited ability of the organ to repair
87 marrow niches in response to remote ischemic injury and migrate to the areas of damage and stimulate
88 a treatment for spasticity in stroke, brain injury and multiple sclerosis patients, who are often un
91 ections, we show that the time delay between injury and polyplex injection directly impacts the magni
92 rvation and correlate the results with graft injury and postoperative graft function in patients unde
94 operties that protect human neutrophils from injury and provides insight into its mode of action beyo
95 We hypothesized that acute regional brain injury and recovery associate with differences in region
101 s the human brain to rewire and recover from injury and sensory deprivation, it can lead to tinnitus
103 le of caspase 3 signaling in mediating spine injury and the modulation of caspase 3 activation may be
105 of resident and recently recruited MPs after injury and unveiled distinct functions of these subsets,
106 ransition' (relevant to ischemia-reperfusion injury) and their effects on the ubiquinone-binding site
107 pia, superficial corneal and/or conjunctival injuries, and orbital fractures accounted for 73.2% of a
108 ods The demographics, clinical presentation, injuries, and radiologic findings of patients reporting
109 results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 to assess th
110 sfunction (EAD), L-GrAFT score, acute kidney injury, and comprehensive complication index were analyz
113 loses most of its normal input after such an injury, and is clearly a major focus of reorganization.
114 ling in homeostatic health, the responses to injury, and new methods to study lung repair and regener
117 the involvement of macrophage AQP3 in liver injury, and provide evidence for mAb inhibition of AQP3-
118 th inflammatory response/disease, organismal injury, and respiratory diseases and were involved in re
120 s, but the effects of this strategy on organ injury are less well studied in critically ill patients
122 nt activation and acute post-ischemic kidney injury are prevented, with additional protection achieve
123 m for better characterizing corneal puncture injuries as seen in a military relevant clinical setting
124 ction in fibrosis after carbon tetrachloride injury, associated with increased HSC death and reduced
126 al outcomes were assessed by American Spinal Injury Association (ASIA), or International Standards fo
128 icroRNAs that control inflammation, neuronal injury, autophagy and vesicular transport genes are obse
129 that transvalvular unloading limits ischemic injury before reperfusion, improves myocardial energy su
131 ibit improved healing following acute tendon injuries, but the driver of this regenerative healing re
132 neration enhancers are not only activated by injury, but surprisingly, they are also actively repress
133 tant in mounting an inflammatory response to injury, but they are also involved in repair of injury.
134 d stellate cell activation, leading to liver injury, by a mechanism involving AQP3-mediated H(2)O(2)
135 ravascular fibrin, vessel caliber, extent of injury, C4d positivity, and inflammatory cell phenotypin
136 t NADPH oxidase 2 (NOX2) generated oxidative injury causes upregulation of a constitutively active fo
138 tine of treated animals show reduced hypoxic injury compared to controls and the kidneys have reduced
144 eration, demonstrated its involvement in non-injury disorders and found multiple ways to block it.
149 maternal TB, all-cause mortality, and liver injury during pregnancy through 12 months postpartum.
150 al factors, even small amounts of myocardial injury (e.g., troponin I >0.03 to 0.09 ng/ml; n = 455; 1
151 sed in studying multiple brain disorders and injuries, e.g., in Parkinson's disease or traumatic brai
152 es with increased mortality and acute kidney injury early after transcatheter aortic valve replacemen
153 zotocin model of hyperglycemia-induced renal injury ENaC activity in hyperglycemic animals was elevat
154 Higher rates of obstetric anal sphincter injury following vaginal birth were found in countries w
155 dings provide further information on orbital injuries from airguns, a theme of growing popularity and
158 out myocardial injury, those with myocardial injury had more electrocardiographic abnormalities, high
161 ns in the postacute phase of traumatic brain injury impede optimal recovery and contribute substantia
162 oduodenoscopy revealed minor mucosal thermal injury in 2 of 36 RF/PF and 0 of 24 PF/PF patients.
163 116 patients (41.4%) and severe acute kidney injury in 32 of 116 (27.6%) patients, which was mostly e
167 N1ICD) and impaired regenerative response to injury in comparison to young (2-3 months old) mice.
172 was continued alleviation of hepatocellular injury in knockout mice despite ongoing carbon tetrachlo
175 bile acids, might mediate parenchymal renal injury in patients with cirrhosis, suggesting that concu
178 soforms in modulating recovery from synaptic injury in SIV infection and suggest their therapeutic ta
179 Regenerative response to skeletal muscle injury in Speg-KO mice was compared with that of WT mice
181 se (AD), its reflection on regional neuronal injury in the context of amyloid pathology remains uncle
182 re organ damage, our understanding of tissue injury in the liver, adrenal glands, and lymphoid tissue
183 international migrants had no excess risk of injury in the past 12 months compared to non-migrants (a
184 erapeutic strategy to attenuate acute kidney injury in transgenic mice receiving contrast material.
185 of PDGFR-alpha in HSCs during chronic liver injury in vivo via regulation of HSC survival and migrat
186 ssage cells to clonal density, to mimic lung injury in vivo, selects for rare subsets of HBECs that a
188 ly conserved metabolic adaptations to severe injury including major trauma, burns, or hemorrhagic sho
189 ased neuronal and network excitability after injury, including increased susceptibility to spreading
191 promoting neuronal recovery.IMPORTANCE Brain injury induced by acute simian (or human) immunodeficien
193 tor 2 (TLR2) signaling is critical for nerve injury-induced activation of spinal cord microglia, but
194 ble and show protection against aneurysm and injury-induced neointimal hyperplasia, diseases linked t
196 nhibition of GT1b synthesis attenuates nerve injury-induced spinal cord microglia activation and pain
197 assayed plasma biomarkers related to tubular injury, inflammation, and fibrosis (KIM-1, TNFR-1, TNFR-
204 interactions pathway in patients with liver injury is indicative of an immune-based mechanism for th
206 mation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective strateg
210 time stroke patients studied at 2 weeks post-injury (mean age 52.8 years, range 22-77; 63 females; 64
212 ized to AngII-induced calcium signaling upon injury might explain results from large, randomized, con
216 functional recovery in vivo in a spinal cord injury model through a unique mechanism of anti-inflamma
217 h in cancer therapy but also an experimental injury model used to examine mechanisms of regeneration
220 zebrafish tail injury and murine acute lung injury models of neutrophilic inflammation, overexpressi
221 lar complications including acute myocardial injury, myocarditis, arrhythmias, and venous thromboembo
222 ultiple organ dysfunction; and direct tissue injury (n = 64, 21.9%) including brain and spinal cord t
223 ommunication defects associated with cardiac injury, namely arrhythmogenesis and progression into hea
224 hts and behaviors (STBs) or nonsuicidal self-injury (NSSI), and relative to adults, research in youth
227 defined as death or significant grey matter injury on MRI according to a previously validated scorin
228 s of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resident renal ma
230 to-severe TBI were assessed at 6 months post injury on the Glasgow Outcome Scale-Extended (GOSE), the
231 resonance imaging findings of vascular brain injury or cerebral atrophy in adult American Indians.
233 mage such as cardiovascular, renal and liver injury or/and multiple organ failure, suggesting a sprea
234 tion (OR, 2.9; 95% CI, 1.3-6.7), acute renal injury (OR, 2.7; 95% CI, 1.3-5.6), and CRP on admission
236 k factors for disparities in traumatic brain injury outcomes between undocumented immigrants and docu
238 cal features had higher rates of aortic root injury (p < 0.001), moderate-to-severe paravalvular regu
240 ence was observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a significant al
242 eria were presenting more than 14 days after injury, previous rupture of the same Achilles tendon, or
244 ting the POOR-get-POORer progression of lung injury relies on two principles: 1) open the lung to min
248 s a trend toward higher risk of acute kidney injury requiring renal replacement therapy in SOT vs. no
251 ory mechanism is lost with acute irradiation injury, resulting in a paucity of tuft cells and acetylc
252 afts can integrate into sites of spinal cord injury (SCI) and generate neuronal relays across lesions
253 after SCI.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) significantly disrupts immunity, thus incre
254 develop adverse LV remodeling following I/R injury secondary to the collateral damage from sustained
257 hile controlling for pre-training behaviors, Injury Severity Score, postgraduate training year, and d
259 e the start of treatment, drug-induced liver injury should be taken into consideration, especially af
261 how Runx1 is specifically upregulated at the injury site during zebrafish heart regeneration, and tha
267 ority, yet current models of traumatic brain injury (TBI) inadequately recapitulate the human immune
268 ., in Parkinson's disease or traumatic brain injury (TBI), and hence it will be useful to the wider n
269 rvation is typically a consequence of tissue injury that disrupts the local blood supply but can also
270 s is a key determinant for early hepatocytes injury, the recruitment of cells of innate immunity exer
272 Compared with patients without myocardial injury, those with myocardial injury had more electrocar
274 aimed at prevention of ischemia/reperfusion injury to allografts based on animal data should be cons
278 isplayed increased expression of parenchymal injury transcripts (eg, hypoxia-inducible factor EGLN1).
279 atherothombotic event), T2MI, or myocardial injury (troponin rise not meeting criteria for myocardia
280 interval {CI}: 1.6, 2.4]; P < .001), carotid injuries versus vertebral artery injuries (49 of 420 [11
283 GFR) and urine albumin excretion, and kidney injury was evaluated by histopathology and gene expressi
287 COVID-19 (n = 375), incidence of acute liver injury was lower in LT recipients (47.5% vs. 34.6%; P =
289 ts are used extensively to model spinal cord injury, we asked if the S1 CST response is conserved in
290 ces across all severities of traumatic brain injury, we combined computational, analytical, and exper
291 In an in vivo model of second organ reflow injury, we found that RvD5 did not reduce lung neutrophi
292 experiences of musculoskeletal symptoms and injury were not significantly different by hospital char
294 utophagy has been implicated in acute kidney injury, which can arise in response to nephrotoxins, sep
295 Gdf5 in tissue remodelling and repair after injury, which may partly underpin its association with O
296 es: 113 [58.2%]); 163 (84%) had acute kidney injury, which was associated variously with dehydration
297 human studies, GFAP, was highest at 6 h post-injury, while no substantial changes were observed in UC
298 tized mice were subjected to traumatic brain injury with a closed-head, free-weight drop method.
300 rther, scRNA sequencing of the HO site after injury with or without immobilization identifies gene si