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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
61 escue microglial activation and white matter injury after TBI.
62 forty-seven genes altered expression in both injury ages (63% of P7SCI data set).
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
65 to discard deceased donors with acute kidney injury (AKI) versus without AKI (30% versus 18%).
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
68                        Ischemic acute kidney injury (AKI), a complication that frequently occurs in h
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
71 sis is a hallmark of overuse musculoskeletal injuries and contributes to functional declines.
72 tions leading to primary and secondary brain injuries and permanent neurological deficits.
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
75                          Prevalence of liver injury and associated clinical characteristics are not w
76 ociated with the development of acute kidney injury and decreased survival.
77                                         Lung injury and development and PH were quantified at differe
78 gy in different organs and various models of injury and disease.
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
82 ia-reperfusion, an event that induces kidney injury and fibrosis.
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
89                       In both zebrafish tail injury and murine acute lung injury models of neutrophil
90  and human lung is associated with oxidative injury and pathogenic inflammation.
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
93 nism by which beta-catenin promotes podocyte injury and proteinuria in glomerular diseases.
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
96                                              Injury and repair caused by the oxygen-induced retinopat
97  increased in end target muscles after nerve injury and repair.
98 ial meniscus (DMM) and after acute cartilage injury and repair.
99      The resulting imbalance between ongoing injury and restitution led to worsening of the Mdr2 KO p
100 uctural outcomes in animal models of retinal injury and retinal degenerative disease.
101 s the human brain to rewire and recover from injury and sensory deprivation, it can lead to tinnitus
102 XR signaling and partially ameliorated liver injury and sinusoidal ischemia in SCD mice.
103 le of caspase 3 signaling in mediating spine injury and the modulation of caspase 3 activation may be
104 d bone marrow involvement, and microvascular injury and thrombosis were also detected.
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
111 stores surfactant homeostasis, prevents lung injury, and improves lung physiology.
112  Glasgow Coma Scale, mechanism and intent of injury, and Injury Severity Score.
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
115 HFD-fed mice by inducing liver inflammation, injury, and p38 activation.
116  PPN such as pain threshold, memory of prior injury, and pain sensitization/desensitization.
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
119                                     Pressure injuries are one of the most frequently occurring, yet p
120 s, but the effects of this strategy on organ injury are less well studied in critically ill patients
121  and during cardiac neovascularization after injury are poorly understood.
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
125                                              Injury-associated risk of painful TMD was elevated in pe
126 al outcomes were assessed by American Spinal Injury Association (ASIA), or International Standards fo
127 tive exhibiting intense symptoms of chilling injury at 6 degrees C.
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
130 n, cytokine storm, and elevations of cardiac injury biomarkers.
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
137                    After a dorsal root crush injury, centrally-projecting sensory axons fail to regen
138 tine of treated animals show reduced hypoxic injury compared to controls and the kidneys have reduced
139    REBOA details, demographics, mechanism of injury, complications, and outcomes were collected.
140                   After surgery or traumatic injury, corneal wound healing can cause a scarring respo
141 fe 4-7 were scored according to standardized injury criteria.
142                           Drug induced liver injury (DILI) is a necro-inflammatory liver disease caus
143  safety concerns, such as drug-induced liver injury (DILI).
144 eration, demonstrated its involvement in non-injury disorders and found multiple ways to block it.
145                                           R3(injury) displayed increased expression of parenchymal in
146 iseases in which direct or indirect podocyte injury drives proteinuria or nephrotic syndrome.
147                           As well as risking injuries due to gastro-intestinal blockage, ingestion of
148 ty with limited evidence of benefit in liver injury due to other causes.
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
156     At later time points following lysosomal injury, Gal3 controlled autophagic responses.
157                                       Higher injury grade (adjusted odds ratio, 2.0 per one-grade inc
158 out myocardial injury, those with myocardial injury had more electrocardiographic abnormalities, high
159 ia around motoneurons axotomized after nerve injuries has been intensely debated.
160                         Further, obstetrical injury has significant deleterious impact on recovery of
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
164          The occurrence rate of acute kidney injury in acute ischemic stroke patients was low and was
165 llular metabolism is a hallmark of ischaemic injury in acute stroke.
166              Repetitive mild traumatic brain injury in American football players has garnered increas
167 N1ICD) and impaired regenerative response to injury in comparison to young (2-3 months old) mice.
168  clinical factors associated with myocardial injury in COVID-19.
169              SF-PreCon markedly reduced MI/R injury in DM mice, as evidenced by improved cardiac func
170  and glycerol transport, and prevented liver injury in experimental animal models.
171 ticoid receptor modulators regulate podocyte injury in experimental models.
172  was continued alleviation of hepatocellular injury in knockout mice despite ongoing carbon tetrachlo
173 that ILCs may be involved in regulating lung injury in lung transplant recipients.
174       Despite the common occurrence of brain injury in patients undergoing extracorporeal membrane ox
175  bile acids, might mediate parenchymal renal injury in patients with cirrhosis, suggesting that concu
176 d impairment, indicating potential for brain injury in regions that control these functions.
177         Lower ADC potentially reflects renal injury in RVD patients, but does not change in response
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
180 e acids in the liver, fails to promote liver injury in the absence of the microbiome in vivo.
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
187  itself is not the cause for direct podocyte injury, in vitro or in vivo.
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
190 on consequence of many forms of neurological injury, including stroke and nerve damage.
191 promoting neuronal recovery.IMPORTANCE Brain injury induced by acute simian (or human) immunodeficien
192        Whether autosis is involved in tissue injury induced under pathologically relevant conditions
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
195 o intestinal development and the dynamics of injury-induced regeneration.
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-
198 , characterized by crystal deposits, tubular injury, inflammation, and fibrosis.
199                          Treatment of tendon injuries is challenging.
200          The paucity of therapies for tendon injuries is due to our limited understanding of the cell
201                                   Myocardial injury is common, but true myocarditis is rare.
202                                 Acute kidney injury is common, with a major effect on morbidity and h
203 fficacy of glucorticoids (GC) for vocal fold injury is highly variable.
204  interactions pathway in patients with liver injury is indicative of an immune-based mechanism for th
205                                         This injury is mitigated by a poorly characterized, maladapti
206 mation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective strateg
207 r Neurological Classification of Spinal Cord Injury (ISNCSCI), examination.
208                           After severe brain injury, it can be difficult to determine the state of co
209 ological, histological, and biochemical lung injury markers.
210 time stroke patients studied at 2 weeks post-injury (mean age 52.8 years, range 22-77; 63 females; 64
211        Early unresolving molecular allograft injury measured via changes in dd-cfDNA may be an early
212 ized to AngII-induced calcium signaling upon injury might explain results from large, randomized, con
213         Finding a window into early podocyte injury might help identify molecular pathways involved i
214              Our tibial fracture orthopaedic injury model in mice recapitulates the major manifestati
215                         We use a dental pulp injury model that exposes the pulp to the outside enviro
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
218 ia in vivo in the DDC-mediated mouse biliary injury model.
219 TBI (rmTBI) using a lateral fluid percussion injury model.
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
225                       Any-stage acute kidney injury occurred in 48 of 116 patients (41.4%) and severe
226 s evaluated in an in vitro model of cellular injury on cortical neurons.
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
229                    Given that a haemorrhagic injury on the battlefield is almost always associated wi
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.
232  are increasingly being requested to confirm injury or to resolve diagnostic uncertainty.
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
235                  By combining radiation with injury, our work reveals a novel connection between dyin
236 k factors for disparities in traumatic brain injury outcomes between undocumented immigrants and docu
237               Disparities in traumatic brain injury outcomes for ethnic minorities and the uninsured
238 cal features had higher rates of aortic root injury (p < 0.001), moderate-to-severe paravalvular regu
239 rophylaxis against postcontrast acute kidney injury (PC-AKI) in 2018 (ESUR 10.0).
240 ence was observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a significant al
241 ed nerve injury, a model of peripheral nerve injury (PNI)-induced neuropathic pain.
242 eria were presenting more than 14 days after injury, previous rupture of the same Achilles tendon, or
243 platelet plug formation at sites of vascular injury (primary hemostasis).
244 ting the POOR-get-POORer progression of lung injury relies on two principles: 1) open the lung to min
245               While postoperative myocardial injury remains a major driver of morbidity and mortality
246                                  Spinal cord injury remains a scientific and therapeutic challenge wi
247 om oxygen transportation to host defense, to injury repair.
248 s a trend toward higher risk of acute kidney injury requiring renal replacement therapy in SOT vs. no
249             Loss of TIPE0 in mice results in injury-resistant enterocytes, that are hyperproliferativ
250                    However, its role in lung injury resolution and the mechanisms by which it regulat
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
255 tion; however, its function in chronic liver injury sequelae, such as fibrosis, is unknown.
256 ortality after TAI was 7.8%, and depended on injury severity (grade IV (free rupture) 20.9%).
257 hile controlling for pre-training behaviors, Injury Severity Score, postgraduate training year, and d
258 a Scale, mechanism and intent of injury, and Injury Severity Score.
259 e the start of treatment, drug-induced liver injury should be taken into consideration, especially af
260         Tissue collected at 7-12 months post-injury showed no significant differences in lesion size,
261 how Runx1 is specifically upregulated at the injury site during zebrafish heart regeneration, and tha
262 ent inhibition was achieved using B4Crry, an injury site-targeted inhibitor of C3 activation.
263                    Following maxillary tooth injury, Smoc2(-/-) mutants had increased osteoclast acti
264  contribute to unanticipated consequences of injury, such as tumorigenesis.
265                      Of 177 eligible firearm injury survivors, 100 were successfully contacted and 63
266 life was significantly reduced among firearm injury survivors.
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
271                             After acute lung injury, they are preferentially localized in regeneratin
272    Compared with patients without myocardial injury, those with myocardial injury had more electrocar
273  but at much higher levels mediates neuronal injury through oxidative stress.
274  aimed at prevention of ischemia/reperfusion injury to allografts based on animal data should be cons
275 ry neurons regenerate their axon after nerve injury to enable functional recovery.
276 ility transition pore opening after ischemic injury to reduce ongoing pathological remodeling.
277 cells undergo dynamic changes in response to injury to regenerate lost cells.
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
281 16) that was similar to that of white matter injury volume (standardized beta = -0.22).
282                This "ventilator-induced lung injury vortex" of the shrinking baby lung is opposed by
283 GFR) and urine albumin excretion, and kidney injury was evaluated by histopathology and gene expressi
284                           The extent of lung injury was identified at 24 h following BOP by assessing
285                                    Bile duct injury was induced by the administration of 3,5-diethoxy
286                     The risk of acute kidney injury was lower between those who either underwent CT a
287 COVID-19 (n = 375), incidence of acute liver injury was lower in LT recipients (47.5% vs. 34.6%; P =
288                         Ischemia-reperfusion injury was modeled in vitro by placing human umbilical v
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
293          All sTBI subjects (n = 24) had mild injuries, whereas eight of the mtTBI subjects had modera
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.
299                                Both surgical injury with HS and counterregulatory hormone (epinephrin
300 rther, scRNA sequencing of the HO site after injury with or without immobilization identifies gene si

 
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