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1 f rib 7 (21.3%, 47 of 221) was most commonly injured.
2 surface only if the cornea was superficially-injured.
3 capable of extensive body regeneration when injured.
4 Among 307 people aboard the flight, 192 were injured; 63 of the injured patients were initially evalu
7 ng drugs have gained popularity for treating injured adult axons, the rationale being that increased
10 tion of recovery neurobiology components for injured adult mammalian spinal cord that are different f
11 9(+) progenitors that were transplanted into injured adult mouse lungs differentiated into all major
14 tored after injury.SIGNIFICANCE STATEMENT In injured and diseased nerves, the transcription factor c-
16 issection to specifically collect individual injured and non-injured nociceptive DRG neurons and to d
18 omponents of the BMP signaling pathway, were injured and then tested for nocifensive responses to a n
20 ur combinatorial strategy in the chronically injured animals prevented a decline in locomotor behavio
22 s were found in cerebrospinal fluid (CSF) of injured animals with a CSF/serum ratio of 20% at peak,
23 spread out over the tissues adjacent to the injured area in certain diseases, including brain tumors
25 s, facilitates the neuronal migration toward injured areas, and shows survival properties due to its
27 onstrate effective siRNA transfection of the injured arterial wall and provide a clinically effective
29 e formation of dystrophic growth cone at the injured axonal tip, the subsequent axonal dieback, and t
33 gthening of 3'UTRs was more prevalent in the injured axons, including the newly discovered alternativ
37 mark problems: in vivo thrombus growth in an injured blood vessel and in vitro thrombus deposition in
39 w-derived G-CSF-responsive cells home to the injured brain and are critical for altering neural proge
40 tion times and increased accumulation in the injured brain compared to generation 4 dendrimers (G4,
41 etitive (r)TBI mouse model and harvested the injured brain extracts from the acute to the chronic pha
48 tivated microglia and damaged neurons in the injured brain, and deliver therapeutics in small and lar
49 of early inflammatory infiltrate within the injured brain, and whether their depletion attenuates se
59 ilities who fall may not be seriously ill or injured, but policies often require immediate transport
60 cents treated at PTCs were more likely to be injured by a blunt than penetrating injury mechanism (91
61 dds of underreporting in the NVSS than those injured by firearms (odds ratio [OR]: 68.2; 95% CI: 15.7
63 dual- and county-level covariates, decedents injured by non-firearm mechanisms had higher odds of und
64 that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT in
65 elets inhibited endothelial recovery in wire-injured carotid arteries, but this effect was also abrog
72 opulation-based, consecutive sample of 67047 injured children and adults served by EMS (1971 rural an
73 ission fibrinolytic derangement is common in injured children and adults, and is associated with poor
76 period of maturation for human NSCs in adult injured CNS is not well defined, posing fundamental ques
77 tion in the adult CNS.SIGNIFICANCE STATEMENT Injured CNS nerves fail to regenerate spontaneously.
80 in vivo High-concentration thrombin directly injured conditionally immortalized human and rat podocyt
84 ate-to-pyruvate ratios were increased in the injured cortex at acute (12/24 hours) and sub-acute (7 d
89 Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrogr
91 ockdown fully reversed MOR expression in the injured DRG and potentiated the morphine effect on pain
92 n of the DNA methyltransferase DNMT3a in the injured DRG neurons via the activation of the transcript
93 KChIP1, and DPP10 were transfected into the injured DRGs (defined as DRGs with injured spinal nerves
97 cating that caErbB2 enhanced regeneration of injured DRs, without aberrantly activating SCs and axons
99 and KKO selectively bound to photochemically injured endothelium at sites where surface glycocalyx wa
106 nd P2 receptors on T cells isolated from the injured heart revealed profound upregulation of the enzy
110 ene expression signature identified severely injured hearts during EVHP (upregulation of c-Jun, 3.19
111 elevations in cardiac Troponin-I in severely injured hearts during EVHP, and may also detect injury a
114 eloid cell numbers markedly increased in the injured hearts, and histamine levels were up-regulated i
115 ignal was found to be 24 +/- 6% lower in the injured hemisphere compared with the non-injured hemisph
116 the injured hemisphere compared with the non-injured hemisphere, while the hyperpolarized bicarbonate
121 1 in the nuclei of renal proximal tubules of injured human kidney allografts, but not in those of sta
125 low, there was responder bias with patients injured in intentional events, younger, and less serious
128 e surrounding surgical resection site can be injured inadvertently due to procedures such as incision
131 ically limits macrophage accumulation in the injured kidney during RAS activation by constraining the
132 Lgals3, Pdgfb, Egf, and Tgfb In comparison, injured kidneys from mice lacking BRP-39 had significant
134 cortex, medulla and pelvis of the normal and injured kidneys, we found that ureteral obstruction not
140 insight into the microscopic behavior of the injured lung and provide a means of testing protective-v
141 ntiinflammatory and pro-resolving effects on injured lung endothelium and alveolar epithelium, includ
146 sp1-EYFP+ CPCs improved the survivability of injured mice and restored the functional performance of
147 Conditional ablation of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately
149 Intraperitoneal inoculation of the thermally injured mice, bypassing the need for translocation, prod
152 type-B receptor 1 (EphB1) is upregulated in injured motor neurons, which in turn can activate astroc
154 s, NMN deamidase reduces NMN accumulation in injured mouse sciatic nerves and preserves some axons fo
155 at trkB.T1 is significantly increased in the injured mouse spinal cord, where it is predominantly fou
159 Such cells failed to accumulate in acutely injured muscle of old mice, known to undergo ineffectual
160 ently proliferate upon injury and regenerate injured muscles, but continually decline during regenera
162 ice exhibited fewer suppressive Tregs in the injured myocardium and decreased expression of the gene
164 lowing MI rescued Treg infiltration into the injured myocardium of YAP/TAZ mutants and decreased fibr
172 ring the endogenous molecules to salvage the injured neighboring cells by regulating apoptosis, infla
174 ich maintains macrophage infiltration to the injured nerve, and sends paracrine signals to activate T
175 ts define novel morphological transitions in injured nerves and show that repair Schwann cells have a
176 elongated cells that build Bungner bands in injured nerves and that such cells can transform to myel
177 red nerve conduit that was applied to bridge injured nerves in a rat sciatic nerve transection model.
178 rowth of axons through the proximal parts of injured nerves repair, Schwann cells gradually lose rege
179 ent with the fact that tumors do not form in injured nerves, although they contain proliferating Schw
183 gy and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic
188 coordinate regulation of gene expression in injured neurons involving multiple pathways was central
190 mediates a cross talk between astrocytes and injured neurons that promotes synaptic recovery in the i
191 s with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic s
192 that axonal fusion restores full function to injured neurons, is dependent on exposure of phospholipi
193 s to form cells that support the survival of injured neurons, promote axon growth, remove myelin-asso
198 cifically collect individual injured and non-injured nociceptive DRG neurons and to define their gene
199 nalysis of the transcriptomic profile of the injured nociceptors revealed oxidative stress as a key b
200 t, several novel transcripts were altered in injured nociceptors, and the global signature of these L
203 Intratracheal delivery of stem cells into injured or diseased lungs can provide a variety of thera
204 that remodeling of the fibronectin matrix in injured or diseased tissue elicits an EDA-dependent fibr
205 ploiting endogenous stem cells to regenerate injured or diseased tissue may circumvent these challeng
207 dily applied to image wound healing in other injured or diseased tissues, or to monitor tissue change
209 however, it is unclear how the type of cells injured or the mechanism of injury activates these pathw
211 investigate that BMSCs deliver miR-9 to the injured pancreas or peripheral blood mononuclear cell (P
213 r topical application, the MSCs homed to the injured parenchyma and improved the neurological functio
216 tometry analyses on a total of 70 critically injured patients (Injury Severity Score [ISS] >/= 25) at
217 med flow cytometry analyses in 34 critically injured patients and compared findings with those of 9 h
218 is still a common cause of death in severely injured patients and is characterized by impairment of o
221 entional events, younger, and less seriously injured patients less likely to participate; therefore,
223 f care, injury severity, and mortality among injured patients served by 9-1-1 emergency medical servi
226 oard the flight, 192 were injured; 63 of the injured patients were initially evaluated at San Francis
227 ared transcriptome findings in 36 critically injured patients with those of 6 patients with minor inj
228 e the longer-term health status of seriously injured patients, identify predictors of outcome, and es
235 l population.SIGNIFICANCE STATEMENT Although injured peripheral nerves contain repair Schwann cells t
236 environment.SIGNIFICANCE STATEMENT Repair of injured peripheral nerves remains a critical clinical pr
238 to CD4(+) T cells following phagocytosis of injured, phosphatidylserine-exposing oligodendroglial ce
240 on of the C5a active receptor (C5aR/CD88) by injured pulp fibroblasts controls the direction of neuri
242 retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presyna
243 oral changes of the elastic stiffness of the injured rat neocortex and spinal cord at 1.5 and three w
244 ate or NMDA was injected directly into crush-injured rat sciatic nerves, ERK1/2 phosphorylation was o
247 at is seen in other mammals, the majority of injured retinal ganglion cells (RGCs) survive with relat
250 of maturation, despite implantation into the injured rodent spinal cord, yet they support delayed fun
252 iously reported that myelin clearance in the injured sciatic nerve proceeds unhindered in the Ccr2(-/
254 1, and CAV1 phosphorylation was increased in injured SECs, resulting in increased GRK2-CAV1 interacti
255 expansions of hepatocyte stem/progenitors at injured sites that are lineage but not fate restricted.
259 d macrophage-specific mRNA directly from the injured spinal cord and performed RNA sequencing to inve
260 n macrophage-specific mRNA directly from the injured spinal cord in mice and performed RNA sequencing
263 majority of myelinating Schwann cells in the injured spinal cord; invasion of peripheral myelinating
266 trix proteins not previously associated with injured spinal tissue, including small proteoglycans inv
268 150 healthy controls and communicative brain-injured subjects in various states of conscious wakefuln
269 propriate inflammatory conditions where they injure the host, leading to the death of the neutrophils
270 A total of 10 Gy irradiation was used to injure the intestinal epithelium and induce subsequent c
272 n reactive nitrogen species damages axons by injuring their mitochondria and inducing demyelination.
274 designed to selectively release morphine in injured tissue and to prevent blood-brain barrier permea
276 fferentiation of stem cells, responsible for injured tissue repair, and simultaneously discourage bac
282 the chemokine receptor CCR2 to gain entry to injured tissues from the bloodstream, are purportedly ne
284 usively intracellular (except in diseased or injured tissues), our data show that schistosomes displa
285 EMS) technicians arriving with intentionally injured trauma patients from January 1 to December 31, 2
288 nd perform the critical tasks of dismantling injured vessels and creating channels for new vascular r
289 d factor (VWF) mediates platelet adhesion to injured vessels by sequestering platelets from blood flo
295 and interaction of all SOC components in the injured VSMCs, where Homer1 interacts with Orai1 and var
296 tion when the concerned spinal segments were injured was studied in 384 patients with clinically comp
299 number of apoptotic chondrocytes within the injured xiphoid cartilage, which was confirmed by TUNEL
300 proportionately sampled group of non-assault-injured youth enrolled from September 2009 through Decem
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