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1 on in recovery of force after an acute nerve crush injury.
2 d of the adult mice with a complete thoracic crush injury.
3 emyelination is severely delayed after nerve-crush injury.
4 ation and delayed RGC loss after optic nerve crush injury.
5 10 is rapidly expressed by macrophages after crush injury.
6  nerves starting between 2 and 3 weeks after crush injury.
7  to a level equivalent of that observed with crush injury.
8 ation in animal models following axotomy and crush injury.
9  protected from degeneration following nerve crush injury.
10 neration following retro-orbital optic nerve crush injury.
11 arly axonal regeneration after sciatic nerve crush injury.
12  of mouse sciatic nerve distal segment after crush injury.
13 egrowth tapered off around 2 weeks after the crush injury.
14 s gangrene, necrotizing fasciitis, and acute crush injury.
15 axons into the spinal cord after dorsal root crush injury.
16 ced regrowth of axons after an in vivo nerve crush injury.
17  lumbar spinal cord, following sciatic nerve crush injury.
18  in mice of both sexes following optic nerve crush injury.
19 nces regeneration of the sciatic nerve after crush injury.
20 ce (C57BL/6J) were unilaterally subjected to crush injury.
21 ances motor nerve regeneration after a nerve crush injury.
22  after 7 d in vivo after a peripheral axonal crush injury.
23 us following either sciatic nerve section or crush injury.
24 extravasation occurs within 3 days following crush injury.
25 unctional recovery after incomplete cervical crush injury; (2) either of these cell types is preferab
26                                  After large crush injuries across the entire spinal cord, ependyma-d
27 y after nerve transection, crush injury, and crush injury after a previous "conditioning" lesion.
28 ave now investigated whether a sciatic nerve crush injury alters the behavioral response in rats to t
29 verse neurological conditions such as spinal crush injuries and Alzheimer's disease.
30                        C57Bl/6 mice received crush injuries and were allowed to survive for 6 weeks t
31 established in vivo models - the optic nerve crush injury and an eIF2B loss of function (LOF) mutant
32 ating that APC can diminish complications of crush injury and leukocyte damage to lung and other tiss
33 terminating inflammation after sciatic nerve crush injury and promoting regeneration.
34 reviously suggested in nerve transection and crush injuries, and now demonstrated in CCI neuropathy,
35 lowing sterile injury, ischemia reperfusion, crush injury, and autoimmune-mediated tissue damage.
36 that severe polytrauma-bone fracture, muscle crush injury, and bowel ischemia-induced a marked increa
37 egenerative ability after nerve transection, crush injury, and crush injury after a previous "conditi
38                               In the carotid crush injury animals, biodistribution analysis confirmed
39                                        After crush injury, animals received either 8.3 mg/kg (332,000
40  C2-C6 spinal cord 3 days after a C3/C4 hemi-crush injury (C3Hc).
41 cidence may be increased as a result of mass crush injury casualties or prolonged evacuation times.
42                                        Nerve crush injury causes partial leakiness of the blood-nerve
43                          After a dorsal root crush injury, centrally-projecting sensory axons fail to
44 ple forms of sciatic nerve injury, including crush injury, chronic constriction injury, and axotomy.
45                          Equivalent moderate crush injuries combined with ablation of reactive astroc
46 sory nerve regeneration achieved after nerve crush injury compared with untreated diabetic rats.
47                RGCs subjected to optic nerve crush injury demonstrated more rapid neurite outgrowth i
48 ral hood ipsilateral or contralateral to the crush injury elicited synaptic responses in RS neurons o
49 uctures and swirling debris inflict numerous crush injuries, fractures, and serious wounds.
50 s surviving blunt and penetrating trauma and crush injuries have subsequent complications that lead t
51                                     Moderate crush injuries in control mice caused focal tissue disru
52 on-adjacent spinal segments after a thoracic crush injury in adult mice.
53 ered by i.v. injection 1 hr post-spinal-cord crush injury in an effort to prevent inflammatory angiog
54   Remyelinated axons were evident 20 d after crush injury in control mice, yet were largely absent in
55       Furthermore, following a sciatic nerve crush injury in male mice, local NMIIi2 administration t
56 mmation and regeneration after sciatic nerve crush injury in mice.
57  after recovery from atrophy evoked by nerve crush injury in mice.
58 regeneration, using a model of sciatic nerve crush injury in mice.
59 administration improves axon densities after crush injury in neonatal cords.
60                                Sciatic nerve crush injury in rats induced expression of the ER chaper
61 tion, acute kidney injury by gentamicin, and crush injury in spinal cord cells.
62 rograde signaling in response to optic nerve crush injury in vivo.
63                                  Optic nerve crush injury induced RGC death as expected, demonstrated
64 ronal death in Nf1+/- mice after optic nerve crush injury is also attenuated by rolipram treatment in
65                 Optic nerve trauma caused by crush injury is frequently used for investigating experi
66 nal regrowth into the distal zone of a nerve crush injury is not markedly impaired in cyclin D1-/- mi
67                                  Optic nerve crush injury leads to rapid elevation of DLK protein, fi
68 when combined with retro-orbital optic nerve crush injury, lengthy growth of severed retinal ganglion
69                                        After crush injury, LRP-1 is lost from the axoplasm and substa
70                         However, optic nerve crush injury-mediated retinal ganglion cell loss evokes
71                Similarly, in the optic nerve crush injury model, MAB228 and AG490 neutralizes dominan
72 ound injured nerves in a mouse sciatic nerve crush injury model, the dExo-loaded pDNH group significa
73                         By using optic nerve crush injury models, recent studies have revealed the ce
74                           In a sciatic nerve crush injury mouse model, we found that phentolamine tre
75  Wistar rats (n=26) underwent either carotid crush injury (mural thrombosis model) or embolic stroke
76 ), myonecrosis due either to polymyositis or crush injuries (n = 12), and septic shock (n = 6); resul
77 his zebrafish TREE target gene expression to crush injuries of neonatal, but not adult, murine spinal
78 om neuronal tissue lysates after spinal cord crush injury of mice.
79 wine model, atherosclerosis was developed by crush injury of one carotid and one femoral artery and i
80 n effects of the growth factor artemin after crush injury of the dorsal spinal nerve roots in rats.
81                       Following a unilateral crush injury of the right trigeminal root, escape behavi
82                         Following unilateral crush injury of the right trigeminal root, HRP labeling
83                             Deceleration and crushing injuries of the chest may traumatize the thorac
84                       Mice received complete crush injury or control laminectomy at either thoracic l
85 ognition of potential complications, such as crushing injuries or nerve damage, must be sought.
86 -induced ocular hypertension and optic nerve crush injury paradigms.
87 ing with or without a right atrial free wall crush injury, respectively.
88 of MMP-9-PEX into sciatic nerves, 24 h after crush injury, robustly increased phosphorylation of ERK1
89                               In response to crush injury, sciatic nerves in scLRP1(-/-) mice showed
90 t of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin genes,
91  cell body to axon predominantly after nerve crush injury, suggesting that it encodes a growth-associ
92 ofile of laser ablation is more similar to a crush injury than the precision removal of individual ce
93                        Following optic nerve crush injury, the mpz:egfp transgene was strongly up-reg
94                            After dorsal root crush injury, the ROCKII(-/-) mice recovered use of the
95 overy occurred in mice after a sciatic nerve crush injury, there was little return of motor function
96           Within 3 days after an optic nerve crush injury to one eye, primary transcript levels of NF
97   Although remote tissue ischemia, such as a crush injury to the hindlimb, may result in P-selectin-m
98                                        After crush injury to the optic nerve, elevated intraocular pr
99 s were generated and subjected to unilateral crush injury to the sciatic nerve.
100                          Here we show that a crush injury to the spinal cord in neonatal mice leads t
101                        One day sciatic nerve crush injury triggered a robust increase in UPR-associat
102                                Sciatic nerve crush injury triggers sterile inflammation within the di
103                                              Crush injury up-regulates kon expression downstream of N
104            Using an infraorbital optic nerve crush injury, we show that reducing beta-catenin-depende
105                                  Spinal cord crush injuries were produced at T9 in two inbred strains
106                                              Crush injuries were produced at the T8 level by using an
107 a high trauma score after earthquake-related crush injury were more likely to remain dialysis-depende
108 n in the dorsal horn reverts to normal after crush injury when regeneration occurs but persists after
109                    Except in one instance of crush injury with progressive intracerebral damage, and
110 ession profiles during development and after crush injury with those of Egr2Lo/Lo Schwann cells revea
111 ured motor neurons, here, we show that after crush injury within the adult murine nervous system of w

 
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