ライフサイエンスコーパス: nerve damage

1 of neurological injury, including stroke and nerve damage.

2 disease progression resulting in less severe nerve damage.

3 ed for any potential correlation with facial nerve damage.

4 e mouse eye increases IOP and leads to optic nerve damage.

5 ntribute to abnormal sensations arising from nerve damage.

6 ere less likely to have postoperative facial nerve damage.

7 lators of the SC regenerative response after nerve damage.

8 tional recovery in patients after peripheral nerve damage.

9 e regeneration and recovery after peripheral nerve damage.

10 essure is associated with glaucomatous optic nerve damage.

11 essure elevations in eyes with minimal optic nerve damage.

12 anslatable therapy to restore function after nerve damage.

13 ute to cellular reorganization after sciatic nerve damage.

14 e patient's condition and to prevent further nerve damage.

15 nd is upregulated following inflammation and nerve damage.

16 perreflexia observed after SCI or peripheral nerve damage.

17 peripheral noxious stimuli, tissue injury or nerve damage.

18 nd spermatic duct function after sympathetic nerve damage.

19 significant axon growth across a site of CNS nerve damage.

20 with clinical symptoms that imply selective nerve damage.

21 s that they innervated both before and after nerve damage.

22 mechanism for Schwann differentiation after nerve damage.

23 coma, all treated eyes had significant optic nerve damage.

24 sease, stroke, kidney failure, blindness and nerve damage.

25 pathic pain is a debilitating consequence of nerve damage.

26 an increased risk of developing glaucomatous nerve damage.

27 ing both phases, and all had extensive optic nerve damage.

28 be bilaterally blind from irreversible optic-nerve damage.

29 ositively correlated with glaucomatous optic nerve damage.

30 specially in patients with preexisting Optic Nerve damage.

31 then tested for their response to peripheral nerve damage.

32 n by early interventions such as receptor or nerve damage.

33 ors in the development of glaucomatous optic nerve damage.

34 uffers from nerve degeneration or peripheral nerve damage.

35 present with different degrees of accessory nerve damage.

36 ppropriate with the lowest risk of articular nerve damage.

37 GA may cause gastrointestinal discomfort and nerve damage.

38 lower vulnerability to esophageal or phrenic nerve damage.

39 es, and neuropathic pain, which is caused by nerve damage.

40 llowed by numbness resulting from peripheral nerve damage.

41 intraocular pressure (IOP) and gradual optic nerve damage.

42 such as intraocular pressure (IOP) and optic nerve damage.

43 r treatment often results in regrowth and/or nerve damage.

44 eased in number for at least two months post-nerve damage.

45 in sensory neurons in response to peripheral nerve damage.

46 o spared peripheral inputs following sensory nerve damage.

47 ize the earliest events of M. leprae-induced nerve damage.

48 rounding either moderate or massive auditory nerve damage.

49 novel, clinically suitable strategy to treat nerve damage.

50 urrently, no clear measures can reduce brain nerve damage.

51 cose elevation, inflammation and even severe nerve damage.

52 y ablation, and there is a trend toward less nerve damage.

53 n preserved the RA while allowing equivalent nerve damage.

54 had no detected effect on glaucomatous optic nerve damage.

55 regenerative response of zebrafish to optic nerve damage.

56 pain, local tissue necrosis, infection, and nerve damage.

57 rates unique, irreversible macular and optic nerve damage.

58 ical modification associated with peripheral nerve damage.

59 ly to prevent or reduce progression of optic nerve damage.

60 in aged individuals recover more slowly from nerve damage.

61 ted nuclear atrophy within 1 day after optic nerve damage.

62 an result in hypoparathyroidism or laryngeal nerve damage.

63 DAMTS10 before clinical indications of optic nerve damage.

64 nuclei undergo the AVD in response to optic nerve damage.

65 acteristics associated with IOP elevation or nerve damage.

66 n accompanied by advanced glaucomatous optic nerve damage.

67 % CI, 0.5%-1.7%]), and nonglaucomatous optic nerve damage (4 individuals [0.7% of those with moderate

68 therapeutic targets, specifically to control nerve damage, a prominent feature of leprosy that has no

69 and can explain both macular holes and optic nerve damage after ocular PBI.

70 However, the incidence of facial nerve damage after TAB is unknown.

71 in D1 (NPD1) and the regeneration of corneal nerves damaged after surgery.

72 Nerve damage although not statistically different betwee

73 Endothelin (ET)-1 can produce nerve damage analogous to that in optic neuropathies suc

74 The extent of nerve damage and age at the time of injury are two of th

75 at desiccation of the corneal surface due to nerve damage and associated loss of BR severely exacerba

76 rk focused on the impact of hyperglycemia on nerve damage and bioenergetics failure, but recent evide

77 investigation of a possible contribution of nerve damage and BR loss to human HSK also appears warra

78 the plasticity that can occur in response to nerve damage and cardiorespiratory disease.

79 nfocal microscopy can identify early corneal nerve damage and change in LC density in children and ad

80 , the relationship between loss of BR due to nerve damage and corneal pathology associated with HSK r

81 Optic nerve damage and death of ganglion cells in the retina w

82 isease progression, and mitigate the risk of nerve damage and disabilities to achieve the WHO goal 'T

83 We assessed optic nerve damage and fovea morphometry by optical coherence

84 es more vulnerable to pressure-induced optic nerve damage and glaucoma development and progression.

85 copy (CCM) has been used to identify corneal nerve damage and increased Langerhans cell (LC) density

86 Vincristine administration induced severe nerve damage and mechanical hypersensitivity that were a

87 er brain and spinal cord disorders involving nerve damage and neuronal cell loss.

88 f ErbB2 RTK-based therapies for both leprosy nerve damage and other demyelinating neurodegenerative d

89 r the actual infectious threat, resulting in nerve damage and permanent disability.

90 traocular pressure (IOP), which causes optic nerve damage and retinal ganglion cell death, is the pri

91 tly increased the number of DBA/2J eyes with nerve damage and RGC loss at an early time point after I

92 fast-to-slow fibre type shift in response to nerve damage and stimulation, but no complete conversion

93 alysis (HD) could lead to glaucomatous optic nerve damage and subsequent visual loss.

94 There was no correlation with facial nerve damage and use of blood thinners, biopsy result, s

95 t public health issue that it leads to optic nerve damage and vision loss.

96 angle glaucoma (POAG) with significant optic nerve damage and visual field loss despite multiple medi

97 disease characterized by irreversible optic nerve damage and visual field loss that leads to visual

98 An OAG was determined based on optic nerve damage and visual field loss.

99 onomic status is associated with worse optic nerve damage and visual field performance at presentatio

100 in expression of PKC betaII contributing to nerve damage, and changes in PKC alpha being a consequen

101 eading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis l

102 t involve retinal ganglion cell death, optic nerve damage, and loss of visual field.

103 ropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups.

104 bnormality, to identify site and severity of nerve damage, and to potentially elucidate mechanisms of

105 ma, macular edema, retinal detachment, optic nerve damage, and vision loss.

106 cular pressure >21 mm Hg, glaucomatous optic nerve damage, and/or glaucomatous visual field loss.

107 muscle, membrane, and humor disorders; optic nerve damage; and eyelid affections.

108 ropathy (DPN) is length-dependent peripheral nerve damage arising as a complication of type 1 or type

109 ere visual dysfunction may result from optic nerve damage as well as from amblyopia arising from anis

110 d given the amount of identifiable tissue or nerve damage, as well as other CNS-derived symptoms, suc

111 efined as the presence of glaucomatous optic nerve damage, associated visual field loss, and elevated

112 the use of OCTA to detect early glaucomatous nerve damage, associated with focal reductions in peripa

113 nal and morphological corneal nerve changes, nerve damage-associated transcriptomic signature in the

114 Infraorbital nerve damage at birth kills neurons and alters anatomica

115 ld result in barotraumatically induced optic nerve damage at the lamina cribrosa.

116 e uncovered a central role for C3 in sensory nerve damage at the morphological and functional levels.

117 lect underlying health conditions, including nerve damage, autonomic and metabolic disorders, and chr

118 an adequate IOP to prevent progressive optic nerve damage, avoiding complications, and preserving vis

119 In contrast to peripheral nerves, damaged axons in the mammalian brain and spinal

120 isons of eyes with different levels of optic nerve damage, based on cup- disc ratio, showed that the

121 to T cell-deficient mice reproduced corneal nerve damage but not epitheliopathy.

122 In nerves damaged by stretching or drying, K+ pulses caused

123 Nerve damage can cause chronic, debilitating problems in

124 Mice with experimental nerve damage can display long-lasting neuropathic pain b

125 Nerve damage can stimulate macrophage infiltration and i

126 istance of 1 mm to prevent inferior alveolar nerve damage caused by three connected implants.

127 In contrast, RFA leads to thermal nerve damage, causing protein denaturation, and suggests

128 noninvasively and detects earlier stages of nerve damage compared with IENF pathology.

129 lower vulnerability to esophageal or phrenic nerve damage compared with RFA.

130 tly reduced the loss of RGCs, lessened optic nerve damage, decreased the number of TUNEL-positive cel

131 human pathogen Mycobacterium leprae, causes nerve damage, deformity and disability in over 200,000 p

132 is dramatically induced in DRG neurons after nerve damage, despite low expression in developing DRG n

133 Glaucomatous optic nerve damage developed in 23% versus 6% (P<0.001) of imp

134 ence, neuroinflammation in PD and peripheral nerve damage due to inflammation in T1R share overlappin

135 f chronic pain that can result from physical nerve damage due to surgery or entrapment.

136 In order to detect glaucomatous optic nerve damages early on and evaluate the severity of glau

137 of acute inflammatory episodes that lead to nerve damage, even after the infecting organisms have be

138 Patients suffering from neuropathic pain, or nerve damage, experience an inversion in the daily modul

139 oA signaling pathway may contribute to optic nerve damage following non-arteritic anterior ischemic o

140 This mechanism could explain the lack of nerve damage from recurrent HSV infection and may provid

141 life, which potentially could lead to optic nerve damage, globe enlargement, and permanent loss of v

142 etiologies, such as local infection, trauma, nerve damage, glossitis, or the enigmatic neuropathic pa

143 s generally diagnosed late when irreversible nerve damage has already taken place.

144 isms involved in noise-induced hair-cell and nerve damage has substantially increased, and preventive

145 However, mechanisms of nerve damage have not been elucidated because of the lac

146 patients with asymmetric glaucomatous optic nerve damage, IL-8 concentration was higher in the AH of

147 late atrophy, initiated either by peripheral nerve damage, immobilization, aging, catabolic steroids,

148 mality and/or evidence of glaucomatous optic nerve damage in >/=1 eye.

149 C3/CD4 T cell axis triggered corneal sensory nerve damage in a mouse model of ocular graft-versus-hos

150 the retina causes glial activation and optic nerve damage in animal models in a manner similar to tha

151 accurate correlation of IOP history to optic nerve damage in animals housed in a light- dark environm

152 and visual field loss consistent with optic nerve damage in at least one eye of the proband.

153 The most critical risk factor for optic nerve damage in cases of primary open-angle glaucoma (PO

154 lar desiccation triggers superficial corneal nerve damage in DED, but proximal propagation of axonal

155 ral nerve microcirculation may contribute to nerve damage in diabetic polyneuropathy (DN).

156 hypotheses regarding hyperglycemia-mediated nerve damage in DN.

157 Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of th

158 s should be considered when evaluating optic nerve damage in experimental laser-induced glaucoma in t

159 contribute to perceptual deficits induced by nerve damage in humans.

160 d IOPs were correlated with quantified optic nerve damage in injected eyes.

161 espite its being a major cause of peripheral nerve damage in leprosy patients, the immunopathogenesis

162 plex disease pathogenesis, the management of nerve damage in leprosy, as in other demyelinating disea

163 flammatory episodes and main contributors to nerve damage in leprosy.

164 n and suggests possible strategies to combat nerve damage in leprosy.

165 s (T1R), are a main contributor to permanent nerve damage in leprosy.

166 macrophages to M. leprae PGL-1 in initiating nerve damage in leprosy.

167 ing central circuitry for vision after optic nerve damage in mature mammals.

168 To evaluate optic nerve damage in mice after laser-induced ocular hyperten

169 s (RGCs) using in vivo models of acute optic nerve damage in mice and rats.

170 r complement in CD4 T cell-dependent corneal nerve damage in multiple disease settings and indicate t

171 c cytotoxicity pathways were dispensable for nerve damage in NOD-B7-2KO mice.

172 The optic nerve damage in nonarteritic anterior ischemic optic neu

173 This study investigated whether peripheral nerve damage in patients with leprosy impairs local cell

174 We have investigated presence of peripheral nerve damage in patients with severe obesity without typ

175 sTNT is a potential indicator for structural nerve damage in T2D.

176 at microangiopathy contributes to structural nerve damage in T2D.

177 ause increased intraocular pressure or optic nerve damage in the C57BL/6J genetic background.

178 Sensory dysfunction due to nerve damage in the foraminal area can occur if the infe

179 roup (P=0.36), there was a trend toward less nerve damage in the irrigated compared with conventional

180 bidity secondary to intraoperative accessory nerve damage, inadvertent injury still often occurs.

181 In areas associated with nerve damage, increased levels of the endocannabinoids,

182 levels increase during neuropathic pain, and nerve damage-induced allodynia is reduced in Epac1-/- mi

183 n in the mouse eye sufficient to cause optic nerve damage induces preferential loss of superior optic

184 Nerve damage is a clinical hallmark of leprosy and a maj

185 del of ocular HSV-1 infection, where sensory nerve damage is a common clinical problem.

186 Evaluation of structural optic nerve damage is a fundamental part of diagnosis and mana

187 Corneal nerve damage is a known component of HSK, but the causes

188 omplete or delayed recovery after peripheral nerve damage is a major health concern in the aging popu

189 sely resembles typical human HSK and suggest nerve damage is an important but largely overlooked fact

190 ing regeneration, the clinical outcome after nerve damage is frequently poor.

191 major consequences of neonatal infraorbital nerve damage is irreversible morphological reorganizatio

192 We further show that nerve damage is reversible and regulated by CD4(+) T cel

193 Nerve damage is the hallmark of Mycobacterium leprae inf

194 raised intraocular pressure (IOP) and optic nerve damage leading to loss of sight.

195 ) exporter channel KCC2 following peripheral nerve damage, leading to increased excitability.

196 after nerve regeneration and may explain how nerve damage leads to chronic pain conditions.

197 At lower levels of nerve damage (lumbar back pain with disc herniation) ass

198 We sought to determine whether early nerve damage may be detected by corneal confocal microsc

199 bility and/or pathophysiologic mechanisms of nerve damage may differ between autonomic and sensory ne

200 Thus, absence of motor recovery after nerve damage may result from a failure of synapse reform

201 mprove visual fields in hemianopia and optic nerve damage, might comprise such a method.

202 s in later RGC death than in traumatic optic nerve damage models.

203 complications, such as crushing injuries or nerve damage, must be sought.

204 = 13), retrobulbar hemorrhage (n = 7), optic nerve damage (n = 4), vascular occlusions (n = 2), pain

205 The nerve damage occurring as a consequence of glucose toxic

206 s of retinal ganglion cells (RGCs) and optic nerve damage, often associated with elevated intraocular

207 were similar across groups with evidence of nerve damage only with radiofrequency.

208 Brain changes in response to nerve damage or cochlear trauma can generate pathologica

209 e when injured, leaving victims of traumatic nerve damage or diseases such as glaucoma with irreversi

210 neous, apparent resolution of pain caused by nerve damage or inflammation, referred to as latent sens

211 of effective medications to halt or reverse nerve damage or promote nerve regeneration, early diagno

212 lowing: darkened choroid, glaucomatous optic nerve damage, or conjunctival hyperemia.

213 Incidence of postoperative facial nerve damage, other complications, and rates of facial n

214 cular pressure and reduce the risk for optic nerve damage over the short to medium term.

215 the duration of fecal incontinence, pudendal nerve damage, patient age, symptom severity, pretreatmen

216 There was a mild median nerve damage periprocedurally that resolved in three mon

217 To identify whether tPA release after nerve damage played a beneficial or deleterious role, we

218 Corneal nerve damage produced by aging, diabetes, refractive sur

219 he causes and consequences of HSK-associated nerve damage remain obscure.

220 e contribution of this pathway to peripheral nerve damage remains poorly explored.

221 Regeneration after peripheral nerve damage requires that axons re-grow to the correct

222 Inflammation and nerve damage result in the up-regulation of TRPV1 transc

223 mimic clinical observations of patients with nerve damage resulting from spinal cord injury and are o

224 illions of patients with leprosy suffer from nerve damage resulting in disabilities as a consequence

225 eference to papers in which animal models of nerve damage resulting in urogenital dysfunction have be

226 aims to define the different types of distal nerve damage, review the anatomy and function of the mos

227 The initiating surgery and nerve damage set off a cascade of events that includes b

228 ry tract dysfunction caused by neuropathy or nerve damage, such as urinary retention or incontinence,

229 greatest at 7 days, with maximum functional nerve damage sustained </=30 days.

230 8-fold while GLUT1 was decreased 1.7-fold in nerve damaged TA.

231 Nerve damage takes place during surgery.

232 cally elevated IOP in the rat produced optic nerve damage that correlated with pressure change (r(2)

233 n (the steroid response) may result in optic nerve damage that very closely mimics the pathologic cou

234 estion of how, in glaucoma or other cases of nerve damage, the glial response can be confined to a ci

235 a possible role for the enzyme in POAG optic nerve damage through citrullination and structural disru

236 monly affected tracts, and illustrate distal nerve damage through diagrams and representative cases f

237 vity are important to consider when inducing nerve damage to create models of urinary incontinence.

238 lar level, allowing even transient tissue or nerve damage to elicit changes in cells that contribute

239 These results show that nerve damage to the CT results in central glial response

240 The specific issues of nerve damage, treatment of local anesthetic toxicity wit

241 dwide, is characterized by progressive optic nerve damage, usually associated with intraocular pressu

242 Optic nerve damage was assessed by stereoscopic slit-lamp biom

243 Optic nerve damage was assessed semiquantitatively in epoxy-em

244 al fibrillary acidic protein expression, and nerve damage was evaluated by activating transcription f

245 Postoperative facial nerve damage was found in 12 patients (16.0%) and 58.3%

246 intraocular pressure (IOP) leading to optic nerve damage was induced by episcleral injection of hype

247 intraocular pressure (IOP) leading to optic nerve damage was induced using the episcleral vein occlu

248 Quantification of optic nerve damage was performed by counting retinal ganglion

249 hydroxylase score, which assesses functional nerve damage, was significantly less after 7 (1+/-1) and

250 role this crystallin plays after peripheral nerve damage, we found that loss of alphaBC impaired rem

251 0, 60, and 90 microg BDNF at the time of the nerve damage were 52%, 81%, 77%, and 70%, respectively.

252 n, mental nerve anatomy, and consequences of nerve damage were evaluated for information pertinent to

253 essure (IOP) was involved in producing optic nerve damage when there was glaucomatous damage to the o

254 and provides objective information on optic nerve damage, which is useful for prognosis.

255 lopment of characteristic glaucomatous optic nerve damage with corresponding visual field defects.

256 ic optic neuropathy (NAION) results in optic nerve damage with retinal ganglion cell (RGC) loss.

257 is a 16.0% incidence of postoperative facial nerve damage with TABs, which recovers fully in over hal

258 sive blood biomarkers specific to peripheral nerve damage would improve management of peripheral nerv

259 the carotid artery include avoiding cranial nerve damage, wound hematoma, and general anesthesia.