ライフサイエンスコーパス: nerve damage

1 essure elevations in eyes with minimal optic nerve damage.

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

3 ute to cellular reorganization after sciatic nerve damage.

4 rounding either moderate or massive auditory nerve damage.

5 nd is upregulated following inflammation and nerve damage.

6 perreflexia observed after SCI or peripheral nerve damage.

7 peripheral noxious stimuli, tissue injury or nerve damage.

8 nd spermatic duct function after sympathetic nerve damage.

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

10 novel, clinically suitable strategy to treat nerve damage.

11 with clinical symptoms that imply selective nerve damage.

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

13 mechanism for Schwann differentiation after nerve damage.

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

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

16 pathic pain is a debilitating consequence of nerve damage.

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

18 be bilaterally blind from irreversible optic-nerve damage.

19 ositively correlated with glaucomatous optic nerve damage.

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

21 then tested for their response to peripheral nerve damage.

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

23 ors in the development of glaucomatous optic nerve damage.

24 cose elevation, inflammation and even severe nerve damage.

25 in sensory neurons in response to peripheral nerve damage.

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

27 n preserved the RA while allowing equivalent nerve damage.

28 had no detected effect on glaucomatous optic nerve damage.

29 regenerative response of zebrafish to optic nerve damage.

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

31 rates unique, irreversible macular and optic nerve damage.

32 ical modification associated with peripheral nerve damage.

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

34 in aged individuals recover more slowly from nerve damage.

35 o spared peripheral inputs following sensory nerve damage.

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

37 DAMTS10 before clinical indications of optic nerve damage.

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

39 acteristics associated with IOP elevation or nerve damage.

40 n accompanied by advanced glaucomatous optic nerve damage.

41 disease progression resulting in less severe nerve damage.

42 ed for any potential correlation with facial nerve damage.

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

44 ntribute to abnormal sensations arising from nerve damage.

45 ere less likely to have postoperative facial nerve damage.

46 lators of the SC regenerative response after nerve damage.

47 tional recovery in patients after peripheral nerve damage.

48 e regeneration and recovery after peripheral nerve damage.

49 essure is associated with glaucomatous optic nerve damage.

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

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

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

53 Nerve damage although not statistically different betwee

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Infraorbital nerve damage at birth kills neurons and alters anatomica

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

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

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

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

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

84 Nerve damage can stimulate macrophage infiltration and i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 hypotheses regarding hyperglycemia-mediated nerve damage in DN.

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

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

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

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

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

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

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

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

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

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

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

117 The optic nerve damage in nonarteritic anterior ischemic optic neu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Nerve damage is the hallmark of Mycobacterium leprae inf

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

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

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

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

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

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

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

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

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

143 The nerve damage occurring as a consequence of glucose toxic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 Nerve damage takes place during surgery.

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

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

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

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

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

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

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

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

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

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

174 Optic nerve damage was assessed semiquantitatively in epoxy-em

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

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

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

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

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

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

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

182 0, 60, and 90 microg BDNF at the time of the nerve damage were 52%, 81%, 77%, and 70%, respectively.

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

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

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

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

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