ライフサイエンスコーパス: sensory neuropathy

1 unrelated patients with hereditary motor and sensory neuropathy.

2 nt with a severe, early-onset proprioceptive sensory neuropathy.

3 intact animals, was absent after large-fiber sensory neuropathy.

4 nced grade 2, and none experienced grade 3/4 sensory neuropathy.

5 levant therapeutic target for HIV-associated sensory neuropathy.

6 increased insulin sensitivity, and previous sensory neuropathy.

7 ompounds that may prevent development of the sensory neuropathy.

8 d were fatigue, constipation, and peripheral sensory neuropathy.

9 nausea or vomiting, headache, and transient sensory neuropathy.

10 ot genotype-specific in hereditary motor and sensory neuropathy.

11 Tooth disease, a severe hereditary motor and sensory neuropathy.

12 prague-Dawley rat strain with an early onset sensory neuropathy.

13 thy with associated radiculopathy and distal sensory neuropathy.

14 nic hyperglycemia results in a predominantly sensory neuropathy.

15 is, manifested clinically as a predominantly sensory neuropathy.

16 or days of therapy and a chronic, cumulative sensory neuropathy.

17 disabling neuropathic pain disorder due to a sensory neuropathy.

18 y contribute to the pathogenesis of diabetic sensory neuropathy.

19 Total dose is limited by development of a sensory neuropathy.

20 hereditary spastic paraplegia and hereditary sensory neuropathy.

21 s potentially efficacious for human diabetic sensory neuropathy.

22 g cells may contribute to the HIV-associated sensory neuropathy.

23 ratory chain and function and resulting in a sensory neuropathy.

24 the invariant presence of a prominent axonal sensory neuropathy.

25 n degeneration in multiple myotomes, without sensory neuropathy.

26 ), which has been associated with hereditary sensory neuropathy.

27 e, and three had a progressive age-dependent sensory neuropathy.

28 ative sensory testing were consistent with a sensory neuropathy.

29 from physiological and structural indices of sensory neuropathy.

30 ediabetic and develop insulin resistance and sensory neuropathy.

31 icantly mitigating oxaliplatin-induced acute sensory neuropathy.

32 in prediabetic mice while protecting against sensory neuropathy.

33 th a dominantly inherited late-onset painful sensory neuropathy.

34 Eleven patients developed grade 3 sensory neuropathy.

35 ebrile seizures and recently (5) small fibre sensory neuropathy.

36 (CMT1C) is a dominantly inherited motor and sensory neuropathy.

37 of cisplatin chemotherapy causes substantial sensory neuropathy.

38 a musculorum (dt) mice results in hereditary sensory neuropathy.

39 trategy for attenuating cisplatin-associated sensory neuropathy.

40 te the importance of this model for study of sensory neuropathy.

41 e may be the initiating event in HIV-induced sensory neuropathy.

42 uninfected patients or HIV patients without sensory neuropathy.

43 complement-targeted therapeutics to mitigate sensory neuropathies.

44 linated, but not myelinated nerve fibres, in sensory neuropathies.

45 le of disrupted ErbB signaling in peripheral sensory neuropathies.

46 fore an excellent model for human hereditary sensory neuropathies.

47 e beneficial in the treatment of large-fiber sensory neuropathies.

48 ic insights into potential etiologies of CMT sensory neuropathies.

49 lications for pain sensitivity in peripheral sensory neuropathies.

50 es and in 1 patient because of a generalized sensory neuropathy; 1 patient refused to continue taking

51 hronic idiopathic axonal polyneuropathy (125 sensory neuropathy, 100 sensory-motor neuropathy) from o

52 vomiting (13%), nausea (11%), and peripheral sensory neuropathy (11%) in arm A, and diarrhea (33%), f

53 included grade 4 neutropenia (24%), grade 3 sensory neuropathy (11%), and grade 4 febrile neutropeni

54 21%), thrombocytopenia (14%), and peripheral sensory neuropathy (12%).

55 treatment-related events included peripheral sensory neuropathy (14%), fatigue/asthenia (13%), myalgi

56 ded neutropenia (24% versus 35%), peripheral sensory neuropathy (17% versus 8%), and anemia (16% vers

57 Grade 3/4 treatment-related sensory neuropathy (21% v 0%), fatigue (9% v 3%), and ne

58 ), febrile neutropenia (35%), and peripheral sensory neuropathy (24%).

59 %), as well as a higher rate of grade 2 to 4 sensory neuropathy (26% vs. 18%); however, they had a lo

60 patients), rash (5 patients), and peripheral sensory neuropathy (3 patients).

61 patients), rash (2 patients), and peripheral sensory neuropathy (3 patients).

62 /vomiting (5%), myalgia/arthralgia (3%), and sensory neuropathy (3%).

63 bocytopenia, 2% and 15%; anemia, 5% and 11%; sensory neuropathy, 3% and 0.8%; fatigue, 5% and 12%; pe

64 related adverse events (AEs) were peripheral sensory neuropathy (30%), peripheral edema (16%), and fa

65 v 25.8%), febrile neutropenia (4.1% v 1.4%), sensory neuropathy (4.1% v 0%), and alopecia (grade 1 or

66 y common groups such as hereditary motor and sensory neuropathy (40/100,000) and mitochondrial disord

67 usion-related reaction (45%), and peripheral sensory neuropathy (44%).

68 nd pyrexia (52% each), nausea and peripheral sensory neuropathy (48% each), and dyspnea (40%) were th

69 , fatigue (6.8% versus 4.5%), and peripheral sensory neuropathy (5.1% versus 2.1%) were more common w

70 ia (2.7% v 3.6%), fatigue (7.9% v 3.4%), and sensory neuropathy (5.5% v 0%).

71 rgent adverse events (TEAEs) were peripheral sensory neuropathy (50%), peripheral edema (32%), and na

72 Common treatment-related toxicities included sensory neuropathy (53%), fatigue (50%), and neutropenia

73 ogic and hematologic, including grade 1 to 2 sensory neuropathy (55%), grade 3 to 4 neutropenia (35%)

74 lated adverse events (TRAEs) were peripheral sensory neuropathy (55.6%), fatigue (51.1%), and alopeci

75 es with HSAN I, 60 individuals with sporadic sensory neuropathy, 6 HSAN II families, 20 Charcot-Marie

76 Peripheral sensory neuropathy (69%), anorexia (63%), nausea (56%),

77 the most common grade >=3 AE was peripheral sensory neuropathy (7%).

78 The most common AEs were peripheral sensory neuropathy (78%), fatigue (44%), and nausea (44%

79 e most common adverse events were peripheral sensory neuropathy (79%), neutropenia (76%), fatigue (74

80 Most common toxicities included sensory neuropathy (80%) and fatigue (64%), with only 27

81 ild to moderate, the most common being acute sensory neuropathy (85%).

82 he brentuximab vedotin group were peripheral sensory neuropathy (94 [56%] of 167 patients vs 25 [16%]

83 sly uncharacterized complex axonal motor and sensory neuropathy accompanied by severe nonprogressive

84 equired that patients have grade 1 or higher sensory neuropathy according to the NCI Common Terminolo

85 found between groups; only grade 2 or higher sensory neuropathy adverse events persisted at 24 months

86 Sensory neuropathy (all grade 1-3) was recorded in 17 (9

87 ions could underlie a fraction of idiopathic sensory neuropathies also diagnosed as chronic idiopathi

88 ing, and potential therapeutic treatment, of sensory neuropathies and a number of neurological diseas

89 n and most frequent of a group of congenital sensory neuropathies and is characterized by widespread

90 he field of axonal CMT and have relevance to sensory neuropathies and motor neuron disorders.

91 tential pathway to therapeutically target in sensory neuropathies and to further explore in other neu

92 ital insensitivity to pain (CIP), hereditary sensory neuropathies and, if autonomic nerves are involv

93 nful neuropathy and 28 without pain, 26 with sensory neuropathy and 24 with sensory and motor neuropa

94 Mutated CCT4/5 subunits cause sensory neuropathy and CCT5 expression is decreased in A

95 A triad of hearing loss, sensory neuropathy and cognitive decline remains as the

96 of three patients experienced a DLT (grade 3 sensory neuropathy and febrile neutropenia).

97 ns were identified in 43 patients (34%) with sensory neuropathy and in none with sensory-motor neurop

98 xanes; such a neuropathy usually presents as sensory neuropathy and is more common with paclitaxel th

99 Sensory neuropathy and neutropenia were more common with

100 Sensory neuropathy and neutropenia were significantly mo

101 eutropenia was 2.3%, and the rate of grade 3 sensory neuropathy and of grade 3 motor neuropathy was 0

102 y adult-onset retinitis pigmentosa, anosmia, sensory neuropathy and phytanic acidaemia.

103 (-/-) mice as an animal model of small fiber sensory neuropathy and provide new insight regarding the

104 ation of results from STZ models of diabetic sensory neuropathy and strongly argues that more refined

105 n important pathogenetic role in nociceptive sensory neuropathy and that C-peptide replacement may be

106 T was grade 3 pharyngolaryngeal dysesthesia, sensory neuropathy, and ataxia at 160 mg/m2.

107 de 3 events of neutropenia (14%), peripheral sensory neuropathy, and hyperkalemia (9% each).

108 n adverse events were fatigue, constipation, sensory neuropathy, and infection; there was no treatmen

109 ea, diarrhea, anorexia, vomiting, peripheral sensory neuropathy, and keratitis/keratopathy.

110 ade 3 hypothyroidism, and grade 3 peripheral sensory neuropathy, and one case of grade 4 pneumonitis.

111 icities included myelosuppression, vomiting, sensory neuropathy, and ototoxicity and were worse with

112 l mechanism for dideoxynucleoside-associated sensory neuropathy, and questions arise about enhanced r

113 s and were characterized by cough, asthenia, sensory neuropathy, anorexia, serum sickness, and hypert

114 Hereditary sensory neuropathies are a class of disorders marked by

115 Late-onset painful sensory neuropathies are usually acquired conditions ass

116 as diabetic and human immunodeficiency virus sensory neuropathies) are characterized by distal axonal

117 c repeat expansions in RFC1 and identify the sensory neuropathy as a common feature in all cases to d

118 ognitive disorders, vacuolar myelopathy, and sensory neuropathies associated with HIV are the most co

119 The sensory neuropathies associated with HIV infection are a

120 he SLC12A6 gene, causes hereditary motor and sensory neuropathy associated with agenesis of the corpu

121 ogical disease (brainstem encephalopathy and sensory neuropathy being common extracerebellar manifest

122 FGFR3 antibodies have been associated with sensory neuropathy, but many questions remain regarding

123 1 (GDAP1) cause severe peripheral motor and sensory neuropathies called Charcot-Marie-Tooth disease.

124 Chronic sensory neuropathy can be dose limiting and may have det

125 monoallelic early-onset hereditary motor and sensory neuropathy caused by de novo mutations, to late-

126 is an uncommon form of hereditary motor and sensory neuropathy caused by mutations in the P(0) myeli

127 T4B) is a demyelinating hereditary motor and sensory neuropathy characterized by abnormal folding of

128 s hereditary motor neuropathy and hereditary sensory neuropathy, collectively termed CMT, are the com

129 , we present the first evidence that chronic sensory neuropathy depends on nonlinear interactions bet

130 athogenic mutations for hereditary motor and sensory neuropathy, distal hereditary motor neuropathy,

131 nosis gene TPP1 and the hereditary motor and sensory neuropathy DNMT1 gene, highlighting the genetic

132 autosomal-dominant disorder that leads to a sensory neuropathy due to mutations in the serine palmit

133 ients), hypokalaemia (six [33%]), peripheral sensory neuropathy (five [28%]), diarrhoea (five [28%]),

134 de 3 or worse adverse events were peripheral sensory neuropathy (four [10%] of 41 patients), neutrope

135 ht [17%] of 48 in the RVd-elotuzumab group), sensory neuropathy (four [8%] of 52 in the RVd group, si

136 of 45), anaemia (five [11%]), and peripheral sensory neuropathy (four [9%]).

137 Peripheral sensory neuropathy grade 3 occurred in two patients trea

138 atients experienced more frequent and severe sensory neuropathy (grade 1 to 4; 8% v 30%).

139 a (9%); 44% had treatment-related peripheral sensory neuropathy (grade 1/2, 40%; grade 3, 4%).

140 fect large nerve fibers; painful small fiber sensory neuropathy has not previously been described in

141 HIV-associated sensory neuropathy (HIV-SN) is currently the most common

142 uman immunodeficiency virus (HIV)-associated sensory neuropathy (HIV-SN) is difficult but needed for

143 uman immunodeficiency virus (HIV)-associated sensory neuropathy (HIV-SN) is the most common neurologi

144 t in human immunodeficiency virus-associated sensory neuropathy (HIV-SN), damaged mtDNA accumulates i

145 me 17p11.2 duplication (hereditary motor and sensory neuropathy-HMSN Ia).

146 The autosomal dominant peripheral sensory neuropathy HSAN1 results from mutations in the L

147 motor neuropathy (HMN, 9.2%), 93 hereditary sensory neuropathy (HSN, 6.1%), 38 sensory ataxic neurop

148 sities in 35 patients confirmed pretreatment sensory neuropathy in 20% and new or worsening neuropath

149 (day 21), consistent with the development of sensory neuropathy in SIV-infected macaques.

150 Febrile neutropenia and sensory neuropathy incidences were similar across groups

151 cy of neurotrophic or regenerative drugs for sensory neuropathies including those caused by HIV, diab

152 compasses axonal and demyelinating motor and sensory neuropathies, including four young patients pres

153 Small fiber sensory neuropathy is a common disorder in which progres

154 HIV-associated sensory neuropathy is a common neurologic comorbidity of

155 IGNIFICANCE STATEMENT Painful HIV-associated sensory neuropathy is a neurological complication of HIV

156 We hypothesized that diabetic sensory neuropathy is associated with activation of apop

157 The painful sensory neuropathy is associated with the use of dideoxy

158 any time, but early in the IBD course, pure sensory neuropathy is more common.

159 jority of patients, the cause of small fiber sensory neuropathy is unknown, and treatment options are

160 eripheral nervous system diseases, including sensory neuropathies, is unclear.

161 they ensheath cause the hereditary motor and sensory neuropathies known as Charcot-Marie-Tooth (CMT)

162 CMT sensory neuropathies lead to impaired peripheral sensiti

163 febrile neutropenia (9%, 3%, 3%; P < .001), sensory neuropathy (< 1%, 7%, 6%; P < .001), and diarrhe

164 nduced by streptozotocin (STZ) resulted in a sensory neuropathy manifest by a decrease in the foot se

165 tment-related adverse events were peripheral sensory neuropathy, nausea, fatigue, neutropenia, and di

166 Since a sensory neuropathy/neuronopathy is identified in all pat

167 e patient in the 1.5 mg/m2 group had grade 3 sensory neuropathy; no grade 3 sensory neuropathy was se

168 Resolution of grade 3/4 peripheral sensory neuropathy occurred after a median period of 5.4

169 Grade 3 sensory neuropathy occurred in 14% of patients, and 22.7

170 lecular genetics of the hereditary motor and sensory neuropathies of autosomal dominant and X-linked

171 The concept of a severe motor-sensory neuropathy of acute onset caused by an immune at

172 hy some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet

173 ed to those of type III hereditary motor and sensory neuropathy or Dejerine-Sottas disease.

174 toplasmic dynein can either result in a pure sensory neuropathy or in a sensory neuropathy with motor

175 cent of RFC1-positive patients had isolated sensory neuropathy or sensory neuropathy with chronic co

176 Sensory neuropathy persisted more often after chemoradio

177 ollow-up of the treatment-related peripheral sensory neuropathy (PSN) showed a significant decrease o

178 HIV-associated sensory neuropathy remains the most common neurological

179 Our study indicates a prominent sensory neuropathy resulting from periaxin gene mutation

180 interventions in preclinical models modulate sensory neuropathy, retinopathy, tumor growth, and muscl

181 lkan Gypsies and termed hereditary motor and sensory neuropathy-Russe (HMSN-R).

182 fects contributing to hearing loss and other sensory neuropathies.SIGNIFICANCE STATEMENT P2X(7) recep

183 e for the important complication of diabetic sensory neuropathy, since hyperglycemia for longer than

184 uman immunodeficiency virus (HIV)-associated sensory neuropathy (SN) is the most common neurological

185 Sensory neuropathy symptoms were more prominent than wer

186 spectively examined the relationship between sensory neuropathy symptoms, falls, and fall-related inj

187 Of the sensory neuropathy symptoms, numbness and tingling were

188 ng side effect of paclitaxel is a peripheral sensory neuropathy that can last days to a lifetime.

189 type, SIMPLE develop a late-onset motor and sensory neuropathy that recapitulates key clinical featu

190 fatigue, depressed consciousness, dizziness, sensory neuropathy, tremor, constipation, dyspnea, hypox

191 Hereditary sensory neuropathy type 1 (HSN1) is a dominantly inherit

192 Hereditary sensory neuropathy type 1 (HSN1) is a rare, slowly progr

193 Hereditary sensory neuropathy type 1 (HSN1, MIM 162400) genetically

194 ed 1-deoxySLs are associated with hereditary sensory neuropathy type 1 and diabetic neuropathy, but t

195 Hereditary sensory neuropathy type 1 is an autosomal-dominant disor

196 ng hereditary spastic paraplegia, hereditary sensory neuropathy type 1, and non-5q spinal muscular at

197 mapped to this region, including hereditary sensory neuropathy type 1, self-healing squamous epithel

198 tly inactivate SPT similar to the hereditary sensory neuropathy type 1-like mutations in Lcb1p.

199 at encodes for SPT subunits cause hereditary sensory neuropathy type 1.

200 palmitoyltransferase (SPT), cause hereditary sensory neuropathy type I .

201 esidues that are mutated to cause hereditary sensory neuropathy type I reside in a highly conserved r

202 Hereditary sensory neuropathy type IA (HSN1A) is a rare neurodegene

203 lar atrophy (SPSMA) and hereditary motor and sensory neuropathy type IIC (HMSN IIC, also known as HMS

204 for which is duplicated in hereditary motor sensory neuropathy type la, can also induce EAN.

205 has been designated as hereditary motor and sensory neuropathy type VI (HMSN VI).

206 ggest that that systemic VCR exposure caused sensory neuropathy via sex-dimorphic mechanisms, leading

207 The severity of the resultant sensory neuropathy was compared with behavioral, physiol

208 r in both arms, as was grade 3 rash, whereas sensory neuropathy was higher in the concurrent arm (15%

209 Sensory neuropathy was identified in nine patients (medi

210 Sensory neuropathy was mild with grade 3 neurotoxicity r

211 Grade 3 sensory neuropathy was more common in the ABI-007 arm th

212 Grade 2 or 3 sensory neuropathy was present in 10 patients (53%) over

213 p had grade 3 sensory neuropathy; no grade 3 sensory neuropathy was seen in the 1.3 mg/m2 group.

214 Sensory neuropathy was seen more commonly than motor axo

215 Sensory neuropathy was the only manifestation in 15 pati

216 Minimal hematologic toxicity and no grade 3 sensory neuropathy were noted.

217 nausea, fatigue, arthralgias, and peripheral sensory neuropathy, were mild to moderate and matched th

218 patients had isolated sensory neuropathy or sensory neuropathy with chronic cough, while vestibular

219 In 4 infants with a new lethal autonomic sensory neuropathy with clinical features similar to fam

220 ith autosomal-recessive hereditary motor and sensory neuropathy with corpus callosum agenesis and men

221 disease, from biallelic hereditary motor and sensory neuropathy with corpus callosum agenesis and men

222 result in a pure sensory neuropathy or in a sensory neuropathy with motor neuron involvement.

223 awling (Swl) mutation display an early-onset sensory neuropathy with muscle spindle deficiency.

224 tive diseases including hereditary motor and sensory neuropathy with proximal dominant involvement (H

225 We produced a dose-dependent large-fiber sensory neuropathy, without detrimental effects on gener