ライフサイエンスコーパス: diabetic neuropathy

1 step polyol pathway previously implicated in diabetic neuropathy.

2 EPCs could reverse various manifestations of diabetic neuropathy.

3 idemia is instrumental in the progression of diabetic neuropathy.

4 postnatal development and are implicated in diabetic neuropathy.

5 ing the same time interval as nonprogressing diabetic neuropathy.

6 eutic approach for the management of painful diabetic neuropathy.

7 ing the protection of erythropoietin against diabetic neuropathy.

8 for pain were analyzed in participants with diabetic neuropathy.

9 ast 50% of individuals with diabetes develop diabetic neuropathy.

10 oot ganglia may prove useful in treatment of diabetic neuropathy.

11 (-/-) mice supported a role for NF-kappaB in diabetic neuropathy.

12 ely diagnose and assess progression of human diabetic neuropathy.

13 terneurons, in the spinal cord is reduced in diabetic neuropathy.

14 of therapeutic intervention in patients with diabetic neuropathy.

15 trosocarbamoil]-D-glucosamine)-induced early diabetic neuropathy.

16 patients with painful compared with painless diabetic neuropathy.

17 to spinal dorsal horn neurons is altered in diabetic neuropathy.

18 contribute to the development of symptoms in diabetic neuropathy.

19 out the potential benefits of these drugs on diabetic neuropathy.

20 nerve injury, optic nerve degeneration, and diabetic neuropathy.

21 fies cellular therapeutic targets to prevent diabetic neuropathy.

22 as diagnosis and treatment of patients with diabetic neuropathy.

23 e investigation of the mechanisms leading to diabetic neuropathy.

24 lycemic control, there are no treatments for diabetic neuropathy.

25 on velocity (NCV) that are characteristic of diabetic neuropathy.

26 ne and tyrosine sites contributes to painful diabetic neuropathy.

27 els of neuropathic pain, including models of diabetic neuropathy.

28 e therapeutic potential for the treatment of diabetic neuropathy.

29 embrane depolarization in sensory neurons in diabetic neuropathy.

30 ogression of heart disease and the impact of diabetic neuropathy.

31 utonomic failure is an integral component of diabetic neuropathy.

32 e therapeutic potential for treating painful diabetic neuropathy.

33 eficient in peripheral nerve microvessels in diabetic neuropathy.

34 in the polyol pathway to the pathogenesis of diabetic neuropathy.

35 s out promise for the effective treatment of diabetic neuropathy.

36 icrovascular ischemia in the pathogenesis of diabetic neuropathy.

37 us stimuli that may model aspects of painful diabetic neuropathy.

38 tributes to neuropathic pain associated with diabetic neuropathy.

39 chanical hyperalgesia is an early symptom of diabetic neuropathy.

40 r endothelial TM expression throughout human diabetic neuropathy.

41 vector may prove useful in the treatment of diabetic neuropathy.

42 on's disease, dementia with Lewy bodies, and diabetic neuropathy.

43 ve approach for reversal of, at least, early diabetic neuropathy.

44 inal inhibitory dysfunction in human painful diabetic neuropathy.

45 g gabapentin therapy for chronic pain due to diabetic neuropathy.

46 of Bax nor levels of Bcl-XL were altered in diabetic neuropathy.

47 greater importance in advanced than in early diabetic neuropathy.

48 aly) on corneal innervation of patients with diabetic neuropathy.

49 investigated the effect of ACE inhibition on diabetic neuropathy.

50 mbar spinal nerves or streptozotocin-induced diabetic neuropathy.

51 stances in the pathogenesis and treatment of diabetic neuropathy.

52 ntrations, associated with hyperglycemia and diabetic neuropathy.

53 the development of therapies for peripheral diabetic neuropathy.

54 ial infarction and to the early diagnosis of diabetic neuropathy.

55 its in the peripheral nerves of experimental diabetic neuropathy.

56 uences in the multifactorial pathogenesis of diabetic neuropathy.

57 have been implicated in the pathogenesis of diabetic neuropathy.

58 o-inositol depletion in the genesis of early diabetic neuropathy.

59 atively similar to that seen in early murine diabetic neuropathy.

60 t feature in nerve biopsies of patients with diabetic neuropathy.

61 g in chronic neurodegenerative diseases like diabetic neuropathy.

62 ive neuropathy, second in prevalence only to diabetic neuropathy.

63 otective effect of Foretinib in experimental diabetic neuropathy.

64 icacy in a subgroup of patients with painful diabetic neuropathy.

65 s a rapid, non-invasive surrogate measure of diabetic neuropathy.

66 ib on cutaneous nerve fibers in experimental diabetic neuropathy.

67 control subjects and patients with painless diabetic neuropathy.

68 troke, parkinsonism, multiple sclerosis, and diabetic neuropathy.

69 nism of the neuroprotective effects of EQ in diabetic neuropathy.

70 nvasive method to assess risk for developing diabetic neuropathy.

71 atment may exert a neuroprotective effect in diabetic neuropathy.

72 from 190 patients with painful and painless diabetic neuropathy.

73 tribute to the clinical phenotype in painful diabetic neuropathy.

74 greater insight into such disease states as diabetic neuropathy.

75 d hepatic steatosis while protecting against diabetic neuropathy.

76 ur individuals were evaluated for a possible diabetic neuropathy.

77 ensory abnormalities produced by the ensuing diabetic neuropathy.

78 oms and reduced QoL in patients with painful diabetic neuropathy.

79 port, a function that may be dysregulated in diabetic neuropathy.

80 d lead to the development of novel drugs for diabetic neuropathy.

81 s (RAGE) in mice was protective in long-term diabetic neuropathy.

82 orsal root ganglia (DRG) of mice, leading to diabetic neuropathy.

83 pathy-resistant," confers susceptibility to, diabetic neuropathy.

84 evaluate the development and progression of diabetic neuropathy.

85 evaluate the development and progression of diabetic neuropathy.

86 l therapeutic approaches to prevent or treat diabetic neuropathy.

87 betic neuropathy than in those with painless diabetic neuropathy.

88 studies to test potential new treatments for diabetic neuropathy.

89 h of MSCs into hindlimb muscles of mice with diabetic neuropathy.

90 tentially responsible for the progression of diabetic neuropathy.

91 imental acute myocardial infarction (MI) and diabetic neuropathy.

92 cribe their potential utility in classifying diabetic neuropathy.

93 n innovative therapeutic option for treating diabetic neuropathy.

94 e pathophysiology and development of painful diabetic neuropathy.

95 a LOX-1 and contribute to the development of diabetic neuropathy.

96 sents in-depth discussions of these atypical diabetic neuropathies.

97 justed HRs were 1.44 (95% CI, 1.27-1.64) for diabetic neuropathy, 1.28 (95% CI, 1.12-1.47) for retino

98 Of 954 patients evaluated for diabetic neuropathy, 104/954 subjects (10.9%) met criter

99 The onset of diabetic neuropathy, a complication of diabetes mellitus

100 y may be accompanied by diabetes and painful diabetic neuropathy, a poorly understood condition that

101 This study shows worsening of diabetic neuropathy across a range of neuropathy measure

102 DR with duration of diabetes, diabetic foot, diabetic neuropathy, agriculture occupation, those under

103 o new efforts to understand the aetiology of diabetic neuropathy, along with new 2017 recommendations

104 fective for short-term management of painful diabetic neuropathy, although their comparative effectiv

105 ic for both large and small fiber peripheral diabetic neuropathies and axonal atrophy of large myelin

106 number of disorders including hereditary and diabetic neuropathies and the neurotoxic side effects of

107 Sural nerve biopsies from 7 patients with diabetic neuropathy and 10 with axonal neuropathy withou

108 standing balance control in 15 patients with diabetic neuropathy and 15 patients with stroke.

109 eutic applications, e.g. in the treatment of diabetic neuropathy and Alzheimer disease.

110 lar performance recovery in rodent models of diabetic neuropathy and Charcot-Marie-Tooth diseases.

111 elated sporadic patient with type 1 painless diabetic neuropathy and chronic itch.

112 and paranodal degenerative changes in type 1 diabetic neuropathy and demonstrate that they are preven

113 entify gene expression signatures related to diabetic neuropathy and develop computational classifica

114 ng the state of research on and treatment of diabetic neuropathy and highlights areas of clinical and

115 ation has been demonstrated in patients with diabetic neuropathy and in animal models.

116 nced glycation endproducts are implicated in diabetic neuropathy and may serve as new therapeutic tar

117 ecently, c-peptide has been shown to improve diabetic neuropathy and nephropathy as well as vascular

118 Somatosensory function declines with diabetic neuropathy and often with stroke, resulting in

119 rence hallmark for future studies on painful diabetic neuropathy and other chronic pain conditions.

120 es of the peripheral nervous system, such as diabetic neuropathy and pain.

121 In treating diabetic neuropathy and postherpetic neuralgia compared

122 PARP activation as an important mechanism in diabetic neuropathy and provides the first evidence for

123 plantation and insulin treatment can relieve diabetic neuropathy and rescue the residual endogenous p

124 MFD over 52 weeks was defined as progressing diabetic neuropathy, and a MFD loss of < or =100 fibers/

125 samples with progressing or non-progressing diabetic neuropathy, and found these were functionally e

126 The abnormalities underlying diabetic neuropathy appear to be multiple and involve me

127 ntion studies and clinical trials of ARIs on diabetic neuropathy appeared disappointing because of ei

128 Surrogate markers of diabetic neuropathy are being actively sought to facilit

129 m, or are part of a generalized process (eg, diabetic neuropathy) are not included within functional

130 duloxetine, while specifically marketed for diabetic neuropathy, are likely to be no better and are

131 l approaches to halt progression and reverse diabetic neuropathy at the earliest stage of the disease

132 be beneficial in the acute complications of diabetic neuropathy, at least in part, via upregulation

133 hese data implicate MAPKs in the etiology of diabetic neuropathy both via direct effects of glucose a

134 tress play a key role in the pathogenesis of diabetic neuropathy, but the mechanisms remain unidentif

135 ith hereditary sensory neuropathy type 1 and diabetic neuropathy, but the molecular basis of their to

136 odynia after chemotherapy, nerve injury, and diabetic neuropathy, but this blockade is abrogated in T

137 blished functional and metabolic deficits of diabetic neuropathy by AR inhibition in general.

138 ed in the pathogenesis of acute experimental diabetic neuropathy, can be reproduced in normal rats by

139 all individuals referred to a tertiary care diabetic neuropathy clinic over 5 years, we define the p

140 Painful diabetic neuropathy commonly affects the peripheral nerv

141 y were demonstrated in patients with painful diabetic neuropathy compared with healthy control subjec

142 defective in both experimental and clinical diabetic neuropathy, contributing to loss of axonal extr

143 Accordingly, we investigated whether diabetic neuropathy could be reversed by local transplan

144 n = 10), (3) healthy controls (n = 20), (4) diabetic neuropathy disease controls (n = 20), and (5) p

145 s) in the sciatic nerves of individuals with diabetic neuropathy (DN) correlate with clinical symptom

146 fit of glucose control on the progression of diabetic neuropathy (DN) have come to controversial resu

147 Diabetic neuropathy (DN) is a common severe complication

148 Diabetic neuropathy (DN) is a prevalent and debilitating

149 nderlying the development and progression of diabetic neuropathy (DN) is essential for the design of

150 Information about the impact of diabetic neuropathy (DN) on outcomes after pancreas tran

151 documented in both experimental and clinical diabetic neuropathy (DN), but its pathogenetic role rema

152 need to understand the mechanisms underlying diabetic neuropathy (DN).

153 arise from damage to nociceptive C fibres in diabetic neuropathy (DN).

154 have been implicated in the pathogenesis of diabetic neuropathy (DN).

155 ation could also be a therapeutic option for diabetic neuropathy (DN).

156 The peripheral nerve of experimental diabetic neuropathy (EDN) is reported to be ischemic and

157 plicated in the pathogenesis of experimental diabetic neuropathy (EDN).

158 cohort of participants with mild to moderate diabetic neuropathy, elevated triglycerides correlated w

159 examine diabetes-induced changes in standard diabetic neuropathy endpoints and innervation of the cor

160 Afterwards, standard diabetic neuropathy endpoints, subbasal corneal nerves a

161 in Nueces County, Texas, who met the Toronto Diabetic Neuropathy Expert Group consensus criteria for

162 Among patients with diabetic neuropathy, foot self-care practice may be insu

163 ucial to successfully address all aspects of diabetic neuropathy, from prevention to treatment.

164 Participants who had painful diabetic neuropathy had a higher percentage of nerve les

165 We discovered that mice with diabetic neuropathy had decreased sirtuin 1 (SIRT1) deac

166 The pathogenetic basis for diabetic neuropathy has been enigmatic.

167 ugh our understanding of the complexities of diabetic neuropathy has substantially evolved over the p

168 inhibitor (ARI) trials for the treatment of diabetic neuropathy have not proven efficacy.

169 DNA methylation patterns in a mouse model of diabetic neuropathy, implicating SAMe in the pathogenesi

170 could be an attractive alternative to treat diabetic neuropathy in humans.

171 cement may be of benefit in treating painful diabetic neuropathy in insulin-deficient diabetic condit

172 of T-channels and the development of painful diabetic neuropathy in leptin-deficient (ob/ob) mice.

173 control effectively halts the progression of diabetic neuropathy in patients with type 1 diabetes mel

174 ts for examining the potential treatments of diabetic neuropathy in preclinical studies.

175 In rodent models of diabetic neuropathy, increased Na(V)1.7 in dorsal root g

176 bitor rosuvastatin has a favorable effect on diabetic neuropathy independent of its cholesterol-lower

177 y neurons prevents and reverses experimental diabetic neuropathy induced by a high fat diet (HFD).

178 Diabetic neuropathy is a common complication of diabetes

179 Diabetic neuropathy is a common form of peripheral neuro

180 Diabetic neuropathy is a debilitating consequence of typ

181 Diabetic neuropathy is a debilitating disorder character

182 Diabetic neuropathy is a loss of sensory function beginn

183 Diabetic neuropathy is a major complication of diabetes

184 These results suggest that painful diabetic neuropathy is associated with altered cell-spec

185 Diabetic neuropathy is associated with increased morbidi

186 Recent evidence suggested that diabetic neuropathy is causally related to impaired angi

187 The most common diabetic neuropathy is distal symmetric polyneuropathy,

188 onventional treatment for painful peripheral diabetic neuropathy is largely symptomatic and often ine

189 Diabetic neuropathy is manifested either by loss of noci

190 Human diabetic neuropathy is multifactorial in etiology, with

191 The pathogenesis of diabetic neuropathy is multifactorial.

192 changes associated with these two models of diabetic neuropathy is not consistent with the proposed

193 c neuropathy, the pathophysiology of painful diabetic neuropathy is not understood.

194 Painful diabetic neuropathy is poorly controlled by analgesics a

195 The pathogeneses of diabetic neuropathy is still unclear.

196 Diabetic neuropathy is the most common diabetic complica

197 r the purpose of this Primer, referred to as diabetic neuropathy) is very common.

198 , higher glycosylated hemoglobin, history of diabetic neuropathy, lower hematocrit, elevated triglyce

199 greater susceptibility of CG/SMG neurons to diabetic neuropathy may be due to a selective inability

200 function of the hepatic vagus, as occurs in diabetic neuropathy, may contribute to diabetic obesity.

201 in sensory nerve amplitude characteristic of diabetic neuropathy measured 4 weeks later, preserved au

202 m skin, the mechanical allodynia worsened in diabetic neuropathy mice, likely due to retrograde degen

203 t ligation of L5 and L6 spinal nerves) and a diabetic neuropathy model (i.e., streptozotocin-induced

204 In the diabetic neuropathy model, ABT-594 (0.3 micromol/kg, i.p

205 the MI model, and in 46% of hindlimbs in the diabetic neuropathy model.

206 hyperalgesia were assessed in the Chung and diabetic neuropathy models, respectively.

207 We hypothesize that diabetic neuropathies, nephropathies and retinopathies d

208 Diabetic neuropathy, nephropathy, and retinopathy cause

209 Our data suggest that diabetic neuropathy occurs in the cornea of type 2 diabe

210 , OSA remained independently associated with diabetic neuropathy (odds ratio, 2.82; 95% confidence in

211 e out of two patients with diabetes develops diabetic neuropathy; of these, 20% experience neuropathi

212 specific treatments and no means to predict diabetic neuropathy onset or progression.

213 hereditary peripheral neuropathies, such as diabetic neuropathy or Charcot-Marie-Tooth diseases, tha

214 vous system (e.g. post-herpetic neuralgia or diabetic neuropathy) or to the central nervous system (e

215 A total of 29.3% (n=85) of diabetic neuropathy patients developed a diabetic foot u

216 nd morphological abnormalities of peripheral diabetic neuropathy (PDN) have been extensively explored

217 -related behaviors characteristic of painful diabetic neuropathy (PDN).

218 e a basis for painful symptoms of peripheral diabetic neuropathy (PDN).

219 VA), heart failure (HF), renal failure (RF), diabetic neuropathy, peripheral arterial disease, reduce

220 tify transcriptional changes associated with diabetic neuropathy progression in human sural nerve bio

221 assify a test set of patients with regard to diabetic neuropathy progression.

222 velop computational classification models of diabetic neuropathy progression.

223 ker of the early development and severity of diabetic neuropathy, providing insights into the pathoph

224 t Score, -3.7 [2.7]; Norfolk Quality of Life-Diabetic Neuropathy questionnaire, -6.5 [4.9]; least-squ

225 l role of ARIs is to slow the progression of diabetic neuropathy rather than to reverse it.

226 cognized as a microvasculopathy, but retinal diabetic neuropathy (RDN), characterized by inner retina

227 asal corneal nerves and that these and other diabetic neuropathy-related defects can be partially to

228 The mechanisms underlying painful diabetic neuropathy remain poorly understood.

229 The quality of the epidemiological data on diabetic neuropathies remains poor for a variety of reas

230 nvestigated the hypothesis that experimental diabetic neuropathy results from destruction of the vasa

231 These findings support the notion that diabetic neuropathy results from microvascular ischemia

232 Experimental diabetic neuropathy results in myelinopathy of dorsal ro

233 strongly argues that more refined models of diabetic neuropathy should replace the use of STZ.

234 remedy these short-comings in the Rochester Diabetic Neuropathy Study (RDNS).

235 med surface area (PISA) with HbA1c in Type 2 Diabetic Neuropathy (T2DN) patients with and without dia

236 oss-sectional study 310 patients with type 2 diabetic neuropathy (T2DN) were randomly selected, and t

237 esions were greater in patients with painful diabetic neuropathy than in those with painless diabetic

238 factors and phenotypes of participants with diabetic neuropathy that can be used in the design of ne

239 sion therefore represents an early change in diabetic neuropathy that could, at least in part, be res

240 over time in slow developing conditions like diabetic neuropathy) that produces neuropathic pain.

241 n can occur concurrently with denervation in diabetic neuropathy The gene mutations for hereditary se

242 To evaluate the development of diabetic neuropathy, the current study examined changes

243 gh pain is experienced by many patients with diabetic neuropathy, the pathophysiology of painful diab

244 logical conditions following nerve injury or diabetic neuropathy, the slightest touch can produce pai

245 e eight sway parameters in the subjects with diabetic neuropathy, the subjects with stroke, and the e

246 ays are implicated in the pathophysiology of diabetic neuropathy, there are no specific treatments an

247 In diabetic neuropathy, there is activation of axonal and s

248 In rats with diabetic neuropathy, there was no significant change in

249 We also used an animal model of painful diabetic neuropathy to demonstrate that blocking T-chann

250 useful in determining the natural course of diabetic neuropathy to identify patients at high risk of

251 of trial (in terms of the natural history of diabetic neuropathy), trial endpoints (reversibility or

252 imental nerve injury and in animal models of diabetic neuropathy TRPV1 is present on neurons that do

253 Patients with diabetic neuropathy typically have decreased sweating in

254 new guidelines for the treatment of painful diabetic neuropathy using distinct classes of drugs, wit

255 indicate that BMDC-PARP expression promotes diabetic neuropathy via BMDC-neuron fusion.

256 Experimental diabetic neuropathy was induced by streptozotocin.

257 Diabetic neuropathy was the most common neuropathy diagn

258 nvier, a characteristic aberration of type 1 diabetic neuropathy, we examined in type 1 BB/Wor and ty

259 ns did not distinguish painful from painless diabetic neuropathy, we identified 11 proteins which pos

260 tify patients with spinally mediated painful diabetic neuropathy who may respond optimally to therapi

261 gene signature of patients with progressive diabetic neuropathy will facilitate the development of n

262 The association between diabetic neuropathy with and without diabetic foot and p

263 periodontal destruction were high in type 2 diabetic neuropathy with diabetic foot.

264 ill focus on recent advances in the field of diabetic neuropathy, with an emphasis on distal symmetri