ライフサイエンスコーパス: diabetic neuropathy

1 inal inhibitory dysfunction in human painful diabetic neuropathy.

2 greater insight into such disease states as diabetic neuropathy.

3 ely diagnose and assess progression of human diabetic neuropathy.

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

5 of therapeutic intervention in patients with diabetic neuropathy.

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

7 patients with painful compared with painless diabetic neuropathy.

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

9 contribute to the development of symptoms in diabetic neuropathy.

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

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

12 fies cellular therapeutic targets to prevent diabetic neuropathy.

13 as diagnosis and treatment of patients with diabetic neuropathy.

14 e investigation of the mechanisms leading to diabetic neuropathy.

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

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

17 ne and tyrosine sites contributes to painful diabetic neuropathy.

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

19 d hepatic steatosis while protecting against diabetic neuropathy.

20 e therapeutic potential for the treatment of diabetic neuropathy.

21 embrane depolarization in sensory neurons in diabetic neuropathy.

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

23 utonomic failure is an integral component of diabetic neuropathy.

24 e therapeutic potential for treating painful diabetic neuropathy.

25 eficient in peripheral nerve microvessels in diabetic neuropathy.

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

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

28 icrovascular ischemia in the pathogenesis of diabetic neuropathy.

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

30 tributes to neuropathic pain associated with diabetic neuropathy.

31 chanical hyperalgesia is an early symptom of diabetic neuropathy.

32 r endothelial TM expression throughout human diabetic neuropathy.

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

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

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

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

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

38 greater importance in advanced than in early diabetic neuropathy.

39 investigated the effect of ACE inhibition on diabetic neuropathy.

40 mbar spinal nerves or streptozotocin-induced diabetic neuropathy.

41 stances in the pathogenesis and treatment of diabetic neuropathy.

42 ntrations, associated with hyperglycemia and diabetic neuropathy.

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

44 its in the peripheral nerves of experimental diabetic neuropathy.

45 uences in the multifactorial pathogenesis of diabetic neuropathy.

46 the development of therapies for peripheral diabetic neuropathy.

47 ur individuals were evaluated for a possible diabetic neuropathy.

48 have been implicated in the pathogenesis of diabetic neuropathy.

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

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

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

52 ensory abnormalities produced by the ensuing diabetic neuropathy.

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

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

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

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

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

58 evaluate the development and progression of diabetic neuropathy.

59 evaluate the development and progression of diabetic neuropathy.

60 l therapeutic approaches to prevent or treat diabetic neuropathy.

61 studies to test potential new treatments for diabetic neuropathy.

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

63 control subjects and patients with painless diabetic neuropathy.

64 tentially responsible for the progression of diabetic neuropathy.

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

66 cribe their potential utility in classifying diabetic neuropathy.

67 n innovative therapeutic option for treating diabetic neuropathy.

68 e pathophysiology and development of painful diabetic neuropathy.

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

70 EPCs could reverse various manifestations of diabetic neuropathy.

71 idemia is instrumental in the progression of diabetic neuropathy.

72 postnatal development and are implicated in diabetic neuropathy.

73 ing the same time interval as nonprogressing diabetic neuropathy.

74 eutic approach for the management of painful diabetic neuropathy.

75 ing the protection of erythropoietin against diabetic neuropathy.

76 tribute to the clinical phenotype in painful diabetic neuropathy.

77 for pain were analyzed in participants with diabetic neuropathy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 In treating diabetic neuropathy and postherpetic neuralgia compared

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 Diabetic neuropathy (DN) is a common severe complication

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

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

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

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

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

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

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

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

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

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

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

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

133 The pathogenetic basis for diabetic neuropathy has been enigmatic.

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

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

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

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

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

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

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

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

142 Diabetic neuropathy is a common complication of diabetes

143 Diabetic neuropathy is a common form of peripheral neuro

144 Diabetic neuropathy is a debilitating consequence of typ

145 Diabetic neuropathy is a major complication of diabetes

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

147 Diabetic neuropathy is associated with increased morbidi

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

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

150 Diabetic neuropathy is manifested either by loss of noci

151 Human diabetic neuropathy is multifactorial in etiology, with

152 The pathogenesis of diabetic neuropathy is multifactorial.

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

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

155 Painful diabetic neuropathy is poorly controlled by analgesics a

156 The pathogeneses of diabetic neuropathy is still unclear.

157 Diabetic neuropathy is the most common diabetic complica

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

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

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

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

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

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

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

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

166 We hypothesize that diabetic neuropathies, nephropathies and retinopathies d

167 Diabetic neuropathy, nephropathy, and retinopathy cause

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

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

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

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

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

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

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

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

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

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

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

179 velop computational classification models of diabetic neuropathy progression.

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

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

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

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

184 The mechanisms underlying painful diabetic neuropathy remain poorly understood.

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

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

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

188 Experimental diabetic neuropathy results in myelinopathy of dorsal ro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 Patients with diabetic neuropathy typically have decreased sweating in

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

205 Experimental diabetic neuropathy was induced by streptozotocin.

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

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

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

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