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1 of polyneuropathy and to detect the onset of diabetic polyneuropathy.
2 ar endothelial growth factor (VEGF) to treat diabetic polyneuropathy.
3  a significant beneficial effect of rhNGF on diabetic polyneuropathy.
4 sticity of neurons may contribute to chronic diabetic polyneuropathy.
5 the evolution of painful sensory symptoms in diabetic polyneuropathy.
6 nt antioxidant that is used in patients with diabetic polyneuropathy.
7  have been implicated in the pathogenesis of diabetic polyneuropathy.
8 CI: 1, 3); multiple sclerosis, 2 (CI: 2, 3); diabetic polyneuropathy, 2 (CI: 1, 3); compressive monon
9 CI: 183, 230); shingles, 140 (CI: 104, 184); diabetic polyneuropathy, 54 (CI: 33, 83); compressive ne
10 n-derived NGF influences the presentation of diabetic polyneuropathy, although metabolic or vascular
11 tin receptor deficient mouse (dbdb) model of diabetic polyneuropathy and 2) superoxide dismutase 1 kn
12 fied sensory and autonomic function in early diabetic polyneuropathy and correlated changes with leve
13 to minimizing the prevalence and severity of diabetic polyneuropathy and makes research into the dele
14 tween participants with painful and painless diabetic polyneuropathy, and there were only minor chang
15 rmacologic therapies for neuropathic pain in diabetic polyneuropathy appear promising.
16  diagnosis of and differential diagnosis for diabetic polyneuropathy are reviewed herein.
17 d-stage kidney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is
18 ts the progression and improves the signs of diabetic polyneuropathy by restoration of a normoglycemi
19 irculation may contribute to nerve damage in diabetic polyneuropathy (DN).
20 ic mechanisms underlying painful symptoms in diabetic polyneuropathy (DPN) are poorly understood.
21 ntify alterations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR)
22 s on magnetic resonance neurography (MRN) in diabetic polyneuropathy (DPN) have found proximal sciati
23 of the metabolic syndrome that contribute to diabetic polyneuropathy (DPN) in type 2 diabetes mellitu
24                                  Large-fiber diabetic polyneuropathy (DPN) leads to balance and gait
25                                              Diabetic polyneuropathy (DPN) renders progressive sensor
26 omote nerve regeneration, early diagnosis of diabetic polyneuropathy, followed by tight glycemic cont
27 e should be useful as a measure of change in diabetic polyneuropathy for purposes of medical practice
28 proved abnormalities in chronic experimental diabetic polyneuropathy, including sensory axon loss, in
29 nomena are major expressions of varieties of diabetic polyneuropathies needing improved assessments f
30            In general, treatment options for diabetic polyneuropathy remain primarily symptomatic.
31  an important measure of overall severity of diabetic polyneuropathy, taking into account both sympto
32 e by which to diagnose and grade severity of diabetic polyneuropathy than does the use of individual
33 erstanding of chronic symmetric sensorimotor diabetic polyneuropathy, the most common and problematic
34                      To estimate severity of diabetic polyneuropathy, the results of the neurological
35 s may address some of the challenges of past diabetic polyneuropathy trials.
36 le to adequately characterize and quantitate diabetic polyneuropathies using only one or two clinical
37    Two hundred thirty-nine participants with diabetic polyneuropathy were recruited from sites in the