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1 toward effects, collectively referred to as 'diabetic complications'.
2 ibutes to the intractability of this serious diabetic complication.
3 Diabetic neuropathy is the most common diabetic complication.
4 as being responsible for development of this diabetic complication.
5 nificant biomarker towards the prediction of diabetic complications.
6 ion reactions, which are the major causes of diabetic complications.
7 ) has been implicated in the pathogenesis of diabetic complications.
8 aradigm shift in our understanding of ocular diabetic complications.
9 been linked to the development of secondary diabetic complications.
10 ion reportedly found in the target organs of diabetic complications.
11 is an important transcriptional regulator of diabetic complications.
12 etes and (2) to assess their contribution to diabetic complications.
13 uscle cell signal transduction contribute to diabetic complications.
14 been linked to the development of secondary diabetic complications.
15 production is central to the development of diabetic complications.
16 thought to contribute to the pathogenesis of diabetic complications.
17 ntial therapeutic roles in the prevention of diabetic complications.
18 t Smad signaling may play a critical role in diabetic complications.
19 through the receptor for AGEs, contribute to diabetic complications.
20 heir receptor, RAGE, to play a major role in diabetic complications.
21 optimal for finding susceptibility genes for diabetic complications.
22 -documented beneficial preventive effects on diabetic complications.
23 mation and protection against development of diabetic complications.
24 e an important factor in the pathogenesis of diabetic complications.
25 rglycemia contributes to the pathogenesis of diabetic complications.
26 been implicated in the etiology of secondary diabetic complications.
27 reactions that are thought to play a role in diabetic complications.
28 y has been implicated in the pathogenesis of diabetic complications.
29 genes that contribute to the pathogenesis of diabetic complications.
30 sm that underlies the development of various diabetic complications.
31 hibitors of AGE formation and development of diabetic complications.
32 ellular membranes and to the pathogenesis of diabetic complications.
33 parameter most consistently associated with diabetic complications.
34 s, without increased risk of readmission for diabetic complications.
35 mine whether PKC-beta inhibition can prevent diabetic complications.
36 collagen are correlated with the severity of diabetic complications.
37 m glycemic control and a strong predictor of diabetic complications.
38 n initiative, which emphasizes prevention of diabetic complications.
39 has been linked to the pathogenesis of some diabetic complications.
40 detection and correction of risk factors for diabetic complications.
41 ht to contribute to the pathogenesis of many diabetic complications.
42 occur in several diseases states, including diabetic complications.
43 ion of these various factors and less severe diabetic complications.
44 ses, e.g., AIDS, cancer, atherosclerosis and diabetic complications.
45 in vascular cells and tissues susceptible to diabetic complications.
46 ic patients before the development of severe diabetic complications.
47 dori-modified proteins in the development of diabetic complications.
48 tablished concomitant factor associated with diabetic complications.
49 tic patients and is thought to contribute to diabetic complications.
50 adical activity underlie the pathogenesis of diabetic complications.
51 new mechanisms underlying the development of diabetic complications.
52 ay contribute to Wnt signaling activation in diabetic complications.
53 st and earlier phase to minimize the risk of diabetic complications.
54 ducts and therefore potentially mitigate the diabetic complications.
55 icyte-endothelial crosstalk in microvascular diabetic complications.
56 of hyperglycemic excursions associated with diabetic complications.
57 ways of using stem cell therapy to overcome diabetic complications.
58 standing the complex pathophysiology of many diabetic complications.
59 fying people at risk of incident diabetes or diabetic complications.
60 usal link between diabetes mellitus (DM) and diabetic complications.
61 way, plays a key role in the pathogenesis of diabetic complications.
62 besity and metabolic syndrome, diabetes, and diabetic complications.
63 n dysfunction and plays an important role in diabetic complications.
64 s novel benchmarks for the future studies of diabetic complications.
65 d to determine the role of TNFalpha in these diabetic complications.
66 n hyperglycemia is a major mechanism causing diabetic complications.
67 (CARHSP1) was identified as a biomarker for diabetic complications.
68 lele is associated with an increased risk of diabetic complications.
69 tabolite-generated ROS in the development of diabetic complications.
70 Thus, lack of B1R and B2R exacerbates diabetic complications.
71 ly with reference to the effect on long-term diabetic complications.
72 mmation and metabolic memory associated with diabetic complications.
73 a novel therapeutic option for treatment of diabetic complications.
74 d glycation end products play major roles in diabetic complications.
75 might also participate in the development of diabetic complications.
76 n enzyme to deglycate proteins implicated in diabetic complications.
77 ixture and high rates of type 2 diabetes and diabetic complications.
78 , have been implicated in the development of diabetic complications.
79 sociated with type 1 and type 2 diabetes and diabetic complications.
80 volvement in development of various vascular diabetic complications.
81 dent risk factor for development of vascular diabetic complications.
82 rsued for treatment of microvascular-related diabetic complications.
83 s being critical for prevention of long-term diabetic complications.
84 factor influencing the development of major diabetic complications.
85 ing disorders are at high risk of developing diabetic complications.
86 ia their receptor, RAGE, play major roles in diabetic complications.
87 g glycation from hyperglycemia as a cause of diabetic complications, a Pseudomonas sp. soil strain co
88 E-mediated diseases, such as those linked to diabetic complications, Alzheimer's disease, and chronic
89 th increased six-month readmission rates for diabetic complications among diabetics and nondiabetics.
90 reemptive identification and anticipation of diabetic complications and comorbidities, along with an
91 hways of crucial importance in propensity to diabetic complications and heart disease in the general
92 various age-associated pathologies, such as diabetic complications and neurodegenerative disorders l
93 ns provide new insights into the etiology of diabetic complications and suggest potential novel thera
94 value of HbA1c is its use as a predictor of diabetic complications and the proven effect of improved
95 Impaired macrophage functions imposed by diabetic complications and the suppressed formation of 1
97 Levels of HbA1c track epidemiologically with diabetic complications, and glycemic control, as reflect
98 disorders, including Alzheimer disease (AD), diabetic complications, and inflammatory conditions.
99 erosis and vascular remodeling after injury, diabetic complications, and neurodegenerative disorders.
100 omics is a reliable source for biomarkers of diabetic complications, and our data suggest that renal
101 at therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular
104 on and cardiac microvascular dysfunction are diabetic complications associated with increased mortali
105 cated in the development of several vascular diabetic complications (atherosclerosis, nephropathy, an
106 mic control, not only to reverse established diabetic complications but also to improve beta-cell sta
107 l decreases the incidence and progression of diabetic complications but increases the incidence of hy
108 elays the onset and slows the progression of diabetic complications but is associated with frequent d
109 ameliorates the progression of microvascular diabetic complications but the procedure is associated w
110 lay a role in many processes underlying late diabetic complications, but efforts to identify genetic
111 fibrosis within 3 months and die because of diabetic complications by 6-7 months after a single inje
112 ent, metformin treatment may protect against diabetic complications by mechanisms independent of its
113 y OGT has been linked to insulin resistance, diabetic complications, cancer and neurodegenerative dis
114 Atherosclerosis, hypertension, obesity, diabetic complications, cancer, benign prostate hyperpla
115 GF therapy may be useful in the treatment of diabetic complications characterized by impaired neovasc
117 he auspices of the NIH, the Animal Models of Diabetic Complications Consortium has worked to address
118 ased O-GlcNAc levels to glucose toxicity and diabetic complications; conversely, acute activation of
119 -dicarbonyl that is thought to contribute to diabetic complications either as a direct toxin or as a
120 , the most common and problematic of chronic diabetic complications, essential for a wide range of me
121 tion end products (AGEs), known promoters of diabetic complications, form abundantly in heated foods
122 t efforts to identify treatments for chronic diabetic complications have resulted in the discovery of
123 chondrial dysfunction has been implicated in diabetic complications; however, it is unknown whether h
124 educing sugars, have been implicated in many diabetic complications; however, their role in diabetic
126 le effectively preventing the development of diabetic complications in animals, results from clinical
127 nomeric peptide that reduces body weight and diabetic complications in rodent models of obesity by ac
129 l therapeutic interventions that may prevent diabetic complications in the presence of hyperglycemia,
130 glutathionylation may play a central role in diabetic complications in vivo where Grx1 is increased.
132 uld provide a novel therapeutic approach for diabetic complications including nephropathy, and other
134 which activates major pathways implicated in diabetic complications, including advanced glycation end
135 n has a critical role in the pathogenesis of diabetic complications, including diabetic nephropathy (
136 lucose is a key factor in the development of diabetic complications, including diabetic nephropathy.
137 OD genetic background may predispose them to diabetic complications, including insulin resistance in
138 istent with a multifactorial pathogenesis of diabetic complications, including roles for metabolic im
139 al drug target because of its involvement in diabetic complications, inflammation, and tumorigenesis.
140 , amyloid beta, and HMGB1 has been linked to diabetic complications, inflammatory and neurodegenerati
144 products is implicated in the development of diabetic complications, little is known about the chemic
146 pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and
147 pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and
148 sorbitol is associated with MI depletion in diabetic complications, no causal relationship has been
151 United States, but the burden and effect of diabetic complications on this group of people is not fu
152 mechanisms may operate in different types of diabetic complications or at different stages of specifi
153 -2001 who developed NODM was used to examine diabetic complications over the first three years posttr
155 BDM, targeting neutrophilic inflammation and diabetic complication pathways to address the greater mo
156 amin E, failed to show beneficial effects on diabetic complications probably because their action is
161 sp. of potential relevance for treatment of diabetic complications resulting from excessive protein
165 cular risk factors confer increased risk for diabetic complications such as peripheral neuropathy, ne
166 primary diabetes and its effects on various diabetic complications, such as diabetic cardiovascular
168 iabetes may predispose to the development of diabetic complications, such as infection and impaired h
169 ficantly decrease or halt the progression of diabetic complications, support the continued applicatio
171 in the study of atherosclerosis and of other diabetic complications, the consortium has created a sys
172 vestigated to understand the pathogenesis of diabetic complications, the increased metabolism of gluc
173 ase, an enzyme linked to the pathogenesis of diabetic complications, the physiological role of FR-1 i
174 been widely studied for their involvement in diabetic complications; these complications are largely
175 enic role of PKCbetaII in the development of diabetic complications, this structure can serve as a te
176 ditis, heart failure, circulatory shock, and diabetic complications to atherosclerosis, arthritis, co
177 increased rates of hospital readmission for diabetic complications traditionally associated with bet
179 act by activating Smad signaling to mediate diabetic complications via both TGF-beta-dependent and -
180 After adjustment for other risk factors and diabetic complications, we found that duration of diabet
181 ole of phagocytic superoxide in the onset of diabetic complications, we used a model of periodontitis
182 ol (hemoglobin A1c [HbA1c]), and presence of diabetic complications were determined at recruitment.
184 nd products (AGEs) have an important role in diabetic complications, with many responses mediated thr
185 the oral glucose tolerance test all predict diabetic complications yet test reliability is better fo
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