ライフサイエンスコーパス: diabetes complication

1 glucose and that pulmonary dysfunction is a diabetes complication.

2 Skeletal muscle myopathy is a common diabetes complication.

3 s a vital role in the progression of various diabetes complications.

4 R) has been implicated in the development of diabetes complications.

5 also measured the presence of self-reported diabetes complications.

6 ol pathway and preventing the development of diabetes complications.

7 t regimens is associated with a high risk of diabetes complications.

8 actices may not be optimal for prevention of diabetes complications.

9 G6PDdef alleles contribute to disparities in diabetes complications.

10 the focus for future prevention attempts for diabetes complications.

11 riability have been associated with incident diabetes complications.

12 g blood glucose control to prevent long-term diabetes complications.

13 s a central mechanism for the development of diabetes complications.

14 l as organ-specific, changes associated with diabetes complications.

15 also associated with increased risk of other diabetes complications.

16 and HbA(1c) may lead to better prevention of diabetes complications.

17 crease in the individual risks of developing diabetes complications.

18 ss, and fibrosis are common features in most diabetes complications.

19 damage 1) contributes to the development of diabetes complications.

20 creased risk of cardiometabolic diseases and diabetes complications.

21 potentially an increase in nonadherence and diabetes complications.

22 eart failure and ischemic heart disease with diabetes complications.

23 ated with increased odds of experiencing all diabetes complications.

24 s the need for additional genetic studies of diabetes complications.

25 ibute to endothelial dysfunction in vascular diabetes complications.

26 and public health interventions can prevent diabetes complications.

27 less so with early stages of non-ophthalmic diabetes complications.

28 ould have translational value for studies of diabetes complications.

29 IL-12 emerged as a critical player in type 2 diabetes complications.

30 may be a potential predictor of the risk of diabetes complications.

31 tasis and separately slow the development of diabetes complications.

32 e progression and have an increased risk for diabetes complications.

33 with no evidence of causal effects on other diabetes complications.

34 ndothelial dysfunction-related microvascular diabetes complications.

35 GEs) in the skin and is a risk indicator for diabetes complications.

36 (amide), for the prevention and treatment of diabetes complications.

37 ators of pathological mechanisms involved in diabetes complications.

38 be an initiating event in the development of diabetes complications.

39 y persistent hyperglycemia and contribute to diabetes complications.

40 rker of glycemic control and risk factor for diabetes complications.

41 upports GV as an independent risk factor for diabetes complications.

42 potential implications for the prevention of diabetes complications.

43 ATP generation in several target tissues of diabetes complications.

44 tential strategy to reduce the likelihood of diabetes complications.

45 athway and were enriched in genes related to diabetes complications.

46 Diabetes remission, relapse, and diabetes complications.

47 d to lncRNA-based therapies for inflammatory diabetes complications.

48 survival of beta-cells, and protects against diabetes complications.

49 re strongly implicated in the development of diabetes complications.

50 ationship between periodontitis severity and diabetes complications.

51 of genetic discoveries for both diabetes and diabetes complications.

52 abolic changes underlying the development of diabetes complications.

53 essive symptoms are strongly associated with diabetes complications.

54 t increased risk of type 2 diabetes and many diabetes complications.

55 fense may play a role in the pathogenesis of diabetes complications.

56 e activation relevant to the pathogenesis of diabetes complications.

57 oposed as a mediator of neurodegeneration in diabetes complications.

58 hs; 22.4%), cancer (21 deaths; 19.6%), acute diabetes complications (19 deaths; 17.8%), and accidents

59 gnosis, the leading cause of death was acute diabetes complications (73.6%), while during the next 10

60 ission trajectories and variation in risk of diabetes complications: a population-based cohort study.

61 pecies may represent an important pathway in diabetes complications and a new mechanism in phagocyte-

62 hat morbidity patterns extend beyond classic diabetes complications and accelerate the onset of sever

63 ring long-term hyperglycemia are involved in diabetes complications and can be estimated by skin auto

64 This can reduce diabetes complications and costs for the health service.

65 d glycaemic control, which reduces long-term diabetes complications and could also improve tuberculos

66 effect than ARBs and ACE inhibitors on these diabetes complications and may be clinically more effica

67 he role of epigenetics and noncoding RNAs in diabetes complications and metabolic memory, and their t

68 diabetes and of poor diabetes outcomes (eg, diabetes complications and mortality).

69 iabetes (T2D) appear to be at a high risk of diabetes complications and other cardiovascular diseases

70 The prevalence and hazard ratios (HRs) of diabetes complications and other cardiovascular diseases

71 Laboratory HbA(1c) does not always predict diabetes complications and our aim was to establish a gl

72 ghts into the biology of glucose regulation, diabetes complications and pathways for treatment strati

73 of periodontal disease on glycaemic control, diabetes complications, and development of type 2 (and p

74 diabetes medication burden, age, presence of diabetes complications, and follow-up duration, and used

75 rglycemia-induced inflammation is central in diabetes complications, and monocytes are important in o

76 cell dysfunction, diabetes pathogenesis, and diabetes complications; and examines the differing outco

77 d chemokines relevant to the pathogenesis of diabetes complications are induced by HG via key signali

78 te the enhanced inflammation associated with diabetes complications are not completely understood.

79 r year from cardiovascular disease or type 2 diabetes complications at current treatment levels, whic

80 sk factors at baseline and at follow-up, and diabetes complications at follow-up.

81 Improved tools for assessing risk for diabetes complication before onset will help in complica

82 s plays a pivotal role in the development of diabetes complications, both microvascular and cardiovas

83 ompound is worthy of further study to lessen diabetes complications but that dosage needs considerati

84 After 20 years' duration, chronic diabetes complications (cardiovascular, renal, or infect

85 glucose control markedly reduced the risk of diabetes complications compared with conventional therap

86 e analyses in the Pittsburgh Epidemiology of Diabetes Complications (EDC) prospective cohort study of

87 ed on evidence from both the Epidemiology of Diabetes Complications (EDC) prospective cohort study of

88 onset type 1 diabetes in the Epidemiology of Diabetes Complications (EDC) Study and was validated usi

89 expectancy of the Pittsburgh Epidemiology of Diabetes Complications (EDC) study cohort and quantify i

90 xamination of the Pittsburgh Epidemiology of Diabetes Complications (EDC) Study cohort, 302 adults (m

91 nce data from the Pittsburgh Epidemiology of Diabetes Complications (EDC) Study to investigate the wi

92 Subjects from the Epidemiology of Diabetes Complications (EDC) Study were clinically exami

93 rein on genetic discoveries for diabetes and diabetes complications, empowered primarily through geno

94 would be expected to reduce DALYs lost from diabetes complications from a median population-weighted

95 confirmed as an independent risk factor for diabetes complications, glycaemic variability can repres

96 Persons born to women with previous acute diabetes complications had a higher CHD risk than those

97 riving, initial cellular response underlying diabetes complications has been held for the past decade

98 an increased frequency of diabetes onset and diabetes complications has been reported in patients fol

99 rs7533564 was not associated with diabetes complications in DCCT/EDIC or with SF in subjec

100 ification of therapy, decreasing the risk of diabetes complications in patients with G6PDdef alleles.

101 ed glucose handling, insulin resistance, and diabetes complications in prediabetic DT/HF mice.

102 ls play a central role in the development of diabetes complications in the retina and nerve.

103 ement of diabetes are critical to reduce the diabetes complications including cardiovascular disease

104 important role in the development of various diabetes complications, including atherosclerosis.

105 xygen species (ROS) are crucial in long-term diabetes complications, including peripheral artery dise

106 that plays a central role in the etiology of diabetes complications, inflammation, and neurodegenerat

107 The risk of long-term diabetes complications is not fully explained by diabete

108 Whether prediabetes is causally related to diabetes complications is unclear.

109 iabetes, but the association with short-term diabetes complications is unclear.

110 Because the role of lncRNAs in diabetes complications is unknown, we further characteri

111 ollment with microvascular and macrovascular diabetes complications is unknown.

112 that a large portion of the genetic risk of diabetes complications is yet to be discovered and empha

113 Diabetic retinopathy (DR), a common diabetes complication leading to vision loss, presents e

114 , with a concomitant 50% to 70% reduction in diabetes complications, may require close monitoring and

115 ations are reexamined, and a new concept for diabetes complications--mitochondrial hormesis--is prese

116 Although some type 1 diabetes complications (mortality, renal failure, and ne

117 Diabetes complications occur at higher rates in individu

118 an HDHP had greater odds of experiencing all diabetes complications (odds ratio [OR], 1.11; 95% CI, 1

119 However, diabetes complications often remain undiagnosed and untr

120 and all hospital admissions related to acute diabetes complications (p = 0.008).

121 rdiovascular disease or microvascular type 2 diabetes complications per 1000 population.

122 abolic memory (MM) is the phenomenon whereby diabetes complications persist and progress after glycem

123 reased odds of potentially preventable acute diabetes complications, potentially because of delayed o

124 The disease does not progress over time, and diabetes complications rarely develop.

125 elevated REDD1 levels in the development of diabetes complications, reflect on limitations of prior

126 ipocalin 2 and galectin 3, two biomarkers of diabetes complications regulated by MR, are increased in

127 aimed at identifying genetic determinants of diabetes complications relied on familial linkage analys

128 Preventing diabetes complications requires monitoring and control o

129 moglobin glycation and have implications for diabetes complications risk and risk assessment.

130 value are a major determinant of the 89% of diabetes complications risk not captured by HbA1c.

131 of HbA(1c) can underestimate or overestimate diabetes complication risks, which may have future clini

132 rs, data on sex, age, income, comorbidities, diabetes complication severity index score, staging of k

133 , the risk increased among those with higher Diabetes Complications Severity Index scores (P = .0002)

134 he Pittsburgh, Pennsylvania, Epidemiology of Diabetes Complications Study of childhood-onset type 1 d

135 Participants from the Epidemiology of Diabetes Complications Study who were free of CAD at stu

136 GN AND Participants from the Epidemiology of Diabetes Complications Study with DNA available were stu

137 rticipants of the Pittsburgh Epidemiology of Diabetes Complications study with Hp genotyping availabl

138 l Pittsburgh Epidemiology of Childhood-Onset Diabetes Complications Study.

139 l roles in the initiation and progression of diabetes complications such as diabetes-associated ather

140 N3K may play a key role in the GGap and thus diabetes complications such that FN3K may be a potential

141 flected established pathogenic mechanisms of diabetes complications, such as elements of Janus kinase

142 hanisms may contribute to the development of diabetes complications, such as nephropathy.

143 es-related cardiometabolic traits and type 2 diabetes complications, suggesting its utility for strat

144 e effective in preventing the progression of diabetes complications than currently available therapie

145 se-lowering therapy, and had a lower risk of diabetes complications than individuals on non-optimal t

146 f people-who were generally at lower risk of diabetes complications-than the BTT.

147 that prediabetes is broadly associated with diabetes complications, the causal inference analysis re

148 For diabetes complications, the median follow-up time was 17

149 type 2 diabetes from the BErgamo NEphrologic Diabetes Complication Trial (BENEDICT), all of whom rece

150 2 diabetic patients from BErgamo NEphrologic DIabetes Complications Trial (BENEDICT).

151 ew of substantial mis-estimation of risks of diabetes complications using existing equations, we soug

152 ubjects, we assessed 16 metabolic status and diabetes complications variables.

153 Information on diabetes complications was obtained from national health

154 The association with acute pregestational diabetes complications was particularly strong, suggesti

155 ; 95% CI, 2.37-4.21) and a greater burden of diabetes complications were associated with higher odds

156 disease duration of 15-25 years and minimal diabetes complications with an age-matched, nondiabetic

157 hypothesized that genetic predisposition to diabetes complications would be more evident among low-r

158 A second approach based on diabetes complications yielded a net value of $6931 per