ライフサイエンスコーパス: macrovascular

1 /d) and microvascular (0.72 [0.61-0.87]) and macrovascular (0.87 [0.82-0.93]) complications (p < 0.00

2 = .02), fewer microvascular (17% vs 22%) and macrovascular (2% vs 9%) invasions (P < .001), and fewer

3 Within OGLD group, Cox regression compared macrovascular (all-cause mortality, myocardial infarctio

4 hypoxia enhances sickle RBC adhesion to both macrovascular and human microvascular ECs via the adhesi

5 effects, but with similar outcomes for other macrovascular and microvascular (cardiac, renal, and ret

6 of endothelial barrier function in pulmonary macrovascular and microvascular cells in vitro and in lu

7 hether these parameters predict the risks of macrovascular and microvascular complications in patient

8 aximum SBP were independent risk factors for macrovascular and microvascular complications in type 2

9 s suggest that while the concept of distinct macrovascular and microvascular complications of diabete

10 d treatment measures are well documented for macrovascular and microvascular complications, little su

11 dative stress proposed to contribute to both macrovascular and microvascular complications.

12 Both coronary macrovascular and microvascular disease are prognostical

13 ie-2 promoter, we have been able to identify macrovascular and microvascular endothelial cells in fou

14 ll type-specific host response mechanisms in macrovascular and microvascular endothelial cells infect

15 and among those age 18 to 25 years; however, macrovascular and microvascular endothelial function in

16 nalysis included 8811 patients without major macrovascular and microvascular events or death during t

17 The association of major macrovascular and microvascular events with SBP variabil

18 ther young binge drinkers (BD) have impaired macrovascular and microvascular function and cardiovascu

19 , greater percentages of mutated HCCs showed macrovascular and microvascular invasion.

20 on outcomes of diabetes, glucose control, or macrovascular and microvascular outcomes.

21 with primary endothelial cells isolated from macrovascular and microvascular sources of varying speci

22 The propensity to evoked macrovascular and microvascular thrombogenesis was also

23 h404, to investigate its effects on diabetic macrovascular and renal injury in streptozotocin-induced

24 compared the replication of HCMV in primary macrovascular aortic EC (AEC) with that in brain microva

25 ng that classical iSS is not associated with macrovascular arterial pathology.

26 n after the diagnosis of diabetes to prevent macrovascular as well as microvascular complications.

27 linical trials have demonstrated significant macrovascular benefits associated with lowering LDL-C in

28 ever, up to 80% of type 2 diabetics die from macrovascular cardiovascular disease.

29 Unlike in macrovascular cells, TSP-1 protein levels are dramatical

30 proliferation of microvascular cells but not macrovascular cells.

31 etinopathy, neuropathy, and nephropathy) and macrovascular (cerebrovascular, coronary artery, and per

32 ired for 72 hours despite restoration of the macrovascular circulation after control of bleeding in t

33 er responses than men in both the micro- and macrovascular circulatory tests, but a similar progressi

34 ed a considerable hypertrophy, indicative of macrovascular compensation in the chronic occlusion mode

35 -standing disease (>3 years) with or without macrovascular complications (-34% and -29%, respectively

36 d a low prevalence of clinically significant macrovascular complications (4% [95% CI, 1%-10%]) that w

37 hypertension) and chronic microvascular and macrovascular complications among people with diabetes p

38 cognizes a leading scientist in the field of macrovascular complications and contributing risk factor

39 cognizes a leading scientist in the field of macrovascular complications and contributing risk factor

40 nt to minimise the risk of microvascular and macrovascular complications and to slow the progression

41 r the U.S. and trend data for neuropathy and macrovascular complications are lacking.

42 USA, for example, substantial reductions in macrovascular complications in adults aged 65 years or o

43 Microvascular and macrovascular complications in diabetes stem from chroni

44 actors in the development of both micro- and macrovascular complications in diabetic patients.

45 Hyperglycemia causes micro- and macrovascular complications in diabetic patients.

46 control over time reduces microvascular and macrovascular complications in human subjects with type

47 delays the progression of microvascular and macrovascular complications in individuals with type 1 d

48 a lower incidence of both microvascular and macrovascular complications in obese patients with type

49 Assessment of microvascular and macrovascular complications in participants 35 years or

50 hould be used for primary prevention against macrovascular complications in patients (both men and wo

51 n may be a therapeutic approach for treating macrovascular complications in patients with diabetes.

52 1c fails to show an unequivocal reduction of macrovascular complications in type 2 diabetes (T2D); ho

53 d indirect costs with both microvascular and macrovascular complications may be appropriate to establ

54 pidemiological data suggest that the risk of macrovascular complications may predate the onset of hyp

55 She has no known microvascular or macrovascular complications of diabetes and is otherwise

56 Pathogenesis of macrovascular complications of diabetes may involve an a

57 Macrovascular complications of diabetes mellitus are a m

58 stress is a common feature of the micro- and macrovascular complications of diabetes, the present fin

59 t of hyperinsulinemia in the pathogenesis of macrovascular complications of diabetes.

60 thogenesis of microvascular, neurologic, and macrovascular complications of diabetes.

61 ntly needed in order to lessen the burden of macrovascular complications of type 1 and type 2 diabete

62 erogenic and may contribute to the excess of macrovascular complications seen in such patients.

63 with diabetes and leads to microvascular and macrovascular complications that cause profound psycholo

64 contribute to a variety of microvascular and macrovascular complications through the formation of cro

65 Macrovascular complications were observed in 44.2 per 10

66 ar complications, the importance of diabetic macrovascular complications will increase.

67 Because no clear threshold exists for macrovascular complications, a formal balancing of direc

68 ts involved in the development of micro- and macrovascular complications, which are the major sources

69 diabetes mellitus and little or no micro- or macrovascular complications, with the aim of preventing

70 scular complications-46.3% versus 11.5%, and macrovascular complications-20.3% versus 5%, respectivel

71 or measurement of the diabetic state and its macrovascular complications.

72 ted receptor gamma (PPAR gamma) could reduce macrovascular complications.

73 effects of statins in diabetes and its micro/macrovascular complications.

74 ts in rapid progression of microvascular and macrovascular complications.

75 scular complications and also contributes to macrovascular complications.

76 orsened risk for premature microvascular and macrovascular complications.

77 Most patients with diabetes die from macrovascular complications.

78 tight glycemic control to reduce micro- and macrovascular complications.

79 therapeutic gap in the treatment of diabetic macrovascular complications.

80 tion had low prevalence of microvascular and macrovascular complications.

81 rongly with risk of future microvascular and macrovascular complications.

82 Markers of cerebral macrovascular (cortical infarcts), microvascular (subcor

83 olve inflammation-mediated microvascular and macrovascular damage, disruption of lipid metabolism, gl

84 ritional effects with reduced micro- but not macrovascular development in the fetal kidney.

85 s significantly lower in subjects with known macrovascular disease (geometric mean [95% CI], 48.7 mic

86 43% increase in the odds of a subject having macrovascular disease (odds ratio 0.57 [95% CI 0.40-0.83

87 relation between grades of microvascular and macrovascular disease (P=0.10).

88 e 16.5 per 1,000), along with 9,746 cases of macrovascular disease and 1,345 cases of microvascular d

89 els of hpIGFBP-1 are closely correlated with macrovascular disease and hypertension in type 2 diabete

90 tic patients with (DM2-MV) and without (DM2) macrovascular disease compared with control subjects.

91 tially contributing to the increased risk of macrovascular disease conferred by cholesterol elevation

92 syndrome (PCOS) who are at increased risk of macrovascular disease display impaired endothelium-depen

93 istance syndrome relate to each other and to macrovascular disease in American Indians in the Strong

94 rent perspective of epigenetic mechanisms of macrovascular disease in diabetes mellitus and highlight

95 y role in the development of both micro- and macrovascular disease in diabetes, and advanced glycatio

96 to the higher incidence of hypertension and macrovascular disease in insulin-resistant patients.

97 approach to the prevention of progression of macrovascular disease in NIDDM is discussed.

98 ationship between coronary microvascular and macrovascular disease in patients with cardiac transplan

99 l on both the development and progression of macrovascular disease in patients with NIDDM.

100 ti-beta2GPI is significantly associated with macrovascular disease in SSc and independently predicts

101 formation and reduce ischemic symptoms from macrovascular disease in the coronary arteries and perip

102 in, at least in part, the increased risk for macrovascular disease in women with PCOS.

103 may partially explain the lower incidence of macrovascular disease in women.

104 In those with diabetes, the extent of macrovascular disease increases and atherosclerotic plaq

105 Macrovascular disease is a major complication of type 2

106 , the relation of glycosylated hemoglobin to macrovascular disease is less clear.

107 Atherosclerotic macrovascular disease is the leading cause of both morbi

108 wth factor release in tissues compromised by macrovascular disease may be important in reducing clini

109 ascular disease events and suggests that the macrovascular disease of type 1 diabetes is at least par

110 ylated IGFBP-1 (lpIGFBP-1) were unrelated to macrovascular disease or hypertension but did correlate

111 ood glycemic control and with no evidence of macrovascular disease or proteinuria were compared with

112 exerts beneficial actions at early stages of macrovascular disease responses to diabetes and dyslipid

113 However, IVUS analysis for macrovascular disease revealed mostly lesser changes wit

114 Macrovascular disease was evaluated from IVUS studies an

115 ammation in type 1 diabetic subjects without macrovascular disease with that in matched control subje

116 e recruited 20 type 2 diabetic patients with macrovascular disease, 14 nondiabetic patients with coro

117 ted IGFBP-1 (hpIGFBP-1) concentration (known macrovascular disease, 45.1 microg/l [35.1-55.2]; no mac

118 cular disease, 45.1 microg/l [35.1-55.2]; no macrovascular disease, 75.8 microg/l [56.2-95.3]; F = 4.

119 hether risk reductions for microvascular and macrovascular disease, achieved with the use of improved

120 e-diabetes carries some predictive power for macrovascular disease, but most of this association appe

121 ates for the prevention of microvascular and macrovascular disease, especially in combination with st

122 er anti-beta2GPI and aCL are correlated with macrovascular disease, including ischemic digital loss a

123 MVD often coexists with or even precedes macrovascular disease, possibly due to shared mechanisms

124 proaches will materially alter the course of macrovascular disease, reduce health care costs, and imp

125 nce, hypertension, hypercholesterolemia, T2D-macrovascular disease, T2D-microvascular disease, T2D-ne

126 diabetic retinopathy, and increased risk of macrovascular disease.

127 cemia, and, consequently, diffuse micro- and macrovascular disease.

128 cteristics, cardiovascular risk factors, and macrovascular disease.

129 f fibrates in treatment of microvascular and macrovascular disease.

130 f fibrates in treatment of microvascular and macrovascular disease.

131 nts with type 2 diabetes who had evidence of macrovascular disease.

132 a major independent risk factor for diabetic macrovascular disease.

133 BP-1 levels are lower in subjects with overt macrovascular disease.

134 have an increased risk of microvascular and macrovascular disease.

135 ations, but it is unknown whether PTX alters macrovascular disease.

136 ttributable to sequelae of microvascular and macrovascular disease.

137 lar complications as well as the response to macrovascular disease.

138 ptor as a new therapeutic target in diabetic macrovascular disease.

139 nd a major risk factor for microvascular and macrovascular disease.

140 cular risk factors, and 35% had a history of macrovascular disease.

141 Micro- and macrovascular diseases are major causes of morbidity and

142 Coronary microvascular and macrovascular diseases were compared.

143 has been shown to have a protective role in macrovascular disorders.

144 Microvascular and macrovascular EC exhibit different biochemical and funct

145 otypic differences between microvascular and macrovascular EC may alter the ability of these cells to

146 d in human umbilical vein EC (HUVEC), aortic macrovascular EC, and cardiac as well as pulmonary micro

147 rface receptors involved in RBC adherence to macrovascular ECs, including vascular cell adhesion mole

148 x with VEGFR2 only in BREC and not in aortic macrovascular endothelial cells (BAEC).

149 or (VEGF) is a potent mitogen for micro- and macrovascular endothelial cells (ECs).

150 on of E-selectin and ICAM-1 was evaluated on macrovascular endothelial cells after stimulation with S

151 rein, we demonstrate in both coronary artery macrovascular endothelial cells and retinal microvascula

152 tube formation in isolated human intestinal macrovascular endothelial cells but did so in human inte

153 thelial cells but did so in human intestinal macrovascular endothelial cells cocultured with NCM460-N

154 expected, the overall activation profiles of macrovascular endothelial cells derived from human pulmo

155 ype voltage-gated Ca2+ channel, whereas lung macrovascular endothelial cells do not express voltage-g

156 scular endothelial cells (HIMEC) to those on macrovascular endothelial cells from human saphenous vei

157 ependent autophagy in both microvascular and macrovascular endothelial cells leading to suppression o

158 As opposed to macrovascular endothelial cells that constitutively expr

159 Here we report a new cell type, macrovascular endothelial cells, that is infectible with

160 ro expression of these adhesion molecules on macrovascular endothelial cells.

161 f endothelial progenitor cells, may precede "macrovascular endothelial dysfunction." Vasa vasorum neo

162 measures of microvascular perfusion but not macrovascular endothelial function.

163 rker of generalized (i.e., microvascular and macrovascular) endothelial dysfunction.

164 (2)), the major product of cyclooxygenase in macrovascular endothelium, mediates its biological effec

165 reference for adhering to microvascular over macrovascular endothelium, whereas CD14(+)CD16(-) monocy

166 t, only IL-6 was an independent predictor of macrovascular events (hazard ratio per SD increase 1.37

167 of SBP variability were 1.54 (0.99-2.39) for macrovascular events and 1.84 (1.19-2.84) for microvascu

168 Whether intensive control of glucose reduces macrovascular events and all-cause mortality in individu

169 on were associated with an increased risk of macrovascular events and death in analyses adjusted for

170 L-6 significantly improved the prediction of macrovascular events and death.

171 vels, add significantly to the prediction of macrovascular events and mortality in individuals with t

172 We found no difference in the risk of macrovascular events between first insulins in the mediu

173 in the risk of death from any cause or major macrovascular events between the intensive-glucose-contr

174 nsive glycemic control does not reduce major macrovascular events in older adults for at least 10 yea

175 Rates of incident macrovascular events were similar when basal insulin was

176 tions, long-term survival, microvascular and macrovascular events, mental health outcomes, and costs.

177 ed their associations with the risk of major macrovascular events, microvascular complications, and m

178 with type 2 diabetes who have a high risk of macrovascular events.

179 g-term benefits with respect to mortality or macrovascular events.

180 d points were death from any cause and major macrovascular events.

181 <10%) significantly improved brachial artery macrovascular flow-mediated vasodilation and microvascul

182 icrovascular (from bone marrow and skin) and macrovascular (from human umbilical vein) endothelial ce

183 Retinal Vessel Analyser (DVA), and systemic macrovascular function by means of flow-mediated dilatio

184 grated improvement in both microvascular and macrovascular function was associated with >/=10% weight

185 b/m donors to db/db recipient mice benefited macrovascular function, insulin sensitivity, and nephrop

186 In macrovascular injury models, hemophilic mice administere

187 cells in murine models of microvascular and macrovascular injury.

188 Cox regression analysis showed that macrovascular invasion (hazard ratio [HR], 4.8; P < 0.00

189 mph node metastasis (HR, 1.78; P = .01), and macrovascular invasion (HR, 2.10; P < .001) were selecte

190 discontinuation (P = 0.004), PS (P < 0.001), macrovascular invasion (P < 0.001), and extrahepatic met

191 serum alpha-fetoprotein levels (P < 0.001), macrovascular invasion (P = 0.001), poor differentiation

192 microvascular [3.07; 1.02-9.24; P = .05] and macrovascular invasion [8.75; 2.15-35.6; P = .002]).

193 DM is associated with macrovascular invasion among a cohort of transplanted HC

194 logy Group performance status of 1-2, and/or macrovascular invasion or extrahepatic metastasis) were

195 rrhosis, esophageal varices, tumor size, and macrovascular invasion to be statistical and independent

196 HCC patients where histologically confirmed macrovascular invasion was found in 20.2% (17/84) of dia

197 prothrombin time, extrahepatic tumor spread, macrovascular invasion, and reason for discontinuation.

198 operative Oncology Group performance status, macrovascular invasion, extrahepatic disease, and alpha-

199 ion due to adverse effects in the absence of macrovascular invasion, extrahepatic metastases, and det

200 ls, P = 0.038; satellite nodules, P < 0.001; macrovascular invasion, P < 0.001; microvascular invasio

201 er alpha-fetoprotein but less satellites and macrovascular invasion; 68% of HBV versus 89% of HCV wer

202 umor-node-metastasis staging systems; had no macrovascular invasion; and showed the lowest metastasis

203 among patients with multinodular, large, and macrovascular invasive HCC, providing acceptable short-

204 T annotation factors metastatic disease (M), macrovascular involvement of all hepatic veins (V) or po

205 m comprehensive understanding of patterns of macrovascular involvement, better perioperative control

206 and can occur in the absence of conventional macrovascular ischemia.

207 However, direct analyses of macrovascular-microvascular relations in the kidney are

208 uggest that VSMC-derived TF is critical in a macrovascular model of arterial thrombosis.

209 as to ascertain whether pioglitazone reduces macrovascular morbidity and mortality in high-risk patie

210 follow-up from the 24-month visit, 407 major macrovascular (myocardial infarction, stroke, or cardiov

211 th immunostaining to identify the micro- and macrovascular networks.

212 xplanation for microvascular dysfunction and macrovascular occlusion in individuals with hyperhomocys

213 e was no benefit regarding the risk of other macrovascular or microvascular (cardiac, renal and retin

214 follow-up of at least 1 year, and evaluated macrovascular or microvascular events.

215 in comparison with pulmonary artery cells of macrovascular origin.

216 easuring patient-important microvascular and macrovascular outcomes, and completed a meta-analysis of

217 uggest a potential benefit from metformin on macrovascular outcomes, even in patients with prevalent

218 ether such therapy had a long-term effect on macrovascular outcomes.

219 No correlations were observed between other macrovascular parameters and microvascular changes after

220 ssociated with the development of micro- and macrovascular pathologies in diabetes mellitus.

221 tic patients commonly have microvascular and macrovascular pathology that influences their perioperat

222 are significantly different in micro- versus macrovascular stenosis.

223 he burden of type 2 diabetes relates more to macrovascular than microvascular complications.

224 so lead to disseminated complement-dependent macrovascular thrombosis.

225 Each vessel in the macrovascular tree exhibits a distinct TLR profile and s

226 ha (TNF-alpha) upregulates Gb3 in both human macrovascular umbilical vein endothelial cells and human