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 action, and inflammation also contributes to macrovascular and microvascular complications of diabete

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

11 y-onset type 2 diabetes have higher rates of macrovascular and microvascular complications with incre

12 -standing diabetes mellitus (DM) can lead to macrovascular and microvascular complications, including

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

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

15 ies found strong familial clustering of both macrovascular and microvascular complications.

16 olinergic systems, accompanied by widespread macrovascular and microvascular damage.

17 Both coronary macrovascular and microvascular disease are prognostical

18 of their contribution to the pathogenesis of macrovascular and microvascular diseases associated with

19 helium-dependent and endothelium-independent macrovascular and microvascular dysfunction, and an incr

20 ic mechanisms and the roles of inflammation, macrovascular and microvascular dysfunction, fibrosis, a

21 cardiac metabolism and calcium homeostasis, macrovascular and microvascular dysfunction, increased c

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

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

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

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

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

27 terized by systemic hypotension and impaired macrovascular and microvascular function accompanied by

28 ed with significant weight loss and improved macrovascular and microvascular function across subgroup

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

30 agonist, normalized blood pressure, improved macrovascular and microvascular function, and prevented

31 and reactive hyperemia (RH) (as measures of macrovascular and microvascular function, respectively)

32 Macrovascular and microvascular functional responses to

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

34 Here, we compared macrovascular and microvascular outcomes in 1,657 patien

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

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

37 The propensity to evoked macrovascular and microvascular thrombogenesis was also

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

39 rage relative risks comprised microvascular, macrovascular, and miscellaneous complications.

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

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

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

43 ascular disease, albeit rigorous evidence of macrovascular benefit did not emerge for over a decade.

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

45 stronger predictor of walking distance than macrovascular blood inflow and ABI.

46 in microvascular reactivity, but not ABI or macrovascular blood inflow, significantly correlated wit

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

48 netic SVD and others), and secondary causes (macrovascular causes, tumor, and other rare causes).

49 4D flow MRI quantified total and regional macrovascular CBF, whereas arterial spin labelling (ASL)

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

51 proliferation of microvascular cells but not macrovascular cells.

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

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

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

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

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

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

58 Devastating macrovascular complications (cardiovascular disease) and

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

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

61 evention and mitigation of microvascular and macrovascular complications and mortality burden.

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

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

64 Macrovascular complications are leading causes of morbid

65 nts, has shown that the burden of micro- and macrovascular complications can be favorably modified de

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

67 Microvascular and macrovascular complications in diabetes stem from chroni

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

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

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

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

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

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

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

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

76 1c fails to show an unequivocal reduction of macrovascular complications in type 2 diabetes (T2D); ho

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

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

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

80 Pathogenesis of macrovascular complications of diabetes may involve an a

81 Macrovascular complications of diabetes mellitus are a m

82 a-associated risks for the microvascular and macrovascular complications of diabetes mellitus over 5-

83 ance (IR) are responsible for the micro- and macrovascular complications of diabetes through differen

84 ed strategy for preventing microvascular and macrovascular complications of diabetes, but its role in

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

86 ated in development of the microvascular and macrovascular complications of diabetes.

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

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

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

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

91 Macrovascular complications such as atherosclerosis, myo

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

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

94 Macrovascular complications were observed in 44.2 per 10

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

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

97 ose, glycosylated hemoglobin A1c, BMI, micro/macrovascular complications, and protein/creatinine rati

98 nicity, diabetes duration, microvascular and macrovascular complications, insurance type, and mean Hb

99 ssociated with accelerated microvascular and macrovascular complications, reduced life expectancy, an

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

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

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

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

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

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

106 scular complications and also contributes to macrovascular complications.

107 se and contributes to both microvascular and macrovascular complications.

108 orsened risk for premature microvascular and macrovascular complications.

109 Most patients with diabetes die from macrovascular complications.

110 described in diabetic patients without overt macrovascular complications.

111 diabetes remain at high risk for micro- and macrovascular complications.

112 ly and leads to burdensome microvascular and macrovascular complications.

113 ts in rapid progression of microvascular and macrovascular complications.

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

115 therapeutic gap in the treatment of diabetic macrovascular complications.

116 tion had low prevalence of microvascular and macrovascular complications.

117 rongly with risk of future microvascular and macrovascular complications.

118 fusion defects on clinical read and no known macrovascular coronary artery disease (n=783), MPR remai

119 rtension, myocardial infarction, stroke, and macrovascular coronary artery disease severity using the

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

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

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

123 ations in cerebral blood flow via micro- and macrovascular dilatation.

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

125 43% increase in the odds of a subject having macrovascular disease (odds ratio 0.57 [95% CI 0.40-0.83

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Macrovascular disease is a major complication of type 2

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

146 Atherosclerotic macrovascular disease is the leading cause of both morbi

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

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

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

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

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

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

153 Macrovascular disease was evaluated from IVUS studies an

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

155 hypertension, dyslipidemia, atherosclerotic macrovascular disease) among children and/or adults with

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

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

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

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

160 sive glycemic control also decreases risk of macrovascular disease, albeit rigorous evidence of macro

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

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

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

164 ingly prevalent, including microvascular and macrovascular disease, obesity, metabolic syndrome, oste

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

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

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

168 diabetic retinopathy, and increased risk of macrovascular disease.

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

170 cteristics, cardiovascular risk factors, and macrovascular disease.

171 f fibrates in treatment of microvascular and macrovascular disease.

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

173 a major independent risk factor for diabetic macrovascular disease.

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

175 have an increased risk of microvascular and macrovascular disease.

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

177 ttributable to sequelae of microvascular and macrovascular disease.

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

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

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

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

182 an duration of diabetes, 6.3 years; 42% with macrovascular disease; 59% had undergone metformin monot

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

184 h in people with diabetes, most notably from macrovascular diseases such as myocardial infarction or

185 Coronary microvascular and macrovascular diseases were compared.

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

187 Microvascular and macrovascular EC exhibit different biochemical and funct

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

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

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

191 , indicating replacement of microvascular by macrovascular ECs.

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

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

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

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

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

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

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

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

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

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

202 As opposed to macrovascular endothelial cells that constitutively expr

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

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

205 Only 6 subjects had a nonpathological study: macrovascular endothelial dysfunction was present in 60%

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

207 measures of microvascular perfusion but not macrovascular endothelial function.

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

209 EC populations in the mouse lung, including macrovascular endothelium (maEC), microvascular endothel

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

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

212 and/or LDL-cholesterol <100 mg/dL) and first macrovascular endpoints (nonfatal myocardial infarction,

213 -group differences in microvascular, but not macrovascular, endpoints.

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

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

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

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

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

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

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

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

222 ere were 233 (40.5%) first microvascular and macrovascular events in intervention and 274 (48.0%) in

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

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

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

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

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

228 idence of between-group differences in first macrovascular events.

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

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

231 <10%) significantly improved brachial artery macrovascular flow-mediated vasodilation and microvascul

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

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

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

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

236 mpanied by impaired diastolic, systolic, and macrovascular functions; cardiac inflammation (increased

237 d study of healthy young adults, we compared macrovascular (i.e. brachial artery flow-mediated dilata

238 0.0001), as well as pathological evidence of macrovascular infiltration and large-vessel occlusion ob

239 Collectively, these findings suggest that macrovascular infiltration and spikes in CTC clusters wi

240 validation cohort, radiological evidence of macrovascular infiltration emerged as the strongest pred

241 rovements in microvascular function, but not macrovascular inflow or ABI, correlate with improvement

242 In macrovascular injury models, hemophilic mice administere

243 cells in murine models of microvascular and macrovascular injury.

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

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

246 Macrovascular invasion (MaVI) defines advanced-stage hep

247 sease (LAD), extrahepatic disease (EHD), and macrovascular invasion (MVI).

248 ment for hepatocellular carcinoma (HCC) with macrovascular invasion (MVI).

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

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

251 h CP class B/C (X(2) = 6.7, p = 0.01), while macrovascular invasion (X(2) = 0.5, p = 0.5) and ECOG sc

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

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

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

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

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

257 TCGA Liver Hepatocellular Carcinoma cohort, macrovascular invasion was present in 5% (n = 17) of tum

258 of metastatic disease, and low prevalence of macrovascular invasion, alpha-fetoprotein >400 ng/mL, AL

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

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

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

262 ratification factors of geographical region; macrovascular invasion, extrahepatic spread, or both; an

263 of six], stratified by geographical region; macrovascular invasion, extrahepatic spread, or both; ba

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

265 Organization tumor grade, microvascular and macrovascular invasion, satellite nodules, and tumor cap

266 Patients in any group could have macrovascular invasion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 in comparison with pulmonary artery cells of macrovascular origin.

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

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

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

285 fit neatly into the historical microvascular/macrovascular paradigm.

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

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

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

289 artiles with microvascular (albuminuria) and macrovascular (peripheral artery disease and coronary ar

290 odels were used to assess the association of macrovascular reactive hyperemic blood inflow within the

291 g the relationship between microvascular and macrovascular risk factors, improving multimodal imaging

292 elevated glucose is ineffective in reducing macrovascular risk in diabetes and suggests new targets

293 Macrovascular shunting was present in 33% of subjects, w

294 are significantly different in micro- versus macrovascular stenosis.

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

296 Endothelial injury and microvascular/macrovascular thrombosis are common pathophysiological f

297 ome that may manifest with microvascular and macrovascular thrombosis.

298 so lead to disseminated complement-dependent macrovascular thrombosis.

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

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