ライフサイエンスコーパス: CAD

1 CAD of latter products (MS(4) experiments) resulted in e

2 CAD was assessed by (1) vessel score (>/=50% reduction i

3 Fine mapping of the 161 CAD loci generated lists of credible sets of single caus

4 studies and one Malay study (Total N = 2,169 CAD cases and 7,376 controls).

5 ipants previously genotyped, totaling 88,192 CAD cases and 162,544 controls.

6 < 5 x 10(-8)) were further evaluated in 291 CAD cases and 1,848 controls of Asian Indians.

7 ed a genome-wide association study in 34 541 CAD cases and 261 984 controls of UK Biobank resource fo

8 Among the 60 CAD genes, the strongest association was with NBEAL1 tha

9 In analysis limited to 60 CAD genes, we detected strong associations with COL4A2/C

10 analytic sample of 184305 individuals (60801 CAD cases [approximately 70% with myocardial infarction]

11 kb regions surrounding these genes in 84,813 CAD cases and 202,543 controls.

12 ct via coronary angiography by calculating a CAD score.

13 er, the association remains significant in a CAD case control population matched for age and sex.

14 We tested a CAD phenotype inclusive of angina (SOFT; ncases = 10,801

15 was to narrow potential mechanisms affecting CAD risk as we hypothesized that the affected genes may

16 ammation associated with atherosclerosis and CAD in men.

17 Spine density was similar among control and CAD cases but was reduced significantly in AD.

18 lative to 1990-2001, atherosclerotic CVD and CAD rates began to decline more rapidly during the 2002-

19 , the seventh member of the IL-1 family, and CAD is unknown.

20 or patients with PAD alone, comorbid PAD and CAD were more likely to be prescribed antiplatelet thera

21 n association analysis between rs3811047 and CAD in two independent populations with 2,501 patients a

22 hospital treatments were compared by sex and CAD status (MI-CAD or MINOCA).

23 ular outcomes were analyzed by age, sex, and CAD status.

24 harmacological efficacies on both stroke and CAD through multi-ingredient, multi-target, multi-functi

25 g mechanism linking DHI's role in stroke and CAD treatment was inflammatory response in the process o

26 rmacological mechanisms of DHI on stroke and CAD treatment.

27 lated 68 common targets shared by stroke and CAD.

28 ver fat but decreased risks for both T2D and CAD.

29 Patients with darker skin types and CAD were younger at diagnosis (mean [SD] age, 40.7 [3.5]

30 ate the impact of sex, CFR, and angiographic CAD severity on adverse cardiovascular events.

31 rdial infarction, and burden of angiographic CAD (P<0.001), they demonstrated greater risk of CVD eve

32 The extent and severity of angiographic CAD were estimated by using the CAD prognostic index, an

33 potentially responsible for coxib-associated CAD risk.

34 imal cutoff point for discriminating between CAD (presence of stenosis) and the non-stenosis conditio

35 ive trait loci of genes correlated with both CAD severity and circulating CXCL5 levels.

36 By CAD/CAM technique, it can correct jaw deformities simult

37 Cinnamyl alcohol dehydrogenase (CAD) catalyzes the final step in monolignol biosynthesis

38 Chronic actinic dermatitis (CAD) is classically described in older, white men, altho

39 D printing translates computer-aided design (CAD) virtual 3D models into physical objects.

40 xed restorations from computer-aided design (CAD)/computer-aided manufacturing (CAM)-fabricated high-

41 raphy (HPLC) with charged aerosol detection (CAD) was investigated for 50 compounds with a wide range

42 utagenesis allows full comparison with dicot CADs and elucidates the potential signature sequence for

43 The association between CACS and different CAD risk factors was determined as well.

44 Primary chronic cold agglutinin disease (CAD) is a well-defined clinicopathologic entity in which

45 ional assessment of coronary artery disease (CAD) ( 1 , 2 ).

46 investigations for coronary artery disease (CAD) (viewed as a positive control) and Alzheimer's dise

47 The prevalence of coronary artery disease (CAD) among patients with refractory out-of-hospital (OH)

48 oci associated with coronary artery disease (CAD) among predominantly Europeans.

49 ion for significant coronary artery disease (CAD) and cardiovascular events.

50 on in patients with coronary artery disease (CAD) and investigate the effects of human L5 on the elec

51 potential to treat coronary artery disease (CAD) and myocardial infarction (MI).

52 levels and risk of coronary artery disease (CAD) and myocardial infarction using mendelian randomiza

53 sis) left main (LM) coronary artery disease (CAD) are at high risk for adverse events; prior studies

54 n studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance

55 vessel or left main coronary artery disease (CAD) had improved long-term outcomes with coronary arter

56 nce and severity of coronary artery disease (CAD) in patients with sign and symptoms of the disease.

57 Coronary artery disease (CAD) is a chronic inflammatory disease.

58 RATIONALE: Coronary artery disease (CAD) is a complex phenotype driven by genetic and enviro

59 Coronary artery disease (CAD) is a leading cause of morbidity and mortality world

60 Coronary artery disease (CAD) is a significant problem during evaluation for live

61 osis of significant coronary artery disease (CAD) is ambiguous, but nuclear myocardial perfusion imag

62 en, yet obstructive coronary artery disease (CAD) is less prevalent in women.

63 Coronary artery disease (CAD) is the leading cause of death, and genetic factors

64 Coronary artery disease (CAD) is the number one cause of death worldwide and invo

65 ncy reduces risk of coronary artery disease (CAD) is unknown.

66 ict the presence of coronary artery disease (CAD) may help reduce the societal burden of CAD.

67 ovascular events in coronary artery disease (CAD) patients and reducing the hs-CRP level may further

68 ents with suspected coronary artery disease (CAD) requiring noninvasive testing.

69 fects and increased coronary artery disease (CAD) risk.

70 timized approach to coronary artery disease (CAD) screening and management in patients undergoing tra

71 Coronary artery disease (CAD) severity was quantified in each subject via coronar

72 ODS AND Obstructive coronary artery disease (CAD) was defined as >/=50% stenosis on angiography by co

73 Comorbid coronary artery disease (CAD) was present in 24.3% of visits.

74 ity for obstructive coronary artery disease (CAD) were randomly assigned to functional testing (exerc

75 fect progression of coronary artery disease (CAD) when compared with transplantation of a kidney-alon

76 underlying cause of coronary artery disease (CAD), a major cause of morbidity and mortality worldwide

77 lerotic CVD (ACVD), coronary artery disease (CAD), and stroke.

78 rol levels, risk of coronary artery disease (CAD), body mass index, as well as risk of asthma.

79 ls in subjects with coronary artery disease (CAD), but its mechanisms of action in subjects without C

80 e susceptibility to coronary artery disease (CAD), cigarettes smoked per day, lung cancer, insulin re

81 Among patients with coronary artery disease (CAD), improvement of lifestyle-related risk factors (LRF

82 for both stroke and coronary artery disease (CAD), its underlying common molecular mechanisms remain

83 ad a higher risk of coronary artery disease (CAD), myocardial infarction (MI) and their risk factors.

84 ell investigated in coronary artery disease (CAD), the knowledge about monocytes and their heterogene

85 ry, and cognition in carotid artery disease (CAD).

86 atients with stable coronary artery disease (CAD).

87 without history of coronary artery disease (CAD).

88 r Disease (PVD) and Coronary Artery Disease (CAD).

89 ndicate obstructive coronary artery disease (CAD).

90 in the detection of coronary artery disease (CAD).

91 tality and incident coronary artery disease (CAD).This study followed 130,473 UK Biobank participants

92 were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a pre

93 The collision-activated dissociation (CAD) fragmentation patterns (obtained in MS(2) and MS(3)

94 exist for collision activated dissociation (CAD) MS/MS based quantification of aminoxyTMT due to the

95 Collisionally activated dissociation (CAD) of these methanol-eliminated adduct ions (MS(3) exp

96 on and collisionally activated dissociation (CAD) provides new insights into the NECD mechanism.

97 Increased spine extent distinguished CAD cases from controls and AD.

98 DNN-CAD classified polyps as neoplastic or hyperplastic in 0

99 DNN-CAD classified polyps with perfect intra-observer agreem

100 and diagnostic time were compared among DNN-CAD, the novice endoscopists, and the expert endoscopist

101 We developed a system called DNN-CAD to identify neoplastic or hyperplastic colorectal po

102 ed diagnosis with a deep neural network (DNN-CAD) to analyze narrow-band images of diminutive colorec

103 In the test set, the DNN-CAD identified neoplastic or hyperplastic polyps with 96

104 ed to test the diagnostic ability of the DNN-CAD vs endoscopists (2 expert and 4 novice), who were as

105 a of 40 patients with angiography documented CAD and 13 patients with no CAD to correlate the QTc int

106 SERMs, even the cationic amphiphilic drugs (CADs), this mechanism led to the endolysosomal calcium a

107 levels allowed for identifying or excluding CAD with >90% predictive value in 42% of subjects.

108 were 1.25 (95% CI, 1.08-1.45; P = .003) for CAD and 1.24 (95% CI, 1.05-1.46; P = .009) for myocardia

109 e SNP (rs2075291, G > T, G185C) in APOA5 for CAD that reached robust genome-wide significance (Meta P

110 t that IL37 is a new susceptibility gene for CAD, which provides a potential target for the preventio

111 fication of causative variants and genes for CAD.

112 We identified 64 novel genetic risk loci for CAD and performed fine mapping of all 161 risk loci to o

113 lysis using 13 SNPs showed a higher risk for CAD (OR 1.87, 95% CI 1.14-3.08).

114 fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral

115 deficiency is associated with lower risk for CAD.

116 osis and suggest new therapeutic targets for CAD.

117 heimer's disease, but a lesser role than for CAD.

118 In arterioles from CAD subjects, H2O2-induced dilation was significantly re

119 n isolated vascular smooth muscle cells from CAD arterioles, although mRNA or total cellular protein

120 eficiency is associated with protection from CAD.

121 with darker and lighter skin types who have CAD.

122 ize the care of patients suspected of having CAD and improve outcomes while reducing overall health c

123 portant role in microvascular dysfunction in CAD or other vascular diseases.

124 rioles, H2O2-induced dilation is impaired in CAD, which is associated with a transition from a combin

125 to 13.9% of all gene sets to be involved in CAD.

126 erapy on circulating inflammation markers in CAD patients.

127 nd other circulating inflammation markers in CAD patients.

128 Photocontact allergy occurs in CAD but is less studied than contact allergy in this exq

129 e involvement of known canonical pathways in CAD was tested by Ingenuity Pathway Analysis.

130 spine density was decreased significantly in CAD and AD compared to controls.

131 1; 95% CI: 1.25, 1.61) and greatly increased CAD incidence (sub-HR: 1.64; 95% CI: 1.39, 1.93) compare

132 echnique, or group B using an individualized CAD/CAM zirconia abutment (CARES abutment; Institut Stra

133 In addition, we investigated known CAD genes previously identified by meta-analysis of GWAS

134 s of SPECT studies among patients with known CAD have not been evaluated previously.

135 ng women than men with severe multivessel/LM CAD.

136 k for events than men with nonobstructive LM CAD (adjusted hazard ratio, 1.78; P=0.017); sex-specific

137 group analysis, women with nonobstructive LM CAD had a nearly 80% higher risk for events than men wit

138 Nonobstructive LM CAD was frequently detected on coronary computed tomogra

139 After excluding those with obstructive LM CAD, 5166 patients were categorized as having normal LM

140 cance of nonobstructive (1%-49% stenosis) LM CAD, including sex-specific differences, has not been pr

141 ed 1,800 patients with 3-vessel or left main CAD to either CABG or DES-PCI.

142 Among patients with 3-vessel or left main CAD, both CABG and DES-PCI were associated with substant

143 CABG for patients with 3-vessel or left main CAD.

144 As SbCAD4 is the only major CAD isoform in bmr6 mutants, replacing SbCAD4 with L119W

145 Our in-depth characterization of two major CAD isoforms, SbCAD2 (Brown midrib 6 [bmr6]) and SbCAD4,

146 The computer-aided design and manufacture (CAD/CAM) technique was used to guide bony mass removal a

147 lithia-based glass-ceramics (e.g., IPS e.max CAD HT).

148 genes affected by coxibs and those mediating CAD risk and points to further mechanisms, which are pot

149 with obstructive coronary artery disease (MI-CAD).

150 ents were compared by sex and CAD status (MI-CAD or MINOCA).

151 tal mortality was lower after MINOCA than MI-CAD (1.1% versus 2.9%; P<0.0001).

152 was associated with lower mortality than MI-CAD.

153 er risk of post-MI death among women with MI-CAD was most pronounced at younger ages.

154 Among patients with MI-CAD, women had higher mortality than men (3.9% versus 2.

155 on to men was restricted to patients with MI-CAD.

156 ncreasingly utilized in patients with milder CAD.

157 This first crystal structure of a monocot CAD combined with enzyme kinetic data and a catalytic mo

158 Multivessel CAD and residual uncontrolled risk factors are strongly

159 density lipoprotein cholesterol, multivessel CAD, diabetes with glycosylated hemoglobin >7%, and pers

160 s likely to have higher grade or multivessel CAD.

161 among patients with diabetes mellitus and MV-CAD in residents of British Columbia, Canada.

162 stents) in diabetic patients with ACS and MV-CAD.

163 with multivessel coronary artery disease (MV-CAD).

164 In diabetic patients with MV-CAD, CABG was associated with a lower rate of long-term

165 This study aims to identify new CAD genetic loci through a large-scale linkage analysis

166 raphy documented CAD and 13 patients with no CAD to correlate the QTc interval respectively.

167 10.4%; severe CAD left untreated: 15.4%; no-CAD: 14.8%; P=0.765).

168 nisms of action in subjects without CAD (non-CAD) when compared with those with CAD remain unknown.

169 endothelium-independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline,

170 tion involves different K(+) channels in non-CAD versus CAD, resulting in an altered capacity for vas

171 g patients at risk because of nonobstructive CAD, provides better prognostic information than functio

172 showed a higher frequency of nonobstructive CAD, whereas men showed a higher frequency of severely o

173 37) occurred in patients with nonobstructive CAD (1%-69% stenosis).

174 lationship between age, sex, and obstructive CAD status and outcomes post-MI has not been established

175 han 50% stenosis, 29 (33.3%) had obstructive CAD (>/=50% stenosis), 7 (8%) with single-vessel disease

176 Prevalence of obstructive CAD and myocardial ischemia was low (11.9% versus 12.7%,

177 a significantly lower burden of obstructive CAD in comparison with men but were not protected from C

178 chest pain with a low burden of obstructive CAD, myocardial ischemia, and events.

179 d a higher frequency of severely obstructive CAD (P=0.002).

180 FR, particularly absent severely obstructive CAD, may represent a novel target for CVD risk reduction

181 rformed in 1126 patients, showed obstructive CAD (>/=50% stenosis) in 814 patients and severe CAD (>/

182 ent predictors of mortality were obstructive CAD, age, baseline systolic blood pressure, history of d

183 deaths occurred in women without obstructive CAD (<50% stenosis).

184 cohort occurred in women without obstructive CAD, a condition often considered benign and without gui

185 rable to angiogram group without obstructive CAD, and both control group I and control group II (P =

186 t guidance for the group without obstructive CAD.

187 ted at 5% FDR in this study explain 21.2% of CAD heritability and identify 243 loci that implicate pa

188 The accuracy of CAD quantification was most significantly improved for h

189 ion in substrate specificity and activity of CAD can result in significant changes in overall composi

190 ic model view on the genetic architecture of CAD.

191 understanding of the genetic architecture of CAD.

192 understanding of the genetic architecture of CAD.

193 noninvasive method for direct assessment of CAD and plaque characterization with high diagnostic acc

194 (CAD) may help reduce the societal burden of CAD.

195 Clinicians should thus be cognizant of CAD in younger women with darker skin types.

196 to describe the prevalence and complexity of CAD and report survival to hospital discharge in patient

197 of perfusion MR imaging in the detection of CAD.

198 1-2, > 2 segments, P = 0.304) and extent of CAD based on Reardon score (0, 1-9, >10, P = 0.224), com

199 Severity or extent of CAD does not impact post-LT survival, if appropriately r

200 ients based on presence, severity, extent of CAD, and cardiac events within 90 days of LT.

201 nd December 2012 in patients with history of CAD defined as having previous myocardial infarction, pe

202 There were 19 373 patients with a history of CAD who underwent SPECT between 1991 and 2012 (mean age,

203 uggest that among patients with a history of CAD, SPECT was being increasingly utilized in patients w

204 r discriminating between different levels of CAD severity (<70%).

205 s associated with a 34% reduction in odds of CAD (odds ratio: 0.66; 95% confidence interval: 0.44 to

206 Co-primary outcomes were the odds of CAD and myocardial infarction.

207 ion correct the proinflammatory phenotype of CAD macrophages.

208 Results The prevalence of CAD was 39% (36 of 92) according to QCA and SPECT and 64

209 17), we studied angiographic progression of CAD between baseline (pretransplant) and follow-up at 7

210 e, SPK recipients had similar progression of CAD long-term compared with LDK recipients.

211 artile range [IQR], 9.1-11.5) progression of CAD occurred at similar rates (10 of 21 cases in the SPK

212 locus, and variants associated with risk of CAD and cholesterol levels.

213 levels was associated with increased risk of CAD and myocardial infarction.

214 Whether the risk of CAD associated with lifelong genetic exposure to increas

215 igher serum calcium may increase the risk of CAD.

216 factors contribute significantly to risk of CAD.

217 ne (rs3811047) confers a significant risk of CAD.

218 In patients undergoing TAVR, screening of CAD with invasive coronary angiography and ad hoc PCI du

219 spective of prerevascularization severity of CAD (P = 0.357), number of segments involved (0, 1-2, >

220 positive association between the severity of CAD and CACS (P<0.001,r=0.781).

221 and the presence as well as the severity of CAD.

222 By digital slicing of CAD, 3D scan, or tomography data, AM builds objects laye

223 ed to large extensively genotyped studies of CAD, MI, diabetes, lipids, glycaemic traits and adiposit

224 ical therapy for prevention and treatment of CAD.

225 l target for the prevention and treatment of CAD.

226 Genetic risk variants of CAD were linked to development of atrial fibrillation, h

227 utments veneered with pressed ceramics or on CAD/CAM zirconia abutments veneered with hand buildup te

228 e the effects of chromosome 9p21 variants on CAD.

229 ality decline was observed in either ACVD or CAD mortality rates after 2002.

230 free controls, 8 controls with AD pathology (CAD), and 21 AD cases.

231 24.8; p < 0.001), and those with no previous CAD (OR: 8.67; p < 0.001).

232 SPECT utilization in patients with previous CAD increased between 1992 and 2003, but then decreased

233 ct a meta-analysis using the two most recent CAD GWAS.

234 rall, patient survival in the revascularized CAD group was comparable to angiogram group without obst

235 Severe CAD was found in 136 patients (22.5%).

236 CAD left untreated (TAVR+PCI: 10.4%; severe CAD left untreated: 15.4%; no-CAD: 14.8%; P=0.765).

237 (>/=50% stenosis) in 814 patients and severe CAD (>/=70% stenosis) in 708 patients.

238 The proportion of severe CAD (>/=70% stenosis) was lower in patients who had hype

239 (13.8%), coronary angiography showed severe CAD that was left untreated.

240 tients without CAD, and patients with severe CAD left untreated (TAVR+PCI: 10.4%; severe CAD left unt

241 Among patients with severe CAD, 53 patients (8.8%) underwent uncomplicated PCI.

242 ND When invasive coronary angiography showed CAD, the treatment strategy and completeness of revascul

243 Significant CAD was defined as stenosis greater than or equal to 50%

244 ing the presence of anatomically significant CAD.

245 e, 58 [9] years), 92 (44.2%) had significant CAD (fractional flow reserve </=0.80).

246 rty-six (84%) of 55 patients had significant CAD, 35 (64%) of 55 had acute thrombotic lesions, and 46

247 atients being reported as having significant CAD (14%, 595 of 4347 vs 23%, 1000 of 4347; P < .001).

248 ied 41% fewer patients as having significant CAD.

249 CTA in detecting hemodynamically significant CAD.

250 Two highly significant CAD loci were identified on chromosome 17q21.2 (NPL scor

251 commonly because of a finding of significant CAD by site but not by core laboratory interpretation (8

252 score to predict the presence of significant CAD.

253 idual families confirmed the six significant CAD loci and identified seven new highly significant lin

254 eath in patients with or without significant CAD, and the independent predictors of death were age (h

255 We identified 25 new SNP-CAD associations (P < 5 x 10(-8), in fixed-effects meta-

256 In stable CAD outpatients, incident MI occurs at a stable rate of

257 ted factors, and related mortality in stable CAD outpatients.

258 led 4,184 unselected outpatients with stable CAD (i.e., MI or coronary revascularization >1 year prev

259 rt period of time, due to physical strength, CAD/CAM fabrication, and low cost.

260 mputed tomographic angiography for suspected CAD and were followed for 5 years.

261 study involving 208 patients with suspected CAD who underwent CCTA, technetium 99m/tetrofosmin-label

262 udy, 748 consecutive patients with suspected CAD, referred for coronary computed tomography angiograp

263 ibute to cognitive impairment in symptomatic CAD, which suggests that subcortical disconnection withi

264 One hundred eight patients with symptomatic CAD but no dementia were included, and a score less than

265 It is widely believed that CAD is a mass detector.

266 angiographic CAD were estimated by using the CAD prognostic index, and CFR was quantified by using po

267 re identified that, when combined with their CAD products (MS(3) experiments), can be used to sequenc

268 were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased s

269 tized, many without an obvious connection to CAD.

270 thways contributing to the susceptibility to CAD in the multi-ethnic populations from Southeast Asia.

271 Complex but treatable CAD was prevalent in patients with refractory OH VF/VT c

272 based on reactions with TMMS and one or two CAD experiments.

273 A total of 604 patients undergoing CAD screening at the time of TAVR procedure were prospec

274 in LT recipients, irrespective of underlying CAD.

275 e chronic inflammatory process that underpin CAD.

276 as their quantities were determined by using CAD and DAD detectors.

277 es different K(+) channels in non-CAD versus CAD, resulting in an altered capacity for vasodilation d

278 ntegrated measure of large- and small-vessel CAD and myocardial ischemia, identifies patients at risk

279 ile the effect of obesity appears to act via CAD.

280 se in calcium was positively associated with CAD (odds ratio (OR) 1.49, 95% confidence interval (CI)

281 gle-nucleotide polymorphisms associated with CAD as a function of their association with low-density

282 nse SNP, rs2075291, in APOA5 associated with CAD at a genome-wide significance level and provided new

283 f rs3811047 is significantly associated with CAD in two independent populations under a recessive mod

284 The high mortality associated with CAD makes the development of medical interventions that

285 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, i

286 ted recently identified loci associated with CAD.

287 cular targets of coxibs for association with CAD.

288 for photosensitivity who were diagnosed with CAD from November 1, 2000, through August 31, 2015, at t

289 ] age, 50.9 [2.3] years) were diagnosed with CAD.

290 duals) that included cases (individuals with CAD and myocardial infarction) and noncases, with baseli

291 a negative association of CXCL5 levels with CAD at an odds ratio (OR) of 0.46 (95% CI, 0.27-0.75).

292 her and correlated with QTc in patients with CAD compared to controls.

293 e considered in first line for patients with CAD requiring therapy.

294 esting should be considered in patients with CAD, with coexistent photocontact allergy occurring in a

295 ieu in the microvasculature of patients with CAD.

296 were ascertained in up to 21,980 people with CAD and 158,200 control subjects.

297 The association of each SNP with CAD and myocardial infarction was weighted by its associ

298 CAD (non-CAD) when compared with those with CAD remain unknown.

299 farction when compared with patients without CAD, and patients with severe CAD left untreated (TAVR+P

300 its mechanisms of action in subjects without CAD (non-CAD) when compared with those with CAD remain u