ライフサイエンスコーパス: CAD

1 CAD (myocardial infarction and its related sequelae).

2 CAD delineations of the area of neoplasm overlapped with

3 CAD discrimination for polygenic risk score, pooled coho

4 CAD events were defined by myocardial infarction or CAD

5 CAD was defined by quantitative coronary angiography (QC

6 ss age strata), ESRD (IRR range, 3.30-9.02), CAD (IRR range, 2.77-10.7), and COPD (IRR range, 5.89-8.

7 linder PAHs decreased following a peak at 10 CAD ATDC but subsequently increased significantly during

8 w systematized information for a total of 51 CAD-associated loci.

9 GPS(CAD) reference distribution using 1,800 CAD cases and 1,163 control subjects newly recruited in

10 the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-

11 93 108), we evaluated associations between a CAD PRS and incident cardiovascular and fatal outcomes.

12 g data from the UK Biobank, we constructed a CAD-GRS based on all known loci, 3 mediating trait-based

13 nly slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C

14 ipid levels and partially overlapping with a CAD PRS.

15 loci, existing evidence suggested additional CAD-associated genes.

16 represent novel therapeutic targets against CAD.

17 rams to gauge the performance of emerging AI CAD systems.

18 giogram examination as control (n = 105) and CAD (n = 116).

19 to stop smoking to limit type 2 diabetes and CAD risk.

20 tithrombotic therapy in patients with DM and CAD.

21 ls (ECFCs) contribute to vascular repair and CAD.

22 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25-1.66, P = 5.63 x 10(-07)), that

23 More than 1700 additional ARIC CAD events have since accrued.

24 revealed that CTRP7 and CTRP15 may serve as CAD markers, while CTRP1 may serve as a marker for the s

25 the design of tandem mass spectrometry-based CAD sequencing strategies for mixtures of lignin degrada

26 of experience from 4 countries to benchmark CAD system performance.

27 or several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body ma

28 The optimal threshold for detecting CAD was a >=67% QCA stenosis in GadaCAD1 and >=63% QCA s

29 mprovement from 90.95 to 98.19% in detecting CAD from healthy controls.

30 Charged aerosol detection (CAD), whose response is proportional to the amount of no

31 ligence (AI)-based computer-aided detection (CAD) systems for use in screening mammography.

32 f PRS) conferred 1.9-fold odds of developing CAD (p < 0.0001).

33 n/Brain Stem, CNS, Computer Aided Diagnosis (CAD), Computer Applications-General (Informatics), Image

34 d 232 patients with cold agglutinin disease (CAD) at 24 centers in 5 countries.

35 ciated with risk of coronary artery disease (CAD) and cancer, whereas the Prudent dietary pattern (PD

36 eated patients with coronary artery disease (CAD) and concomitant type 2 diabetes mellitus (T2DM), T2

37 ts with obstructive coronary artery disease (CAD) are at high risk for cardiovascular disease (CVD) e

38 Because rates of coronary artery disease (CAD) are substantially higher among South Asians, a GPS

39 utes to the risk of coronary artery disease (CAD) can be evaluated as a risk score of multiple varian

40 Coronary artery disease (CAD) causes mortality and morbidity worldwide.

41 Coronary artery disease (CAD) events have been associated with certain antiretrov

42 is associated with coronary artery disease (CAD) events in the general population.

43 icare patients with coronary artery disease (CAD) have been a significant focus of value-based paymen

44 sk scores (PRS) for coronary artery disease (CAD) identify high-risk individuals more likely to benef

45 sk scores (PRS) for coronary artery disease (CAD) identify individuals at higher risk who derive incr

46 ment in severity of coronary artery disease (CAD) in 52% (82 of 159) of all cases.

47 5 as a biomarker of coronary artery disease (CAD) in a real-world clinical practice setting.

48 Applied to coronary artery disease (CAD) in both the WGHS and in JUPITER (N = 8,749), a rand

49 Coronary artery disease (CAD) is a major cause of morbidity and mortality worldwi

50 th before and after coronary artery disease (CAD) is established.

51 hing a diagnosis of coronary artery disease (CAD) is more difficult than it would seem.

52 Coronary artery disease (CAD) is more frequent among individuals with dysglycemia

53 ediction models for coronary artery disease (CAD) is uncertain.

54 atients with stable coronary artery disease (CAD) is unknown.

55 chanisms underlying coronary artery disease (CAD) loci and find molecular biomarkers for CAD.

56 ed were enriched in coronary artery disease (CAD) loci, and this result has specific implications for

57 tates for detecting coronary artery disease (CAD) prior to the current studies.

58 essing the risks of coronary artery disease (CAD) remains controversial.

59 sess for high-grade coronary artery disease (CAD) requiring revascularization.

60 ional mechanisms of coronary artery disease (CAD) risk, as well as the functional regulation of chrom

61 omic loci affecting coronary artery disease (CAD) risk.

62 ociated with higher coronary artery disease (CAD) risk.

63 pathophysiology in coronary artery disease (CAD) that may shed light upon potential diagnostic bioma

64 Evaluation of coronary artery disease (CAD) using coronary computed tomography angiography (CCT

65 ients with unstable coronary artery disease (CAD), and their recruitment to inflamed arteries is impl

66 e associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular f

67 eart failure (CHF), coronary artery disease (CAD), cerebrovascular accidents (CVA), chronic obstructi

68 In other forms of coronary artery disease (CAD), however, it has been controversial whether PCI red

69 raphic diagnoses of coronary artery disease (CAD).

70 ly in patients with coronary artery disease (CAD).

71 to as having stable coronary artery disease (CAD).

72 al causal effect on coronary artery disease (CAD).

73 ble risk factor for coronary artery disease (CAD).

74 th of patients with coronary artery disease (CAD).

75 ed lifetime risk of coronary artery disease (CAD).

76 tes and multivessel coronary artery disease (CAD).

77 isk factors causing coronary artery disease (CAD).

78 Disrupt CAD III (NCT03595176) was a prospective, single-arm mult

79 red to collisionally activated dissociation (CAD) on a series of agrochemicals.

80 bjected to collision-activated dissociation (CAD; MS(2) experiments).

81 In patients with DM with established CAD, secondary prevention with antiplatelet drugs is an

82 In patients with DM without established CAD, primary prevention with aspirin is not routinely ad

83 Cases had a first CAD event during 01.01.2000-31.12.2017.

84 10(-36), OR = 0.95 [95% CI: 0.94-0.96], for CAD; P = 3.35 x 10(-6), OR = 0.96 [95% CI: 0.95-0.98] fo

85 LGE imaging had high diagnostic accuracy for CAD in 2 phase 3 clinical trials.

86 (CAD) loci and find molecular biomarkers for CAD.

87 For 27 genes we infer they are causal for CAD, and for 10 further genes we judge them most likely

88 to affect a number of treatment choices for CAD.

89 luding 5 studies, the pooled RR (95% CI) for CAD in the lowest compared with the highest circulating

90 at TG itself is not a causal risk factor for CAD, but it's shown as a risk factor due to pleiotropic

91 ure television watching is a risk factor for CAD.

92 SNPs showed that TG is not a risk factor for CAD.

93 each of the three potential risk factors for CAD including low density lipoprotein cholesterol (LDL-c

94 suggesting it as one of the risk factors for CAD.

95 iable and multivariable odds ratios (OR) for CAD from conditional logistic regression analyses.

96 is not reliable in screening LT patients for CAD.

97 recommendations and management patterns for CAD primary prevention.

98 P5 may serve as an independent predictor for CAD.

99 A genome-wide PRS for CAD comprising 6 579 025 genetic variants was evaluated

100 c analyses to determine whether high PRS for CAD identifies higher-risk individuals, independent of b

101 A high PRS for CAD is associated with elevated risk for recurrent MACE

102 In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiab

103 in the placebo group was related to PRS for CAD: 17.0% for high PRS patients (>90th percentile) and

104 a 201-variant polygenic risk score (PRS) for CAD and tested for interaction with diabetes prevention

105 as strongly associated with reduced risk for CAD (beta = -0.315, OR = 0.729 per 1 SD (equivalent to 1

106 ing the full datasets, an increased risk for CAD (beta = 0.184, OR = 1.2 per 1 SD (equivalent to 89 m

107 strongly associated with increased risk for CAD (beta = 0.396,OR = 1.486 per 1 SD (equivalent to 38

108 Compared with the middle quintile, risk for CAD was most pronounced for those in the top 5% of the G

109 or individuals at different genetic risk for CAD.

110 ve performance of a polygenic risk score for CAD based on summary statistics from published genome-wi

111 Polygenic risk score for CAD, pooled cohort equations, and both combined.

112 thin healthy limits is a useful strategy for CAD prevention remains to be seen.

113 Testing for CAD differed by LVEF: 53% in HF with reduced EF (LVEF <=

114 for new-onset HF did not receive testing for CAD either during the hospitalization or in the 90 days

115 ew-onset HF, 6672 (39%) received testing for CAD, including 3997 (23%) during the index hospitalizati

116 ption of guideline recommended therapies for CAD as well as clinical outcomes (emergency department p

117 on imaging shows promise as a new tracer for CAD detection and assessment of women, obese patients, a

118 ECFCs from CAD patients that smoke did not respond to FIR in most c

119 their structures were examined using further CAD experiments (MS(n) experiments wherein n = 2-5).

120 ndividuals onto this static ancestry and GPS(CAD) reference distribution using 1,800 CAD cases and 1,

121 Next, a static ancestry and GPS(CAD) reference distribution was built using whole-genome

122 e-wide association study to derive a new GPS(CAD) for South Asians.

123 The new GPS(CAD) has been developed and tested using 3 distinct Sout

124 ronounced for those in the top 5% of the GPS(CAD) distribution-ORs of 4.16, 2.46, and 3.22 in the Sou

125 The GPS(CAD), containing 6,630,150 common DNA variants, had an o

126 This GPS(CAD) was validated in 7,244 South Asian UK Biobank parti

127 .4% versus 10.2%, P<0.0001), have high-grade CAD (0.5% versus 6.5%, P<0.0001), and receive revascular

128 ssociation between CAC and 90-day high-grade CAD and revascularization were assessed.

129 PET/CT patients unlikely to have high-grade CAD or require revascularization within 90 days and unli

130 nd 559 underwent CATH (69%), of whom 10% had CAD requiring PCI.

131 ean age was 60 years, and 11,020 (23.4%) had CAD.

132 ay be recommended for statin therapy if high CAD PRS were considered a guideline-based risk-enhancing

133 all, low serum Mg was associated with higher CAD risk after adjustment for demographics, lifestyle fa

134 ow circulating Mg was associated with higher CAD risk than was higher Mg.

135 An opportunity may exist to improve CAD prevention efforts by integrating both genetic and c

136 for future clinical detection and improving CAD risk assessment.

137 d miRNAs, down-regulation of miR-548aq-3p in CAD ECFCs after FIR treatment was observed in FIR-respon

138 AR duration were associated with low BDNF in CAD.

139 f periodontal viruses such as EBV and CMV in CAD patients with periodontitis suggesting it as one of

140 f CTRPs (CTRP1, CTRP5, CTRP7, and CTRP15) in CAD.

141 as CTRP7 and CTRP15 levels were decreased in CAD patients compared to the non-CAD group.

142 and platelets were significantly elevated in CAD individuals compared to controls.

143 he down-regulation of miR-548aq-3p by FIR in CAD ECFCs, we demonstrated through overexpression and kn

144 el biomarker for therapeutic usage of FIR in CAD patients.

145 the role of non-obstructive CAD patients in CAD diagnostics.

146 community to reconsider the role of T2DM in CAD.

147 biomarkers for indication of FIR therapy in CAD patients.

148 e of BDNF as a potential diagnostic value in CAD that might lead to clinical application.

149 er a median follow-up of 27 y, 2131 incident CAD cases accrued.

150 he examined models, there were 6272 incident CAD events over a median of 8 years of follow-up.

151 tic associations with prevalent and incident CAD between men and women were investigated among 317 50

152 For both prevalent and incident CAD, the associations of comprehensive and genome-wide G

153 we observed a 2.4x higher risk for incident CAD comparing men with high genetic risk to men with low

154 African American) were followed for incident CAD through 2017.

155 rt equations, and both combined for incident CAD.

156 We generated a novel sphingolipid-inclusive CAD risk score, termed SIC, that demarcates patients wit

157 terolemia associates with severely increased CAD risk, it remains less clear to what extent a high po

158 ncreasing variants associates with increased CAD risk.

159 ascular risk factors depending on individual CAD genetic risk profile.

160 ctions or two in MS(3) experiments involving CAD of products formed upon ion-molecule reactions) and

161 use of CAC in PET/CT patients without known CAD in identifying patients unlikely to need revasculari

162 Herein, we leverage CAD-induced oxocarbenium ion generation to trigger ultra

163 ied a sex-interaction whereby the inverse Mg-CAD association was much stronger among women than men.

164 s (ARIC) Study article that evaluated the Mg-CAD association, based on 319 events occurring over 4-7

165 We developed a hybrid ResNet-UNet model CAD system using 5 independent endoscopy data sets.

166 by changes in gene expression in one or more CAD-relevant tissues.

167 .80 * 10(-84)), and the corresponding motif "CAD" captured the risk association of DQ2.5 (OR 2.10, P

168 L quintile had univariable and multivariable CAD event OR=0.56 (95% confidence interval, 0.35-0.91) a

169 sensitivity and specificity for multivessel CAD was 87.4% and 73.0%.

170 In patients with multivessel CAD and diabetes, CABG was associated with improved long

171 obstructive disease: 6.1 per 1,000 PY for no CAD to 34.7 per 1,000 PY for 3-vessel disease).

172 guishes non-obstructive CAD patients from no CAD patients is associated with higher precision, sugges

173 Functional analysis of non-CAD-associated loci implicate genes involved in cardiac

174 ecreased in CAD patients compared to the non-CAD group.

175 and may help with comprehensive noninvasive CAD diagnostics.Supplemental material is available for t

176 l [CI], 0.79-2.33; P = 0.298; nonobstructive CAD, HR, 1.53; 95% CI, 0.84-2.77; P = 0.161; and signifi

177 higher risk than presence of nonobstructive CAD.

178 of this study was to evaluate if obstructive CAD provides predictive value beyond its association wit

179 c profile that distinguishes non-obstructive CAD patients from no CAD patients is associated with hig

180 goal to identify the role of non-obstructive CAD patients in CAD diagnostics.

181 estimation of the likelihood of obstructive CAD by combining a pre-test probability (PTP) model (Dia

182 dels predicted the prevalence of obstructive CAD more accurately in the validation cohorts than the P

183 00, and >1,000), the presence of obstructive CAD was not associated with higher risk than presence of

184 erating characteristic curves of obstructive CAD: for the PTP model, 72 (95% confidence intervals [CI

185 ther they have nonobstructive or obstructive CAD.

186 ation of patients with suspected obstructive CAD.

187 rrelated with the tube formation activity of CAD ECFCs enhanced by FIR.

188 sure the BDNF level in the classification of CAD from healthy controls.

189 e primary endpoint (MACE) comprised death of CAD, nonfatal myocardial infarction, ischemic stroke, or

190 d specificity of gadobutrol for detection of CAD by assessing myocardial perfusion and late gadoliniu

191 Diagnosis of CAD can be approached in two ways: detection of ischemia

192 more suitable biomarker for the diagnosis of CAD patients, whereas CTRP5 may serve as an independent

193 ysis demonstrated superior discrimination of CAD by flurpiridaz PET versus SPECT in the overall popul

194 deeper insights into the genetic etiology of CAD and demonstrate knowledge gaps where further researc

195 is especially important in the evaluation of CAD in immune-driven conditions with increased cardiovas

196 as the first-line test for the evaluation of CAD, the ISCHEMIA trial also resulted in some interestin

197 thermore, by integrating the risk factors of CAD in our analysis, we were able to investigate the cli

198 Identification of typical features of CAD-associated lymphoproliferative disorder in the bone

199 applications of genetic risk score (GRS) of CAD.

200 ng age, male gender, and personal history of CAD (P < 0.05 for all).

201 Patients, without a history of CAD and no elevation in troponin, referred for PET/CT at

202 redictive factors for the vascular lesion of CAD and represent novel therapeutic targets against CAD.

203 or diagnosis of severity of vessel-lesion of CAD patients.

204 as a marker for the single-vessel lesion of CAD.

205 rized as having a low clinical likelihood of CAD, as compared with 11% with the PTP model.

206 ssification of patients to low likelihood of CAD, who need no further testing.

207 of effective, patient-centered management of CAD in patients with T2DM, with emphasis on the emerging

208 m BDNF concentration and blood parameters of CAD achieved significant improvement from 90.95 to 98.19

209 The prevalence of CAD was 27.8% defined by a >=70% QCA stenosis.

210 ive interventions improve CRFs regardless of CAD genetic risk and delivers hypothesis-generating data

211 markers causally associated with the risk of CAD within genomic regions known to be associated with C

212 at were causally associated with the risk of CAD.

213 cal utility of CCTA across various stages of CAD, from the detection of early subclinical disease to

214 on should be considered in future studies of CAD, and GRSs should not be assumed to perform equally w

215 ube length) capacities in a subpopulation of CAD ECFCs.

216 6514 within the BSN gene exert its effect on CAD through central nervous system-lifestyle risk factor

217 A3, ILF3, and N4BP2L2) exert their effect on CAD through height.

218 r of novel loci that have a causal impact on CAD including C5orf38, SF3A3, DHX36, and MRPL33.

219 entifying appropriate candidates for optimal CAD medical therapy and revascularization.

220 nts were defined by myocardial infarction or CAD mortality.

221 r demographics, lifestyle factors, and other CAD risk factors than was higher serum Mg (HR Q1 compare

222 Through our CAD-centered multiomics data analysis approach, we ident

223 d search approach, applied to two phenotypic CAD profiles.

224 A case-control sample of 15 947 prevalent CAD cases and equal number of age and sex frequency-matc

225 Additionally, among prevalent CAD cases, we found an evidence of an inverse associatio

226 baseline subsamples of UK Biobank: prevalent CAD cases (N = 10 287) and individuals without CAD (N =

227 on was found for ischaemic stroke [prevalent CAD (OR 0.78; 95% CI 0.67, 0.90); without CAD (OR 1.09;

228 e CAD PRS strongly associated with prevalent CAD (odds ratio: 1.4 per SD increase in PRS; p < 0.0001)

229 In the present study, we aimed to prioritize CAD-relevant genes based on cumulative evidence from the

230 FIR treatment was observed in FIR-responsive CAD ECFCs by RT-qPCR.

231 n-regulated, respectively, in FIR-responsive CAD ECFCs in both genders.

232 to be men (78% vs. 73%) and had more severe CAD.

233 5% CI, 0.84-2.77; P = 0.161; and significant CAD, HR, 1.96; 95% CI, 0.93-4.15; P = 0.080). Post-LT ou

234 ss echocardiography in detecting significant CAD was 37%.

235 ronary angiography could exclude significant CAD.

236 entifying patients with ACP with significant CAD in the ED setting and reduce unnecessary downstream

237 For stable CAD, PCI did not reduce mortality (RR, 0.98 [95% CI, 0.8

238 0 consecutive patients with suspected stable CAD who had undergone coronary computed tomographic angi

239 syndrome; and (4) patients with truly stable CAD with no recent infarct.

240 in non-ST elevation MI compared with stable CAD patients.

241 For patients with stable CAD, PCI shows no evidence of an effect on any of these

242 The concept of 'stable' CAD is misleading for two important reasons: the continu

243 In dispelling the myth of 'stable' CAD, we explore the pathophysiology of the disease and t

244 to explore associations between subclinical CAD and cumulative exposure to the 10 most frequently us

245 The following subclinical CAD endpoints were analyzed separately: CAC score >0, an

246 and the prevalence and extent of subclinical CAD.

247 n ion-molecule reactions) and the subsequent CAD in the MS(3) experiments were the most important lim

248 GE in adult patients with known or suspected CAD.

249 years of age, 53% were male) with suspected CAD were assessed by stress CMR and followed over a medi

250 ulticenter cohort of patients with suspected CAD, presence of UMI or RMI portended an equally signifi

251 amples from patients treated for symptomatic CAD including non-ST elevation MI, along with healthy ag

252 and independently associated with long-term CAD risk in ARIC and in a meta-analysis with other prosp

253 05) in the cardiac samples of the CAD+P than CAD only (25% and 47.2%, respectively).

254 The CAD PRS strongly associated with prevalent CAD (odds rat

255 The CAD risk associated with a high polygenic load for lipid

256 The CAD system achieved higher accuracy than any of the indi

257 The CAD system classified images as containing neoplasms or

258 The CAD system identified the optimal site for biopsy of det

259 idence of an inverse association between the CAD PRS and risk of all-cause death (OR 0.91; 95% CI 0.8

260 et 5 (80 patients and images) values for the CAD system vs those of the general endoscopists were 88%

261 athways were determined by comparison of the CAD mass spectra measured for undeuterated and deuterate

262 vely, P <0.05) in the cardiac samples of the CAD+P than CAD only (25% and 47.2%, respectively).

263 ulatory variants that mediate binding of the CAD-associated transcription factor TCF21 with ChIPseq s

264 isease-associated TGFB1-SMAD3 pathway to the CAD-associated FN1 gene through a response QTL that modu

265 The TL-CAD association remained significant when adjusting only

266 unctional group characterization compared to CAD.

267 easurement was 9.4 (5.9-13.8) years prior to CAD event.

268 unravel the functional mechanisms underlying CAD loci and to identify novel molecular biomarkers.

269 In unstable CAD, PCI also reduced cardiac death (RR, 0.69 [95% CI, 0

270 diac death, and MI in patients with unstable CAD.

271 with angiographic evidence of 2- or 3-vessel CAD who were treated with either PCI or isolated CABG fr

272 A genome-wide CAD PRS was applied to 47,108 individuals across 3 U.S.

273 -for-service patients >=65 years of age with CAD (mean [SD] age, 75.3 [7.7] years; 39.7% female) care

274 ars before, is independently associated with CAD events after adjusting for multiple traditional and

275 w that these QTLs are highly associated with CAD GWAS loci and correlate to lead SNPs where they show

276 It is unknown whether TL is associated with CAD in PLWH.

277 rd an inflammatory phenotype associated with CAD progression is unknown.

278 ation between eQTLs and loci associated with CAD using SMR/HEIDI approach.

279 genomic regions known to be associated with CAD.

280 on studies revealed 163 loci associated with CAD.

281 t for 18 out of these loci, association with CAD can be explained by changes in gene expression in on

282 ted the association of smoking behavior with CAD (OR 1.24, 95% CI: 1.12-1.37, P = 2 x 10-5), but not

283 zard rates (HR) for mortality increased with CAD severity (normal CATH, HR, 1.35; 95% confidence inte

284 was significantly lower in individuals with CAD (30.69 +/- 5.45 ng/ml) than controls (46.58 +/- 7.95

285 rotic cardiovascular events in patients with CAD and DM.

286 sence of AGE-autoantibodies in patients with CAD and that in parallel to the AGEs themselves, they ma

287 e, termed SIC, that demarcates patients with CAD independently and more effectively than conventional

288 A total of 60 patients with CAD indicated for coronary artery bypass graft surgery (

289 ocioeconomically disadvantaged patients with CAD perform worse on some clinical outcomes, despite pro

290 s periprocedural management of patients with CAD undergoing non-cardiac surgery, including those trea

291 sive risk factor management in patients with CAD, there is mounting evidence that the mechanism by wh

292 In symptomatic patients with CAD, very low hs-cTn concentrations, including hs-cTnI c

293 viously in mostly asymptomatic patients with CAD, was assessed.

294 Flurpiridaz F 18 Injection in Patients with CAD; NCT01347710).

295 are fee-for-service patients >=65 years with CAD at outpatient practices participating in the the Pra

296 nt CAD (OR 0.78; 95% CI 0.67, 0.90); without CAD (OR 1.09; 95% CI 1.04, 1.15), heterogeneity P < 0.00

297 We matched 1-3 PLWH controls without CAD events on sex, age, and observation time.

298 D cases (N = 10 287) and individuals without CAD (N = 393 108), we evaluated associations between a C

299 % CI 0.85, 0.98) compared with those without CAD (OR 1.01; 95% CI 0.99, 1.03) and heterogeneity P = 0

300 mically disadvantaged populations have worse CAD outcomes, and if this reflects the delivery of lower