ライフサイエンスコーパス: SCD

1 SCD cases were adjudicated by a group of physicians thro

2 SCD during intense exertion occurred in 61% of cases; AR

3 SCD incidence was 1.86 per 1000 person-years.

4 SCD may be prevented by implantable cardioverter-defibri

5 SCD may represent a new target for therapeutic intervent

6 SCD prevention strategies are hampered by over-reliance

7 In Mali, Cameroon, and Ivory Coast, 2407 SCD patients (1751 SS or sickle beta-zero-thalassemia [S

8 While 22 of 32 SCD eyes (68.8%) had retinopathy on biomicroscopy, by UW

9 inase type I-alpha regulatory subunit) in 58 SCD patients (P = 7.9 x 10 - 7) and 58 HapMap Yoruba sam

10 hy on biomicroscopy, by UWFA 4 of 24 (16.7%) SCD eyes had peripheral arterial occlusion (Goldberg I),

11 ents on raw microscopy image datasets from 8 SCD patients (over 7,000 single RBC images) through a 5-

12 Our initial objective was to derive a SCD prediction model using the ARIC cohort and validate

13 ell transplantation approach to generating a SCD model in PKCdelta-deficient mice.

14 X2(-/-)/SCD, six NADPHox-deficient mice on a SCD; (4) NOX2(-/-)/HFD, six NADPHox-deficient mice on a

15 primary composite outcome of SCD or aborted SCD among consecutive referrals with dilated cardiomyopa

16 ing after the index hospitalization for ACS, SCD was associated with recurrent myocardial infarction

17 ibitor targeting MIF's tautomerase activity (SCD-19) significantly reduces the inflammatory response

18 clinical pharmaceutical research addressing SCD and the new and old drugs in the pipeline make it re

19 The main outcome was physician-adjudicated SCD.

20 prospectively recruited pediatric and adult SCD patients and healthy controls in Cameroon, Ivory Coa

21 onal multicenter registry, we identified all SCD cases, matched to living controls by age, sex, conge

22 n clusters of S/TQ motifs that constitute an SCD domain.

23 In contrast, an SCD-associated UBIAD1 variant inhibited reductase ERAD,

24 In an SCD mouse model, we observed increased AHR and higher le

25 n between entorhinal cortical tau burden and SCD was largely unchanged after accounting for Abeta bur

26 After adjustment for age, sex, country, and SCD phenotype, a low hemoglobin level was significantly

27 xamine consequences of UBIAD1 deficiency and SCD-associated UBIAD1 on reductase ERAD and cholesterol

28 The AD, MCI, and SCD groups were divided into a sex- and age-matched trai

29 AD, conversion of MCI to AD, stable MCI, and SCD with good to excellent accuracy and AUC values.

30 The link between myofilaments and SCD has been known for over 25 years, but identifying mu

31 associations between arterial stiffness and SCD-related vascular complications.

32 inflammatory responses between wild-type and SCD animals during infection, SCD mice continued to dete

33 tion between echocardiographic variables and SCD, adjusting for Framingham risk score variables, coro

34 d 352,656 non-AF patients without antecedent SCD/VAs were identified.

35 we develop a personalized approach to assess SCD risk in post-infarction patients based on cardiac im

36 al factors must be considered when assessing SCD in clinically healthy older adults.

37 To examine associations between SCD and global Abeta and tau burdens in regions of inter

38 In the first 30 days after CABG, SCD (n=5) accounted for 7% of all deaths.

39 ped from this model and yielded a calculated SCD probability ranging from 0.1% to 56.7% (C statistic,

40 In conclusion, SCD patients with the FCGR2Cnc-ORF polymorphism have ove

41 note is the overrepresentation of conserved SCD-containing proteins involved in pathways related to

42 tage of transferred globin necessary to cure SCD is currently not known.

43 vascular incidents and sudden cardiac death (SCD) are among the leading causes of premature death in

44 den cardiac arrest and sudden cardiac death (SCD) are terms often used interchangeably.

45 Sudden cardiac death (SCD) from arrhythmias is a leading cause of mortality.

46 ough the occurrence of sudden cardiac death (SCD) in a young person is a rare event, it is traumatic

47 knowledge of causes of sudden cardiac death (SCD) in athletes and its precipitating factors is necess

48 The risk of sudden cardiac death (SCD) in patients with heart failure after coronary arter

49 primary prevention of sudden cardiac death (SCD) in those with a left ventricular ejection fraction

50 Sudden cardiac death (SCD) is a devastating event afflicting 350 000 Americans

51 Sudden cardiac death (SCD) is a major cause of mortality in adult congenital h

52 Sudden cardiac death (SCD) is the leading cause of mortality in athletes durin

53 Sudden cardiac death (SCD) is the most devastating manifestation of ventricula

54 ographic predictors of sudden cardiac death (SCD) within 2 population-based cohorts.

55 s an elevated risk for sudden cardiac death (SCD), and implantable cardioverter-defibrillators (ICDs)

56 val is associated with sudden cardiac death (SCD).

57 an increased risk for sudden cardiac death (SCD).

58 t an increased risk of sudden cardiac death (SCD).

59 thy is associated with sudden cardiac death (SCD).

60 subjects with subjective cognitive decline (SCD) after using the W score method to remove confoundin

61 een reports of subjective cognitive decline (SCD) and biomarkers of early Alzheimer disease (AD) path

62 patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), Alzheimer's disea

63 Changes in stearoyl-coenzyme A desaturase (SCD) expression and activity were evaluated in the ovalb

64 atty-acid synthase, stearoyl-CoA desaturase (SCD)-1, and apoB.

65 ild-type (WT) mice fed a standard chow diet (SCD); WT/HFD, six WT mice fed a HFD; NOX2(-/-)/SCD, six

66 ion could be reproduced in the two different SCD murine models to ascertain the underlying mechanisms

67 children with SCD, cluster 1 differentiated SCD severity using a published scoring index.

68 serious complication of sickle cell disease (SCD) and a leading cause of hospitalization and death in

69 a life-long symptom in sickle cell disease (SCD) and a predictor of disease progression and mortalit

70 obinopathies, including sickle cell disease (SCD) and beta-thalassemia.

71 5%-77% of children with sickle cell disease (SCD) and occurs even in the absence of asthma.

72 lation, we assessed two sickle cell disease (SCD) cohorts for genetic associations with plasma EPO, b

73 Sickle cell disease (SCD) complications are associated with increased morbidi

74 anced correction of the sickle cell disease (SCD) genetic defect in patient-specific induced Pluripot

75 aso-occlusive episodes, sickle cell disease (SCD) has continued to be treated primarily with analgesi

76 the pathophysiology of sickle cell disease (SCD) in a NRF2 knockout (SCD/NRF2(-/-)) transgenic mouse

77 f newborn screening for sickle cell disease (SCD) in sub-Saharan Africa and other resource-limited ar

78 Sickle cell disease (SCD) is a hematological disorder leading to blood vessel

79 Sickle cell disease (SCD) is a highly complex genetic blood disorder in which

80 Sickle cell disease (SCD) is a major global health concern.

81 Sickle cell disease (SCD) is a severe genetic blood disorder characterized by

82 blood genetic disease, sickle cell disease (SCD) leads to a chronic vasculopathy with multiple organ

83 scous" subphenotypes of sickle cell disease (SCD) patients is based on North American studies.

84 Patients with sickle cell disease (SCD) suffer from intense pain that can start during infa

85 Sickle cell disease (SCD), a congenital hemolytic anemia that exacts terrible

86 In sickle cell disease (SCD), abnormal adhesion of RBCs to endothelial cells is

87 revent complications of sickle cell disease (SCD), access to care is not universal.

88 (S1P) is detrimental in Sickle Cell Disease (SCD), but the mechanistic basis remains obscure.

89 pain conditions such as sickle cell disease (SCD), for which patients may require opioid analgesics t

90 of adult patients with sickle cell disease (SCD), particularly those with the homozygous genotype.

91 In sickle cell disease (SCD), treatment of recurrent vasoocclusive episodes, lea

92 Sickle cell disease (SCD)-associated nephropathy is a major source of morbidi

93 rtance in patients with sickle cell disease (SCD).

94 rials for patients with sickle cell disease (SCD).

95 ent vasoconstrictor, in sickle cell disease (SCD).

96 oal in the treatment of sickle cell disease (SCD).

97 th clinical severity in sickle cell disease (SCD).

98 10% of adolescents with sickle cell disease (SCD).

99 Systemic circulatory dysfunction (SCD) was estimated by plasma renin (PRC) and copeptin (P

100 associated with Schnyder corneal dystrophy (SCD), a human disorder characterized by corneal accumula

101 showed good to excellent discrimination for SCD risk (c-statistic 0.820 in ARIC and 0.745 in CHS).

102 hma patients and controls were evaluated for SCD expression and activity.

103 s have identified Meis1 as a risk factor for SCD.

104 nary disease were important risk factors for SCD/VAs.

105 ning effective therapeutic interventions for SCD.

106 lop and validate a risk prediction model for SCD (HCM Risk-SCD [hypertrophic cardiomyopathy risk-SCD]

107 g the overall cost of screening newborns for SCD and thus increasing the practicality of universal ne

108 nstrated similar and accurate prediction for SCD using both the original, uncalibrated score and the

109 ive ability of these ICD recommendations for SCD in ACHD patients.

110 h MWT>/=35 mm did not have a higher risk for SCD (hazard ratio, 0.22; 95% confidence interval, 0.03-1

111 A model developed to calculate the risk for SCD in trials with systematic collection of left ventric

112 ut identifying mutation carriers at risk for SCD is still a challenge and currently the only effectiv

113 icular to identify those at highest risk for SCD.

114 ths, suggesting that risk stratification for SCD should occur early in the postoperative period, part

115 m the direct, pathophysiologic substrate for SCD.

116 n is, to date, the only curative therapy for SCD, but its application is limited by availability of a

117 ct that we will soon have new treatments for SCD.

118 form variations of 12,727 genes derived from SCD blood mononuclear cells.

119 HDAd/EBV transduction of keratinocytes from SCD patients resulted in footprint-free iPSCs with high

120 Greater SCD was associated with increasing entorhinal cortical t

121 477) surgical ventricular reconstruction had SCD; 311 died of other causes.

122 Patients who had SCD and those who did not die were younger and had fewer

123 For patients at high SCD risk, prophylactic insertion of implantable cardiove

124 eversing vasoocclusion in nude and humanized SCD mouse models of acute vasoocclusive episodes using i

125 tivity and 83.3% specificity, and identified SCD newborns with 100.0% sensitivity and 70.7% specifici

126 vasively by echocardiography, helps identify SCD patients at risk for pulmonary hypertension, but def

127 eports that some of these treatments improve SCD-related pulmonary hypertension.

128 ameters to clinical characteristics improves SCD risk prediction.

129 In SCD mice, 0.025, 0.05, or 0.1 mg/kg MEK1/2 inhibitor als

130 art rate, increased more rapidly with age in SCD patients and was higher in SCD than in control adult

131 ariation of FCGR and RBC alloimmunization in SCD.

132 hological role of imbalanced Lands' cycle in SCD erythrocytes, novel molecular basis regulating Lands

133 hroblast-secreted factor that is elevated in SCD, mediates AHR.

134 and treatment of vaso-occlusive episodes in SCD.

135 Loss of NRF2 function in SCD/NRF2(-/-) mice produced greater splenomegaly with re

136 y with age in SCD patients and was higher in SCD than in control adults.

137 hat plasma EPO elevation with hydroxyurea in SCD is independent of hypoxic responses and that genetic

138 ading to vaso-occlusion and tissue injury in SCD has now resulted in a burgeoning effort to identify

139 Mean cf-PWV was lower in SCD patients (7.5+/-2.0 m/s) than in controls (9.1+/-2.4

140 PWV and AI are deeply modified in SCD patients in comparison with healthy controls.

141 mmatory cytokines, and adhesion molecules in SCD mice.

142 g therapies to reduce pulmonary morbidity in SCD.

143 sodes (VOE), the major cause of morbidity in SCD.

144 a major cause of morbidity and mortality in SCD patients.

145 profile predictive of these poor outcomes in SCD.

146 rent treatment of moderate to severe pain in SCD is mostly reliant upon opioids; however, long-term u

147 understanding of the pathobiology of pain in SCD.

148 preventive strategies to ameliorate pain in SCD.

149 protection from diverse renal pathologies in SCD mice, and suggest that long-term ETA receptor antago

150 Although the pulmonary artery pressure in SCD patients with pulmonary hypertension is only moderat

151 of exclusively targeting the ETA receptor in SCD.

152 diated pathogenic metabolic reprogramming in SCD and novel therapeutic avenues.

153 conclusion, severe anemia at steady state in SCD patients living in West and Central Africa is associ

154 We assessed arterial stiffness in SCD patients and looked for associations between arteria

155 ressing optimal IVF management during VOE in SCD.

156 While asthma increases SCD morbidity and mortality, the mechanisms underlying t

157 hydroxyurea) and validated it in independent SCD patients (n = 183, P = 0.018).

158 t ventricular fibrosis with exercise-induced SCD reinforces the need for early detection and abstinen

159 wild-type and SCD animals during infection, SCD mice continued to deteriorate and failed to resolve

160 hat do not necessarily interact to influence SCD endorsement.

161 58; P = .001), and no interaction influenced SCD (beta = -0.36; 95% CI, -0.34 to 0.09; P = .25).

162 ickle cell disease (SCD) in a NRF2 knockout (SCD/NRF2(-/-)) transgenic mouse model.

163 ent-binding protein-beta, pyruvate kinase L, SCD-1, and DGAT1, key transcriptional factors and enzyme

164 t multiple underlying pathways that motivate SCD that do not necessarily interact to influence SCD en

165 ity of PLA2 but not LPCAT in human and mouse SCD erythrocytes.

166 single-crystal diamond substrate (4 x 4 muG-SCD MEA) for real-time monitoring of exocytotic events f

167 easing the practicality of universal newborn SCD screening programs in resource-limited settings.

168 or genetic disease by cascade screening, no SCD has occurred over a median follow-up of 5.6 years (5

169 ment of effective, low-cost, and noninvasive SCD risk stratification tools is necessary.

170 D); WT/HFD, six WT mice fed a HFD; NOX2(-/-)/SCD, six NADPHox-deficient mice on a SCD; (4) NOX2(-/-)/

171 rious locations throughout the Indian Ocean (SCD).

172 In total, 41% of SCD cases and 17% of controls had an ICD recommendation

173 experience the majority, as many as 80%, of SCD events, which occur in the setting of more preserved

174 rtant opportunity to understand the basis of SCD and AD risk.

175 ytosis, key pathophysiological biomarkers of SCD.

176 ow-up of 23.6 years, a total of 346 cases of SCD were identified.

177 This study investigated causes of SCD and their association with intensive physical activi

178 tate hemolysis and vascular complications of SCD among sub-Saharan African patients.

179 for the prevention of renal complications of SCD.

180 , may also play a role in the development of SCD vasculopathy.

181 ge 0-22 years) with a discharge diagnosis of SCD and either ACS or pneumonia.

182 nt knowledge relevant to the epidemiology of SCD and to strategies for prevention, resuscitation, and

183 cking PKCdelta despite full establishment of SCD phenotypes.

184 aimed to identify important risk factors of SCD/VAs among AF patients.

185 A unique feature of SCD is vaso-occlusive crises (VOCs) characterized by epi

186 About half of SCD-related pulmonary hypertension patients have precapi

187 of vaso-occlusive episodes, the hallmark of SCD.

188 ease the dissemination and implementation of SCD treatment guidelines are warranted as is comparative

189 method was used to estimate the incidence of SCD accounting for the competing risk of other deaths.

190 The cumulative incidence of SCD and cardiovascular death was examined according to t

191 The 5-year cumulative incidence of SCD was 8.5%.

192 nt study was to investigate the incidence of SCD/VAs amongst patients with and without AF.

193 Inhibition of SCD in mice promoted airway hyper-responsiveness.

194 Inhibition of SCD reduced surfactant protein C expression and suppress

195 to these guidelines, whereas the majority of SCD victims remained unrecognized.

196 m desaturation index (an indirect measure of SCD) was significantly reduced in nonobese asthma patien

197 rstanding about the underlying mechanisms of SCD in patients with sarcomeric mutations will also allo

198 A minority of SCD cases had an ICD recommendation according to these g

199 ed pain in a targeted knockin mouse model of SCD (TOW mouse) that exclusively expresses human alleles

200 We sought to develop a predictive model of SCD among US adults.

201 of nephropathy in a humanized mouse model of SCD.

202 algesic effect in transgenic mouse models of SCD and cancer as well as complete Freund's adjuvant-ind

203 he prespecified primary composite outcome of SCD or aborted SCD among consecutive referrals with dila

204 d the temporal trends in the pathogenesis of SCD.

205 rs that contribute to the pathophysiology of SCD.

206 o T-peak remained the strongest predictor of SCD (per 1-SD increase: hazard ratio, 1.21; 95% confiden

207 ncidence, timing, and clinical predictors of SCD after CABG.

208 s used to examine and identify predictors of SCD.

209 ded to optimize management and prevention of SCD in this population.

210 ssify the phenotype and genotype profiles of SCD in a consecutive series of victims of SCD in Norther

211 The numerically greatest monthly rate of SCD was in the 31- to 90-day time period.

212 Red blood cells (RBCs) of SCD patients have diverse shapes that reveal important b

213 was associated with a 49% increased risk of SCD (hazard ratio, 1.49; 95% confidence interval, 1.01-2

214 athy and an LVEF >/=40% at increased risk of SCD and low risk of nonsudden death who may benefit from

215 improve, consequently decreasing the risk of SCD and obviating the need for an ICD.

216 stimulating hormone and FT4 with the risk of SCD by using an age- and sex-adjusted Cox proportional-h

217 Therefore, those at high risk of SCD may gain longevity from successful implantable cardi

218 The monthly risk of SCD shortly after CABG among patients with a low left ve

219 The risk of SCD with the QT interval is driven by prolongation of th

220 vere LV systolic dysfunction at high risk of SCD.

221 between MWT and the estimated 5-year risk of SCD.

222 ine the relation between MWT and the risk of SCD.

223 In conclusion, the risk of SCD/VAs amongst AF patients was 1.64-fold higher compare

224 The increased risk of SCD/VAs in AF patients was consistently observed in diff

225 The annual risk of SCD/VAs was higher in AF than non-AF groups (0.97% versu

226 dative stress and the phenotypic severity of SCD.

227 lobin (HbS) synthesis as well as sickling of SCD erythroid cells under hypoxic conditions.

228 NRF2 loss impaired survival of SCD pups during gestation and in the first 2 months of l

229 s therapeutic potential for the treatment of SCD.

230 Among victims of SCD as a first cardiac event (n=2697), the proportion wi

231 of SCD in a consecutive series of victims of SCD in Northern Finland.

232 Proportion of SCDs associated with hypertensive heart disease with lef

233 hinal cortical, and inferior temporal tau on SCD, controlling for age, sex, educational attainment, a

234 Transduced primary normal or SCD human HSCs expressing the lineage-specific BCL11A sh

235 nheritance of HPFH with beta-thalassemia- or SCD-associated gene mutations alleviates their clinical

236 e profiles of the segmental order parameters SCD((i)) as a function of acyl segment position (i).

237 ventricular fibrosis most strongly predicted SCD during exertion.

238 prediction equation was better at predicting SCD than the 2013 American College of Cardiology/America

239 assessment may have the potential to prevent SCD and avoid unnecessary ICD implantations.

240 val to its individual components will refine SCD prediction in the community.

241 We restrict SCD hereafter to cardiac arrest due to ventricular fibri

242 M Risk-SCD [hypertrophic cardiomyopathy risk-SCD]).

243 te a risk prediction model for SCD (HCM Risk-SCD [hypertrophic cardiomyopathy risk-SCD]).

244 age, 33 years; 81% men), there was a single SCD end point (annual rate, 0.2%; 95% confidence interva

245 xisting methods that can be adapted to solve SCD, which consider only one of segmentation quality or

246 Mutations of the genes in the SREBP-SCD pathway reduce satiety quiescence.

247 than did those who died of causes other than SCD.

248 hoc whole-brain analysis also indicated that SCD was predominantly associated with greater tau burden

249 Our model reveals that SCD exhibits substantial heterogeneity even within a par

250 trategies against influenza infection in the SCD population.

251 Model performance was assessed in the SCD-HeFT cohort (Sudden Cardiac Death in Heart Failure T

252 Among participants in the SCD-HeFT who had a repeated EF assessment during the cou

253 y testing by IEF, without missing any of the SCD newborns in the studied cohort.

254 A subset of 1902 participants (75.4%) of the SCD-HeFT had a repeated assessment of EF a mean (SD) of

255 Only the SCD prediction model, however, demonstrated similar and

256 Furthermore, we evaluated whether the SCD prediction equation was better at predicting SCD tha

257 tory chromatin interactions in heart tissue (SCD, SLF2 and MAPK8).

258 fects, thus increasing the susceptibility to SCD.

259 dy, DNA samples from 2 cohorts of transfused SCD patients were combined (France and The Netherlands).

260 at both genetic and bone marrow-transplanted SCD mice had greater mortality in response to influenza

261 he art related to defibrillation in treating SCD, including a brief history of the evolution of defib

262 Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), which randomly assigned 2521 patients to plac

263 Moreover, T( *)cr proportional, variant -SCD, where SCD is a recently proposed "sequence charge d

264 Application of the AD versus SCD discrimination map for prediction of MCI subgroups r

265 zed to predict ventricular fibrillation (VF)/SCD during follow-up.

266 The primary outcome was SCD as adjudicated by a blinded committee.

267 1640 cardiovascular deaths, 513 (31.3%) were SCD.

268 Patients were SCD adults at risk of early death despite standard-of-ca

269 r, T( *)cr proportional, variant -SCD, where SCD is a recently proposed "sequence charge decoration"

270 Sixteen adolescents with SCD, aged 10-19 years (mean age 14.9 years), and 5 age-e

271 ore-frequent retinopathy in adolescents with SCD.

272 n and death in both children and adults with SCD.

273 transplantation for children and adults with SCD.

274 er the index event that were associated with SCD after NSTE ACS were identified.

275 nce interval, 1.06-1.34) was associated with SCD and not any of the other components in separate mode

276 parameters is independently associated with SCD in the general population.

277 trical cardiac disorders are associated with SCD in young athletes, the majority of which can be iden

278 o address various mechanisms associated with SCD.

279 ry evaluation for conditions associated with SCD.

280 ies cholesterol accumulation associated with SCD.

281 c peptide were most strongly associated with SCD.

282 val are responsible for its association with SCD.

283 patterns of antibiotic use for children with SCD hospitalized for ACS and to determine whether receip

284 a third cohort of West African children with SCD, cluster 1 differentiated SCD severity using a publi

285 et to T-peak, and T-peak to T-wave end) with SCD in 12 241 participants (54+/-5.7 years; 26% black; 5

286 dition to episodic acute pain, patients with SCD also report chronic pain.

287 Included were 3627 patients with SCD and 943 controls.

288 translational implications for patients with SCD and warrant a large-scale prospective clinical study

289 Patients with SCD experience disproportionately greater morbidity and

290 tion of oral THU-decitabine to patients with SCD was safe in this study and, by targeting DNMT1, upre

291 ng cohorts consisting of adult patients with SCD were recruited and prospectively followed.

292 HbF), hematopoietic cells from patients with SCD were treated with a lentivirus expressing the ZF-Ldb

293 ularization had a negative relationship with SCD (HR, 0.75; 95% CI, 0.58-0.98; P = .03).

294 both children and adults, respectively, with SCD and highlight potential associated molecular pathway

295 agnosis converted to AD versus subjects with SCD (AUC, 0.84; P < .01) and fair performance for patien

296 , and 36 had no follow-up; 100 subjects with SCD; and 26 healthy control subjects.

297 ciation of ACLF with SI was higher than with SCD.

298 .85-1.95 ng/dL) and including only witnessed SCDs as outcome.

299 /6J mice were distributed in four groups: WT/SCD: six wild-type (WT) mice fed a standard chow diet (S

300 better outcomes after resuscitation of young SCD patients.