ライフサイエンスコーパス: SCD

1 SCD attributable to ACM affects men predominantly, most

2 SCD incidence was higher in nonmetropolitan versus metro

3 SCD is caused by mutations in UBIAD1, which utilizes ger

4 SCD mice manifested sinusoidal ischemia, progressive hep

5 SCD mice were systemically challenged with nanogram quan

6 SCD mice with deficiency of LDLR (Ldlr(-/-), SCD(bmt) mi

7 SCD prevalence in adults aged >= 45 years correlates wit

8 SCD-associated UBIAD1 resists GGpp-induced release and i

9 (SCD-HeFT 10 Year Follow-up [SCD-HeFT10 Yr]; NCT01058837)

10 benefits accrued from genetically deleting 1 SCD allele, providing target validation.

11 Year 1 SCDs correlated with wheat-specific (rho = 0.55, P = .00

12 lative proportion of SCD events was 9.1% (14 SCD, 25 resuscitated sudden cardiac arrests, and 14 abor

13 important mechanism for BC hearing, and (2) SCD facilitates the flow of sound volume velocity throug

14 ed microparticles (MPs) from the blood of 23 SCD patients (HbSS) of which 11 were on, and 12, off hyd

15 During follow-up (median 6.3 years), 52 SCDs and 49 non-SCDs occurred.

16 ithin 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, et

17 Our objective was to develop and validate a SCD risk prediction model in pediatric hypertrophic card

18 tated sudden cardiac arrests, and 14 aborted SCD).

19 uscitated sudden cardiac arrest, and aborted SCD, that is, appropriate shock following primary preven

20 treated ventricular tachycardia; or aborted SCD), syncope, 24-hour premature ventricular complexes c

21 clinical predictors with LTVA (SCD, aborted SCD, sustained, or implantable cardioverter-defibrillato

22 perienced LTVA including 15 with SCD/aborted SCD (1.7%).

23 nt AF-related SCD, especially because the AF-SCD relationship is in part driven by heart failure.

24 most common substrates for SCD-making the AF-SCD relationship particularly challenging to address.

25 P(SV) - P(ST)) before and after creating an SCD.

26 ubjects achieved the primary end point of an SCD of 4443 mg of WP or greater (P < .0001); median SCDs

27 OIT-treated subjects were desensitized to an SCD of 7443 mg of WP; 3 (13%) achieved sustained unrespo

28 related differences in central adiposity and SCD (stearoyl-CoA desaturase)-1 enzyme activity index.

29 nce supporting an association between AF and SCD.

30 iciency of PCSK9 (Pcsk9(-/-), SCD(bmt)), and SCD mice with deficiency of LDLR (Ldlr(-/-), SCD(bmt)).

31 r removing individuals diagnosed with CF and SCD, we assessed heterozygosity effects at our lead vari

32 Motor phenotypes, brain cytopathology, and SCD-related lipid changes were quantified in 5b- versus

33 correlated with visceral and hepatic fat and SCD-1 activity in both groups.

34 Lower visceral fat and SCD-1 activity may contribute to the paradoxical associa

35 In multivariate models, visceral fat and SCD-1 were associated with total fasting TRLP concentrat

36 n sensitivity, hepatic and visceral fat, and SCD-1 levels.

37 Hepatic fat, insulin sensitivity index, and SCD-1 were similar in black women and lower than in whit

38 e with AD mortality rates, AD prevalence and SCD prevalence.

39 he knock-in humanized mouse model of SCD and SCD patient blood, we sought to mechanistically characte

40 ent clinical trials for beta-thalassemia and SCD are showing promising outcomes: patients were able t

41 s translationally regulated targets USP3 and SCD repressed proliferation-revealing a dedicated tRNA-r

42 n in lung arterioles of SCD mice in vivo and SCD human blood in microfluidics in vitro.

43 w in lung arterioles of SCD mice in vivo and SCD human blood in microfluidics in vitro.Conclusions: T

44 ramedullary hematopoiesis in anemias such as SCD.

45 Consistent with clinical audiograms, SCD increased BC-driven P(DIFF) below 1 kHz.

46 Thus, an orally available SCD inhibitor potently ameliorates PD phenotypes, positi

47 re essential for moving genome editing based SCD treatment into clinical practice.

48 f studies are investigating the link between SCD and the very early stages of Alzheimer's disease and

49 Per1/Per2 dKO mice transplanted with SCD BM (SCD -> Per1/Per2 dKO) displayed severe irradiation sensi

50 Both SCD patients had pronounced hemolysis and depleted plasm

51 Prolonged reduction of brain SCD activity prevented PD-like neuropathology in multipl

52 The proportion of deaths caused by SCD was not different between HF quartiles (P=0.91), and

53 d, we sought to mechanistically characterize SCD-associated hepato-pathophysiology applying our recen

54 The cumulative SCD incidence at 5 years was 9.7% (95% CI, 3.3%-16.2%) i

55 profiling of risk for sudden cardiac death (SCD) and prevention and intervention of cardiac diseases

56 s the leading cause of sudden cardiac death (SCD) in children and young adults.

57 (LTPA) and the risk of sudden cardiac death (SCD) in coronary artery disease patients is not well kno

58 Sudden cardiac death (SCD) in the young is devastating.

59 The risk of sudden cardiac death (SCD) is high early after myocardial infarction (MI).

60 mias, that can lead to sudden cardiac death (SCD) within minutes.

61 r arrhythmias (VA) and sudden cardiac death (SCD).

62 is a leading cause of sudden cardiac death (SCD).

63 with increased risk of sudden cardiac death (SCD).

64 h an increased risk of sudden cardiac death (SCD).

65 The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first m

66 patients with subjective cognitive decline (SCD) or mild cognitive impairment (MCI) can serve to pre

67 AD prevalence, subjective cognitive decline (SCD) prevalence, and oral health data.

68 The term subjective cognitive decline (SCD) was conceived in 2014 to describe this condition.

69 tudied the World Health Organization-defined SCDs autopsied in the POST SCD study (Postmortem Systema

70 by patients with superior canal dehiscence (SCD).

71 A after U[(13)C]-PA treatment, demonstrating SCD activity in PHT cells.

72 oth peripheral blood and bone marrow-derived SCD HSPCs, a significant reduction in sickling of red bl

73 catalyzed by stearoyl-coenzyme A desaturase (SCD) activity.

74 e trial of a stearoyl-coenzyme A desaturase (SCD) inhibitor ("5b") that prevented alphaS-positive ves

75 ey lipogenic enzyme stearoyl-CoA desaturase (SCD) and that SCD is required for MITF(High) melanoma ce

76 active inhibitor of stearoyl-CoA desaturase (SCD).

77 A-generating enzyme stearoyl-CoA-desaturase (SCD) was protective.

78 therapeutic approach in sickle cell disease (SCD) and beta-thalassemia.

79 and kidney function in sickle cell disease (SCD) and report that (1) acute elevations in heme lead t

80 a-thalassemia (TDT) and sickle cell disease (SCD) are severe monogenic diseases with severe and poten

81 ed to the hospital with sickle cell disease (SCD) crisis.

82 Persons with sickle cell disease (SCD) exhibit subjective hypersensitivity to cold and hea

83 Children with sickle cell disease (SCD) experience cognitive deficits even when unaffected

84 Sickle cell disease (SCD) is a genetic disorder caused by a single point muta

85 Sickle cell disease (SCD) is a worldwide hematological disorder causing painf

86 Sickle cell disease (SCD) is associated with chronic activation of coagulatio

87 Sickle cell disease (SCD) is caused by a variant hemoglobin molecule that pol

88 rate that patients with sickle cell disease (SCD) on hydroxyurea have lower cerebral oxygen extractio

89 in (HbS) play a role in sickle cell disease (SCD) pathogenesis.

90 ial cells (ECs) from 60 sickle cell disease (SCD) patients.

91 Sickle cell disease (SCD) results from a hemoglobin (Hb) mutation betaGlu6 ->

92 bidity and mortality in sickle cell disease (SCD), but preventive, diagnostic, and therapeutic option

93 rial function occurs in sickle cell disease (SCD), due in part to low nitric oxide (NO) bioavailabili

94 , including people with sickle cell disease (SCD), exhibit a greater prevalence of OSAS.

95 ystic fibrosis (CF) and sickle cell disease (SCD), respectively.

96 lature of patients with sickle cell disease (SCD).

97 jor clinical concern in sickle cell disease (SCD).

98 th heme levels in mouse sickle cell disease (SCD).

99 e beneficial effects in sickle cell disease (SCD).

100 ir development to treat sickle cell disease (SCD).

101 and hospitalization in sickle cell disease (SCD); however, only 4 therapies (hydroxyurea, l-glutamin

102 affecting patients with sickle cell disease (SCD); however, the molecular mechanism of sickle cell he

103 ention and intervention of cardiac diseases, SCD remains a major cause of death.

104 ansplantation (BMT) was performed from donor SCD mice to wild-type, PCSK9-deficient, and LDLR-deficie

105 The centers of the stable cavitation dose (SCD) maps obtained by PCI and the corresponding centers

106 gnant hypertrophic cardiomyopathy with early SCD even in the absence of hypertrophy.

107 t ventricular hypertrophy on echocardiogram, SCD occurred, myocyte disarray was found on autopsy hear

108 red blood cells, engraftment of gene-edited SCD HSPCs in vivo and the importance of reducing off-tar

109 gas chromatography and were used to estimate SCD-1 indices.

110 ival analysis investigating the age at first SCD in carriers of the mutation.

111 SS, 34 HbS variant (Goldberg staging 0-3 for SCD eyes), and 24 control eyes (total 48 children, aged

112 be developed as novel therapeutic agents for SCD.

113 idence, trends, causes, and risk factors for SCD in the young.

114 overall cost of screening and management for SCD, thus increasing the practicality of smartphone-base

115 onal laboratory-based diagnostic methods for SCD are time-consuming, complex, and cannot be performed

116 Information System registry was reviewed for SCD in people aged 1 to 35 years from 2000 to 2016 in Au

117 Inactive patients had increased risk for SCD compared with active patients (hazard ratio, 2.45 [9

118 igher (n=839, 34 events), increased risk for SCD was encountered in highly active patients (hazard ra

119 e this outcome may overestimate the risk for SCD, we aimed to specifically predict life-threatening V

120 cular disease and those at elevated risk for SCD.

121 utility to identify individuals at risk for SCD.

122 tery disease patients had increased risk for SCD.

123 ay be sufficient for risk stratification for SCD.

124 art failure-the 2 most common substrates for SCD-making the AF-SCD relationship particularly challeng

125 eatening VA (LTVA) as a closer surrogate for SCD.

126 of smartphone-based screening technique for SCD in low-resource settings.

127 to serve as a disease-modifying therapy for SCD.

128 oxyurea, in lieu of transfusion therapy, for SCD patients with abnormal transcranial Doppler results,

129 MPs were collected from SCD patients and compared with MPs isolated from healthy

130 ere developed to predict 5-year freedom from SCD.

131 t, and LDLR-deficient recipients to generate SCD controls (Pcsk9(+/+), SCD(bmt)) with preserved PCSK9

132 diatric hypertrophic cardiomyopathy to guide SCD prevention strategies.

133 Baseline specimens from individuals who had SCD or MCI revealed that NT1 tau, but not tau measured u

134 ination could identify individuals at higher SCD risk in large, free-living populations with and with

135 However, SCD affected the individual scalae pressures in unexpect

136 ography with suppressed conductometry (HPIEC-SCD) coupled to Q-Exactive Orbitrap high resolution mass

137 observed in transplanted macaques and human SCD CD34(+) cells.

138 imaging of the lung in transgenic humanized SCD mice and in vitro imaging of SCD patient blood flowi

139 leading to intrahepatic bile accumulation in SCD mouse liver.

140 opexin deficiency as a risk factor of AKI in SCD and hemopexin replacement as a potential therapy.

141 ests that red cell alarmins may cause AKI in SCD, however, the sterile inflammatory process involved

142 PCSK9 is associated with worsened anemia in SCD mice due to increased hemolysis.

143 ab, and voxeletor) are currently approved in SCD.

144 OSAS is relatively common in SCD populations, with hypoxia as a key manifestation, an

145 een associated with vaso-occlusive crises in SCD.

146 oimaging biomarkers for cognitive decline in SCD.

147 We discovered that hemopexin deficiency in SCD is associated with a compensatory increase in alpha-

148 NO production, becomes acutely deficient in SCD patients with vaso-occlusive pain episodes (VOE).

149 ors explained ~65% of the race difference in SCD.

150 ctors that may explain racial differences in SCD risk in the general population.

151 by the presence of LPS at a nanogram dose in SCD but not control human blood.

152 ed serum cytokines (IFNgamma, IL27, IL10) in SCD mice.

153 e-dependent lung vasoocclusion and injury in SCD.Methods: In vivo imaging of the lung in transgenic h

154 orylation and ubiquitination are involved in SCD pathogenesis and provide further insight into the mu

155 ated liver injury and sinusoidal ischemia in SCD mice.

156 at excess heme is directed to the kidneys in SCD in a process involving A1M causing AKI, whereas exce

157 Data on V/Q scanning are limited in SCD.

158 r gut microbiome contributes to bone loss in SCD mice.

159 a pectoris class interaction was observed in SCD risk (P=0.019 in highly active patients).

160 that this receptor is a mediator of pain in SCD.

161 to 10-fold higher A1M-to-hemopexin ratio in SCD compared with healthy controls.

162 rovides evidence that MPs play a key role in SCD pathophysiology by triggering a proinflammatory phen

163 apies most frequently associated with SCR in SCD patients.

164 rfusion with repeated thermal stimulation in SCD are indicative of autonomic hypersensitivity in the

165 e potential to reduce thromboinflammation in SCD crisis patients.

166 rotein phosphorylation and ubiquitination in SCD patients than in controls.

167 g platelet EVs promote lung vasoocclusion in SCD.

168 In healthy individuals, SCD patients, and patients treated with pharmacologic Hb

169 (bmt) mice) had similar anemia as Ldlr(+/+), SCD(bmt) mice despite higher serum cholesterol.

170 SCD mice with deficiency of LDLR (Ldlr(-/-), SCD(bmt) mice) had similar anemia as Ldlr(+/+), SCD(bmt)

171 SCD mice with deficiency of LDLR (Ldlr(-/-), SCD(bmt)).

172 prespecified clinical predictors with LTVA (SCD, aborted SCD, sustained, or implantable cardioverter

173 of 21 were desensitized after 1 year (median SCD, 7443 mg of WP; nonsignificant vs low-dose VWG OIT).

174 4443 mg of WP or greater (P < .0001); median SCDs were 4443 and 143 mg, respectively.

175 Significantly, the MITF-SCD axis suppresses metastasis, inflammatory signaling,

176 and home-based test to diagnose and monitor SCD and reduce mortality in resource-limited settings.

177 ion between LTPA and the risk of SCD and non-SCD in patients with coronary artery disease.

178 ssociation was observed between LTPA and non-SCD; those with high LTPA had the lowest risk for non-SC

179 e with high LTPA had the lowest risk for non-SCD.

180 ow-up (median 6.3 years), 52 SCDs and 49 non-SCDs occurred.

181 crovascular blood flow in lung arterioles of SCD mice in vivo and SCD human blood in microfluidics in

182 neutrophil aggregation in lung arterioles of SCD mice in vivo and SCD human blood in microfluidics in

183 The high burden of SCD and the racial-gender disparities observed in our st

184 The most common cause of SCD was coronary artery disease (40%), followed by sudde

185 ne demographics, circumstances, and cause of SCD were obtained from coronial and police reports, alon

186 sity are risk factors for specific causes of SCD in the young.

187 as the time from diagnosis to a composite of SCD events at 5-year follow-up: SCD, resuscitated sudden

188 information for the clinical counselling of SCD patients.

189 An early-stage and timely diagnosis of SCD can help in the effective management of the disease.

190 rtia mechanism, and the simulated effects of SCD were similar to the experimental findings.

191 g strategy might exploit the essentiality of SCD for tumor growth, while avoiding toxicity associated

192 These mice share many features of SCD patients, including persistent inflammation and hype

193 Activation of coagulation is a hallmark of SCD.

194 n inverse association, and family history of SCD had no association with SCD.

195 c humanized SCD mice and in vitro imaging of SCD patient blood flowing through a microfluidic system

196 Incidence of SCD in the young and specifically coronary artery diseas

197 which contributes to hepatobiliary injury of SCD.

198 tudy (Postmortem Systematic Investigation of SCD) to determine whether premortem characteristics coul

199 was associated with increased likelihood of SCD from cardiomegaly (odds ratio, 1.08 [95% CI, 1.05-1.

200 ppa B (NF-kappaB) activation in the liver of SCD mice inhibited farnesoid X receptor (FXR) signaling

201 s do not fully address the manifestations of SCD, which arise from a complex network of interdependen

202 n burden, the mechanisms and risk markers of SCD are not as well defined for women.

203 Using the knock-in humanized mouse model of SCD and SCD patient blood, we sought to mechanistically

204 ects of PCSK9 deficiency in a mouse model of SCD.

205 Studies in animal models of SCD have shown that coagulation contributes to the chron

206 Conversely, overexpression of SCD or exogenous administration of its C16:1 and C18:1 p

207 Recent advances in the pathophysiology of SCD have led to an understanding that many of the conseq

208 has not been proven a reliable predictor of SCD.

209 y the incidence and additional predictors of SCD early after MI in a contemporary nationwide setting.

210 The 5-year cumulative proportion of SCD events was 9.1% (14 SCD, 25 resuscitated sudden card

211 Proportion of SCD related to sudden arrhythmic death syndrome increase

212 Proportion of SCD related to sudden arrhythmic death syndrome increase

213 s to compare the lifetime cumulative risk of SCD among blacks and whites, and to evaluate the risk fa

214 an association between LTPA and the risk of SCD and non-SCD in patients with coronary artery disease

215 edicted both all-cause mortality and risk of SCD independently of other risk indicators.

216 ysis among symptomatic patients, the risk of SCD was increased in highly active and inactive patients

217 Follow-up of SCD-HeFT patients to 11 years demonstrated heterogenous

218 The majority (70%) of SCDs occurred in previously undiagnosed individuals.

219 pients to generate SCD controls (Pcsk9(+/+), SCD(bmt)) with preserved PCSK9 status, SCD mice with def

220 (-/-), SCD(bmt) mice compared to Pcsk9(+/+), SCD(bmt) mice consistent with greater hemolysis.

221 (-/-), SCD(bmt) mice compared to Pcsk9(+/+), SCD(bmt) mice, anemia was more severe in Pcsk9(-/-), SCD

222 neys contained increased iron in Pcsk9(-/-), SCD(bmt) mice compared to Pcsk9(+/+), SCD(bmt) mice cons

223 cholesterol levels were lower in Pcsk9(-/-), SCD(bmt) mice compared to Pcsk9(+/+), SCD(bmt) mice, ane

224 mice, anemia was more severe in Pcsk9(-/-), SCD(bmt) mice.

225 D mice with deficiency of PCSK9 (Pcsk9(-/-), SCD(bmt)), and SCD mice with deficiency of LDLR (Ldlr(-/

226 Genetic or pharmacological SCD inhibition ameliorated toxicity in alphaS-overexpres

227 diomyopathy manifested a malignant phenotype-SCD occurred in 30 (53%) of 57 affected individuals at a

228 anization-defined SCDs autopsied in the POST SCD study (Postmortem Systematic Investigation of SCD) t

229 While the role of AF in predicting SCD in the general population appears limited and not es

230 sudden arrhythmic death (SAD) among presumed SCDs.

231 entions for AF will be effective in reducing SCD only if there is a causal association between these

232 ears to be of interest to prevent AF-related SCD, especially because the AF-SCD relationship is in pa

233 ociated with coronary artery disease-related SCD (odds ratio, 1.44 [95% CI, 1.24-1.67]; P<0.001).

234 Incidence of coronary artery disease-related SCD decreased from 2001-2003 to 2013-2015 (P<0.001).

235 specifically coronary artery disease-related SCD has declined in recent years.

236 definite, probable, or possible HCM-related SCD (estimated 140 740 HCM person-years of observation).

237 ght to estimate the incidence of HCM-related SCD and its association with exercise in a large unselec

238 The incidence of HCM-related SCD in the general population 10 to 45 years of age is s

239 d microscopic features (definite HCM-related SCD).

240 (95% CI, 0.24-0.44) for definite HCM-related SCD, 0.33 per 1000 HCM person-years (95% CI, 0.34-0.62)

241 4-0.62) for definite or probable HCM-related SCD, and 0.39 per 1000 HCM person-years (95% CI, 0.28-0.

242 y the coroner, we identified all HCM-related SCDs in individuals 10 to 45 years of age between 2005 a

243 definite, probable, and possible HCM-related SCDs, respectively, were identified, corresponding to es

244 erroptosis of stearoyl-CoA desaturase (SCD1, SCD), an enzyme that catalyzes the rate-limiting step in

245 +/+), SCD(bmt)) with preserved PCSK9 status, SCD mice with deficiency of PCSK9 (Pcsk9(-/-), SCD(bmt))

246 e avoiding toxicity associated with systemic SCD inhibition.

247 nzyme stearoyl-CoA desaturase (SCD) and that SCD is required for MITF(High) melanoma cell proliferati

248 Epidemiological studies have shown that SCD and ventricular arrhythmias are more likely to occur

249 The SCD maps were found to be linearly correlated with the (

250 The SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) r

251 ion method for capturing RBC images from the SCD patients in normoxia and hypoxia conditions.

252 the extended treatment group survival of the SCD-HeFT cohort.

253 r the 1,855 patients alive at the end of the SCD-HeFT trial were collected between 2010 and 2011.

254 contrast MITF(Low) cells are insensitive to SCD inhibition.

255 isms through which AF may promote or lead to SCD, as well as the existing epidemiological evidence su

256 In a 2-week multiple dose study using Townes SCD mice, 23 showed a 37.8% (+/-9.0%) reduction in sickl

257 ghted microvascular benefits in the training SCD patients compared with nontraining patients, includi

258 d cell (RBC) membrane proteins of transgenic SCD mice.

259 oral therapy specifically developed to treat SCD by modulating the affinity of hemoglobin (Hb) for ox

260 r was recently approved by U.S. FDA to treat SCD.

261 The median study follow-up time until SCD was 11.3 years.

262 (SCD-HeFT 10 Year Follow-up [SCD-HeFT10 Yr]; NCT01058837).

263 composite of SCD events at 5-year follow-up: SCD, resuscitated sudden cardiac arrest, and aborted SCD

264 Our study provides a validated SCD risk prediction model with >70% prediction accuracy

265 ividual scalae pressures in unexpected ways: SCD increased P(SV) below 1 kHz, but had little effect o

266 patients experienced LTVA including 15 with SCD/aborted SCD (1.7%).

267 xacerbates the complications associated with SCD and provides pertinent information for the clinical

268 LTPA was not associated with SCD in patients with Canadian Cardiovascular Society gra

269 nificantly and independently associated with SCD risk after mutually controlling for cardiac risk fac

270 ore range, 0-4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37-1

271 clinical and genetic factors associated with SCD.

272 amily history of SCD had no association with SCD.

273 ow significant independent associations with SCD risk in apparently low-risk populations.

274 performed for 20 samples from children with SCD at baseline and during a hospitalization for either

275 mically contiguous networks in children with SCD compared with controls, even when differences are no

276 Children with SCD have similar retinal thickness but less dense vascul

277 we tested our hypothesis that children with SCD would have decreased functional connectivity, and th

278 ves mitochondrial function, 12 children with SCD-VOE (13.6 +/- 3 years; 67% male; 75% hemoglobin-SS)

279 esting in healthy controls and children with SCD.

280 changes during acute events in children with SCD.

281 nd reduces oxidative stress in children with SCD/VOE.

282 ing medical conditions in an individual with SCD who actively seeks medical help.

283 However, the majority of individuals with SCD will not show progressive cognitive decline.

284 nd dementia is increased in individuals with SCD.

285 molysis and AKI in both humans and mice with SCD.

286 o patients - one with TDT and the other with SCD - received autologous CD34+ cells edited with CRISPR

287 nd subcortical networks in participants with SCD compared with controls.

288 usion independence, and (in the patient with SCD) elimination of vaso-occlusive episodes.

289 We exposed 17 patients with SCD and 16 control participants to a sequence of predete

290 gene expression profiles among patients with SCD hospitalized for VOC and ACS episodes to better unde

291 ma from prospectively followed patients with SCD or MCI who remained cognitively stable, converted to

292 Furthermore, patients with SCD showed a greater progressive decrease in blood flow

293 of stimulus application, with patients with SCD showing significantly stronger vasoconstriction (P =

294 aterial in circulating PMos of patients with SCD, and their frequency was further increased during ac

295 r lipid-lowering strategies in patients with SCD, as well as for potential novel modifiers of anemia

296 x and Roche assays in baseline subjects with SCD and MCI.

297 Because those with SCD have dysautonomia, we anticipated that thermal expos

298 ed that Per1/Per2 dKO mice transplanted with SCD BM (SCD -> Per1/Per2 dKO) displayed severe irradiati

299 criminated between patients with and without SCD events with a c-statistic of 0.75 and 0.76, respecti

300 A trend toward worse SCD/VT/VF (p = 0.062) and DHF/HTx/VAD (p = 0.061) was fo