ライフサイエンスコーパス: RHD

1 RHD and RHCE are a pair of duplicated genes located with

2 RHD cases were predominantly Black (66%), Admixed (24%),

3 RHD complications and mortality rates were higher for ur

4 RHD is estimated to affect 33.4 million people and resul

5 Another 32 (6.1%) RHD cases harbored large gene-disrupting CNVs that were

6 For GWAS, 2548 RHD cases and 2261 controls (3301 women [69%]; mean age

7 splasia (RHD) and replicated findings in 330 RHD cases from two independent cohorts.

8 dertaken in 1263 Aboriginal Australians (398 RHD cases; 865 controls).

9 All together, 55/522 (10.5%) RHD cases harbored 34 distinct known genomic disorders,

10 ascertainment using retrospectively acquired RHD displayed high levels of agreement with CEC adjudica

11 After RHD diagnosis, 27% developed heart failure within 5 year

12 ications was highest in the first year after RHD diagnosis: heart failure incidence rate per 100 pers

13 lleles may confer protective effects against RHD.

14 Although RHD-HIV comorbid individuals have higher rates of stroke

15 Among RHD cases, 34% were asymptomatic, 26% had prior valve su

16 There was significant evidence for an RHD maternal-fetal genotype incompatibility, and the inc

17 ); the DVIcE transcripts are derived from an RHD gene where exons 4 and 5 are replaced by RHCE equiva

18 at the DVICe transcripts are derived from an RHD gene where exons 4-6 have been replaced with RHCE eq

19 nd RHD genes and have defined the site of an RHD-specific deletion located in this intron.

20 lymorphisms, while it has been shown that an RHD gene deletion can generate the D-negative phenotype.

21 antiproliferative or apoptotic activity, and RHD-defective (K83N, N109D) mutant RUNX1 conferred resis

22 igenous population has high rates of ARF and RHD allowed us to examine current disease incidence and

23 stralians in the Northern Territory, ARF and RHD incidence and associated mortality remain very high.

24 ARF and RHD incidence rates, ARF recurrence rates, progression r

25 rates from ARF to RHD to heart failure, and RHD survival and mortality rates were calculated for Nor

26 The molecular association between HLA and RHD was investigated in patients with defined clinical o

27 troke, their similar all-cause mortality and RHD care quality metrics (such as retention in care) com

28 that recruits the motor adaptor protein and RHD family member JIP4 to lysosomes.

29 acterize the difference between the RHCE and RHD antigens.

30 We have analyzed intron 4 of the RHCE and RHD genes and have defined the site of an RHD-specific d

31 the theoretical results, the human RHCE and RHD genes are considered.

32 nature implicating activity of HMG (TCF) and RHD (NF-kappaB) transcription factor family members in c

33 in these same regions, whereas few, if any, RHD patients with normal timing had similar lesion distr

34 important new prognostic information for ARF/RHD.

35 ssess the emerging role of GWAS in assessing RHD, outlining both the advantages and disadvantages of

36 The median age at RHD diagnosis in Indigenous people was young, especially

37 nzyme A-disulfide reductase isoform (BaCoADR-RHD) containing a C-terminal RHD domain; this is the fir

38 trast to the B. anthracis CoADR, the BaCoADR-RHD isoform does not catalyze the reduction of coenzyme

39 Borderline RHD was identified in children at both low and high risk

40 Children with mild definite and borderline RHD showed 26% and 9.8% echocardiographic progression an

41 The proportion of cases borderline RHD who progressed to definite RHD was 11.3% (95% CI 6.9

42 e interval, 6.0-12.0]) and 66 for borderline RHD (prevalence, 16.7 per 1000 [95% confidence interval,

43 e RHD, and 5 met the criteria for borderline RHD.

44 e more likely to have definite or borderline RHD than low-risk children (adjusted odds ratio, 5.7 [95

45 Proportion with definite or borderline RHD was 5.52% (95% CI, 4.70-6.47); proportion with defin

46 of the index test for definite or borderline RHD was 70.4% (95% CI, 62.2-77.8), specificity was 78.1%

47 f those with mild definite RHD or borderline RHD, more advanced disease category, younger age, and mo

48 one of the largest single-country childhood RHD prevalence studies and the first to be conducted in

49 years, 69% were women, and 82% had clinical RHD.

50 of the American Heart Association to combat RHD, we hope to inspire others to collaborate, communica

51 generating the D- phenotype to the complete RHD gene deletion described previously.

52 generating the D- phenotype to the complete RHD gene deletion described previously.

53 In contrast, RHD interfered with online corrections to the final posi

54 th sickle cell disease who have conventional RHD gene(s) and are transfused with units from Black don

55 with left (LHD) and right hemisphere damage (RHD).

56 Using linked data (RHD register, hospital, and mortality data) for resident

57 retention in care-possibly by decentralizing RHD services-would have the greatest impact on uptake of

58 Definite RHD progressed in 7.5% (95% CI 1.5-17.6) of the cases, w

59 Definite RHD tends to progress or remain stable over time.

60 World Heart Federation criteria for definite RHD (prevalence, 8.6 per 1000 [95% confidence interval,

61 children, none met the criteria for definite RHD, and 5 met the criteria for borderline RHD.

62 ldren with both borderline and mild definite RHD are at substantial risk of progression.

63 Of those with mild definite RHD or borderline RHD, more advanced disease category, y

64 expected in our population, and no definite RHD was identified in the low-risk group.

65 The prevalence of definite RHD in high-risk Indigenous Australian children approxim

66 (55.4%) with possible, probable, or definite RHD; 18 (13.8%) with congenital heart disease; and 40 (3

67 ia, is highly accurate to recognize definite RHD and provides the first tool for risk stratification,

68 Of children with moderate-to-severe definite RHD, 47.6% had echocardiographic progression (including

69 This study suggests that definite RHD, as defined by the World Heart Federation criteria,

70 es borderline RHD who progressed to definite RHD was 11.3% (95% CI 6.9-16.5).

71 95% CI, 4.70-6.47); proportion with definite RHD was 3.23% (95% CI, 2.61-3.98).

72 ables independently associated with definite RHD were assigned point values proportional to their reg

73 ters were elevated in children with definite RHD.

74 s reflecting residential heating deployment (RHD): pre-RHD, intra-RHD, and post-RHD periods.

75 We used these guidelines to determine RHD prevalence in a large cohort of Ugandan school child

76 After a first ARF diagnosis, 61% developed RHD within 10 years.

77 at increase or reduce the risk of developing RHD.

78 Rheumatic heart disease (RHD) affects ~40 million people and claims nearly 300 00

79 Rheumatic heart disease (RHD) after group A streptococcus (GAS) infections is her

80 een associated with rheumatic heart disease (RHD) and rheumatic fever (RF).

81 tic fever (ARF) and rheumatic heart disease (RHD) and the effect of comorbidities and demographic fac

82 tic fever (ARF) and rheumatic heart disease (RHD) are autoimmune sequelae of upper respiratory infect

83 he global burden of rheumatic heart disease (RHD) from echocardiographic population-based studies.

84 ines in deaths from rheumatic heart disease (RHD) in Africa over the past 30 years, it remains a majo

85 Rheumatic heart disease (RHD) is a complication of group A streptococcal infectio

86 Rheumatic heart disease (RHD) is a leading cause of premature death and disabilit

87 aphic screening for rheumatic heart disease (RHD) is becoming more widespread, but screening studies

88 I associations with rheumatic heart disease (RHD) may have been due to inaccuracies of serological ty

89 Rheumatic heart disease (RHD) remains a major public health problem worldwide.

90 edge for >70 years, rheumatic heart disease (RHD) remains the most common cause of cardiovascular mor

91 -risk patients with rheumatic heart disease (RHD) who were undergoing valve replacement surgery (VRS)

92 which may evolve to rheumatic heart disease (RHD) with persistent cardiac valve damage.

93 Rheumatic heart disease (RHD), an autoinflammatory heart disease, was recently de

94 RF) and its sequel, rheumatic heart disease (RHD), continue to cause a large burden of morbidity and

95 ymptomatic cases of rheumatic heart disease (RHD), facilitating access to treatment.

96 clinically detected rheumatic heart disease (RHD).

97 diagnosis of latent rheumatic heart disease (RHD).

98 ce a high burden of rheumatic heart disease (RHD).

99 early diagnosis of rheumatic heart disease (RHD).

100 Rabbit hemorrhagic disease (RHD) is a veterinary disease that affects the European r

101 c regulation of LYTL tubules by two distinct RHD proteins and pRAB effectors, acting as opposing moto

102 (RHD) of RelA, but not to the more divergent RHDs of p50/NF-kappaB1, p52/NF-kappaB2, or RelB.

103 ation domain called the Rel homology domain (RHD) and a C-terminal transactivation domain (TAD).

104 ysis revealed that the runt homology domain (RHD) and a C-terminal transcriptional repression domain

105 MsRel2B contain only a Rel homology domain (RHD) and lack the ankyrin-repeat inhibitory domain.

106 interacted with Relish-Rel-homology domain (RHD) but not with Dorsal-RHD.

107 on of p50 with a mutant Rel-homology domain (RHD) defective for DNA binding led to synergistic activa

108 erminal portion of the Runt homology domain (RHD) in AML1 proteins and determined that the N-terminal

109 ator of G protein signaling homology domain (RHD) is highly correlated with establishment of the acti

110 Importantly, the reticulon homology domain (RHD) mediates the assembly of the various Pex30 complexe

111 hat interacted with the Rel homology domain (RHD) of NF-ATp was identified with the use of a two-hybr

112 C25 interacted with the Rel Homology domain (RHD) of p65/RelA and promotes the degradation of p65/Rel

113 enic phenotype upon the Rel homology domain (RHD) of RelA, but not to the more divergent RHDs of p50/

114 hat is dependent on the Rel homology domain (RHD) of RelB.

115 ral similarity with the Rel homology domain (RHD) of the mammalian transcription factor NF-kappaB.

116 membrane-embedded reticulon homology domain (RHD) of the RTNs is sufficient to functionally support v

117 e that stability of the Rel homology domain (RHD) within the N-terminal portion of the NF-kappa B 1 p

118 NX1 required an intact runt homology domain (RHD), a domain where most leukemia-associated point muta

119 amino acids called the Rel Homology Domain (RHD), which governs DNA binding, dimerization, and bindi

120 contains an N-terminal Rel homology domain (RHD), which is responsible for DNA binding and regulated

121 main and the N-terminal Rel homology domain (RHD).

122 teraction of the RUNX1 Runt-Homology-Domain (RHD) with the core-binding factor beta protein (CBFbeta)

123 Rhodanese homology domains (RHDs) play important roles in sulfur trafficking mechani

124 proteins contain reticulon homology domains (RHDs) that have unusually long hydrophobic segments and

125 on through their reticulon homology domains (RHDs).

126 el-homology domain (RHD) but not with Dorsal-RHD.

127 branching pattern of the right hepatic duct (RHD) was typical in 55.3% of subjects.

128 fDNA and dry chemistry qPCR method for fetal RHD genotyping is feasible, as it achieved 100% sensitiv

129 vidence-based strategies for rheumatic fever/RHD prevention, (3) access to essential medications and

130 imple echocardiographic score applicable for RHD screening with potential to predict disease progress

131 ultrasound (FCU) to a reference approach for RHD screening in a school children population.

132 port of the known polygenic architecture for RHD, overtransmission of a polygenic risk score from una

133 d optimal discrimination and calibration for RHD diagnosis in the derivation and validation cohorts (

134 lobal awareness, resources, and capacity for RHD control.

135 evention and secondary and tertiary care for RHD are lower than for primary prevention, and benefits

136 hensively describe the treatment cascade for RHD in Uganda to identify appropriate targets for interv

137 A1-DQB1 is the major genetic risk factor for RHD in Aboriginal Australians studied here.

138 sent an approach for active case finding for RHD, including the use of screening and confirmatory cri

139 group of Australian children at low risk for RHD.

140 efine the first cell cycle-specific role for RHD proteins.

141 ning new perspectives for mass screening for RHD in low-resource settings.

142 s acceptable sensitivity and specificity for RHD detection when compared with the state-of-the-art ap

143 rio log-linear modeling approach to test for RHD maternal-fetal genotype incompatibility and to disti

144 andomized treatment effects ascertained from RHD versus traditional clinical evaluation and adjudicat

145 is preferentially recognized by T cells from RHD patients and demonstrates that exposure to streptoco

146 avert 74 000 (UI 50 000-104 000) deaths from RHD and ARF from 2021 to 2030 in the AU, reaching a 30.7

147 in randomized control trials determined from RHD and CEC resulted in similar point estimates.

148 ripheral blood mononuclear cells (PBMC) from RHD patients to human myocardial proteins in a T-cell We

149 are associated with risk or protection from RHD and that these associations appear to be stronger an

150 tion in the age-standardised death rate from RHD in 2030, compared with no increase in coverage of in

151 By introducing point mutations in the GRK5 RHD-kinase domain interface, we show with both in silico

152 s with focal left (LHD) or right hemisphere (RHD) lesions and control subjects performed two time per

153 e a gene conversion event generates a hybrid RHD-RHCE-RHD gene; the second (in individuals of DVIccEe

154 In two individuals we have found hybrid RHD-RHCE-RHD transcripts in both DVICe and DVIcE haploty

155 Renal agenesis and hypodysplasia (RHD) are major causes of pediatric chronic kidney diseas

156 in 192 individuals with renal hypodysplasia (RHD) and replicated findings in 330 RHD cases from two i

157 dney tissue can lead to renal hypodysplasia (RHD), but the underlying causes of RHD are not well unde

158 n of the less common haplotypes, but only if RHD lies 3' of RHCE, i.e. the order is C-E-D.

159 improved secondary prophylaxis; a decline in RHD incidence is expected to follow.

160 he residual Indigenous survival disparity in RHD patients, which persisted after accounting for comor

161 ewed toward larger gene-disrupting events in RHD cases compared to 4,733 ethnicity-matched controls (

162 o serving as a global champion and leader in RHD care and prevention.

163 nd clinical trials of preventive measures in RHD-endemic settings.

164 APHs play a previously unrecognized role in RHD membrane curvature stabilization.

165 For Indigenous RHD patients, the relative survival rate was 88.4% at 10

166 higher among Indigenous than non-Indigenous RHD patients (hazard ratio, 6.55; 95% confidence interva

167 can occur in D-positive patients who inherit RHD genetic variants encoding partial D antigen expressi

168 uals we have identified an apparently intact RHD gene.

169 ial heating deployment (RHD): pre-RHD, intra-RHD, and post-RHD periods.

170 ucosan was 9.2 times higher during the intra-RHD period compared to the pre-RHD period, correlating w

171 During the intra-RHD period, PM(2.5) levels were significantly higher tha

172 DTT assay levels during the intra-RHD were 2.1 times higher than those observed during the

173 Latent RHD is a heterogeneous diagnosis with variable disease o

174 emains unclear, the initial change in latent RHD may be evident during the first 1 to 2 years followi

175 llin prophylaxis on the trajectory of latent RHD.

176 Blinded review confirmed 227 cases of latent RHD: 164 borderline and 63 definite (42 mild, 21 moderat

177 Children with moderate to severe latent RHD have poor outcomes.

178 Children with latent RHD and >/=1 year of follow-up were included.

179 outcomes of a cohort of children with latent RHD and identify risk factors for unfavorable outcomes.

180 ratification, assigning children with latent RHD to low, intermediate, or high risk based on echocard

181 Cee) illustrates the presence of full-length RHD transcripts, which have a point mutation at nucleoti

182 erage of interventions to control and manage RHD could accelerate progress towards eradication in AU

183 Lower socioeconomic groups had more RHD (2.7% versus 1.4%; P=0.036) and more advanced diseas

184 e confirmed the interaction between MsDorsal-RHD and MsRel2-RHD, and suggesting that Dorsal and Rel2

185 More importantly, co-expression of MsDorsal-RHD with MsRel2-RHD suppressed activation of several M.

186 interaction between MsDorsal-RHD and MsRel2-RHD, and suggesting that Dorsal and Rel2 may form hetero

187 y, co-expression of MsDorsal-RHD with MsRel2-RHD suppressed activation of several M. sexta AMP gene p

188 Using a multiplex RHD typing assay, which combines a reverse polymerase ch

189 digrees with isolated familial, nonsyndromic RHD and screened for mutations in candidate genes involv

190 rdiography detected 3 times as many cases of RHD as auscultation: 72 (1.5%) versus 23 (0.5%; P<0.001)

191 ysplasia (RHD), but the underlying causes of RHD are not well understood.

192 this Rh null background, any combination of RHD or RHCE complementary DNAs could be reintroduced to

193 graphy-based screening improves detection of RHD in endemic regions.

194 The sensitivity of FCU for the detection of RHD was 83.7% (95% confidence interval, 73.3-94.0) for n

195 the class III region is a key determinant of RHD susceptibility offering important new insight into p

196 teria for the echocardiographic diagnosis of RHD.

197 nce of RHD and 9 studies on the evolution of RHD lesions.

198 e distribution was determined in 2 groups of RHD patients (n=88) and a control group (n=59).

199 rt a genome-wide association study (GWAS) of RHD susceptibility in 1,163 South Asians (672 cases; 491

200 rt a genome-wide association study (GWAS) of RHD susceptibility in 2,852 individuals recruited in eig

201 ng molecular mimicry as the key mechanism of RHD pathogenesis.

202 L as genes implicated in the pathogenesis of RHD.

203 wever, PBMC from a significant percentage of RHD patients (40%) responded to a discrete band of myoca

204 h rheumatogenic GAS caused the percentage of RHD patients responding to the 50- to 54-kDa myocardial

205 The prevalence of RHD across WHO regions remains high.

206 icipant) reporting data on the prevalence of RHD and 9 studies on the evolution of RHD lesions.

207 We aimed to establish the prevalence of RHD in high-risk Indigenous Australian children using th

208 The prevalence of RHD varied inversely with the level of a country's incom

209 The pooled prevalence of RHD was 26.1 per mille (95%CI 19.2-33.1) and 11.3 per mi

210 The highest prevalence of RHD was noted among studies which used the WHF diagnosti

211 ening echocardiography hinges on the rate of RHD progression and the ability of penicillin prophylaxi

212 ated with a 1.4-fold increase in the risk of RHD (odds ratio 1.43, 95% confidence intervals 1.27-1.61

213 Given the role of RHD in membrane shaping, our findings offer a mechanisti

214 scriptional control, we analyzed a series of RHD mutations in S2 cells and embryos.

215 Overall, our review supports the use of RHD as a potential alternative source for clinical outco

216 mple size, these findings support the use of RHD genotyping as a precise and effective alternative or

217 ing of a World Health Assembly resolution on RHD in 2018 now mandates a coordinated global response.

218 little evidence that the incidence of ARF or RHD had declined.

219 with left or right hemisphere damage (LHD or RHD), we examined the ability: (i) to plan reaching move

220 We also analyzed the role of other RHD genes and the plant hormones auxin and ethylene in R

221 ) encodes Rh CcEe antigens, while the other (RHD) the D antigen.

222 ported phospho-acceptor sites within the p65 RHD.

223 sion of IkappaB kinase beta (IKKbeta) or p65-RHD causes nuclear translocation of NFATc1, and expressi

224 Overexpression of the p65-RHD disrupts the association between endogenous p65 and

225 this phenotype is not generated by a partial RHD gene deletion, but occurs by a similar mechanism to

226 type) was proposed to be caused by a partial RHD gene deletion.

227 Physcomitrella patens RHD SIX-LIKE1 (PpRSL1) and PpRSL2 transcription factors

228 A disease of the poor, RHD is one of the most neglected diseases.

229 per procedure with a total of 72 D-positive RHD genotyped units transfused, with no anti-D restimula

230 ployment (RHD): pre-RHD, intra-RHD, and post-RHD periods.

231 ng residential heating deployment (RHD): pre-RHD, intra-RHD, and post-RHD periods.

232 ing the intra-RHD period compared to the pre-RHD period, correlating with elevated levels of elementa

233 -affinity RNA aptamers against a recombinant RHD-CBFbeta complex.

234 he RHD required to stabilize the recombinant RHD-CBFbeta complex and thus will further aid exploring

235 plexes differed from that in wild-type c-Rel-RHD/p50 complexes, and correlated with activated transcr

236 owed that co-expression of MsFkh with Relish-RHD did not have an additive effect on the activity of m

237 In addition to previously reported RHD-causing genes, we found that two affected brothers w

238 conversion event generates a hybrid RHD-RHCE-RHD gene; the second (in individuals of DVIccEe phenotyp

239 wo individuals we have found hybrid RHD-RHCE-RHD transcripts in both DVICe and DVIcE haplotypes.

240 ection might be working to maintain the RHCE/RHD antigen variation in the two-locus system.

241 f progression from ARF to RHD to severe RHD, RHD complication rates (heart failure, endocarditis, str

242 tes of progression from ARF to RHD to severe RHD, RHD complication rates (heart failure, endocarditis

243 echocardiographically diagnosed subclinical RHD is needed.

244 Four drugs under development targeting RHD were identified (Rozrolimupab, Roledumab, Atorolimum

245 soform (BaCoADR-RHD) containing a C-terminal RHD domain; this is the first structural representative

246 nd faster secondary peak velocities, and the RHD group produced deficits in final error only.

247 ternal-fetal genotype incompatibility at the RHD locus in schizophrenia.

248 1 patient-father pairs were genotyped at the RHD locus.

249 ences (amino acids (aa) 323-422) between the RHD and TAD as a REL inhibitory domain (RID) because del

250 pparently inhibitory interaction between the RHD and the CTD and eliminate both activation and repres

251 To determine if the RHD has a direct role in transcriptional control, we ana

252 plicate previous findings that implicate the RHD locus in schizophrenia, and the candidate-gene desig

253 est of switching nonspatial attention in the RHD but not the LHD patients, despite attention deficits

254 y of the known CNV disorders detected in the RHD cohort have previous associations with developmental

255 1*0103-DQB1*0603 haplotype was absent in the RHD sample.

256 ffect from a high-risk allele at or near the RHD locus and from a direct maternal effect alone.

257 ssociation with schizophrenia at or near the RHD locus nor any evidence to support the role of matern

258 gene transfer using cDNA transcripts of the RHD and RHCE genes resulted in the isolation of K562 clo

259 by 25 A from the active-site Cys514' of the RHD domain from the complementary subunit.

260 Overexpression of the RHD domains of MsDorsal and MsRel2 in Drosophila melanog

261 critical role of the unique structure of the RHD for the survival of p50 during proteosomal processin

262 CR assays assume the complete absence of the RHD gene in D- phenotypes.

263 a pair of primers located in exon 10 of the RHD gene, we have analyzed 357 different genomic DNA sam

264 A total of 27.3% of the RHD patients had hypoalbuminemia.

265 At the C-terminal end of the RHD, each protein has a nuclear localization signal (NLS

266 nteraction surfaces on opposite faces of the RHD.

267 reagents that target a novel surface on the RHD required to stabilize the recombinant RHD-CBFbeta co

268 he p50 and RelA family members show that the RHD consists of two regions: an N-terminal section which

269 duction in ARF recurrence indicates that the RHD control program has improved secondary prophylaxis;

270 sent the first direct demonstration that the RHD gene encodes the D and G antigens and the RHCE gene

271 study provides increasing evidence that the RHD locus increases schizophrenia risk through a materna

272 provide some of the first evidence that the RHD plays an active role in transcriptional regulation i

273 These bind to the RHD subunit and disrupt its interaction with CBFbeta, wh

274 iomyocytes, and this interaction maps to the RHD within p65.

275 the transfer of reducing equivalents to the RHD, with the swinging pantetheine arm serving as a ca.

276 portion of the NF-kappa B 1 protein when the RHD is destabilized.

277 hosphorylation of serine residues within the RHD modulates transcriptional activity in a cis-acting e

278 reaction (PCR) primer, which straddles this RHD-specific sequence, and a pair of primers located in

279 urrence rates, progression rates from ARF to RHD to heart failure, and RHD survival and mortality rat

280 ence rates, rates of progression from ARF to RHD to severe RHD, RHD complication rates (heart failure

281 Progression to RHD was also highest (incidence, 35.9) in the first year

282 Consistent with this, two RHD-defective RUNX1 proteins lacked any antiproliferativ

283 METHODS AND Using data from the Uganda RHD Registry (n=1504), we identified the proportion of p

284 al history study conducted under the Ugandan RHD registry.

285 individuals diagnosed with ARF and 1248 with RHD in 1997 to 2013 (94.9% Indigenous).

286 l trials compared outcome ascertainment with RHD and CEC in patients with or at risk of cardiovascula

287 tations in genes known to be associated with RHD in 7/202 case subjects.

288 ng the causes and mechanisms associated with RHD susceptibility and development.

289 To identify genes associated with RHD, we performed an exome-wide association study with 1

290 Children with RHD were older (10.1 versus 9.3 years; P=0.002).

291 rs; 49.6% male), 49 (4%) were diagnosed with RHD by the reference approach.

292 In an additional affected individual with RHD and a congenital heart defect, we found a homozygous

293 Patients living with RHD and HIV in Uganda are a relatively young, predominan

294 Lesion overlays of patients with RHD and impaired timing showed that 100% of the patients

295 f antibiotic prophylaxis among patients with RHD in Uganda.

296 deficits were controlled, only patients with RHD showed time perception deficits.

297 tudy included 1782 consecutive patients with RHD who were undergoing VRS to explore the relationship

298 1-year mortality after VRS in patients with RHD, which might have additive prognostic value to Euro

299 e-exome sequencing in 202 case subjects with RHD and identified diagnostic mutations in genes known t

300 as retention in care) compared to those with RHD alone suggest rheumatic heart disease defines their