ライフサイエンスコーパス: RV

1 RV acute mechanical circulatory support now represents a

2 RV and RV/TLC improved at 6 months.

3 RV cardiac resynchronization therapy carried significant

4 RV dysfunction is a strong, independent predictor of arr

5 RV dysfunction is associated with reduced systemic paras

6 RV dysfunction was defined as right ventricular ejection

7 RV dysfunction was independently predictive of the prima

8 RV ejection fraction and peak oxygen uptake predicted mo

9 RV ejection fraction was assessed in 112 patients with P

10 RV end-systolic remodeling index (RVESRI) was defined by

11 RV likely causes less structural damage and yet is a sig

12 RV mechanical synchrony improved: septal-to-lateral RV m

13 RV systolic dysfunction was defined as reduced RV ejecti

14 RV systolic stretch fraction reflecting the ratio of myo

15 RV T1 correlated inversely with RV outflow tract gradien

16 RV, but not LV, T1 were higher in patients than in contr

17 RV-induced mucous metaplasia, ILC2 expansion, airway hyp

18 RVs and intact myofibers were laser microdissected from

19 RVs formed coincident with silica bead uptake in a proce

20 RVs fused with lysosomes, whereas associated phagosomes

21 RVs were detected in 97 (57%) of 171 exacerbation sample

22 RVs, RSV-B, and HCoV-OC43 infected ciliated cells and ca

23 to 39) to 37 mm (IQR, 33 to 41) (P < .001), RV-FAC decreased from 39% (IQR, 33% to 44%) to 34% (IQR,

24 Overall, 57 of 570 (10%) RV-positive patients were viremic, and all were children

25 Within the 3 RV species, multiple divergent genotypes encode diverse

26 eft ventricular ejection fraction, 45+/-6%), RV dysfunction provided an adjusted hazard ratio of 4.2

27 More than 1 out of 7 RV-infected children aged <10 years hospitalized with CA

28 minor-group members of rhinovirus species A (RV-A) are correlated with the inception and aggravation

29 Tissues were infected with RV-A55, RV-A49, RV-B48, RV-C8, and RV-C15; respiratory EV-D68; influenza

30 Tissues were infected with RV-A55, RV-A49, RV-B48, RV-C8, and RV-C15; respiratory EV-D68; i

31 Little is known about RV viremia and its value as a diagnostic indicator in pe

32 tion) confirmed pacing from a late activated RV area.

33 ion requiring covered stent (n=2), and acute RV dysfunction with flash pulmonary edema.

34 iew, we discuss the pathophysiology of acute RV failure and both the mechanism of action and clinical

35 hocardiography was repeated, with additional RV pressure-volume measurements, along with lung, RV his

36 o Italiano Malattie Ematologiche dell'Adulto RV-MM-PI-209, and Intergroupe Francophone du Myelome 200

37 long-term stability of CD8(+) T cells after RV transduction by comparing the durability of T cells t

38 All RV-A strains show high rates of amino acid substitutions

39 , the search has continued through alternate RV pacing sites, minimizing RV pacing, biventricular pac

40 Although RV-A was the most common RV species detected from respir

41 artery velocity time integral (P=0.006), and RV maximum +dP/dt (P<0.001), and decrease in RV index of

42 But more than that, RV-A and RV-C are the dominant causes of hospitalization category

43 cted with RV-A55, RV-A49, RV-B48, RV-C8, and RV-C15; respiratory EV-D68; influenza virus H3N2; RSV-B;

44 etermined by RV outflow tract dimension, and RV and left ventricular (LV) systolic function were dete

45 Adults with repaired tetralogy of Fallot and RV dysfunction (RV ejection fraction [EF] <50%) but with

46 pertrophy, RV fibrosis, RV inflammation, and RV alpha-7 nicotinic acetylcholine receptor and muscarin

47 addition to age, NT-proBNP serum levels, and RV size.

48 es were independently associated with LV and RV T1 on multivariable analysis.

49 RV and RV/TLC improved at 6 months.

50 Early life aeroallergen sensitization and RV wheezing had additive effects on asthma risk at adole

51 ions in indexed RV end-diastolic volumes and RV end-systolic volumes (RVESVi) (indexed RV end-diastol

52 Severe OMR was defined as RV>/=60 mL.

53 FYCO1 accumulates at RVs, and rare missense variants in FYCO1 are overreprese

54 FYCO1 colocalized at RVs with autophagic proteins such as MAP1LC3 and SQSTM1

55 s were infected with RV-A55, RV-A49, RV-B48, RV-C8, and RV-C15; respiratory EV-D68; influenza virus H

56 is more powerful than existing family-based RV association methods, particularly for the analysis of

57 y was to investigate the association between RV morphology and risk of incident AF.

58 heart disease and right bundle branch block, RV cardiac resynchronization therapy carried multiple po

59 cadherin-related family member 3 (CDHR3) by RV-C as its cellular receptor creates a direct phenotypi

60 ar (LV) systolic function were determined by RV fractional area change (RV-FAC) and LV ejection fract

61 The RV size was determined by RV outflow tract dimension, and RV and left ventricular

62 L-33 and TSLP expression are also induced by RV infection in immature mice and are required for maxim

63 ntify a novel mechanism of IFN subversion by RV and reveal an unexpected protective effect of RV infe

64 Residual volume/total lung capacity (RV/TLC) ratio decreased at 6 months and remained unchang

65 we describe an optimized mouse CD8(+) T-cell RV transduction protocol that uses simple and rapid Perc

66 ere determined by RV fractional area change (RV-FAC) and LV ejection fraction (LVEF), respectively.

67 Although RV-A was the most common RV species detected from respiratory specimens (48.8%),

68 Mean ECHO-derived RV was on average 17.1 mL larger than the MRI-derived RV

69 average 17.1 mL larger than the MRI-derived RV (P<0.05).

70 increased RV native T1 suggestive of diffuse RV fibrosis, for which volume loading seems to be a risk

71 rm future studies of the recently discovered RV-C, which also appears to exacerbate asthma in adults

72 In chronic Chagas disease, RV systolic dysfunction is more commonly associated with

73 strain-dependent host responses and diverse RV disease phenotypes.IMPORTANCE Genetic variation among

74 ired tetralogy of Fallot and RV dysfunction (RV ejection fraction [EF] <50%) but without severe valvu

75 lic dysfunction, although isolated and early RV dysfunction can also be identified.

76 pid Percoll density centrifugation to enrich RV-susceptible activated CD8(+) T cells.

77 All viruses, except RV-B48 and HCoV-OC43, altered cilia beating and mucocili

78 nical data exploring the utility of existing RV acute mechanical circulatory support devices.

79 d RV stiffness, RV hypertrophy, RV fibrosis, RV inflammation, and RV alpha-7 nicotinic acetylcholine

80 These results show that pre-HCT BAL fluid RV positivity was a predictor for allo-LSs.

81 , whereas the association was attenuated for RV mass (hazard ratio, 1.16 per SD; 95% confidence inter

82 that inhibit inflammation have efficacy for RV-induced wheezing, whereas the anti-RSV mAb palivizuma

83 een 2004 and 2014, in whom real-time PCR for RV was performed in nasopharyngeal aspirates (NPAs) and

84 ntact ventricular septum deemed suitable for RV decompression have a high reintervention burden altho

85 adults hospitalized with CAP were tested for RV by real-time reverse-transcription polymerase chain r

86 rows, their role as mechanical therapies for RV failure will depend less on the technical ability to

87 Weekly nasal mucus samples were analyzed for RVs, and respiratory symptoms and asthma exacerbations w

88 Screening for RVs before HCT might identify patients at risk for allo-

89 s), which shrink within 20 min of formation, RVs persisted around bead-containing phagosomes.

90 Sera from RV-positive children and adults hospitalized with CAP we

91 Optimal thresholds for ventricular function (RV EF <30%: hazard ratio, 3.90; 95% CI, 1.84-8.26; P < .

92 nce interval, 1.03-1.32; P=0.02) and greater RV mass (hazard ratio, 1.25 per SD; 95% confidence inter

93 Higher RV ejection fraction and greater RV mass were associated with an increased risk of AF in

94 nor-group viruses are similar to major-group RV-A, from which they were derived, although they tend t

95 of many serotypes of major- and minor-group RVs.

96 t 3 LL-37 quartiles were less likely to have RV (eg, aOR, 0.5 [lowest quartile]; Pall quartiles </= .

97 Higher RV ejection fraction and greater RV mass were associated

98 s with available spirometry (n=2540), higher RV ejection fraction and mass remained significantly ass

99 rs, including incident heart failure, higher RV ejection fraction (hazard ratio, 1.16 per SD; 95% con

100 ms, P<0.001) and female patients had higher RV T1 compared with males (1051+/-79 versus 1017+/-68 ms

101 0.85; P=0.02) and more likely to have higher RV end-diastolic pressure (HR, 1.07; 95% CI, 1.00-1.15;

102 espective left ventricular parameter, higher RV ejection fraction remained significantly associated w

103 very in comparison with patients with higher RV ejection fraction.

104 ings, surgical defect area estimated by HRCM-RV, and observed surgical defect area.

105 ndheld RCM with radial video mosaicing (HRCM-RV) offers accurate presurgical assessment of LM and LMM

106 mor clearance in each quadrant based on HRCM-RV findings were calculated and compared with the surgic

107 size and area, LM and LMM area based on HRCM-RV findings, surgical defect area estimated by HRCM-RV,

108 0.67-0.84 mm; P < .001) larger than the HRCM-RV estimate.

109 Thus, mapping of LM using HRCM-RV can help spare healthy tissue by reducing the number

110 ty-two patients underwent imaging using HRCM-RV, and 22 patients with 23 LM or LMM lesions underwent

111 Mapping of LM and LMM with HRCM-RV estimated defects that were similar to but slightly s

112 SD) surgical defect area estimated with HRCM-RV was 6.34 (4.02) cm2 and the mean (SD) area of surgica

113 not rescue an SA11 reassortant with a human RV strain AU-1 NSP2 gene, which differs from that of SA1

114 SA11 reassortants with NSP2 genes from human RV strains Wa or DS-1 were efficiently rescued and exhib

115 y, and reduced RV stiffness, RV hypertrophy, RV fibrosis, RV inflammation, and RV alpha-7 nicotinic a

116 d an unbiased proteomic approach to identify RV proteins in sIBM that included a novel protein involv

117 more on improved algorithms for identifying RV failure, patient monitoring, and weaning protocols fo

118 generation of mucous metaplasia in immature RV-infected mice involves a complex interplay among the

119 ic function of the VP1 polymerase.IMPORTANCE RVs cause diarrhea in the young of many animal species,

120 Losartan did not significantly improve RV EF in comparison with placebo (+0.51%; 95% confidence

121 lysis, losartan was associated with improved RV EF in a subgroup (n=30) with nonrestrictive RV and in

122 We sought to evaluate changes in RV function after temporary RV cardiac resynchronization

123 RV maximum +dP/dt (P<0.001), and decrease in RV index of myocardial performance (P=0.006).

124 tylcholinesterase activity were evaluated in RV (n=11) and lungs (n=7) from patients with PAH undergo

125 dle branch block QRS morphology, increase in RV filling time (P=0.002), pulmonary artery velocity tim

126 213 proteins were enriched by >1.5 -fold in RVs compared to controls and included proteins previousl

127 lular volume, but show evidence of increased RV native T1 suggestive of diffuse RV fibrosis, for whic

128 PYR improved survival, increased RV contractility, and reduced RV stiffness, RV hypertrop

129 left ventricular end-systolic volume index, RV, and OMR category (severe versus moderate), and the E

130 immediate and midterm reductions in indexed RV end-diastolic volumes and RV end-systolic volumes (RV

131 nd RV end-systolic volumes (RVESVi) (indexed RV end-diastolic volume pPVR versus immediately after PV

132 ellular and viral events in early infection (RV 217/Early Capture HIV Cohort [ECHO] study).

133 term follow-up, indicating ongoing intrinsic RV functional improvement after PVR.

134 ing, and weaning protocols for both isolated RV failure and biventricular failure.

135 left ventricular ejection fraction, isolated RV systolic dysfunction was found in 7 (4.4%) patients,

136 sent in 142 patients (49%): 113 had isolated RV involvement and 29 had evidence of LV dysfunction.

137 1, 1.7), and 1.4 g (95% CI: 0.4, 2.5) larger RV mass among former smokers, current smokers, and perso

138 anical synchrony improved: septal-to-lateral RV mechanical delay decreased (P<0.001) and signs of RV

139 L/m(2), mean 148 mL/m(2)) volumes, and lower RV and left ventricular (LV) ejection fractions compared

140 , 18.6; 95% CI, 5.3-65.2; P<0.001) and lower RV area (odds ratio, 0.81; 95% CI, 0.72-0.91; P<0.001).

141 Patients with PAH with lower RV ejection fraction (<41%) had a significantly reduced

142 essure-volume measurements, along with lung, RV histological, and protein analyses.

143 Mean RV values decreased at 6 months but increased at 12 mont

144 hrough alternate RV pacing sites, minimizing RV pacing, biventricular pacing, left ventricular (LV) p

145 (IFNRs) in vitro In a suckling mouse model, RV effectively blocked STAT1 activation and transcriptio

146 NR degradation was conserved across multiple RV strains that differ in their modes of regulating IFN

147 The ability of EW murine RV to inhibit multiple IFN types led us to test protecti

148 ty in controls, mice infected with EW murine RV were substantially protected against mortality follow

149 EF in a subgroup (n=30) with nonrestrictive RV and incomplete remodeling (QRS fragmentation and prev

150 with BrS, conduction delay in RVOT, but not RV or left ventricle, correlated to the degree of J-ST p

151 lated death in children worldwide and 95% of RV-associated deaths occur in Africa and Asia where RV v

152 that allows long-term in vivo assessment of RV-transduced T cells.

153 We found positive associations of RV mass and, to a lesser extent, end diastolic volume wi

154 st-TPVR, there were 2 late deaths because of RV failure and 1 cardiac transplantation because of prog

155 Omalizumab decreased the duration of RV infection (11.2 d vs. 12.4 d; P = 0.03) and reduced p

156 nt with omalizumab decreased the duration of RV infections, viral shedding, and the risk of RV illnes

157 nd reveal an unexpected protective effect of RV infection on endotoxin-mediated shock in suckling mic

158 don may have coemerged with the evolution of RV-C and helped shape modern human genomes against the v

159 nally, omalizumab decreased the frequency of RV illnesses (risk ratio, 0.64; 95% confidence interval,

160 ery (up to 60%), as well as the frequency of RV-transduced cells ( approximately sixfold over several

161 sents an important step in the management of RV failure and provides an opportunity to rapidly stabil

162 confers optimal chances of normalization of RV function.

163 Presence of RV dysfunction was not significantly different in patien

164 Progression of RV disease was associated with depolarization criteria a

165 ssion was used to verify the relationship of RV systolic dysfunction with age, sex, functional class,

166 infections, viral shedding, and the risk of RV illnesses.

167 nical delay decreased (P<0.001) and signs of RV dyssynchrony pattern were significantly abolished.

168 calize to viroplasms, which are the sites of RV RNA synthesis, by expressing the mutant form as a gre

169 The incremental values of RV free wall longitudinal strain and RVESRI to risk scor

170 Molecular detection of RVs from the upper respiratory tract can be prolonged, c

171 tive tool for elucidating the involvement of RVs in the etiology of complex traits.

172 Losartan had no significant effect on RV dysfunction or secondary outcome parameters in repair

173 therapy carried multiple positive effects on RV mechanics, synchrony, and contraction efficiency.

174 t have a statistically significant impact on RV EF in subgroups with symptoms, restrictive RV, RV EF<

175 did not appear to reduce residual dyspnea or RV dysfunction in these patients.

176 rences in residual pulmonary hypertension or RV dysfunction.

177 -knockout mice with sham HeLa cell lysate or RV.

178 such as MAP1LC3 and SQSTM1 in sIBM and other RV myopathies.

179 In contrast with other RV species, RV-C infections were highly associated with

180 In PAH RV samples, alpha-7 nicotinic acetylcholine receptor was

181 1.2 d vs. 12.4 d; P = 0.03) and reduced peak RV shedding by 0.4 log units (95% confidence interval, -

182 ctional and morphological indicators of poor RV function were seen, many of which were similar to eff

183 Primary end point was reintervention post-RV decompression; secondary end points included circulat

184 ng preferences of individual 2A(pro) predict RV genotype-specific targeting of NPC pathways and cargo

185 Larger preoperative RV outflow tract scar was associated with a smaller impr

186 However, occurrence of primary RV dysfunction in Chagas disease remains controversial.

187 There was no association between progressive RV/LV structural disease and newly developed ECG TFC.

188 rdiac transplantation because of progressive RV dysfunction and tricuspid regurgitation.

189 iated with a smaller improvement in post-PVR RV/left ventricular ejection fraction.

190 The q-RV interval at the RV free wall pacing site (mean 77.2%

191 val, increased RV contractility, and reduced RV stiffness, RV hypertrophy, RV fibrosis, RV inflammati

192 systolic dysfunction was defined as reduced RV ejection fraction based on predefined cutoffs account

193 , PYR reduced pulmonary vascular resistance, RV afterload, and pulmonary vascular remodeling, which w

194 V EF in subgroups with symptoms, restrictive RV, RV EF<40%, pulmonary valve replacement, or QRS fragm

195 Retroviral (RV) expression of genes of interest (GOIs) is an invalua

196 Rhinovirus (RV) infection of 6-d-old mice, but not mature mice, caus

197 duction associated with enhanced rhinovirus (RV) and respiratory syncytial virus (RSV) replication.

198 Early life rhinovirus (RV) wheezing illnesses and aeroallergen sensitization in

199 iratory syncytial virus (RSV) or rhinovirus (RV), including coinfections with other viruses.

200 agent of bronchiolitis, whereas rhinovirus (RV) is most commonly detected in wheezing children there

201 The RNA rhinoviruses (RV) encode 2A proteases (2A(pro)) that contribute essent

202 Rhinoviruses (RVs) are ubiquitous respiratory pathogens that often cau

203 Rhinoviruses (RVs), respiratory enteroviruses (EVs), influenza virus,

204 TANCE Most colds are caused by rhinoviruses (RVs).

205 Human rhinoviruses (RVs) of the A, B, and C species are defined agents of th

206 Rotavirus (RV) is the leading cause of diarrhea-related death in ch

207 -sensitive (ts) mutants of simian rotavirus (RV) strain SA11 have been previously created to investig

208 Rotaviruses (RVs) can evolve through the process of reassortment, whe

209 The regulation by rotaviruses (RVs) of antiviral pathways mediated by multiple IFN type

210 in subgroups with symptoms, restrictive RV, RV EF<40%, pulmonary valve replacement, or QRS fragmenta

211 recovery intervals prolongation in the RVOT, RV, or left ventricle.

212 Mean (SD) RV ejection fraction (EF) was 44% (10%), and mean (SD) L

213 ate with restricted reassortment into simian RV strain SA11.

214 Previously, a mutant simian RV (SA11-tsC) that replicates worse at higher temperatur

215 e interval [CI], 0.28-091; P=0.027), smaller RV length (HR, 0.94; 95% CI, 0.89-0.99; P=0.027), and </

216 In contrast with other RV species, RV-C infections were highly associated with viremia and

217 RV contractility, and reduced RV stiffness, RV hypertrophy, RV fibrosis, RV inflammation, and RV alp

218 Murine EW strain RV infection transiently activated intestinal STAT1 at 1

219 We aimed to study RV systolic function in patients with Chagas disease usi

220 pport pumps specifically designed to support RV failure have been introduced into clinical practice.

221 after primary repair (n=4) or after surgical RV revalvulation for significant pulmonary regurgitation

222 mpathetic activity by PYR improved survival, RV function, and pulmonary vascular remodeling in experi

223 t bundle branch block by atrial-synchronized RV free wall pacing in complete fusion with spontaneous

224 Worsening of systemic RV dysfunction or tricuspid regurgitation was seen in 12

225 effect in symptomatic patients with systemic RV dysfunction.

226 Worsening systemic RV function and tricuspid regurgitation may develop afte

227 Temporary RV cardiac resynchronization therapy was applied in the

228 luate changes in RV function after temporary RV cardiac resynchronization therapy.

229 tanding the deleterious effects of long-term RV apical pacing in vulnerable populations has created t

230 Here, we find that RV degrades the types I, II, and III IFN receptors (IFNR

231 iratory pathogen identified, suggesting that RV-C viremia may be an important diagnostic indicator in

232 But more than that, RV-A and RV-C are the dominant causes of hospitalization

233 The RV size was determined by RV outflow tract dimension, an

234 The RV-GDT has increased power by efficiently incorporating

235 assess associations within a family, and the RV extension combines the single-variant GDT statistic o

236 The q-RV interval at the RV free wall pacing site (mean 77.2% of baseline QRS dur

237 ve response of the cholinergic system in the RV.

238 atients with cardiogenic shock involving the RV.

239 Given the capability of the RV-GDT to adequately control for population admixture or

240 disease to illustrate the application of the RV-GDT.

241 lated genetic data, we demonstrated that the RV-GDT method has well-controlled type I error rates, ev

242 The quantified thresholds (RV EF <30% and LV EF <45%) may be implemented in noninva

243 Alterations to RV structure may represent a mechanism by which long-ter

244 e overall procedure from T-cell isolation to RV transduction takes 2 d, and enrichment of activated T

245 s may impair autophagic function, leading to RV formation in sIBM patient muscle.

246 ols for evaluating the host cell response to RV infections in real time and suggests that differentia

247 pted) were identified based on the RVESRI to RV systolic pressure relationship.

248 hat blocking IgE decreases susceptibility to RV infections and illness.

249 ersus 21 mm Hg; P=0.02) and higher post-TPVR RV sphericity index (median 0.88 versus 0.52; P=0.004).

250 METHODS AND Neonates undergoing RV decompression for pulmonary atresia with intact ventr

251 eptum and 28 with virtual atresia) underwent RV decompression at median 3 (25th-75th, 2-5) days of ag

252 viruses expressing each of six commonly used RV reporter genes.

253 enesis is unknown; however, rimmed vacuoles (RVs) are a constant feature.

254 ermed these structures "renitence vacuoles" (RVs).

255 generated for the detection of rare-variant (RV) associations in families.

256 cations in patients with retinal vasculitis (RV).

257 tivation timings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were

258 Outcomes after right ventricle (RV) decompression in infants with pulmonary atresia with

259 , atrium and SV but not the right ventricle (RV).

260 larger left (P = .023) and right ventricles (RV; P = .002), and worse RV function (P < .001).

261 s recommended to quantify right ventricular (RV) and left ventricular (LV) function.

262 g with atrial synchronous right ventricular (RV) apical pacing, the search has continued through alte

263 te to long-term pulmonary right ventricular (RV) dysfunction in patients after surgery for congenital

264 isease, which can lead to right ventricular (RV) dysfunction.

265 years, had higher indexed right ventricular (RV) end-diastolic (range 85-326 mL/m(2), mean 148 mL/m(2

266 Right ventricular (RV) end-systolic dimensions provide information on both

267 We report right ventricular (RV) filling and ejection abnormalities in IUGR young adu

268 asympathetic activity and right ventricular (RV) function in patients with PAH, and the potential the

269 Although it is known that right ventricular (RV) function is dependent on LV health, the IUGR right v

270 n II receptor blockers on right ventricular (RV) function is still unknown.

271 Right ventricular (RV) impairment is postulated to be responsible for promi

272 Right ventricular (RV) morphology has been associated with drivers of atria

273 therapy for dysfunctional right ventricular (RV) outflow tract conduits.

274 Right ventricular (RV) size and systolic function between baseline and last

275 s symptomatic benefit and right ventricular (RV) volume reduction.

276 n of left ventricular and right ventricular (RV) volumes was performed from standard cine imaging.

277 Respiratory virus (RV) has been suggested to play a role in the pathogenesi

278 that during infection in vitro and in vivo, RVs significantly deplete IFN type I, II, and III recept

279 nderwent MRI to quantify regurgitant volume (RV) of OMR by subtracting the aortic forward flow volume

280 nd postbronchodilator FEV1, residual volume (RV), and total lung capacity (TLC) were determined at ba

281 The primary outcome was RV EF change, determined by cardiovascular MRI in intent

282 specimens (48.8%), almost all viremias were RV-C (98.2%).

283 ciated deaths occur in Africa and Asia where RV vaccines (RVVs) have lower efficacy.

284 tein variants) and the efficiency with which RV-C can infect cells.

285 indings are consistent with a model in which RVs, as persistent MPs, prevent fusion between damaged p

286 We quantified associations with RV mass, end-diastolic volume, and ejection fraction aft

287 9 versus 21+/-12 ms; P=0.0005) compared with RV or left ventricle.

288 LV T1 correlated with RV T1 (r=0.45, P<0.001), cardiopulmonary bypass (r=0.30,

289 ed for 96 patients (175 eyes) diagnosed with RV from 2003 to 2013.

290 As experience with RV devices grows, their role as mechanical therapies for

291 ated with outpatient wheezing illnesses with RV and aeroallergen sensitization in early life.

292 Tissues were infected with RV-A55, RV-A49, RV-B48, RV-C8, and RV-C15; respiratory E

293 RV T1 correlated inversely with RV outflow tract gradient (r=-0.28, P=0.02).

294 l loss and complications among patients with RV were similar to reported rates in noninfectious uveit

295 greatest for young children who wheeze with RV infections.

296 sted for all viral etiologies, wheezing with RV (odds ratio = 3.3; 95% CI, 1.5-7.1), but not respirat

297 tissue or when mutated cause myopathies with RVs.

298 to identify proteins that accumulate within RVs.

299 d right ventricles (RV; P = .002), and worse RV function (P < .001).

300 er a mean (SD) follow-up of 6.4 (2.5) years, RV outflow tract dimension increased from 35 mm (interqu