ライフサイエンスコーパス: RV

1 RV also induced lung mRNA and protein expression of pro-

2 RV dysfunction (hazard ratio [HR]: 2.57; 95% confidence

3 RV dysfunction increased stepwise in relation to RV cham

4 RV failure showed lower oxidative phosphorylation (moder

5 RV failure was characterized by an increase in 4HNE addu

6 RV function improved as measured by central venous press

7 RV indices provided additional risk stratification beyon

8 RV infection increased the numbers of bronchial mucosal

9 RV infection of 6-day-old immature mice causes mucous me

10 RV infection was also associated with more severe diseas

11 RV recovery was defined as improvements in central venou

12 RV RNA was found in 88.9% of monocytes from infected HG

13 RV-A and RV-C, therefore, induce qualitatively different

14 RV-C induced higher expression of CCL24 (eotaxin-2) than

15 100 (RVd n=52, RVd-elotuzumab n=48) patients were enrolled be

16 OR, not available; AFE, approximately 100%), RV (OR, 7.1 [95% CI, 3.7-13.6]; AFE, 86%) and CoV (OR, 2

17 n peripheral blood mononuclear cells from 11 RV-infected hypogammaglobulinemia patients, 7 RV-infecte

18 y 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 p

19 sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.

20 100 (RVd n=52, RVd-elotuzumab n=48) patients were enrolled between Oct

21 V-infected hypogammaglobulinemia patients, 7 RV-infected control subjects, and 14 noninfected control

22 Among 115 subjects (49%) positive for a RV, 37% (42 of 115) had discordant sample pairs.

23 In addition to the 11 group A RV segment-specific (+)RNAs [(+)ssRNAs], a chimeric plas

24 PE is safe and highly effective at achieving RV recovery.

25 h clinical deterioration at follow-up, acute RV dysfunction, with or without deep vein thrombosis, is

26 Adverse RV remodeling predicts mortality in COVID-19 independent

27 In multivariate analysis, adverse RV remodeling conferred a >2-fold increase in mortality

28 dilation; the prognostic utility of adverse RV remodeling in COVID-19 patients is uncertain.

29 elevations; the predictive value of adverse RV remodeling was similar irrespective of whether analys

30 se of this study was to test whether adverse RV remodeling (dysfunction/dilation) predicts COVID-19 p

31 ath was greatest among patients with adverse RV remodeling and positive biomarkers and was lesser amo

32 Patients without adverse RV remodeling were more likely to survive to hospital di

33 tive mAbs, had neutralizing activity against RV-A15.

34 O) was demonstrated to be protective against RV dilatation in patients with repaired tetralogy of Fal

35 Cellular binding and entry by all RV-C, which trigger these episodes, is mediated by the f

36 CDHR3 EC1 contacts C15a, and presumably all RV-Cs, in a unique cohesive footprint near the threefold

37 g (r = -0.53, P < 0.01) when compared to all RV functional and haemodynamic parameters.

38 An RV LGE volume of 25 cm(3) had 72% sensitivity and 81% sp

39 massive or massive pulmonary embolism and an RV/LV diameter ratio >=0.9 on chest computed tomography.

40 whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-gamma

41 T-cell memory responses induced by RV-A and RV-C in children with and without asthma.Methods: Periph

42 without asthma were lower for both RV-A and RV-C while retaining the pattern of gene expression and

43 RV-A and RV-C, therefore, induce qualitatively different T-cell r

44 members of two distinct RV species, RV-A and RV-C.

45 ative species-specific responses to RV-A and RV-C.

46 Four compounds showed broad-spectrum EV and RV activity and inhibited contemporary strains of emergi

47 nary arterial hypertension, RV fibrosis, and RV failure.

48 nts with pulmonary arterial hypertension and RV failure, RVfib had increased PDK1 expression.

49 Our results demonstrated that the LV and RV of human donor hearts have distinct responses to cold

50 Samples of left and right ventricle (LV and RV) free wall collected from 32 Wistar rats were subject

51 cant relationship between measures of PR and RV volumes in patients after TOF repair with concomitant

52 ng of LV forward flow, filling pressure, and RV function allowed categorization of patients hospitali

53 memory that promotes collagen production and RV fibrosis.

54 lations were observed between PRF or PRV and RV ejection fraction (r = -0.04; p = 0.87 and r = -0.03;

55 lic pressure, RV/left ventricular ratio, and RV fractional area change.

56 nged terminal activation duration (TAD), and RV enlargement by echocardiogram, and together with JUP

57 4D flow derived tricuspid stroke volume and RV blood flow KE E/A ratio.

58 In patients with arrhythmogenic RV cardiomyopathy presenting with recurrent ventricular

59 ntly present in patients with arrhythmogenic RV cardiomyopathy who have progressive RV dilation.

60 ar effects and provide evidence to associate RVs affecting the transcriptome with human traits.

61 iR-21/221 knockdown significantly attenuated RV but not LV fibroblast proliferation.

62 However, ML-based RV still faces challenges in prediction accuracy and pro

63 fter adjusting for age, gender, and baseline RV/LV ratio, pulmonary artery systolic pressure, and mod

64 t, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of

65 ified a novel, biological difference between RV and LV fibroblasts that might underlie distinctions i

66 Both RV E-wave KEi(EDV) (r = -0.3, P = 0.04) and A-wave KEi(E

67 ith those without asthma were lower for both RV-A and RV-C while retaining the pattern of gene expres

68 4 distinct endotypes-mainly characterized by RV species, microbiome, and type 2 cytokine (T2) respons

69 d compare T-cell memory responses induced by RV-A and RV-C in children with and without asthma.Method

70 ouble-stranded RNA (dsRNA), was inhibited by RV.

71 Infection by Rhinovirus-C (RV-C), a species of Picornaviridae Enterovirus, is stron

72 d cardiomyocytes isolated from normal canine RV and LV to cyclic overstretch and aldosterone.

73 patients and infected non-HG controls carry RV RNA.

74 tes of discordance were observed for certain RVs.

75 ctivation of the IL-17A pathway.Conclusions: RV-C induced memory cells with a lower IFN-gamma-type re

76 do not enable the rescue of all cultivatable RV strains.

77 o D-RVd or RVd induction (4 cycles), ASCT, D-RVd or RVd consolidation (2 cycles), and lenalidomide or

78 he end of post-ASCT consolidation, favored D-RVd vs RVd (42.4% vs 32.0%; odds ratio, 1.57; 95% confid

79 dian CD34+ cell yield was 8.2 x 106/kg for D-RVd and 9.4 x 106/kg for RVd, although plerixafor use wa

80 responses deepened; sCR rates improved for D-RVd vs RVd (62.6% vs 45.4%; P = .0177), as did minimal r

81 The addition of daratumumab (D) to RVd (D-RVd) in transplant-eligible NDMM patients was evaluated.

82 Four patients (3.8%) in the D-RVd group and 7 patients (6.8%) in the RVd group progres

83 Patients (N = 207) were randomized 1:1 to D-RVd or RVd induction (4 cycles), ASCT, D-RVd or RVd cons

84 More infections occurred with D-RVd, but grade 3/4 infection rates were similar.

85 though plerixafor use was more common with D-RVd.

86 logic adverse events were more common with D-RVd.

87 in the RVfib of patients with decompensated RV failure (n=11) versus control (n=7).

88 V) lead length was associated with decreased RV sensing (beta = -0.012 mV, P = .05) and reduced RV ca

89 d by mutagenesis studies with four different RV-C genotypes.

90 Infants are infected with many different RV strains per year.

91 asmids encoding capsid proteins of different RV A types.

92 cient replication of members of two distinct RV species, RV-A and RV-C.

93 in the activity of the endogenous Drosophila RV, gypsy, in the nervous system.

94 avage of multiple intestinal caspases during RV infection is mediated by the IFN-STAT1 signaling path

95 erent intestinal interferon receptors during RV infection eliminates several innate and inflammatory

96 Further, IFNAR1 stimulation during RV infection significantly repressed a set of virus-indu

97 Here, we found that during RV infection in vitro, both virus-infected and uninfecte

98 ients were randomly assigned (1:1) to either RVd or RVd-elotuzumab.

99 duced inflammation, was also prevented in EW RV-infected mice.

100 g mice using the highly infectious murine EW RV strain.

101 The simian RRV strain, but not murine EW RV, uniquely triggers the cleavage of both extrinsic and

102 Kinetic studies indicated that sustained EW RV replication and IFN induction in the small intestine

103 Experimental RV infection induces bronchial mucosal eosinophilia and

104 nfection baseline and following experimental RV infection in 17 Global Initiative for Chronic Obstruc

105 d phospho-pyruvate dehydrogenase expression, RV fibrosis, and hypertrophy and improved RV function.

106 Finally, RV strain-specific STAT1 regulation also likely determin

107 Finally, RV-infected 6-day-old mice showed reduced IL-1beta mRNA

108 inflammation and mucous metaplasia following RV infection by suppressing epithelial cell innate cytok

109 54% were positive for any virus and 39% for RV.

110 in bivariable analyses after controlling for RV LGE volume (OR, 1.14; P=0.003).

111 ssion of CXCL9, 10, and 11 was not found for RV-C.

112 Of 122 infants hospitalized for RV bronchiolitis (median age, 4 months), we identified 4

113 ed imaging markers have future potential for RV diastolic assessment.

114 Palmitoylation of STING was not required for RV-A16 replication, nor was the C-terminal tail of STING

115 LDs and may be the virus factor required for RV-induced LD formation.

116 r RV-C are lower than responses specific for RV-A, suggesting poor immunity to this species.Objective

117 noviruses (RVs), although those specific for RV-C are lower than responses specific for RV-A, suggest

118 8.2 x 106/kg for D-RVd and 9.4 x 106/kg for RVd, although plerixafor use was more common with D-RVd.

119 ghts on the interaction between LA function, RV hypertension, and myocardial fibrosis in SCA.

120 these findings demonstrate that the healthy RV is not merely a passive conduit, but actively partici

121 y suppresses the replication of heterologous RV strains.

122 nfection with a STAT1-sensitive heterologous RV strain induced IFN-stimulated transcripts, inflammato

123 (from 60.6 +/- 14.2 to 33.8 +/- 10.7 mm Hg), RV/left ventricular ratio (from 1.19 +/- 0.33 to 0.87 +/

124 ure at screening that associated with higher RV/TLC% predicted values.

125 cytokines were also suppressed by homologous RV, as was intestinal damage in response to endotoxin.

126 In contrast to infection with homologous RV, infection with a STAT1-sensitive heterologous RV str

127 VP3 from homologous RVs relies on its 2'-5'-phosphodiesterase (PDE) domain t

128 ecovered the simian RV RRV strain, the human RV CDC-9 strain, a reassortant between murine RV D6/2 an

129 s developed pulmonary arterial hypertension, RV fibrosis, and RV failure.

130 We aimed to identify RV bronchiolitis endotypes and examine their longitudina

131 We applied STAAR to identify RVs associated with four lipid traits in 12,316 discover

132 n, RV fibrosis, and hypertrophy and improved RV function.

133 Short-term ICS/LABA treatment improves RV/TLC% predicted in severe COPD.

134 In RV during early PAH, especially proteins associated with

135 s markedly upregulated miR-21 and miR-221 in RV fibroblasts but not in LV fibroblasts nor cardiomyocy

136 e model adjusted R(2) for absolute change in RV/LV ratio, pulmonary artery systolic pressure, modifie

137 To study 1-year changes in RV remodeling, functional status, and quality of life, w

138 There were no differences in RV volumes and ejection fraction between patients with a

139 re accompanied by more extensive fibrosis in RV-HF than LV-HF.

140 nt ventricular tachycardia, >10% increase in RV endocardial surface area of bipolar voltage consisten

141 re associated with a significant increase in RV volume (bipolar: Spearman rho, 0.6965, P=0.006; unipo

142 There was a significant increase in RV volumes (percentage increase, 28%; 206 mL [IQR, 170-2

143 e previously identified two forms of NSP2 in RV-infected cells, a cytoplasmically dispersed form (dNS

144 the most, at 4- and 2-fold, respectively, in RV-HF versus RV-Control.

145 role of mitochondrial metabolism of RVfib in RV fibrosis in human and experimental pulmonary arterial

146 Echocardiographic assessment included RV-to-left ventricular diameter ratio within 4 hours of

147 of clinical and imaging variables, including RV function, both TRF (adjusted hazard ratio [AHR] per 1

148 redictors of inducible VT included increased RV LGE (odds ratio [OR], 1.15; P=0.001 per cm(3)), incre

149 IL-1RA, anti-IL-1beta, or NLRP3 KO increased RV-induced type 2 cytokine immune responses, ILC2 number

150 However, only a small number of individual RV strains have been recovered to date.

151 e in mean z scores for LV, left atrium (LA), RV, interventricular septum, and LV posterior wall diame

152 Mean z scores for LV, LA, RV, interventricular septum, and LV posterior wall diame

153 n, the human CDC-9 strain, and a murine-like RV strain, which is suitable for both in vitro and in vi

154 ) had a worse prognosis than those with lone RV (p < 0.0001).

155 dict the observed risk in patients with lone RV but underestimated the risk in those with LV involvem

156 0.16 versus 1.36+/-0.15, P<0.0001) and lower RV inflow/outflow ratio (P<0.001), as compared to men.

157 HCT candidates or recipients had URT and LRT RV testing within 3 days.

158 ls were used to analyze risk factors for LRT RV detection.

159 etween URT and lower respiratory tract (LRT) RV detection is not well characterized.

160 iar biventricular adaptation, with higher LV/RV (1.41+/-0.16 versus 1.36+/-0.15, P<0.0001) and lower

161 A progressive increase in LV/RV dimensions was observed in women from those engaged i

162 muVs and 31 +/- 7 ms; both p < 0.05) and LVs+RV pacing (to 108 +/- 37 muVs; p < 0.05; and 29 +/- 8 ms

163 9%, respectively) and larger than during LVs+RV pacing (11 +/- 9%; p < 0.05).

164 combination with right ventricular (RV) (LVs+RV), BiV, and HB pacing was performed in 27 patients und

165 Mean RV-to-left ventricular diameter ratio decreased from bas

166 otent form of oxidative stress, in mediating RV hypertrophy and failure in congenital heart disease i

167 ed lower oxidative phosphorylation (moderate RV hypertrophy, 287.6+/-19.75 versus RV failure, 137.8+/

168 cantly improve rescue efficiency of multiple RV strains.

169 V CDC-9 strain, a reassortant between murine RV D6/2 and simian RV SA11 strains, and several reassort

170 ethods have supported the recovery of murine RV, impeding the study of RV replication and pathogenesi

171 ients and healthy individuals during natural RV infection.

172 , and inflammatory functions, during natural RV intestinal infection.IMPORTANCE Rotavirus is a highly

173 (RV) systolic pressure <40 mm Hg, and normal RV function by echocardiography.

174 t healthy ageing requires maintaining normal RV intra-cavity blood flow as quantified using KE method

175 dian progression-free survival was observed (RVd 33.64 months [95% CI 19.55-not reached], RVd-elotuzu

176 The ability of RV to suppress IFN-mediated receptors likely impacts int

177 has been applied to enhance the accuracy of RV prediction.

178 The replication capacity of RV in the small bowel is substantially due to its abilit

179 has not been fully studied in the context of RV infection in vivo Here, we present both in vitro and

180 ce ones demonstrating the greatest degree of RV dilatation.

181 an understanding to previous discoveries of RV activation in ALS affected patients.

182 served regions located on capsid proteins of RV A viruses, mice were sequentially vaccinated with DNA

183 Replication of RV-A serotypes was strictly dependent on STING, whereas

184 cross-reactivity against multiple strains of RV A viruses by ELISA, including strains A1A, A1B, A15,

185 recovery of murine RV, impeding the study of RV replication and pathogenesis in an in vivo suckling m

186 revealed a shared binding epitope on VP1 of RV-A15 for several neutralizing mAbs.

187 e that each signal informs unique classes of RVs.

188 Our results link thousands of RVs to diverse molecular effects and provide evidence to

189 The impact on RV remodeling, functional status, and quality of life ov

190 ngly, we aimed to assess the impact of PR on RV size and function in this population.

191 of the impact of pulmonary regurgitation on RV size and function.

192 ption of this protein or its binding site on RV-C.

193 r NRLP3-/- mice were inoculated with sham or RV-A1B.

194 or RVd induction (4 cycles), ASCT, D-RVd or RVd consolidation (2 cycles), and lenalidomide or lenali

195 ts (N = 207) were randomized 1:1 to D-RVd or RVd induction (4 cycles), ASCT, D-RVd or RVd consolidati

196 ere randomly assigned (1:1) to either RVd or RVd-elotuzumab.

197 right ventricular (RV) pacing, particularly RV apical pacing, can have deleterious effects on cardia

198 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on d

199 V-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.

200 tation information), a scalable and powerful RV association test method that effectively incorporates

201 ressure, pulmonary artery systolic pressure, RV/left ventricular ratio, and RV fractional area change

202 genic RV cardiomyopathy who have progressive RV dilation.

203 Most patients with progressive RV dilatation (8/14, 57%) had moderate (2 patients) or s

204 RVd 33.64 months [95% CI 19.55-not reached], RVd-elotuzumab 31.47 months [18.56-53.98]; hazard ratio

205 tial for the rescue of other hard-to-recover RV strains such as low-replicating attenuated vaccine ca

206 sing (beta = -0.012 mV, P = .05) and reduced RV capture threshold (beta = -0.002 V, P < .01) immediat

207 rains, and several reassortants and reporter RVs.

208 fic, as murine STING (mSTING) did not rescue RV-A16 replication in STING-deficient cells.

209 we have uncovered repressors of retrovirus (RV) activity as modifiers of CHMP2BIntron5 toxicity.

210 ovirus (HMPV), adenovirus (AdV), rhinovirus (RV), bocavirus (BoV), and coronavirus (CoV).

211 lammation following experimental rhinovirus (RV)-16-induced COPD exacerbations and its relationship t

212 Data are scarce on the role of rhinovirus (RV) infections in this patient group.

213 Young children with rhinovirus (RV) infection-particularly bronchiolitis-are at high ris

214 Rhinoviruses (RVs) are the main cause of the common cold worldwide.

215 Human rhinoviruses (RVs) are positive-strand RNA viruses that cause respirat

216 ightened antibody responses to rhinoviruses (RVs), although those specific for RV-C are lower than re

217 Rotavirus (RV) replication in viroplasms requires interactions betw

218 ans or animals.IMPORTANCE Group A rotavirus (RV) remains as the single most important cause of severe

219 Our understanding of how rotavirus (RV) subverts host innate immune signaling has greatly in

220 e(Haemophilus)T2(low); endotype C, virus(RSV/RV)microbiome(Streptococcus)T2(low); and endotype D, vir

221 Severe RV dysfunction was indicated by elevated end-diastolic p

222 In its most severe form, there is severe RV hypoplasia and poorly developed OFT resulting in earl

223 eassortant between murine RV D6/2 and simian RV SA11 strains, and several reassortants and reporter R

224 system, we successfully recovered the simian RV RRV strain, the human RV CDC-9 strain, a reassortant

225 ation of members of two distinct RV species, RV-A and RV-C.

226 higher expression of CCL24 (eotaxin-2) than RV-A in the responses of children with and without asthm

227 ls with a lower IFN-gamma-type response than RV-A without T-helper cell type 2 (Th2) upregulation.

228 We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous m

229 ition of the molecular interface between the RV-Cs and their receptors provides new avenues that can

230 of the left ventricle and historically, the RV has even been referred to as a 'passive conduit' of l

231 ion-related genes were down-regulated in the RV and while oxidative phosphorylation genes were activa

232 ichloroacetate, at therapeutic levels in the RV, reduced phospho-pyruvate dehydrogenase expression, R

233 Mouse-adaptive mutations in the RV-A16 2C protein allowed for robust replication in cell

234 sing conductance catheters inserted into the RV to generate real-time PV loops.

235 load, LV growth greatly outpaces that of the RV during postnatal stages.

236 stinctions in pathological remodeling of the RV in biventricular HF.

237 Similarly, the RV demonstrated a significant, threefold increase in lus

238 We found that the RV-A15-specific mAbs, but not the cross-reactive mAbs, h

239 translocation of NFkappaB (p65), whereas the RV showed increased cell death close to the endocardium

240 here were no treatment-related deaths in the RVd group and one death in the RVd-elotuzumab group for

241 the D-RVd group and 7 patients (6.8%) in the RVd group progressed; respective 24-month progression-fr

242 grade 3-5 infections (four [8%] of 52 in the RVd group, eight [17%] of 48 in the RVd-elotuzumab group

243 and motor neuropathy (one [2%] of 52 in the RVd group, four [8%] of 48 in the RVd-elotuzumab group).

244 , sensory neuropathy (four [8%] of 52 in the RVd group, six [13%] of 48 in the RVd-elotuzumab group),

245 deaths in the RVd group and one death in the RVd-elotuzumab group for which study treatment was liste

246 52 in the RVd group, six [13%] of 48 in the RVd-elotuzumab group), and motor neuropathy (one [2%] of

247 2 in the RVd group, eight [17%] of 48 in the RVd-elotuzumab group), sensory neuropathy (four [8%] of

248 52 in the RVd group, four [8%] of 48 in the RVd-elotuzumab group).

249 dings directly link endosomal dysfunction to RV de-repression in an FTD-ALS model without TDP-43 path

250 ysfunction increased stepwise in relation to RV chamber size (p = 0.007).

251 representative species-specific responses to RV-A and RV-C.

252 .Measurements and Main Results: Responses to RV-A showed higher expression of IFNG and STAT1 compared

253 R-21 and miR-221 upregulation is specific to RV cellular response to mechanical and hormonal stimuli

254 gesting a role for 2C in recruiting STING to RV-A replication organelles.

255 The addition of daratumumab (D) to RVd (D-RVd) in transplant-eligible NDMM patients was eva

256 Commonly used RV association tests have limited scope to leverage vari

257 Reverse vaccinology (RV) is a milestone in rational vaccine design, and machi

258 have enabled the analysis of rare variants (RVs) associated with complex phenotypes.

259 ying functional, large-effect rare variants (RVs).

260 leads to an underdeveloped right ventricle (RV) and outflow tract (OFT).

261 The failing right ventricle (RV) does not respond like the left ventricle (LV) to gui

262 eft ventricle (LV, n=4) and right ventricle (RV, n=4) after 0, 4, and 8 hours of cold storage in hist

263 ne or in combination with right ventricular (RV) (LVs+RV), BiV, and HB pacing was performed in 27 pat

264 nd valve hemodynamics and right ventricular (RV) assessment, as well as lung ultrasound.

265 changes of arrhythmogenic right ventricular (RV) cardiomyopathy are limited.

266 Right ventricular (RV) dilatation persisted at follow-up in 92% of particip

267 ut greater indexed LV and right ventricular (RV) dimensions as compared to males.

268 onfers augmented risk for right ventricular (RV) dysfunction and dilation; the prognostic utility of

269 and mortality because of right ventricular (RV) failure.

270 Knowledge of right ventricular (RV) function has lagged behind that of the left ventricl

271 patients (10%), isolated right ventricular (RV) involvement was found in 58 (41%), biventricular in

272 Additionally, right ventricular (RV) lead length was associated with decreased RV sensing

273 Right ventricular (RV) outflow tract obstruction (RVOTO) was demonstrated t

274 Conventional right ventricular (RV) pacing, particularly RV apical pacing, can have dele

275 d advanced liver disease, right ventricular (RV) systolic pressure <40 mm Hg, and normal RV function

276 uted tomographic-measured right ventricular (RV)-to-left ventricular diameter ratio in massive and su

277 oderate RV hypertrophy, 287.6+/-19.75 versus RV failure, 137.8+/-11.57 pmol/[secxmL]; P=0.0004), and

278 4- and 2-fold, respectively, in RV-HF versus RV-Control.

279 2 cytokine (T2) response: endotype A, virus(RV-C)microbiome(mixed)T2(low); endotype B, virus(RV-A)mi

280 )microbiome(mixed)T2(low); endotype B, virus(RV-A)microbiome(Haemophilus)T2(low); endotype C, virus(R

281 Streptococcus)T2(low); and endotype D, virus(RV-C)microbiome(Moraxella)T2(high).

282 requently infected with respiratory viruses (RVs) in the upper respiratory tract (URT), but the conco

283 3-month ICS/LABA treatment, residual volume (RV)/total lung capacity (TLC)% predicted was reduced com

284 of post-ASCT consolidation, favored D-RVd vs RVd (42.4% vs 32.0%; odds ratio, 1.57; 95% confidence in

285 es deepened; sCR rates improved for D-RVd vs RVd (62.6% vs 45.4%; P = .0177), as did minimal residual

286 s for ruling-out and ruling-in inducible VT, RV LGE >10 cm(3) was 100% sensitive and >36 cm(3) was 10

287 hocardiographic abnormality at follow-up was RV function deterioration (12 patients), followed by LV

288 pes was strictly dependent on STING, whereas RV-B serotypes were notably less dependent.

289 h dyssynchronous ventricular activation with RV apical pacing.

290 ient characteristics were only assessed with RV infection due to low number of other viruses.

291 lation and (ii) vNSP2 S313D colocalizes with RV-induced LDs without NSP5, suggesting that vNSP2 phosp

292 r expression of IFNG and STAT1 compared with RV-C, and significant expression of CXCL9, 10, and 11 wa

293 Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased n

294 In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed

295 bosis was diagnosed in 5 of 12 patients with RV failure.

296 sceptible to 4HNE-adduction in patients with RV failure.

297 Daratumumab with RVd induction and consolidation improved depth of respon

298 dence suggests clinical heterogeneity within RV bronchiolitis.

299 etter clinical condition, but they had worse RV function.

300 rer clinical grade are associated with worse RV function.