ライフサイエンスコーパス: VF

1 VF did not satisfy programmed detection criteria in 9 pa

2 VF progression is defined as either a confirmed progress

3 VF progression was reached if either the event or trend

4 VF termination was only successful for configurations in

5 VF tests were conducted using the Humphrey 24-2 Swedish

6 VF was assessed every 6 months.

7 VF was assessed with the VF-11 questionnaire validated u

8 VF was defined by a plasma viral load >1000 copies/mL >/

9 VF was induced electrically, and after short-duration VF

10 The proportion of enrollees undergoing >/=1 VF test, FP, OOI, and no testing of any type in the 2 ye

11 A total of 1828 VF results from 1235 normal eyes of 830 study subjects w

12 d scotoma area were calculated with the 10-2 VF as the clinical reference standard.

13 s, to our knowledge, the association of 10-2 VF damage with vision-related quality of life (QOL) has

14 The 10-2 VF model showed a stronger association with NEI VFQ-25 s

15 en the Amsler grid scotoma area and the 10-2 VF parameters (mean deviation [MD], scotoma extent [numb

16 Standardized binocular 24-2 and 10-2 VF sensitivities were calculated for each patient.

17 linear regression model, with binocular 10-2 VF sensitivity as the independent variable.

18 Association of binocular 24-2 and 10-2 VF sensitivity with Rasch-calibrated NEI VFQ-25 scores.

19 ive responses >15%), had undergone only 10-2 VF testing, had VF defects not typical of glaucoma, or h

20 -4.01; P = .001) sensitivities, but the 10-2 VF univariable model showed an almost 2-fold better fit

21 An abnormal 10-2 VF was defined as >/=3 adjacent points at P < 0.01 with

22 Among eyes with an abnormal 10-2 VF, regression analyses were performed between the Amsle

23 with glaucoma with the entire range of 24-2 VF damage completed the National Eye Institute Visual Fu

24 ity of vision relative to patients with 24-2 VF damage may have damage on the central field missed by

25 ociation with NEI VFQ-25 score than the 24-2 VF model.

26 n-related QOL disproportionate to their 24-2 VF status may exhibit 10-2 damage overlooked by the 24-2

27 visual function as measured by 24-2 and 10-2 VFs in patients with primary open-angle glaucoma and to

28 visual acuity (VA) were evaluated, and 24-2 VFs were obtained to calculate average integrated VF (IV

29 A total of 10 262 VFs from 1538 eyes of 909 subjects with suspect or manif

30 s with suspect or manifest glaucoma and >/=5 VF examinations.

31 atients with a VF defect in 1 eye also had a VF defect in their fellow eye.

32 Sixty-four percent of patients with a VF defect in 1 eye also had a VF defect in their fellow

33 Patients with a VF endpoint had a median rim area rate that was nearly 3

34 These experiments demonstrate active VF movement with fusion events as well as transient inte

35 The mean rate of change for all VF locations slowed from -2.5+/-9.3%/year before surgery

36 Alternatively, VF could result from abnormal excitation by PVEM, overla

37 f glaucoma surgery (r = 0.148; P = .023) and VF MD of the better eye (r = -0.284; P < .001) and worse

38 with nontraumatic OHCA, vascular access, and VF/VT anytime after >/=1 shock(s) were prospectively ran

39 V, inferior NFL quadrant thickness, age, and VF PSD.

40 domains showed that sigmaNS association and VF localization phenotypes of G3BP1 do not occur solely

41 sive and standardized ocular examination and VF assessment using a Humphrey Field Analyzer II (Carl Z

42 disc demonstrated glaucomatous features, and VF data were combined with optic disc grading to determi

43 were found between the blood flux index and VF mean deviation (Spearman rho = 0.44; P = .045) and RN

44 ombinant (r)TC-muNS viruses were rescued and VF formation, colocalization with associating virus prot

45 ted with the corresponding GCC thickness and VF sensitivity (P < 0.003).

46 Patients with open-angle glaucoma and VFs obtained from reliable examinations (defined as <30%

47 The annual VF decline rate was 5% in patients from the genetic isol

48 early VF, but the regular pattern emerges as VF progressed.

49 earchers have been unable to directly assess VF dynamics from virus-produced muNS.

50 he virulence factors of pathogenic bacteria (VF 0073-ClpE, VF0124-LPS, and VF0350-BSH).

51 The best, VF-EX2, does so with a signal-to-noise ratio nearly doub

52 zard ratio (SHR) of the associations between VF and patient clinical and demographic factors, taking

53 ere were no significant correlations between VF clusters and Modified Glaucoma Symptom Scale subscale

54 mediated their respective relations between VF (as a potential primary exposure) and CVD risk factor

55 e found some benefit in performing binocular VF testing, because the results correlated more closely

56 han the detection rate of 41.8% and 27.3% by VF.

57 ersion to perimetric glaucoma was defined by VF pattern standard deviation (PSD) or glaucoma hemifiel

58 elation with mean deviation of the 4 central VF points (rho = -0.420; P < .001).

59 Scores of central VF defects in the better eye and inferior hemisphere def

60 n full-thickness macular measures or central VF parameters and CS at 6 cpd.

61 n for the better eye was between the central VF cluster and total Compressed Assessment of Ability Re

62 The central VF cluster in the better eye was positively correlated w

63 severity-specific standards for classifying VF reliability for clinical or research applications.

64 Rasch analysis was used to convert VF-11 questionnaire scores to estimated interval measure

65 rence in a porcine model of commotio cordis, VF has been suggested to arise from abnormal repolarizat

66 ATP-inactivated potassium channels curtailed VF occurrence in a porcine model of commotio cordis, VF

67 ize at different locations of a 16.2 degrees VF were recorded.

68 9.6%) of the glaucoma suspect eyes developed VF damage.

69 ONL classification among eyes that developed VF damage was 23.5% for Cirrus and 32.4% for Spectralis.

70 Patients who developed VF/SCD had a lower prevalence of SCN5A gene mutations (p

71 detrimental impact on both near and distance VF, public health strategies to increase uptake of presb

72 persisted over 1 to 2 minutes (long-duration VF [LDVF]).

73 ion was assessed after initial long-duration VF by attempting to reinduce VF.

74 a(+) current inhibition during long-duration VF reduces the susceptibility to subsequent refibrillati

75 METHODS AND Long-duration VF was induced electrically in Langendorff-perfused rabb

76 taneous termination of initial long-duration VF was observed (66.67%; P=0.01).

77 duced electrically, and after short-duration VF (10 seconds) and LDVF (7 minutes), shocks of increasi

78 d patterns in LDVF but not in short-duration VF.

79 sualize VFs, evidence is provided of dynamic VF movement and interactions at least partially dependen

80 ce that the -CHF2 and -CH2 F chain ends in E/VF copolymer generated by (phosphinoarenesulfonate)PdR c

81 threshold sensitivity deterioration at each VF location as a function of time.

82 the chaotic pattern was predominant in early VF, but the regular pattern emerges as VF progressed.

83 Binocular tests of visual function (Esterman VF score, binocular VA) were added to the CIGTS protocol

84 es were utilized to infect cells and examine VF dynamics using live-cell microscopy.

85 ants), 55 eyes (46 participants) experienced VF conversion during 41 +/- 23 months of follow-up.

86 ltageFluors targeted by esterase expression (VF-EXs) report single spikes in cultured mammalian neuro

87 n orthoreovirus (MRV) forms viral factories (VFs), which are sites of viral transcription, translatio

88 oplasmic structures, termed virus factories (VFs), where viral transcription, translation, and replic

89 ing randomized treatment, virologic failure (VF), or death by 6 months.

90 luated risk factors for virological failure (VF) in a logistic regression model adjusted for repeated

91 igated risk factors for virological failure (VF) of bPI-based ART in the combined study arms.

92 ied in individuals with virological failure (VF) while receiving a boosted PI (PI/r)-containing regim

93 factors of CVD, namely excess visceral fat (VF), elevated blood pressure, insulin resistance, and at

94 entricular tachycardia (VT) or fibrillation (VF).

95 such a therapy could terminate fibrillation (VF) and identify which combinations of light-sensitive i

96 r tachycardia (VT)/ventricular fibrillation (VF) and Brugada syndrome-related symptoms, and 72 (group

97 llation of initial ventricular fibrillation (VF), it is crucial to prevent refibrillation to ensure s

98 iques to terminate ventricular fibrillation (VF).

99 PVEM) and, rarely, ventricular fibrillation (VF).

100 r tachycardia (VT)/ventricular fibrillation (VF).

101 icular tachycardia/ventricular fibrillation (VF).

102 nalyzed to predict ventricular fibrillation (VF)/SCD during follow-up.

103 t-of-hospital (OH) ventricular fibrillation (VF)/ventricular tachycardia (VT) cardiac arrest is unkno

104 Monocular visual field (VF) and visual acuity (VA) tests were performed at basel

105 rmine whether those with worse visual field (VF) damage have fewer home hazards.

106 n cells and associated central visual field (VF) defects in glaucoma, even in early stages.

107 glaucoma with single-hemifield visual field (VF) defects may provide insight into the pathophysiology

108 rimetry was used to assess for visual field (VF) defects.

109 drusen in eyes with or without visual field (VF) defects.

110 sure (IOP; >/= or <22 mmHg) or visual field (VF) loss pattern at diagnosis (peripheral loss only or e

111 OP) (>/=22 or <22 mm Hg) or by visual field (VF) loss pattern at diagnosis (peripheral loss only or e

112 ge, sex, intraocular pressure, visual field (VF) mean deviation (MD), number of antiglaucoma medicati

113 To evaluate visual field (VF) progression and rate of glaucomatous VF loss in pati

114 FL), and test duration (TD) on visual field (VF) reliability at different stages of glaucoma severity

115 ) affect the global indices of visual field (VF) results in nonglaucomatous eyes.

116 herence tomography (SDOCT) and visual field (VF) results were recorded.

117 l complex (GCC) thickness, and visual field (VF) sensitivity.

118 interobserver agreement using visual field (VF) testing and optical coherence tomography (OCT) softw

119 ly diagnosed OAG who underwent visual field (VF) testing, fundus photography (FP), other ocular imagi

120 coherence tomography (OCT) and visual field (VF).

121 ing, 24-2 standard achromatic visual fields (VF), and CS measurement on the same day were enrolled.

122 PD) values of 11,449 reliable visual fields (VFs) that are defined as clinically unaffected based on

123 etinography (ffERG), Goldmann visual fields (VFs), and spectral-domain optical coherence tomography.

124 quently deposited in headwater valley fills (VF).

125 2-SO3 -5-MeC6 H3 )P, inserts vinyl fluoride (VF) to form (PO(Bp,OMe) )PdCH2 CHF2 (lutidine) and inser

126 eement was substantial to almost perfect for VF software (overall kappa [95% CI], 0.59 [0.46-0.72] to

127 ed by FDOCT are the strongest predictors for VF progression among the measurements considered.

128 of HIV-infected adolescents at high risk for VF might help to improve treatment success in this group

129 r a significant (P < .05) negative slope for VF index (VFI).

130 the importance of microtubule stability for VF fusion during MRV infection.

131 ng ICDs failed to deliver timely therapy for VF from April 2015 to January 2017 at 4 institutions.

132 generic programming can prevent therapy for VF.

133 During infection, MRV forms VFs that play a critical role in virus infection but rem

134 The printout pages from VF progression software and OCT progression software fro

135 Binocular visual function (VF and VA) and VR QOL.

136 The fraction of functional VF was determined by CDA-GVF.

137 nded on continuity of the ventral funiculus (VF) along the S2-L2 segments.

138 ective: To model the process of glaucomatous VF decay over the entire perimetric range from normal to

139 can predict the development of glaucomatous VF loss in glaucoma suspects and preperimetric glaucoma

140 ld (VF) progression and rate of glaucomatous VF loss in patients with primary angle-closure glaucoma

141 t that the measured behavior of glaucomatous VF loss to perimetric blindness is nonlinear and that it

142 rmined using chromatic dark-adapted Goldmann VFs (CDA-GVFs).

143 ) 1.6 (+/-0.3) dB (group I), and 36 eyes had VF defects with MD -13.7 (+/-10.4) dB and PSD 7.2 (+/-3.

144 5%), had undergone only 10-2 VF testing, had VF defects not typical of glaucoma, or had undergone cat

145 Eyes with glaucoma and single-hemifield VF defect and normal eyes underwent scanning using an op

146 HIV VF occurred frequently during the study period (14%-36%)

147 r study may allow clinicians to estimate how VF results are affected by varying degrees of unreliabil

148 Trab group, 57% of eyes had >/=10 improving VF locations postoperatively.

149 To evaluate agreement in VF and OCT software among 5 glaucoma specialists.

150 zed activity were previously demonstrated in VF that persisted over 1 to 2 minutes (long-duration VF

151 of age) there was a significant increase in VF compared with the reference group of children aged 12

152 ble fundus images and Visual Function Index (VF-11) data available were included in the analyses for

153 as transient interactions between individual VFs and demonstrate the importance of microtubule stabil

154 ulnerable window for commotio cordis-induced VF that exists both in time and in space.

155 ts potential role in commotio cordis-induced VF.

156 37 889 patients with OHCA, 3026 with initial VF/VT and 1063 with initial nonshockable-turned-shockabl

157 ere obtained to calculate average integrated VF (IVF) sensitivity.

158 attern only emerged occasionally during late VF.

159 Second-line VF was frequent in this setting.

160 Questionnaire results of 152 patients (mean VF MD, -8.03 +/- 7.86 dB [better eye] and -16.06 +/- 10.

161 We measured VF with MRI.

162 s and correlations among blood flow metrics, VF thresholds, and clinical optical coherence tomography

163 ulfilled the inclusion criteria of 5 or more VFs and 5 years or more of follow-up.

164 : -0.18 dB) and increased in the lower nasal VF region (ADSP: 0.14 dB).

165 By targeting PLE to neurons, VF-EX2 can interrogate the neuromodulatory effects of se

166 RFamide neuropeptide VF (NPVF) is expressed by neurons in the hypothalamus an

167 vertebrate hypothalamic RFamide neuropeptide VF (NPVF) regulates sleep in the zebrafish, a diurnal ve

168 Thirty-three eyes had a normal VF with average mean deviation (MD) -0.96 (+/-1.2) dB an

169 icantly with all binocular approximations of VF, with r values ranging from 0.31 (worse-eye mean devi

170 objective diagnosis of RP and assessment of VF defects.

171 ematic effect on the spatial distribution of VF sensitivity.

172 nd X-Pb-X bond angles, sees the formation of VF color centers whose radiative decay ultimately leads

173 The incidence of VF on second-line ART was 12.9 per 100 person-years (n =

174 Cumulative incidence of VF was estimated and competing risk regression was used

175 eight mutants, likely as a result of loss of VF formation or important virus protein interactions.

176 ed with ranolazine or GS-967 at 2 minutes of VF.

177 duction correlated with the excess number of VF locations that exhibited long-term improvement postop

178 nts) with similar baseline damage, number of VF tests, and follow-up was used to address possible reg

179 Further, the onset of VF was not observed with an upregulation of SERCA, a pot

180 d ratio: 3.7) were independent predictors of VF/SCD during follow-up.

181 100 person-years (n = 23), and prevalence of VF at censoring was 17.8%.

182 Proportions of VF locations decaying or improving before and after surg

183 The overall mean rate of VF change for these patients was -0.12+/-0.51 dB/year ov

184 was noted in 15.8%, and the overall rate of VF loss was -0.12+/-0.51 dB/year.

185 Visual field progression and rate of VF loss.

186 articipants had significantly higher risk of VF or death (adjusted hazard ratio [aHR], 1.90; 95% conf

187 The most common sector of VF progression was the superior arcuate area (65%).

188 nt groundwork for future in-depth studies of VF dynamics and host cell interactions.IMPORTANCE MRV ha

189 tein muNS comprises the structural matrix of VFs and is involved in recruiting other viral proteins t

190 stribution, follow-up duration, or number of VFs between those who showed progression and those who d

191 onsecutive adult patients with refractory OH VF/VT cardiac arrest requiring ongoing cardiopulmonary r

192 was prevalent in patients with refractory OH VF/VT cardiac arrest who also met criteria for continuin

193 , 41 years vs. 54 years; P < 0.001) based on VF and 18 years earlier based on VA (median age, 54 year

194 and implicit times on ERG, mean deviation on VF, central subfield mean thickness, and total macular v

195 th uncorrected presbyopia, and its impact on VF, respectively.

196 m (asystole, pulseless electric activity, or VF/VT).

197 correction was associated with worse overall VF and reduced ability to perform individual near and di

198 neity = .01) for POAG with early paracentral VF loss (433 cases; quintile 5 vs quintile 1 MVRR = 0.56

199 93; 95% CI, 1.09-3.43) and early paracentral VF loss (MVRR, 2.27; 95% CI, 1.32-3.88).

200 sk, particularly POAG with early paracentral VF loss at diagnosis.

201 nd = .02) and 0.52 for POAG with paracentral VF loss (95% CI, 0.29-0.96; P for trend < .001).

202 trend < .001) than for POAG with peripheral VF loss only (835 cases; quintile 5 vs quintile 1 MVRR =

203 ng the epicardium, PVEM can reliably provoke VF if, and only if, the mechanical stimulation site over

204 a repeated effective procedure for recurrent VF.

205 ischarge in patients experiencing refractory VF/VT cardiac arrest treated with a novel protocol of ea

206 nts presenting with initial shock-refractory VF/VT were previously reported.

207 s from treatment of initial shock-refractory VF/VT with these drugs.

208 on subsequently developing shock-refractory VF/VT.

209 l long-duration VF by attempting to reinduce VF.

210 (74 eyes of 64 patients) with >/=4 reliable VF measurements before and after trabeculectomy and at l

211 re glaucoma patients with 5 or more reliable VF tests and with 5 years or more of follow-up.

212 ucoma suspect eyes that developed repeatable VF damage.

213 acral CPGs excite ventral clusters of sacral VF neurons to deliver the ascending drive required for d

214 e the activity of lumbar networks via sacral VF neurons provides a novel way to recruit rostral lumba

215 th PACG being managed in a hospital setting, VF progression was noted in 15.8%, and the overall rate

216 Mild, moderate, and severe VF loss were defined by a mean deviation of -6.00 dB or

217 of some concerns increased with more severe VF loss, prior glaucoma surgery, or younger age.

218 patients who had mild, moderate, and severe VFs was 72 (28.9%), 78 (31.3%), and 99 (39.8%), respecti

219 a-F elimination of Pd(beta-F-alkyl) species, VF or E insertion of the resulting (PO)PdF species, and

220 rates to withhold therapy, including strict VF episode termination rules, enhancements to minimize T

221 To study VFs, researchers have focused on visualizing the nonstru

222 Subjective VFs of RP patients were determined using chromatic dark-

223 d rat hearts by burst pacing until sustained VF was induced.

224 rillation/pulseless ventricular tachycardia [VF/VT]) during resuscitation.

225 P: -0.11 dB) and increased in upper temporal VF areas (ADSP: 0.19 dB).

226 ith blue light never successfully terminated VF, illumination of red light-sensitive ion channels wit

227 d that OCT detected progression earlier than VF in both PG and GS/PPG groups.

228 had significantly higher detection rate than VF in mild PG (63.1% vs. 38.7%, P < .001), but not in mo

229 OCT is more sensitive than VF for the detection of progression in early glaucoma.

230 For the VF locations with an initial sensitivity of 26 dB or gre

231 nonstructural protein muNS, which forms the VF matrix.

232 Interrupting the VF abolished the rhythm and replaced it by slow unstable

233 light was relatively constant throughout the VF.

234 ith G3BP1 and relocalization of G3BP1 to the VF periphery play roles in SG disruption to facilitate M

235 aging of S1-S2 neurons, back-labeled via the VF, revealed that approximately 40% responded to METH, m

236 nt among the 5 glaucoma specialists with the VF progression software was moderate (kappa, 0.48; 95% C

237 VF was assessed with the VF-11 questionnaire validated using Rasch analysis.

238 The VFs of each patient were divided into 5 clusters: nasal,

239 volved in recruiting other viral proteins to VF structures.

240 We compared time to VF or death, death, and CD4% and growth changes using in

241 HIV-infected AYAs are vulnerable to VF, especially during the transition period.

242 ructural protein sigmaNS, which localizes to VFs via association with VF nucleating protein, muNS.

243 The localization of SG proteins to VFs was dependent on polysome dissociation and occurred

244 rameters and failure of modern ICDs to treat VF.

245 ents with newly diagnosed OAG are undergoing VF testing in the 2 years after initial OAG diagnosis, a

246 Odds ratios (OR) of undergoing VF testing, FP, OOI, or none of these tests in the 15 mo

247 rance with newly diagnosed OAG who underwent VF, FP, and OOI were 63%, 22%, and 54%, respectively, wh

248 atients were excluded if they had unreliable VFs (fixation losses >33% and false-positive responses >

249 engths were delivered every 10 seconds until VF was terminated.

250 Untreated VF despite recommended programming accounted for 56% of

251 0 ambulatory patients, 5 died from untreated VF, 4 had cardiac arrests requiring external shocks, and

252 revious attempts have been made to visualize VF dynamics in live cells, but due to current limitation

253 FlAsH-EDT2 biarsenical reagent to visualize VFs, evidence is provided of dynamic VF movement and int

254 lar tachycardia-ventricular fibrillation (VT-VF).

255 PCI in 407974 patients hospitalized after VT/VF OHCA from January 1, 2000, through December 31, 2012,

256 2012, coronary angiography and PCI after VT/VF OHCA increased in patients with STE (53.7% to 87.2%,

257 ng the 407974 patients hospitalized after VT/VF OHCA, 143688 (35.2%) were selected to undergo coronar

258 ated AES leading to ECG normalization and VT/VF noninducibility in all patients.

259 leading to ECG pattern normalization and VT/VF noninducibility.

260 ablation results in ECG normalization and VT/VF noninducibility.

261 f 2.9 years, 254 (24%) patients developed VT/VF.

262 ia or pulseless ventricular fibrillation (VT/VF).

263 ventricular tachycardia and fibrillation (VT/VF).

264 ed incremental prognostic information for VT/VF over clinical and echocardiographic parameters (C sta

265 d survival to discharge have increased in VT/VF OHCA survivors from event to hospitalization.

266 d SHR hearts revealed that H2 O2 -induced VT/VF arose spontaneously from focal activations at the bas

267 ion, the susceptibility to stress-induced VT/VF increases.

268 mptoms, and 72 (group 2) having inducible VT/VF without ECG documentation at the time of symptoms.

269 strain remained independent predictors of VT/VF (anterior: hazard ratio, 1.08 [1.03-1.13]; P=0.001; i

270 in the inferior myocardial wall predicted VT/VF (hazard ratio, 1.05 [1.00-1.11]; P=0.039).

271 ardiac defibrillator shocks for recurrent VT/VF episodes.

272 age/sex-matched normotensive rats (NR) to VT/VF during challenge with oxidative stress (H2 O2 ; 0.15

273 increased susceptibility of SHR hearts to VT/VF, patch clamped isolated SHR ventricular myocytes deve

274 significantly associated with ICD-treated VT/VF (adjusted hazard ratio, 3.98; 95% confidence interval

275 SVT were also associated with ICD-treated VT/VF (adjusted hazard ratio, 9.22; 95% confidence interval

276 ICD-treated VT/VF was associated with NSVT runs at a rate >200 beats pe

277 ere more highly predictive of ICD-treated VT/VF.

278 Patients with VT/VF had significantly lower left ventricular ejection fra

279 n the overall population of patients with VT/VF OHCA (46.9% to 60.1%, P for trend < .001) in those wi

280 a significant proportion of patients with VT/VF OHCA, especially those without STE, do not undergo co

281 nd survival to discharge in patients with VT/VF OHCA.

282 dial walls compared with patients without VT/VF (anterior-strain, -7.7% versus -8.8%; P<0.001; latera

283 recovery of replicating reoviruses in which VFs can be labeled in live cells via introduction of a T

284 Tuberculosis treatment was associated with VF (SHR, 11.50 [95% confidence interval, 3.92-33.74]; P

285 as used to explore variables associated with VF improvement.

286 haracteristics significantly associated with VF were low educational attainment and lack of autonomy

287 Tuberculosis was associated with VF; therefore, novel approaches to optimize the effectiv

288 which localizes to VFs via association with VF nucleating protein, muNS.

289 vation of cation-nonselective channels, with VF induction requiring PVEM overlap with the trailing ed

290 about socioeconomic factors correlated with VF MD of the better eye (r = -0.245; P = .003) and age (

291 oncern about visual symptoms correlated with VF MD of the better eye (r = -0.258; P = .001) and worse

292 l population variation, and correlation with VF and GCC thickness.

293 th glaucoma, with strong correspondence with VF loss and RNFL thinning.

294 enced gag and/or gp41 in 61 individuals with VF on a PI/r (n = 40) or NNRTI (n = 20) containing regim

295 in an MRI-based human ventricular model with VF induced by rapid pacing; light sensitisation via syst

296 en were more commonly found in patients with VF defects.

297 Eyes with and without VF defects were compared with regard to retinal nerve fi

298 ics of ONHD between patients with or without VF defects.

299 cantly different in patients with or without VF defects.

300 umbers were not lower for persons with worse VF damage, suggesting that individuals with more advance