ライフサイエンスコーパス: VF

1 VF mean deviation (VF-MD) was simulated by NFLP mean dev

2 VF rate increases over time in patients with left ventri

3 VF testing does not influence IOP as measured with a non

4 VF was defined as a confirmed VL >=200 copies/mL or any

5 VF was independently lower among participants with basel

6 VF-Home can return a high level of short-term compliance

7 VF-Home gave greater fixation loss but a similar level o

8 VF-Home uptake was excellent, with 88% of participants s

9 ter (Eyecatcher) and were asked to perform 1 VF home assessment per eye, per month, for 6 months (12

10 Stage 1 VF defects are the earliest detectable and involve the i

11 From 2 initial datasets of 672 123 VF results from 213 254 eyes and 350 437 samples of clin

12 up of 64 months, 20 disc photographs, and 16 VF tests.

13 were 1) macular function as measured by 10-2 VF and 2) CS as measured by the Freiburg Visual Acuity a

14 mparison between abnormal points on the 10-2 VF and OCT probability maps.

15 t-based progression algorithm using the 10-2 VF can identify eyes experiencing more rapid MD progress

16 relation between facial recognition and 10-2 VF MD (P < .0001 better, worse eye).

17 The 10-2 VF MD remained a significant predictor of facial recogni

18 Better and worse eye was determined by 10-2 VF mean deviations (MDs).

19 The number of eyes experiencing 10-2 VF progression based on "possible" and "likely" progress

20 For the validation analysis, 10-2 VF results from ADAGES performed on at least 5 visits we

21 The 10-2 VF results from MAPS were obtained during 4 test-retest

22 ld (VF) test, as well as the PSD of the 10-2 VF, will miss central glaucomatous damage confirmed with

23 h based upon OCT probability maps and a 10-2 VF.

24 ed simulated VF agreed well with actual 24-2 VF in terms of both the location and severity of glaucom

25 The NFLP-CD and 24-2 VF maps were divided into 8 corresponding sectors using

26 Comparing simulated and actual 24-2 VF maps, the worst sector was in the same or adjacent lo

27 The median 24-2 VF MD was -6.8 dB (interquartile range [IQR], -4.9 to -1

28 f the 126 (65%) better eyes (defined by 24-2 VF MD) had evidence of macular damage, while the remaini

29 Before and after home monitoring, 2 VF assessments were performed in clinic using standard a

30 Stage 2 VF defects include 2 distinguishable levels of severity

31 Stage 3 involves progression of stage 2 VF defects to complete loss of inferior and superior hem

32 Between the 2 VF tests, TD values were correlated more strongly in cen

33 ) group (45 eyes/patients) had 24-2 and 10-2 VFs and optical coherence tomography (OCT) scans twice w

34 visual fields (VFs) on 8077 subjects, 13 231 VFs from the most recent visit of each patient were incl

35 e horizontal meridian) occurred in 41 of 234 VFs (17.5%), stage 2b (inferior altitudinal with superio

36 nd stage 3 (total loss) occurred in 5 of 234 VFs (2.1%).

37 with superior arcuate) occurred in 6 of 234 VFs (2.6%), and stage 3 (total loss) occurred in 5 of 23

38 c (inferior altitudinal defect) in 11 of 234 VFs (4.7%).

39 e inferior paracentral defect) in 112 of 234 VFs (47.9%), and stage 1c (inferior altitudinal defect)

40 ll inferior paracentral defect) in 22 of 234 VFs (9.4%), stage 1b (large inferior paracentral defect)

41 Of 234 VFs in 37 eyes of 23 subjects, inferior defects were mos

42 otographs with >2 years of follow-up and >=5 VFs.

43 uare deviation (RMSD) of TD values at all 52 VF locations.

44 Participants were tasked with performing 6 VF examinations from home, at weekly intervals, using a

45 le VFs were analyzed, with an average of 3.6 VFs per eye.

46 ged in series (median length and duration, 9 VFs over 48 months).

47 LP-MD had better reproducibility than actual VF-MD and holds promise for improving glaucoma monitorin

48 ivities and compared these results to actual VF sensitivities.

49 loss, (2) moderate VF loss, or (3) advanced VF loss.

50 r within a maximum of 5 min before and after VF testing.

51 There was no significant change in IOP after VF testing, with IOP's 15.14 +/- 4.00 mmHg before and 14

52 king history seemed to be protective against VF deterioration.

53 mmonly used glaucoma progression algorithms (VF index slope, mean deviation slope, and pointwise line

54 er radiofrequency ablation in both cases and VF terminated spontaneously shortly after ablation in on

55 heric difference correlation between FPL and VF (Spearman's rho = 0.770) was significantly (P < 0.001

56 6 hpi compared to 0.22 mum/s at 22 hpi), and VF coalescence was dependent on an intact microtubule ne

57 heric difference correlation between LPA and VF (rho = 0.595).

58 The differences between NFLP-MD and VF-MD in early, moderate, and severe glaucoma stages wer

59 ed optic disc photography every 3 months and VF testing every 4 months.

60 The association between ODH and VF progression rate globally and within a sector was cal

61 an the correlation between NFL thickness and VF MD (rho = 0.760).

62 ejection fraction, 30+/-10%) had both VT and VF and met inclusion criteria.

63 n; and (3) computationally derived archetype VF loss patterns.

64 Inclusion of archetype VF loss patterns and TD values based on first VF improve

65 Affected outcome metrics, such as VF motion correlation, intervocalization interval, and p

66 er therapies: the ASCO-Value Framework (ASCO-VF) and the ESMO-Magnitude of Clinical Benefit Scale (ES

67 assessed countries except France using ASCO-VF (p=0.56 for the USA, p=0.47 for England, p=0.26 for S

68 urs, we assessed clinical benefit using ASCO-VF and ESMO-MCBS.

69 ole-body plethysmography were used to assess VF motion, swallow function, vocal function, and respira

70 initiation of antiretroviral therapy and at VF in participants who went on to develop M184V/I.

71 gree of VF damage was defined by the average VF sensitivity within the integrated VF (IVF).

72 ldren with PCG reported significantly better VF and VRQoL than secondary childhood glaucoma patients.

73 treated PCG experience significantly better VF and VRQoL than those with secondary childhood glaucom

74 were used to assess the associations between VF damage and accumulation of activity across 6 3-hour i

75 est for cross-sectional associations between VF damage and activity fragmentation.

76 icant increase in dominant frequency between VF onset and termination but none of the other parameter

77 There was good concordance between VFs measured at home and in the clinic (r = 0.94, P < .0

78 Binocular VF defects were quantified with the DSpecs testing strat

79 nocular Humphrey VFs to estimate a binocular VF index (OU-VFI).

80 The diagnostic binocular VF testing with the DSpecs was comparable to the integra

81 Twenty patients with known binocular VF defects were tested using static test images, followe

82 Binocular VFs were derived from monocular Humphrey VFs to estimate

83 The model that was trained on both VF and clinical data (AUC, 0.89-0.93) showed better diag

84 ained on VF data and another trained on both VF and clinical data, were tested.

85 -MD had better diagnostic accuracy than both VF-MD and overall NFL thickness and may be useful for ea

86 The POAG groups were matched by VF mean deviation (MD).

87 These may reduce VA or cause VF defects unrelated to papilledema, emphasizing the imp

88 wo glaucomatous eyes with ADRVDs had central VF loss.

89 ibited inferior rather than superior central VF loss (P = 0.032).

90 topographically corresponding to the central VF loss and macular ganglion cell complex thinning.

91 Thirteen eyes (59.1%) with central VF loss had ADRVDs topographically corresponding to the

92 found in any of the 12 eyes without central VF loss.

93 a progression algorithms given 4 consecutive VF results for each participant.

94 attern deviation maps were used to determine VF deterioration.

95 VF mean deviation (VF-MD) was simulated by NFLP mean deviation (NFLP-MD).

96 Discrete VFs initially formed from each virus that subsequently c

97 VP1-GFP11 and PBG98-VP1-TC viruses, discrete VFs initially formed from each input virus that subseque

98 r in persons with and without M184V/I during VF on a TDF/XTC/NNRTI-containing regimen.

99 Radiofrequency ablation was performed during VF in 2 patients.

100 Each VF had fixation losses (FLs) of 33% or less, false-negat

101 linear regression on the sensitivity at each VF location over time and then selecting the largest and

102 We entered VF data from the most recent visit of glaucomatous and n

103 r mixed-effects models were used to evaluate VF progression.

104 within discrete cytoplasmic virus factories (VFs) that may represent a barrier to genome mixing.

105 ate in discrete cytoplasmic virus factories (VFs).

106 of 1445 individuals with virologic failure (VF).

107 0 copies/mL), confirmed virological failure (VF) (2 consecutive viral loads >1000 copies/mL), and vir

108 progression, sectors with 1 ODH had a faster VF progression rate than those with no ODH (P < 0.017) a

109 Sectors with >8 ODH had faster VF progression than all other groups (all P < 0.001).

110 ve analysis of the ventricular fibrillation (VF) dynamics for every heart was carried out by measurin

111 ve measures of the ventricular fibrillation (VF) ECG waveform can assess myocardial physiology and pr

112 Studies of ventricular fibrillation (VF) in humans are limited because of the short available

113 Ventricular fibrillation (VF) optical mapping was performed in Langendorff-perfuse

114 ischaemia-induced ventricular fibrillation (VF).

115 aturity and is associated with visual field (VF) defects and optic disc cupping.

116 Visual field (VF) defects in the glaucoma eyes were classified into in

117 Glaucoma clinical trials using visual field (VF) endpoints currently require large sample sizes becau

118 The visual field (VF) index was used for the vertical axis as the function

119 ed a gaze-contingent simulated visual field (VF) loss paradigm, in which participants experienced a v

120 Visual field (VF) loss severity is associated with higher driving simu

121 relationship with the central visual field (VF) loss.

122 had perimetric glaucoma, with visual field (VF) mean deviation (MD) of -5.14+/-4.25 decibels (dB).

123 predictors of time-to-incident visual field (VF) progression was computed with the TD OCT and the syn

124 .79 +/- 0.30 in both eyes, and visual field (VF) results were -9.89 +/- 11.52 dB in both eyes.

125 iber layer scans, >=5 reliable visual field (VF) results, and follow-up of >=4 years.

126 oned into 8 sectors to match 8 visual field (VF) sectors.

127 T-derived models, we predicted visual field (VF) sensitivities and compared these results to actual V

128 D) metric, based upon the 24-2 visual field (VF) test, as well as the PSD of the 10-2 VF, will miss c

129 ate the influence of automated visual field (VF) testing on intraocular pressure (IOP) in patients wi

130 Baseline in-clinic visual field (VF) was recorded with the Humphrey Field Analyser (HFA,

131 Study (UKGTS) investigated the visual field (VF)-preserving effect of medical treatment in open-angle

132 rence tomography with the 10-2 visual field (VF).

133 ce used for home monitoring of visual field (VF-Home) by glaucoma patients.

134 ntral corneal thickness [CCT], visual field [VF], and OCT) were extracted and binary logistic (backwa

135 ing glaucoma progression from visual fields (VFs) alone are discordant and have tradeoffs.

136 Of 31 591 visual fields (VFs) on 8077 subjects, 13 231 VFs from the most recent v

137 luding visual acuity (VA) and visual fields (VFs) were collated from medical records.

138 Visual fields (VFs) were measured using standard automated perimetry an

139 enerations with corresponding visual fields (VFs).

140 (96% porosity), followed by vacuum-filtered (VF) networks (33% porosity).

141 F loss patterns and TD values based on first VF improved the prediction of the global test-retest var

142 y from 3 categories of features of the first VF: (1) base parameters (age, mean deviation, pattern st

143 84 aqueous humor (AH) and/or vitreous fluid (VF) samples.

144 (RLN) is responsible for normal vocal-fold (VF) movement, and is at risk for iatrogenic injury durin

145 e apply a single-molecule vectorial folding (VF) assay in which an engineered superhelicase Rep-X seq

146 VF and VRQoL compared to PCG (difference for VF, -0.83; 95% confidence interval [CI], -1.34 to 0.31;

147 vious) was associated with a reduced HR, for VF deterioration (HR, 0.59; 95% CI, 0.37-0.93; P = 0.023

148 eatment with latanoprost reduced the HR, for VF deterioration by 58% (HR, 0.42; 95% CI, 0.27-0.67; P

149 VF loss at baseline were at higher risk for VF progression.

150 Reliability and global indices from VF-Home were compared to in-clinic outcomes.

151 Among patients resuscitated from VF/pVT OHCA with ST-segment elevation on their postresus

152 Conversely, among patients resuscitated from VF/pVT OHCA without ST-segment elevation on their postre

153 Global VF organization quantified by causality pairing index sh

154 Global VF progression rate was calculated using linear regressi

155 more strongly associated with greater global VF progression compared with those occurring within the

156 st variability than using traditional global VF indices alone.

157 With global VF analysis, eyes with ODH in 2 different sectors of the

158 ol was independently associated with greater VF loss and worse neurocognitive performance, suggesting

159 the UKGTS, treatment with latanoprost halved VF deterioration risk.

160 levation >=2 mmHg had a significantly higher VF test duration (P = 0.002).

161 Human VF fibroblasts (HVOX) were treated with three commonly-e

162 ese findings were further confirmed in human VF.

163 Humphrey VF defects resulting from TED-CON are most often inferio

164 dentified patients with progressive Humphrey VF defects secondary to TED-CON.

165 lar VFs were derived from monocular Humphrey VFs to estimate a binocular VF index (OU-VFI).

166 s to track the location and movement of IBDV VFs, in order to better understand the intracellular dyn

167 0% in AH samples [n = 69]; 66% versus 63% in VF samples [n = 82], respectively).

168 unction despite no significant difference in VF scores.

169 Injury, resulting in VF paralysis, may contribute to subsequent swallowing, v

170 e by PCR-based tests was higher than that in VF by culturing (62% vs 48%, respectively; n = 94; P = 0

171 cture can capture local and global trends in VFs over time.

172 The previously incessant VFs in these 2 patients did not recur afterward.

173 Cox regression modeling for time to incident VF progression was 1.09 (95% confidence interval [CI], 1

174 superior optic nerve thinning with inferior VF defects, suggest PVL.

175 average VF sensitivity within the integrated VF (IVF).

176 led that RLN transection created ipsilateral VF paralysis that did not recover by 13 weeks postsurger

177 glaucoma dashboard, developed using a large VF dataset containing a broad spectrum of visual deficit

178 forms and effect of ablation in long-lasting VF in patients with left assist devices.

179 Long-lasting VF may be modified or even terminated by ablation.

180 us 12-lead ECG of 5 episodes of long-lasting VF occurring in 3 patients with left ventricular assist

181 Longitudinal VFs from 287 eyes with glaucoma were used to validate th

182 The POAG groups had matched VF MD (-3.1 +/- 2.5 dB paracentral vs. -2.3 +/- 2.0 dB p

183 , pattern standard deviation (PSD), and mean VF sectoral pattern deviation (PD) from SD OCT data.

184 In predicting mean VF sectoral PD, deep learning models achieved high accur

185 augmentation profiles based on the measured VF.

186 g, we used a longitudinal data set of merged VF and clinical data to assess the performance of a conv

187 s, either with: (1) no VF loss, (2) moderate VF loss, or (3) advanced VF loss.

188 The diagnostic monocular VF testing algorithm was comparable to standard automate

189 The sequence of monocular VF was tested and customized image remapping was carried

190 The monocular VF was used to calculate remapping parameters with a cus

191 intersection of both datasets with 4 or more VF results and corresponding baseline clinical data (cup

192 We previously identified neuropeptide VF (NPVF) and the hypothalamic neurons that produce it a

193 deos and three pictures, either with: (1) no VF loss, (2) moderate VF loss, or (3) advanced VF loss.

194 standard and CNN prediction of incident non-VFs.

195 g statistical significance), and less normal VF results and superior paracentral defect.

196 g (MRI), optical coherence tomography (OCT), VF, and optic disc photographs were reviewed.

197 Degree of VF damage was defined by the average VF sensitivity with

198 lar global functional severity, an extent of VF loss into different hemifields, and characteristic lo

199 Moreover, we show that the main features of VF dynamics in a treated failing heart are not affected

200 e effectively individualize the frequency of VF testing to the individual patient.

201 We evaluated a comprehensive group of VF measures with and without ongoing compressions to det

202 ine's beneficial effects on the incidence of VF caused by 120 min regional ischaemia were contrasted

203 y is completed) did not vary across level of VF damage.

204 At worse levels of VF damage, glaucoma patients demonstrate shorter, more f

205 ere performed over a median of 24 minutes of VF.

206 ponent was calculated with a linear model of VF measurements over time.

207 A reverse order of VF defect progression was noted in 15 eyes with improvin

208 fields, and characteristic local patterns of VF loss.

209 lar global, hemifield, and local patterns of VF loss.

210 RNFLT change became a stronger predictor of VF progression.

211 but no significant difference in the rate of VF loss was seen after tube shunt implantation and trabe

212 The incidence rate of VF was 7.0, 2.0, and 0.5 per 100 person-years among part

213 Slow rates of VF loss were observed after randomized surgical treatmen

214 The longitudinal sequence of VF defects from the 37 eyes of 23 patients was analyzed.

215 defect, and the association between type of VF defect and CMvD was evaluated.

216 We observed that the combined use of VF and OCT endpoints led to a 31-33% reduction in sample

217 ter understand the intracellular dynamics of VFs during a coinfection.

218 Home monitoring of VFs is viable for some patients and may provide clinical

219 The average number of VFs decreased from a mean of 60 to 5 per cell between 10

220 clusion criteria-specifically the removal of VFs with high false-positive and false-negative rates an

221 ent illumination had no observable effect on VF measurements (r = 0.07, P = .320).

222 In order to provide new information on VF trafficking during dsRNA virus coinfection, we rescue

223 No progression on VF or OCT was noted in the index case over almost 4 year

224 learning models, one exclusively trained on VF data and another trained on both VF and clinical data

225 ability than a model exclusively trained on VF results (AUC, 0.79-0.82; P < 0.001).

226 In organized VF with high causality pairing index values, GC vector m

227 articipants, both paracentral and peripheral VF loss groups showed reduced VD (P < 0.001 and P = 0.00

228 more strongly in central than in peripheral VF locations (intraclass coefficient, 0.66-0.89; P < 0.0

229 Monocular peripheral VF defects were measured and defined with a head-mounted

230 r TD sensitivity in the outermost peripheral VF locations was predictive of higher global variability

231 Compared with POAG eyes with peripheral VF loss, the paracentral group showed reduced peripapill

232 A mixed-effects model (MEM) and a pointwise VF progression analysis of pattern deviation were used t

233 inear models were used to estimate pointwise VF progression rates, which were then averaged to produc

234 hase analysis and further tested in previous VF optical mapping recordings of coronary perfused donor

235 years and involved, among other procedures, VF testing and intraocular pressure (IOP) measurement at

236 progression criteria: at least 3 progressing VF locations on 2 or 3 consecutive tests ("possible" or

237 n slow VF loss in glaucoma or if progressive VF loss results in activity restriction.

238 measurements in predicting all quantitative VF metrics.

239 tify eyes with GVFD and predict quantitative VF mean deviation (MD), pattern standard deviation (PSD)

240 baseline factors associated with more rapid VF loss.

241 d first with medical therapy underwent rapid VF progression compared with those treated first with SL

242 M had no adverse effects, but did not reduce VF incidence.

243 Mexiletine 1 uM reduced VF incidence to 0% but had adverse effects on atrioventr

244 1 with CNVM) had distinctive retina-related VF defects at presentation.

245 We selected 2 reliable VFs per eye measured with the Humphrey Field Analyzer (S

246 A total of 436 reliable VFs were analyzed, with an average of 3.6 VFs per eye.

247 ng video signals to fit within the remaining VF in real time.

248 seen peripheral targets within the remaining VF.

249 late that Birnaviridae reassortment requires VF coalescence.IMPORTANCE Reassortment is common in viru

250 Regarding the largest sectoral VF progression, sectors with 1 ODH had a faster VF progr

251 s with diabetes, higher IOP, and more severe VF loss at baseline were at higher risk for VF progressi

252 OCTA-based simulated VF agreed well with actual 24-2 VF in terms of both the

253 apable of consistently identifying simulated VF loss, despite it being of a magnitude likely easily d

254 xperienced a variable magnitude of simulated VF loss based on longitudinal data from a real glaucoma

255 c dB scale and converted to sector simulated VF deviation maps.

256 The simulated VF loss caused some statistically significant effects in

257 d to determine if physical activity can slow VF loss in glaucoma or if progressive VF loss results in

258 Small VFs moved faster than large (average 0.57 mum/s at 16 hp

259 Some VF parameters varied from patient to patient and from le

260 ce: (4) functional progression in a "stable" VF with structure-function correlation, (5) functional p

261 e horizontal midline to involve the superior VF.

262 Supplementing VF results with clinical data improves the model's abili

263 eated failing heart is more prone to sustain VF than the normal heart, and is at least as susceptible

264 and is at least as susceptible to sustained VF as the untreated failing heart.

265 and cognition (verbal fluency language task, VF) and affect (anxiety) in both groups as well as disea

266 ity (0.63 dB pooled standard deviation) than VF-MD (1.03 dB).

267 had a significantly higher sensitivity than VF-MD (P < .001) and overall NFL thickness (P = .031).

268 Here, we evaluated the hypothesis that VF loss severity and neurocognitive performance interact

269 We hypothesize that VF coalescence is required for the reassortment of the B

270 erlying mechanism remains unknown given that VFs may act as a barrier to genome mixing.

271 The VF defects were analyzed by 2 independent reviewers and

272 mHg before and 14.98 +/- 3.33 mmHg after the VF (P = 0.4).

273 d." We used density-based clustering and the VF decomposition method called "archetypal analysis" to

274 hese questionnaires were used to compare the VF and VFQoL between the 2 groups.

275 2) = 0.12), whether based on duration of the VF test (P = 0.18) or the MD (P = 0.7) after adjustment

276 sing multivariate analysis, no effect of the VF test on IOP was found (global model fit R(2) = 0.12),

277 thickness (CCT), mean deviation (MD) of the VF, VF test duration and filtration surgery on IOP fluct

278 the affected hemisphere corresponding to the VF hemifield of more severe loss, which was used to calc

279 The VFs were excluded if visual acuity <20/400 or loss of >=

280 The VFs were included if the false-positive rate was <=20% a

281 ittle to restore physiologic function of the VFs.

282 01), and live cell imaging revealed that the VFs were highly dynamic structures that coalesced in the

283 These VFs and their interactions with the host are represented

284 n sample size requirements compared to using VF endpoints alone for various treatment effect sizes.

285 Clinical and treatment variables (VF, surgical interventions, medications) were not indepe

286 ckness (CCT), mean deviation (MD) of the VF, VF test duration and filtration surgery on IOP fluctuati

287 hat adds to our understanding of dsRNA virus VF trafficking.

288 m exchanger as predominant phenotypes for VT/VF.

289 alternans was greater (by 80%, P<0.05) in VT/VF(+) versus VT/VF(-) STIM1-KD hearts.

290 ielded c-statistics of 0.90 for sustained VT/VF (95% CI, 0.76-1.00) and 0.91 for mortality (95% CI, 0

291 re trained to 2 end points: (1) sustained VT/VF or (2) mortality at 3 years.

292 Susceptibility to VT/VF (ventricular tachycardia/fibrillation) is difficult t

293 eater (by 80%, P<0.05) in VT/VF(+) versus VT/VF(-) STIM1-KD hearts.

294 cal glaucoma damage with good agreement with VF.

295 was to identify risk factors associated with VF deterioration.

296 The FPL had excellent correlation with VF MD (Spearman's rho = -0.843), which was significantly

297 thinning was most prominent superiorly, with VF defects more notable inferior and homonymous.

298 ocalized with VP3 and dsRNA, consistent with VFs.

299 its, was associated with significantly worse VF progression than sectors with moderate or only 1 obse

300 ildhood glaucoma to be associated with worse VF and VRQoL compared to PCG (difference for VF, -0.83;