ライフサイエンスコーパス: disease stage

1 onse system, stratified by mutation type and disease stage.

2 derate/advanced (n = 14) groups according to disease stage.

3 se that can be designed to identify the Lyme disease stage.

4 amyotrophic lateral sclerosis from the early disease stage.

5 for these diseases, with therapy adjusted to disease stage.

6 obal Initiative for Chronic Obstructive Lung Disease stage.

7 ing in amyotrophic lateral sclerosis at late disease stage.

8 vel of FL produced >/=1 dB of DeltaMD at any disease stage.

9 otrophic lateral sclerosis patients in early disease stage.

10 leep quality resembling signs of a prodromal disease stage.

11 trophy progresses further during the chronic disease stage.

12 Oncology Group performance status, age, and disease stage.

13 depth, ulceration of the primary lesion, and disease stage.

14 stratified according to centre and clinical disease stage.

15 y although therapeutic benefit may depend on disease stage.

16 ses in intrinsic excitability that depend on disease stage.

17 echanism that groups patients based on their disease stage.

18 s a high risk of distant metastasis at every disease stage.

19 HCV, with efficacy dependent on genotype and disease stage.

20 tive, the sensitivity was 100% regardless of disease stage.

21 data on the immune status of this particular disease stage.

22 gs was observed in patients at a less severe disease stage.

23 lack of cancer-specific information such as disease stage.

24 +) T cells emerged as positive correlates of disease stage.

25 ggesting a role of Th17.1 cells in the early disease stage.

26 rve does not plateau at an early symptomatic disease stage.

27 ple myeloma with poor prognosis and advanced disease stage.

28 ty' rather than as a marker of disability or disease stage.

29 y transplanted into G93A mice at symptomatic disease stage.

30 e with a worse progression-free survival and disease stage.

31 rly T(2) prolongation occurs at a reversible disease stage.

32 AMD, but only in patients with a less severe disease stage.

33 notype development is different at different disease stages.

34 compartment occurred as early as preinvasive disease stages.

35 the identification of patients at different disease stages.

36 driving cellular compartments at the various disease stages.

37 on, likely representing in early Alzheimer's disease stages.

38 ic markers for early infection detection and disease stages.

39 ipheral inflammation occurs early at the MCI disease stages.

40 rsodeoxycholic acid, may be effective at all disease stages.

41 ents are dramatically less effective at late disease stages.

42 broader age spectrum and patients of various disease stages.

43 amyloid-beta species across brain areas and disease stages.

44 luence plasma drug concentrations in the two disease stages.

45 t treatment stratification at early and late disease stages.

46 in patients with parkinsonism, even at early disease stages.

47 in intermediate monocyte subsets in advanced disease stages.

48 istribution of HBV genotypes among different disease stages.

49 s and a myostatin inhibitor in mice at later disease stages.

50 es in a DTI metric that reflect distinct ALS disease stages.

51 survival of rods and cones at early and late disease stages.

52 nd uncovered additional heterogeneity within disease stages.

53 nts with multiple sclerosis (MS) at distinct disease stages.

54 We then treated mice at early, mid, or late disease stages.

55 dicating their greater usefulness in earlier disease stages.

56 ssive increase in human brain in preclinical disease stages.

57 purified native mouse podocytes during early disease stages.

58 d glaucomatous patients with a wide range of disease stages.

59 iatum of R6/1 mice during the presymptomatic disease stages.

60 otective mainly for preclinical and clinical disease stages.

61 al target for HIV-1 infection throughout all disease stages.

62 oth GLUT and SGLT transporters in health and disease stages.

63 optimal use of imaging methods at different disease stages.

64 free of HF risk factors or structural heart disease (Stage 0), 52% were categorized as Stage A, 30%

65 ormer Global Initiative for Obstructive Lung Disease stage 0 smokers predicted structural and physiol

66 ed as Global Initiative for Obstructive Lung Disease stage 0).

67 obal Initiative for Chronic Obstructive Lung Disease stage 1, where each exacerbation was associated

68 ns were observed with (68)Ga-PSMA-11 in both disease stages (113 for (18)F-rhPSMA-7 and 124 for (68)G

69 205 uninsured patients with chronic HCV had disease staging, 145 (70.7%) had teleconsultation review

70 uated by the provider, 55.3% underwent liver disease staging, 15.0% initiated treatment, 12.0% comple

71 Within each disease stage, 1q gain was associated with inferior EFS

72 obal Initiative for Chronic Obstructive Lung Disease stage 2 and 3 subjects.

73 I, 4.28-79.4 for 3-4 quadrants vs no preplus disease), stage 2 ROP (OR, 4.13; 95% CI, 2.13-8.00 vs no

74 d diagnosis for certain categories (eg, plus disease, stage 2 disease or worse, and treatment-requiri

75 BW and prematurity, the presence of preplus disease, stage 2 ROP, retinal hemorrhage, and the need f

76 ation rate and lowest rate of chronic kidney disease (>=stage 3) from year 1 onwards until study end.

77 Measurements: Chronic kidney disease (stages 3 and 4) was defined as an estimated glo

78 oportion of HRS2 patients had chronic kidney disease stage 3 (CKD3) at 3 (53.8% vs 28.4%; P = 0.007)

79 a in 20/46 (43%) patients and chronic kidney disease stage 3 or above in 42/49 (86%) patients.

80 etiapine had reduced rates of chronic kidney disease stage 3 or more severe, following adjustment for

81 in decade 1 demonstrated advanced stages of disease (stage 3B or worse) compared with 20% of eyes in

82 ficant difference in rates of chronic kidney disease stage 4 or more severe, type 2 diabetes mellitus

83 obal Initiative for Chronic Obstructive Lung Disease stage 4 versus stage 1 COPD (P < 0.0001).

84 ease, including patients with chronic kidney disease stages 4 or 5 (CKD 4/5).

85 22 patients with chronic kidney disease stage 5 undergoing intermittent hemodialysis tre

86 minimisation program, stratified by centre, disease stage according to FIGO guidelines, and age.

87 : validation of non-invasive tests for liver disease staging; additional immunopathogenesis studies i

88 , there were no differences in biomarkers by disease stage after 12 months of ART (n = 438; P > .05),

89 mpact of major clinical variables, including disease stage, age of disease onset and accelerated brai

90 r of RFS and OS and associated strongly with disease stage (AJCC 8(th) Edition Staging Manual).

91 as hyperlipidemia, smoking, medication, and disease stage, all of which affect the thiol redox state

92 litis, sleep disorders vary according to the disease stage along with other neuropsychiatric symptoms

93 with anti-NMDAR encephalitis after the acute disease stage and 25 healthy control subjects underwent

94 response system and stratified according to disease stage and baseline PD-L1 status of tumour cells.

95 These findings show that both disease stage and cell type must be considered when deve

96 +) myeloid cells, IL30 levels increased with disease stage and correlated with recurrence.

97 Patients were stratified at randomisation by disease stage and ECOG performance status.

98 n technique, randomisation was stratified by disease stage and geographical region.

99 Knees were matched according to radiographic disease stage and patient sex and age.

100 were significantly associated with advanced disease stage and poor patient prognosis (P<0.01).

101 erm (>/=2 years) symptoms, adjusted for Lyme disease stage and severity at diagnosis.

102 Disease stage and smoking history are often used in curr

103 that tumor GRP78 expression correlates with disease stage and that anti-GRP78 AutoAb levels parallel

104 tatus of the heart may vary depending on the disease stage and that treatment should be initiated bef

105 scovery of novel biomarkers that may reflect disease stage and therapeutic response.

106 clerosis, including lipid breakdown at early disease stages and activation of anaplerotic pathways to

107 tinct bacterial populations in the different disease stages and also depending on the level of inflam

108 Inflammation is typically present in all disease stages and associated with the development of fi

109 accumulations distributed differently across disease stages and brain areas, while N-terminally trunc

110 ink motor microcircuit pathology to specific disease stages and clinical phenotypes.

111 tment of OPSCC are outlined for a variety of disease stages and clinical scenarios.

112 sed experimental platforms that recapitulate disease stages and clonal architecture.

113 ction of diffuse myocardial disease in early disease stages and complements late gadolinium enhanceme

114 ties in cancer cells exists across different disease stages and even in the same patient, with increa

115 mally' treat retinal degeneration at various disease stages and examined the long-term efficacy of ge

116 ease-associated astrocytes appeared at early disease stages and increased in abundance with disease p

117 ecause epileptic activity can occur at early disease stages and might contribute to pathogenesis.

118 eptide (PepVF) to capture sensitivity in all disease stages and OspC for early Lyme disease.

119 -20% in early disease stages to -61% in late disease stages and preceded fibrosis.

120 imited accuracy of neuroimaging in the early disease stages and the absence of molecular biomarkers,

121 ship between these networks across different disease stages and their association with brain connecti

122 Neurogranin was increased at early CJD disease stages and was a good prognostic marker of survi

123 This loss of richness correlated with disease stages and was particularly marked in patients w

124 hese areas, combined with efforts related to disease staging and emerging mechanistic data from clini

125 tron emission tomography is a useful tool in disease staging and follow-up.

126 es require valid biomarkers for standardized disease staging and for evaluation of progression and th

127 ated healthcare system provides non-invasive disease staging and minimizes hepatology clinic utilizat

128 ntial information for accurate evaluation of disease staging and progression, yet the poor cellular u

129 uted in August 2017 to improve efficiency of disease staging and promote lifestyle modification.

130 uch improvements could lead to more accurate disease staging and robust measurements of changes in ta

131 D) and defined its association with advanced disease-stage and poor clinical outcomes.

132 0% within 1 year of diagnosis (regardless of disease stage), and 20% per year thereafter, chronic pre

133 ined the effect of ageing, HIV infection (by disease stage), and their interaction on five neurocogni

134 subgroups defined by prior transplantation, disease stage, and cytogenetics, with prognostic superio

135 ng abnormalities in SCA2 differ depending on disease stage, and interventions targeted towards correc

136 Randomisation was stratified by GCIG group, disease stage, and outcome and timing of surgery.

137 key clinical variables (e.g., tumor subtype, disease stage, and patient survival time) and other mole

138 stratified, in a block size of two, by age, disease stage, and performance status.

139 ratified by induction regimen, pre-induction disease stage, and response post-transplantation.

140 nts were stratified according to GCIG group, disease stage, and timing and outcome of cytoreductive s

141 in hypoxia tracer uptake, even in the early disease stages, and a 45-fold elevation in ROS expressio

142 s benefit molecular diagnosis, evaluation of disease stages, and also play a central role in fundamen

143 t-specific differences in infectivity across disease stages, and on the epidemic level we considered

144 ly occurring in both initial and progressive disease stages, and preventing truncation may be an effe

145 n about the transition from acute to chronic disease stages, and the factors and mechanisms that shap

146 s critical for HIV prevention, screening and disease staging, and monitoring antiretroviral therapy (

147 r imaging could be used for early detection, disease staging, and prognostication, as well as for ass

148 italisation for heart failure; annual kidney disease stages; and cardiovascular and nonvascular death

149 Predictors of genital shedding were HIV disease stage, antiretroviral regimen, and genital ulcer

150 terval [CI], 1.82-4.17) and to undergo liver disease staging (aOR, 1.92; 95% CI, 1.02-2.86) than pati

151 n levels and mitochondrial function as early disease stages are initiated.

152 and prognostic markers used in more advanced disease stages are not applicable) will lead to the iden

153 es and the implications for TB diagnosis and disease staging are poorly understood.

154 d variables such as age of disease onset and disease stage as well alterations of structural brain ma

155 a and full-length amyloid-beta, depending on disease stage as well as brain area, and determined how

156 y pathways was reduced in the lungs at later disease stages as were splenocyte IL12/23p40 and IFN-gam

157 on-free and overall survival was assessed by disease stage at diagnosis in pregnant patients and comp

158 duced in Brazil in 2004, but their effect on disease stage at diagnosis is unclear.

159 y stratified by sex, CD4 cell count, and WHO disease stage at enrolment in care and initiation of ant

160 istent with the interocular disparity of the disease stage at presentation.

161 irometry results and modified Hoehn and Yahr disease stage at screening were used for stratification

162 the more affected anterior node and, at the disease stage at which we studied these patients, appear

163 Promisingly, NOD mice given transient late disease stage BAFFR-Fc monotherapy were rendered T1D res

164 y begin as an astrogliopathy at a very early disease stage but neuronal lesions gradually take over a

165 neys, and total kidneys of mice at different disease stages by using a personal genome machine and RN

166 lantation (alloHSCT) outcomes by disease and disease stage can limit statistical power.

167 atment intent occurred in 65.5% of subjects, disease stage changed in 65.5%, and management plans cha

168 ponents were quantified, and were related to disease stage, clinical severity, and MECP2 mutation typ

169 rsodeoxycholic acid (UDCA)-responding, early-disease stage cohort.

170 Treatment decisions should also consider disease stage, comorbidities, and patient preferences.

171 ted antiretroviral therapy (ART) at advanced disease stages, continue to have increased age-related m

172 rly inflammation, as well as mild and severe disease stages, could be distinguished.

173 This proliferation persisted into the late disease stage (day 56 post-immunization), indicating the

174 An obstacle in such an approach is that disease stage-defining biomarkers are still lacking.

175 Here, we determined disease stage-dependent changes in myocardial efficiency

176 f neurological disturbances independently of disease stage determined by current criteria.

177 tion for improving detection and accuracy of disease stage diagnosis.

178 tterns, which are characteristic of advanced disease stages, during a much earlier presymptomatic pha

179 llagen FSR in NAFLD increased with advancing disease stage (e.g., higher in NASH than nonalcoholic fa

180 stem cell (iPSC) lines capturing a range of disease stages encompassing preleukemia, low-risk MDS, h

181 dative phosphorylation was observed at early disease stage, even before the appearance of disease phe

182 ity of normalization was not associated with disease stage, FIGO score, or baseline hCG.

183 ce costs were directly related to increasing disease stages from 0 to 4 (p<0.001).

184 sue samples that were collected at different disease stages from desmoglein 2-mutant mice, a well cha

185 s stratified by International Staging System disease stage, geographical region, and age.

186 s showed that patients at an advanced severe disease stage had a higher frequency of terminally diffe

187 Because patients with different liver disease stages have been treated with great success incl

188 vious injections and blood transfusions, HIV disease stage, hepatitis B and hepatitis C status, and C

189 obal Initiative for Chronic Obstructive Lung Disease stage higher than 1 (odds ratio = 1.96 [95% CI =

190 age based on the following categories: liver disease stage, HIV co-infection, prescriber type, and dr

191 riteria for sofosbuvir with respect to liver disease staging, HIV co-infection, prescriber type, and

192 ion in the colon biopsy tissues at different disease stages, hyperplasia, dysplasia, and cancer, and

193 ortality among participants with early-stage disease (stages I and II; HR, 1.61; 95% CI, 1.26 to 2.04

194 obal Initiative for Chronic Obstructive Lung Disease stage I to II) before and after treatment with f

195 s of 500 cells per muL or more, and with WHO disease stage I, had the highest life expectancies.

196 obal Initiative for Chronic Obstructive Lung Disease stage I-IV COPD, and smoking and never-smoking c

197 obal Initiative for Chronic Obstructive Lung Disease) stages I-IV: 9.4, 42.5, 37.5, and 10.5%, respec

198 Localized disease (stage IE or IIE) was commonly treated with exte

199 obal Initiative for Chronic Obstructive Lung Disease stage II subjects with COPD and as controls 20 s

200 obal Initiative for Chronic Obstructive Lung Disease stage II-IV COPD and persistent symptoms and/or

201 obal Initiative for Chronic Obstructive Lung Disease stage II-IV were enrolled.

202 obal Initiative for Chronic Obstructive Lung Disease stage II-IV) underwent hyperpolarized (129)Xe MR

203 6 PD patients who were divided into three PD disease stages (IIa, III, and IV) according to the Unifi

204 1; 95% CI, 1.26 to 2.04), but not late-stage disease (stages III and IV; HR, 1.05; 95% CI, 0.91 to 1.

205 g of localized, disseminated, and persistent disease stages, impacting several organ systems through

206 Results: PSMA PET/CT changed the disease stage in 135 of 197 (69%) patients (upstaging in

207 evel of CENPA expression correlates with the disease stage in a large cohort of patients.

208 gly correlated with NF-kappaB activation and disease stage in clinical specimens of ovarian cancer.

209 n mouse models of cancer and with increasing disease stage in primary human cancers.

210 onducting quality-controlled trials for this disease stage in the multi-institutional setting.

211 s, Abeta and p-tau were quantified across AD disease stages in parietal cortex.

212 e dyed pig esophagus and images of different disease stages in the human esophagus were analyzed, sho

213 NIR-AF could be a marker for disease staging in choroideremia, and could be used for

214 Pre-HCT disease staging included 10-color multiparametric flow c

215 grade, involvement of lymphovascular space), disease stage (including myometrial invasion), patients'

216 causes of death were progression to advanced disease stage, including complications of stem-cell tran

217 ts were found progressively increased as the disease stage increased in severity.

218 s (HCV) in 2009, incremental annual costs by disease stage, incremental total Medicare HCV payments i

219 hat were enhanced early and blunted at later disease stages, indicating evolving responses along the

220 was consistent with or without SEER-Medicare disease stage information (weighted kappa >/= 0.81).

221 ic, history and examination, laboratory, and disease staging information were shown using descriptive

222 As previously observed, late disease stage-initiated anti-CD20 monotherapy did not in

223 severe, and usually persist beyond the acute disease stage, interfering with patients' recovery and q

224 ying an important role in progression of the disease stage is of great interest.

225 While the histopathology of the different disease stages is well characterized, the cause underlyi

226 Disease staging is a method for measuring the progressio

227 ularly when treatments are given at advanced disease stages, is controversial.

228 problem, but little is known about its early disease stages, its effects on biological processes or t

229 obal Initiative for Chronic Obstructive Lung Disease stage IV COPD lungs with TLOs.Measurements and M

230 plant included having pretreatment extent of disease stage IV lesions and a longer waiting list time

231 a statistical framework that models distinct disease stages (locoregional recurrence, distant recurre

232 the number of chemotherapy cycles received, disease stage, lymph node sampling procedure, performanc

233 that therapeutic interventions at the early disease stage may be effective at alleviating the myopat

234 e lesions, and their relationship to earlier disease stages may be greatly underestimated.

235 s, diverse microglial reactions at different disease stages may open new avenues for therapeutic inte

236 Randomisation was stratified by disease stage, menopausal status, hormone-receptor statu

237 of the head and neck who have advanced nodal disease (stage N2 or N3) and who have received chemoradi

238 analysis, cardiac involvement, advanced Mayo disease stage, neuropathic involvement, and liver involv

239 ) had stage II, and 439 (30%) had stage IIIA disease (stage of disease data were missing for 43 patie

240 ATPase isoform 1 (SPCA1) correlated with the disease stage of PV.

241 olution of the biomarkers, and (iii) predict disease stages of 57 animals that were naturally infecte

242 bition of CXCR4 and PAI-1 in ALI and various disease stages of IPF.

243 In this early disease stage, only the CTC status was an independent, p

244 entified in all patients, independent of the disease stage or presence of widespread changes on autof

245 ignificantly larger than differences between disease stages or models.

246 odocytes of patients with DN, independent of disease stage, or BTBR ob/obmice, a model of type 2 diab

247 use this ordering to estimate the molecular disease stage-or disease pseudotime-for each sample.

248 hysematous and normal voxels with increasing disease stage (P < 0.001).

249 p<0.0001), and were diagnosed at an earlier disease stage (p=0.006, chi(2) test for trend).

250 e (p=0.029), imaging modality (p=0.019), and disease stage (p=0.025) on sensitivity as well as of pos

251 increased risk of death after adjusting for disease stage [PAM negative, HR = 13.8 (CI: 4.2-45.5)].

252 tulate that these lesions define preclinical disease stages, preceding the formation of protein aggre

253 ch remained significant after adjustment for disease stage, prior clinical suspicion, and primary tre

254 ia which may be helpful in the assessment of disease staging, qualification to HSCT and follow-up.

255 alue of MSIS-29 for survival time at earlier disease stages requires further investigation.

256 oro-parietal hypometabolism, while the later disease stages show overlapping brain atrophy and hypome

257 occurrence of these changes at a reversible disease stage shows the clinical potential of this CMR m

258 Furthermore, disease stage significantly moderated neuroanatomical di

259 ates, all lacking GPL, predominated at later disease stages, some showing variation within rough morp

260 re robust, stable, disease specific, or even disease stage specific.

261 ve cryopreservation, and exhibit ductal- and disease-stage-specific characteristics.

262 s iPSC-based approach can be used to uncover disease-stage-specific responses to drugs.

263 hnologies in oncology might misclassify true disease stage, spuriously informing disease management a

264 OTATATE PET that did not alter the patient's disease stage (stage IV) because the patient had 11 addi

265 At the early disease stage, subchondral bone plate thinning and reduc

266 At the late disease stages, subchondral bone plate thickened concomi

267 In late disease stages, subchondral bone sclerosis has been link

268 In later disease stages T2* changes involved deeper cortical lami

269 g action, together with careful selection of disease stage targets and dosing strategies may overcome

270 , which is considered to be the peak age for disease stages that require timely intervention.

271 ated as in Sweden, given their age, sex, and disease stage, the largest increase in resectional surge

272 Otherwise, at early disease stages, the synaptic physiology phenotype appear

273 o balance, on the basis of comorbidities and disease staging, the potential immediate benefits of tre

274 .0001) and the difference increased from one disease stage to the next.

275 This reduction ranged from -20% in early disease stages to -61% in late disease stages and preced

276 subtype is likely to be attainable at early disease stages to prognosticate clinical course and desi

277 istent sequence of OCT features from earlier disease stages to the end stage of RORA could be found,

278 onse system, stratified by mutation type and disease stage, to receive oral dabrafenib (150 mg twice

279 equences to having moderate disease and that disease stage transitions can be anticipated.

280 We also show that disease stage transitions, both reversal and progression

281 The effect of immunotherapy type, disease stage, tumor histology, and concurrent chemother

282 Disease stage, tumor response, and MDD at diagnosis did

283 ngle-predictor Cox regression analysis, age, disease stage, tumor weight, somatic TP53 mutations, and

284 ion with a random element stratified by age, disease stage, tumour site, and country.

285 ed NRM were non-VRE BSI, older age, advanced disease stage, UCB allograft, - mismatch, comorbidity in

286 Overall survival, disease staging using international scales, time period

287 motor, executive and behavioural scales and disease staging using the King's college staging system.

288 Before ablation, disease stage was evaluated, to identify active (AM) ver

289 creased Abeta accumulation and cell death as disease stage was higher.

290 Median age was 34 years; disease stage was I or III in 53.3% and 46.7% of women,

291 Disease stage was known for 30 733 (85.8%) of 35 823 men

292 Retinal disease staging was done by indirect funduscopy and FAG

293 Focusing on progressive disease stages, we could then demonstrate that pHERV-W E

294 The change of chronic kidney disease stages were recorded and compared with baseline

295 drusen score), pigmentary abnormalities, and disease staging were also evaluated.

296 Fundus features specific for diagnosis and disease staging were retrospectively characterized by sy

297 8alpha plays distinct roles depending on the disease stages, which may set the stage for investigatin

298 alterations in gut microbiome that parallel disease stages with maximal changes in ACLF.

299 HIV disease staging with referral laboratory-based CD4 cell

300 s more generalisable across cancer types and disease stages, with good indices for screening and case