ライフサイエンスコーパス: disease onset

1 the contribution of atopic sensitization to disease onset.

2 tibody repertoires of an Ebola survivor from disease onset.

3 ts or in homozygous juveniles prior to liver disease onset.

4 , and 43% were still ambulant 20 years after disease onset.

5 due to potential application in forecasting disease onset.

6 ntify at-risk populations earlier to prevent disease onset.

7 most likely not due to factors downstream of disease onset.

8 ables, and assessed the effect of postponing disease onset.

9 ific IgM and IgG antibodies within a week of disease onset.

10 IRAK4 reduced the expression of IRGs during disease onset.

11 ficile in the host gut are prerequisites for disease onset.

12 ng pathways up to two decades prior to overt disease onset.

13 tions of genes affecting TB invasion provoke disease onset.

14 of the mir-17~92 cluster in LMC-MNs prior to disease onset.

15 ich corresponded to 255 days (228-287) after disease onset.

16 3 can successfully lower microgliosis before disease onset.

17 ogression, as well as a characteristic rapid disease onset.

18 remains unchanged by PrP(C) reduction after disease onset.

19 highest prevalence of nephrotic syndrome at disease onset.

20 e to aquarium zoanthid corals shortly before disease onset.

21 leads to paralysis and death 2-5 years after disease onset.

22 activation with tranexamic acid also delayed disease onset.

23 ) of 188 men, at a maximum of 548 days after disease onset.

24 t can be effective when applied months after disease onset.

25 have provided insight into the mechanisms of disease onset.

26 als at high risk for schizophrenia promoting disease onset.

27 d that this regulation is impaired during MS disease onset.

28 significant inverse correlation with age at disease onset.

29 gated for their potential in preventing this disease onset.

30 ar surfaces play a major role in determining disease onset.

31 synaptic functions independently from age of disease onset.

32 d might represent promising tools to predict disease onset.

33 en when therapy was initiated 36 hours after disease onset.

34 on (r = -0.58, P = 0.01) but not with age at disease onset.

35 seen in animals that succumbed with delayed disease onset.

36 cells was able to halt EAE progression after disease onset.

37 s, and patients die within a few years after disease onset.

38 d not correlate with survival time or age of disease onset.

39 egration in AD patients with a wide range of disease onset.

40 mygdala, caudate and cortex is predictive of disease onset.

41 isease progression if treatment occurs after disease onset.

42 nts and at-risk relatives of patients before disease onset.

43 rmacological inhibition of JAK1 also delayed disease onset.

44 evels, shorter disease duration, and earlier disease onset.

45 sen disease activity and might contribute to disease onset.

46 onset with those who started 4-6 years after disease onset.

47 ssed at hospital discharge and one-year post-disease onset.

48 pies aimed at SPN synapse function, prior to disease onset.

49 nd IgG antibodies as early as week one after disease onset.

50 n B cell-tropic Epstein-Barr virus (EBV) and disease onset.

51 gher lifetime risk, and 4 to 9 years earlier disease onset.

52 n change during cellular differentiation and disease onset.

53 s (early) or 4-6 years (late) after clinical disease onset.

54 ble existing models for testing drugs before disease onset.

55 nd Year 4 in Hispanics after end-stage renal disease onset.

56 orylated TDP-43 levels and an earlier age of disease onset.

57 onset multiple sclerosis (MS), followed from disease onset.

58 The median survival time was 26 years from disease onset.

59 ts in >1 ALS gene, and these individuals had disease onset 10 years earlier (p = 0.0046) than subject

60 At a median time of 16.8 years after disease onset, 10.7% (95% confidence interval [CI] = 7.2

61 atients (404 women [68.9%]; mean [SD] age at disease onset, 33.6 [9.4] years), HLAGB was higher than

62 rioration) included at baseline: late age of disease onset (49.5 vs 45 years, P = .05), presence of v

63 Moreover, we show that post-disease-onset administration of the type 2 diabetes medi

64 At hospital discharge and one-year post-disease onset, adverse outcomes were identified in 17.7%

65 mmunological tolerance with aging suppresses disease onset after late young adulthood in mice.

66 rman's rho = 0.32, p < 10(-16)); and (3) the disease onset age and heritability are negatively correl

67 mechanisms similar to those responsible for disease onset also contribute to the rate of disease pro

68 ions of recombinant APRIL before and even at disease onset also had an effect.

69 mice, we showed that antibiotics given after disease onset ameliorated systemic autoimmunity and kidn

70 Systemic administration of TRAILPEG after disease onset ameliorated the severity of inflammatory a

71 mice with clenbuterol, which was started at disease onset, ameliorated motor function and extended s

72 nt is a rare hypomorphic allele with a later disease onset, amenable to therapeutic intervention.

73 The mean age was 6.4 years at disease onset and 9.3 years at time of initial presentat

74 Mice showed a significant delay in disease onset and a reduction in disease severity follow

75 th a progressive evolution of WM damage from disease onset and a transient, early increase in GM volu

76 d without IVIG, we evaluated these scores at disease onset and at the time of the latest examination.

77 essed clinical manifestation and symptoms at disease onset and calculated case fatality rates (CFRs).

78 n were seen in 4% and contributed to earlier disease onset and cardiac events.

79 ility and disease features, including age at disease onset and clinical symptoms.

80 f ambulation after a median of 7 years after disease onset and demonstrates little interindividual va

81 e, sex, disease duration, age at Parkinson's disease onset and disease duration.

82 enuated inversion recovery (FLAIR) images at disease onset and during follow-up.

83 implementation of preventive measures before disease onset and halt progression.Objectives: To invest

84 istory group, an association between delayed disease onset and HLA-DQ8 carriage was observed (p < 0.0

85 known about whether such alterations precede disease onset and how they relate to risk and prodromal

86 gene therapy approach significantly delayed disease onset and increased survival of ALS mice.

87 under CD11b promoter, significantly delayed disease onset and increased survival of SOD1(G93A) mice.

88 The latency between disease onset and initiation of immunotherapy was signif

89 te elimination of endogenous MIF accelerated disease onset and late disease progression and shortened

90 te elimination of endogenous MIF accelerated disease onset and late disease progression, as well as s

91 ver with a maximum period of 4 weeks between disease onset and microbiological characterization.

92 s information is increasingly used to detect disease onset and monitor disease progression during ear

93 k at different PRS levels, and the impact on disease onset and on prediction together with clinical r

94 h an unexpected role of the immune system in disease onset and pathogenesis; however, the role of cyt

95 Disease onset and perpetuation are mediated by periphera

96 The temporal molecular changes that lead to disease onset and progression in Alzheimer's disease (AD

97 kinase domain of TBK1 differentially affect disease onset and progression in an ALS mouse model.

98 ignaling is part of the mechanism underlying disease onset and progression in dyW-/- mice.

99 as a potential prognostic blood biomarker of disease onset and progression in Huntington's disease.

100 ding the causal processes that contribute to disease onset and progression is essential for developin

101 s a pioneer transcription factor involved in disease onset and progression through both androgen rece

102 th the goal of obtaining fresh insights into disease onset and progression under specific stimuli, pa

103 ta into mathematical models that can predict disease onset and progression, identify biomarkers, esta

104 is considerable inter-patient variability in disease onset and progression, which can confound the re

105 y a key role in accelerating or decelerating disease onset and progression.

106 and the dynamic changes of methylomes during disease onset and progression.

107 of measures to quantitatively monitor early disease onset and progression.

108 Its deregulation is strongly linked to disease onset and progression.

109 ffs in cancer-related proteins-may influence disease onset and progression.

110 Alzheimer's disease, inextricably linked to disease onset and progression.

111 entrations may provide useful information on disease onset and progression.

112 production of ROS is critically important in disease onset and progression.

113 V2/9-MIF demonstrated a significant delay in disease onset and prolonged survival compared with their

114 minogen, the key fibrinolytic enzyme, delays disease onset and protects from the development of the p

115 Plg(-)) mice developed significantly delayed disease onset and reduced disease severity compared with

116 hese animals display a significantly earlier disease onset and reduced overall survival, compared to

117 Disease onset and severity are codetermined by genotype.

118 d be used to reduce the critical gap between disease onset and start of treatment.

119 tively recruited within 3 months of clinical disease onset and studied with MRI scans of the brain an

120 Disease onset and survival were recorded, and weight and

121 Lack of outcome measures sensitive to disease onset and symptom severity hamper evaluation of

122 presymptomatic states, calibrated to data on disease onset and test frequency from the Diamond Prince

123 rea and beta-cell mass are maintained before disease onset and that production of proinsulin increase

124 reventive therapy), shorten the time between disease onset and treatment initiation (case finding and

125 es in HD CSF are significantly elevated upon disease onset and with the progression of neuropathologi

126 ignaling-deficient mice demonstrated earlier disease onset and worsened severity that was associated

127 uced mice reduced disease incidence, delayed disease onset, and diminished the clinical disability, i

128 accinations, had no defined port of entry at disease onset, and had symptoms lasting for 6 months.

129 o mouse models of autoimmune diabetes delays disease onset, and its administration in mice paralysed

130 rvention to slow the pace of cellular aging, disease onset, and neuropathology, particularly in older

131 had normal or mildly altered serum C3, late disease onset, and poor renal survival.

132 e of vitiligo risk, vitiligo triggering, and disease onset, and provide suggestions for future direct

133 e interanimal variability in neuropathology, disease onset, and tau prion formation in the PS19 mice

134 etween the markers of microbial exposure and disease onset, and we considered for controls the same t

135 is, with at least 6 years of follow-up since disease onset, and who started the high-efficacy therapy

136 D-19 patients at different time points after disease-onset, and seropositive sera to other human coro

137 ction (CDI), but the factors associated with disease onset are poorly understood.

138 in an immunocompromised adult presenting at disease onset as bilateral hearing loss.

139 erity, they did not exhibit the delay in EAE disease onset, as seen in mice with plasminogen deficien

140 g increased disability), at 6-10 years after disease onset, assessed with a linear mixed-effects mode

141 inal clinical information for 1354 patients (disease onset at >3 months and <20 years of age): 612 ha

142 CEBPA germline mutations, with variable AML disease onset at 59 and 27 years, respectively.

143 neutralizing IgG to SARS-CoV-2 10 days after disease onset, (b) SARS-CoV-2 persisted longer in those

144 ) or clinically isolated syndrome (CIS) with disease onset before 18 years of age and duration of les

145 ated motor and sensory disturbance scores at disease onset, before IVIG, 1 week and 1 month after the

146 qMotor can be used to assess early disease onset, before paralysis, as well as disease prog

147 ss CD1d and that iNKT cells critically delay disease onset but become functionally impaired upon dise

148 kinase activity in all cells also accelerate disease onset but extend the lifespan of SOD1 mice.

149 sorders are intimately linked with premature disease onset but the underlying mechanisms remain poorl

150 used not only to assist in the diagnosis of disease onset, but may also be useful as an outcome meas

151 Infection-like symptoms often herald disease onset, but no pathogen or immune defect has been

152 ld still worsen in a CAG-driven manner after disease onset, but these CAG-related progressive changes

153 ypothetical preventive strategies that delay disease onset by 1, 2 and 3 years, respectively.

154 to ameliorate disease severity and to delay disease onset by blocking effector T cell activation.

155 atic expansion proposed to drive the rate of disease onset by eliciting a pathological process that u

156 y high levels of miR-204 in RPE can mitigate disease onset by preventing generation of oxidative stre

157 outcomes included ascertainment of symptoms/disease onset by questionnaire from birth through age 13

158 el of human Adrenomyeloneuropathy, preceding disease-onset by one year.

159 nificantly stronger associations with age-at-disease-onset, clinical progression, amyloid deposition,

160 cohort is unique as it is the furthest from disease onset comprehensively studied to date (mean year

161 Clinical disease onset comprises synovitis and systemic comorbidi

162 ly, in severely affected patients with early disease onset due to point mutations in the PLP1 gene, a

163 beta42 in cortical areas was associated with disease onset, duration and cognitive scores.

164 ed to anticipate immunologic intervention at disease onset (early allergen immunotherapy) or even ear

165 ta-catenin pathway in CNS endothelium before disease onset exacerbates the clinical presentation of E

166 tions in gut microbiota, resulting in either disease onset/exacerbation due to a "poor" diet or prote

167 increasing doses of MSC-Exo starting at the disease onset for 7 consecutive days.

168 Estimated durations of time to RRT after disease onset for 99% of the nonglomerular and glomerula

169 Patients varied in the age of the disease onset (from 22 to 38 years) and severity of the

170 e investigated the route of infection and of disease onset, from airway exposure, colonization, and b

171 ease have revealed that the treatments after disease onset have little benefit on patient cognition.

172 r mucosa positivity was determinant of later disease onset; however, blood presence increased the ris

173 or EMG activity might be an early measure of disease onset; (ii) alterations in locomotor patterning

174 ere low (<40%) within the first 5 days after disease onset, immunoglobulin (Ig) M, IgA, and total ant

175 ution at the neuromuscular junction, delayed disease onset, improved motor function and preserved mot

176 dicted future diabetes up to 12 years before disease onset in 3 distinct human cohorts.

177 amilial AD (FAD)-associated phenotypes after disease onset in a mouse model of FAD.

178 fficacy of laminin-111 protein therapy after disease onset in a mouse model of LAMA2-CMD.

179 ime course more closely mimics the timing of disease onset in affected patients.

180 cations occurring in the first 2 years after disease onset in both groups.

181 h AD younger than 5 years within 6 months of disease onset in comparison with adults with AD or psori

182 tion studies typically ignore possible later disease onset in currently healthy subjects and assume t

183 FF and combined BAFF/APRIL inhibition delays disease onset in diverse murine lupus strains, although

184 Disease onset in females occurred across all age groups,

185 so been found to be a modifier of the age at disease onset in frontotemporal dementia patients with T

186 ymorphisms in TMEM106B are thought to modify disease onset in frontotemporal dementia, but its relati

187 that aberrant gene expression precedes overt disease onset in HD, identifies the Elk-1 transcription

188 ase progression in prion diseases or predict disease onset in healthy individuals at risk of disease.

189 PrP suppression extends survival and delays disease onset in intracerebrally prion-infected mice in

190 on at cervical and lumbar levels just before disease onset in mice expressing a familial amyotrophic

191 ase progression using 3 criteria showed that disease onset in PS19 mice is too variable to obtain rel

192 iated with genetic anticipation (ie, earlier disease onset in successive generations), although the d

193 ation between PCV13 vaccination and Kawasaki disease onset in the 4 weeks after vaccination nor of an

194 ng its accelerated buildup, the early age of disease onset in the population, and the high case fatal

195 nges in Huntington's disease are seen before disease onset in the premanifest stage around the striat

196 an absolute beta-cell loss may be causal for disease onset in these patients.

197 e (alpha-NETA) that significantly suppressed disease onset in vivo.

198 tayed in the region during the week prior to disease onset, in 2015.

199 ts showed laminin-111 treatment after muscle disease onset increased life expectancy, promoted muscle

200 E did not prevent hyperglycemia, accelerated disease onset, increased its incidence, and worsened ins

201 ine temporal changes in gene expression from disease onset involving phagosome formation as well as n

202 ily self-care activities; and younger age at disease onset is a major predictor for faster disease pr

203 efficacy therapy commenced within 2 years of disease onset is associated with less disability after 6

204 How these risk factors interact to drive disease onset is currently unknown.

205 ls in events initiating and/or precipitating disease onset is largely unknown.

206 nd the development of therapies that prevent disease onset is limited by the lack of adjuvant-free ex

207 Consistent with this mechanistic diversity, disease onset is unpredictable and phenotypic variabilit

208 prediction of severe cGVHD, in particular at disease onset, is therefore of high importance for ensui

209 with multiple sclerosis, in whom biological disease onset likely started many years prior to the imm

210 ed in another sample of 399 German CP cases (disease onset <60 y of age) and 1,633 controls ( P = 0.0

211 Thus, alteration of the IL-13 pathway at disease onset may lead to the progression of the autoimm

212 year of follow-up until the tenth year after disease onset (mean EDSS score 2.3 [SD 1.8] vs 3.5 [SD 2

213 e first study to compare metal levels before disease onset, minimizing reverse causation.

214 n the signs of neurological illness, time to disease onset, morphology of cerebral alpha-synuclein de

215 Putamen dopamine terminal loss at disease onset most likely exceeds that of the nigral cel

216 remission of proteinuria within 12 months of disease onset occurred in 24.5% and 16.5% of children, r

217 phase but increase significantly after acute disease onset on cardiomyocyte death and fibrotic myocar

218 regardless of whether coffee consumption at disease onset or 5 or 10 years prior to disease onset wa

219 nship between structural measures and age at disease onset or degree of seizure control.

220 n into two subgroups according to the age at disease onset or disease state, we again obtained no sig

221 Time until disease onset or last examination, time from disease ons

222 sed biomarkers that target various stages in disease onset or progression are also discussed.

223 anisms in linking environmental factors with disease onset, our goal was to conduct a systematic revi

224 ic CAG.CTG expansion (P = 0.004) and delayed disease onset (P = 0.003) in both Huntington's disease a

225 Additional changes occurred at clinical disease onset (P450) for S and FR MU.

226 Treatment after disease onset potently blocks progression of disease and

227 t and type of data needed to train effective disease onset predictive models using longitudinal elect

228 226 and GtQ226 mice had distinct kinetics of disease onset, prion conformations, and distributions of

229 Past this tipping point, disease onset progresses rapidly.

230 expansions in affected tissues contribute to disease onset, progression and severity.

231 and then challenged with rhinovirus to model disease onset, progression, and chronicity.

232 that circadian rhythms may have an effect on disease onset, progression, and resolution.

233 We observed that dC+dT delayed disease onset, prolonged life span of Tk2-deficient mice

234 n B cell epitopes, antigen presentation, and disease onset provides insight into the pathogenic mecha

235 al anomalies in HD decades prior to clinical disease onset, providing a greater understanding of neur

236 ce of subcerebral projection neurons delayed disease onset, reduced weight loss and motor impairment,

237 In SOD1(G93A) mice, loss of HIPK2 delays disease onset, reduces cell death in spinal motor neuron

238 cellular and molecular mechanisms leading to disease onset remain largely unknown.

239 se, specific changes within MNs that trigger disease onset remain unclear.

240 reducing poly(GR) level in adult mice after disease onset rescued poly(GR)-induced neurotoxicity.

241 nterval 72-160) and 294 days (212-399) after disease onset, respectively.

242 al data suggest a correlation between age at disease onset, response to sodium channel blockers and t

243 Notably, initiation of ASO treatment after disease onset restored myelination, MNCV, and CMAP almos

244 Treatment after disease onset resulted in the reversal of clinical and h

245 aspinal delivery of recombinant APRIL before disease onset, shortly reduced EAE symptoms.

246 ddress the question whether a younger age at disease onset should prompt per se a more "aggressive" t

247 Delaying treatment until after disease onset showed modest benefit, though this effect

248 rapy for certain AD-related phenotypes after disease onset.SIGNIFICANCE STATEMENT The study presented

249 experimental autoimmune encephalomyelitis at disease onset significantly reversed disease severity, r

250 Furthermore, disease onset sites were associated with disease progres

251 lume may be linked to processes that precede disease onset, such as inflammation, while decreased ICV

252 Changes occur before disease onset, suggesting that ATG16L1 T300A contributes

253 Disease onset, symptoms and mortality span a broad spect

254 ease progression, and shorter survival after disease onset than ALS patients without C9ORF72 expansio

255 ariants in the enriched regions have earlier disease onset than patients who have HCM with variants e

256 Importantly, prior to disease onset, the gut microbiome of infants that later

257 In the sixth year after disease onset, the mean EDSS score was 2.2 (SD 1.6) in t

258 gnaling (IIS) offers a possibility to retard disease onset through induction of metabolic changes tha

259 1 in laforin (Epm2a)-deficient LD mice after disease onset to determine whether LD can be halted in m

260 Time from disease onset to four autonomic symptoms (constipation,

261 y, or number of steps, of factors related to disease onset trigger is important prior deciding to stu

262 e aim to find clues on the complexity of the disease onset trigger of the different NDs expressed in

263 disease onset or last examination, time from disease onset until death or last examination, or age at

264 Intramuscular gene therapy post-disease onset using an adeno-associated viral 6 (AAV6) v

265 oduce small amounts of insulin decades after disease onset, very few beta-cells persist within their

266 nterferon beta was started within 5 years of disease onset vs later (HR, 0.77; 95% CI, 0.61-0.98; P =

267 ing glaucoma development 4 to 7 years before disease onset was 0.77 (95% confidence interval [CI], 0.

268 evelopment approximately 1 to 3 years before disease onset was 0.88 (95% CI, 0.86-0.91).

269 transplanted patients, 5-year survival after disease onset was 100% (41 of 41).

270 Mean age of disease onset was 49.7+/-12.3 years (mean+/-SD) for all

271 The dysfunction at disease onset was accompanied by increased expression of

272 Earlier disease onset was associated with less severe disease.

273 n at disease onset or 5 or 10 years prior to disease onset was considered.

274 ion carrier in the asymptomatic phase and at disease onset was included as well.

275 ular function and remodeling and that age of disease onset was later in individuals from haplogroups

276 Median age at disease onset was lower in southern Europe (3.5 years, I

277 or 1) and an IQ of at least 85, when age at disease onset was older than 4 years, or when MRI severi

278 The total motor disturbance score at disease onset was significantly lower in EGPA patients w

279 and response to therapy are not available at disease onset, we based the initial diagnostic approach

280 how peripheral infection could contribute to disease onset, we inoculated wild-type C57BL/6 mice and

281 of AD can be present several decades before disease onset, we investigated whether effects of polyge

282 study visit occurred more than 12 years from disease onset were excluded.

283 ly isolated syndrome (CIS) within 4 years of disease onset were recruited from 15 paediatric MS centr

284 ith LEMS, occurring within three months from disease onset, were collated to produce a DELTA-P score

285 ry NS patients presented a tendency to early disease onset when compared with the other groups (P = 0

286 Loss of Ripk1 accelerated disease onset, whereas combined deletion of caspase-8 an

287 ng which muscles will exhibit early and late disease onset, whereas DUX4 may worsen the muscle phenot

288 with the respective subtype of UCD and early disease onset, whereas height of the initial peak plasma

289 eased inflammation and precipitated clinical disease onset, whereas overexpression of IL-10 in microg

290 collected from NOD/ShiLtJ female mice after disease onset, whereas these drastic changes did not occ

291 In vivo, JNK inhibition prevents disease onset, while MEK/ERK inhibition in mice lacking

292 Preventive strategies that delay disease onset with 1 to 3 years could theoretically redu

293 cted cognitive impairment within 10 years of disease onset with an area under the curve (AUC) of more

294 s most prominent during the first week since disease onset with an average increase of 13%, but then

295 dels can predict glaucoma development before disease onset with reasonable accuracy.

296 ed high-efficacy therapies within 2 years of disease onset with those who started 4-6 years after dis

297 ands (SMG) from NOD/ShiLtJ female mice after disease onset, with 5-LOX and 12/15-LOX being downregula

298 s differ greatly in how long they live after disease onset, with the nature and severity of the disea

299 ases SOD1 aggregation, and accelerates early disease onset without affecting lifespan.

300 athways promoting microglial action prior to disease onset would inform potential preventative interv