ライフサイエンスコーパス: disease onset

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

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

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

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

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

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

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

8 isease progression if treatment occurs after disease onset.

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

10 rmacological inhibition of JAK1 also delayed disease onset.

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

12 evant transcript isoforms were low even near disease onset.

13 ain abnormalities that may be present before disease onset.

14 e of the advanced disease state in humans at disease onset.

15 athogenesis and develop predictive models of disease onset.

16 spitals, Geneva, Switzerland, on day 5 after disease onset.

17 were measured from samples collected before disease onset.

18 with computed tomography (CT) 2-6 days after disease onset.

19 rbidities, season, study site, and timing of disease onset.

20 ated in the skin of cpdm mice prior to overt disease onset.

21 ed haemoglobin, glycaemic level, and time of disease onset.

22 k of developing psychotic disorders prior to disease onset.

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

24 ional features like asymmetry of weakness at disease onset.

25 isease and the role of modulating factors on disease onset.

26 ncy and location of edema, as well as age at disease onset.

27 by autosomal dominant heritability and early disease onset.

28 istent or chronic, and of severe bleeding at disease onset.

29 ge, sex, and residential area at the time of disease onset.

30 to INK4 inhibitors, resulting in accelerated disease onset.

31 vent disease, as well as suppress EAMG after disease onset.

32 k alleles is strongly associated with age at disease onset.

33 ipsilateral to hNPC transplants made before disease onset.

34 spinal cord of SOD1 (G93A) ALS mice prior to disease onset.

35 between HLA-A*24 and islet autoantibodies at disease onset.

36 g the cell infiltrates at the early phase of disease onset.

37 de levels in patients with T1D 2 years after disease onset.

38 vival, regardless of the clinical pattern of disease onset.

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

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

41 highest prevalence of nephrotic syndrome at disease onset.

42 e to aquarium zoanthid corals shortly before disease onset.

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

44 activation with tranexamic acid also delayed disease onset.

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

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

47 have provided insight into the mechanisms of disease onset.

48 als at high risk for schizophrenia promoting disease onset.

49 significant inverse correlation with age at disease onset.

50 gated for their potential in preventing this disease onset.

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

52 synaptic functions independently from age of disease onset.

53 d might represent promising tools to predict disease onset.

54 nalyses of survival outcomes, such as age-at-disease-onset.

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

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

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

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

59 ll eight patients (five women; median age at disease onset 59 years [range 52-76]) had abnormal sleep

60 Age at disease onset abstracted from medical records among part

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

62 Our analysis found no evidence that age at disease onset, age at treatment start, drug dosage, or m

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

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

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

66 eveloped isolated psychiatric episodes, 5 at disease onset and 18 during relapse.

67 ntiactin antibodies (AAA) were determined at disease onset and 379 other times during the follow-up e

68 th at least 2 serum samples collected before disease onset and 613 controls matched to cases on age,

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

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

71 l variables, including disease stage, age of disease onset and accelerated brain ageing on the signat

72 ic symptoms in major depression, but earlier disease onset and accelerated brain ageing promoted misc

73 As clinical disease onset and activity of IgAN often coincide with m

74 ng PD with GBA mutations have earlier age at disease onset and are more likely to demonstrate cogniti

75 es to these autoantigens appear years before disease onset and are widely used as predictive markers.

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

77 mice with PHCCC NPs every three days delayed disease onset and decreased disease severity compared wi

78 HTT detected is associated with proximity to disease onset and diminished cognitive and motor functio

79 ease course-related variables such as age of disease onset and disease stage as well alterations of s

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

81 t cigarette smoking may increase Alzheimer's disease onset and exacerbate its features and thus, may

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

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

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

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

86 a genetically determined trait that predates disease onset and may act as a risk factor contributing

87 al-1(-/-) mice also exhibited an accelerated disease onset and more severe arthritis characterized by

88 Although disease onset and mortality are delayed, disease duratio

89 regulated DNA modification, could influence disease onset and progression because it functions as an

90 Deletion of endophilin-B1 accelerated disease onset and progression in 6-month-old APPswe/PSEN

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

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

93 he role of these proteinaceous aggregates in disease onset and progression is still uncertain.

94 microglia), but not in T cells, facilitated disease onset and progression through multiple pathways.

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

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

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

98 in pancreatic cancer and is associated with disease onset and progression.

99 lluminating inflammatory pathways related to disease onset and progression.

100 vents in the vascular tissue responsible for disease onset and progression.

101 ication of new markers for the monitoring of disease onset and progression.

102 d disease specimens can provide insight into disease onset and progression.

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

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

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

106 1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, sugges

107 transporter 2 (EAAT2) overexpression delays disease onset and prolongs survival, and ceftriaxone inc

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

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

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

111 Disease onset and severity are codetermined by genotype.

112 e evaluated and tested for autoantibodies at disease onset and successively (mean 3.2 [2-6] times) af

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

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

115 ers to disease is important in understanding disease onset and the development of therapeutic agents.

116 yeast correlates with the approximate age of disease onset and the severity of symptoms observed in h

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

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

119 ore advanced phases of the disease (i.e., at disease onset and years after diagnosis).

120 ressive multiple sclerosis within 6 years of disease onset, and 24 control subjects were analysed.

121 decreased mortality in the first 2 wk after disease onset, and also reduced the severity of symptoms

122 sis, provided significant protection against disease onset, and attenuated inflammatory reactions in

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

124 on also prevents loss of motor axons, delays disease onset, and extends survival of JNPL3 mice by 3 m

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

126 gnosis regardless of the clinical pattern of disease onset, and its reassessment at 6 months appears

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

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

129 reast cancer samples that, though present at disease onset, are not evident from a single primary tum

130 ard ratios for shorter survival using age at disease onset as a continuous variable and sex, clinical

131 ion axotomy in both mSOD1 subgroups prior to disease onset as a method to standardize the axonal disc

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

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

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

135 trapolating our equation to model the age of disease onset, (B) testing it on a second patient data s

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

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

138 18 months, stratified by trial site, area of disease onset (bulbar vs other areas), and previous use

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

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

141 GAS6 did not delay disease onset, but significantly reduced the clinical sc

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

143 imitations or reflect a different pattern of disease onset by phenotype.

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

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

146 Clinical disease onset comprises synovitis and systemic comorbidi

147 In addition, an earlier age of disease onset correlated with significantly greater numb

148 oportional hazards regression to use time-to-disease onset data.

149 e 1 diabetes (T1D) by immune intervention at disease onset depends on the restoration of insulin secr

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

151 All the patients had disease onset during early childhood.

152 mechanism, computing probabilities of mtDNA disease onset, efficacy of clinical sampling strategies,

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

154 OD1-shRNA resulted in a significant delay of disease onset, expansion of lifespan, enhanced survival

155 those with large deletions had the earliest disease onset, followed by those with missense, frameshi

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

157 evere bilateral phenotypes featured by early disease onset, frequently at birth.

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

159 features between genotypes, including age at disease onset, gender, family history, progressive exter

160 genotype was associated with an older age of disease onset [>40 years; 30.6% vs 13.2%; odds ratio (OR

161 In most patients, at disease onset, >90% of antibodies binding to the PTP dom

162 -)CD303(-) type 1 myeloid dendritic cells at disease onset had a significant predictive value.

163 Better insight into factors that influence disease onset has direct implications for preventive mea

164 However, BDNF treatment after disease onset has not been reported to improve neuronal

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

166 ted with aHUS, but the mechanisms triggering disease onset have remained unresolved.

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

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

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

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

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

172 potential in clonogenic assays, and delayed disease onset in a mouse xenograft model of leukemia.

173 s (P = .02) with a trend toward older age at disease onset in AQP4-Ab-positive patients (44.9 vs 32.3

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

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

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

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

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

179 d tumor-suppressive miRNAs are implicated in disease onset in murine models of Notch-driven T-cell le

180 Islet autoantibodies detected at disease onset in patients with type 1 diabetes are signs

181 ained functional and anatomical rescue after disease onset in patients.

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

183 ediated toxicity to motor neurons and delays disease onset in SOD1G93A mice.

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

185 , CA-CDI, and "indeterminate" (classified as disease onset in the community, 4-12 weeks from hospital

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

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

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

189 specific for T4p2553 are detected before the disease onset in thyroid-draining cervical lymph nodes o

190 ven by allergic sensitization, and may imply disease onset in utero, with clinical presentation later

191 e survival in a murine AML model and delayed disease onset in xenograft models.

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

193 th collagen-induced arthritis it facilitated disease onset, increased disease incidence and severity,

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

195 el of FTD, administration of salsalate after disease onset inhibited p300 activity, lowered levels of

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

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

198 is of the EFACTS cohort suggest that earlier disease onset is associated with larger numbers of GAA r

199 Most frequently the disease onset is congenital or during childhood.

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

201 l sclerosis (ALS) pathogenesis suggests that disease onset is initiated by a peripheral pathological

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

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

204 eurofibrillary tangle (NFT) pathology during disease onset is unknown.

205 The mechanism for delayed glomerular disease onset is unknown.

206 tic targeting of Cxcr4 in murine T-ALL after disease onset led to rapid, sustained disease remission,

207 stigation include those described by side of disease onset (left or right body side), predominant cog

208 Patients with disease onset <18 years were identified from a prospecti

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

210 hort was subdivided into three groups: early disease onset (</=14 years), intermediate onset (15-24 y

211 Early disease onset (<10 years) was very frequent in our cohor

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

213 unusual PD phenotype characterized by early disease onset, moderate response to levodopa, rapid prog

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

215 At disease onset, most of the patients with LAR had moderat

216 At disease onset, no strong association was found between p

217 continuum ranging from neonatal to childhood disease onset, normal to delayed early development and s

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

219 A total of 56 patients with a mean age at disease onset of 15.3 years (range, 3-28 years), a mean

220 range, 11-62 years), with a mean (SD) age at disease onset of 16 (8) years (age range, 3-50 years) an

221 cate the rs6918698GG genotype with an age of disease onset of greater than 40 years in Crohn's diseas

222 We analyzed 144 patients with a disease onset of less than age 17 years using a systemat

223 Treatment of SJL/J mice with AZD1480 delays disease onset of PLP-induced relapsing-remitting disease

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

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

226 patients were regular smokers at the time of disease onset or at diagnosis (ever-smokers).

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

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

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

230 , and it is unknown whether they occur after disease onset or represent potential markers of genetic

231 ested in mice showed no clear attenuation in disease onset or severity versus controls.

232 mogenesis in vivo revealed no differences in disease onset or survival rates, and Emu-Myc-driven lymp

233 bracketing the phrenic motor nucleus before disease onset, or exposed to acute intermittent hypoxia

234 nificantly associated with a 7-year delay in disease onset (P < 0.0001) regardless of SERPING1 mutati

235 T carriers exhibited a significantly delayed disease onset (P < 0.001) and did not need long-term tre

236 having PD with GBA mutations were younger at disease onset (P = .04) and were more likely to demonstr

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

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

239 y independent of relapses and can occur with disease onset (primary progressive) or can be preceded b

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

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

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

243 pulations suggests that it occurs only after disease onset, rather than representing a vulnerability

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

245 (WT-hSOD1) with ALS mutant hSOD1 accelerates disease onset relative to mice expressing only mutant pr

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

247 Although the genetic determinants underlying disease onset remain unclear, epigenetic modifications i

248 The latency period between exposure and disease onset remains uncertain.

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

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

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

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

253 during embryogenesis or in young mice after disease onset revealed that the rescue associated with d

254 ein by competing for protective factors, but disease onset seems to be most accelerated when WT-hSOD1

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

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

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

258 d between pathological and clinical grade at disease onset (tau=0.034, P=0.6).

259 bling and polyfocal neurological symptoms at disease onset than adults with MS.

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

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

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

263 In multivariate analysis, disease onset to diagnosis of >1 month (P < .0001), olde

264 Average delay from ocular disease onset to uveitis service referral was 755.3 days

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

266 ation between repeat size and survival after disease onset using Cox proportional hazards regression

267 Disease onset varied with gender, occurring in male chil

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

269 ples from the overall cohort, survival after disease onset was 4.8 years (IQR 3.0-7.4) in the group w

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

271 essor in Emicro-myc lymphomagenesis, because disease onset was accelerated by heterozygosity for Suz1

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

273 Earlier disease onset was associated with less severe disease.

274 When disease onset was before the first decade, 31% had SPG4

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

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

277 Age of disease onset was inversely correlated with the number o

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

279 on activation gene 1 knockout) mice although disease onset was modestly delayed.

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

281 Disease onset was symptomatic in 610 patients (79%), whi

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

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

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

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

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

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

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

289 of experimental autoimmune uveitis prevented disease onset, whereas monocyte depletion at the resolut

290 godendrocyte marker genes preceding clinical disease onset, whereas neuroinflammatory markers progres

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

292 cantly reduced skin inflammation and delayed disease onset, whereas systemic immunological disease pe

293 ation results in a more rapid progression of disease onset, whereas the incubation time in bats inocu

294 ved a loss in BSCB integrity within a day of disease onset, which paralleled the infiltration of GFP(

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

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

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

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

299 Death occurred 4 months after disease onset without any tumor detected.

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