ライフサイエンスコーパス: CFS

1 CFS also connected the hubs of within-frequency-synchron

2 CFS had 12 diminished miRNAs after exercise.

3 CFS of LAB strains showed statistically inhibitor effect

4 CFS sequences are sensitive to perturbation of replicati

5 CFS was diagnosed in 41.5% (22/53) and ICF in 13.2% (7/5

6 CFS, as diagnosed by Centers for Disease Control and Pre

7 1, P < 0.001), SANDE (R = -0.56, P < 0.001), CFS (R = -0.36, P = 0.001), and BCVA (R = -0.30, P = 0.0

8 We collected blood samples from 100 CFS patients and 200 self-reported healthy volunteers fr

9 equivalent between nonexercise GWI (n = 22), CFS (n = 43) and control (n = 22) groups.

10 of Lactococcus lactis subsp. lactis and 25% CFS of Leuconostoc lactis. subsp. cremoris.

11 senteroides subsp. cremoris (20%) whilst 25% CFS of Leu. mes. subsp. cremoris and Lc. lactis subsp. l

12 /1:1) and 25% (2.5 ml CFS+7.5 ml medium/1:3) CFS and the control without CFS were prepared.

13 Blood and saliva were collected from 39 CFS cases and 9 healthy control subjects.

14 We examined cerebrospinal fluid from 43 CFS patients using polymerase chain reaction techniques,

15 of CFS of Streptococcus thermophilus and 50% CFS of Pediococcus acidophilus inhibited tyramine produc

16 y Escherichia coli was also inhibited by 50% CFS of Lactococcus lactis subsp. lactis and 25% CFS of L

17 The inhibitor effect of 50% CFS of P. acidophilus was the highest on tyramine produc

18 The stimulation effects of 50% CFS of S. thermophilus and Lc. lactis subsp. lactis were

19 ke microdeletions that reduce fragility at a CFS in cultured cells and suggests that similar conditio

20 erize dietary diversity from home foods in a CFS efficacy trial and determine whether supplementation

21 Adolescent CFS is associated with enhanced sympathetic nervous acti

22 Although CFS instability leads to chromosome gaps and breaks and

23 sagreement, and reactivity was similar among CFS subjects and negative controls.

24 icate significant disability among ADCLS and CFS patients and many important differences between thes

25 trol study comparing patients with ADCLS and CFS to each other and to both healthy controls and contr

26 ) are hot spots of chromosomal breakage, and CFS breakage models involve perturbations of DNA replica

27 eristics were similar for VAS(O), AMS-C, and CFS vs a score of 5 or greater on the LLQS (positive LRs

28 cific predictors of induced CNV hotspots and CFS loci.

29 on, pathogenic immune cell infiltration, and CFS scores.

30 aded relationship between exposure level and CFS risk.

31 fferent between healthy control subjects and CFS patients.

32 fferent between healthy control subjects and CFS patients.

33 significant improvement in both symptoms and CFS score (all P < 0.05).

34 g view that the association between XMRV and CFS likely reflects contamination of laboratories and re

35 tion mechanism, it is not known how CNVs and CFSs are related or why some genomic loci are much more

36 plication stress, resulting in both CNVs and CFSs as different manifestations of perturbed replicatio

37 re we compare large sets of de novo CNVs and CFSs in several experimental cell systems to each other

38 gile sites (CFS), the stability of ERFSs and CFSs is similarly dependent on the replication-stress re

39 We first show that CNV hotpots and CFSs occurred at the same human loci within a given cult

40 th an unprecedented opportunity to associate CFSs with features of their local genomic contexts.

41 ichment of microsatellite and QP elements at CFS regions contributes to fragility by perturbing repli

42 associated with DNA:RNA hybrid formation at CFS-FRA16D, and inhibition of DNA:RNA hybrid formation s

43 is required for repair of DSBs occurring at CFS-derived AT-rich sequences.

44 We demonstrated that Pol eta accumulated at CFSs upon partial replication stress and could efficient

45 Moreover, lack of histone acetylation at CFSs may contribute to the defective response to replica

46 ine treatment reduced chromosome breakage at CFSs.

47 nts stabilizing stalled replication forks at CFSs and hence facilitates CFS cleavage by MUS81-EME1.

48 alocus deletion and inactivation of genes at CFSs and perhaps elsewhere in the genome.

49 , the molecular basis for the instability at CFSs is poorly understood.

50 matin conformation in genomic instability at CFSs.

51 ndings do not support an association between CFS and MLV-related viruses, including XMRV, and the off

52 did not show significant differences between CFS and controls or ADCLS and controls.

53 number, and HHV-7 viral copy number between CFS patients and healthy controls.

54 Complete bilateral CFS clearance was noted in 8 of 28 patients (29%) treate

55 uorescein staining (CFS), complete bilateral CFS clearance, dry eye-related symptoms as measured by t

56 lowest contrast target rendered invisible by CFS, but also for higher contrast targets, which were vi

57 tigue or whether they relate to other common CFS symptoms (e.g., chronic pain, lower psychomotor spee

58 eglect were most effective in discriminating CFS cases from controls.

59 tical activity in higher visual areas during CFS, but the role of primary visual cortex (V1) is still

60 NCD2 protein is required to ensure efficient CFS replication and provide mechanistic insight into how

61 fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a multisystem disease, the pathogenesis of wh

62 re, chromatin at the most commonly expressed CFS, the FRA3B, is more resistant to micrococcal nucleas

63 0 kb region of the most frequently expressed CFS, FRA3B.

64 lication forks at CFSs and hence facilitates CFS cleavage by MUS81-EME1.

65 stress in spinalized preparations following CFS and AFS.

66 ly sessions of footshock (chronic footshock, CFS), six accommodation sessions followed by one exposur

67 fect your activity (ordinal scale 0-3)?" For CFS, moderate to severe reduction in daily activities ha

68 rior arcuate FA may serve as a biomarker for CFS.

69 lescents (mainly women) met the criteria for CFS 6 months following infectious mononucleosis; the fig

70 nts meeting accepted diagnostic criteria for CFS and found MLV-like virus gag gene sequences in 32 of

71 Disease Control and Prevention criteria for CFS.

72 r some patients meeting case definitions for CFS, whereas evidence for other treatments and harms is

73 a trend toward statistical significance for CFS (P = .05), LRF (P = .087), and CF (P = .074).

74 CDDP, and it has borderline significance for CFS, CF, and LRF.

75 Cs, B cells, T cells, or plasma derived from CFS patients.

76 ipheral blood mononuclear cells (PBMCs) from CFS patients, we identified DNA from a human gammaretrov

77 The gag and env sequences from CFS patients were more closely related to those of polyt

78 RV) susceptible to inactivation by sera from CFS patients and healthy controls, which suggested that

79 Lumbar punctures were performed in GWI, CFS and control subjects after (i) overnight rest (nonex

80 However, CFSs are undercharacterized at the molecular level and t

81 n modification patterns within the six human CFSs with the highest levels of breakage, and their surr

82 ive binding of RAD51 to CFS loci and impairs CFS expression.

83 Erlotinib did not, however, improve CFS in high-risk patients with LOH-positive or high-EGFR

84 duced skin rash was associated with improved CFS (P = .01).

85 othesis of reactivation of HHV-6 or HHV-7 in CFS.

86 hood trauma to neuroendocrine dysfunction in CFS remains obscure.

87 onally mediated immune cell dysregulation in CFS and ADCLS, at least outside of periods of acute symp

88 Significant improvements in CFS and patient symptomatology after DED treatment were

89 athetic outflow and systemic inflammation in CFS but has a concomitant negative effect on physical ac

90 ct mechanisms for post-exertional malaise in CFS and START and STOPP phenotypes of GWI.

91 we described similar clinical phenotypes in CFS patients and alternatively diagnosed chronic Lyme sy

92 ntial involvement of Y-family polymerases in CFS maintenance to include polymerase kappa.

93 Bilateral white matter atrophy is present in CFS.

94 lateral white matter volumes were reduced in CFS (mean +/- standard deviation, 467 581 mm(3) +/- 47 6

95 nism for the neuromuscular pathology seen in CFS.

96 ring S phase at replication forks stalled in CFS regions to suppress CFS instability by preventing ch

97 w-dose clonidine is not clinically useful in CFS.

98 esolve this controversy on the role of V1 in CFS and also begin characterizing the computational proc

99 in the original study that reported XMRV in CFS patients.

100 udy shows that Giardia duodenalis may induce CFS persisting as long as five years after the infection

101 cytogenetically defined aphidicolin-induced CFSs (aCFSs) to that of nonfragile sites, using multiple

102 L. johnsonii CFS significantly reduced IDO activity in HT-29 intestin

103 ith LOH-positive status (P < .001) and lower CFS (P = .01).

104 nscribed genes, the CNV hotpots that matched CFSs specifically corresponded to the largest active tra

105 ty and fatigue duration, cytokines of 192 ME/CFS patients and 392 healthy controls were measured usin

106 a more symptomatic subset of the broader ME/CFS population.

107 clinical criteria are available to define ME/CFS, yet none of the current diagnostic methods have bee

108 case definitions have been used to define ME/CFS; a ninth, recently proposed by the Institute of Medi

109 and 23 women) met diagnostic criteria for ME/CFS by Institute of Medicine, Canadian, and Fukuda crite

110 tion of dangerous diagnostic criteria for ME/CFS, as well as preventing patients from making informed

111 ne and recommending proven treatments for ME/CFS, because of potential implications for future commis

112 stionnaires to measure illness domains of ME/CFS and to evaluate patient heterogeneity overall and be

113 ine's preprocessed data were regressed on ME/CFS severity plus covariates for age, sex, race, and an

114 halomyelitis or chronic fatigue syndrome (ME/CFS), the data are limited and contradictory.

115 cephalomyelitis/chronic fatigue syndrome (ME/CFS).

116 serum cytokines could be associated with ME/CFS and correlated with disease severity and fatigue dur

117 rted symptoms differentiate patients with ME/CFS from healthy controls under study conditions but hav

118 asures that best distinguish persons with ME/CFS from those in the comparison groups and detect subgr

119 upward linear trend that correlated with ME/CFS severity: CCL11 (Eotaxin-1), CXCL1 (GROalpha), CXCL1

120 r illnesses that share some features with ME/CFS were enrolled in comparison groups.

121 equately tested to identify patients with ME/CFS when diagnostic uncertainty exists.

122 oups and detect subgroups of persons with ME/CFS who may have different underlying causes.

123 tial description of the 471 patients with ME/CFS who were enrolled in stage 1.

124 xpert clinicians to care for persons with ME/CFS; 4) collect biospecimens for future hypothesis testi

125 hicle achieved a 19% reduction in their mean CFS score (P = .11).

126 2.5%, achieved a 46% reduction in their mean CFS score (P = .12 compared with vehicle and P < .001 co

127 , 5%, achieved a 17% reduction in their mean CFS score (P = .88 compared with vehicle and P = .33 com

128 ifferent concentrations which were 50% (5 ml CFS+5 ml medium/1:1) and 25% (2.5 ml CFS+7.5 ml medium/1

129 % (5 ml CFS+5 ml medium/1:1) and 25% (2.5 ml CFS+7.5 ml medium/1:3) CFS and the control without CFS w

130 length polymorphism was confirmed for 68% of CFS diSSRs even though these repeats were nestled among

131 e chromosome segregation and accumulation of CFS-associated DNA damage in G1 cells.

132 olomics to gain insights into the biology of CFS.

133 LV)-related virus gene sequences in blood of CFS patients.

134 Despite extensive research into a cause of CFS, no definitive etiology has been determined; however

135 Both concentration of CFS of Streptococcus thermophilus and 50% CFS of Pedioco

136 s stall within the AT-rich fragility core of CFS, leading to dormant origin activation.

137 play a causative role in the development of CFS, and whether they represent a threat to the blood su

138 for FANCD2 as a trans-acting facilitator of CFS replication, in the absence of exogenous replicative

139 ldhood trauma as an important risk factor of CFS.

140 endocrine dysfunction, a hallmark feature of CFS, appears to be associated with childhood trauma.

141 Although the mechanism of CFS expression has not been fully elucidated, one known

142 Despite symptom overlap of CFS, GWI and other illnesses in their differential diagn

143 a contributing factor in the pathogenesis of CFS.

144 hat are implicated in the pathophysiology of CFS, including the hypothalamic-pituitary-adrenal axis.

145 n determined; however, a large percentage of CFS patients note an acute infectious event that trigger

146 and to devise targets for the prevention of CFS.

147 The prognosis of CFS is better in adolescents than in adults.

148 The risk of CFS conveyed by childhood trauma further increased with

149 s associated with a 6-fold increased risk of CFS.

150 TLR4 inhibition decreased the severity of CFS and significantly reduced the mRNA expression of IL-

151 patients have a similar phenotype to that of CFS patients.

152 use of antiretrovirals for the treatment of CFS does not seem justified at present.

153 onse to replication stress characteristic of CFSs, leading to the genetic instability characteristic

154 to the genetic instability characteristic of CFSs.

155 Although the characteristics of CFSs that render them vulnerable to stress are associate

156 These data are relevant to the expression of CFSs and provide insights into TIN2, which is compromise

157 on is a characteristic epigenetic pattern of CFSs, and chromatin within CFSs might be relatively more

158 To investigate the unusual sensitivity of CFSs to APH-induced replication stress, we examined repl

159 tern may underlie the unusual sensitivity of CFSs to replication interference.

160 The great majority of FHIT and other CFS-associated gene rearrangements in tumors are submicr

161 d viral copy number were compared to patient CFS symptom severity.

162 erebrospinal fluid, because in some patients CFS is thought to be a brain disorder.

163 lication, the cellular pathways that protect CFSs during replication remain unclear.

164 associated nuclease activities in protecting CFSs in mammalian cells.

165 Recently, CFS has been associated with xenotropic murine leukemia

166 ntly more effective than vehicle at reducing CFS scores (P </= 0.05).

167 echanistic insight into how FANCD2 regulates CFS stability.

168 istence of checkpoint-blind under-replicated CFS regions in mitosis, detectable as FANCD2-associated

169 oped assays in mammalian cells that revealed CFS-derived AT-rich sequences and inverted Alu repeats (

170 tes AMS), and the clinical functional score (CFS; >/=2 indicates AMS) compared with the Lake Louise Q

171 with conserved upstream flanking sequences (CFS).

172 ering, in which contactless flash sintering (CFS) is achieved using plasma electrodes.

173 Common fragile sites (CFS) are chromosomal regions that exhibit instability du

174 from late-replicating common fragile sites (CFS), the stability of ERFSs and CFSs is similarly depen

175 enomic regions, namely common fragile sites (CFS).

176 ry structures, such as common fragile sites (CFSs) and palindromic repeats.

177 Chromosomal common fragile sites (CFSs) are genetically unstable regions of the genome tha

178 Common fragile sites (CFSs) are genomic regions that are unstable under condit

179 Common fragile sites (CFSs) are hot spots of chromosomal breakage, and CFS bre

180 Common fragile sites (CFSs) are loci that preferentially exhibit metaphase chr

181 Chromosomal common fragile sites (CFSs) are unstable genomic regions that break under repl

182 ation intermediates at common fragile sites (CFSs) during early mitosis to trigger DNA-repair synthes

183 Common fragile sites (CFSs) represent large, highly unstable regions of the hu

184 s and duplications and common fragile sites (CFSs) seen as breaks on metaphase chromosomes are distin

185 eres that resemble the common fragile sites (CFSs), and the association of sister telomeres.

186 d for the stability of common fragile sites (CFSs), whose rearrangements are considered a driving for

187 The function of cell-free solutions (CFSs) of lactic acid bacteria (LAB) on tyramine and othe

188 nding that Pol delta dissociates at specific CFS sequences is significant, since dissociation of the

189 assessed using corneal fluorescein staining (CFS) and the cotton thread test (CTT).

190 Corneal fluorescein staining (CFS) was performed to evaluate clinical disease progress

191 Corneal fluorescein staining (CFS) was performed to evaluate clinical disease severity

192 outcomes were corneal fluorescein staining (CFS), complete bilateral CFS clearance, dry eye-related

193 acuity (BCVA), corneal fluorescein staining (CFS), tear break-up time, and Schirmer test.

194 nd points were corneal fluorescein staining (CFS), tear film break-up time (TBUT), Schirmer test resu

195 participants in the Cleveland Family Study (CFS), followed by gene-based association and additional

196 L. johnsonii culture cell-free supernatant (CFS) with affinity-purified IDO and HT-29 intestinal epi

197 Complementary food supplements (CFSs) can enhance growth where stunting is common, but s

198 ion forks stalled in CFS regions to suppress CFS instability by preventing checkpoint-blind under-rep

199 Using continuous flash suppression (CFS) in the MRI scanner, we manipulated visual awareness

200 stion, we used continuous flash suppression (CFS) to present the MIB stimulus outside visual awarenes

201 cedure, called continuous flash suppression (CFS), has been proposed as an ideal way of studying awar

202 res invisible: continuous flash suppression (CFS), which obliterates input into ventral temporal regi

203 o an improvement in colostomy-free survival (CFS).

204 survival (DFS, OS, colostomy-free survival [CFS]), CF, and relapse (locoregional failure [LRF], dist

205 achieved by cross-frequency phase synchrony (CFS).

206 s of patients with Chronic Fatigue Syndrome (CFS) after the infection.

207 e used to diagnose chronic fatigue syndrome (CFS) and idiopathic chronic fatigue (ICF).

208 % of patients with chronic fatigue syndrome (CFS) compared with 3.7% of healthy controls.

209 many patients with chronic fatigue syndrome (CFS) harbor a retrovirus, xenotropic murine leukemia-rel

210 Illness (GWI) and Chronic Fatigue Syndrome (CFS) have similar profiles of pain, fatigue, cognitive d

211 of postinfectious chronic fatigue syndrome (CFS) in adolescents.

212 rostate cancer and chronic fatigue syndrome (CFS) in recent years.

213 Chronic fatigue syndrome (CFS) is a complex, heterogeneous disease characterized b

214 Chronic fatigue syndrome (CFS) is a debilitating disease of unknown etiology that

215 phalomyelitis (ME)/chronic fatigue syndrome (CFS) is a debilitating multisystem condition affecting m

216 Chronic fatigue syndrome (CFS) is a disabling condition with unknown disease mecha

217 Chronic fatigue syndrome (CFS) is a multisystem disorder characterized by prolonge

218 Chronic fatigue syndrome (CFS) is a serious systemic illness of unknown cause.

219 phalomyelitis (ME)/chronic fatigue syndrome (CFS) is based on clinical criteria, yet there has been n

220 Chronic fatigue syndrome (CFS) is characterized by severe fatigue persisting for >

221 d DNA samples from chronic fatigue syndrome (CFS) patients and healthy controls.

222 Chronic fatigue syndrome (CFS) remains poorly understood.

223 d by patients with chronic fatigue syndrome (CFS).

224 to play a role in chronic fatigue syndrome (CFS).

225 phalomyelitis (ME)/chronic fatigue syndrome (CFS).

226 age of humans with chronic fatigue syndrome (CFS).

227 ) of patients with chronic fatigue syndrome (CFS).

228 d of patients with chronic fatigue syndrome (CFS).

229 ersially linked to chronic fatigue syndrome (CFS).

230 nt risk factor for chronic fatigue syndrome (CFS).

231 phalomyelitis (ME)/chronic fatigue syndrome (CFS).

232 recasts from NOAA's Climate Forecast System (CFS).

233 o- and electroencephalography, we found that CFS was load-dependently enhanced between theta and alph

234 developed in this study, we hypothesize that CFS origins may be less efficient, and that APH treatmen

235 We infer that CFS is based on modulating the gain of neural responses,

236 We propose that CFS integrates processing among synchronized neuronal ne

237 ere has been no direct evidence showing that CFS instability or replication stress can generate large

238 The CFS asks a single question: "overall if you had any symp

239 ample, global GMV did not differ between the CFS and healthy control groups.

240 In the CFS population, FA was increased in the right arcuate fa

241 the samples they used shows that some of the CFS peripheral blood mononuclear cell (PBMC) DNA prepara

242 tive than methylprednisolone in reducing the CFS score at week 10 (55% vs. 23% reduction, respectivel

243 mean ratio, 0.69; P = .02) compared with the CFS placebo group.

244 Chromatin at most of the CFSs analyzed has significantly less histone acetylation

245 pinalized preparations following exposure to CFS but not AFS.

246 pite the heterogeneity of factors leading to CFS, the cellular metabolic response in patients was hom

247 t previous evidence linking XMRV and MLVs to CFS is likely attributable to laboratory contamination.

248 on site causes excessive binding of RAD51 to CFS loci and impairs CFS expression.

249 Attempts to treat CFS have been largely ineffective primarily because the

250 egorically congruent primes suppressed under CFS facilitate categorization of tools but have no effec

251 izing the computational processes underlying CFS.

252 ted food by bacteria, it is advisable to use CFS for food and food products.

253 Using CFS as our main end point, we did not find an advantage

254 Typically, small-volume CFS is followed by discontinuous purification; however,

255 lume continuous-flow synthesis (small-volume CFS) offers a number of benefits for use in small-scale

256 ell suited for integration with small-volume CFS.

257 nes (DEGs) were found to be significant when CFS or ADCLS cases were compared to controls.

258 Our data support a model whereby CFS expression during cellular stress is due to a combin

259 ly reported to be XMRV/MLV-positive (14 with CFS) and from 15 healthy donors previously determined to

260 nction were similar between adolescents with CFS following infectious mononucleosis and recovered con

261 A referred sample of 176 adolescents with CFS was assessed for eligibility; 120 were included (34

262 V-7 viral copy number did not correlate with CFS symptom severity.

263 lood collected from 25 adults diagnosed with CFS and 13 ADCLS patients, comparing these cases to 25 m

264 ory confirmed giardiasis were diagnosed with CFS.

265 Only individuals with CFS and with childhood trauma exposure, but not individu

266 Individuals with CFS reported significantly higher levels of childhood tr

267 od trauma exposure, but not individuals with CFS without exposure, exhibited decreased salivary corti

268 Males with CFS were 53 (+/-2.8) y old (mean +/- SEM; range, 21-67 y

269 and NAA/Cr differences between patients with CFS and 26 sex-, age-, and education-matched healthy con

270 valuated blood samples from 61 patients with CFS from a single clinical practice, 43 of whom had prev

271 testing could not distinguish patients with CFS from adolescents who have recovered from infectious

272 At baseline, patients with CFS had a lower number of steps per day (P < .001), digi

273 Neuroimaging studies of patients with CFS have revealed alterations in prefrontal brain morpho

274 Patients with CFS showed abnormalities in 20 metabolic pathways.

275 Fifteen patients with CFS were identified by means of retrospective review wit

276 Thereafter, patients with CFS were randomized 1:1 to treatment with low-dose cloni

277 alternative US laboratory), 25 patients with CFS, 25 matched healthy controls, and 11 SLE controls.

278 In patients with CFS, right anterior arcuate FA increased with disease se

279 es is found in other groups of patients with CFS, whether these viruses play a causative role in the

280 on fatigue severity in female patients with CFS.

281 solateral prefrontal cortex of patients with CFS.

282 solateral prefrontal cortex of patients with CFS.

283 on were further analyzed in 55 patients with CFS/ME and 75 healthy blood donors, using quantitative p

284 on in peripheral blood from 25 patients with CFS/ME diagnosed according to the Centers for Disease Co

285 erase chain reaction data from patients with CFS/ME revealed 7 subtypes with distinct differences in

286 ene expression in the blood of patients with CFS/ME.

287 TS: A case-control study of 113 persons with CFS and 124 well control subjects identified from a gene

288 reduction in fatigue severity in women with CFS and severe fatigue.

289 e ratio (NAA/Cr) in a group of 89 women with CFS.

290 50 women aged 18 to 59 years with CFS and severe fatigue leading to functional impairment.

291 on replication stress, RECQ5 associates with CFSs in early mitosis through its physical interaction w

292 iments, we show that Pol delta pauses within CFS sequences are sites of enzyme dissociation, and diss

293 enetic pattern of CFSs, and chromatin within CFSs might be relatively more compact than that of the N

294 ific repetitive DNA sequence elements within CFSs to the inhibition of DNA synthesis by replicative a

295 ciently replicate non-B DNA sequences within CFSs.

296 5 ml medium/1:3) CFS and the control without CFS were prepared.

297 The 3-year CFS rates in placebo- and erlotinib-treated patients wer

298 The 3-year CFS was significantly lower for LOH-positive compared wi

299 an follow-up period of 50 months, the 5-year CFS rates were 69.6%, 82.4%, 77.1%, and 72.7% in arms A,

300 ing the 2 x 2 factorial analysis, the 5-year CFS was 76.5% versus 75.0% (P = .37) in groups A and B v