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 and PAC networks had distinct spectral patterns and

3 CFS had 12 diminished miRNAs after exercise.

4 CFS more than when normalised for apparent contrast, and

5 CFS of LAB strains showed statistically inhibitor effect

6 CFS skeletal muscle cells were shown to oxidise galactos

7 CFS stability may be compromised by incomplete DNA repli

8 CFS study highlight the role of high, rather than low sp

9 CFS) has explored these effects, showing similar biases

10 CFS, and shows that the visibility of facial expressions

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

12 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

13 who were stratified by 2000 Kansas GWI, 1994 CFS, and 1990 FM criteria.

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

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

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

17 /1:1) and 25% (2.5 ml CFS+7.5 ml medium/1:3) CFS and the control without CFS were prepared.

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

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

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

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

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

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

24 Adolescent CFS is associated with enhanced sympathetic nervous acti

25 95% confidence interval (CI), 1.24-8.14] and CFS 6/7 aOR 6.10 (95% CI, 2.26-16.45) compared with CFS

26 , n = 196), FM (3.9 +/- 1.4 kg, n = 56), and CFS (5.8 +/- 2.1 kg, n = 170) compared to controls (7.2

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

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

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

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

31 symptoms were equivalent for GWI, CFS/FM and CFS.

32 ssure thresholds of 4.0 kg to define GWI and CFS/FM (specificity 0.85, sensitivities 0.80 and 0.83, r

33 cific predictors of induced CNV hotspots and CFS loci.

34 Pain, fatigue, quality of life, and CFS symptoms were equivalent for GWI, CFS/FM and CFS.

35 lective noncardiac surgery using the mFI and CFS.

36 fferent between healthy control subjects and CFS patients.

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

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

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

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

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

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

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

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

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

46 ng translocations and copy number changes at CFSs in cancers.

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

48 ws some mechanistic differences from that at CFSs, being dependent on RAD51, SLX1, and POLD3.

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

50 ished protocol showed no differences between CFS/ME patients and healthy controls in any of the compo

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

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

53 Both CFS and PAC networks coupled theta and alpha oscillation

54 oups, with treatment effect mainly driven by CFS score.

55 /- 1.6 kg, mean +/- SD, n = 70), followed by CFS/FM (3.1 +/- 1.4 kg, n = 196), FM (3.9 +/- 1.4 kg, n

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

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

60 fatigue syndrome/Myalgic Encephalomyelitis (CFS/ME).

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

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

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

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

65 respectively), 4.5 kg for FM, and 6.0 kg for CFS.

66 urrently be offered as a diagnostic test for CFS/ME.

67 vs. 84 +/- 5; p < 0.001), less often frail (CFS > 4; 38% versus 49%; p < 0.001) but evidenced higher

68 ome measures were the prevalence of frailty (CFS 5-7) and its association to mortality at 90 days pos

69 tality was directly associated with frailty: CFS 5 adjusted odds ratio (aOR) 3.18 [95% confidence int

70 ent substrates by skeletal muscle cells from CFS patients (n = 9) and healthy controls (n = 11) using

71 as previously been shown in blood cells from CFS patients.

72 ipheral blood mononuclear cells (PBMCs) from CFS/ME patients (10) and healthy controls (13).

73 e, and CFS symptoms were equivalent for GWI, CFS/FM and CFS.

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

75 Therefore, women with GWI, CFS and FM have systemic hyperalgesia compared to sedent

76 on of a 3.4 kb AT-DRS derived from the human CFS FRA16C into a chromosomally stable region within the

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

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

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

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

81 lls derived from skeletal muscle biopsies in CFS patients and healthy controls to look at cellular bi

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

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

84 Improvements in CFS score, rescue medication use, key VKC symptoms (phot

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

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

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

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

89 Bilateral white matter atrophy is present in CFS.

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

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

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

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

94 hese results provide evidence for interareal CFS and PAC being 2 distinct mechanisms for coupling osc

95 Interestingly, CFS and crude ethyl acetate extracts of PUFSTP35 (Bacill

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

97 e mapping of core fragility regions in known CFSs and identification of novel fragile sites.

98 ssociations are not replicated by the larger CFS cohort within the UK Biobank.

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

100 Many CFSs are enriched with AT-dinucleotide rich sequences (A

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

102 ME/CFS has historically presented in outbreaks, often has a

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

104 sting evidence that genetic factors alter ME/CFS risk before concluding that most ME/CFS candidate ge

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

106 For both cohorts, ME/CFS patients had an excess of individuals without a mild

107 idence that it has a heritable component, ME/CFS has not yet benefited from the advances in technolog

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

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

110 At baseline, those who developed ME/CFS had more physical symptoms and immune irregularities

111 tifying three groups: those who developed ME/CFS, those who developed severe ME/CFS (meeting >1 set o

112 immune data collected prior to developing ME/CFS..

113 iomarkers or laboratory tests to diagnose ME/CFS.

114 ter, 55 of the 238 (23%) met criteria for ME/CFS and 157 (66%) were asymptomatic.

115 al of developing a reliable biomarker for ME/CFS and to demonstrate the utility of our platform for p

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

117 algorithms, we developed a classifier for ME/CFS patients capable of identifying new patients, requir

118 IM) annually, and 9-12% meet criteria for ME/CFS six months later.

119 nctive microRNA expression signatures for ME/CFS through a provocation challenge is essential for the

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

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

122 ating microRNA expression in severely ill ME/CFS patients before and after an innovative stress chall

123 cell types that are causally involved in ME/CFS disease.

124 istent with ongoing immune alterations in ME/CFS that may illuminate the mechanism behind this diseas

125 To investigate immune metabolism in ME/CFS, we isolated CD4+ and CD8+ T cells from 53 patients

126 nd mitochondrial DNA (mtDNA) variation in ME/CFS.

127 nvestigate the role of mtDNA variation in ME/CFS.

128 r ME/CFS risk before concluding that most ME/CFS candidate gene associations are not replicated by th

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

130 errations observed in numerous studies of ME/CFS blood cells offer the opportunity to develop a diagn

131 . illuminate bioenergetic derangements of ME/CFS T cell subsets.

132 anism important to the pathophysiology of ME/CFS.

133 lly provide us with a unique indicator of ME/CFS.

134 We sought to determine predictors of ME/CFS.

135 ysical or mental stress, is a hallmark of ME/CFS.

136 ie the complex neuroimmune dysfunction of ME/CFS.

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

138 eloped ME/CFS, those who developed severe ME/CFS (meeting >1 set of criteria) and those who were asym

139 pear significantly associated with severe ME/CFS (p < 0.05).

140 testing patients with moderate to severe ME/CFS patients and healthy controls.

141 and behavioral symptoms while the severe- ME/CFS group had higher levels of IL-12 and lower levels of

142 Students with severe-ME/CFS were compared to students who were asymptomatic at t

143 cephalomyelitis/chronic fatigue syndrome (ME/CFS) involves severe fatigue, unrefreshing sleep, and co

144 cephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex chronic disease, rooted in multi-syste

145 cephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease with no known cause or mechani

146 cephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystem illness that lacks effecti

147 cephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multisystemic disease of unknown

148 cephalomyelitis/chronic fatigue syndrome (ME/CFS) is a highly debilitating disease with heterogeneous

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

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

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

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

153 We found that ME/CFS CD8+ T cells had reduced mitochondrial membrane pote

154 e is essential for the elucidation of the ME/CFS pathophysiology, and lead to accurate diagnoses, pre

155 The ME/CFS samples' response to the hyperosmotic stressor obser

156 r team has evaluated, for the first time, ME/CFS miRNomes in peripheral blood mononuclear cells (PBMC

157 Time 2 (when they developed IM), the two ME/CFS groups tended to have more autonomic complaints and

158 4+ and CD8+ T cells from 53 patients with ME/CFS and 45 healthy controls.

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

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

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

162 CD4+ and CD8+ T cells from patients with ME/CFS had reduced glycolysis at rest, whereas CD8+ T cells

163 Patients with ME/CFS had significant correlations between measures of T c

164 RNA expression signatures associated with ME/CFS in response to PEM induction and reports microRNA ex

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

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

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

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

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

170 ith clinical improvement in patients with ME/CFS.

171 of specific immune cells in patients with ME/CFS.

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

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

174 % (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

175 etry correlated with symptoms in GWI but not CFS or FM.

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

177 olomics to gain insights into the biology of CFS.

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

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

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

181 for GWI females, and aid in the diagnosis of CFS.

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

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

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

185 The strength of CFS networks was also predictive of cognitive performanc

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

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

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

189 ze MiDAS and to what extent the fragility of CFSs and RFSs arises by shared or distinct mechanisms.

190 ll allow for a more comprehensive mapping of CFSs and pave the way for investigating mechanisms promo

191 ) is employed to complete the replication of CFSs in early mitosis.

192 icantly associated with the primary outcome (CFS adjusted odds ratio, OR, 2.51, 95% confidence interv

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

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

195 associated nuclease activities in protecting CFSs in mammalian cells.

196 nt was a mean composite score that reflected CFS, rescue medication use (dexamethasone 0.1% 4 times d

197 echanistic insight into how FANCD2 regulates CFS stability.

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

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

200 frailty assessed by Clinical Frailty Scale (CFS) were documented.

201 sing the progressive Clinical Frailty Score (CFS): 1 (very fit) to 7 (severely frail).

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

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

204 S and late-replicating common fragile sites (CFS) are equally fragile in response to aphidicolin.

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

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

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

208 Common fragile sites (CFSs) are genomic regions prone to breakage under replic

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

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

211 Common fragile sites (CFSs) are regions susceptible to replication stress and

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

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

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

215 ructures that resemble common fragile sites (CFSs)-but how they are formed is not known.

216 are many features with common fragile sites (CFSs; which are found in all individuals), they are indu

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

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

219 acy, including corneal fluorescein staining (CFS) score.

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

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

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

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

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

225 FE and intracellular cell-free supernatants (CFS) exhibited potential inhibitory activities towards a

226 study were to assess cell-free supernatants (CFS) of 16 strains of these bacteria cultures on S. scle

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

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

229 Here, we used continuous flash suppression (CFS) to assess whether the modulatory effect of gaze dir

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

231 ) or by n:m-cross-frequency phase synchrony (CFS).

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

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

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

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

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

237 ME), also known as Chronic Fatigue Syndrome (CFS) is a debilitating condition.

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

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

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

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

242 Chronic fatigue syndrome (CFS) patients often suffer from severe muscle pain and a

243 Chronic fatigue syndrome (CFS) remains poorly understood.

244 War Illness (GWI), Chronic Fatigue Syndrome (CFS), and fibromyalgia (FM).

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

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

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

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

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

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

251 rent cell types supports the hypothesis that CFS is a systemic disease.

252 We propose that CFS integrates processing among synchronized neuronal ne

253 Results show that CFS skeletal muscle cells are unable to utilise glucose

254 It has previously been shown that CFS skeletal muscle cells have lower levels of ATP and h

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

256 The CFS identified 297 (42.3%) with frailty, the mFI 257 (36

257 The CFS of X. szentirmaii inhibited > 98% of fungus growth f

258 The CFS was easier to use, required less time and had less m

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

260 sessments before surgery should consider the CFS over the mFI as accuracy was similar, but ease of us

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

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

263 Among the 16 strains, the CFS of X. szentirmaii showed the highest fungicidal effe

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

265 the X. szentirmaii cultures as well as their CFS on the protection of soybean seeds against the white

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

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

268 We report that analogous to CFSs, fragile telomeres in BLM-deficient cells involved

269 Several features were suggested to underlie CFS instability, however, these features are prevalent a

270 erefore, the molecular mechanisms underlying CFS instability remain unclear.

271 izing the computational processes underlying CFS.

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

273 Previous research using CFS has demonstrated that fearful facial expressions are

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

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

276 ell suited for integration with small-volume CFS.

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

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

279 aOR 6.10 (95% CI, 2.26-16.45) compared with CFS 1.

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

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

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

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

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

285 Patients with CFS showed abnormalities in 20 metabolic pathways.

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

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

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

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

290 on fatigue severity in female patients with CFS.

291 solateral prefrontal cortex of patients with CFS.

292 solateral prefrontal cortex of patients with CFS.

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

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

295 50 women aged 18 to 59 years with CFS and severe fatigue leading to functional impairment.

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

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

298 ciently replicate non-B DNA sequences within CFSs.

299 5 ml medium/1:3) CFS and the control without CFS were prepared.

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

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