ライフサイエンスコーパス: PMF

1 PMF analysis resolved the PM10 data with four source fac

2 PMF analysis successfully extracted 11 factors from mass

3 PMF attributed 55 to 80% of the measured dust flux to th

4 PMF induced the expression of SHP-1 and was linked to th

5 PMF is characterized by bone marrow megakaryocytic proli

6 PMF may be associated with somatic mutations in JAK2, MP

7 PMF yielded a three-factor solution: cooking OA (COA), h

8 PMF-conditioned medium increased the migration and tubul

9 , we compared survival from diagnosis of 100 PMF patients receiving ruxolitinib within COMFORT-2 with

10 imensional positive matrix factorization (3D-PMF), showing that PBOA represented the main OMCOARSE so

11 The diagnosis of 661 PMF patients with a bone marrow biopsy at presentation w

12 confidence interval [CI], 1.4-2.2), and 5.9 PMF (n = 267; HR, 4.5; 95% CI, 3.5-5.7).

13 mma occurs only when FoF1 operates against a PMF-induced torque; the effect disappears when PMF is el

14 H20 is required for a PMF-dependent conformational change, suggesting that the

15 GhoT reduces metabolism by reducing ATP and PMF and that this reduction in metabolism is important f

16 CMB and PMF analyses indicate that deca technical mixtures are t

17 tions in the triple-negative cases of ET and PMF by applying whole-exome sequencing (WES) on paired t

18 suggest that triple-negative cases of ET and PMF do not represent a homogenous disease entity.

19 a significant proportion of familial ET and PMF nonmutated for JAK2 carry a somatic mutation of CALR

20 stically highly significantly between ET and PMF.

21 port a differential diagnosis between ET and PMF.

22 eas CALR and MPL mutants are found in ET and PMF.

23 cting the pathogenesis of CALR-mutant ET and PMF.

24 aberrantly expressed in lower-risk MDSs and PMF.

25 died the function of this axis in normal and PMF CD34(+) cells.

26 These formulations based on SHSs and PMF met all the requirements to be considered as CBEs; t

27 th liquid feces significantly reduced TA and PMF compared to the reference.

28 cythemia vera, essential thrombocytosis, and PMF samples compared with healthy controls.

29 Combining WSE with bulk species as PMF inputs also produced five factors.

30 ine) in the mass spectra were used to assign PMF factors to biomass burning, traffic, and smoking emi

31 bution of the A3669G allele differed between PMF patients and 2 healthy control populations (odds rat

32 results show epigenetic differences between PMF and polycythemia vera/essential thrombocytosis and r

33 ogy of palm oil (PO) and mid-fraction blend (PMF) was investigated in this study.

34 sed FLC predicted shortened survival in both PMF and MDS, independent of age, creatinine, and other c

35 entration predicts inferior survival in both PMF and MDS.

36 and signaling processes that are mediated by PMF-coupled energetics at the cell membrane.

37 The inhibition of STAT3 by PMF was reversible.

38 Qualitative trends in the computed PMF can be understood based on the stress field distribu

39 The computed PMF indicates that the central hydrophobic region provid

40 ins in the region around the minimum of each PMF.

41 In multivariate analysis, early PMF and the JAK2V617F mutation emerged as independent fa

42 patients/year, P = .01) in WHO-ET and early PMF, respectively.

43 ns, particularly arterial, was seen in early PMF compared with ET.

44 t myelofibrosis was 3% in ET and 9% in early PMF, but no transformation into acute leukemia was obser

45 fined ET and 35 patients (16%) showing early PMF.

46 cross-validated RMSE than those from either PMF or CTM alone.

47 Excessive PMF is known to limit the turnover of HCOs, but the mole

48 A 7-factor PMF solution was identified using speciated OMM and bulk

49 lysis and (2) positive matrix factorization (PMF) analysis of aerosol mass spectrometer (AMS) data.

50 resolved from positive matrix factorization (PMF) analysis of organic mass spectral data obtained fro

51 analyzer, (2) positive matrix factorization (PMF) analysis to separate the gas- and particle-phase si

52 tigations and Positive Matrix Factorization (PMF) analysis, we deduce that Red Sea Deep Water (RSDW)

53 evaluated by positive matrix factorization (PMF) and principal component analysis (PCA).

54 Positive matrix factorization (PMF) applied to organic aerosol (OA) data yielded 5 fact

55 Positive Matrix Factorization (PMF) applied to the data set revealed a factor indicativ

56 t of PM(2.5), positive matrix factorization (PMF) coupled with a bootstrap technique for uncertainty

57 (SVOC) data, positive matrix factorization (PMF) coupled with a bootstrap technique was applied to t

58 Positive matrix factorization (PMF) has been applied to single particle ATOFMS spectra

59 MB) model and positive matrix factorization (PMF) in order to quantify PBDE sources and debromination

60 y resolved by positive matrix factorization (PMF) of aerosol mass spectrometer data collected in area

61 resolved from positive matrix factorization (PMF) of AMS organic aerosol spectra collected from low-N

62 rtioned using positive matrix factorization (PMF) of data collected from aerosol mass spectrometry de

63 ated into the positive matrix factorization (PMF) receptor model to form a receptor-oriented hybrid m

64 ach, based on positive matrix factorization (PMF) shows that the COA factor was clearly linked to loc

65 xamined using positive matrix factorization (PMF) to apportion PCB sources in the air, water, and per

66 t tool called Positive Matrix Factorization (PMF) to identify the sources of PCBs to the atmosphere i

67 Positive matrix factorization (PMF) was applied to identify and apportion indoor and ou

68 ortionment by Positive Matrix Factorization (PMF) was carried out to interpret the real-world driving

69 Positive matrix factorization (PMF) was used for apportioning sources of atmospheric pa

70 e this issue, Positive Matrix Factorization (PMF) was used to identify the dominant sources of gas-ph

71 Positive matrix factorization (PMF) was used to resolve PM0.1 source contributions from

72 t study using positive matrix factorization (PMF), performed on long-term PM2.5 chemical speciation d

73 e analyzed by positive matrix factorization (PMF), yielding three conventional factors: hydrocarbon-l

74 examined with positive matrix factorization (PMF).

75 analyzed with Positive Matrix Factorization (PMF).

76 analyzed via Positive Matrix Factorization (PMF).

77 resolved from positive matrix factorization (PMF).

78 ormed from a polarization maintaining fiber (PMF).

79 molecular mass and peptide mass fingerprint (PMF) by matrix-assisted laser desorption/ionization time

80 ately 33 years for ET, 24 for PV, and 15 for PMF.

81 ceptor A3669G is a susceptibility allele for PMF: it contributes to confer the phenotype of excess my

82 g the survival impact of newer therapies for PMF, which are currently being tested in these patient s

83 the combination of potential of mean force (PMF) and stress field calculations.

84 h umbrella sampling/potential of mean force (PMF) calculations as a function of the distance between

85 Potential of mean force (PMF) calculations confirm that the observed motion is th

86 Potential of mean force (PMF) calculations utilizing the multistate empirical val

87 n investigated with potential of mean force (PMF) calculations.

88 d to calculate the potentials of mean force (PMF) for a variety of restrained relative orientations o

89 The potentials of mean force (PMF) from adaptive biasing force (ABF) molecular dynamic

90 as confirmed by the potential of mean force (PMF) measurements.

91 ed to construct the potential of mean force (PMF) of the ligand and calculate the corresponding bindi

92 ns to calculate the potential of mean force (PMF) profiles for translocation of the four DNA nucleoti

93 ion permeation, the potential of mean force (PMF) was calculated for displacing a single Na(+) ion al

94 as indicated by the potential of mean force (PMF).

95 Furthermore, the proton-motive force (PMF) across the inner-membrane acts at distinct stages o

96 aratus utilizes ATP and proton motive force (PMF) as the energy source to transport component protein

97 sin (pR) to control the proton-motive force (PMF) in vivo by illumination.

98 transport, however, the proton motive force (PMF) is not required to keep P(i) in the periplasm.

99 ative bacteria uses the proton motive force (PMF) of the cytoplasmic membrane to energize active tran

100 lecular motor that uses proton-motive force (PMF) to drive the synthesis of ATP from ADP and Pi.

101 arvest and transmit the proton motive force (PMF) to outer membrane transporters.

102 Pvd) by coupling to the proton motive force (PMF) via the inner membrane (IM) protein TonB1.

103 mpounds that target the proton motive force (PMF), uncouplers, represent one possible class of compou

104 hemical gradient termed proton motive force (PMF), which provides the driving force for the adenosine

105 P and the disruption of proton motive force (PMF).

106 le maintaining a viable proton motive force (PMF).

107 r and the transmembrane proton motive force (PMF).

108 by a pump powered by a proton motive force (PMF).

109 the host cell under the proton motive force (PMF).

110 a normal mitochondrial proton motive force (PMF).

111 cA, in concert with the proton motive force (PMF).

112 The mitochondrial protonmotive force (PMF) is an electrochemical gradient that powers ATP synt

113 s on the plasma membrane protonmotive force (PMF), such as high external potassium to reduce the elec

114 ation (TA) and particulate matter formation (PMF) up to 49%, through lower ammonia emission, but incr

115 egetable fats by blending palm mid fraction (PMF) and tropical butters coming from shea, mango kernel

116 ated by blending SHSs and palm mid fraction (PMF) were studied and compared with those from cocoa but

117 mixing PDAGS with either palm mid fraction, PMF (PDAGS/PMF), palm olein, POL(PDAGS/POL) or sunflower

118 in fibronectin (FN) by BM stromal cells from PMF patients correlates with fibrosis and disease severi

119 3 levels are decreased in CD34(+) cells from PMF patients, and the NOL3 locus is deleted in a subset

120 A) expression profiles in CD34(+) cells from PMF patients.

121 similarities with primary CD34(+) cells from PMF patients.

122 Strikingly, further PMF calculations demonstrate that the mutation V174A dec

123 e in terms of the ability of CIV to generate PMF.

124 Reverse operation generates PMF via ATP hydrolysis.

125 Our results reveal a novel genetic PMF-like mouse model and identify a tumor suppressor rol

126 In PMF (n = 428), but not in ET (n = 576), survival and bla

127 In PMF, JAK2/CALR/MPL mutational status is prognostically i

128 In PMF, type 1 or type 1-like CALR mutations are associated

129 , 20%, and 3% in ET, and 60%, 25%, and 7% in PMF.

130 th increased creatinine, and advanced age in PMF (P < .001) and hemoglobin less than 10 g/dL in MDS (

131 on, SRSF2 mutations are relatively common in PMF, cluster with IDH mutations, and are independently p

132 uggest that megakaryocytes drive fibrosis in PMF and that targeting them with AURKA inhibitors has th

133 ontribute to the induction of BM fibrosis in PMF, and inhibiting fibrocyte differentiation with SAP m

134 ay a role in the induction of BM fibrosis in PMF.

135 plicing machinery are predominantly found in PMF and are implicated in the development of anemia or p

136 In contrast, aberrantly methylated genes in PMF were involved in inflammatory pathways and were enri

137 f JARID2 may contribute to MK hyperplasia in PMF.

138 Aberrant hypomethylation in PMF was seen to occur in non-CpG island loci, showing fu

139 promising strategy to reduce inflammation in PMF.

140 onal targets for therapeutic intervention in PMF.

141 ere, we have revealed that megakaryocytes in PMF show impaired maturation that is associated with red

142 we demonstrate that NF-E2 is mislocalized in PMF cells and that aberrant NF-E2 localization discrimin

143 d prognostic relevance of SRSF2 mutations in PMF.

144 rvival prolongation has actually occurred in PMF.

145 stic Scoring System-adjusted hazard ratio in PMF was 1.9 (95% CI, 1.3 to 2.7), and was 6.3 (95% CI, 2

146 that "triple negative" mutational status in PMF is an important adverse risk factor for blast transf

147 roborates a role of paracrine stimulation in PMF disease progression, underlines the importance of ta

148 URKA) represents a new therapeutic target in PMF.

149 Recent clinical trials in PMF patients with intermediate-2 or high IPSS risk have

150 e treatments, and have started to be used in PMF.

151 of P(i) into the periplasm across the OM is PMF-dependent and can be enhanced by light energy.

152 ributes to BM megakaryocytosis in JAK2V617F+ PMF.

153 1 integrin to megakaryocytosis in JAK2V617F+ PMF.

154 le Sprague-Dawley rats elicited long-lasting PMF (>120 min), an effect prevented by pretreatment with

155 k252a affected late PMF (>/= 90 min) only.

156 RSP is unable to counterbalance CPF-mediated PMF depletion by cellular metabolic adaptations, resulti

157 from diminished generation of mitochondrial PMF by CIV and limits the level of CIV activity required

158 inks spatiotemporal control of mitochondrial PMF to cellular metabolic changes that mediate behavior

159 megakaryocytes and stromal cells in 3 murine PMF models.

160 ombocythemia (ET) and primary myelofibrosis (PMF) are chronic diseases characterized by clonal hemato

161 ythemia vera (PV) and primary myelofibrosis (PMF) CD34(+) cells with low doses of RG7112 and Peg-IFNa

162 mbocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-negative myeloproliferative

163 syndromes (MDSs) and primary myelofibrosis (PMF) generally becomes resistant to available treatments

164 thermore, even though primary myelofibrosis (PMF) has a markedly worse prognosis than essential throm

165 Patients with primary myelofibrosis (PMF) have substantially reduced life expectancy, whereas

166 Primary myelofibrosis (PMF) is a clonal hematologic malignancy characterized by

167 Primary myelofibrosis (PMF) is a fatal neoplastic disease characterized by clon

168 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MPN) that leads t

169 Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by m

170 Primary myelofibrosis (PMF) is characterized by bone marrow fibrosis, myeloprol

171 Primary myelofibrosis (PMF) is characterized by fibrosis, ineffective hematopoi

172 ombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutations.

173 ion-age patients with primary myelofibrosis (PMF) that integrates clinical, cytogenetic, and mutation

174 mbocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants are found in ET and PM

175 ith early/prefibrotic primary myelofibrosis (PMF) with presenting thrombocythemia.

176 plastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neoplasm characterized by pro

177 patients affected by primary myelofibrosis (PMF), a well-known pathological situation caused by alte

178 patients with PV and primary myelofibrosis (PMF), and that "triple negative" mutational status in PM

179 polycythemia vera and primary myelofibrosis (PMF), are a heterogeneous group of myeloid-derived chron

180 ion for patients with primary myelofibrosis (PMF), but information on its net advantage over conventi

181 rombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohort of 892 consecutive pa

182 s in the treatment of primary myelofibrosis (PMF), there are recent indications that the survival of

183 ment in patients with primary myelofibrosis (PMF).

184 marrow (BM) milieu in primary myelofibrosis (PMF).

185 ombocythemia (ET) and primary myelofibrosis (PMF).

186 ival of patients with primary myelofibrosis (PMF).

187 mbocythemia (ET), and primary myelofibrosis (PMF).

188 ns in both MDS-RS and primary myelofibrosis (PMF).

189 in 499 patients with primary myelofibrosis (PMF).

190 to an MPN resembling primary myelofibrosis (PMF).

191 ombocythemia (ET) and primary myelofibrosis (PMF).

192 mbocythemia (ET), and primary myelofibrosis (PMF).

193 s defines 2 stages of primary myelofibrosis (PMF): prefibrotic/early (pre-PMF) and overt fibrotic (ov

194 thrombocythemia (ET); primary myelofibrosis (PMF); and MPN, unclassifiable (MPN,U).

195 and when excited in cells with intact native PMF generation systems increased motor speed beyond the

196 was shown to be sufficient to replace native PMF generation, and when excited in cells with intact na

197 K2, CALR, and MPL (so-called triple-negative PMF).

198 y that pervanadate suppressed the ability of PMF to inhibit the phosphorylation of STAT3, suggesting

199 the PDAGS were reduced with the addition of PMF, POL and SFO.

200 FN is increased in plasma and BM biopsies of PMF patients as compared with healthy controls, correlat

201 of patients belonging to these categories of PMF.

202 uxolitinib may modify the natural history of PMF.

203 n of GATA1 effectively rescued maturation of PMF megakaryocytes.

204 Isosolid phase diagrams of mixtures of PMF/SHS showed eutectic formation for SHS 65 and SHS 80,

205 ntitumor activity in vivo in mouse models of PMF.

206 ar mutations involved in the pathogenesis of PMF have been extensively investigated, the sequential e

207 lay a central role in the pathophysiology of PMF.

208 However, extended periods of PMF loss led to stepwise increases in rotation rate upon

209 Rates of PMF-attributable mortality at 5 and 10 years were signif

210 Survival of PMF is steadily improving, except in patients in poor-ri

211 U patients specified upon follow-up as ET or PMF with 92% accuracy.

212 49 additional triple-negative cases of ET or PMF.

213 d Peg-IFNalpha 2a for the treatment of PV or PMF patients with the intent of altering their natural h

214 sufficient to ameliorate fibrosis and other PMF features in vivo.

215 ic/early (pre-PMF) and overt fibrotic (overt PMF) phase.

216 urvival was significantly shortened in overt PMF (7.2 vs 17.6 years), with triple negativity for driv

217 IDH1/2, EZH2) were more represented in overt PMF.

218 Compared with pre-PMF, overt PMF was enriched in patients with anemia, thrombocytopen

219 More patients with overt PMF were in higher International Prognostic Scoring Syst

220 PDAGS/PMF and PDAGS/SFO crystallised in beta'+beta polymorphs

221 18:1 were the dominant fatty acids for PDAGS/PMF and PDAGS/POL, while C18:1 and C18:2 were dominant i

222 Binary mixtures of PDAGS/PMF had better structural compatibility and full miscibi

223 GS with either palm mid fraction, PMF (PDAGS/PMF), palm olein, POL(PDAGS/POL) or sunflower oil, SFO (

224 The results gave indication that PDAGS: PMF at 50%:50% and 60%:40% (w/w) were the most suitable

225 myelofibrosis (PMF): prefibrotic/early (pre-PMF) and overt fibrotic (overt PMF) phase.

226 Compared with pre-PMF, overt PMF was enriched in patients with anemia, thr

227 ity to disease progression compared with pre-PMF.

228 diagnosis between ET and early, prefibrotic PMF can be challenging but is critical because clinical

229 cially in distinguishing ET from prefibrotic PMF and masked PV.

230 d surface latches the substrate and promotes PMF-driven transport.

231 HOS at pH 10.5, where the bulk protonmotive (PMF) force is low.

232 s, we have measured the effects of a reduced PMF on root and hypocotyl growth, ATP-induced skewed roo

233 s, patients with intermediate-2 or high-risk PMF clearly benefit from allogenic SCT.

234 For example, the small PMF barrier, which is approximately 1 kcal/mol independe

235 er PMF2 software and the newer EPA-sponsored PMF 3.0 software were employed.

236 away from the flagellar motor, showing that PMF presence is necessary for continued motor integrity,

237 The PMF analysis revealed four resolved factors at each site

238 The PMF in PM eyes has characteristic morphologic SD-OCT fea

239 The PMF method predicted that the R14A mutation in HsTX1 wou

240 The PMF method resolved seven dust sources with distinct com

241 The PMF results are validated by PBDE manufacturing records,

242 The PMF results were confirmed by examining three samples th

243 etion by small interfering RNA abolished the PMF-induced constitutive and inducible STAT3 inhibition.

244 corneal power (R = 0.49; P = 0.002), and the PMF height correlated strongly and inversely with the ax

245 ting, as predicted, a close link between the PMF and potassium uptake at the plasma membrane.

246 ably affect the physical content of CIV, the PMF generated by CIV was also lower than normal.

247 Indeed, SDP rapidly collapses the PMF as measured by fluorometry and flow cytometry, which

248 Collapsing the PMF is an ideal mechanism for a toxin involved in cannib

249 rane proteins, in addition to collapsing the PMF.

250 Comparing the PMF values of different systems, we obtain a relative ra

251 By rapidly dissipating the PMF, we propose that this leak state may enable cytochro

252 However, the PMF well depth is reproduced poorly by a simple continuu

253 the 3 MPN drivers and play a key role in the PMF pathogenesis.

254 icant correlation with the axial length, the PMF severity and keratometry established in this study s

255 tail AHA2's specific role in maintaining the PMF during seedling growth.

256 Arrest was not due to collapse of the PMF and did not require the presence of ExbD or TonB.

257 CIV activity required for maintenance of the PMF and growth under aerobic conditions.

258 anions pair with chemiosmotic cations of the PMF and millions of accumulated P(i) pairs could influen

259 The depth of the potential well of the PMF was shown to depend approximately linearly on the bu

260 The OCT characteristics of the PMF were analyzed and the PPCIs were compared and correl

261 le in the pathogenesis and morphology of the PMF.

262 ical potential (DeltapH) compositions of the PMF.

263 fusions are not affected by substrate or the PMF, although TatB-YFP oligomerization does require TatC

264 Removing the PMF causes TatA complexes to dissociate, except in strai

265 ve been experimentally demonstrated with the PMF lengths of 75 cm and 20 cm respectively in the range

266 l power in both groups of eyes, and with the PMF severity in PM eyes.

267 Within the PMF subgroup, cases with ASXL1 disruptions formed an epi

268 s were generally consistent across the three PMF solutions.

269 ly "turn off" mitochondrial function through PMF dissipation in tissues with light.

270 Pathogenicity is thus likely attributable to PMF-mediated paracrine stimulation of mouse myeloid cell

271 AML was of mouse origin, confined to PMF-xenografted mice, and contained multiple clonal inte

272 l of influence of the CTM versus traditional PMF was varied using a weighting parameter applied to an

273 Transient PMF disruption events from loss of illumination caused m

274 otB stator proteins, we found that transient PMF disruption leads to reversible stator diffusion away

275 It is unknown how or where transient PMF changes are sensed and signaled due to the lack of p

276 export apparatus consists of a transmembrane PMF-driven export gate and a cytoplasmic ATPase complex

277 to stepwise increases in rotation rate upon PMF return as stators returned to the motor.

278 features that would not be identified using PMF alone, without sacrificing fit to observations.

279 ment of PCDD/F sources was carried out using PMF.

280 FliJ allows the gate to efficiently utilize PMF to drive flagellar protein export but it remains unk

281 e characterized the effects of rapid in vivo PMF changes on the flagellar motor.

282 F-induced torque; the effect disappears when PMF is eliminated by an uncoupler.

283 aberrant promoter hypermethylation, whereas PMF is an epigenetically distinct subgroup characterized

284 istent with a mechanochemical model in which PMF-driven motors, similar to bacterial flagella stator

285 ) subjects with ET and in 6 of 20 (30%) with PMF, whereas 52 cases of polycythemia vera had nonmutate

286 /661 (4%) patients with ET, 10/187 (5%) with PMF, and 7/44 (16%) patients with post-ET myelofibrosis.

287 tearin (used as reference) were blended with PMF to evaluate their potential use in CBEs formulation.

288 n PM eyes, the PPCI strongly correlated with PMF height (R = 0.68; P<0.0001), inverse axial length (R

289 A total of 802 patients diagnosed with PMF in four European countries were compared for the pre

290 bone marrow and spleens of individuals with PMF contain large numbers of atypical megakaryocytes tha

291 n and differentiation of megakaryocytes with PMF-associated mutations and had potent antifibrotic and

292 Methods The study included 805 patients with PMF age </= 70 years recruited from multiple Italian cen

293 were documented in 33% of 240 patients with PMF and 46% of 74 patients with MDS.

294 cation for transplantation-age patients with PMF and integrate prognostically relevant clinical, cyto

295 is study, we show that BM from patients with PMF harbors an abundance of clonal, neoplastic collagen-

296 nd was significantly higher in patients with PMF or post-ET myelofibrosis compared with those with ET

297 on of 2 distinct categories of patients with PMF where increased grades of fibrosis are associated wi

298 In patients with PMF who were studied by cytokine profiling, the prognost

299 nd 0.21 (95% CI, 0.18 to 0.25) in those with PMF.

300 ions define distinct disease entities within PMF.