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1                                              PMF also significantly potentiated the apoptotic effects
2                                              PMF analysis resolved the PM10 data with four source fac
3                                              PMF analysis successfully extracted 11 factors from mass
4                                              PMF evolution is rapid, incessant, and driven by positiv
5                                              PMF induced the expression of SHP-1 and was linked to th
6                                              PMF inhibited both constitutive and interleukin-6-induci
7                                              PMF is characterized by bone marrow megakaryocytic proli
8                                              PMF may be associated with somatic mutations in JAK2, MP
9                                              PMF-conditioned medium increased the migration and tubul
10 , we compared survival from diagnosis of 100 PMF patients receiving ruxolitinib within COMFORT-2 with
11                                In total, 127 PMF patients were studied; comparison with normal contro
12 imensional positive matrix factorization (3D-PMF), showing that PBOA represented the main OMCOARSE so
13                         The diagnosis of 661 PMF patients with a bone marrow biopsy at presentation w
14  confidence interval [CI], 1.4-2.2), and 5.9 PMF (n = 267; HR, 4.5; 95% CI, 3.5-5.7).
15 mma occurs only when FoF1 operates against a PMF-induced torque; the effect disappears when PMF is el
16                        H20 is required for a PMF-dependent conformational change, suggesting that the
17  GhoT reduces metabolism by reducing ATP and PMF and that this reduction in metabolism is important f
18                                      CMB and PMF analyses indicate that deca technical mixtures are t
19 tions in the triple-negative cases of ET and PMF by applying whole-exome sequencing (WES) on paired t
20 suggest that triple-negative cases of ET and PMF do not represent a homogenous disease entity.
21  a significant proportion of familial ET and PMF nonmutated for JAK2 carry a somatic mutation of CALR
22 stically highly significantly between ET and PMF.
23 port a differential diagnosis between ET and PMF.
24 eas CALR and MPL mutants are found in ET and PMF.
25 cting the pathogenesis of CALR-mutant ET and PMF.
26       Pathogenetic mechanisms in PV, ET, and PMF include stem cell-derived clonal myeloproliferation
27 onent of diagnostic criteria for PV, ET, and PMF, but its prognostic utility is limited.
28 died the function of this axis in normal and PMF CD34(+) cells.
29 spectrometry, the PB and BM plasma of PV and PMF patients was shown to contain reduced amounts of int
30         These formulations based on SHSs and PMF met all the requirements to be considered as CBEs; t
31 th liquid feces significantly reduced TA and PMF compared to the reference.
32 cythemia vera, essential thrombocytosis, and PMF samples compared with healthy controls.
33           Combining WSE with bulk species as PMF inputs also produced five factors.
34 ine) in the mass spectra were used to assign PMF factors to biomass burning, traffic, and smoking emi
35 bution of the A3669G allele differed between PMF patients and 2 healthy control populations (odds rat
36  results show epigenetic differences between PMF and polycythemia vera/essential thrombocytosis and r
37 K/ERK inhibition delayed, but did not block, PMF.
38 sed FLC predicted shortened survival in both PMF and MDS, independent of age, creatinine, and other c
39 entration predicts inferior survival in both PMF and MDS.
40 and signaling processes that are mediated by PMF-coupled energetics at the cell membrane.
41                   The inhibition of STAT3 by PMF was reversible.
42           Qualitative trends in the computed PMF can be understood based on the stress field distribu
43                                 The computed PMF indicates that the central hydrophobic region provid
44 ins in the region around the minimum of each PMF.
45              In multivariate analysis, early PMF and the JAK2V617F mutation emerged as independent fa
46  patients/year, P = .01) in WHO-ET and early PMF, respectively.
47 ns, particularly arterial, was seen in early PMF compared with ET.
48 t myelofibrosis was 3% in ET and 9% in early PMF, but no transformation into acute leukemia was obser
49 fined ET and 35 patients (16%) showing early PMF.
50  cross-validated RMSE than those from either PMF or CTM alone.
51 on).We hypothesized that other GsPCRs elicit PMF, specifically serotonin-7 (5-HT7) receptors, which a
52                                    Excessive PMF is known to limit the turnover of HCOs, but the mole
53  of long-lasting phrenic motor facilitation (PMF), but via unique mechanisms (BDNF independent TrkB t
54                                   A 7-factor PMF solution was identified using speciated OMM and bulk
55 lysis and (2) positive matrix factorization (PMF) analysis of aerosol mass spectrometer (AMS) data.
56 resolved from positive matrix factorization (PMF) analysis of organic mass spectral data obtained fro
57 analyzer, (2) positive matrix factorization (PMF) analysis to separate the gas- and particle-phase si
58  evaluated by positive matrix factorization (PMF) and principal component analysis (PCA).
59               Positive matrix factorization (PMF) applied to organic aerosol (OA) data yielded 5 fact
60               Positive Matrix Factorization (PMF) applied to the data set revealed a factor indicativ
61 t of PM(2.5), positive matrix factorization (PMF) coupled with a bootstrap technique for uncertainty
62  (SVOC) data, positive matrix factorization (PMF) coupled with a bootstrap technique was applied to t
63               Positive matrix factorization (PMF) has been applied to single particle ATOFMS spectra
64 MB) model and positive matrix factorization (PMF) in order to quantify PBDE sources and debromination
65 y resolved by positive matrix factorization (PMF) of aerosol mass spectrometer data collected in area
66 resolved from positive matrix factorization (PMF) of AMS organic aerosol spectra collected from low-N
67 ated into the positive matrix factorization (PMF) receptor model to form a receptor-oriented hybrid m
68 ach, based on positive matrix factorization (PMF) shows that the COA factor was clearly linked to loc
69 xamined using positive matrix factorization (PMF) to apportion PCB sources in the air, water, and per
70 t tool called Positive Matrix Factorization (PMF) to identify the sources of PCBs to the atmosphere i
71               Positive matrix factorization (PMF) was applied to identify and apportion indoor and ou
72 ortionment by Positive Matrix Factorization (PMF) was carried out to interpret the real-world driving
73               Positive matrix factorization (PMF) was used for apportioning sources of atmospheric pa
74 e this issue, Positive Matrix Factorization (PMF) was used to identify the dominant sources of gas-ph
75               Positive matrix factorization (PMF) was used to resolve PM0.1 source contributions from
76 t study using positive matrix factorization (PMF), performed on long-term PM2.5 chemical speciation d
77 e analyzed by positive matrix factorization (PMF), yielding three conventional factors: hydrocarbon-l
78  analyzed via Positive Matrix Factorization (PMF).
79 resolved from positive matrix factorization (PMF).
80 examined with positive matrix factorization (PMF).
81 ormed from a polarization maintaining fiber (PMF).
82                                     Finally, PMF inhibited proliferation and induced apoptosis of MM
83 ately 33 years for ET, 24 for PV, and 15 for PMF.
84 ceptor A3669G is a susceptibility allele for PMF: it contributes to confer the phenotype of excess my
85                    Mayo Clinic databases for PMF were used to identify patients with available bone m
86 g the survival impact of newer therapies for PMF, which are currently being tested in these patient s
87  the combination of potential of mean force (PMF) and stress field calculations.
88 h umbrella sampling/potential of mean force (PMF) calculations as a function of the distance between
89                     Potential of mean force (PMF) calculations confirm that the observed motion is th
90                     Potential of mean force (PMF) calculations utilizing the multistate empirical val
91 n investigated with potential of mean force (PMF) calculations.
92 d to calculate the potentials of mean force (PMF) for a variety of restrained relative orientations o
93 ed to construct the potential of mean force (PMF) of the ligand and calculate the corresponding bindi
94 ns to calculate the potential of mean force (PMF) profiles for translocation of the four DNA nucleoti
95 ion permeation, the potential of mean force (PMF) was calculated for displacing a single Na(+) ion al
96 a method based on a potential of mean force (PMF) with restraining potentials to compute the binding
97 as indicated by the potential of mean force (PMF).
98 x rotation is driven by proton motive force (PMF) and depends on actin-like MreB cytoskeletal filamen
99 aratus utilizes ATP and proton motive force (PMF) as the energy source to transport component protein
100 sin (pR) to control the proton-motive force (PMF) in vivo by illumination.
101 ative bacteria uses the proton motive force (PMF) of the cytoplasmic membrane to energize active tran
102  and ExbD couple the CM proton motive force (PMF) to active transport of iron-siderophore complexes a
103 lecular motor that uses proton-motive force (PMF) to drive the synthesis of ATP from ADP and Pi.
104 arvest and transmit the proton motive force (PMF) to outer membrane transporters.
105 Pvd) by coupling to the proton motive force (PMF) via the inner membrane (IM) protein TonB1.
106 mpounds that target the proton motive force (PMF), uncouplers, represent one possible class of compou
107 hemical gradient termed proton motive force (PMF), which provides the driving force for the adenosine
108 P and the disruption of proton motive force (PMF).
109 le maintaining a viable proton motive force (PMF).
110 r and the transmembrane proton motive force (PMF).
111  by a pump powered by a proton motive force (PMF).
112 the host cell under the proton motive force (PMF).
113 cA, in concert with the proton motive force (PMF).
114 s on the plasma membrane protonmotive force (PMF), such as high external potassium to reduce the elec
115 ation (TA) and particulate matter formation (PMF) up to 49%, through lower ammonia emission, but incr
116 egetable fats by blending palm mid fraction (PMF) and tropical butters coming from shea, mango kernel
117 ated by blending SHSs and palm mid fraction (PMF) were studied and compared with those from cocoa but
118  mixing PDAGS with either palm mid fraction, PMF (PDAGS/PMF), palm olein, POL(PDAGS/POL) or sunflower
119 3 levels are decreased in CD34(+) cells from PMF patients, and the NOL3 locus is deleted in a subset
120 similarities with primary CD34(+) cells from PMF patients.
121 A) expression profiles in CD34(+) cells from PMF patients.
122                          Strikingly, further PMF calculations demonstrate that the mutation V174A dec
123                  Reverse operation generates PMF via ATP hydrolysis.
124           Our results reveal a novel genetic PMF-like mouse model and identify a tumor suppressor rol
125                                           In PMF (n = 428), but not in ET (n = 576), survival and bla
126                                           In PMF, JAK2/CALR/MPL mutational status is prognostically i
127                                           In PMF, survival and quality of life are significantly wors
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  specific cytokine-phenotype associations in PMF and a prognostically relevant plasma cytokine signat
132 on, SRSF2 mutations are relatively common in PMF, cluster with IDH mutations, and are independently p
133 uggest that megakaryocytes drive fibrosis in PMF and that targeting them with AURKA inhibitors has th
134 ontribute to the induction of BM fibrosis in PMF, and inhibiting fibrocyte differentiation with SAP m
135 ay a role in the induction of BM fibrosis in PMF.
136 plicing machinery are predominantly found in PMF and are implicated in the development of anemia or p
137  In contrast, aberrantly methylated genes in PMF were involved in inflammatory pathways and were enri
138 f JARID2 may contribute to MK hyperplasia in PMF.
139                  Aberrant hypomethylation in PMF was seen to occur in non-CpG island loci, showing fu
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 fusion status to predict overall survival in PMF.
149 URKA) represents a new therapeutic target in PMF.
150              The unmet need for treatment in PMF dictates a different approach for assessing the ther
151                    Recent clinical trials in PMF patients with intermediate-2 or high IPSS risk have
152 anslation both blocked 5-HT7 agonist-induced PMF, confirming a requirement for TrkB synthesis and act
153 3K/AKT pathway blocked 5-HT7 agonist-induced PMF, whereas MEK/ERK inhibition delayed, but did not blo
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 kine abnormalities in primary myelofibrosis (PMF) and examines their phenotypic correlates and progno
157 ombocythemia (ET) and primary myelofibrosis (PMF) are chronic diseases characterized by clonal hemato
158 ythemia vera (PV) and primary myelofibrosis (PMF) CD34(+) cells with low doses of RG7112 and Peg-IFNa
159 mbocythemia (ET), and primary myelofibrosis (PMF) constitute the BCR-ABL1-negative myeloproliferative
160 thermore, even though primary myelofibrosis (PMF) has a markedly worse prognosis than essential throm
161         Patients with primary myelofibrosis (PMF) have substantially reduced life expectancy, whereas
162                       Primary myelofibrosis (PMF) is a clonal hematologic malignancy characterized by
163                       Primary myelofibrosis (PMF) is a fatal neoplastic disease characterized by clon
164                       Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by m
165                       Primary myelofibrosis (PMF) is characterized by bone marrow fibrosis, myeloprol
166                       Primary myelofibrosis (PMF) is characterized by fibrosis, ineffective hematopoi
167 ombocythemia (ET) and primary myelofibrosis (PMF) lacking JAK2 and MPL mutations.
168 ion-age patients with primary myelofibrosis (PMF) that integrates clinical, cytogenetic, and mutation
169 mbocythemia (ET), and primary myelofibrosis (PMF) whereas CALR and MPL mutants are found in ET and PM
170 ith early/prefibrotic primary myelofibrosis (PMF) with presenting thrombocythemia.
171 plastic stem cells of primary myelofibrosis (PMF), a myeloproliferative neoplasm characterized by pro
172  patients with PV and primary myelofibrosis (PMF), and that "triple negative" mutational status in PM
173 polycythemia vera and primary myelofibrosis (PMF), are a heterogeneous group of myeloid-derived chron
174 ion for patients with primary myelofibrosis (PMF), but information on its net advantage over conventi
175 rombocythemia (ET) or primary myelofibrosis (PMF), first investigating a cohort of 892 consecutive pa
176 s in the treatment of primary myelofibrosis (PMF), there are recent indications that the survival of
177 ombocythemia (ET) and primary myelofibrosis (PMF).
178 ival of patients with primary myelofibrosis (PMF).
179 mbocythemia (ET), and primary myelofibrosis (PMF).
180 ns in both MDS-RS and primary myelofibrosis (PMF).
181  in 499 patients with primary myelofibrosis (PMF).
182 mbocythemia (ET), and primary myelofibrosis (PMF).
183 ombocythemia (ET) and primary myelofibrosis (PMF).
184 mbocythemia (ET), and primary myelofibrosis (PMF).
185  to an MPN resembling primary myelofibrosis (PMF).
186 ment in patients with primary myelofibrosis (PMF).
187 s defines 2 stages of primary myelofibrosis (PMF): prefibrotic/early (pre-PMF) and overt fibrotic (ov
188 thrombocythemia (ET); primary myelofibrosis (PMF); and MPN, unclassifiable (MPN,U).
189 and when excited in cells with intact native PMF generation systems increased motor speed beyond the
190 was shown to be sufficient to replace native PMF generation, and when excited in cells with intact na
191 K2, CALR, and MPL (so-called triple-negative PMF).
192 y that pervanadate suppressed the ability of PMF to inhibit the phosphorylation of STAT3, suggesting
193  the PDAGS were reduced with the addition of PMF, POL and SFO.
194 of patients belonging to these categories of PMF.
195 tumorigenesis, we investigated the effect of PMF on this pathway.
196 uxolitinib may modify the natural history of PMF.
197 n of GATA1 effectively rescued maturation of PMF megakaryocytes.
198       Isosolid phase diagrams of mixtures of PMF/SHS showed eutectic formation for SHS 65 and SHS 80,
199 ntitumor activity in vivo in mouse models of PMF.
200 lay a central role in the pathophysiology of PMF.
201                 However, extended periods of PMF loss led to stepwise increases in rotation rate upon
202                                     Rates of PMF-attributable mortality at 5 and 10 years were signif
203                                  Survival of PMF is steadily improving, except in patients in poor-ri
204 U patients specified upon follow-up as ET or PMF with 92% accuracy.
205 49 additional triple-negative cases of ET or PMF.
206 d Peg-IFNalpha 2a for the treatment of PV or PMF patients with the intent of altering their natural h
207  sufficient to ameliorate fibrosis and other PMF features in vivo.
208 ic/early (pre-PMF) and overt fibrotic (overt PMF) phase.
209 urvival was significantly shortened in overt PMF (7.2 vs 17.6 years), with triple negativity for driv
210 IDH1/2, EZH2) were more represented in overt PMF.
211                 Compared with pre-PMF, overt PMF was enriched in patients with anemia, thrombocytopen
212                     More patients with overt PMF were in higher International Prognostic Scoring Syst
213                                        PDAGS/PMF and PDAGS/SFO crystallised in beta'+beta polymorphs
214 18:1 were the dominant fatty acids for PDAGS/PMF and PDAGS/POL, while C18:1 and C18:2 were dominant i
215                     Binary mixtures of PDAGS/PMF had better structural compatibility and full miscibi
216 GS with either palm mid fraction, PMF (PDAGS/PMF), palm olein, POL(PDAGS/POL) or sunflower oil, SFO (
217      The results gave indication that PDAGS: PMF at 50%:50% and 60%:40% (w/w) were the most suitable
218 3'-dihydroxy-3,6,7,8,4'-pentamethoxyflavone (PMF), from the leaves of the Thai plant Gardenia obtusif
219 3'-dihydroxy-3,6,7,8,4'-pentamethoxyflavone (PMF), that has the ability to inhibit STAT3 activation.
220  myelofibrosis (PMF): prefibrotic/early (pre-PMF) and overt fibrotic (overt PMF) phase.
221                            Compared with pre-PMF, overt PMF was enriched in patients with anemia, thr
222 ity to disease progression compared with pre-PMF.
223  diagnosis between ET and early, prefibrotic PMF can be challenging but is critical because clinical
224 cially in distinguishing ET from prefibrotic PMF and masked PV.
225 d surface latches the substrate and promotes PMF-driven transport.
226 HOS at pH 10.5, where the bulk protonmotive (PMF) force is low.
227 s, we have measured the effects of a reduced PMF on root and hypocotyl growth, ATP-induced skewed roo
228 s, patients with intermediate-2 or high-risk PMF clearly benefit from allogenic SCT.
229                       For example, the small PMF barrier, which is approximately 1 kcal/mol independe
230                            Like PRF and SPF, PMF is produced by a multigene family characterized by g
231 er PMF2 software and the newer EPA-sponsored PMF 3.0 software were employed.
232 e used RT-PCR in mental gland cDNA to survey PMF sequences from three genera of plethodontid salamand
233                                We found that PMF suppressed NF-kappaB activation induced by inflammat
234  away from the flagellar motor, showing that PMF presence is necessary for continued motor integrity,
235          Overall, these results suggest that PMF is a novel blocker of STAT3 activation and thus may
236                                          The PMF analysis revealed four resolved factors at each site
237                                          The PMF in PM eyes has characteristic morphologic SD-OCT fea
238                                          The PMF method predicted that the R14A mutation in HsTX1 wou
239                                          The PMF results are validated by PBDE manufacturing records,
240                                          The PMF results were confirmed by examining three samples th
241 etion by small interfering RNA abolished the PMF-induced constitutive and inducible STAT3 inhibition.
242 corneal power (R = 0.49; P = 0.002), and the PMF height correlated strongly and inversely with the ax
243 ting, as predicted, a close link between the PMF and potassium uptake at the plasma membrane.
244 utants were defective in supporting both the PMF-dependent formaldehyde cross-link between the peripl
245            Indeed, SDP rapidly collapses the PMF as measured by fluorometry and flow cytometry, which
246                               Collapsing the PMF is an ideal mechanism for a toxin involved in cannib
247 rane proteins, in addition to collapsing the PMF.
248                                Comparing the PMF values of different systems, we obtain a relative ra
249                   By rapidly dissipating the PMF, we propose that this leak state may enable cytochro
250                                 However, the PMF well depth is reproduced poorly by a simple continuu
251 the 3 MPN drivers and play a key role in the PMF pathogenesis.
252 icant correlation with the axial length, the PMF severity and keratometry established in this study s
253 tail AHA2's specific role in maintaining the PMF during seedling growth.
254        Arrest was not due to collapse of the PMF and did not require the presence of ExbD or TonB.
255 t structural and biochemical features of the PMF protein (i.e., secretion signal, cysteine residues,
256       The depth of the potential well of the PMF was shown to depend approximately linearly on the bu
257               The OCT characteristics of the PMF were analyzed and the PPCIs were compared and correl
258         Furthermore, the practicality of the PMF-based method for larger systems is validated by agre
259 hat differently structured exposition of the PMF-based method with restraining potentials and outline
260 le in the pathogenesis and morphology of the PMF.
261 ical potential (DeltapH) compositions of the PMF.
262 fusions are not affected by substrate or the PMF, although TatB-YFP oligomerization does require TatC
263                                 Removing the PMF causes TatA complexes to dissociate, except in strai
264         This work also demonstrates that the PMF-based method with restraining potentials provides an
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 Pathogenicity is thus likely attributable to PMF-mediated paracrine stimulation of mouse myeloid cell
270         AML was of mouse origin, confined to PMF-xenografted mice, and contained multiple clonal inte
271 pathway and thus only indirectly responds to PMF, probably via ExbD.
272 ding of signalling mechanisms giving rise to PMF may guide development of novel therapeutic strategie
273 l of influence of the CTM versus traditional PMF was varied using a weighting parameter applied to an
274                                    Transient PMF disruption events from loss of illumination caused m
275 otB stator proteins, we found that transient PMF disruption leads to reversible stator diffusion away
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.

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