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1 MPD can successfully design multiplex PCR experiments su
2 MPD contains >3500 phenotype measurements or traits rele
3 MPD flipping is highly specific.
4 MPD houses a wealth of strain characteristics data to fa
5 MPD improvements and updates since our last NAR report a
6 MPD increased glucose metabolism in most brain regions f
7 MPD integrates quantitative phenotype, gene expression a
8 MPD is also a facility for query, analysis and in silico
9 MPD is reproduced in primary and secondary recipient mic
10 MPD maintains a growing collection of standardized refer
11 MPD MCs exhibited increased migratory behavior in respon
12 MPD provides a community data repository and a platform
13 .53 mg/L [p < .01]) and postoperative day 2 (MPD 71.97 mg/L [p < .01], 35.18 mg/L [p < .05], 63.76 mg
16 ment is clearly indicated in patients with a MPD diameter of >/=5 mm and the 2012 guidelines should b
19 urvival associated with chronic stage Alox15 MPD are all reversible upon treatment with a PI3-K inhib
22 is single-center, retrospective analysis, an MPD diameter of 7.2 mm was identified as an optimal cuto
23 cy for malignant neoplasms was highest at an MPD diameter cutoff of 7.2 mm (area under the receiver o
24 irin to treat patients with BCS caused by an MPD seems to be safe and effective and avoids the risks
25 new management algorithm, which included an MPD diameter of 7.2 mm or greater as one of the high-ris
28 esection is recommended for patients with an MPD diameter of 10.0 mm or greater, which is characteriz
31 s in dose-response characteristics, i.e., as MPD dose increased, evoked sensory inputs decreased.
32 atistical correlations were observed between MPD diameter and clinical and/or IPMN features such as a
33 with the Flt3 kinase inhibitor AC220 blocks MPD development by targeting Flt3(+) multipotent progeni
44 combination with the PI3K inhibitor corrects MPD by disrupting a protein complex involving p85alpha,
49 algorithm, Marginalized Posterior Decoding (MPD), which explicitly accounts for uncertainties, is le
51 19 in oncogenic KIT is sufficient to develop MPD by recruiting p85alpha, SHP2, and Gab2 complex to on
52 the preoperative (median paired difference [MPD] 1.97 mg/L [p < .05], 0.29 mg/L, 1.56 mg/L [p < .01]
54 b-value DW images is useful to differentiate MPD from benign alterations, performing substantially be
55 ging is a promising tool for differentiating MPD from benign lesions, with high accuracy, and supplem
57 ranch-duct IPMN) to MPD involvement, diffuse MPD dilation, increase of MPD diameter, absence of extra
63 30% more cancers in small cysts than dilated MPD or MN and half of the cancers without either of thes
64 e when either the mean position of the disc (MPD) fell below the 95% confidence limit of each eye's i
66 is and develop a myeloproliferative disease (MPD) characterized by profound thrombocytosis, megakaryo
67 ndispensable for myeloproliferative disease (MPD) development, and SYK overexpression promotes overt
68 as a model of a myeloproliferative disease (MPD) driven by wild-type Flt3, in the present study, we
69 usly that lethal myeloproliferative disease (MPD) in mice mediated by persistently activated STAT5 (S
75 delphia-negative myeloproliferative disease (MPD), were retrospectively evaluated to characterize the
76 AML blast cells, myeloproliferative disease (MPD)-like AML relapsed characterized by cells that did n
81 and induces a myeloid proliferative disease (MPD) with features of megakaryoblastic leukemia in a mur
84 nitiated both a myeloproliferative disorder (MPD) and B-lymphoid leukemia, whereas BCR-ABL(P210)-tran
85 ), CD8(+)) or a myeloproliferative disorder (MPD) at increased rates and with shorter latencies than
86 ors of MEK in a myeloproliferative disorder (MPD) initiated by inactivating Nf1 in mouse bone marrow
88 y presents as a myeloproliferative disorder (MPD) that evolves to acute myeloid leukemia and/or lymph
92 for developing myeloproliferative disorders (MPD), including juvenile myelomonocytic leukemia (JMML).
97 patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these dis
103 patients with myeloproliferative disorders (MPDs) who acquired the JAK2-V617F somatic mutation in th
104 patients with myeloproliferative disorders (MPDs), including polycythemia vera, essential thrombocyt
105 in the chronic myeloproliferative disorders (MPDs), polycythemia vera (PV), idiopathic myelofibrosis
106 Patients with myeloproliferative disorders (MPDs), such as essential thrombocythemia (ET) have incre
110 y estimating the mean phylogenetic distance (MPD) among species and by comparing empirical phylogenet
111 ize of mean pairwise phylogenetic distances (MPD) and phylogenetic diversity (PD) increased significa
114 interacts with the membrane-proximal domain (MPD), a domain of ADAM17 involved in its dimerization an
115 suggest that oral administration of low-dose MPD improves spatial learning and memory in both male an
116 iple myeloma where the maximum planned dose (MPD) was carfilzomib 20 mg/m2 days 1 and 2 of cycle 1 an
117 t size >30 mm, dilated main pancreatic duct (MPD) >6 mm, mural nodule (MN) and "positive" cytology as
119 pancreatic system is a main pancreatic duct (MPD) diameter of 5.0 mm or greater on computed tomograph
121 gnancy associated with main pancreatic duct (MPD)-involved intraductal papillary mucinous neoplasm (I
122 cause of microcephalic primordial dwarfism (MPD), a phenotype characterized by prenatal-onset extrem
123 a new method, molecular population dynamics (MPD), to describe the intricate equilibrium among non-B
125 esting that ICSBP deficiency is adequate for MPD, but additional genetic lesions are required for AML
126 " do not fulfill the diagnostic criteria for MPD but have features suggestive of a latent form based
127 a support lowering the accepted criteria for MPD diameter when selecting patients for resection vs su
128 ther trisomy for Aml1/Runx1 is essential for MPD, we restored disomy at the Aml1/Runx1 locus in the T
129 ts with pleural abnormalities suspicious for MPD underwent whole-body positron emission tomography (P
131 reshold to differentiate benign lesions from MPD with DW MR imaging was 1.52 x 10(-3) mm(2)/sec, with
132 HSCs expressing Shp2D61Y do not generate MPD in recipient animals upon transplantation, whereas S
133 ter locomotor activity, while the two higher MPD doses (2.5 and 10.0 mg/kg) elicited increase in loco
137 show that MEK inhibitors are ineffective in MPD, but induce objective regression of many Nf1-deficie
142 le of FTKs in causing disease progression in MPDs by inducing chromosomal instability through the pro
144 Furthermore, the presence of pruritus in MPDs was statistically correlated with a greater number
147 nsduced bone marrow into BALB/c mice induces MPD reminiscent of human PV, characterized by erythrocyt
151 T pathway in some patients with JAK2V617F(-) MPD, suggesting that constitutive activation of this sig
163 ificant overlap with CMPD (classified as MDS/MPD), but the diagnostic assignment may be challenging.
165 bone marrow from 270 patients with MDS, MDS/MPD, and CMPD for the presence of JAK2 V617F mutation us
166 re found in around three-fourths of MDS, MDS/MPD, and sAML (vs 59%, 37%, 53% by MC; in 8% of patients
167 d in 20% of MDS, 23% of sAML, and 35% of MDS/MPD patients, a lesion resulting in copy-neutral loss of
169 features consistent with the provisional MDS/MPD-U entity refractory anemia with ringed sideroblasts
173 ulants like amphetamine and methylphenidate (MPD) are used to treat attention deficit hyperactivity d
174 erties of acute and chronic methylphenidate (MPD) on neurons of the prefrontal cortex (PFC) and cauda
175 nvestigating the effects of methylphenidate (MPD) are using behavioral and biochemical approaches.
179 h eligible eyes) measured using the modified MPD-Visucam 200 (Carl Zeiss Meditec) and the modified He
184 ek inhibition did not correct the neoplastic MPD characteristic of these mutant mice, regardless of t
186 luding cases with minimal noncircumferential MPD involvement has been challenged because these show c
187 demonstrate that functional abnormalities of MPD MCs probably lead to pruritogenesis in patients with
188 imental day 1 and an acute administration of MPD (0.6, 2.5, or 10.0 mg/kg, i.p.) on experimental day
191 al responses after chronic administration of MPD suggests that the sensory evoked responses on experi
192 and nigrostriatal systems with the amount of MPD-induced behavior (stereotypy and locomotion) show th
194 PD flippase recognizes the dolichol chain of MPD, preferring a saturated alpha-isoprene to unsaturate
199 mmunication with MPD, extent and diameter of MPD dilatation, calcifications, and vascular encasement.
201 fferents are involved in the acute effect of MPD as well as in its chronic effects such as behavioral
202 n modulated the acute and chronic effects of MPD and hence suggests that PFC glutamatergic afferents
203 to investigate the dose-response effects of MPD on sensory evoked potentials recorded from the PFC a
205 rophysiological studies about the effects of MPD on spontaneous electrical activity; however, there i
206 c-/- stem cells did not develop evidence of MPD despite the presence of increased number of immature
209 volvement, diffuse MPD dilation, increase of MPD diameter, absence of extra pancreatic cysts, elevate
210 hallenge doses (0.6, 2.5, and 10.0 mg/kg) of MPD on experimental day 1 elicited dose-response attenua
212 ill provide insight into the pathogenesis of MPD and could help develop specific therapeutic approach
215 rentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor pr
219 a establish Lnk as a bona fide suppressor of MPD in mice and raise the possibility that Lnk dysfuncti
220 ntify 12/15-LO as an important suppressor of MPD via its role as a critical upstream effector in the
230 s a topological probe to selectively oxidize MPD molecules in the outer leaflet of the reconstituted
232 r understanding human biology and pathology; MPD facilitates research that uses the mouse to identify
233 Chronic myeloid leukemia (CML) is a Ph(+) MPD that is defined on the basis of its molecular lesion
234 ase gene, JAK2, in the predominance of Ph(-) MPD patients and has highlighted JAK2 as a therapeutic i
235 l focus on the comparison of Ph(+) and Ph(-) MPDs, drug discovery and development efforts targeting t
243 leukemia, whereas somatic Shp2E76K produces MPD in vivo that transforms into full-blown leukemia.
247 xture prior to reconstitution indicated that MPD flippase (i) is not a Con A-binding glycoprotein and
249 soluble isoprenyl monophosphates showed that MPD flippase recognizes the dolichol chain of MPD, prefe
253 sumed on experimental days 2 and 6 after the MPD maintenance dose followed by 3 days of washout.
255 OD as measured with the modified HRA and the MPD-Visucam was not modified after 6 months of lutein an
257 sults from the phase 2 dose expansion at the MPD, focusing on the 52 patients enrolled in the MPD coh
258 directed hematopoietic differentiation, the MPD-iPS cell-derived hematopoietic progenitor (CD34(+)CD
261 ppressing erythropoiesis that results in the MPD-like AML show significantly reduced ability to induc
262 of the present study were to investigate the MPD dose-response characteristics on locomotor activity
265 thin the thioredoxin motif C600XXC603 of the MPD and results in a drastic structural change between a
266 roved search and navigational aspects of the MPD application, developed several web-enabled data anal
267 tivity and negative predictive value) of the MPD diameter on CT or MRI as a prognostic factor for mal
274 A JavaScript web application utilizing the MPD Perl package provides a convenient platform for user
275 ith biochemical results firmly validates the MPD analyses, which, we expect, can be widely applicable
278 ties are involved in the pathogenesis of the MPDs and that aberrant Mpl expression may be a common de
279 GM-CSF receptor to initiate and sustain this MPD by generating Nf1 mutant hematopoietic cells lacking
282 interval (from isolated branch-duct IPMN) to MPD involvement, diffuse MPD dilation, increase of MPD d
283 mutation in pan hematopoietic cells leads to MPD as a result of aberrant activation of hematopoietic
284 posure affects brain function in response to MPD as measured by glucose metabolism in a rodent model.
285 m overall but produced a reduced response to MPD in the nucleus accumbens in a rostral/caudal gradien
290 de a mechanistic framework for understanding MPD flipping, as well as a biochemical basis for identif
291 6 mg/L [p < .01]), postanesthesia care unit (MPD 2.83 mg/L, 2.22 mg/L [p < .05], 2.53 mg/L [p < .01])
293 on, septa, mural nodules, communication with MPD, extent and diameter of MPD dilatation, calcificatio
295 occurs in a high proportion of patients with MPD and is of use in the characterization of latent MPD
296 rgery for IPMN, there were 320 patients with MPD involvement, 238 patients with mixed-type IPMN, and
297 based on the cause of BCS: 17 patients with MPDs received hydroxyurea/aspirin; 5 received warfarin;
300 tion, whereas Shp2E76K-expressing HSCs yield MPD as well as acute leukemia in recipient animals.
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