ライフサイエンスコーパス: MPD

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

14 Since our last NAR reporting in 2007, MPD has added more community-contributed data covering m

15 Main-duct IPMNs with a MPD between 5 and 9 mm already bear a significant risk o

16 ment is clearly indicated in patients with a MPD diameter of >/=5 mm and the 2012 guidelines should b

17 In contrast to the acquired MPDs, mutations of the erythropoietin receptor and throm

18 Remarkably, the evolution of Alox15 MPD to leukemia is associated with additional regulation

19 urvival associated with chronic stage Alox15 MPD are all reversible upon treatment with a PI3-K inhib

20 An MPD diameter of 5.0 to 9.0 mm is not an indication for i

21 An MPD diameter of 7.2 mm or greater was also an independen

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

26 In mice, ICSBP deficiency induces an MPD that progresses to AML over time, suggesting that IC

27 capitulated the human disease by inducing an MPD with rare lymphoid involvement.

28 esection is recommended for patients with an MPD diameter of 10.0 mm or greater, which is characteriz

29 s to analyze cancer risk in patients with an MPD diameter of less than 10 mm.

30 An appropriate MPD diameter on preoperative CT or MRI to predict malign

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

34 dities, patient choice, and early/borderline MPD dilation (42%, 51%, and 7%, respectively).

35 and settings, or in some cases, retrieved by MPD staff from public sources.

36 The data show that JAK2(V617F) can cause MPDs in mice.

37 he obligate binding partner of LIG4, causing MPD.

38 therapeutic strategy to treat 8p11 stem cell MPD.

39 Based on our criteria for childhood MPD, we identified 34 patients with sporadic thrombocyth

40 Chronic MPD administration resulted in attenuation of the PFC's

41 behavioral sensitization elicited by chronic MPD administration.

42 gnancies resembling characteristics of CMML, MPD-like myeloid leukemia, and MDS.

43 ctly inhibits oncogenic JAK2 in constraining MPD development.

44 combination with the PI3K inhibitor corrects MPD by disrupting a protein complex involving p85alpha,

45 Currently MPD contains about 1400 phenotypic measurements contribu

46 The Mouse Phenome Database (MPD) is an open source, web-based repository of phenotyp

47 The Mouse Phenome Database (MPD; phenome.jax.org) was launched in 2001 as the data c

48 enzyme, mevalonate phosphate decarboxylase (MPD) and IPK.

49 algorithm, Marginalized Posterior Decoding (MPD), which explicitly accounts for uncertainties, is le

50 Five minimal phagocytic determinants (MPDs) of K/R(X)(1-2)KKK in Tulp1 N-terminus were defined

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]

53 used to study the effects of three different MPD doses on the response to sensory inputs.

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

56 Diffuse MPD dilation, serum CA19-9, serum alkaline phosphatase,

57 ranch-duct IPMN) to MPD involvement, diffuse MPD dilation, increase of MPD diameter, absence of extra

58 In logistic regression, diffuse MPD dilation, serum CA19-9 and serum alkaline phosphatas

59 g measure of WB mean parenchyma diffusivity (MPD).

60 Dilated MPD, MN, and HGA were independent predictors of malignan

61 MN and dilated MPD were highly specific (>90%), but insensitive (39%-44

62 Presence of mural nodules, dilated MPD (>10-mm diameter), or thick septa at CT or MRCP may

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

65 mutation develop myeloproliferative disease (MPD) and a block in early B-lymphocyte development.

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

70 ion gene induces myeloproliferative disease (MPD) in mice.

71 vity and induces myeloproliferative disease (MPD) in vivo by HSC transformation.

72 val in vitro and myeloproliferative disease (MPD) in vivo.

73 ukemia (JMML), a myeloproliferative disease (MPD) of early childhood.

74 e in determining myeloproliferative disease (MPD) phenotype.

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

77 eart defects and myeloproliferative disease (MPD).

78 yed the onset of myeloproliferative disease (MPD).

79 (JMML), a fatal myeloproliferative disease (MPD).

80 ndrome (MDS) and myeloproliferative disease (MPD).

81 and induces a myeloid proliferative disease (MPD) with features of megakaryoblastic leukemia in a mur

82 ic JAK2-induced myeloproliferative diseases (MPDs) in mice.

83 ions, and 67 had malignant pleural diseases (MPDs); 57 of 67 had MPM.

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

87 re described in myeloproliferative disorder (MPD) patients.

88 y presents as a myeloproliferative disorder (MPD) that evolves to acute myeloid leukemia and/or lymph

89 cy results in a myeloproliferative disorder (MPD) with increased mature neutrophils.

90 ML), which is a myeloproliferative disorder (MPD).

91 Myeloproliferative disorders (MPD) are stem cell-derived clonal diseases arising as a

92 for developing myeloproliferative disorders (MPD), including juvenile myelomonocytic leukemia (JMML).

93 ), overlap MDS/myeloproliferative disorders (MPD), MPD, and acute myeloid leukemia.

94 patients with myeloproliferative disorders (MPD).

95 ically related myeloproliferative disorders (MPD).

96 ly in atypical myeloproliferative disorders (MPD).

97 patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these dis

98 Because myeloproliferative disorders (MPDs) are a frequent cause of Budd-Chiari syndrome (BCS)

99 Myeloproliferative disorders (MPDs) are characterized by a clonal expansion of myeloid

100 Myeloproliferative disorders (MPDs) are characterized by cytokine hypersensitivity and

101 Myeloproliferative disorders (MPDs) are clonal malignancies that arise from hematopoie

102 Myeloproliferative disorders (MPDs) are thought to be clonogenic diseases arising at t

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

107 osome-negative myeloproliferative disorders (MPDs).

108 ion in various myeloproliferative disorders (MPDs).

109 ation of these myeloproliferative disorders (MPDs).

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

112 Mannose-phosphate-dolichol (MPD) is a multifunctional glycolipid that is synthesized

113 The isolated membrane proximal domain (MPD) of ADAM17 binds to PS but not to phosphatidylcholin

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

118 t IPMN patients with a main pancreatic duct (MPD) diameter of >/=10 mm.

119 pancreatic system is a main pancreatic duct (MPD) diameter of 5.0 mm or greater on computed tomograph

120 ved reformations along main pancreatic duct (MPD) were generated.

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

124 IPMN underwent primary surveillance, 70 for MPD-involved, mixed-type IPMN.

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

130 of JAK2(V617F) and to develop treatment for MPDs.

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

134 d rechallenged with saline and the identical MPD doses as on experimental day 1.

135 well as a biochemical basis for identifying MPD flippase.

136 and the role of additional genetic events in MPD disease pathogenesis.

137 show that MEK inhibitors are ineffective in MPD, but induce objective regression of many Nf1-deficie

138 evated levels of IL-31 were also observed in MPD CD3(+) cell-conditioned media.

139 the role of descending glutamate from PFC in MPD elicited behavioral sensitization.

140 to 9 mm, malignancy rate was 59%, whereas in MPD diameter more than 10 mm, it was 73%.

141 lelic mutations of Egr1 were not observed in MPDs in Egr1(+/-) mice.

142 le of FTKs in causing disease progression in MPDs by inducing chromosomal instability through the pro

143 role in the development of pruritogenesis in MPDs.

144 Furthermore, the presence of pruritus in MPDs was statistically correlated with a greater number

145 ch receptors may play unappreciated roles in MPDs.

146 ignificant sensitivity of TEL-PDGFRB-induced MPD to the dosage of Stat5a.

147 nsduced bone marrow into BALB/c mice induces MPD reminiscent of human PV, characterized by erythrocyt

148 r data suggest that oncogenic Ptpn11 induces MPD by aberrant activation of HSCs.

149 at cooperates with lipid kinases in inducing MPD.

150 ective hematopoiesis model for investigating MPD pathogenesis.

151 T pathway in some patients with JAK2V617F(-) MPD, suggesting that constitutive activation of this sig

152 rding was resumed before and after 2.5 mg/kg MPD administration.

153 All three groups received 2.5 mg/kg MPD for 6 days (from ED 9 to ED 14), followed by a 3-day

154 for the next five days with daily 2.5 mg/kg MPD to elicit behavioral sensitization.

155 ED 19, a rechallenge injection of 2.5 mg/kg MPD was given and locomotor activity was recorded.

156 On ED's 9 through 14, 2.5 mg/kg MPD was given, followed by a 4-day washout period (ED 15

157 Latent MPD was missed in a substantial number of our subjects b

158 is of use in the characterization of latent MPD in BCS.

159 ll expansion, induction of bcl-2, and lethal MPD.

160 k-/- mice spontaneously developed a CML-like MPD.

161 Maximum MPD and/or branch-duct diameter were not significant.

162 myelomonocytic leukemia (CMML; 48%) and MDS/MPD-unclassifiable (38%).

163 ificant overlap with CMPD (classified as MDS/MPD), but the diagnostic assignment may be challenging.

164 lodysplastic/myeloproliferative disease [MDS/MPD]) and 76 controls.

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

168 nesis of a clonal process in a subset of MDS/MPD, including CMML.

169 features consistent with the provisional MDS/MPD-U entity refractory anemia with ringed sideroblasts

170 res with the development of BCR-ABL-mediated MPD.

171 TEL-PDGFRB-mediated MPD was incompletely penetrant in TPiGFP-->Stat5b(-/-) m

172 Methylphenidate (MPD) is widely prescribed for attention-deficit/hyperact

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.

176 Since methylphenidate (MPD) is widely used to treat attention disorders, we wan

177 It is known that methylphenidate (MPD) (also known as Ritalin), a drug used to treat atten

178 f these, 50 were excluded because of minimal MPD involvement.

179 h eligible eyes) measured using the modified MPD-Visucam 200 (Carl Zeiss Meditec) and the modified He

180 Most MPD patients have a gain of function mutation in Janus k

181 rlap MDS/myeloproliferative disorders (MPD), MPD, and acute myeloid leukemia.

182 (> 10-fold lower rate) compared with natural MPD.

183 JAK2 V617F-positive and JAK2 V617F-negative MPDs.

184 ek inhibition did not correct the neoplastic MPD characteristic of these mutant mice, regardless of t

185 nagement algorithm that incorporated the new MPD diameter cutoff was evaluated.

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

189 sensitization to repeated administration of MPD in adult male Sprague-Dawley rats.

190 sults showed that repeated administration of MPD induced behavioral sensitization.

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

193 Severe attenuation of MPD by STAT5aDeltaN(S711F) was reversed by H2k/bcl-2 tra

194 PD flippase recognizes the dolichol chain of MPD, preferring a saturated alpha-isoprene to unsaturate

195 The core of MPD is implemented in C for speed and uses a hashed geno

196 capabilities, leading to the development of MPD.

197 )) fully protects against the development of MPD.

198 ity, and accuracy of PET/CT for diagnosis of MPD were 100%, 35.3%, and 64.5%.

199 mmunication with MPD, extent and diameter of MPD dilatation, calcifications, and vascular encasement.

200 The lowest dose of MPD (0.6 mg/kg, i.p.) failed to alter locomotor activity

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

204 however, there is none about the effects of MPD on sensory inputs.

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

207 gic abnormalities including a severe form of MPD that resembles human JMML.

208 As such, the natural history of MPD-involved IPMN is poorly understood.

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

211 ys 41-45, offspring received 10mg/kg i.p. of MPD or saline.

212 ill provide insight into the pathogenesis of MPD and could help develop specific therapeutic approach

213 other genes involved in the pathogenesis of MPD were investigated in JAK2 wild-type patients.

214 The pathophysiology of MPD-associated pruritus is unclear.

215 rentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor pr

216 their exclusion has led to a redefinition of MPD IPMN (MD-IPMN).

217 s Guidelines recommend surgical resection of MPD-involved IPMN in fit patients.

218 A stereoisomer of MPD was weakly translocated (> 10-fold lower rate) compa

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

221 TP-independent transbilayer translocation of MPD from the inner to the outer leaflet.

222 Treatment of MPD on experimental day 10 resulted in further decrease

223 In addition, the lesser severity of MPDs initiated from old BCR-ABL(P210)-transduced BM cell

224 F) has greatly advanced our understanding of MPDs.

225 tween Met66 allele status and T1-LV, NWMV or MPD.

226 with phenotypically classified ET and other MPDs.

227 ; these cases may subsequently develop overt MPD.

228 Eleven of 41 subjects developed overt MPD (8/11 essential thrombocythemia, 3/11 PV) after the

229 rved for the subsequent development of overt MPD.

230 s a topological probe to selectively oxidize MPD molecules in the outer leaflet of the reconstituted

231 ter saline and 0.6, 2.5, and 10 mg/kg, i.p., MPD administration.

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

236 The three main Ph(-) MPDs are polycythemia vera (PV), essential thrombocythem

237 The key features of these Ph(-) MPDs are an increased red blood cell mass in PV, a high

238 erapeutic intervention in JAK2V617F-positive MPDs.

239 time points, but not 1 month postoperative (MPD 2.72 mg/L, -0.66 mg/L, 1.10 mg/L).

240 We present MPD, a software package that automates the design of mul

241 lesion of prefrontal cortex (PFC) prevented MPD elicited behavioral sensitization.

242 The somatic mutation Shp2D61Y produces MPD in vivo but fails to induce acute leukemia, whereas

243 leukemia, whereas somatic Shp2E76K produces MPD in vivo that transforms into full-blown leukemia.

244 As a result, MPD phenotypes are markedly ameliorated in Ptpn11(D61G/+

245 We have demonstrated that MPD mast cells (MCs) are involved by the malignant proce

246 We found that MPD MCs released significantly greater amounts of prurit

247 xture prior to reconstitution indicated that MPD flippase (i) is not a Con A-binding glycoprotein and

248 Here we show that MPD-flippase activity can be reconstituted in large unil

249 soluble isoprenyl monophosphates showed that MPD flippase recognizes the dolichol chain of MPD, prefe

250 the mice were treated, thus suggesting that MPD is driven by additional signaling pathways.

251 The MPD was characterized by an elevated white blood cell co

252 The MPD-derived iPS cells containing the mutation appeared n

253 sumed on experimental days 2 and 6 after the MPD maintenance dose followed by 3 days of washout.

254 In comparison with primary AML, the MPD-like AML showed significantly reduced aggressiveness

255 OD as measured with the modified HRA and the MPD-Visucam was not modified after 6 months of lutein an

256 CRd at the MPD was well tolerated with robust, rapid, and durable r

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

259 In the MPD cohort, overall response rate (ORR) was 76.9% with m

260 focusing on the 52 patients enrolled in the MPD cohort.

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

263 IPMNs involving the MPD harbor a high likelihood of malignancy and different

264 s underwent resection for IPMN involving the MPD.

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

268 This conformational change of the MPD putatively acts as a molecular switch, facilitating

269 The molecular identity of the MPD translocator (MPD flippase) is not known.

270 oss of beta c-/- reduced the severity of the MPD, but did not abrogate it.

271 ive imaging with regard to morphology of the MPD, were correlated with final histopathology.

272 n factor hnRNP LL are compared to reveal the MPD of different species.

273 interactive Tool Demo available through the MPD homepage.

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

276 When the MPD diameter was 5 to 9 mm, malignancy rate was 59%, whe

277 as revealed apparent heterogeneity among the MPDs.

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

280 Over time this MPD progresses to acute myeloid leukemia (AML), suggesti

281 However, the same three MPD doses elicited significant attenuation of sensory in

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

286 erents of PFC in behavioral sensitization to MPD is discussed.

287 effects such as behavioral sensitization to MPD.

288 ailed to exhibit behavioral sensitization to MPD.

289 molecular identity of the MPD translocator (MPD flippase) is not known.

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])

292 n our population suggests that children with MPD may be managed by tailored approaches.

293 on, septa, mural nodules, communication with MPD, extent and diameter of MPD dilatation, calcificatio

294 splasia and invasive carcinoma in IPMNs with MPD involvement was 68%.

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;

298 ably lead to pruritogenesis in patients with MPDs.

299 ment of antipruritus drugs for patients with MPDs.

300 tion, whereas Shp2E76K-expressing HSCs yield MPD as well as acute leukemia in recipient animals.