ライフサイエンスコーパス: HPC

1 HPC activation is involved in the response of the liver

2 HPC blood plasma levels were also compared to known in v

3 HPC-PFC interactions have rarely been studied in monkeys

4 HPCs and HPC-expressing adipokines (e.g., adiponectin, r

5 HPCs are bipotent liver stem cells that can self-replica

6 HPCs are known to be bipotential cells, capable of formi

7 HPCs are thought to play an important role in liver rege

8 HPCs derived from RUNX1a hPSCs show enhanced expansion a

9 HPCs were the major source of Wnt ligands.

10 rs of HSCs, hematopoietic progenitor cell-1 (HPC-1), HPC-2, and Lin(-)Sca-1(+)c-Kit(+) subpopulations

11 Cs, hematopoietic progenitor cell-1 (HPC-1), HPC-2, and Lin(-)Sca-1(+)c-Kit(+) subpopulations.

12 We attribute the revived activity with 3-HPC to the alpha-effect, where tandem electronegative at

13 omparison with 2D monolayer culture and a 3D HPC-only model, our 3D triculture model shows both pheno

14 on a single workstation or in parallel on a HPC cluster.

15 ypropyl cellulose-graft-poly (acrylic acid) (HPC-g-PAA) as a template and was coated with PDA to cons

16 conspicuously show the presence of activated HPC response and proliferation.

17 rent review highlights the role of activated HPCs in both hepatic regeneration and fibrosis during li

18 In addition, HPC TF initiated factor Xa generation without exogenous

19 regulating the stemness properties of adult HPCs and reveal a previously unrecognized link between E

20 After HPC transplantation, new red cell antibodies were seen i

21 All HPC-7 data sets are freely available both through standa

22 As not all HPCs are, or can be, chemically analyzed, the applicatio

23 However, not all HPCs in the aorta, vitelline and umbilical arteries, and

24 ed the incidence of such complications among HPC transplant recipients with sickle cell disease.

25 On multivariate regression analysis, HPC was the most important variable associated with pean

26 MSC proliferation, collagen deposition, and HPC supportive function, suggesting LGL BM infiltration

27 tions of RBPJ during biliary development and HPC-associated biliary regeneration after hepatectomy.

28 As platelet-activating factor and HPC share structural semblances and both induce killing

29 HPCs and HPC-expressing adipokines (e.g., adiponectin, resistin,

30 on of the portal inflammatory infiltrate and HPC/DR niche in NAFLD will shape future functional studi

31 ic brain profiling analysis revealed PFC and HPC changes in various molecular pathways associated wit

32 ed the proliferation of MF CD34(+) cells and HPCs in a dose-dependent fashion.

33 (BM) and the retention of activated HSCs and HPCs but not of quiescent HSCs in their BM niches.

34 rt-term GC pretreatment of human CB HSCs and HPCs promoted SDF-1-CXCR4-axis-mediated chemotaxis, homi

35 opoietic stem and progenitor cells (HSCs and HPCs) remains elusive.

36 population of MF-HPCs, while sparing another HPC subpopulation as well as MF-SCs.

37 nct memories for individual events, anterior HPC and posterior MPFC integrate across memories.

38 that neural representations in left anterior HPC correspond with model predictions of concept organiz

39 (+)Lin(-) cells and all classes of assayable HPCs (colony-forming unit-megakaryocyte [CFU-MK], CFU-gr

40 Theta-band HPC-PFC synchrony was stronger after errors, was driven

41 Before HPC transplantation, three patients had antibodies incom

42 Phase-amplitude coupling between HPC theta and gamma oscillations strongly and specifical

43 and frequency-specific interactions between HPC and PFC of monkeys learning object pair associations

44 normal heart development requires bilateral HPCs to undergo a critical behavioral and phenotypic tra

45 n recordings of neural activity from the BLA-HPC-mPFC circuit during fear conditioning, extinction, a

46 Hepatoprotection by HPC was significant in wild-type and A1, A2A, and A3 AR

47 ger after correct trials, was driven more by HPC and increased with learning.

48 oduction of IL-5 and IL-13, but not IL-4, by HPCs.

49 stem and in primary ex vivo-cultured CD34(+) HPCs.

50 eration and differentiation of human CD34(+) HPCs.

51 us replication in fibroblasts and in CD34(+) HPCs for latency.

52 ding to its entry receptor, EGFR, in CD34(+) HPCs initiates early events necessary for successful lat

53 HIV-1 infection frequency of Lin(-)/CD34(+) HPCs from bone marrow, if it occurred, was <.003% (highe

54 results strongly suggest that Lin(-)/CD34(+) HPCs in bone marrow are not a source of persistent HIV-1

55 required for successful infection of CD34(+) HPCs by HCMV.IMPORTANCE HCMV establishes lifelong persis

56 Gene expression profiling of CD34(+) HPCs from 7 ARV-exposed and 6 control newborns revealed

57 GFR signaling following infection of CD34(+) HPCs may also contribute to changes in hematopoietic pot

58 assessed whether thalassemia patient CD34(+) HPCs could be transduced with a globin lentiviral vector

59 gene transfer in thalassemia patient CD34(+) HPCs, which we will implement in the first US trial in p

60 conventional hematopoietic progenitor cell (HPC) compartment.

61 CD34(+) hematopoietic stem/progenitor cell (HPC) compartment.

62 her specific haematopoietic progenitor cell (HPC) subsets reside in distinct niches defined by the su

63 Haemopoietic progenitor cell (HPC) transplantation can cure sickle cell disease.

64 differentiation of hepatic progenitor cells (HPC) has not been investigated, and little is known abou

65 iation of putative hepatic progenitor cells (HPC) residing in the canals of Hering and/or metaplasia

66 signaling in hematopoietic progenitor cells (HPC), myeloid-derived suppressor cells (MDSC), and dendr

67 aling affects hepatic progenitor/oval cells (HPCs) and beta-adrenoceptor agonism will expand HPCs to

68 emergence of hematopoietic progenitor cells (HPCs) and positively regulates expression of mesoderm an

69 Hematopoietic progenitor cells (HPCs) are central to hematopoiesis as they provide large

70 d numbers of hematopoietic progenitor cells (HPCs) at the expense of repopulating hematopoietic stem

71 pulations of hematopoietic progenitor cells (HPCs) derived from human embryonic stem cells (hESCs).

72 Foxl1(+) hepatic progenitor cells (HPCs) differentiate into cholangiocytes and hepatocytes

73 decisions of adult hepatic progenitor cells (HPCs) has not been resolved.

74 zing CD34(+) hematopoietic progenitor cells (HPCs) in adults with beta-thalassemia major.

75 Hematopoietic progenitor cells (HPCs) in the bone marrow of human immunodeficiency virus

76 In CD34(+) hematopoietic progenitor cells (HPCs) infected in vitro, disruption of the 23- and 19-kD

77 as assayable hematopoietic progenitor cells (HPCs) irrespective of the JAK2 and calreticulin mutation

78 ields of mesenchymal heart progenitor cells (HPCs) move from the anterior lateral plate mesoderm to t

79 infection in hematopoietic progenitor cells (HPCs) or CD14 (+) monocytes.

80 ar sources such as hepatic progenitor cells (HPCs) to regenerate hepatocytes in various contexts of f

81 c homing of haematopoietic progenitor cells (HPCs) via the blood is critical for normal T-cell develo

82 function of hematopoietic progenitor cells (HPCs), and myeloid and erythroid hyperplasia.

83 s on healthy hematopoietic progenitor cells (HPCs), bioartificial matrixes from rat tail or purified

84 rent loss of hematopoietic progenitor cells (HPCs), leading to fatal BM aplasia.

85 the fate of the DR hepatic progenitor cells (HPCs), regulating the balance between liver repair and f

86 l entry into CD34(+) human progenitor cells (HPCs), resulting in distinct cellular trafficking and nu

87 ived CD34(+) hematopoietic progenitor cells (HPCs), which include eosinophil lineage-committed progen

88 hly dividing hematopoietic progenitor cells (HPCs), which produce all blood cell lineages.

89 the activation of hepatic progenitor cells (HPCs), which then participate in the restoration of the

90 cells (HSCs)/hematopoietic progenitor cells (HPCs).

91 CB HSCs and hematopoietic progenitor cells (HPCs).

92 ived CD34(+) hematopoietic progenitor cells (HPCs).

93 n in CD34(+) hematopoietic progenitor cells (HPCs).

94 aining bipotential hepatic progenitor cells (HPCs).

95 s (HSCs) and hematopoietic progenitor cells (HPCs).

96 s (HSCs) and hematopoietic progenitor cells (HPCs).

97 latently in hematopoietic progenitor cells (HPCs).

98 al human HSC/hematopoietic progenitor cells [HPCs], revealing that several chemokine ligands (CXCL1-4

99 s treated with hexadecylpyridinium chloride (HPC).

100 transition to affect hematopoietic cluster, HPC, and HSC formation.

101 Halogenated phenolic compounds (HPCs) including hydroxylated polychlorobiphenyls (OH-PCB

102 ation of the halogenated phenolic compounds (HPCs).

103 ational power of high performance computing (HPC) and cloud resources, we demonstrated that the metho

104 ands of cores on high-performance computing (HPC) architectures; made them robust and portable to nex

105 igently adapt to high performance computing (HPC) cluster.

106 llelization on a high performance computing (HPC) cluster.

107 migrated to any high-performance computing (HPC) environment.

108 dent of existing high-performance computing (HPC) infrastructures.

109 nfigure links to high-performance computing (HPC) resources, view and manage output, apply analysis a

110 ing and utilizes high performance computing (HPC) techniques.

111 ironment (XSEDE) high-performance computing (HPC) virtual system, iPlant cloud data storage resources

112 work, including high performance computing (HPC), bioinformatics support, multistep workflows, updat

113 when concept updating is most consequential, HPC is functionally coupled with prefrontal regions.

114 lls and osteoblasts, results in constitutive HPC mobilization and a loss of B-lymphoid progenitors, b

115 sponse between household peanut consumption (HPC; used as an indirect marker of environmental peanut

116 These data provide a framework for defining HPC lineage potential, elucidate a molecular contributio

117 Gata factors, compared with Gata2-dependent HPCs.

118 uce long-term survival of murine ESC-derived HPCs without the overexpression of HoxB4, a homeobox tra

119 , thrombin generation was dependent on donor HPC TF expression in a model of HPC transplantation.

120 but striking accumulation of HSCs and early HPCs that are defective in multilineage reconstitution,

121 Significant increases in mature eosinophil, HPC, and eosinophil lineage-committed progenitor cell co

122 SNS catecholamines expand HPCs, which are both targets and sources of Wnt ligands.

123 s) and beta-adrenoceptor agonism will expand HPCs to reduce AILI.

124 ssociated weak inducer of apoptosis expanded HPCs and protected against AILI.

125 cells failed to recognize HLA-A2-expressing HPCs but became anergic.

126 h we could trace and delete Foxl1-expressing HPCs and their descendants (Foxl1-Cre;Rosa(YFP/iDTR)-ind

127 n, data management, and scaling analyses for HPC-acknowledging that data science skills will be requi

128 y that governs thymic EC differentiation for HPC homing.

129 ct concentrations reported in literature for HPCs of 0.05-10000 nM.

130 We investigated the requirement for Foxl1(+) HPCs in recovery from liver injury in mice.

131 s of Foxl1-Cre;Rosa(YFP/iDTR) mice, Foxl1(+) HPCs and/or their descendants are required for the devel

132 ortal EC population with features that guide HPC homing.

133 betaR) directly controls thymic ECs to guide HPC homing.

134 ted a cohort of 52 SFTs/hemangiopericytomas (HPCs) by whole-exome sequencing (one case) and multiplex

135 factor (TF) expression in mouse hepatocytes (HPCs) and evaluated its role in mouse models of HPC tran

136 Miltefosine [hexadecylphosphocholine (HPC)] is the only orally bioavailable drug for the disea

137 on prefrontal cortex (PFC) and hippocampal (HPC) tissue from Df(16)A(+/-) mice, a model of the 22q11

138 re, our aim is to determine how hippocampal (HPC) object representations are organized and updated to

139 (aWK) similarly in the RSC and hippocampus (HPC) but not in ACA.

140 lateral amygdala (BLA) with the hippocampus (HPC) and medial prefrontal cortex (mPFC) during fear exp

141 mple, face-name), for which the hippocampus (HPC) and prefrontal cortex (PFC) are critical.

142 dies have mainly implicated the hippocampus (HPC) in this process, it is unknown which cell type(s) o

143 hough theories suggest that the hippocampus (HPC) is dedicated to represent specific episodes while t

144 ry or neurotoxic lesions of the hippocampus (HPC), medial dorsal striatum (DSM), or lateral dorsal st

145 prefrontal cortex (PFC) and the hippocampus (HPC)-regions critical for sensory associations-of monkey

146 iPSC-derived hepatic progenitor cells (hiPSC-HPCs) in a 3D environment that depicts the physiological

147 gel-based triculture model that embeds hiPSC-HPCs with human umbilical vein endothelial cells and adi

148 pic and functional enhancements in the hiPSC-HPCs over weeks of in vitro culture.

149 nsion and differentiation of CB CD133(+) HSC/HPC after 8-day culture on a 3D scaffold.

150 tion and differentiation of the CD133(+) HSC/HPC subset from human umbilical CB.

151 tion and differentiation of the CD133(+) HSC/HPC.

152 hematopoietic stem and progenitor cells (HSC/HPC) in ex vivo culture with cytokines and small molecul

153 play a role in the maintenance of normal HSC/HPC cell fates, including survival and self-renewal.

154 ne or small molecule on the expansion of HSC/HPC is a laborious and expensive process.

155 of hematopoietic stem/progenitor cells (HSCs/HPCs).

156 in hematopoietic stem/progenitor cells (HSCs/HPCs).

157 e reactive oxygen species production in HSCs/HPCs that coincides with pronounced defects in function.

158 These effects of LCP4 on MF HSCs/HPCs were associated with inhibition of JAK-STAT activit

159 ablishes the reconstitution capacity of HSCs/HPCs that express activated beta-catenin.

160 ite instability accumulation in normal human HPCs associated with the loss of MLH1 protein expression

161 ut sample treatment, hydroxypropylcellulose (HPC) coated capillary was used to prevent analyte adsorp

162 ) in Gfi-1(-/-) mice did not rescue impaired HPC function or erythropoiesis.

163 hanical stress within the HFR and changes in HPC migratory behaviors.

164 individual roles of HGF/MET and EGF/EGFR in HPC self-renewal and binary cell fate decision.

165 resolution promoter-enhancer interactomes in HPC-7 cells.

166 ially used to investigate SNS involvement in HPC physiology.

167 ctivity of casein kinase 2 (CK2) observed in HPC and in MDSC could be responsible for the phosphoryla

168 task goals change, object representations in HPC can be organized in new ways, resulting in updated c

169 have suggested that HIV genomes detected in HPCs arise from T-cell contamination.

170 Donors with detectable HIV DNA in HPCs received their diagnosis significantly more recentl

171 cell populations phenotypically enriched in HPCs and HSCs show expression of Gata2, there has been n

172 fies with mature virions and is expressed in HPCs upon virus entry although its expression at the tim

173 h a significant allergen-induced increase in HPCs expressing TSLPR, CD127, and ST2.

174 in the establishment of latent infection in HPCs.

175 Interestingly, while DPY30 knockdown in HPCs impaired their differentiation into the myelomonocy

176 the underlying endoderm, we find that MET in HPCs can be accelerated in response to microenvironmenta

177 To test whether MET in HPCs was responsive to purely physical mechanical cues,

178 ogue 1 (MLH1) and MutS homologue 2 (MSH2) in HPCs and colony-forming cell-derived clones (CFCs) from

179 We hypothesized that loss of MMR occurs in HPCs as a process of human aging.

180 Stable knockdown of ACTN4 by shRNA in HPCs significantly reduces dexamethasone-mediated induct

181 These Gata2-independent HPCs exhibit a different functional output and genetic p

182 tories and traction generation of individual HPCs, we find that the onset of MET correlates with a pe

183 xon 4 mRNA is expressed in latently infected HPCs.

184 es (IE1x4) is expressed in latently infected HPCs.

185 The absence of infected HPCs provides strong evidence that the HIV-1 infection f

186 genome-wide data sets, this study integrates HPC-7 data into a genomic resource on par with ENCODE ti

187 ession was significantly reduced in isolated HPCs and liver homogenates from TF(flox/flox)/albumin-Cr

188 atecholamine SNS neurotransmitters, isolated HPCs, and immature ductular 603B cells were initially us

189 r-dependent multipotent progenitor cell line HPC-7 represents a well-recognized cell line model for H

190 of T potential by CD34(++)CD38(lo)lineage(-) HPCs, the later age-dependent production decline of prot

191 Dbh-/- mice lacking catecholamines had low HPC numbers, reconstituted by ISO.

192 he recovery phase to delete Foxl1-Cre-marked HPCs and their descendants.

193 Foxl1-Cre-marked HPCs were required for the development of cholangiocytes

194 t cholangiocytes arose from Foxl1-Cre-marked HPCs.

195 esulted in the depletion of the number of MF HPCs that were JAK2V617F(+) Moreover, the degree of huma

196 itor treatment affects a subpopulation of MF-HPCs, while sparing another HPC subpopulation as well as

197 genates from TF(flox/flox)/albumin-Cre mice (HPC(DeltaTF) mice) compared with TF(flox/flox) mice (con

198 Moreover, HPCs generated from RUNX1a EBs possess >/=9-week repopul

199 Isolated mouse HPCs expressed low levels of TF that clotted factor VII-

200 These results suggest that mouse HPCs constitutively express cell surface TF that mediate

201 hat is associated with defective multipotent HPCs.

202 itical and specific regulator of multipotent HPCs during cytokinesis and thus essential for multiline

203 potential but failed to produce multipotent HPCs and lineage-defined blood cells.

204 e three clinical trials of non-myeloablative HPC transplantation at the National Institutes of Health

205 esulted in canonical Wnt signaling in nearby HPCs, thus maintaining expression of Numb (a cell fate d

206 F receptor in the leishmanicidal activity of HPC.

207 ) reduced binding of a fluorescent analog of HPC, 2) decreased TNF-alpha production, and 3) lower mil

208 This study presents a meta-analysis of HPC burdens in human and wildlife tissues, including OH-

209 From this integrated analysis of HPC polarity and mechanics, we propose that normal heart

210 eration by coordinating the fate decision of HPC and clarifies the molecular mechanisms involved.

211 Because liver protective effects of HPC are negated when the A2B receptor is nonfunctional,

212 In this paper, study of the feasibility of HPC to diminish the counts of pollen is undertaken.

213 stically significant with fewer incidents of HPC exceeding 10 cfu per mL in samples following WSP imp

214 ent on donor HPC TF expression in a model of HPC transplantation.

215 s) and evaluated its role in mouse models of HPC transplantation and acetaminophen (APAP) overdose.

216 supported by molecular dynamic simulation of HPC docking into PAF receptor and by comparison of its l

217 We strongly advise further study of HPC blood levels in the general population, children, an

218 esting intricate links between activation of HPCs and fibrogenesis.

219 Furthermore, allotransplantation of HPCs from APAP+ISO-treated mice to other APAP-injured mi

220 es revealed a temporal bias in commitment of HPCs that recapitulates discrete waves of lineage differ

221 We found that the development of HPCs and erythropoiesis, but not HSC function, was rescu

222 anced cell-cycle entry of HSCs, expansion of HPCs, and defects in long-term engraftment, mimicking th

223 CGD, increased cycling of HSCs, expansion of HPCs, and impaired long-term engraftment capacity were f

224 of RhoA results in a cytokinesis failure of HPCs manifested by an accumulation of multinucleated cel

225 asthmatic responses increased lung homing of HPCs may be orchestrated by TSLP and IL-33 through an IL

226 etal tissues contained the highest levels of HPCs.

227 re to TSLP and IL-33 primed the migration of HPCs to a potent progenitor cell chemoattractant, stroma

228 lly, GR and ACTN4 interact in the nucleus of HPCs.

229 ches, and become activated when the pools of HPCs decrease.

230 dition to regeneration, the proliferation of HPCs also determines the appearance of a ductular reacti

231 only a modest reduction in the proportion of HPCs that were JAK2V617F(+) or had a chromosomal abnorma

232 gesting that CD1d is a negative regulator of HPCs.

233 l an even greater toxicological relevance of HPCs.

234 collaborate to increase the self-renewal of HPCs through activation of the extracellular signal-regu

235 mmunications direct the cellular response of HPCs to fibrogenic stimuli, but also identify novel pote

236 The numbers and cycling status of HPCs in the BM and spleen of different strains of cd1d(-

237 c zebrafish model, we identified a subset of HPCs, responsive to Notch signaling, that retains its ca

238 Colony formation by immature subsets of HPCs was greatly enhanced when normal, but not cd1d(-/-)

239 Treatment of HPCs with an inhibitory TF antibody or a cell-impermeabl

240 atenin pathway (CWP) in the action of ISO on HPC expansion and comparison of ISO with the current sta

241 the functional effects of these cytokines on HPCs.

242 populations and characterized the effect on HPCs.

243 ctures (local desktop, cloud environments or HPC clusters).

244 he other hand, heterogeneous photocatalysis (HPC) arose as a promising technology for reducing the le

245 ptor (GR) in the nucleus of human podocytes (HPCs), a key cell type in the glomerulus critical for ki

246 We show that while posterior HPC and anterior MPFC maintain distinct memories for ind

247 DPY30 promotes HPC proliferation by directly regulating the expression

248 rthermore, we demonstrate that RBPJ promotes HPC differentiation toward cholangiocytes in vitro and b

249 In control mice, AILI raised HPC numbers, further increased by ISO, with attenuation

250 ytokine signaling in mice with X-CGD reduced HPC numbers but had only minor effects on the repopulati

251 nd/or protein inputs (locally or on a remote HPC cluster), predict gene structures and gene structure

252 ata analysis workflows by integrating remote HPC resources and efficient data management with ease of

253 s bed, crib rail, and play area and reported HPC over 1 and 6 months.

254 to explore the relationship between reported HPC and peanut protein levels in an infant's home enviro

255 cellular outcomes of these Notch-responsive HPCs in hepatocyte regeneration.

256 supports B-lymphoid progenitors and retains HPCs in the bone marrow, and that expression of CXCL12 f

257 classic pleuropulmonary SFT and deep-seated HPC are separate entities that share common features but

258 mpers competition for CPU time in the shared HPC environment, and jobs submitted during quiet periods

259 ikely initiating molecular events driving SN-HPC tumorigenesis, which places SN-HPC among the growing

260 Sinonasal hemangiopericytoma (SN-HPC) is an uncommon, site-specific, low-grade mesenchyma

261 myoid cell neoplasms were also absent in SN-HPC; thus, the molecular pathogenesis of SN-HPCs remaine

262 riving SN-HPC tumorigenesis, which places SN-HPC among the growing family of beta-catenin-driven mese

263 -HPC; thus, the molecular pathogenesis of SN-HPCs remained unknown.

264 f soft tissue and sinonasal tract origin, SN-HPCs were recently shown to lack recurrent NAB2-STAT6 fu

265 an index case, we analyzed a total of six SN-HPCs for mutations within the amino-terminal region of t

266 ar staining of the tumor cells in all six SN-HPCs.

267 hanistic studies examined effects of non-SNS HPC expansion on AILI, involvement of the canonical Wnt/

268 CD133-sorted HPCs and CD133-depleted bone marrow cells were purified

269 Specifically, HPCs isolated at later time points showed reduced capaci

270 rified human collagen were found to suppress HPC differentiation and proliferation.

271 CL), and RBPMS is not expressed in syntaxin (HPC-1)-immunoreactive cells in the inner nuclear layer (

272 When rats learned one task, HPC and DSL selectively supported spatial navigation and

273 However, when rats learned both tasks, HPC and DSL additionally supported the behavior incongru

274 We have determined that HPC-II exists in an iron(IV) hydroxide state up to pH 11

275 s to mortar specimens with the evidence that HPC is able to reduce the amount of pollen grains.

276 MPFC) generalizes, other accounts posit that HPC can also integrate related memories.

277 The results show that HPC (heterotrophic plate counts), representing microbiol

278 These data indicate for the first time that HPCs induce T-cell anergy, a unique characteristic of iP

279 By contrast, the HPC showed little evidence of learning-related changes i

280 Exposure to donor antigens from the HPC graft and new red cell antibodies induced by transfu

281 unknown which cell type(s) or regions of the HPC might be essential for synaptic consolidation.

282 that poor delivery of signals 1 and 2 by the HPCs mediated T-cell anergy.

283 Concomitantly, the HPCs show a drastically increased death associated with

284 ylation and ethylation, respectively, of the HPCs in the mussel extracts.

285 cytokinesis, and programmed necrosis of the HPCs, and loss of RhoA results in a cytokinesis failure

286 litates the process of producing therapeutic HPCs from hPSCs.

287 These HPCs poorly express major histocompatibility complex (MH

288 taR signalling results in a defect in thymic HPC homing, suggesting the feedback regulation of thymic

289 posure to peanut is most likely to be due to HPC.

290 e the contribution of portal inflammation to HPC differentiation and NAFLD pathogenesis.

291 after errors, was driven primarily by PFC to HPC directional influences and decreased with learning.

292 , which develop within the YS in parallel to HPCs but can be specified in the E8.5 Runx1-null embryo

293 ion was dramatically reduced in APAP-treated HPC(DeltaTF) mice compared with APAP-treated control mic

294 edian age, 47 years) and represented typical HPCs from deep soft tissue with a more aggressive phenot

295 eceptor-deficient macrophages and mice under HPC treatment.

296 rgic neurons in either the dorsal or ventral HPC.

297 arallel with behavioral performance, whereas HPC neurons reflected feedback about whether trial-and-e

298 sociative learning may occur in PFC, whereas HPC may guide neocortical plasticity by signaling succes

299 ng toward HSC fate but not in all cells with HPC fate, have implications for current reprogramming st

300 roles in the behavior of HSCs compared with HPCs and is essential for the maintenance of adult hemat