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1 -alpha partially and transiently rescued the myeloid and lymphoid abnormalities found in NHD13(+) Tg
2 s are accumulated to the same degree in both myeloid and lymphoid acute leukemia cells, paralleling t
3 ermediates correlated with the levels of the myeloid- and lymphoid-associated transcription factors m
6 igher in treated pups than in controls; both myeloid and lymphoid cell chimerism increased because of
8 These results show that FL can affect both myeloid and lymphoid cell lineages in vivo and further d
9 in long-term allogeneic repopulation of both myeloid and lymphoid cell lineages were observed in reci
10 -sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph
11 ly activated in both transiently transfected myeloid and lymphoid cell lines by the 80-bp gene fragme
12 the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell ly
13 ctin ligands on granulocytes, monocytes, and myeloid and lymphoid cell lines, and not on peripheral b
17 tect clonal cytogenetic markers in different myeloid and lymphoid cell types of the peripheral blood
18 autophagy contributes to differentiation of myeloid and lymphoid cell types, coordinates multicellul
21 ession, thereby providing protection to both myeloid and lymphoid cells against L. monocytogenes-indu
22 es with Imatinib against BCR/ABL-transformed myeloid and lymphoid cells and increases survival in a m
23 ude that CD45 is regulated differentially in myeloid and lymphoid cells and that sequences critical t
26 etected constitutively in both primary human myeloid and lymphoid cells by Northern blot hybridizatio
27 ctional data, EMSA demonstrated that in both myeloid and lymphoid cells C/EBPbeta binds specifically
28 monstrated significantly higher infiltrating myeloid and lymphoid cells compared with GBM, MED, or NT
29 lity to shape the transcriptome of activated myeloid and lymphoid cells controlling diverse biologica
31 to the same cellular chromosomal DNA site in myeloid and lymphoid cells descended from a common HSC p
32 tat5 in maintaining a normal balance between myeloid and lymphoid cells during hematopoiesis, and we
34 gainst wild-type cells in the development of myeloid and lymphoid cells in in vivo reconstitution ass
35 er 21 to 413 days, percentages of donor type myeloid and lymphoid cells in recipient blood were measu
36 reased L. monocytogenes-induced apoptosis of myeloid and lymphoid cells in the spleen that are requir
37 dicating that FcgammaRIIb expression on both myeloid and lymphoid cells is regulated by the naturally
39 y, PU.1(-/-) mice that are unable to develop myeloid and lymphoid cells received bone marrow transpla
40 thro-myeloid cells and pre-B cells, and both myeloid and lymphoid cells seem to be derived from the C
41 Transient transfection experiments in both myeloid and lymphoid cells showed an increase in CCR5 pr
42 higher level of chimerism and generated both myeloid and lymphoid cells that contained molecular or c
43 microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeosta
44 ilized CD34(+) cells with Neo(R) gene marked myeloid and lymphoid cells up to 32 months after transpl
45 rd distinct HLA type and donor and recipient myeloid and lymphoid cells were identified after 8 to 10
46 have a potential to differentiate in vivo to myeloid and lymphoid cells, and (4) have a high prolifer
48 as been shown in a wide range of circulating myeloid and lymphoid cells, but their role in normal hem
49 lement receptors (CRs), expressed notably on myeloid and lymphoid cells, play an essential function i
51 ool of NF-kappaB transcriptional activity in myeloid and lymphoid cells, which is believed to be seco
70 highly proliferating and serially replatable myeloid and lymphoid colony-forming cultures could be es
72 tential hematopoietic stem cells into common myeloid- and lymphoid-committed progenitors establishes
74 In addition, evidence for the existence of myeloid and lymphoid DC lineages and their different fun
75 (i) reduces the numbers of Langerhans cells, myeloid and lymphoid DC, and activated CD4(+) T cells in
77 ombinant Adv readily targets transduction of myeloid and lymphoid DCs in the draining popliteal lymph
78 ch resulted in depletion of 88-95% of mature myeloid and lymphoid DCs, with less depletion (75%) of p
80 ha transgenic reporter was activated in both myeloid- and lymphoid-derived PDCs at a level comparable
82 is known about the function of FOG-1 during myeloid and lymphoid development or how FOG-1 expression
88 controlling hematopoietic stem cell biology, myeloid and lymphoid differentiation and lymphocyte effe
91 now know that Gfi1 is primarily important in myeloid and lymphoid differentiation, whereas Gfi1b is c
95 Our data indicate that Cbfb is required for myeloid and lymphoid differentiation; but does not play
97 d infiltrating hematopoietic cells including myeloid and lymphoid elements that impact tumor growth,
98 onal maturation of promyelocytes (erythroid, myeloid, and lymphoid [EML]-derived promyelocytes) deriv
99 tment because recipients displayed increased myeloid and lymphoid engraftment and because sunitinib-t
100 bust (>80% human chimerism) and reproducible myeloid and lymphoid engraftment, with T cells arising 1
101 s, and sunitinib enhanced marrow, peripheral myeloid, and lymphoid engraftment after BMT in Rag1(-/-)
102 well as hematopoietic genes; MPPs coexpress myeloid and lymphoid genes; CMPs coexpress myeloerythroi
103 essor that plays a critical role during both myeloid and lymphoid haematopoietic lineage commitment.
106 econdary and tertiary recipients, as well as myeloid and lymphoid hematopoietic progenitor subsets an
108 d temporal and spatial relationships between myeloid and lymphoid immune responses in wild-type C57BL
110 umor antigen that is aberrantly expressed in myeloid and lymphoid leukemia and in this issue of Blood
111 granulate when challenged with primary acute myeloid and lymphoid leukemia blasts; and (5) Vdelta2 ce
113 hnique to compare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at l
114 echanism by which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate t
115 mosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner gen
119 plays distinct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, vali
120 rapid death of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytot
123 epitope is presented on the surface of both myeloid and lymphoid leukemic cells from male HLA-B*2705
126 mportance of the Bcr/Abl-Grb2 interaction to myeloid and lymphoid leukemogenesis in vivo is unclear.
129 quent genetic changes in infant leukemias of myeloid and lymphoid lineage and in treatment-induced se
131 PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutel
132 miR-17-92-overexpressing mice are capable of myeloid and lymphoid lineage differentiation, and recapi
134 tern in that it is expressed on cells of the myeloid and lymphoid lineage, suggesting that it plays a
135 lineage short-term progenitors reconstituted myeloid and lymphoid lineages at 1 month but were suppla
136 he hematopoietic flow from stem cells toward myeloid and lymphoid lineages during development and adu
137 of cytokines to induce differentiation into myeloid and lymphoid lineages following AAV infection, t
138 ematopoietic development with segregation of myeloid and lymphoid lineages from multipotent progenito
139 ent), compared with negligible expression in myeloid and lymphoid lineages in blood, BM, spleen, and
140 lta/Delta) HSCs contributed normally to both myeloid and lymphoid lineages in both primary and second
143 tained these high transduction levels in all myeloid and lymphoid lineages, including early progenito
144 characterized by a maturation arrest in the myeloid and lymphoid lineages, leading to early onset, r
145 of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone m
146 ntiate into more specific progenitors of the myeloid and lymphoid lineages, ultimately leading to dif
161 tment, self-renewal and differentiation into myeloid and lymphoid lineages; however, the proper diffe
162 gests that the segregation of the erythroid, myeloid, and lymphoid lineages may not always be an earl
163 s confer a graft-versus-malignancy effect in myeloid and lymphoid malignancies and in metastatic rena
164 elapse rates, whereas patients with advanced myeloid and lymphoid malignancies had high relapse rates
166 igning improved strategies for treating both myeloid and lymphoid malignancies in this high-risk popu
167 neral terms, we review specific use cases in myeloid and lymphoid malignancies to highlight the utili
168 , we review recent major genetic advances in myeloid and lymphoid malignancies, the impact of these f
172 These data suggest that Delta-1 can enhance myeloid and lymphoid marrow-repopulating ability and pro
175 cation recognizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abn
176 sive molecular disease detection in selected myeloid and lymphoid neoplasms, with a focus on the curr
177 y developed hematologic malignancies of both myeloid and lymphoid origin with myeloid malignancies di
178 uently rearranged in human leukemias of both myeloid and lymphoid origin, encodes a member of the Ets
180 1a regulates hematopoietic stem cells (HSC), myeloid and lymphoid populations, while its paralog, Gfi
181 tentiality is conserved until segregation of myeloid and lymphoid potential has recently been challen
184 gen expression leads to reduced apoptosis of myeloid and lymphoid progenitor cells, and a propensity
185 gand to primitive hematopoietic cells and to myeloid and lymphoid progenitor cells, in contrast to th
187 h the MegE potential of downstream committed myeloid and lymphoid progenitors and with their ability
189 asts alters the differentiation potential of myeloid and lymphoid progenitors leading to development
190 NA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-X(L) and Bcl-2
191 differential capacity to generate committed myeloid and lymphoid progenitors, and diminished lymphoi
192 ved lineage-specific DNA methylation between myeloid and lymphoid progenitors, characterized immature
196 ineage precursors were bipotential, yielding myeloid and lymphoid progeny, whereas most that were c-k
197 ings implicate MyD88 as the key initiator of myeloid and lymphoid proliferation in HLH, and suggest t
204 rn blood, liver, and spleen, were assayed as myeloid and lymphoid repopulating abilities relative to
206 s support a role for relative proportions of myeloid and lymphoid transcripts in tuberculosis outcome
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