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1 activated in each focus, consistent with its monoclonality.
2 -cell subpopulations revealed no evidence of monoclonality.
3 onal mechanism by which T cells can maintain monoclonality.
4 ents that can ensure thymocyte expansion and monoclonality.
5 elped to understand the mechanism leading to monoclonality.
6  colitis-associated neoplasms to show lesion monoclonality.
7 fied in all crypts across the lesion showing monoclonality.
8 blood cell counts histology, T-cell receptor monoclonality, and host transferability.
9 onoclonal cell type in plaque and learn when monoclonality arises, we studied X chromosome inactivati
10                              One solution is monoclonality, but this option still leaves room for exp
11                           We also noted that monoclonality characterized AH lesions in younger as com
12                                              Monoclonality could arise by somatic mutation, selection
13                                              Monoclonality could arise either by 1) proliferation of
14               Recently, technology to assess monoclonality has allowed the distinction between cellul
15                                  We detected monoclonality in 20/21 (95%) T-cell lymphoma cases, wher
16                        It is time-consuming, monoclonality is not guaranteed, and the number of clone
17 n patches raises the possibility that plaque monoclonality may arise by expanding a pre-existing clon
18      PCR of D/J IgH gene segments proved the monoclonality of infiltrating B cells, which strongly co
19 antibody-producing hybridoma clones, ensured monoclonality of sorted cells, and reduced development t
20 unoglobulin gene rearrangements document the monoclonality of the tumor.
21 nant PTLD, as assessed by histopathology and monoclonality of the tumor.
22 earrangement of the Ig heavy chain indicated monoclonality or oligoclonality in all lymphomas, some o
23 Analysis of Ig gene rearrangements indicates monoclonality or oligoclonality in these populations, su
24 ed clone survival while lengthening times to monoclonality, suggesting that Tgfbeta signaling control
25 ghter colonies by serial dilution, verifying monoclonality using the Humara assay.
26                                              Monoclonality was demonstrated by immunoglobulin light-c
27                                              Monoclonality was observed in a few infiltrates in the p
28                                              Monoclonality was verified by the identification of a si

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