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1 trations of hCG 6 months after evacuation of hydatidiform mole.
2 concentrations 6 months after evacuation of hydatidiform mole.
3 orms are derived from the precursor lesions, hydatidiform moles.
4 hat these tumors are not related to complete hydatidiform moles.
5 ostic methods for accurate classification of hydatidiform moles.
6 nal-triploidy and the development of partial hydatidiform moles.
7 , NLRP7 and NLRP2, cause familial biparental hydatidiform mole and multilocus imprinting disturbance,
8 e genome-wide restriction maps of a complete hydatidiform mole and three lymphoblast-derived cell lin
9 iform moles (purely androgenetic in complete hydatidiform moles and diandric triploid in partial hyda
10 emalignant disorders of complete and partial hydatidiform mole, and the malignant disorders of invasi
12 haliana, Drosophila melanogaster and a human hydatidiform mole cell line (CHM1) from SMRT sequencing.
13 sed 77 twin pregnancies, comprising complete hydatidiform mole (CHM) and healthy co-twin, to ascertai
18 diagnosis, routine morphologic assessment of hydatidiform moles continues to suffer from interobserve
25 development of the conceptus into a complete hydatidiform mole in which extraembryonic trophoblastic
26 istinguishable from an androgenetic complete hydatidiform mole, in which abnormal extra-embryonic tis
27 eotide polymorphism markers in most complete hydatidiform moles indicating that these tumors are not
29 iform moles and diandric triploid in partial hydatidiform moles) is a fundamental genetic event leadi
31 niparental tissues of germline origin, i.e., hydatidiform moles (paternal origin) and complete ovaria
33 sentation of the paternal genome in sporadic hydatidiform moles (purely androgenetic in complete hyda
35 esent evidence of homozygosity of a complete hydatidiform mole using 20 diallelic markers distributed
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