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N Takagi

Publications and source records attributed to N Takagi.

At least 289 records · Page 16Linked to original sources
PubMed1982

Sensitive high-performance liquid chromatographic method for prostaglandins using a fluorescence reagent, 4-bromomethyl-7-acetoxycoumarin.

High-performance liquid chromatography of prostaglandins is developed in which a fluorescence reagent, 4-bromomethyl-7-acetoxycoumarin is used to perform the high-sensitivity detection. The reagent reacts with prostaglandins and related compounds to form the ester derivatives, which are separated using a reversed-phase system. Each labeled compound eluted from the column is successively hydrolyzed to the fluorescent coumarin derivative, and this fluorophore is introduced into a flow-through fluorometer. Prostaglandins can be determined in the range of at least 1 nmol to 5 pmol, and the detection limit is about 10 fmol. This system is applied to the analysis of prostaglandins in human seminal fluid.

Chromatography, High Pressure Liquid↗
PubMed1982

Regional and temporal changes in the pattern of X-chromosome replication during the early post-implantation development of the female mouse.

We have made a detailed study of the X-chromosome replication pattern during the period when X-inactivation is occurring in the mouse embryo. Our observations show unequivocal regionalization of the embryo with respect to the temporal X-chromosome. The switch from isocyclic to allocyclic replication occurs in the embryonic ectoderm at approximately 6 days of development and is random with respect to parental origin of the X-chromosome. In the extra-embryonic tissues, however, the switch to allocyclic replication has apparently occurred prior to 5.3 days of development and almost exclusively involves the paternally-derived X-chromosome. Since these findings are consistent with results obtained in biochemical studies of X-chromosome activity in female embryos, we conclude that there is a close temporal relationship between the cytogenetic and biochemical manifestations of the X-inactivation process. In addition, we have observed a pattern of early paternal X-chromosome replication, transitory in some cases, that is unique to extra-embryonic tissues. These results suggest that there may be some differences in the mechanism by which X-inactivation occurs in the extra-embryonic tissues as compared with the embryonic ectoderm.

Animals↗
PubMed1982

Influence of strain difference on the karyotypic changes in N-nitroso-N-butylurea--induced mouse lymphomas.

Karyotypes were analyzed in 44 cases of mouse lymphomas induced by continuous oral administration of N-nitroso-N-butylurea (NBU): 14 cases of C57BL/6JKok, 6 from LT/sv, 5 from MT/Hok, 2 from (AKR/MsHok x T1Ct)F1, 2 from (AKR/MsHok x CBA/H-T6Hok)F1, and 15 from the first backcross generation of (CBA/Hok x CBA/H-T6Hok)F1 to CBA/Hok. Thirty-six were thymic lymphomas (TLs) and the remaining 8 nonthymic lymphomas (NTLs). No chromosome abnormality was found in 8 NTLs, whereas modal cells were karyotypically changed in 13 TLs. Unlike the situation in NTLs, chromosomally abnormal cells were always present in the remaining 23 TL cases in which modal cells showed no apparent deviation from the constitutional host karyotype. A total of 31 independent karyotypic changes were identified in 26 cytogenetically abnormal major clones from 19 TLs. Although trisomy 15 was the most frequent karyotypic change, being present in 9 TLs, its incidence was substantially low compared with experimentally induced murine TLs so far reported. Furthermore, 6 of the 9 trisomy 15 clones clustered to (CBA x T6)F1 x CBA. Thus, it seems probable that the genetic background of the host animals has a profound influence upon the frequency of trisomy 15 in TLs.

Animals↗
PubMed1981

Effect of fatty acids and monoglycerides on permeability of lipid bilayer.

The effect of fatty acids and monoglycerides on barrier properties of liposomal membranes prepared from egg phosphatidylcholine was investigated. The incorporation of these lipids as liposomal membrane components induced the alteration of the permeability to less permeable liposomally entrapped drugs, sulfanilic acid and procainamide ethobromide (PAEB). Monoolein caused greatly increased permeability of both drugs and unsaturated fatty acids markedly enhanced the release rate of PAEB, while saturated fatty acids caused a small increase in the release rate. Electron spin resonance (ESR) investigation with 5-nitroxide stearic acid showed that fatty acids disordered the hydrophobic region of the lipid bilayer and the disordering effect of unsaturated fatty acids was greater than that of saturated ones. It was demonstrated that the incorporated fatty acids and monoglycerides interacted with the polar region of the membranes by ESR study with cholestane label and 1H-NMR study. These results indicated that the increase in the membrane permeability caused by fatty acids and monoglycerides associated with the disorder in the membranes' interior and the interaction of the incorporated lipid with the polar head group of phospholipid.

Electron Spin Resonance Spectroscopy↗
PubMed1981

Karyotypic changes in serial transfers of leukemic cells of AKR mouse.

Four spontaneous AKR leukemias (T67, T68, T70, and T74) with a modal chromosome number of 40 were transplanted serially to syngeneic mice in order to assess the significance of trisomy 15 and other karyotypic changes in the development of leukemia. In T67 and T70, the chromosomally normal cell disappeared completely or decreased considerably in frequency at the first passage in vivo. The karyotype of the modal cells changed continuously in T67 during transplantation, conserving trisomy 17, while the pseudodiploid cells with trisomy 15 and monosomy X were stable from the first to the seventh transplant generations of T70. In contrast to these results, the primary cell population of T68 and T74 with modal cells having a normal karyotype remained essentially unchanged throughout 7 or 15 transplant generations, despite the occurrence of aneuploidy, which included trisomy 15 or trisomy 17 in low frequencies. It is thus evident that the diploid cell is compatible with being leukemic and that neither trisomy 15 nor trisomy 17 is necessary for the initiation and progression of AKR leukemia, although the former was detected in three of four primary leukemias used for this experiment and in all four during transplantation.

Aneuploidy↗
PubMed1980

Primary and secondary nonrandom X chromosome inactivation in early female mouse embryos carrying Searle's translocation T(X; 16)16H.

By means of a cytological technique involving 5-bromodeoxyuridine, acridine orange, and fluorescence microscopy, the asynchronously replicating, hence genetically inactivated, X chromosome was identified in 6- to 8-day embryos from female mice heterozygous for Searle's translocation T(X;16)16H (abbreviated as T16H) mated with either karyotypically normal males or males carrying Cattanach's translocation T(X;7)1Ct in order to analyse the way in which the total inactivation of the normal X is achieved in adult T16H heterozygotes. Embryos examined included 9 Xn/X(7);16/16, 3 X 16/Xn;16x/16, 12 X16/X(7); 16x/16, 5 X16/Xn;16/16, 8 X16/X(7); 16/16 and 2 Xn/Y; 16x/16/16. In these notations X16, 16x, X(7) and Xn represent Searle's X with the centromeric segment of the X, Searle's X with the centomeric segment of chromosome 16, Cattanach's X with insertion of a chromosome 7 segment, and normal X, respectively. The X(7) exerted no apparent effect upon embryonic development up to the 8th day of gestation and X chromosome inactivation. -- The asynchronously replicating X was the Xn in X16/Xn;16x/16 and X(7) in X16/X(7);16x/16 embryos except a small number of cells on day 6 (13/493) and on day 7 (1/886) in which almost the entire 16x replicated asynchronously. The X16, on the other hand, never showed replication asynchrony. That the X16 is indeed unable to become inactivated was indicated by the observation that the X16 as well as Xn or X(7) did not replicate asynchronously in Xn/X16;16/16 and X16/X(7);16/16 embryos X16-inactive cell lines, if occurring, should have been genetically less unbalanced than any other cell line in such embryos. It is highly likely therefore that the ultimate inactivation pattern in T16H heterozygotes has been accomplished by (1) the inability of the X16 to become inactive; (2) inactivation in favor of the Xn; and (3) rapid elimination of 16x-inactive cells. Severe growth retardatin and early death of X16/Xn;16/16 and X16/X(7);16/16 embryos having no inactive X suggested that functional X disomy is detrimental to embryogenesis. These embryos further indicated that the concurrence of at least two X chromosomal loci separated by the T16H breakpoint is necessary for the homologous X chromosome becoming inactivated.

Animals↗
PubMed1978

Androgenesis as a cause of hydatidiform mole.

Q-band chromosome studies were done in 3 molar conceptuses and their parents, with special attention to six pairs of chromosomes (No. 3, 13--15, 21, and 22) in which polymorphic variants occur frequently. Those six pairs of chromosomes were uniformly homomorphic in moles, whereas at least one of them was heteromorphic in both paternal and maternal cells. Closer analyses provided evidence strongly suggesting that the moles inherited two morphologically identical haploid sets from the father and none from the mother. Thus androgenesis seemed causally related to pathogenesis of complete hydatidiform moles.

Adult↗