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Biomedical subjects

N Wake

Publications and source records attributed to N Wake.

102 records · Page 6Linked to original sources

Specific cytogenetic changes in ovarian cancer involving chromosomes 6 and 14.

Cytogenetic studies were performed in 12 papillary serous adenocarcinomas of the ovary. Of the more than 19 clonal structural chromosome abnormalities observed in these cancers, 6q- and 14q+ were found to be the most frequent. Both markers coexisted in the cells of eight cases; in the other four cases, either a 6q- or 14q+ was present. In at least six cases, the additional segment on the long arm of chromosome 14 appeared to originate, on the basis of the chromosomal quantity and fluorescence pattern, from the missing part of chromosome 6. This suggested that the 6q- and 14q+ markers had arisen as a result of a reciprocal translocation at Bands q21 and q24, respectively, i.e., t(6;14)(q21;q24). However, it is uncertain in the remaining six cases whether an identical type of translocation was responsible for the formation of the markers. Thus, abnormalities involving chromosomes 6 and 14 seem to be specifically associated with papillary serous adenocarcinoma of the ovary.

Adenocarcinoma, Papillary↗

Human lymphocyte antigen expression in hydatidiform mole: androgenesis following fertilization by a haploid sperm.

Thirteen hydatidiform moles (complete moles) and lymphocytes from each parent were analyzed for human lymphocyte antigen (HLA-A and HLA-B specificities). It was demonstrated that molar tissues expressed homozygous A and B specificities which were identical to those of the father and not those of the mother. It was concluded that androgenesis was responsible for the pathogenesis of most cases of complete mole. There was homozygous expression of paternal HLA specificities which were heterozygous for A locus and/or B locus in eight of nine cases of complete mole. This suggests that these hydatidiform moles developed from an egg which was fertilized by a haploid sperm which duplicated its own chromosomes after meiosis.

Adult↗

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↗

Cytologic evidence for preferential inactivation of the paternally derived X chromosome in XX mouse blastocysts.

A total of 941 mouse blastocysts obtained from two types of crosses in which one of parents carried Cattanach's X/autosome translocation was studied cytogenetically by quinacrine mustard fluorescence. The rearranged X (Xt) and the normal X (Xh) were distinguished by size. Karyotype analysis was successful in 721 embryos, of which 205 were heterozygous for Cattanach's translocation. A single heterochromatic and brightly fluorescent X chromosome was identified in 154 metaphase spreads from 89 blastocysts consisting of 32--96 cells. The paternally derived X chromosome (Xp) was heterochromatic in 87% and 88% of the informative cells from the crosses XnXn x XtY and XtXn x XnY, respectively. This preferential choice of Xp at the blastocyst stage might have an important bearing upon the preponderance of cells with an inactive Xp in the chorion and yolk-sac splanchnopleure.

Animals↗

New neonatal problems of blood coagulation and fibrinolysis. I. The change of plasmin inhibitor levels in the newborn infant.

"Hemorrhage in the newborn" has long been recognized as merely a result of vitamin K deficiency. However, it is also recognized that fibrinolysis, especially the correlation between the plasminogen-activator and plasmin-inhibitors, play an important role in this disease during the neonatal period. With this in mind, we compared thromboelastograms (TEG) from samples with and without urokinase (plasminogen-activator). In 13 out of 15 newborn infant blood-samples (prior to and after addition of urokinase) the thromboelastogram showed the pattern of a consumption coagulopathy. The change in the concentration of plasmin-inhibitor during the neonatal period was also measured using alpha2-macroglobulin, alpha1-antitrypsin and antithrombin III with M-partigen-plates. The value of alpha2-macroglobulin showed normal adult levels but the value of alpha1-antitrypsin and antithrombin III did not even reach half of the adult level. During the newborn period, the plasmin-inhibitor shows a remarkable lowering tendency and it may be surmised that with such a lowering tendency plasmin-inhibitor may constitute an exceptionally large handicap when the activator is working. This is especially true in the case of lung hemorrhage since the activator arises from a severe pathological state in the lungs and in addition because this is complicated by the lowering of plasmin-inhibitor. These results indicate that the low level of plasmin-inhibitors work synergistically with the high value of activator. The low level of antithrombin III could be the reason for coagulation disorders such as disseminated intravascular coagulation, (DIC).

Antithrombins↗

New neonatal problems of blood coagulation and fibrinolysis. II. Thromboplastic effect of amniotic fluid and its relation to lung maturity.

Pulmonary hyaline membrane disease in newborn infants is considered an abnormality in the alveolar lining layer. Quantitative analysis of this surfactant is necessary for the intrauterine diagnosis of lung maturity of the fetus. The presence of surfactant in amniotic fluid has been demonstrated by the shaking method [1]. But it is also well known that amniotic fluid has a thromboplastic effect [3,6]. In order to compare the correlation between the shaking method and the thromboplastic effect of the amniotic fluid, recalcification time and partial thromboplastin time were measured with and without amniotic fluid using an aggregation-meter. In each of 15 cases, a shortening of these times was recorded after the addition of amniotic fluid after the 30th week of pregnancy. In all cases the addition of amniotic fluid resulting in shortening these times. Surfactant seems to have enhancing effect on the coagulation. These results demonstrate the presence of surfactant in amniotic fluid in agreement with the results of the shaking method. Although these methods are of limited utility as quantitative assays for surfactant, they are of sufficient accuracy and of great value for clinical diagnosis.

Amniotic Fluid↗

The propensity to malignancy of dispermic heterozygous moles.

Complete hydatidiform moles may originate from either the fertilization of an empty egg by a haploid sperm followed by duplication (producing a monospermic, homozygous mole) or the fertilization of such an egg by two haploid sperms (producing a dispermic, heterozygous mole). This difference in the mechanism leading to the formation of complete moles raises the question of whether the risk of subsequent malignancy is influenced by the zygosity of the mole. We have compared the incidence of postmolar sequelae in patients with homozygous and heterozygous moles. Using chromosomal heteromorphisms, human lymphocyte antigen (HLA) and phosphoglucuromutase 1 (PGM1) polymorphisms, we established the androgenetic origin of complete mole in 84 of 91 cases. Homozygosity was confirmed in 51 moles, and we found ten heterozygous moles. Five of ten patients with heterozygous moles developed postmolar trophoblastic disease, whereas only two of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional five patients showed signs of degenerating residual trophoblasts). The XY sex chromosome constitution of the two in vitro choriocarcinoma cell lines examined here provides further evidence of the propensity to malignancy of heterozygous moles.

Choriocarcinoma↗

Significance of postoperative irradiation for stage III lung cancer.

The significance of postoperative irradiation for stage III lung cancer was analyzed in 30 patients. Radiation was given to 15 of the patients and the remaining 15 did not receive any radiation therapy following surgical intervention. A total dose of 40 to 70 Gy was given to the radiation group with a fraction dose of 2 Gy five times a week using cobalt 60 gamma-ray or linac 10 MV X-ray. There was no significant difference of survival time between these two groups. However, in analyzing modes of operation, radiation seemed to improve the survival rate in patients who underwent curative or relatively curative operations (P = 0.1), while the patients who underwent non-curative operations did not receive any benefit from the postoperative irradiation. Some reasons for the ineffectiveness in cases of non-curative operation are discussed.

Adenocarcinoma↗