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Biomedical subjects

S Honma

Publications and source records attributed to S Honma.

At least 217 records · Page 12Linked to original sources

[Immunohistologic characterization of lymphoid cells infiltrating dysgerminoma of the ovary].

Dysgerminoma of the ovary is composed of cells that resemble primordial germ cells morphologically and connective tissue stroma with lymphoid cell infiltration, the degree of which has been discussed in correlation with the prognosis. In order to characterize the lymphoid cells histochemically, a sensitive immunoperoxidase technique was applied on serial tumor tissue sections. Monoclonal antibodies used in this study were anti-HLA-ABC, anti-HLA-DR, anti-HLe-1 (leukocytes), anti-Leu-1,-4(pan T cells), anti-Leu-2a (killer/suppressor T cells), anti-Leu-3a (helper/inducer T cells), anti-Leu-12,-14 (B cells), anti-Leu-M3 (monocytes/macrophages) and OKT-10 (myeloid and lymphoid precursors, thymocytes, activated T and B cells). Lymphoid cells identified morphologically on sections stained with hematoxylin-eosin were HLe-1 positive, and were therefore thought to originate in bone marrow. Most of them were also positive for Leu-1,-4, and they were composed of nearly equal numbers of Leu-2a positive cells and Leu-3a positive cells. Furthermore, the majority of the lymphoid cells were HLA-DR positive, consisting of a large number of OKT-10 positive cells and a small number of Leu-12,-14 positive cells and Leu-M3 positive cells which were mainly found in connective stroma encapsulating tumor tissue. Taken together, the lymphoid cells in the connective stroma were considered to be activated T cells. Tumor cells themselves lacked reactivity with anti-HLA-ABC or anti-HLA-DR, while lymphoid cells and connective stroma were HLA-ABC positive.

Dysgerminoma↗

[Establishment and characterization of two histologically differentiated human uterine endometrial carcinoma cell lines from the same patient--a correlation between grade of morphological differentiation and HLA antigens].

The cell lines designated KKNS-I and KKNS-II were derived from the metastatic lesions in the lymph nodes of endometrial adenocarcinoma. The KKNS-I cells were small spindle or polygonal in shape and showed a jig-saw puzzle-like arrangement with a tendency to pile up. The KKNS-II cells were polygonal in shape, and larger than the KKNS-I. They appeared to be arranged like a pavement. The modal number of the two cell lines was 46 without marker chromosome. Calculating from the growth curves, the doubling times for the KKNS-I and the KKNS-II cells were 35 hours and 60 hours, respectively. The tumors obtained from the nude mouse inoculated with the KKNS-I and the KKNS-II were a poorly differentiated endometrial adenocarcinoma and a well differentiated endometrial adenocarcinoma in histology, respectively. The volume of estrogen receptor and progesterone receptor in the KKNS-II were more than that in the KKNS-I cells. HLA-ABC antigens were detected in both the cells, but HLA-DR antigens were detected in only some populations of KKNS-II cells. These data suggest a relationship between the HLA-DR antigens and the degree of differentiation of the endometrial adenocarcinoma.

Adenocarcinoma↗

Defective enzyme causes lecithin-cholesterol acyltransferase deficiency in a Japanese kindred.

Lecithin-cholesterol acyltransferase mass levels and activity and apolipoproteins A-I, A-II, B and D were measured in a Japanese family who have a familial lecithin-cholesterol acyltransferase deficiency. This analysis was performed to gain insight into the molecular basis of the enzyme deficiency and to compare findings in this family with other families with familial lecithin-cholesterol acyltransferase deficiency. The mass of the enzyme in plasma was determined by a sensitive double antibody radioimmunoassay, and enzyme activity was measured by using a common synthetic substrate comprised of phosphatidylcholine, cholesterol and apolipoprotein A-I liposomes prepared by a cholate dialysis procedure. The lecithin-cholesterol acyltransferase-deficient subject had an enzyme mass level that was 35% of normal (2.04 micrograms/ml, as compared with an average normal level of 5.76 +/- 0.95 micrograms/ml in 19 Japanese subjects) and an enzyme activity of less than 0.1% of normal (0.07 nmol/h per ml, as compared with normal levels of 100 nmol/h per ml). This subject also had lower levels of apolipoproteins: apolipoprotein A-I was 53 mg/dl (42% of normal), apolipoprotein A-II was 10.6 mg/dl (31% of normal), apolipoprotein B was 68 mg/dl (68% of normal), and apolipoprotein D was 3.6 mg/dl (60% of normal). The three obligate heterozygotes had enzyme mass levels ranging from 65% to 100% of normal and enzyme activity levels ranging from 23% to 65% of normal (23.4, 56.8, and 64.7 nmol/h per ml, respectively). The proband's sister had an enzyme mass level of 6.55 micrograms/ml (114% of normal) and an enzyme activity of only 64.8 nmol/h per ml (65% of normal), suggesting that she was also a heterozygote for lecithin-cholesterol acyltransferase deficiency. The obligate heterozygotes and the sister had normal apolipoprotein levels. We conclude that the lecithin-cholesterol acyltransferase deficiency in this family is due to the production of a defective enzyme that is expressed in the homozygote as well as in the heterozygotes, and, further, that this family's mutation differs from that reported earlier for other Japanese lecithin-cholesterol acyltransferase-deficient families.

Female↗

Response curve, free-running period, and activity time in circadian locomotor rhythm of rats.

Phase response curves (PRC) for the spontaneous locomotor rhythm were constructed by applying short light pulses to rats in constant darkness (DD). The offset of locomotor activity as well as the onset was taken as a phase reference (offset PRC vs. onset PRC). The amount of phase shift yielded by light pulses was evaluated on the next day of pulse treatment (immediate PRC) and also after completion of a new steady state (steady state PRC). Significant differences in shape were observed between the onset and offset PRCs as well as between the immediate and steady state PRCs. In the immediate onset PRC, an area under the phase advance part (A) was absent, while it was present in the immediate offset PRC. In contrast, the steady state PRCs for activity onset and offset were essentially the same. The shape of steady state PRC depended on the free-running period in DD (tau). In the PRCs of long tau rhythms, the range covered by the phase delay area (D) was lengthened without changing its amplitude, resulting in a larger D/A ratio. A strong positive correlation was detected between tau and activity time (alpha). The steady state PRC shapes also depended on alpha; the D/A ratio was larger in a long alpha rhythm than in a short alpha. These results are in good agreement with the hypothesis that the circadian locomotor rhythm of nocturnal rodents is regulated by two coupled oscillators.

Animals↗

[HLA antigen on the trophoblast of normal pregnancy].

The mechanism of fetal survival as a semiallograft in the uterus remains to be clarified. In this context, the expression of HLA antigen on the trophoblast which stands between the mother and the fetus is the main problem, because HLA antigen plays an important role in immunological reaction to an allograft. For this purpose, 41 pregnant uteri (6-18 weeks of gestation) were examined immunohistochemically (avidin-biotin-peroxidase complex method) using monoclonal antibodies to HLA antigens. Troma 1, a rat monoclonal antibody, was used as a trophoblast marker in immunohistochemical studies. The results were as follows: HLA-A,B,C is not expressed on syncytiotrophoblast and villous cytotrophoblast. HLA-A,B,C is expressed on nonvillous cytotrophoblast which exists in cytotrophoblastic cell column, cytotrophoblastic shell, and endometrium. HLA-DR is not expressed on any trophoblast. The absence of HLA antigen on syncytiotrophoblast and villous cytotrophoblast seems to be essential for the survival of the fetus. But it is proved that some trophoblasts express HLA-A,B,C on their cell surface and they are adjacent to endometrial cells or maternal blood. From these findings, it seems that fetal HLA antigen might be recognized by the mother and there might be an exquisite immune escape mechanism in decidua.

Antibodies, Monoclonal↗

[The metabolism of testosterone in the central nervous system (1). Analysis of testosterone metabolites in the anterior pituitary and hypothalamus using gas chromatography-mass spectrometry (GC-MS), and subcellular localization of testosterone converting enzyme].

The aim of this study was to identify accurately the structure of testosterone metabolites in the anterior pituitary and hypothalamus for the investigation of the mechanism of androgen action in the central nervous system. Tissue homogenate and cellular fraction of male rat anterior pituitary and hypothalamus were incubated with testosterone-4-14C and testosterone-19-CD3 (14C/D3 = 1) in the presence of NADH and NADPH. The incubation media were extracted, and they were separated using thin layer chromatography (TLC). Using autoradiogram of TLC, four main radioactive fractions were found on the TLC. The TFA or TMS derivatives of every fraction were analyzed using GC-MS. The main metabolites in the anterior pituitary were identified as 5 alpha-androstan-17-ol 3-one; androst-4-ene-3, 17-dione, 5 alpha-androstane-3 alpha, 17 beta-diol, 5 alpha-androstane-3 beta, 17 beta-diol, androst-4-ene-3 alpha, 17 beta-diol and androst-4-ene-3 beta, 17 beta-diol. The result in the hypothalamus was the same as that in the pituitary. The subcellular localization of metabolites in the anterior pituitary was as follows: 5 alpha-androstan-17-ol-3-one, 5 alpha-androstane-3 alpha, 17 beta-diol and 5 alpha-androstane-3 beta, 17 beta-diol were found in microsome; 5 alpha-androstane-3 alpha, 17 beta-diol and androst-4-ene-3 alpha, 17 beta-diol were found in soluble fraction. The result in the hypothalamus was the same as that in the pituitary.

Androstane-3,17-diol↗

Feeding-associated corticosterone peak in rats under various feeding cycles.

Features of the anticipatory (prefeeding) corticosterone peak under restricted feeding were examined in rats by forcing them to various feeding schedules. Meal feeding appears specific in inducing the anticipatory corticosterone peak, since other regular manipulations such as daily cleaning of the rat cage and sampling of vaginal smear were without effect. Under meal intervals of 22,24, and 26 h, the phase relation of prefeeding hormone peak to meal was 30 min, 2.5 h, and 4.5 h, respectively. When the interval was extended to 30 h, a hormone peak appeared not immediately but several hours before meal, and when it was shortened to 18 h, hormone peak was not observed before meal but appeared when regular meal was omitted; the interval between a preceding meal and the hormone peak was similarly 18-20 h in both cases. On the other hand, a single meal feeding had a bidirectional immediate effect on plasma hormone levels, namely, a postprandial elevation of the basal hormone level and a postprandial reduction of the already elevated prefeeding hormone level under restricted feeding. Both effects were observed alternately when rats were fed twice a day for 2 wk. It is concluded that the 24-h pattern of plasma corticosterone level in rats under restricted feeding is determined primarily by the interaction of three different factors: a light- entrainable circadian rhythm, a separate oscillation associated with meal feeding, and a bidirectional effect of a single meal.

Animals↗

Dissociation of circadian rhythms in rats with a hypothalamic island.

Complete isolation of the medial basal hypothalamus, including the suprachiasmatic nuclei in the isolated island, from the rest of the central nervous system was performed in rats. The circadian rhythm of plasma corticosterone level remained essentially intact in 5 of 16 rats with complete islands, whereas that of spontaneous locomotor activity was decomposed into ultradian bursts in 15 rats, resulting in a clear dissociation of the two rhythms in four rats. One rat, whose circadian rhythm of both variables persisted after the hypothalamic isolation, showed a diurnal activity. The 24-h patterns of plasma corticosterone of the other rats could be characterized as either episodic or continuously low throughout the day. A prefeeding corticosterone peak was detected under restricted feeding in rats with episodic fluctuations but not in those with continuously low hormone levels. It is concluded that the hypothalamic island includes the fundamental structures necessary for the manifestation of the entrained circadian rhythm of plasma corticosterone in rats under ad libitum feeding, whereas it contains only a part of that for spontaneous locomotor activity. The coupling pathways from the circadian oscillator(s) to these overt rhythms seem to be separate in the central nervous system, and the circadian rhythm of plasma corticosterone is not a direct consequence of that of locomotor activity.

Animals↗

Ethosecretogram: relation of behavior to plasma corticosterone in freely moving rats.

An ethosecretogram, which illustrates the phase relation between animal behavior and plasma hormone levels, was constructed in conscious rats. A catheter was placed into the right atrium in male rats 2 days before blood sampling. Plasma corticosterone levels were monitored individually through the catheter every 5 min over a period of several hours under freely moving conditions on an Animex, which records spontaneous locomotor activity. The results showed that the bursts of locomotor activity were temporally correlated with those of plasma corticosterone level, the peak of the former preceding the hormone peak by 15 min. Regarding the type of locomotor activity, feeding and grooming were significantly correlated with the subsequent hormone elevation, whereas drinking was not. In a separate series of experiments, effects of feeding and drinking on plasma corticosterone levels were examined in conscious rats that had been fasted or water deprived for 24 or 48 h. In both cases, feeding induced a more pronounced elevation than drinking, although locomotor activity counts per se increased more sharply in the latter. It is concluded that in the ethosecretogram specific types of locomotor activity such as feeding and grooming induce a phase-locked elevation of plasma corticosterone under freely moving conditions.

Animals↗

Selective depression of prefeeding corticosterone peak in rat by sodium pentobarbital injection.

Dependency of prefeeding corticosterone peak on the time of meal supply and effects of an anesthetic, sodium pentobarbital, on both prefeeding and light-entrainable circadian hormone peaks were examined in rats. The prefeeding hormone peak which developed under restricted feeding was more prominent when rats had access to meal in the evening than in the morning. However, the increment of the hormone level above the baseline was greater in the morning than in the evening. An intraperitoneal injection of pentobarbital depressed the prefeeding hormone peak to the baseline level of circadian excursion at both times of day, but did not affect the light-entrainable circadian rise of the hormone level. It is concluded that the magnitude of prefeeding corticosterone peak under restricted feeding depends on the time of day and the mechanism behind the hormone peak was different from that underlying the light-entrainable circadian rhythm in that the former is sensitive to pentobarbital while the latter is insensitive to it.

Animals↗

Effects of elimination of maternal circadian rhythms during pregnancy on the postnatal development of circadian corticosterone rhythm in blinded infantile rats.

The influence of maternal circadian rhythms on fetal circadian oscillations during pregnancy was examined. Circadian rhythms of spontaneous locomotor activity and plasma corticosterone level in pregnant rats were eliminated by bilateral lesions of the suprachiasmatic nuclei (SCN) at different stages of gestation and the postnatal manifestation of the circadian corticosterone rhythm was examined in individual pups. Effective lesions of SCN at day 3 of gestation resulted in an abortion in all rats examined. Rats whose SCN were lesioned at day 10 or 17 of gestation maintained their pregnancies. At term, pups were removed by Cesarean operation and immediately blinded by bilateral ocular enucleation; they were reared by unoperated foster mother afterwards. All pups from SCN lesioned mothers showed a clear free running circadian rhythm of plasma corticosterone levels after the 4th week of postnatal life. Furthermore, the circadian rhythm that developed in pups from SCN-lesioned mother at day 10 of gestation (G10 pups) was always phase-delayed about 4 h as compared with that in pups from mothers whose SCN were lesioned at day 17 of gestation (G17 pups) and in pups from sham-operated mothers (S pups). It is concluded that the circadian hormone rhythmicity develops in normal fashion postnatally when the maternal SCN are effectively lesioned after day 10 of gestation. The phase-angle difference in the circadian rhythm between G10 pups and G17 or S pups suggests that fetal circadian oscillation is entrainable at least after day 10 of gestation.

Animals↗