Acute fatty liver of pregnancy with hyperlipidemia, acute hemorrhagic pancreatitis and disseminated intravascular coagulation.
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Biomedical subjects
Publications and source records attributed to H Minakami.
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The effect of progesterone on pulsatile and basal release of gonadotrophins was studied in 10 hypogonadal women. The day before progesterone treatment, control blood samples were obtained at 15 min intervals between 15.00 and 20.00 h. The next day, 50 mg of progesterone was administered im at 06.00 h and blood samples again were obtained at 15 min intervals between 15.00 and 20.00 h. Serum progesterone levels were 28.4 +/- 4.4 ng/ml at 15.00 h, 24.2 +/- 3.9 ng/ml at 17.30 h and 20.7 +/- 2.5 ng/ml (mean +/- SD) at 20.00 h. Progesterone prolonged the interval between LH pulses from 85 +/- 27 to 155 +/- 55 min (mean +/- SD), augmented their amplitude 2-fold, and caused average declines in LH and FSH concentrations of 27 and 15%, respectively. The results suggest that progesterone suppresses the mean levels of LH and FSH concentrations by acting in the brain to decrease the pulse frequency of gonadotrophin-releasing hormone.
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Several investigators have reported that CB-154 induces ovulation in patients with normoprolactinemic anovulation as well as those with hyperprolactinemic amenorrhea. In the present research, the ovulation-inducing effects of CB-154 were studied in normoprolactinemic subjects with special reference to the feedback effect of estradiol on LH release. Thirty female subjects aged 20 approximately 32 years with ovulatory disturbances were studied. Basal serum PRL, LH and FSH were determined by radioimmunoassay, and both hyperprolactinemic and hypergonadotropic anovulatory patients were excluded. A 2mg dose of estradiol benzoate was administered intramuscularly to each subject and 8ml samples of venous blood were taken at 0, 6, 24, 30, 48, 54, 72, 78 hr. The subjects under study were divided into two groups, A and B, according to the effect the estradiol benzoate had an LH release. Group A subjects (nine in all) failed to show any positive feedback release of LH in response to the estradiol benzoate. Group B subjects (twenty-one in all) showed a more than twofold increase in circulating LH as compared with the initial serum LH value, and this was taken as an indication of positive feedback release. All the subjects in group B were given clomiphene (50 approximately 100mg daily for five days). The clomiphene therapy was effective in eleven subjects, and four became pregnant (three in the first or second cycle of treatment and one in the third). The therapy was ineffective in the remaining six subjects, four of whom were diagnosed as suffering from polycystic ovary syndrome. Clomiphene was judged to be effective when the subjects undergoing therapy with this drug ovulated during three successive treatment cycles, and ineffective when the subjects did not fulfill this criterion (criterion for effectiveness of clomiphene). With the exception of four cases of polycystic ovary syndrome and three pregnancies which occurred in the first or second cycle, the rate of effectiveness of clomiphene in group B was 12 out of 14. It was concluded from these results that clomiphene was effective in group B subjects except in cases of polycystic ovary syndrome. Treatment with clomiphene alone was effective in none of the seven subjects in group A. However, administration of CB-154 for several weeks prior to and during the clomiphene treatment cycle (combined therapy of CB-154 and clomiphene) led to remarkably improved ovulation rates in five subjects in group A. Four patients in group A were selected, and given estradiol benzoate prior to (control) and during (study) CB-154 administration. In each case administration of CB-154 elicited marked positive feedback release of LH as compared with the control period, that is to say, CB-154 transformed group A patients into group B patients. This effect of CB-154 may explain why therapy combining CB-154 and clomiphene improved ovulation rates in group A...
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In order to elucidate the positive feedback mechanism of estrogen on gonadotropin release in women, the responses of plasma LH and FSH to the constant infusion of estradiol-17 beta for a prolonged period were studied. The infusion was initiated on various days of the follicular phase and maintained for 36-66 hr at a constant rate of 500 or 1,000 microgram/24 hr. When the stimulus of estradiol was sustained for more than 30 hr in the women of the middle or late follicular phase, a positive feedback effect to elicit gonadotropin surges was observed during the maintenance of the infusion. In contrast, the stimulus of estrogen was ineffective in the early follicular phase, even if sustained for a longer period up to 66 hr. Gonadotropin levels, also, increased after the end of infusion. The magnitude of the responses, however, was much smaller, as compared to spontaneous preovulatory gonadotropin surges. In all cases, the effect of estradiol was greater for LH than for FSH. It is suggested that: 1) Preovulatory gonadotropin surges are triggered by estrogen increments rather than the withdrawal of the negative feedback effect of estrogen. 2) Low levels of estrogen for a certain period of the early follicular phase may play an important role in priming the control system which responds to the positive feedback effect of estrogen.
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Four male infants with early neonatal infection caused by coxsackievirus B3 (presumed in one case) exhibited severe thrombocytopenia and liver dysfunction at presentation. The three infants who were administered human normal immunoglobulin within 3 days of disease onset survived, while the fourth infant, who received the preparation 6 days after disease onset, died.
The purpose of this study was to examine evidence for the presence of activated leukocytes in the fetal membranes from patients with preterm delivery. Polymorphonuclear leukocytes in fetal membranes from seven patients with preterm delivery (26-32 weeks of gestation) were analysed using transmission electron microscopy and ultrastructural enzyme-histochemistry for peroxidase and alkaline phosphatase. A large number of leukocytes accumulated in the fetal membranes from preterm deliveries. Phagosome, phagocytosis of cell debris, attachment of primary granules to the phagosomal membrane and cell surface projections were observed in fetal membrane leukocytes from preterm delivery but not in peripheral blood leukocytes. Peroxidase and alkaline phosphatase activity was demonstrated on the plasma membrane of the phagosomes. Morphological and enzyme-histochemical observation indicated that polymorphonuclear leukocytes in the fetal membrane in patients with preterm delivery were stimulated or activated. Such activated leukocytes may play a role in the pathophysiology or pathogenesis of preterm delivery.
The purpose of the present study was to examine morphological evidence for the presence of phagocytosing chorion laeve trophoblasts in fetal membranes from patients who had undergone chorioamnionitis-related preterm delivery. Chorion laeve trophoblasts from six patients, who underwent preterm delivery (28-34 weeks of gestation) complicated with chorioamnionitis, were analysed using transmission electron microscopy and ultrastructural enzyme-histochemistry for acid phosphatase, and compared with those from gestational age-matched chorioamnionitis-negative controls. Cytosomal cell projections, phagosomes, phagocytosis of degenerated cells and cell debris, attachment or fusion of lysosomes to the phagosomal membranes and phagosomal membranes positive for acid phosphatase staining were characteristically observed much more frequently in trophoblasts with chorioamnionitis than those without. The results indicated that chorion laeve trophoblasts in fetal membranes from patients having undergone chorioamnionitis-related preterm delivery underwent phagocytosis. Such phagocytosing trophoblasts may play a role in the pathophysiology or pathogenesis of infection-related preterm delivery.
It has been suggested that histologic subtype of ovarian cancer is a factor that determines the chemoresponsiveness of tumor. In this study, we wanted to clarify the prognostic significance of histologic subtype and its correlation to expression of chemoresistance-related proteins (CRPs) in ovarian cancer. A total of 93 stage II-IV ovarian cancers, where the proportion of serous, endometrioid, mucinous, and clear cell subtype was 61.3%, 14.0%, 7.5%, and 17.2%, respectively, were investigated for glutathione S-transferase-pi (GST-pi), MDR (multidrug resistance)-1, and p53 expression using immunohistochemistry. GST-pi expression was detected in 62.4% of the tumors and was not related to histologic subtype of tumor. MDR-1 expression was observed in 12.9% of the tumors tested and was more frequently detected in clear cell adenocarcinomas than other histologic subtypes of tumor (10/ 16 vs. 2 / 77, P < 0.001). P53 expression was found in 49.1% of serous, 53.8% of endometrioid, and 50% of mucinous adenocarcinomas. In contrast, none of 16 clear cell adenocarcinomas showed positive p53 staining. In univariate analysis, no direct correlations were found between CRPs and overall survival. Histology of mucinous/clear cell tumors (P = 0.0063), as well as FIGO stage III/IV (P = 0.0091) and residual tumor >or= 2 cm (P = 0.0045), was found to have independent prognostic value in multivariate analysis. In conclusion, histologic subtype proved to be the significant independent prognostic factor in addition to FIGO stage and residual tumor in stage II-IV ovarian cancer. GST-pi, MDR-1, and p53 expression pattern is closely related to histologic subtype of ovarian cancer, although they are not significant predictors of survival.
A 25-year-old pregnant Japanese woman was diagnosed with idiopathic hyperamylasemia. The administration of a beta-stimulant caused a further increase in the serum levels of pancreas-type amylase and lipase.The patient's hyperamylasemia concomitant with elevated serum levels of lipase, elastase 1, and trypsin lasted over a 4 year-period, in which the patient remained asymptomatic. It is possible that the pancreas in some women with the idiopathic hyperamylasemia can respond to a beta-adrenoceptor stimulation with respect to pancreatic enzyme secretion.