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Background: We have previously demonstrated that prophylactic administration of melatonin to pregnant rats can protect against ischemia/reperfusion (I/R)-induced oxidative cerebral damage in fetal rats. However, the effects of maternal administration of melatonin after an ischemic episode on the brains of neonatal rats exposed to oxidative stress in utero have not been evaluated., Objectives: The purpose of the present study was to investigate whether maternal administration of melatonin after an ischemic episode can prevent oxidative cerebral damage in neonatal rats., Methods: The utero-ovarian arteries were occluded bilaterally for 30 min in female Wistar rats on day 16 of pregnancy to induce fetal ischemia. Reperfusion was achieved by releasing the occlusion and restoring circulation. Melatonin solution (10 mg/kg) or vehicle was injected intraperitoneally at 0, 1, 3, 6, and 12 h after reperfusion. After surgery, melatonin solution (20 microg/ml) or vehicle was administered freely via drinking water up to vaginal delivery. Control rats underwent a sham operation. We collected brain tissue from neonatal rats that were delivered naturally and measured the respiratory control index (RCI) as indicators of mitochondrial respiratory activity. Histological evaluation was performed on the cornu ammonis (CA1) and CA3 regions of the hippocampus., Results: I/R significantly reduced the RCI, but melatonin administration at postreperfusion hour 0 or 1 reversed I/R-induced reductions in the RCI. In contrast, melatonin administration at postreperfusion hours 3-12 had no protective effect. Histological analysis revealed a decrease in the ratio of normal to whole pyramidal cell number in the CA1 and CA3 regions in the I/R group. While melatonin administration within 3 h protected against degeneration, administration 6 h after reperfusion failed to protect., Conclusions: These results suggest that maternal administration of melatonin within 1 h after an ischemic/oxidative episode can prevent I/R-induced oxidative cerebral damage in neonatal rats.

Background: To explore predictors of functional improvement or decline in instrumental activities of daily living (IADL) among community-dwelling older people., Methods: Of all the residents (>or=65 years, n = 1,673) living in Yoita town, Niigata prefecture, Japan, in 2000, 1,544 subjects who participated in the baseline interview survey (T1) were followed up until 2002 (T2). A wide range of variables obtained in T1 was entered into the model predicting functional improvement or decline in IADL., Results: Among 1,274 individuals who participated in both T1 and T2, 105 subjects showed improvement, 194 decline, and the remaining 975 showed stability in IADL. Multiple logistic regression analyses indicated that good self-rated health and cognitive function (MMSE >or=24) at T1 were good predictors of both improvement and protection against decline in IADL. Independence in basic activities of daily living predicted improvement in IADL. Advanced age and poor walking ability predicted decline in IADL., Conclusions: Good self-rated health and cognitive function predicted both improvement and protection against decline in IADL. Thus, intervention programs aiming at maintaining both good self-rated health and cognitive function should be able to improve IADL., ((c) 2008 S. Karger AG, Basel.)

To determine the incidence and etiology of childhood thrombocytosis, over 15,000 platelet counts in 7,539 patients performed at a single regional hospital were reviewed. When thrombocytosis was defined as > or =500 x 10(9)/l of platelet counts, the condition could be diagnosed in 6.0% (456 cases) of the patients. All patients were classified as having secondary thrombocytosis. The incidence of thrombocytosis dramatically changed throughout child development; it was 12.5% in neonates, peaked to 35.8% in 1-month-old infants and then returned to 12.9% in 6- to 11-month-old infants. Thereafter, it gradually decreased with age to only 0.6% in 11- to 15-year-old children. Frequent causes of thrombocytosis included infection (67.5%), Kawasaki disease (9.4%), prematurity (7.7%) and iron deficiency anemia (6.4%). Thrombocytosis was an incidental finding in a substantial population of early infants. Thrombocytosis as a reaction to several types of infection and Kawasaki disease was more common in children under 7 years old, while autoimmune disease and tissue damage were major causes in children aged 11-15 years. No child had thromboembolic complications. These findings indicate that childhood thrombocytosis is a benign condition and its incidence and etiology seem to depend on age., (Copyright 2004 S. Karger AG, Basel)

Defects in the cell-mediated immune system may play a role in the pathogenesis or progression of pelvic endometriosis. Possible mediators include macrophages, interleukins-1 and -6, and tumor necrosis factor-alpha. More recent work points to the involvement of adhesion molecules and growth factors. To clarify the pathogenesis of endometriosis, we compared the characteristics of soluble intercellular adhesion molecule-1 (soluble ICAM-1) and hepatocyte growth factor (HGF) in women with and without endometriosis. We found that, in patients with endometriosis, the concentrations of soluble ICAM-1 in peritoneal fluid increased and interfered with the activity of natural killer cells. We also found that HGF secretion was significantly increased in cultured endometrial stromal cells, and that HGF stimulated the proliferation and migration of, and morphogenic changes in, endometrial epithelial cells. HGF and ICAM-1 play important roles in the initiation and regulation of endometriotic lesions on the microenvironment level. The increased secretion of HGF by eutopic endometrial stromal cells may contribute to the pathogenesis of endometriosis, whereas the increased levels of soluble ICAM-1 may impair natural killer cell activity and accelerate the progression of the disease.

The authors report a rare case of clinically occult thyroid carcinoma that initially manifested as a metastatic mediastinal tumor with tracheal stenosis. A curative operation was performed by complete removal of the tumor through a median sternotomy approach combined with resection of the tracheal invasion. Histopathological examination revealed transition of a well-differentiated papillary carcinoma into a poorly differentiated component in the lesion invading the trachea, which suggested that this transition might have rendered the tumor more aggressive, leading to tracheal invasion.

We investigated apoptosis in 37 human ovaries from normally cycling women to determine the mechanism of the various stages of follicular atresia and the regression of corpus luteum in human. Apoptosis was examined by 3'-hydroxy nick end-labeling, by immunostaining of an apoptosis-related antigen, Le(y) and by cell death-related genes, bcl-2. Immunoreactivity for Le(y) and nick end-labeling reactive cells were not observed in the follicular and luteal phases, except for scattered cells in the degenerating corpus luteum. On the other hand, immunoreactivity for bcl-2 was observed in the granulosa cells of antral follicles. These results indicated that apoptosis is not obvious through follicular maturation and luteal regression. This may be due to the relatively long process of human follicular growth and atresia.

Adrenocorticotropic hormone (ACTH), beta-lipotropin (beta-LPH) and beta-endorphin (beta-EP) were measured simultaneously in maternal plasma at delivery. Mean concentrations of beta-LPH and beta-EP in maternal plasma at delivery were significantly higher than those in normal control. There were significant positive correlations among ACTH, beta-LPH and beta-EP concentrations, respectively. These data suggest that beta-LPH and beta-EP were elevated during delivery and in parallel with each other.

Luteinizing hormone-human chorionic gonadotropin (LH-hCG), follicle-stimulating hormone(FSH), beta-human chorionic gonadotropin (beta-hCG), estradiol, cortisol and testosterone levels were determined in cord venous serum and the correlation of birth weights with those hormone levels was investigated in 32 male and 35 female fetuses. There were significant negative correlations between LH-hCG or FSH levels and birth weights in the male fetus. Also there was a significant positive correlation between LH-hCG levels and birth weights in the female fetus. This data suggests that there is a sex difference during the development of the pituitary-gonadal axis.

The pituitary endocrine function in 4 anencephalic infants was studied by measuring the concentrations of growth hormone, prolactin, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in umbilical venous serum. There was no significant difference in hormone levels between the anencephalic and normal infants. The response of FSH and LH was negative after administration of 10 micrograms of luteinizing hormone-releasing hormone. The TSH levels after administration of 50 micrograms of TRH elevated about 4- to 6-fold over pre-administration levels. These results indicate that the hypothalamo-pituitary axis of the human fetus initiates its function from mid-pregnancy; TSH may have an autoregulating system of the pituitary itself.

Human plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) were measured simultaneously by radioimmunoassay in 4 women with regular menstrual cycle (4 follicular phase and 4 luteal phase), 5 normal men and 10 term fetuses. Mean plasma beta-EP level in the total samples of 8 women was 30.7 +/- 5.8 pg/ml (+/- SE), significantly (p less than 0.03) higher than the beta-EP level in men (12.2 +/- 2.0 pg/ml). There was no significant sex difference in fetal plasma beta-EP level. These data suggest that the existence of sex differences for beta-EP secretion and release, and opioid peptides secretion and release mechanism might change with sexual maturation, due to changing sex steroids secretion.

Cord venous growth hormone (GH) were measured by radioimmunoassay in 88 infants and 11 anencephalic infants. The mean GH levels decreased gradually from midgestation, preterm to term fetus. There was a significant (p less than 0.01) sex difference in the GH level of term fetuses. Anencephalic infants had low GH levels. There was a significant (p less than 0.01) negative correlation between the cord GH level and birth weight in the normal infant. These data suggest that there is a sex difference for fetal GH secretion and that GH is not so important for fetal growth, but the hypothalamus plays an essential role in the regulation of fetal GH secretion.

We measured maternal venous (MV), umbilical arterial (UA), and umbilical venous (UV) cortisol levels of 180 pregnancies at term. The cortisol level of MV was higher than that of UA and UV in all deliveries. The cortisol levels of three samples had no difference between the induced labor group and the spontaneous onset of labor group regardless of delivery mode. In spontaneous vaginal delivery the cortisol levels of three individual samples were significantly higher in primipara than in multipara. The positive correlations were observed in any modes of deliveries between the cortisol levels of MV and UA, and MV and UA and UV. These data suggest that the fetus may produce cortisol by itself and maternal cortisol may inflow to the fetus.