Worsening of systemic lupus erythematosus-associated thrombocytopenia after administration of gonadotropin-releasing hormone analog.
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Adult↗
Biomedical subjects
M Ichijo
Publications and source records attributed to M Ichijo.
Platelet aggregation inhibiting activity of human placental chorioepithelial brush border membrane vesicles--the role of alkaline phosphatase.
Human placental chorioepithelial brush border membrane, which is in direct contact with maternal blood flow, has platelet aggregation inhibiting activity. In the present study, the mechanism of this action has been examined in relation to ADP (adenosine diphosphate) degrading activity and alkaline phosphatase activity of brush border membrane vesicles (BBMV). BBMV prepared from human early and term placental villi, inhibited platelet aggregation induced by ADP. BBMV had potent ADP degrading (ADPase) activity. ADP was quickly degraded by BBMV. ADP degrading activity of BBMV was not so different between early and term placenta. Alkaline phosphatase activity of late placental BBMV was about three times greater than that of early placental BBMV. On the other hand, ADP degrading activity of late placental BBMV was almost the same as that of early placental BBMV. Inhibiting activity of platelet aggregation induced by ADP and ADP degrading activity of BBMV, were not inhibited by levamisole (alkaline phosphatase inhibitor).
Adenosine Diphosphate↗
Detection and localization of interleukin-8 mRNA and protein in human placenta and decidual tissues.
It has been reported that interleukin-8 (IL-8) is secreted from the placental and decidual tissues and that IL-8 levels in the amniotic fluids are significantly elevated by chorioamnionitis or labor pain. The present study was aimed at defining the localization of IL-8 mRNA as well as IL-8 protein at the feto-maternal interface using in situ hybridization and immunohistochemical staining. Both IL-8 mRNA and protein were localized in cytotrophoblast, syncytiotrophoblast and Hofbauer cells of the placenta, decidual stromal cells, decidual lymphocytes and endometrial gland cells. IL-8 secretion from glandular cells has not previously been reported. In addition, we confirmed IL-8 mRNA expression and secretion of IL-8 by an endometrial cancer cell line (Ishikawa) using the reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) methods, respectively.
Base Sequence↗
Presynaptic glutamate receptors facilitate release of norepinephrine and 5-hydroxytryptamine as well as dopamine in the normal and ischemic striatum.
We investigated the effects of selective glutamate (Glu) agonists on the release of monoamine neurotransmitters and their implication in the enhanced monoamine release in cerebral ischemia. In the striatum of anesthetized Sprague-Dawley rats, in vivo microdialysis was performed and the release of excitatory amino acids (Glu and aspartate (Asp)) and monoamines (dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT)) was measured by high-performance liquid chromatography with an electrochemical detector. (1) Forebrain ischemia by 4-vessel occlusion generated significant correlations between the Glu and Asp levels and the DA, NE and 5-HT levels (r = 0.922-0.967, P < 0.01, n = 6). (2) L-Glu and its selective agonists (N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and kainate (KA)) evoked a simultaneous release of striatal DA, NE and 5-HT in a dose-dependent manner (P < 0.01, ANOVA, n = 8). The maximal monoamine release evoked by the Glu agonists showed different magnitudes in the order of DA >> NE > 5-HT (118-, 16- and 9-fold from the baseline levels by 62.5 mM L-Glu, respectively). Each Glu agonist exerted a different magnitude of transmitter release and the order of agonist efficacy was different among NE, 5-HT and DA release: AMPA = KA > L-Glu = NMDA for DA release, AMPA > L-Glu = NMDA = KA for NE release, and L-Glu = NMDA = KA = AMPA for 5-HT release.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A study of CD45RO, CD45RA and CD29 antigen expression on human decidual T cells in an early stage of pregnancy.
The decidua is the place where the fertilized egg is implanted and where the immunocompetent cells of the mother come into direct contact with genetically disparate cells of the conceptus. Although the T cells in the decidua are exposed to fetal antigens, the fetus is not rejected by maternal immunocompetent cells. In the present study, we examined surface markers to determine whether the T cells in the human decidua are naive T cells without or memory T cells with a history of antigen stimulation. Although few T cells were present in the decidua, as compared to the peripheral blood, CD45RO+, CD29+ and CD45RA- CD4+ T cells as well as CD45RO+, CD29+ and CD45RA- CD8+ T cells, which are considered to be memory T cells, were in the majority, with only small numbers of CD45RO-, CD29- and CD45RA+ CD4+ and CD8+ cells, which are naive T cells, present. Also, the decidual mononuclear cells secreted IL-2 and IL-4. Since IL-4 is secreted only by memory T cells, it is suggested that in the decidua memory T cells increase in number and secrete cytokines, thereby in some way influencing the phenomenon of fertility.
Antigens, CD↗
Macrophage colony-stimulating factor induces the growth and differentiation of normal pregnancy human cytotrophoblast cells and hydatidiform moles but does not induce the growth and differentiation of choriocarcinoma cells.
In the present study, we examined whether or not macrophage colony-stimulating factor (M-CSF; CSF-1) is involved in the growth and differentiation of human chorionic, hydatidiform mole and choriocarcinoma cells. M-CSF promotes the growth of early gestation chorionic cells, hydatidiform mole cells, and a human term placenta cell line (tPA30-1). However, the growth of choriocarcinoma cells, BeWo, Jar, Jeg-3, and NUC-1, was not influenced at all by M-CSF. M-CSF promoted the secretion of human chorionic gonadotropin (hCG) and human placental lactogen (hPL), which are secreted from differentiated trophoblast, from early gestation chorionic cells and from hydatidiform mole cells. However, the secretion of hCG and hPL from choriocarcinoma cells was not affected by M-CSF. When M-CSF localization was examined by immunohistochemical staining, M-CSF was detected in chorionic and hydatidiform mole cells, but was absent in choriocarcinoma cells. These results suggest that the growth and differentiation of normal chorionic and hydatidiform mole cells are M-CSF-dependent, while the growth and differentiation of choriocarcinoma cells are not.
Base Sequence↗
Renal impairment in very low birthweight infants following antenatal indomethacin administration.
Three cases of neonatal renal insufficiency in very low birthweight (VLBW) infants following repeated antenatal administration of indomethacin to prevent premature labor are reported. Three pregnant women received indomethacin (total doses of 150-850 mg) for 3-14 days from admission until delivery. The gestational ages and birthweights of the infants ranged from 24 to 28 weeks and 612 to 1432 g, respectively. Oliguria, early onset of hyperkalemia and prolonged renal dysfunction occurred after birth. Renal failure did not improve in one infant. Despite the efficacy of indomethacin for tocolysis in premature labor, VLBW infants born after repeated maternal administration near the time of delivery may have developed impairment of the premature kidney.
Adult↗
Expression of granulocyte colony-stimulating factor and its receptor at the fetomaternal interface in murine and human pregnancy.
Granulocyte colony-stimulating factor (G-CSF) is a cytokine which regulates proliferation and differentiation of neutrophilic granulocytes, and its receptor (G-CSF-R) is a member of the hemopoietic growth factor receptor family. We studied the expression of G-CSF and G-CSF-R at the fetomaternal interface in murine and human pregnancy. Immunohistochemical analysis and in situ hybridization indicated that both G-CSF and G-CSF-R are expressed in mouse spongiotrophoblasts and placental labyrinths, and human placental cytotrophoblasts and syncytiotrophoblasts. They were also detected in mouse decidual basalis cells and endometrial epithelial cells, and human decidual stromal cells and endometrial gland cells. These results suggest that G-CSF plays a role in decidual and placental functions by autocrine and paracrine mechanisms.
Abortion, Induced↗
The effect of interleukin 2 and transforming growth factor-beta 2 (TGF-beta 2) on the proliferation and natural killer activity of decidual CD16- CD56bright natural killer cells.
The present study, using flow cytometry, demonstrated that CD16- CD56bright natural killer (NK) cells, which are abundant in the decidua, have both interleukin-2 receptor alpha (IL-2R alpha) and interleukin-2 receptor beta (IL-2R beta). The NK activity and DNA synthesis of CD16- CD56bright NK cells were markedly elevated even by treatment with small amounts of IL-2. These results indicate that decidual CD16- CD56bright NK cells possess a high-affinity receptor for IL-2. Transforming growth factor-beta 2 (TGF-beta 2), which is contained in the decidua and is thought to serve as a major immunosuppressive factor, reduced the NK activity of decidual CD16- CD56bright NK cells, but it hardly affected the IL-2-induced augmentation of the NK activity or DNA synthesis of decidual CD16- CD56bright NK cells. The conclusion has therefore been reached that once IL-2 is produced in the decidua, the IL-2-induced potentiation of the NK activity of decidual CD16- CD56bright NK cells cannot be suppressed by TGF-beta 2.
Antigens, CD↗
Transacting activities of the E7 genes of several types of human papillomavirus.
In accordance with previous reports by others, the E7 gene of human papillomavirus (HPV) 16, considered to be etiologically associated with cervical cancer, transactivated the E2 promoter of adenovirus. This promoter, however, was equally stimulated by the E7 gene of HPV1, a skin type HPV never associated with human malignancy. A variety of promoters were tested to see the effect of the E7 genes of low-risk and high-risk type HPVs. The result indicated that there was no obvious relationship in the levels of transactivation or transrepression by the E7 gene between low-risk and high-risk types. It has been suggested that the binding of the E7 protein to the product of retinoblastoma susceptibility gene (pRb) is the underlying mechanism by which the E7 protein transactivates the E2 promoter. Therefore, the association of the E7 protein and pRb alone did not seem to fully explain the mechanism by which this protein participates in the activation of transcription and induction of human malignancies.
Adenoviridae↗
Family study of women showing development of antibody to human T-cell leukemia virus I and assessment of the risk of vertical transmission of the virus to their children.
When pregnant women were tested for antibody to human T-cell leukemia virus-I, some were found to be positive although they had been negative during the previous pregnancy. In these women, HTLV-I infection was found from pedigree studies to have been acquired from their mothers rather than from their husbands. Furthermore, some of them had apparently remained HTLV-I antibody-negative for long periods after infection. When the breast-fed children of these women, in whom HTLV-I was acquired from their mothers but who were in an HTLV-I antibody-negative state, were also examined for evidence of HTLV-I infection, none was found.
Carrier State↗
Elevation of amniotic fluid interleukin 6 (IL-6), IL-8 and granulocyte colony stimulating factor (G-CSF) in term and preterm parturition.
We determined the levels of inflammatory cytokines such as interleukin 6 (IL-6) granulocyte-colony stimulating factor (G-CSF) and IL-8 in the amniotic fluids from women with premature or term delivery. Cytokines were detectable even in the absence of apparent infection (group 1), but much higher cytokine levels were found in cases of intrauterine infection, particularly in cases of premature delivery (group 2). In cases of term delivery (groups 3-5), all of the cytokine levels showed c. 3- to 4-fold increase during labor pain (group 4) and an 8- to 13-fold increase in the presence of endotoxin (group 5), in comparison with the levels in cases where neither factor was present (group 3). Regarding infection, the cytokine levels were 20- to 30-fold higher in chorioamnionitis-positive premature delivery group (group 2), than in the infection-negative group (group 1). All the cytokines were simultaneously induced in amniotic fluid by labor pain and infection, and a significant positive correlation was observed among these three cytokine levels. In-vitro culture system and immunohistochemical study indicated that the cytokines in the amniotic fluid appeared to originate from trophoblasts and decidual cells. Thus, infection and labor pain may trigger the production of inflammatory cytokines at term as well as premature delivery and the determination of these cytokine levels will be a good indication for the prediction of the presence of intrauterine infection.
Amniotic Fluid↗
Cytokine production by CD16-CD56bright natural killer cells in the human early pregnancy decidua.
Using a cell sorter, CD16-CD56bright natural killer (NK) cells were sorted from decidual mononuclear cells at an early stage of pregnancy. These cells were examined by the reverse transcriptase-polymerase chain reaction (RT-PCR) method for their expression of mRNA coding for the following 12 cytokines: IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and leukemia inhibitory factor (LIF). Although mRNA coding for every cytokine was detected in decidual mononuclear cells, mRNAs coding for only G-CSF, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, and LIF were detected in CD16-CD56bright NK cells. Also, the supernatant of CD16-CD56bright NK cell cultures was found to contain G-CSF, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, and LIF. These findings indicate that CD16-CD56bright NK cells produce many different cytokines and that these cytokines may play an important role in a successful pregnancy.
Antigens, CD↗
Transforming growth factor-beta (TGF-beta) in human milk.
The amount of TGF-beta contained in human whey was studied by the colony formation of NRK47F cells. It was noted that a factor inducing colony formation did exist in human whey, and its action was neutralized when anti-TGF-beta antibodies were introduced. This suggests that TGF-beta does exist in human whey. In colostrum, the total amount of TGF-beta was 1365.7 +/- 242.9 ng/ml, of which the active form comprised 728.1 +/- 248.7 ng/ml (n = 21). In late milk, the total TGF-beta was 952.5 +/- 212.6 ng/ml, with an active form of 178.7 +/- 157.3 ng/ml. Thus human milk contains a large amount of active TGF-beta. Furthermore, it was revealed by the reverse transcriptase polymerase chain reaction that mRNAs coding TGF-beta 1 and TGF-beta 2 exist in human milk cells. These results suggest that both TGF-beta 1 and TGF-beta 2 exist in human milk.
Base Sequence↗
T-cell receptors are expressed but down-regulated on intradecidual T lymphocytes.
PROBLEM: Dietl et al. considered "intradecidual T cell tolerance towards fetal antigens" with their observation that intradecidual T cells lack immunohistochemically detectable amounts of T cell receptor (TCR) molecules while expressing normal amounts of CD3 molecules during early normal pregnancy (Am J Reprod Immunol. 1990; 24:33-36). METHOD: To reevaluate these findings we examined the TCR and CD3 expression on intradecidual T cells using flow cytometry. CONCLUSIONS: In our study, all intradecidual CD3+ T cells expressed either TCR alpha beta or TCR gamma delta. However, the expression of the CD3/TCR complex on intradecidual T cells was down-regulated. The level of CD3/TCR complex expression on intradecidual T cells was about two-thirds of that on peripheral blood T cells. Further, the proportions of alpha beta+ and gamma delta+ cells in CD3+ cells did not significantly differ between decidua and peripheral blood.
Decidua↗
Correlations of leuko-araiosis with cerebral atrophy and perfusion in elderly normal subjects and demented patients.
CT images of leuko-araiosis in brain slices were quantified according to volumes of reduced Hounsfield units in frontal periventricular white matter in groups of elderly patients with multi-infarct dementia (MID, n = 23) and dementia of the Alzheimer type (DAT, n = 16). Volumes of leuko-araiosis, estimates of atrophic cerebral tissue, and local cerebral perfusion utilising inhalation of xenon gas as the indicator were correlated on the same CT slices. Ratios of frontal leuko-araiosis to total brain tissue volume were similar for patients with MID and DAT (mean 5.7 (SD 2.1)% v 6.5 (3.2%)), and both were significantly greater than ratios in elderly normal volunteers (3.1(1.3)%, 0 < 0.001). Cerebral atrophy (measured as the ratio of volumes of cerebrospinal fluid to total brain area) for DAT patients was 17.0 (6.7)%, which was greater than for MID patients (12.5 (5.4)%; p < 0.05) and both types of patients showed more cerebral atrophy than did age matched, elderly normal subjects. Cerebral perfusion was decreased in all regions measured in patients with MID and DAT compared with elderly normal subjects. Multi variate regression analyses correlated frontal leuko-araiosis with reductions of local cerebral blood flow in subcortical grey matter (p < 0.025) in patients with vascular dementia but not in those with DAT. These quantitative measures implicate decreased perfusion due to atherosclerosis in territories supplied by the deep penetrating cerebral arteries in the pathogenesis of leuko-araiosis in patients with vascular dementia, but suggest a different pathogenesis for leuko-araiosis in Alzheimer's disease.
Aged↗
Human macrophage colony-stimulating factor induces the differentiation of trophoblast.
When human cytotrophoblastic cells in the early stage of pregnancy were cultured in a serum-free medium in the presence of human macrophage colony-stimulating factor (M-CSF), the cytotrophoblastic cells fused and formed a typical syncytiotrophoblast which had a dense distribution of microvilli revealed under an electron microscope. On the other hand, cytotrophoblasts incubated with anti-M-CSF antibody showed hardly any syncytiotrophoblast formation. Following this finding, we studied the differentiation of chorionic cells from the viewpoint of hormone secretion. When cytotrophoblasts were incubated in the presence of M-CSF, the supernatant of the culture showed an increase in human chorionic gonadotropin and human placental lactogen levels in proportion to the concentration of M-CSF added. When cytotrophoblasts were incubated in the presence of anti-M-CSF antibody or anti-fms antibody, human chorionic gonadotropin and human placental lactogen secretion were suppressed. Thus, M-CSF was morphologically and endocrinologically found to induce the differentiation of chorionic cells.
Cell Differentiation↗
Localization and production of human macrophage colony-stimulating factor (hM-CSF) in human placental and decidual tissues.
The localization of the human macrophage colony-stimulating factor (hM-CSF) in human trophoblast cells (syncytiotrophoblast and cytotrophoblast), decidual stromal cells, decidual lymphocytes, macrophages, and endometrial gland cells during the early stage of pregnancy was determined by the immunohistochemical examination and in situ hybridization. A large amount of hM-CSF was detected in the supernatant of the primary cultured cytotrophoblasts and decidual stromal cells. The decidual stromal cells secreted approximately 2 to 20 times as much hM-CSF as the trophoblast cells. Northern blot analysis showed that the placental and decidual tissues expressed the 4.0 kb hM-CSF-mRNA, however a larger amount of hM-CSF-related mRNA was found in the decidual than in the placental tissue. We also demonstrated the localization of hM-CSF mRNA expression in human decidual macrophages and CD16- CD56+ NK cells using the RT-PCR method. These findings indicate that hM-CSF is produced by decidual stromal cells, decidual macrophages, decidual CD16- CD56+ NK cells, and endometrial gland cells, as well as by trophoblasts. This increased production of hM-CSF may play a role in decidual function and placental function by the autocrine and paracrine system.
Antigens, CD↗