Masato Miyama

Positron emission tomography using 2-[18F] fluoro-2-deoxy-d-glucose in the diagnosis of uterine leiomyosarcoma: A case report

Abstract The preoperative diagnosis of uterine leiomyosarcoma (LMS) is very difficult. Magnetic resonance (MR) imaging is usually used for it; however, precise diagnosis by MR imaging is limited to typical LMS with coagulative tumor cell necrosis. We presented a case of LMS that was diagnosed preoperatively by positron emission tomography (PET) using 2-[ 18 F] fluoro-2-deoxy-d-glucose (FDG).

Successful preoperative diagnosis of massive ovarian edema aided by comparative imaging study using magnetic resonance and ultrasound.

Massive ovarian edema (MOE) is a rare disease. Therefore, preoperative diagnostic method of massive ovarian edema (MOE) has not been established. We have succeeded in making a preoperative diagnosis of MOE aided by ultrasonogram and magnetic resonance imaging (MRI) and the patients ovaries were preserved. Characteristics and proposed diagnostic imaging criteria for MOE are discussed.

Increased Natural Killer Cell Activities in Patients Treated with Gonadotropin Releasing Hormone Agonist

Natural killer (NK) cell activity in patients treated with gonadotropin-releasing hormone agonists (GnRH-a) was studied. The subjects were 8 patients with endometriosis (6 with ovarian endometrial cyst, 2 with adenomyosis) and 3 patients with uterine leiomyoma. Changes in serum estradiol (E2) concentration and NK cell activity in peripheral blood were analyzed before and after GnRH-a treatment (buserelin 900 μg/day for 4–5 months). NK cell activity was determined by 51Cr release assay and E2 by radioimmunoassay. NK cell activity before GnRH-a treatment was 37.7 ± 19.0%, and after therapy activity increased significantly to 50.8 ± 18.2%. However, no significant correlation between the increase in NK cell activity and the decrease in E2 concentration was found. Results indicate that the standard GnRH-a treatment for endometriosis and uterine leiomyoma might increase NK cell activity. The etiology of the increase of NK activity with GnRH-a treatment is likely related to factors other than E2 concentration.

Production and physiological function of granulocyte colony-stimulating factor in non-pregnant human endometrial stromal cells

Effects of granulocyte colony-stimulating factor (G-CSF) on proliferation and differentiation of normal human endometrial stromal cells were investigated in an in vitro decidualization culture of stromal cells. Unstimulated stromal cells secreted little prolactin and G-CSF, whereas 8-Br-cAMP-stimulated stromal cells secreted higher levels. There was no relationship, however, between the levels of prolactin and G-CSF secreted from the stimulated cells. Detectable levels of prolactin secretion were not found in two of six stromal cell cultures stimulated with 8-Br-cAMP; however, these two culture supernatants contained high concentrations of G-CSF. Co-stimulation of the stromal cells with 8-Br-cAMP and G-CSF enhanced prolactin secretion from the stimulated cells in a G-CSF concentration-dependent manner without any change in viable cell numbers. However, G-CSF did not affect prolactin secretion or viable cell numbers of 8-Br-cAMP-stimulated decidualized cells. These results indicate that G-CSF enhances cAMP-mediated decidualization of human endometrial stromal cells in an autocrine or paracrine fashion.

Plasma Granulocyte Colony Stimulating Factor Concentrations in Pregnant Women

We measured the plasma granulocyte colony stimulating factor (G-CSF) concentrations in pregnant women to evaluate the association between G-CSF and increased neutrophil counts that has been observed during pregnancy. We examined 96 pregnant and 10 nonpregnant women. The G-CSF concentrations were assayed using a sandwich enzyme immunoassay. The G-CSF concentrations in pregnant women were significantly higher at all times than those of nonpregnant women. The G-CSF concentrations were also significantly higher during than before labor. The plasma G-CSF concentrations were positively correlated with the neutrophil counts during the 3rd trimester only. In conclusion, increased G-CSF concentrations may be related to the increases in neutrophil counts in pregnant women, especially during the 3rd trimester.

Interleukin-11 enhances cell survival of decidualized normal human endometrial stromal cells.

High expression of interleukin-11 (IL-11) and the IL-11 receptor alpha chain in developing decidual cells in mice has been reported ,and mice lacking IL-11 receptor expression have been reported to show impaired implantation owing to defective decidualization. However ,the direct effect of IL-11 on endometrial stromal cells has not been studied. In this study ,we examined the direct effects of IL-11 on normal human endometrial stromal cells using an in vitro decidualization assay system. IL-11 enhanced cell viability and prolactin secretion of 8-Br-cAMP-induced decidualized cells but not of nonstimulated stromal cells. IL-11 dose-dependently enhanced the viability of stromal cells co-stimulated with 8-Br-cAMP and IL-11 without any significant effect on prolactin secretion from the cells. The extracellular matrix did not affect the effect of IL-11 on the viability of 8-Br-cAMP-stimulated stromal cells. These results indicate that IL-11 enhances the viability of 8-Br-cAMP-stimulated stromal cells and of decidualized stromal cells ,and that the cell survival signals generated by IL-11 are independent of those generated by the extracellular matrix. IL-11 produced locally in decidual tissues may enhance the viability of decidualized stromal cells and possibly protect against cell damage during embryo implantation and trophoblastic invasion.

Enhanced Fas/CD95-mediated apoptosis by epidermal growth factor in human endometrial epithelial cells

Epidermal growth factor (EGF) has been reported to regulate apoptosis in various cell lineages. Throughout the menstrual cycle overexpression of the EGF receptor in the secretory epithelium and constitutive expression of EGF in all types of endometrial cells were identified by immunohistochemical study of normal human endometrial tissues. However, it is not known whether EGF also regulates endometrial apoptosis. This study examined the regulatory functions of EGF in endometrial apoptosis by using a human endometrial epithelial cell line HHUA which is susceptible to Fas-mediated apoptosis. Although EGF alone did not affect the cell growth of HHUA, EGF pretreatment of HHUA enhanced Fas-mediated growth suppression and Fas-mediated DNA fragmentation in the cells. Flowcytometric analyses demonstrated that EGF did not induce Fas expression on the cell surface while expressions of the EGF receptor were down-regulated. These results suggest that EGF may enhance apoptotic susceptibility of the endometrial epithelium, especially in the secretory epithelium.

Production and function of human decidual granulocyte-colony stimulating factor (G-GSF)

Summary G-CSF is a hematopoietic factor, which induces differentiation and proliferation of immature granulocytes. During pregnancy, decidual tissue produces G-CSF and the receptor for G-CSF is expressed on chorionic villous tissues. This study attempted to determine the cell population responsible for G-CSF production in decidual tissue and the influence of G-CSF on trophoblast cells. Immunostaining and in situ hybridization showed that both the decidual cells and macrophages in the decidual tissue were sources of G-CSF. With 50 ng of G-CSF the [ 3 H] thymidine uptake was 11,100±2,200 DPM and the control uptake was 7,970±1,820 DPM. G-CSF induced an increase of [ 3 H] thymidine uptake of cytotrophoblast cells 1.4 times than that of control. It is concluded that the decidual cells and macrophages were sources of G-CSF in the decidual tissue, and G-CSF might induce decidualization and promote trophoblast cell proliferation.

Identification of the granulocyte colony stimulating factor (G-CSF) producing cell population in human decidua and its biological action on trophoblasts

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic factor, which induces differentiation and proliferation of immature granulocytes. During pregnancy, decidual tissue produces G-CSF and the receptor for G-CSF is expressed on chorionic villous tissues. This study attempted to determine the cell population responsible for G-CSF production in decidual tissue and the influence of G-CSF on trophoblasts. Immunostaining and in situ hybridization showed that both the decidual cells and macrophages in the decidual tissue were sources of G-CSF. With 50 micrograms of G-CSF, the [3H] thymidine uptake was 11,100 +/- 2,200 DPM and the control uptake was 7,970 +/- 1,820 DPM. G-CSF induced proliferation of trophoblasts 1.4-fold higher than that of control. It is concluded that the decidual cells and macrophages were sources of G-CSF in the decidual tissue, and G-CSF promoted trophoblast cell proliferation.