In blood vessels of the chorionic villi of mouse placenta, primitive macrophages first emerged at 10 days of gestation, then differentiated and matured into fetal macrophages. After emigration into the chorionic villous mesenchymal stroma, they ingested fluid-like stromal materials and transformed into Hofbauer cells. In our observation of their differentiation and maturation, no promonocytes or monocytes were detected. In the culture of cell suspensions from the placenta with LP3-conditioned medium, CFU-GM was confirmed, but in the culture with the mouse bone marrow stromal cell line (ST2) the primitive/fetal macrophage population occurred predominantly before the development of the monocyte/macrophage population. Proliferative potential of the primitive and fetal macrophages is slight. With the progress of gestation, the monocyte/macrophage population appeared in the chorionic villous stroma, forming a heterogeneous population of placental macrophages in the late fetal stage.

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Summary Thymidine phosphorylase (TP) is associated with angiogenesis and the progression of solid tumours. High intracellular levels of this enzyme indicate increased chemosensitivity to pyrimidine antimetabolites. TP gene expression in 56 cases of epithelial ovarian cancer (27 of serous, 10 mucinous, 12 endometrioid, five clear cell and two undifferentiated) were analysed by polymerase chain reaction of RNA after reverse transcription. These included eight of low malignant potential. Twenty were stage I, four stage II, 27 stage III and five stage IV. The level of TP gene expression was presented by the relative yield of the TP gene to the β2-microglobulin gene. TP gene expression ranged from 0.19 to 5.38 (median 0.93). The value of TP gene expression in stage III-IV was significantly higher than that of TP gene expression in stage I-II (P = 0.0005). Histological grade significantly associated with TP gene expression (P = 0.008), but histological subtype did not (P = 0.166). A follow-up study of 34 cases after complete resection of the primary tumours by surgical operation was performed. TP gene expression of the cases with recurrence showed significantly higher levels compared to cases without recurrence (P = 0.049). Survival data were available for 47 of the 56 patients. The prognosis of the patients with high TP gene expression (equal to, or greater than, median) was to be significantly worse than patients with low TP gene expression (less than median) (P = 0.021). The TP gene expression level may play one of the key roles in the biology of ovarian epithelial cancer and define a more aggressive tumour phenotype. A new therapeutic intervention mediated by TP protein activity is anticipated.

The pathogenesis of pelvic endometriosis has been studied by using scanning electron and light microscopy, observing the surface structure of bluish lesions obtained from 26 patients during laparotomy. Paraffin sections included another 17 tissue samples of endometriosis, based on immunohistochemical responses to epithelial membrane antigen, keratin and vimentin. Ultrastructurally, the surface epithelial cells could not be detected in 13 out of 17 pelvic peritoneal endometriosis samples. In one case in which the surface peritoneal cells were seen histologically to dip into the subperitoneal stroma, many surface peritoneal infoldings were observed, and ciliated cells were detected at the edge of these infoldings. Ovarian endometriosis was composed of three types of cells, none of which had any cilia. These findings were observed in continuity with adjacent normal mesothelial cells. No characteristic structure of the endometrial surface was observed for the bluish lesion, but the gland surface of endometriosis located in the subperitoneal stroma initially had ciliated cells. The immunoreactions in both the columnar mesothelial cells with surface peritoneal infoldings and the glands of endometriotic tissues were similar to those of normal endometrial glands, but different from those of normal mesothelial cells. Pelvic endometriosis might originate by a process of metaplasia from the pelvic peritoneum.

Background: Porous diaphragm syndrome is caused by a defect in the diaphragm. The defect may induce pleural effusion in a patient with an ovarian tumor. Case Report: A 59-year-old Japanese woman with an ovarian tumor and right hemothorax underwent thoracotomy and presented with a fenestra in the right diaphragm through which bloody fluids were flowing from the peritoneal cavity into the pleural space. Following suturing of the fenestra, laparotomy revealed intraabdominal bleeding due to torsion of an ovarian tumor. Conclusion: This is the first report in which the diaphragmatic defect was identified in a patient with an ovarian tumor and hemothorax. Porous diaphragm syndrome may be involved in the pathophysiology of right pleural effusion observed in other medical conditions such as Meigs’ syndrome, ovarian hyperstimulated syndrome, and ovarian cancer.