[en] Placental mesenchymal dysplasia (PMD) is an uncommon vascular anomaly of the placenta characterized by placentomegaly with multicystic placental lesion on ultrasonography and mesenchymal stem villous hyperplasia on histopathology. Placental mesenchymal dysplasia should be considered in the differential diagnosis of cases of multicystic placental lesion such as molar pregnancy, chorioangioma, subchorionic hematoma, and spontaneous abortion with hydropic placental changes. However, lack of high-velocity signals inside the lesion and a normal karyotype favor a diagnosis of PMD. PMD must be differentiated from gestational trophoblastic disease because management and outcomes differ. We report the case of an 18-year-old female at 15 weeks of gestation with sonographic findings suggestive of placental mesenchymal dysplasia. The diagnosis was confirmed on histopathology.

[en] Highlights: • Unknown patterning mechanisms subdivide early trophoblast into two regions. • These are extraembryonic ectoderm (ExE) and ectoplacental cone (EPC). • Identifying ExE-EPC border/distinguishing entire ExE from EPC not addressed before. • These are prerequisites to grasping trophoblast patterning and were addressed here. • We identified ExE-EPC border and discovered unique features of entire ExE and EPC. The early stages of mouse placentogenesis (placenta formation) involve poorly understood patterning events within polar trophectoderm-derived trophoblast, the progenitor of all placental trophoblast cell types. By early postimplantation [embryonic day 5.5 (E5.5)], this patterning causes early trophoblast to become subdivided into extraembryonic ectoderm (ExE) and ectoplacental cone (EPC). A prerequisite to understanding this patterning requires knowing the location of ExE-EPC border and being able to distinguish the entire ExE from EPC at E5.5/E6.5, a time when the proamnioitic cavity within ExE is not fully established. However, these issues are unknown, as they have not been directly addressed. Here, we directly addressed these using trophoblast explant culture to functionally test for the location of ExE-EPC border, combined with phenotypic characterization of trophoblast proximal and distal to it. We show for the first time that the proximal-distal level of ExE-EPC border within E5.5/E6.5 trophoblast coincides with where Reichert's membrane (outermost basement membrane of conceptus) inserts into early trophoblast and with the proximal limit of extraembryonic visceral endoderm (primitive endoderm derivative covering part of early trophoblast). Based on these novel findings, we discovered that (a) the entire E5.5/E6.5 ExE can be distinguished from EPC because it is epithelial and specifically expresses Erf and Claudin4 and (b) at E5.5/E6.5, the entire EPC differs from ExE in that it is not epithelial and specifically expresses Snail. This work is expected to contribute to understanding the cellular and molecular basis of early trophoblast patterning during placentogenesis.

[en] Twin-twin transfusion syndrome (TTTS) is a severe complication of monozygotic (identical) twins, which share one single monochorionic placenta. It is caused by placental anastomoses which link the two fetoplacental circulations of the twins and allow a chronic net inter-twin transfusion to develop between the fetuses. Clinical presentation of TTTS manifestations has been classified into five different stages. In this paper, we used our computational model of TTTS and examined the possible differences between chronic and rapidly increasing inter-twin transfusion in the simulated TTTS staging sequence. Our results suggest that rapid alterations in the net inter-twin transfusion, e.g. due to thrombosis of placental anastomoses, may produce a different staging sequence than in TTTS caused by chronic inter-twin transfusion. These results may aid an improved knowledge of TTTS pathophysiology under conditions of a rapidly changing cardiovascular function, and contribute to the planning of optimal intervention under such circumstances. (note)

[en] The morphogenesis of experimental deciduomata and the genesis of polyploidy in this tissue were studied by radioautographic and ultrastructural techniques in the rat. The growth is effected by mitotic renewal of diploid cells which are in post-synthetic resting period. They themselves organize by forming cellular strings. The level of Polyploidy is determined by the modality of division. Mitotic divisions without cytodieresis lead to a substantial pool of binucleated cells (2n + 2n) in mesometrial and antimesometrial areas. Mitotic divisions for binucleated cells with a single spindle can create tetraploid mononucleated cells. This mitotic type of division limits the polyploidy to 4 n in mesometrial cells. In antimesometrial area the evolution continues above 4 n nuclei by means of endomitosis, without any filiation between mono-and binucleated cells. In some respects, this evolution agrees with results obtained in hepatic tissue in the rat

[en] The purpose of this study was to evaluate the efficacy of transvaginal color Doppler sonography (TVCDS) in the diagnosis of retained placenta. 24 cases pathologically diagnosed retained placenta and underwent TVCDS before treatment were included in this study. The clinical findings, TVCDS findings, and pathological findings were reviewed retrospectively. We evaluated size, location, echo character, and myometrial invasion with gray scale. Presence, grade (1-3), location, peak systolic velocity (PSV), and resistive index (RI) of blood flow in retained placenta were observed. In transvaginal sonography, 21 cases had cystic changes and heterogeneous echo texture in retained placenta. The sizes of retained placenta were 1.4-6.4 cm (mean 3.4 cm ), and 17 cases demonstrated myometrial invasion. In TVCDS, 19 cases showed blood flow in retained placenta but 5 cases did not. Most blood flows were grade 2 and located in either periphery or both periphery and center of the mass. PSV were 15.4-99.3 cm/sec (mean 47.33 ± 22.75 cm/sec ) and RI were 0.17-0.43 (mean 0.31 ± 0.07). RI of blood flow inretained placenta negatively correlated with the size (p=0.033<0.05). Retained placenta demonstrated with TVCDS shows blood flow of high velocity and low impedance. TVCDS may be a useful tool in the diagnosis of retained placenta.

No abstract available

[en] Objective: To investigate the value of detection of HPL-expressing intermediate trophoblasts in endometrial specimens for diagnosis of intrauterine and ectopic pregnancies. Methods: The examined specimens included: (1) Group I, 35 specimens with suspected intermediate trophoblast in decidua (2) Group II, 30 specimens with decidua-like plump endometrial stroma cells and/ or A-S phenomena in glandular epithelium (3) 30 specimens from proven intrauterine pregnancies serving as controls. Histochemistry (SP method) was used for HPL detection in all these specimens. Results: In the 30 proven intrauterine pregnancies, decidua and villa were present in all the specimens. Only 24 of the 30 were found to be HPL(+) with 6 HPL negatives (20%). In Group I , 28 of the 35 specimens were found to be HPL(+) and all of 28 were from intrauterine pregnancies: Of the 7 HPL negative cases, 5 were later confirmed as with ectopic pregnancy, the remaining 2 were with intrauterine pregnancy. In Group II, 22 of 30 specimens were HPL(+) and all were from intrauterine pregnancy. Of the 8 HPL negative cases, 6 were later confirmed as with ectopic pregnancy and 2 were with intrauterine pregnancy. Combining the data from Group I and II, we could see that in the total 15 HPL negative cases, 11 were with ectopic pregnancy (11/15=73.3%) and 4 were with intrauterine pregnancy (4/15=26.7%). Conclusion: In specimens of intrauterine contents, demonstration of HPL (+) cells could be regarded as confirmative evidence of intrauterine pregnancy. However, the reverse did not hold true. Many of the HPL negative specimens were from intrauterine pregnancies (in this study 4/15 or 26.7%). Therefore, in HPL negative cases, there was a high possibility of ectopic pregnancy but further examinations were required to ascertain the diagnosis. (authors)

[en] Diagnostic ultrasound has become one of the most useful tools in the practice of obstetrics. It has been of particular utility in the placental localization. We analyzed 34 patients of placenta previa scanned by ultrasound. The results were as follows; 1. The age of patient ranged from 22 to 39 years, showing the highest incidence in 26 to 30 years. 2. The accuracy of correct localization was 70.6%. 3. Among 13 cases diagnosed by ultrasound as total placenta previa, 2 cases were partial placental previa and 1 was low-lying placenta at the time of delivery. 4. Among 9 cases diagnosed by ultrasound as partial placenta previa, 1 case was total placenta previa and 1 case was low-lying placenta and 1 case was upper segment placenta. 5. Among 10 cases diagnosed by ultrasound as low-lying placenta, 2 cases were partial placenta previa. 6. Among 2 cases diagnosed by ultrasound as upper segment placenta, 1 case was total placenta previa and 1 case was partial placenta previa. 7. Among 9 cases done serial ultrasound, 3 cases revealed that the placenta migrates toward fundus in the course of pregnancy. Therefore, the placental scanning should be repeated in the last month before term to decide the mode of delivery. Conclusively, ultrasonography is the imaging modality of choice in the evaluation of placenta localization because it provides speedy and repeatable way without any known risk to both mother and fetus itself. Careful performance and accurate interpretation should be needed for more correct placental localization.

[en] Highlights: • Significantly higher Follistatin-like 3 levels were detected in patients with preeclampsia. • Hypoxia increased the expression of FSTL3 in trophoblast. • Follistatin-like 3 involved in invasion and migration of trophoblast functions. • Down-regulation of Follistatin-like 3 affected trophoblast lipids metabolism. Preeclampsia is a main cause of maternal and perinatal mortality and morbidity. The expression of follistatin-like 3 (FSTL3) is enhanced in maternal serum and placenta of preeclamptic women. However, whether FSTL3 is involved in the pathophysiologic of preeclampsia has not been clarified yet.

No abstract available