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Simcha Yagel

Publications and source records attributed to Simcha Yagel.

28 records · Page 2Linked to original sources

Route of delivery of fetuses with structural anomalies.

Our ability to diagnose fetuses with congenital anomalies has dramatically increased over the past two decades and with improved surgical treatment for some defects, more women may choose to continue their pregnancies. Antenatal management is thus of increasing relevance. The literature on route of delivery suggests the following conclusions. Babies with neural tube defects presenting by the breech benefit from caesarean section but there is no clear evidence that cesarean improves outcome in those with a vertex presentation. When the size of the sac exceeds 6 cm, cesarean section may be justified to decrease the risk of disruption. Vaginal delivery is desirable in all other cases to reduce maternal morbidity. Cystic hygroma: cesarean section offers optimal conditions for management of large anterior lymphangiomas that can obstruct the airway. Sacrococcygeal teratoma: the current approach is based on the size of the tumor. In a fetus with a tumor of less than 5 cm, vaginal delivery may be attempted. Ventral wall defects: there is no conclusive evidence that cesarean section is beneficial for fetuses with omphalocele. Gastroschisis: because of the heterogeneity of the studies, it is difficult to assess the net impact of mode of delivery. There is no evidence of significant differences in outcome among fetuses delivered by the vaginal versus the abdominal route. Trauma to the abdominal viscera can occur during either route, and careful delivery is thus mandated.

Abnormalities, Multiple↗

[Prenatal diagnosis of developmental congenital malformations--the limitations of ultrasound scanning].

Prenatal diagnosis of congenital malformations is a major goal of obstetric sonography. Although significant progress has been made in the ability to detect fetal anomalies by ultrasound, some fetal anomalies cannot be detected during second trimester routine ultrasound scanning. Among the "undiagnosed anomalies" are many fetal anomalies that follow a developmental course in-utero and have a late-onset sonographic appearance, and hence cannot be diagnosed early in pregnancy or during the traditional mid-second trimester scan. Several mechanisms cause in-utero development of fetal malformations, and the developmental course of each fetal anomaly depends on the cause, mechanism, extent and timing of the insult. In some cases the destructive or disruptive event might occur at a relatively advanced gestational age and thus go undiagnosed. Some malformations are the result of an early insult but are manifested and detected late, while others have a "late onset". This concept of the developmental natural course of fetal anomalies in-utero, must be recognized and lead to a new nomenclature for fetal malformations. In this review we describe some developmental fetal malformations and discuss the clinical, diagnostic and medicolegal implications.

Congenital Abnormalities↗

Regulation of trophoblast invasion: from normal implantation to pre-eclampsia.

Conversion of the maternal spiral arteries into larger competent vessels is one of the essential steps in the development of the normal placenta. This process is apparently dependent on the invasion by trophoblasts of the sub-endometrial area and the spiral arteries. Preeclampsia is characterized by shallow trophoblast invasion and unconverted narrow spiral arteries. This leads to fetal hypoxia that causes endothelial injury that eventually manifest as maternal hypertension, edema, and proteinuria. The following steps have been shown to be involved in the breakthrough of the trophoblasts from the uterine cavity into the decidua and the spiral arteries: trophoblast targeting, adhesion, and detachment from the extracellular matrix (ECM), invasion of the ECM and maternal vessels by proteolysis. Abnormal expression and activity of these molecules may explain in part some of the molecular mechanisms leading to abnormal placentation and the development of preeclampsia.

Animals↗

Single umbilical artery stenosis associated with intrauterine fetal death post-transfusion.

Single umbilical artery is among the most common funicular vascular anomalies. In contrast, umbilical artery stenosis is rare, and has only been reported in three-vessel cords. We describe a case of single umbilical artery stenosis in a fetus with no associated malformations. Intrauterine fetal death occurred at 28 weeks' gestation following cordocentesis and intravascular transfusion for Rhesus alloimmunization. Single umbilical artery stenosis may place the fetus at increased risk, particularly in cases requiring interventions involving cord manipulation.

Adult↗

Evaluating the risk of tuberous sclerosis in cases with prenatal diagnosis of cardiac rhabdomyoma.

OBJECTIVE: To evaluate the prenatal parameters that increase the risk of tuberous sclerosis in prenatal management of fetal cardiac tumors suspected as rhabdomyoma. METHODS: The study was a retrospective survey of 18 documented cases in which cardiac rhabdomyoma was suspected during pregnancy. The following parameters were evaluated as possible risk factors associated with tuberous sclerosis: tumor size, isolated or multiple, and family history of tuberous sclerosis. RESULTS: Eighteen documented cases in which cardiac rhabdomyoma was found during pregnancy were evaluated. Of these cases, seven (39%) had proven tuberous sclerosis and 11 were found to be non-associated tuberous sclerosis tumors. When combining the present data with previous series, cases with diagnosis of tuberous sclerosis had equal mean tumor size to those with normal outcome. Family history of tuberous sclerosis in the presence of cardiac rhabdomyoma almost invariably ended with tuberous sclerosis (86%). All other cases with diagnosis of tuberous sclerosis and no family history had all multiple cardiac tumors. CONCLUSION: The present data suggest that 39% of in utero suspected cardiac rhabdomyoma would have tuberous sclerosis. Family history and multifocality remain the strongest predictors of tuberous sclerosis, whereas size of the cardiac tumor can not reliably be used to predict tuberous sclerosis in prenatal counseling.

Adult↗

Localization of heparanase in normal and pathological human placenta.

Degradation of extracellular matrix (ECM) components is critical for invasion. Heparan sulphate proteoglycans are abundant in the ECM of the placenta and the decidua, hence their degradation may disassemble the matrix and facilitate placentation and trophoblast invasion. This study investigates the expression of heparanase in normal and pathological placentation using RT-PCR, in-situ hybridization and immunohistochemistry analysis to detect heparanase in specific cells of the placenta and at the fetal-maternal interface throughout pregnancy. Heparanase was observed in villous cytotrophoblasts (CT), syncytial trophoblasts (ST) and in intermediate trophoblast cell columns in normal first trimester, molar and ectopic pregnancies. The heparanase protein was preferentially expressed in the endothelium of fetal capillaries, and to a much lesser extent in larger fetal vessels. Extravillous trophoblasts (EVT) invading the decidua and the maternal vessels were also heparanase positive. In the second and third trimesters, villous CT remained heparanase positive whereas ST showed variable heparanase expression. EVT invading the placental implantation site were also positively stained. A similar pattern was observed in samples obtained from pre-eclamptic placentae and from placenta accreta. Our results indicate consistent expression of heparanase in normal and abnormal placenta, in small fetal vessels and in a variety of trophoblast subpopulations with different invasive potentials.

Female↗

Pivotal role of CEACAM1 protein in the inhibition of activated decidual lymphocyte functions.

Lymphocytes in direct contact with embryonic extravillous trophoblasts constitute more than 40% of decidual cells and appear to play major roles in implantation and early gestation. A unique subset of NK cells, making up 70-80% of decidual lymphocytes, express high levels of CD56 but lack CD16. We have recently demonstrated a novel class I MHC-independent inhibitory mechanism of NK cell cytotoxicity that is mediated by CEACAM1 homotypic interactions. This mechanism is used by some melanoma cells to avoid attack, mainly by CD16(-) NK cells. We now demonstrate that CEACAM1 is expressed on primary extravillous trophoblasts and is upregulated on the vast majority of IL-2-activated decidual lymphocytes, including NK, T, and NKT cells. Importantly, we present evidence that CEACAM1 interactions inhibit the lysis, proliferation, and cytokine secretion of activated decidual NK, T, and NKT cells, respectively. In vivo analysis of decidual lymphocytes isolated from cytomegalovirus-infected (CMV-infected) pregnant women revealed a dramatic increase in the expression of CEACAM1. Finally, we suggest that a novel ligand for this adhesion molecule is present on the surface of CMV-infected fibroblasts. These combined results demonstrate a major role for the CEACAM1 protein in controlling local decidual immune responses.

Antigens, CD↗

The human fetal venous system: normal embryologic, anatomic, and physiologic characteristics and developmental abnormalities.

OBJECTIVE: The introduction of high-resolution ultrasonography combined with color-coded Doppler imaging offered a breakthrough in the evaluation of the human fetal venous system, considerably enhancing our understanding of fetal venous circulation in normal physiologic conditions, as well as providing us the ability to study circulatory changes in abnormal circumstances. The purpose of this study was to describe the normal anatomic development and complex of anomalies of the human fetal venous system and to review recently published series of these anomalies. METHODS: Normal embryologic and anatomic development is described. An English language literature search of recent MEDLINE listings was performed to glean data from recently published series reporting prenatal diagnosis of the various anomalies and their associated malformations. RESULTS: Anomalies of the human fetal venous system occur sporadically, often associated with cardiac or other malformations. The pathophysiologic mechanisms leading to abnormal in utero development of the human venous system remain largely undetermined. On the basis of the type of vein involved, embryologic precursor, and etiologic correlation (primary or secondary), classification into 4 major groups is described. CONCLUSIONS: Prenatal evaluation of fetuses found to have anomalies of the venous system should include a careful search for cardiac anomalies, including pulmonary venous drainage, and a detailed anatomic survey of the umbilical, portal, hepatic, and ductal systems to determine aberrant communication and, if possible, to discover clues to systemic diseases or thromboembolic phenomena.

Ductus Arteriosus↗