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F Debieve

Publications and source records attributed to F Debieve.

6 recordsLinked to original sources
PubMed2006

[Dissection of renal artery aneurysm in a pregnant woman with Elhers-Danlos disease type IV].

Recall the clinical signs and personal and family medical history suggestive of Elhers-Danlos syndrome, mainly type IV. Review of literature and presentation of a clinical case observed in a female patient with Elhers-Danlos disease type IV who developed dissection of a renal artery during pregnancy. The prevalence of the syndrome is increasing, reaching, according to the latest publications 1/5,000 births. It is important to determine the type of syndrome to assess prognosis. In the classic type and in the hyper mobile type, pregnancy is generally well tolerated although certain complications linked to connective tissue dysfunction such as pelvic instability, premature delivery, bleeding postpartum and perineal lacerations, may develop. Ehlers-Danlos syndrome can be associated with serious and even fatal complications for these patients: vascular dissection or uterine rupture. It is important for obstetricians to be aware of the clinical signs and symptoms suggestive of Elhers-Danlos syndrome in a pregnant patient and to know the diagnostic possibilities and potential risks. If a typeIV syndrome is diagnosed, it is very important to inform the patient about the potential implications for pregnancy and maternal health, as well as the risk of transmission to the child and the possibility of antenatal diagnosis.

Adult↗
PubMed2002

Control of the human inhibin alpha chain promoter in cytotrophoblast cells differentiating into syncytium.

Inhibins are dimeric proteins consisting of a common alpha subunit linked to one of the beta subunits, beta A or beta B. During pregnancy, the placenta is the main source of inhibin A production and the in-vitro transformation of cytotrophoblast cells into syncytium is associated with an inhibin alpha subunit mRNA up-regulation. In this study, the 5' region of the human inhibin alpha gene was isolated and sequenced. Three transcription initiation sites were identified. When transiently transfected in trophoblast cells with a luciferase reporter vector, the sequence displayed promoter activity. DNase I footprinting and electrophoretic mobility shift assay (EMSA) analysis showed a specific DNA-protein interaction in the promoter when using cytotrophoblast nuclear proteins. This interaction was weaker with syncytiotrophoblast nuclear proteins. Moreover, the deletion of this DNA-protein interaction region suppressed the promoter activity. In an attempt to identify this factor, the potential binding of known factors delta EF1, AP1 and NFE2 were excluded by competition EMSA experiments. We suggest that it may correspond to an undescribed protein interaction. The identification of the human inhibin alpha promoter could help in understanding the mechanisms modulating inhibin gene transcription. Moreover, the identification of a factor, whose presence is related to the trophoblast cell differentiation state, could help in understanding the transformation of cytotrophoblast cells into syncytium.

Animals↗
PubMed2001

Vascular endothelial growth factor and placenta growth factor concentrations in Down's syndrome and control pregnancies.

Vascular endothelial growth factor (VEGF) and placenta growth factor (PLGF) are considered to play important roles in angiogenesis and vascular permeability during placental development. Since trisomy 21 placentae show trophoblastic hypoplasia and hypovascularity, we investigated PLGF and VEGF synthesis in Down's syndrome pregnancies. Maternal serum was collected from 102 euploid and 24 trisomy 21 pregnancies between 15 and 20 weeks gestation and tested for these two factors by enzyme-linked immunosorbent assays. Protein extracts from 15 normal and six trisomy 21 placentae were also tested. VEGF was not detected in maternal serum, while PLGF increased significantly with gestational age. Serum PLGF, transformed as a multiple of the gestational age median (MoM), in Down's syndrome pregnancies was significantly lower than in euploid controls (mean 0.67 +/- 0.043 MoM versus 1.00 +/- 0.047 MoM, analysis of variance F = 11.605, P < 0.001 ). Both VEGF and PLGF were detected in placental protein extracts without variation according to gestational age. Down's syndrome placentae had significantly less PLGF compared to normal placentae (Mann-Whitney, P < 0.05 ) but no difference was observed in placental VEGF content (Mann-Whitney, P = 0.94 ). Considering the biological properties of PLGF, this decrease may provide new insights into the mechanism(s) leading to the structural and functional anomalies described in trisomy 21 placentae.

Adult↗
PubMed2000

Inhibin and activin production and subunit expression in human placental cells cultured in vitro.

Inhibins and activins are dimeric proteins, with each subunit being one of three related protein subunits (alpha, betaA or betaB). The mRNA levels of these subunits were studied quantitatively during in-vitro differentiation of human cytotrophoblast cells into syncytium, using Northern blot analysis and semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. The corresponding protein concentrations were determined by specific enzyme-linked immunosorbent assays for inhibin A, B, pro alphaC and activin A in cellular protein extracts and culture medium (n = 5). Immunofluorescence studies showed syncytium formation after 48 h. The alpha subunit was present before plating and increased at 48 h (P<0.001) while the betaA subunit was weak before plating and increased at 24 h. The betaB subunit was not detected. With respect to corresponding protein synthesis, inhibin A (alpha + betaA) had risen after 48 h in cellular protein extract and after 72 h in culture medium, while activin A (betaA + betaB) was detected after 24 h, with no significant variations in culture medium. There was a good correlation between inhibin A and alpha subunit expression (r = 0.736, P<0.001), as well as between activin A and betaA subunit expression (r = 0.755, P<0.001). This study showed that mRNA expression parallels protein synthesis of inhibin and activin in trophoblast cells. Inhibin A synthesis appears to be dependent on alpha subunit mRNA expression, rather than on the betaA subunit which controls activin A synthesis. This study has also shown that isolated cytotrophoblast cells do not produce dimeric inhibin. However, during the transformation of cytotrophoblast cells into syncytium, betaA subunit mRNA expression may be an indicator of cell aggregation, while alpha subunit mRNA expression may be an indicator of cell fusion.

Activins↗
PubMed2000

Gonadotropins, prolactin, inhibin A, inhibin B, and activin A in human fetal serum from midpregnancy and term pregnancy.

Using specific enzyme-linked immunosorbent assays we measured inhibin A, inhibin B, and activin A in relation to LH, FSH, and PRL in normal human fetal midpregnancy serum obtained by in utero cord venipuncture (n = 25) and compared these results to those in fetal serum from term pregnancies (n = 23). We also tested serum from fetuses with intrauterine growth retardation (n = 6) or trisomy 21 (n = 6). We found no measurable inhibin A, except in three midpregnancy males (3 of 14). Inhibin B, however, was detected in midpregnancy male fetuses (167+/-67 pg/mL) and was higher than that in females (16+/-12 pg/mL). It was present in male term fetuses (125+/-32 pg/mL), but not in females. The activin A levels did not significantly differ between term and midpregnancy males and females. LH and FSH were detected in midpregnancy male fetuses (4.4+/-3.3 and 0.77+/-0.49 mIU/mL, respectively), with higher levels in females (33.0+/-23.2 and 54.4+/-27.7 mIU/mL, respectively), and were suppressed at term. PRL did not exhibit sexual difference, but showed a higher level at term (322.4+/-113.8 ng/mL) than at midpregnancy (33.0+/-26.1 ng/mL). Comparison of inhibin B with FSH levels showed correlation coefficients of -0.565 at midpregnancy vs. +0.445 at term. Serum from fetuses with intrauterine growth retardation or trisomy 21 did not show any different hormonal profiles. These data suggest that inhibin B is probably an additional factor in FSH inhibition at midpregnancy, whereas activin A is not associated with any change in the different studied populations. We speculate that inhibin A could be a method to detect maternal blood contamination in cord venipuncture.

Activins↗