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L Cedard

Publications and source records attributed to L Cedard.

138 records · Page 8Linked to original sources
PubMedDate not supplied

Characterization of specific low-density lipoprotein binding sites in human term placental microvillous membranes.

Purified microvillous membranes prepared from normal term human placenta were studied for their ability to bind specifically low-density lipoprotein (LDL). Electron microscopic examination of the membrane preparations revealed essentially microvilli-like structures, and the enzyme analyses a 14-17-fold enrichment in the membrane markers 5'-nucleotidase and alkaline phosphatase. The binding of [125I]LDL was dependent on time, temperature, pH and protein concentration; it was saturable with a low capacity (130.4 +/- 22.2 ng/mg of membrane protein) and presented a high affinity (apparent Ka 6.12 +/- 1.32 micrograms protein per ml). These high-affinity binding sites were specific for LDL (high-density lipoprotein induced less competition than unlabelled LDL) and were sensitive to pronase digestion. Unlike the binding of LDL to other tissues, the [125I]LDL binding to microvillous membranes did not require divalent cations. The presence of specific LDL receptors on the placental microvillous membranes, located at the effective site of exchange between the maternal blood and the placental tissue, supports the concept that human placenta utilizes LDL-cholesterol for its progesterone synthesis.

Female↗
PubMedDate not supplied

Acetylated low density lipoprotein endocytosis by human syncytiotrophoblast in culture.

Low density lipoproteins (LDL) were chemically modified (acetyl LDL) and then conjugated to colloïdal gold (gold acetyl LDL), firstly, to visualize the acetyl LDL binding sites, and secondly, to demonstrate a possible internalization by human syncytiotrophoblast in culture. Cells were obtained by a trypsin DNase method followed by a Percoll gradient centrifugation. After 3 days of culture the syncytiotrophoblast characterization was performed by using ultramicroscopy, immunohistochemistry, and by studying the secretion of gestational hormones during culture. Binding experiments showed gold acetyl LDL attached to the membrane with random distribution. After incubation at 37 degrees C, gold acetyl LDL was internalized by the syncytiotrophoblast following the classical receptor mediated endocytosis process and a non-specific internalization process. These results suggest the existence in the placenta of a 'scavenger pathway' concomittant of the classical LDL internalization. This phenomenon may be related to the high amount of cholesterol required by the human placenta for its cellular growth and intensive progesterone synthesis.

Cells, Cultured↗
PubMedDate not supplied

[Deficiency in placental sulfatase. Description of a recent case].

Synthesis of oestrogens occurs, during the greater part of pregnancy, in the placenta starting with two fetal precursors: DHA-S and 16 OH DHA-S. In the case of a deficit in sulphatase, an enzyme which is mainly localised in the placenta, these precursors cannot be transformed so that the level of oestrogens stays very low, without the level of secretion of progesterone being altered. Faced with such hormonal abnormalities it is worth while remembering the diagnosis of placental enzyme deficiency. In fact, this abnormality has no repercussions on the progress of the pregnancy and carries no danger for the fetus. It is therefore unnecessary to carry out untimely treatments thinking: fetal distress or adrenal agenesis be it primary or secondary (due to anencephaly) will occur. The diagnosis depends on simple dynamic tests: the mother receives an injection of free DHA and DHA-S, and enzyme study of the placenta can be confirmed in vitro. There seems to be a link between this abnormality and the sex of the fetus. All cases were followed by the birth of a normal boy. Finally, placental suphatase deficiency is rare, but it would appear that increased usage of hormone levels will reveal a rising number of such cases.

Adult↗
PubMedDate not supplied

[Orange colored cells in the amniotic fluid. Statistical evaluation of 504 samples].

The authors have made a statistical evaluation of 504 estimations of the percentage of orange coloured cells in the liquor amnii. They have been able to draw up a curve of the means which confirms the value of this method. Orange coloured cells of fetal origin first appear after about 28 to 30 weeks. The rise in the percentage which is gradually progressive between the 30th and 37th weeks becomes sharp at the 38th week. The gradients of the curve of the means between the 37th and 38th week is comparable to that of the ratio lecithin/sphingomyelin. It is different from that of creatinaemia which is steeper. False-positive results are rare: at 2 p. 100 they seem to correspond to an advance in fetal maturation which may be spontaneous or may be brought about by treatment. False-negative results are commomer: 13 p. 100. The percentage of orange coloured cells should be viewed in conjunction with other tests for maturity. The technique is simple but the results may be vitiated by the minutae of preservation, of taking or of staining the cells which are described. Orange coloured cells maintain their value in pathological pregnancies and in particular in those where the fetuses are small for dates, for the percentage of orange coloured cells agrees more with the age of the fetus than with its weight.

Amniocentesis↗