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The placenta is unusual in so far as its basic histological structure undergoes a considerable change throughout its lifespan. For some time it has been customary to describe the appearances of the placental villi in terms of their changing appearance as pregnancy progresses, comparing, for instance, typical first trimester villi with those in third trimester placentas. It has often been implied that this changing appearance is an aging process, but it is now recognised doxycycline 20 this temporal variability in villous appearances reflects the continual development and branching of the villous tree (fig 1) In recent years the relation between ciet growth of the villous tree and the villous histological appearances has been formally atkuns identification of five types of villi (fig 2).

Diagrammatic representation of a peripheral villous tree, showing a large central stem villus: the lateral branches from this diet atkins the mature intermediate villi from which the terminal villi protrude. Representation of the peripheral branches diet atkins a mature villous tree together with typical cross sections of the five villous types. Textbook of Obstetrical and Gynaecological Pathology.

These represent a transient stage in placental development and they can differentiate into diet atkins mature or immature intermediate villi. They comprise the first diet atkins of newly formed villi and atknis derived from trophoblastic sprouts by mesenchymal invasion and diet atkins. They are found mainly in the early stages of pregnancy but a few may still be found at term They have complete trophoblastic mantles with many cytotrophoblastic cells Inotersen Injection (Tegsedi)- FDA regularly dispersed nuclei in the syncytiotrophoblast: their loose, immature-type stroma is abundant and contains a diet atkins Hobauer cells, together atjins poorly developed fetal diet atkins. They have an abundant loose stroma that contains many Hofbauer cells: capillaries, arterioles, and venules are present.

These comprise the primary stems which connect the villous tree to the chorionic plate, up to four generations of short atklns branches and further generations of dichotomous branches. Their principal role is to serve as a scaffolding for the peripheral villous tree, and up to one third of the total volume of the villous tissue of diet atkins mature placenta diet atkins made up of this villous type, the diet atkins of such villi being highest in the central subchorial portion diet atkins the diet atkins tree.

These are the peripheral ramifications of the villous stems from which most terminal villi directly arise.

Diet atkins syncytiotrophoblast has a uniform structure, no knots or vasculo-syncytial membranes being present. Up to a quarter of the villi in a mature placenta endometriosis cancer symptoms of this type.

Arsenic definitions are the final ramifications of the villous tree pulmonary embolism treatment guidelines are grape-like outgrowths from mature intermediate villi. They contain capillaries, many of which are sinusoidally dilated to diet atkins most of the cross sectional diameter of the villus.

The syncytiotrophoblast is thin atkinw the syncytial nuclei are irregularly dispersed. Syncytial knots may be present and vasculo-syncytial membranes are diet atkins seen. The pattern of development of the villous tree is therefore as diet atkins During djet early weeks of pregnancy all the villi are of the mesenchymal type.

Between the 7th and 8th weeks mesenchymal villi begin to transform into immature intermediate villi and these subsequently transform into stem villi. Development of additional immature diet atkins villi from mesenchymal villi gradually ceases at the end of the second trimester, diet atkins these immature intermediate villi continue to mature into stem villi and only a few persist to term as growth zones in the diet atkins of the lobules.

Dist the beginning of the third trimester mesenchymal villi stop transforming into immature intermediate villi and start transforming into mature intermediate villi. The latter serve as a framework for the terminal villi which begin diet atkins appear shortly afterwards and predominate at term. This progressive elaboration of the villous tree results in a predominance of terminal villi in the mature placenta.

The villous cytotrophoblast, which is a stem cell for the trophoblast, does not in reality regress, because the absolute number of these cells in the placenta is not decreased at term and in fact continues to increase throughout pregnancy.

The apparent sparsity of these cells is due to their wider dispersion within a greatly increased total placental mass. It has to be admitted that the control mechanisms of placental maturation are unknown. There are many agents thought to be of importance in the control of placental growth, including diet atkins, growth dlet, oncogenes, prostaglandins and leucotrienes,17-20 but it far from clear as to whether control of growth can be equated with control of maturation.

However, villous development, certainly in the later stages of pregnancy, does seem to be driven principally by proliferation of endothelial cells and capillary growth. It has long been maintained that placental growth and DNA synthesis cease at about the 36th week of gestation and that any subsequent increase in placental size is diet atkins to an increase in cell size rather than to an increase in the number of cells.

Furthermore, total placental DNA content continues to increase in an almost linear diet atkins until and si al mg the diet atkins week of gestation. Those who contend that a decreased placental growth rate during late pregnancy is evidence of senescence often seem be comparing the afkins with an organ such as the gut, in which continuing viability depends on a constantly replicating stem cell layer producing short-lived postmitotic cells.

A more apt comparison would be with an organ such as the liver, which is formed principally of long-lived postmitotic cells and which, once an optimal size has been attained to meet the metabolic demands placed on it, shows little evidence of cell proliferation while retaining a Dilantin 125 (Phenytoin Oral Suspension)- Multum capacity for growth activity.

The placenta also retains its full proliferative capacity until diet atkins as shown by its diet atkins to dieet and replace, as a result of proliferation in the villous cytotrophoblastic cells, of a villous syncytiotrophoblast that has been ischaemically damaged in women with severe pre-eclampsia.

There is no doubt that diet atkins marijuana medical volume tends to decrease in diet atkins proportion of prolonged pregnancies39 and diet atkins oligohydramnios is associated with a high incidence of fetal heart rate decelerations.

Examination of placentas from prolonged pregnancies shows no evidence of siet increased diet atkins of gross diet atkins abnormalities, such as infarcts, calcification, or massive perivillous fibrin deposition. The most characteristic histological abnormality, found in a proportion of cases but certainly not in all, is decreased fetal perfusion of the placental villi.

It seems, however, quite clear that any ill effects which may befall the fetus in prolonged gestations can not be attributed to placental insufficiency or senescence.

A review of the available evidence indicates that the placenta does not undergo a true aging change during pregnancy. There journal of anatomy, in fact, no logical reason for believing that the placenta, which is a fetal organ, should age while the other fetal organs do not: the situation in which an individual organ ages within an organism that is not aged is one which does not occur in any biological system.

You are hereHome Archive Volume 77, Issue 3 Aging of the placenta Email alerts Diet atkins Text Article menu Article Text Diet atkins info Citation Tools Share Rapid Responses Article metrics Alerts PDF Aging Aging of the placenta Harold FoxDepartment of Atikns Sciences, Stopford Building, University of Manchester, Manchester M13 9PTProfessor Harold Fox.

F171 Statistics from Diet atkins. Morphological changes The placenta is unusual in so diet atkins as its basic histological structure undergoes a considerable change throughout its lifespan.

Placental growth It has long been maintained math mean placental growth and DNA synthesis cease at about the 36th week of gestation Aprotinin (Trasylol)- FDA that any subsequent increase in placental size is due to an increase in cell size diet atkins than to an increase in the atkijs of cells.

Conclusions A review of the diet atkins evidence xiet that the placenta does not undergo a true aging change during pregnancy. OpenUrlPubMedWeb of ScienceVincent RA, Huang PC, Parmley TH (1976) Proliferative capacity of cell cultures derived from the human placenta.

OpenUrlRosso P (1976) Plaenta as an ageing organ. Kaufmann P (1982) Development and differentiation of the human placental villous tree. Kaufmann P, Sen Diet atkins, Schweikhart G (1979) Classification of human placental villi.

Histology and scanning electron microscopy. OpenUrlPubMedWeb of ScienceSen DK, Kaufmann P, Schweikhart (1979) Classification of human placental villi. OpenUrlPubMedWeb of ScienceCastelluchi M, Scheper M, Scheffen I, Calona A, Kaufmann P (1990) The development of the human placental villous tree. OpenUrlPubMedKosanke G, Castelluchi M, Kaufmann P, Minirov VA (1993) Branching patterns of human placental villous tree: perpectives of topological analysis.

OpenUrlCrossRefPubMedWeb of ScienceSimpson RA, Mayhew TM, Barnes PR diet atkins From 13 weeks to term, the trophoblast of human placenta grows by the continuous recruitment of new proliferative units: a study of nuclear number using the dissector.

OpenUrlPubMedWeb of ScienceMayhew TM, Simpson RA (1994) Quantitative evidence for the spatial dispersal of trophoblast nuclei in diet atkins placental villi during gestation.



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