Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLACENTA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1979

[Clinical aspects and morphology of placenta increta and placenta percreta (two case examples) (author's transl)].

The cases of a female patient with placenta increta and of another patient with placenta percreta and rupture of the uterus are presented. Both women were 41 years old, multiparae and had a history of multiple abortions as well as a Caesarean section. In both cases a Caesarean section, followed by a hysterectomy and supracervical amputation of the uterus respectively was done. Frequency, clinical aspects, histology and aetiology of the above described disorders of placentation are discussed.

Adult↗
PubMed1976

In vitro perfusion studies of the human placenta. IV. Some characteristics of the glucose transport system in the human placenta.

In vitro perfusion studies of glucose transport in the human placenta show saturation kinetics at high glucose concentrations and competitive inhibition of glucose transfer by the nonmetablizable glucose analog 3-O-methyl-alpha-D glucopyranoside. These characteristics provide further evidence that glucose is transported by a facilitated diffusion process in the human placenta.

Biological Transport↗
PubMed1991

Chorioallantoic placenta formation in the rat: II. Angiogenesis and maternal blood circulation in the mesometrial region of the implantation chamber prior to placenta formation.

Rat gestation sites were examined on days 7 through 9 of pregnancy by light microscopy and transmission and scanning electron microscopy to determine the extent of vascular modifications in the vicinity of the mesometrial part of the implantation chamber (mesometrial chamber). At a later time, the mesometrial chamber is, in conjunction with the uterine lumen, the site of chorioallantoic placenta formation. On day 7, in the vicinity of the mesometrial chamber, vessels derived from a subepithelial capillary plexus and venules draining the plexus were dilating. By early day 8, this network of thin-walled dilated vessels (sinusoids) was further enlarged and consisted primarily of hypertrophied endothelial cells with indistinct basal laminas. Sinusoids were frequently close to the mesometrial chamber's luminal surface which was devoid of epithelial cells but was lined by decidual cell processes and extracellular matrix. By late day 8, cytoplasmic projections of endothelial cells extended between healthy-appearing decidual cells and out onto the mesometrial chamber's luminal surface, and endothelial cells were sometimes found on the luminal surface indicating that endothelial cells were migrating. The presence of maternal blood cells in the mesometrial chamber lumen suggested that there was continuity between the chamber and blood-vessel lumens. On day 9, the mesometrial chamber was completely lined with hypertrophied endothelial cells, and sinusoid lumens were clearly continuous with the lumen of the mesometrial chamber. Mesometrial sinusoids and possibly the mesometrial chamber lumen were continuous with vessels in vicinity of the uterine lumen that were fed by mesometrial arterial vessels. Clearing of the mesometrial chamber lumen during perfusion fixation via the maternal vasculature indicated the patency of this luminal space and its confluence with mesometrial arterial vessels and sinusoids. The conceptus occupied an antimesometrial position in the implantation chamber on days 7 through 9, and it was not in direct contact with uterine tissues in the vicinity of the mesometrial chamber. These observations suggest that angiogenesis, not trophoblast invasion or decidual cell death, plays a major role in the opening of maternal vessels into the mesometrial chamber lumen before the formation of the chorioallantoic placenta.

Animals↗
PubMed2004

Major histocompatibility antigen expression on the bovine placenta: its relationship to abnormal pregnancies and retained placenta.

In viviparous animals, regulation of expression of major histocompatibility complex (MHC) class I antigens by the trophoblast cells, which constitute the outermost layer of the placenta, seems to be critical for maternal immunological acceptance of an allogeneic fetus. Cattle are unusual in this regard, since the bovine trophoblast cells, in specific regions of the uterine/placental interface, normally express MHC class I antigens during the third trimester of gestation. This expression appears to be biologically relevant as MHC class I compatibility between a cow and her fetus has been associated with an increased incidence of placental retention. We have found significant differences in lymphocyte populations, cytokine production, and trophoblast cell apoptosis in the placentomes of MHC-compatible and -incompatible pregnancies at parturition. This suggests that maternal immunological recognition of fetal MHC class I proteins triggers an immune/inflammatory response that contributes to placental separation at parturition in cattle. Early in pregnancy, a complete shutdown of MHC class I expression by trophoblast cells appears to be critical for normal placental development and fetal survival. In bovine somatic cell nuclear transfer (SCNT) pregnancies, there is an extremely high rate of fetal loss between days 30 and 90 of pregnancy. We have shown that in bovine SCNT pregnancies, between days 34 and 63 of gestation, there is both abnormal expression of MHC class I antigens by trophoblast cells and an abnormal accumulation of lymphocytes within the uterine stroma. Consequently, it is likely that activation of the maternal mucosal immune system, within the uterus at the same time when placentomes are being established, interferes with the process of placentome development and leads to immune-mediated abortion. Our data suggest that bovine MHC-compatible pregnancies provide a unique model for studying regulation of the uterine immune system, as well as immune-mediated placental rejection.

Abortion, Veterinary↗
PubMed1996

Localisation of placenta growth factor (PIGF) in human term placenta.

Placenta growth factor (PlGF) is a growth factor which belongs to the vascular endothelial growth factor (VEGF) family and is known to bind to the fms-like tyrosine kinase receptor (flt-1). Using Western blot analysis a 50 kDa band was identified in placental protein extract which corresponded to PlGF homodimer. Immunoreactive PlGF was localised to the vasculosyncytial membrane and in the media of large blood vessels of the placental villi, while staining within the mesenchyme was weak and diffuse. There was moderate staining for PlGF in discrete cells in the chorion and no staining in the epithelial layer of the amnion. The maternal decidual cells showed strong staining for PlGF immunoreactive protein. PlGF mRNA was predominantly expressed by the vasculosyncytial membrane of villous trophoblast, whilst there was no apparent expression of PlGF mRNA within the villous mesenchyme. These results suggest that PlGF may be an important paracrine factor for vascular endothelial cells in placental angiogenesis and an autocrine mediator of trophoblast function.

Blotting, Western↗
PubMed1992

[Pathology of the placenta. XII. Tumors of the umbilical cord and placenta].

Benign and malignant tumours of the umbilical cord and placenta are the topics covered in Part XII of this general account under the above heading. Angiomas, angiofibromas and teratomas, all of them of rare occurrence, are the benign tumours, with the chorioangioma being the best known of them. The trophoblast tumours proper include chorionic epitheliomas and choriocarcinomas. While histological differentiation is not possible between these two, they still are biologically benign or malignant. They may develop in the wake of normal pregnancy or abortion or hydatidiform mole. Southeast Asia is a geographically preferred region for hydatidiform mole and chorionic epithelioma. Differentiated growth behaviours of trophoblast tumours are attributable to immunological aspects. It is certainly a rare event to have a high degree of tissue compatibility (HLA antigens) between tumour and maternal organism. This may at least offer an explanation for the low incidence of choriocarcinomas in the northern hemisphere. In Southeast Asia, efforts should be made to clear up the causative background of high incidence of hydatidiform mole, since the latter most probably is the basis for development of choriocarcinoma.

Choriocarcinoma↗
PubMed1991

[Pathology of the placenta. V. Circulatory disorders of the placenta. Fetal vascular system].

Discussed are circulatory disorders as well as pathologico-anatomic findings recordable from fetal vessels of the placenta. Thorough reference is first made to obliterative endoarteritis of the greater arteries. Its forms are described, with formal and causative pathogenesis being discussed. Conclusive coverage of causative pathogenesis has proved to be possible only for unambiguously determined inflammatory manifestations (rubella, lues). The second major complex covers alterations to greater and minor fetal vessels which are characterized by central parietal thrombosis (possibly associated with fetal asphyxia) and peripherally disseminated intravasal coagulation (associated with peripartal shock or other conditions). Included in the latter group of alterations are congenital pulmonary hyaline membranes (perhaps also some membranes of postnatal origin) which are, as well, considered as shock equivalent.

Asphyxia Neonatorum↗
PubMed1991

[Pathology of the placenta. IV. Maturation disorders of the placenta under special clinical conditions].

In Part IV of this review of placental pathology, reference is made to impaired maturation of the placenta under special clinical conditions. Foetal erythroblastosis is only of minor importance, in that context, today, while similar placental alterations may result from foetal hydrops of different genesis, including immunological causes. A detailed account is given of diabetic impairment of maturation together with possible placental diagnosis of diabetes. Cases of diabetes mellitus with concomitant EPH gestosis were found to be more strongly determined for placental differentiation by EPH gestosis. Reference, finally, is made to disturbed placental differentiation under conditions of EPH gestosis with or without concomitant impairment of intervillous circulation.

Erythroblastosis, Fetal↗
PubMedDate not supplied

[Associated placenta praevia and placenta accreta. Clinical case].

Personal experience of a case of placenta praevia and accreta is reported. In agreement with other authorities, it is thought that since the condition is not immediately apparent, it should always be suspected when hemorrhaging occurs in the 7th-9th month of pregnancy. It is also confirmed that rapid diagnosis and radical treatment will generally prevent serious problems.

Adult↗
PubMed1989

Immunoactive products of human placenta. I. An immunoregulatory factor obtained from explant cultures of human placenta inhibits CTL generation and cytotoxic effector activity.

Supernatants were prepared from short-duration explant cultures of term human placentas obtained after cesarean delivery. These supernatants inhibited murine and human mixed lymphocyte reactions, as well as CTL generation. The effects were reversed by an excess of IL-2-containing medium. Similarly, the material inhibited human natural killer cytotoxicity against K 562 targets. The material was subjected to gel-filtration chromatography on an ACA 44 or Bio-Gel A15m column. The apparent MW of the MLR-CML material was about 60-70 kDa, whereas the NK inhibiting activity was eluted in high-MW components (greater than 200 kDa) as well as in the 50-kDa range. The relevance of this material in local immunoregulation during human pregnancy is discussed.

Adjuvants, Immunologic↗
PubMed2004

The dynamic placenta: II. Hypothetical model of a fetus driven transplacental water balance mechanism producing low apparent permeability in a highly permeable placenta.

In vitro and isotopic studies in vivo have reported the paradox that the human placenta is highly permeable, water exchanging at 3.6 litres per hour at 35 weeks of gestation, but clinical measurements in vivo show net transfer is minimal, around 2 ml/day. Current theories are based on osmotic pressure balances, but changes in maternofetal hydrostatic pressure change much faster than osmotic factors could respond. An alternative explanation might be that net transfer is not in fact the result of passive mechanisms, but is actively controlled by the fetus itself. The fetus is well equipped to monitor changes in blood volume, such as via sensors in venous and atrial stretch receptors to control ANF and hence urine production. Transplacental water regulation requires modification of transvillus pressures. Placental sub-chorial arteries and veins (of extra-embryonic origin) have different sensitivities from fetal body tissues to some vasoactive substances, and stem villous veins have unusually well developed vascular smooth muscle. It is thus theoretically possible for the fetus to modify subchorial venous resistances, and hence villous capillary pressure with a suitable circulating placental venous constrictive agent. A computer modelling study was undertaken using a fictitious placental venous constricting agent "fictensin", considered to be released by the fetus in proportion to disturbance of vascular volume. The effective placental permeability fell in proportion to the tightness of this fetal control mechanism, suggesting that the apparent placental permeability measured in vivo is a measure of fetal control, not true permeability. However, the range of compensatory pressures that the fetus can produce by this means is limited and failure of such a mechanism could allow flooding or dehydration of the feto-placental unit. This may shed new light on disorders such as polyhydramnios and fetal hydrops.

Animals↗
PubMedDate not supplied

Expression of human placenta alkaline phosphatase in placenta during pregnancy.

To clarify the expression of PLAP during the course of pregnancy, the amount of PLAP mRNA and its activity in normal placental villi were measured. Both PLAP and its mRNA were found in placentae of as early as 7 weeks of gestation, and they continued to increase throughout pregnancy. But they showed different patterns of increase. The amount of PLAP mRNA began to increase dramatically around 13th week and probably continued to increase gradually until term. PLAP activity per gram of villi showed a gradual increase from around 13th week and a marked increase was observed after about 20th week. PLAP levels in sera from pregnant women were also measured, and they showed a pattern of increase imilar to that of PLAP activity per gram of villi. The continuous increase in the expression of PLAP throughout pregnancy suggests that PLAP may play a role in feto-maternal metabolism and placental differentiation.

Alkaline Phosphatase↗
PubMedDate not supplied

Stereological studies on the true thickness of the villous membrane in human term placentae: a study of placentae from high-altitude pregnancies.

Stereological principles were used to calculate functionally significant dimensions of the human villous membrane, its arithmetic mean thickness (Ta) and its harmonic mean thickness (Th). The former is proportional to tissue mass and oxygen consumption, the latter to diffusional resistance. For a group of 15 term placentae from uncomplicated pregnancies at high altitude, the average values were Ta = 4.44 micron, Th = 3.56 micron and Ta/Th = 1.26. The latter figure provides a useful quantitative expression for the efficiency of the membrane in gas and metabolite diffusion. It implies that vasculosyncytial membranes and syncytial knots decrease resistance to diffusion by 26 per cent, compared with that of a membrane with uniform thickness throughout. The methods are simple to apply and provide better estimates of true thickness than do measurements confined to thin sections.

Altitude↗
PubMed2002

Bovine retained placenta: hormonal concentrations in fetal and maternal placenta.

The aim of this study was to evaluate the relationship between the occurrence of retention of the fetal membranes (RFM) and the hormonal concentrations of progesterone, estradiol-17beta, prostaglandin E(2) (PGE(2)), prostaglandin F(2alpha) (PGF(2alpha)), oxytocin (OT), oxytocin receptor (OT-R), endothelin-1 and angiotensin II (Ang II) in the placental tissues of cattle. Parturition was induced in nine Holstein cows by a single injection of PGF(2alpha) on Day 274 of gestation. Six out of nine cows in the induced group did not release the fetal membranes within 12 h after parturition and served as the RFM group, and the remaining three cows in that group, which released their fetal membranes within 12 h, served as the non-RFM group. Five other cows calved spontaneously and served as controls. The placental tissues were collected immediately (0 h) and at 6 h after parturition. The hormonal concentrations were measured by enzyme immunoassay in maternal and fetal placental tissues from RFM, non-RFM and control cows. There were no differences in P4 and E2 concentrations among the RFM, non-RFM and control groups. The mean PGF(2alpha) concentration of the RFM group was lower than those of the non-RFM and control groups in the maternal part of the placenta. In maternal tissues, the OT and OT-R concentrations in the RFM group were lower than those at 0 and 6 h after parturition in the non-RFM group. Additionally, the Ang II concentration of the RFM group in both the maternal and fetal parts of placental tissues tended to be higher than those of the other groups. In conclusion, the present results suggest that ET-1 and Ang II may play differential tissue-specific roles in the placental unit that may amplify the local endocrinological cascade involving OT, OT-R and PGF(2alpha) interactions which are necessary for normal placental separation in the cow.

Animals↗
PubMed1986

Immunoactive products of placenta. V: Soluble factors from murine placenta can block effector stages of maternal antipaternal cell-mediated immunity.

Supernatants from short-term cultures of placental or trophoblast-enriched cell suspensions derived from 14-17-day isopregnant mice display suppressive activity on NK lysis in vitro. The soluble factor is produced by trypsin-sensitive cells and requires protein synthesis. Its activity is destroyed by treatment with insoluble trypsin. The suppression is not strain restricted, but appears species-restricted. The factor acts at the level of the NK effectors themselves. Furthermore, such supernatants also are able to inhibit CTL-mediated lysis at the effector stage, in an MHC nonrestricted, nonspecific fashion. The effect is not seen with supernatants from control fetal tissues. At least two mechanisms could be involved: inhibition of homing toward allogeneic targets, and a direct effect on effector cell lytic action. These factors could play an important role in protecting the placenta from the deleterious effects of maternal antipaternal immunity and could explain the survival of the fetus in a presensitized maternal host.

Animals↗
PubMed1991

[Determination of the copper content in healthy placenta and placenta in gestosis using atomic absorption spectrophotometry].

Several complications in pregnancy seem to be related to the fluctuations of serum copper. In particular, values of serum copper over the normal range, have been associated to pregnancies complicated by EPH-gestosis. In this study we have evaluated the copper concentration in samples of placenta from 15 gravidas affected by EPH-gestosis and from 15 healthy gravidas with atom absorption spectrophotometry. The results of our study confirm the presence of an elevated copper concentration in the EPH-gestosis patients group (mean value: 196 micrograms/100 g of placental tissue). We can hypothesize that the result is due to a reduced copper uptake from the fetus.

Copper↗
PubMed1991

[Pathology of the placenta. VIII. Asphyxial infiltrates of the placenta].

Asphyxial infiltrates of the afterbirth (umbilical cord and placenta) are believed to be non-inflammatory round-cell to leucocytic infiltrates on the following sites: wall of greater vessels of umbilical cord, chorionic membrane, and, less often, stem villi as well as in the chorionic membrane proper. There has also been cellular to primarily leucocytic subchorial demarcation, usually between chorionic plate and Langhans fibrin or even in Langhans fibrin. Also recorded were parietal thrombi in greater arteries of chorionic membrane and stem villi, usually in concomitance round-cell infiltration of the arterial wall in the sense of asphyxial infiltrates. Those alterations are considered to be an entity associated to intra-uterine foetal asphyxia, with extended duration of parturition being though to play a particular role as a trigger factor of asphyxia. The author's own investigations of such alterations to afterbirths from high-risk pregnancies as well as to a consecutive series of newborns without increased risk have shown for either group that no statistical relationship existed between high-risk factors of asphyxia prior to or during labour, on the one hand, and such asphyxial infiltrates, on the other, not even in cases of prolonged labour. While we are not in a position at present to clearly define this complex in terms of genetic causality, we should like to maintain it under the heading of "asphyxial infiltrates" for the purpose of placental diagnosis.

Chorion↗
PubMed1990

[Pathology of the placenta. III. Maturation disorders of the placenta].

Normal maturation of the placenta (signs of maturation) and disorders in maturation are covered in the third part of this account of placental pathology. Impairment of maturation should be related to pregnancy age and intrauterine fetal development. A historic account is given of various classifications so far applied to impaired placental maturation, and a new setup is recommended for introduction to routine diagnosis.

Embryonic and Fetal Development↗