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PubMed1988

Human amnion as a bioprosthesis for bile duct reconstruction in the pig.

Despite technical advances in management, the complication of late stricture formation and biliary sepsis still occur in bile duct reconstruction. In an attempt to avoid bilioenteric anastomosis, which bypasses the biliary sphincter mechanism, various biologic and artificial materials have been employed clinically and experimentally to replace the damaged bile duct. No satisfactory biliary replacement material has yet been found. In the experimental model of bile duct stricture that has been presented, human amnion bile duct injuries mimicking those seen in clinical practice were repaired using human amnion as a free graft. Noncircumferential duct loss appeared to be satisfactorily repaired using amnion, and the amnion repair was found to be as good as or superior to plastic repair; however, circumferential duct loss was not adequately repaired with the amnion graft.

Alkaline Phosphatase↗
PubMed1996

The expression of cyclooxygenase-2 (COX-2) in amnion and decidua following spontaneous labor.

OBJECTIVE: Prostaglandins production rises dramatically during term and preterm labor. The source of this production is thought to be the fetal membranes and maternal decidua. The enzyme responsible for the conversion of arachidonic acid to the prostaglandins and related endoperoxides is variously known as prostaglandin synthase or cyclooxygenase (COX). An inducible form of this enzyme, COX-2, has been described in several tissues. The purpose of this study was to investigate a possible role for COX-2 in labor by comparing the COX-2 content in amnion and decidua from laboring and non-laboring patients. STUDY DESIGN: Fetal membranes from seven normal labor and ten elective cesarean sections at term were collected immediately following delivery. The maternal age and gravity were similar between the groups. The amnion and decidua were identified, washed in sterile saline, frozen in liquid nitrogen and stored in -70 degrees C. COX-2 expression was determined using Western Blot analysis with a purified COX-2 antibody. A scanning densitometer was used to quantify the bands. Results were expressed as mean +/-S.D. ng/50 micrograms protein. RESULTS: The concentration of COX-2 in amnion of laboring women showed a twofold increase (240.0 +/- 17.6 vs. 120.7 +/- 5.1) compared to the non-labored group (p < 0.05). The concentration in the decidua showed no significant increase during labor (38.1 +/- 7.5 vs. 26.4 +/- 2.1, p > 0.05). CONCLUSION: We evaluated the role of COX-2 in normal labor. Our study demonstrates that COX-2 is significantly induced in the amnion following spontaneous labor. These findings suggest that the induction of amnion COX-2 may be involved in the process of human labor.

Amnion↗
PubMed1997

Action of immunoregulatory agents on 5-HETE production by cultured human amnion cells.

Labor in women is associated with increased amniotic fluid prostaglandin (PG) concentrations. AF of women with term and preterm labor also contains elevated concentrations of arachidonic acid metabolites from the lipoxygenase pathway including 5-hydroxyeicosatetraenoic acid (5-HETE). We and others have shown that 5-HETE production within the uterus is increased by inflammatory cytokines. The purpose of this study was to determine whether 5-HETE production is regulated by immunotherapeutic agents that inhibit prostaglandin E2 (PGE2) production, such as interleukin-10 (IL-10) and cyclosporin A (CsA). Cultured confluent amnion cells were incubated for 16 hr with IL-10 (1 100 ng/ml), CsA (1 1000 ng/ml), or controls. Additional incubation of IL-10 and CsA (both at 10 and 100 ng/ml) were conducted on amnion cells in the presence and absence of interleukin-1 beta at 1 ng/ml. 5-HETE was measured by radioimmunoassay and cellular protein determined. IL-1 beta stimulated amnion cell 5-HETE production as expected. However, 5-HETE production by amnion cells was significantly inhibited by incubation with IL-10 and CsA, and both significantly attenuated 5-HETE production in response to IL-1 beta. We speculate that the inhibitory effect of IL-10 and CsA on amnion cell 5-HETE production is at the level of substrate release or inhibition of 5-lipoxygenase and that the use of these agents during pregnancy may not adversely affect pregnancy outcomes.

Amnion↗
PubMed1998

Production of prostanoids via increased cyclo-oxygenase-2 expression in human amnion cells in response to low molecular weight hyaluronic acid fragment.

Increased concentrations of hyaluronic acid (HA) have been found in serum and at uterine cervix at term. In its native form, HA exists as a high molecular weight (MW) polymer, but during parturition a lower MW HA fragment accumulates. The aim of this study was to investigate the regulatory mechanisms responsible for increased amnion prostanoid production and cyclo-oxygenase (COX) expression in response to HA. Human term amnion cells in culture were exposed to native HA polymer (MW 2.2x106) and its fragment (MW 3.5x104). We have determined levels of prostanoids, prostaglandins E2 and F2alpha, in conditioned media using specific immunoassays. Expression of COX-1 and COX-2 was examined with Western blot. Results were analyzed for statistical significance with Mann-Whitney U-test. Human amnion cells treated with HA fragment (100 nmol/l) produced significantly more PGE2 (2.3+/-0.21 (mean+/-S.D.) pg/106 cells/24 h) than controls (0.34+/-0.03) or high MW HA-treated cells (1.2+/-0.21). Protein levels of COX-2, but not COX-1, were substantially increased in amnion cells treated with HA fragment. HA fragment-mediated prostanoid production is markedly diminished by pretreatment with indomethacin. Our results indicate that HA fragment, rather than physiologic native HA polymer, induces amnion cell-derived prostanoid production via increased COX-2 expression. COX-2-mediated prostanoid production is likely a key physiologic event in HA fragment-mediated cervical ripening and the labor onset.

Amnion↗
PubMedDate not supplied

Interleukin-1 alpha, epidermal growth factor, and transforming growth factor-beta exhibit differential kinetics on endothelin-1 synthesis in amnion cells.

OBJECTIVE: To investigate the effects of three cytokines, interleukin-1 alpha (IL-1 alpha), epidermal growth factor (EGF), and transforming growth factor-beta (TGF-beta), on the regulation of endothelin-1 (ET-1) mRNA and protein production in human amnion cells. METHODS: Human amnion cells were harvested from uncomplicated pregnancies undergoing elective cesarean delivery at term and grown in primary monolayer culture. Cells were treated with IL-1 alpha, EGF, and TGF-beta for dose-response and time course experiments. Northern analysis was used to determine ET-1 mRNA expression, and enzyme-linked immunosorbent assay was used for ET-1 peptide determination. RESULTS: Interleukin-1 alpha, EGF, and TGF-beta induced the expression of ET-1 mRNA and protein in a dose- and time-dependent fashion. The kinetics of ET-1 mRNA production did not differ markedly with respect to the inducing cytokine, but the kinetics of ET-1 protein production was quite different. Interleukin-1 alpha and EGF stimulated a rapid increase in ET-1 that peaked by 24 hours, and the levels declined to just above the detection limit by 72 hours. In contrast, TGF-beta-stimulated cells showed modest ET-1 production at early times (4-24 hours) and then gradually increased and peaked at 72 hours. CONCLUSIONS: Cytokines modulate the expression of ET-1 mRNA and its cognate protein in human amnion cells. The differential kinetics of ET-1 peptide expression in amnion cells suggests that ET metabolism as well as synthesis contribute to the net expression of endothelin in amnion.

Amnion↗
PubMedDate not supplied

Cyclooxygenase inhibitors decrease apoptosis initiated by actinomycin D, cycloheximide, and staurosporine in amnion-derived WISH cells.

Apoptosis is a process by which external or developmental factors induce a specific series of events leading to cell death. Recently, apoptotic cells have been described in rat amnion membrane at late gestation, suggesting apoptosis may be involved in membrane rupture. Mechanisms controlling amnion cell apoptosis are unknown. The objective of this study was to investigate whether cyclooxygenase and prostaglandins are integral to apoptosis in amnion, as reported in intestinal epithelial cells and renal mesangial cells. Amnion-derived WISH cells underwent apoptosis in a dose- and time-dependent manner after incubation with actinomycin D, cycloheximide, or staurosporine, as determined by cell viability, DNA fragmentation analysis, and fluorescent in situ fragmentation analysis. Cells cultured with increasing doses of these agents also demonstrated concomitant increases in prostaglandin E2 output. WISH cell coincubation with these agents and the cyclooxygenase inhibitors indomethacin or piroxicam resulted in dose-dependent decreases in both prostaglandin E2 and apoptosis. Cultures incubated with 0.5 microgram/mL actinomycin D showed 80.7% cell apoptosis after 12 hours compared with 1.1% in untreated cultures. After 24 hours incubation with actinomycin D, 0.8% of the original cell number remained attached to the plate. In cultures coincubated with 0.5 microgram/mL actinomycin D and 100 mumol/L indomethacin, only 19.2%, 24.7%, and 39.3% of the cells were found to be apoptotic after 12, 24, and 48 hours in culture, respectively. Similar trends were observed after the use of cycloheximide or staurosporine in combination with indomethacin or prioxicam. These data suggest that cyclooxygenase and/or prostaglandins play a role in programmed cell death of amnion-derived WISH cells in culture.

Amnion↗
PubMedDate not supplied

Prostanoid stimulation of cytokine production in an amnion-derived cell line: evidence of a feed-forward mechanism with implications for term and preterm labor.

OBJECTIVE: To test the hypothesis that amnion cytokine production might be regulated by prostanoids. METHODS: Amnion-derived WISH cells were treated with a range of prostanoids and their effects on production of interleukin (IL)-6 and IL-8 were determined by enzyme-linked immunosorbent assay and Northern analysis. The effects of thromboxane inhibitors on cytokine production by term primary amnion explants also were examined. RESULTS: Prostaglandin (PG)A2, PGD2, PGF2 alpha, PGE2, PGJ2, and the PGI2 analogue carbaprostacyclin (1-1000 nmol/L) exhibited no significant effects on cytokine production. However, the thromboxane A2 (TXA2) agonist U46619 and carbocyclic (c)TXA2 both stimulated WISH cytokine production with similar potencies under basal or cytokine-stimulated conditions. Significant stimulation of IL-6 production was observed at concentrations > or = 8 nmol/L (P < .05 by analysis of variance), whereas IL-8 production was stimulated significantly but to a lesser extent. The effects of U46619 and cTXA2 were rapid; maximal stimulation of cytokine production occurred within 4 to 8 hours of treatment. U46619 augmented IL-1 beta-stimulated IL-6 and IL-8 mRNA expression within 2 hours of treatment. In amnion explants inhibitors of TX synthesis and action abrogated the stimulatory effects of IL-1 beta on cytokine production. CONCLUSION: These results are consistent with the presence of a feed-forward loop in amnion involving TXA2 and cytokines, which could play a significant role in the progression of the inflammatory response involved in the mechanism of infection-driven preterm labor.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2002

Rhythmic contractions in chick amnio-yolk sac and snake amnion during embryogenesis.

The rhythmic movements of fetal membranes in chick and reptile embryos were studied to explore the developmental role of the extra-embryonic motor activity. In the snakes Lamprophis fuliginosus and Elaphe radiata, rhythmic contractions of amnion inside the developing egg were recorded from the 11th incubation day until pre-hatching stages (ca. day 60-72). The duration of these contractions averaged 2.02+/-0.27 min. The frequency ranged from 2 to 6 per 10 min and averaged 4.61+/-0.57 per 10 min. A tendency of frequency to increase toward the end of embryogenesis was observed. Lowering the temperature from 28 to 20 degrees C significantly decreased the frequency of amnion contractions to 2.85+/-0.91 per 10 min. The isolated snake amnion retained its capacity for spontaneous contraction. Noradrenaline inhibited, acetylcholine stimulated and serotonin did not affect the rhythmic activity of the isolated snake amnion. Similar effects were found when these agents were applied into the snake amniotic cavity. In the chick, yolk sac rhythmic contractions were recorded from the fifth until the 12th incubation days. The duration of these contractions ranged from 15 to 60 s, their frequency averaged 11.8+/-3.18 per 10 min and depended on temperature. The low temperature threshold was approximately 30 degrees C. After surgical removal of the amnion and embryo, the yolk sac continued contracting inside the egg. The yolk sac rhythmic contractions likely participate in the space movement of the embryo inside the egg during embryogenesis.

Amnion↗
PubMed1995

Activation of phospholipase D in cultured human amnion cells.

The regulation of phospholipase D (PLD) activity in the human amniotic membrane was examined using primary cultures of amnion cells. Cultured amnion cells were labelled with [3H]oleic acid, and PLD activity was determined as the amount of [3H]phosphatidylethanol (PEt) produced during incubation in the presence of 0.1% ethanol. PLD activity in cultured amnion cells was activated by addition of arginine vasopressin and oxytocin. PLD activity was also stimulated by treatment was arachidonic acid, the product of phospholipase A2 (PLA2), and phospholipase C (PLC). These results indicate that PLD in amnion cells is activated by substances present in amniotic fluid, and that cross-talk between phospholipases A2, C and D may occur in amnion cells.

Amnion↗
PubMed2001

A single nucleotide polymorphism in the matrix metalloproteinase-1 (MMP-1) promoter influences amnion cell MMP-1 expression and risk for preterm premature rupture of the fetal membranes.

Interstitial collagen gives fetal membranes tensile strength, and membrane rupture has been attributed to collagen degradation. A polymorphism at -1607 in the matrix metalloproteinase-1 (MMP-1) promoter (an insertion of a guanine (G)) creates a core Ets binding site and increases promoter activity. We investigated whether this polymorphism is functionally significant for MMP-1 expression in amnion cells and whether it is associated with preterm premature rupture of the membranes (PPROM). The 2G promoter had >2-fold greater activity than the 1G allele in amnion mesenchymal cells and WISH amnion cells. Phorbol 12-myristate 13-acetate (PMA) increased mesenchymal cell nuclear protein binding with greater affinity to the 2G allele. Induction of MMP-1 mRNA by PMA was significantly greater in cells with a 1G/2G or 2G/2G genotype compared with cells homozygous for the 1G allele. When treated with PMA, the 1G/2G and 2G/2G cells produced greater amounts of MMP-1 protein than 1G/1G cells. A significant association was found between fetal carriage of a 2G allele and PPROM. We conclude that the 2G allele has stronger promoter activity in amnion cells, that it confers increased responsiveness of amnion cells to stimuli that induce MMP-1, and that this polymorphism contributes to the risk of PPROM.

Amnion↗
PubMed2006

S100B protein expression in the amnion and amniotic fluid in pregnancies complicated by pre-eclampsia.

Our aim was to investigate the expression of S100B protein in the amnion and to assess the amniotic fluid concentration in pregnancies complicated by pre-eclampsia. Samples were obtained from women who developed pre-eclampsia (n = 7), pre-eclampsia with intrauterine growth retardation (IUGR) (n = 4), normotensive IUGR (n = 7) and gestational hypertension (n = 4) during pregnancy and healthy controls who delivered at term (n = 35). To determine the difference in the expression of S100B in the amnion, we performed immunohistochemistry, western blot analysis and RT-PCR. Using enzyme-linked immunosorbent assay (ELISA), we assessed the S100B concentration in amniotic fluid. The S100B mRNA expression in the amnion of pre-eclamptic patients and patients with pre-eclampsia with IUGR was significantly higher than that in the control. The amniotic fluid S100B protein concentration of the pre-eclampsia and normotensive IUGR cases was significantly higher than that of the control. This study shows that amnion could be a source responsible for the increased concentration of S100B in amniotic fluid. In pre-eclampsia, reactive oxygen species (ROS) are generated by oxidative stress. Some pathological conditions that develop during pregnancy and are related to hypoxic stress can affect the elevation of S100B concentration in the amnion.

Adult↗
PubMed1995

92-kDa gelatinase (matrix metalloproteinase-9) is induced in rat amnion immediately prior to parturition.

The fetal membranes undergo striking changes in structure before delivery that involve catabolism of the extracellular matrix. To investigate the role of specific enzymes in this process, we examined gelatinase activities in rat amnion, visceral yolk sac placenta, and placenta and amniotic fluid between Days 18-21 of pregnancy. Matrix metalloproteinase (MMP)-2 was present in amnion on all days, and its activity increased slightly on Day 21. The 92-kDa gelatinase, MMP-9, was not detected on Days 18-20 but appeared by the morning of Day 21. There was a marked increase in MMP-9 mRNA in the amnion on Day 20, preceding the appearance of MMP-9 activity. Western blotting confirmed an increase in MMP-9 protein in amnion on Day 21. MMP-2 and MMP-9 activities were detected in extracts of whole yolk sac placenta, placenta, and amniotic fluid, but there were no striking changes in these gelatinases between Days 18 and 21. However, the capsular regions of the visceral yolk sac placentae, which thin and rupture during labor, did show higher MMP-9 activity on Day 21 than on Days 18 and 20. We suggest that the striking increase in MMP-9 expression in amnion and possibly the capsular region of the visceral yolk sac placenta approximately 12 h prior to delivery is responsible, in part, for the alterations in the structure of these fetal membranes before parturition.

Amnion↗
PubMed1998

Cellular specificity of interleukin-1beta-stimulated expression of type-2 prostaglandin H synthase in human amnion cell cultures.

Interleukin-1beta (IL-1beta) has been shown in numerous studies to increase prostaglandin output by cultures of human amnion cells. This is due to an increase in the expression of type-2 prostaglandin H synthase (PGHS-2), the inducible form of the enzyme, in these cultures. Amnion consists of an epithelial layer of cells and a subepithelial mesenchymal layer of cells. The purpose of the present study was to determine the cell-type(s) responsible for the IL-1beta-induced PGHS-2 expression in amnion cultures. Amnion was obtained at term after elective Cesarean section or vaginal delivery. Tissues were dispersed with collagenase, and cells were plated in multichamber culture slides and cultured for 7 days in media supplemented with 10% fetal bovine serum. Cell types were characterized with antisera to keratin (epithelial cells) and vimentin (mesenchymal cells). Cultures contained both cell types, and the proportion of these varied considerably from one culture to another. Cells were treated with various concentrations of IL-1beta for 6 or 24 h and were then fixed in 4% paraformaldehyde. The fixed cells were permeabilized with Triton and examined by immunohistochemistry for PGHS-2 protein using specific antisera, and PGHS-2 mRNA was localized by in situ hybridization using a specific oligonucleotide probe. The cell type(s) expressing PGHS-2 was characterized using double labeling with antisera to keratin (epithelial cell marker) and vimentin (mesenchymal cell marker). IL-1beta was found to increase expression of immunoreactive PGHS-2 and PGHS-2 mRNA. This increased expression was found to occur only in the vimentin-positive cells and not the epithelial cells. These results highlight the potential importance of the subepithelial cells in the mesenchymal layer of amnion in the formation of prostaglandins during pregnancy and possibly in preterm labor with infection.

Amnion↗
PubMed2000

Increased apoptosis in human amnion is associated with labor at term.

PROBLEM: To characterize whether increased apoptosis in human amnion was associated with labor at term. METHOD OF STUDY: Human amnion were obtained from term patients with vaginal delivery (n = 5) or who underwent elective Cesarean section (C/S) without labor (n = 5). Apoptosis was performed by the TUNEL (Terminal dUTP Nuclear End Labeling) assay. All nucleated cells stained with propidium iodide in the amnion epithelial cells were identified in red fluorescence. TUNEL positive apoptotic nuclei were identified in green fluorescence. Five random fields of each specimen were blindly counted by investigators. The percentage of apoptotic nuclei of total nuclei (apoptotic index) was calculated and compared between the two groups (25 microscopic fields for each group, respectively). RESULTS: Patients with term labor had a significantly higher mean apoptotic index in amnion epithelial cells than that with elective C/S without labor (27.3 +/- 4.1% versus 3.6 +/- 1.6%, P < 0.001). CONCLUSIONS: Our data indicate that apoptosis in human amnion is significantly increased and associated with labor at term.

Amnion↗
PubMed1987

Comparison of the specific binding of cortisol in human amnion, amniotic fluid, and plasma.

The purpose of this study was to compare the specific cortisol-binding protein found associated with human amnion with specific cortisol binding in human amniotic fluid and plasma. The electrophoretic mobility on polyacrylamide gels of the specific cortisol binding in amnion, amniotic fluid, and maternal plasma was identical. The influence of pH on cortisol binding activity was similar in all tissues and the cortisol binding was immunoprecipitable by a polyclonal antibody raised against human corticosteroid-binding globulin. The interaction of the cortisol binding protein with concanavalin A was studied in preterm amniotic fluid, term amniotic fluid, term amnion, and plasma from pregnant women at term and women under oral contraceptive treatment. Binding to concanavalin A was similar in term amnion and term amniotic fluid but was less than that found with both preterm amniotic fluid and term plasma. These results indicate that the cortisol binding protein associated with human amnion has similar characteristics to plasma corticosteroid-binding globulin, but that its state of glycosylation appears to be more like that of the cortisol binding protein in term amniotic fluid rather than in plasma.

Amnion↗
PubMed2006

Amnion cells engineering: a new perspective in fetal membrane healing after intrauterine surgery?

In this study we aimed to set up an in vitro culture of the rabbit amnion in order to support in vivo fetal membrane healing capacity following fetoscopy. Fetal membranes were collected from a mid-gestational rabbit, and cultured on collagen support material for 14 days. 34 rabbits at 22-23 days gestational age (GA) underwent fetoscopy. The entry site was randomly allocated to 4 closure technique study groups: group I, human amnion membrane (n = 23); group II, collagen foil (n = 16); group III, collagen plug (n = 19), and group IV, collagen plug with cultured amnion cells (n = 19). In all groups membrane access sites were additionally sealed with fibrin sealant, and the myometrium was closed with sutures. Fetal survival, amnion membrane integrity, and the presence of amniotic fluid were evaluated at 30 days GA. Cultures showed good survival in the collagen support material. Increased cellularity, survival and proliferations were observed. The amnion at the access site resealed in 58-64% of cases in groups II-IV, but none of the tested techniques was significantly better than the other. Histological examination indirectly revealed the anatomic repair of the membranes, since no entrapment of the membranes could be demonstrated in the myometrial wound.

Amnion↗
PubMed1996

A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor.

Fetal membranes usually rupture during the process of labor. Premature fetal membrane rupture occurs not infrequently and is associated with significant fetal and maternal morbidity. The mechanisms of normal and pathologic fetal membrane rupture are not well understood. We have examined structural and biochemical changes in the rat amnion as labor approaches in order to characterize this process in normal pregnancy. Here we report that before the onset of active labor the amnion epithelial cells undergo apoptotic cell death which encompasses degradation of 28S ribosomal subunit RNA and associated P proteins and fragmentation of nuclear DNA. Concurrent with these cellular changes, the amnion type I collagen matrix is degraded with the accumulation of three-quarter length type I collagen fragments in extraembryonic fluid, characteristic of the cleavage of fibrillar collagen by interstitial collagenase. Western blot and immunohistochemical analyses confirmed that interstitial collagenase protein appears in association with the loss of amnion type I collagen. We conclude that amnion epithelial cells undergo a process of programmed cell death associated with orchestrated extracellular matrix degradation which begins before the onset of active labor. Thus, fetal membrane rupture is likely to be the result of biochemical changes as well as physical forces.

Amnion↗
PubMed2007

The effect of mechanical stretch on cyclooxygenase type 2 expression and activator protein-1 and nuclear factor-kappaB activity in human amnion cells.

Stretch of the uterus plays a role in parturition. Uterine stretch also leads to stretch of the fetal membranes, including the amnion, an important source of prostaglandin E2 (PGE2). We tested the hypothesis that stretch of the amnion leads to increased cyclooxygenase (COX)-2 expression and PGE2 synthesis and investigated the mechanisms involved. We obtained amnion from women undergoing term elective cesarean section and isolated amnion epithelial cells. These cells were subjected to 11% static stretch. Stretch increased COX-2 expression and PGE2 production. EMSA studies showed that stretch increased both activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) DNA binding at 1 and 6 h. In contrast, IL-1beta increased both AP-1 and NF-kappaB DNA binding at 1 h only. Chromatin immunoprecipitation studies confirmed that stretch increased binding of NF-kappaB to the COX-2 promoter in vivo. Stretch had no effect on inhibitory-kappaBalpha (IkappaBalpha) levels at the early time points but caused a decrease at 4 h. IL-1beta stimulation decreased IkappaBalpha levels after 30 min. MG132, a proteasome inhibitor, inhibited only the second stretch-induced increase in NF-kappaB binding. This suggests that stretch initially activates NF-kappaB via a nonclassical pathway, which does not involve the inhibitory-kappa kinase-induced degradation of IkappaBalpha. The second peak of NF-kappaB activation may be mediated by the classical mechanism. Stretch of the amnion may contribute to increased expression of COX-2- and other AP-1- and NF-kappaB-regulated genes with the onset of labor in the human.

Amnion↗