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1  captured during evolution for a function in placentation.
2 first pregnancies, is associated with faulty placentation.
3 ion and those associated with aberrations of placentation.
4            Oxygen is a critical regulator of placentation.
5 zation, and embryonic PPARdelta is vital for placentation.
6 nsor to direct trophoblast cell fates during placentation.
7 maternal role of COUP-TFII in regulating the placentation.
8 emodeling of arterioles, a hallmark of human placentation.
9 irst step of implantation and, subsequently, placentation.
10 villous trophoblasts (EVTs) influences human placentation.
11 terine wall is characteristic of hemochorial placentation.
12 PAR2 and PAR3 in the invasive phase of human placentation.
13  regulates trophoblast invasion during early placentation.
14 giogenesis are hallmarks of implantation and placentation.
15 d permits the unique arrangement for primate placentation.
16  understanding factors that lead to abnormal placentation.
17 ng neural tube closure, digit septation, and placentation.
18 vivo and that HIF is essential for mammalian placentation.
19 pivotal to understanding normal and abnormal placentation.
20  successful endovascular invasion and normal placentation.
21  of the CEBP and GATA families essential for placentation.
22 tein dysregulation in EVT cells during early placentation.
23 se, was unable to activate matriptase during placentation.
24 aptured by eutherian mammals, with a role in placentation.
25 tment of pregnancy loss mediated by abnormal placentation.
26 eclampsia, a syndrome arising from defective placentation.
27  FMVD regulation in normal and dysfunctional placentation.
28 ene that has evolved a function in eutherian placentation.
29  that allowed an extended period of intimate placentation.
30 in that have been captured for a function in placentation.
31 in that have been captured for a function in placentation.
32 kely critical during the beginning stages of placentation.
33 lated lineages in the presence or absence of placentation.
34 e imaging modalities for diagnosing abnormal placentation.
35 invasion is a fundamental component of human placentation.
36 ternal-fetal immune mechanism that regulates placentation.
37 igin, ancestrally captured for a function in placentation.
38 s morbidity increased in cases with abnormal placentation.
39 th placenta previa with and without abnormal placentation.
40 ce in angiogenic growth factors and abnormal placentation.
41 NK-trophoblast interactions may lead to poor placentation.
42  is required for successful implantation and placentation.
43 reproduction scheme involving viviparity and placentation.
44 e decidua are important regulators of normal placentation.
45 ng KIR on maternal dNK may be beneficial for placentation.
46 in that have been captured for a function in placentation.
47 roductive character in apes, highly invasive placentation.
48 estigation of the involvement of NK cells in placentation.
49 iron metabolism is associated with defective placentation.
50 stemic inflammatory state as well as shallow placentation.
51  the first trimester, optimizing hemochorial placentation.
52 theria species that have a different form of placentation.
53 to delineate hypoxia-sensitive events during placentation.
54 myometrial invasion and the type of abnormal placentation (73.5% and 47%, respectively).
55 ivity and specificity in diagnosing abnormal placentation (97-100% and 94-100%, respectively).
56 ary, maternal hypoxia during early stages of placentation activates the invasive endovascular trophob
57 e most significant risk factors for abnormal placentation, added to risk factors known for placenta p
58 show that the essential function of HAI-1 in placentation and all other embryonic processes is to res
59      PE is strongly associated with abnormal placentation and an excessive maternal inflammatory resp
60 ified as having USs exhibit epitheliochorial placentation and are in the Ruminantia and Suidae orders
61 selective FOXO1 knockdown leads to defective placentation and compromised embryo development, similar
62 inical inflammatory state that impairs early placentation and development of its blood supply.
63 eins lead directly or indirectly to abnormal placentation and fetal death.
64 ial growth factor, and, ultimately, abnormal placentation and fetal death.
65 gnancy-compatible immunovascular role during placentation and fetal development.
66 scular modification are implicated in normal placentation and fetal growth in humans, our findings su
67  addition to the role of uterine NK cells in placentation and fetal growth, other uterine ILCs (uILCs
68  molecular and genomic changes that underlie placentation and find that two distinct evolutionary mec
69 ble importance both for the study of healthy placentation and for the investigation of the potential
70 ntiation of trophoblasts and helps in normal placentation and formation of vascular exchange interfac
71                               Thus, invasive placentation and gestational fetal growth are not requir
72 etween maternal and fetal cells during early placentation and highlights novel avenues for research t
73 cations including low birth weight, abnormal placentation and increased risk for rare imprinting diso
74 rrations in embryo spacing, decidualization, placentation and intrauterine embryonic growth, manifest
75 of decidualized endometrium is essential for placentation and is tightly regulated and involves troph
76 origin that have been co-opted for a role in placentation and likely contribute to the remarkable div
77 nic balance in pregnancy and induce abnormal placentation and maternal hypertension.
78  deregulating processes associated with good placentation and maternal spiral artery remodeling.
79 hat endocannabinoid signaling is critical to placentation and pregnancy success in humans and implica
80  proinflammatory molecules inducing abnormal placentation and premature labor.
81 eptor 4 (Par4) from the mother allows normal placentation and prevents fetal loss.
82  pregnancy for species with epitheliochorial placentation and some but not all Laurasiatheria species
83  demonstrate both clade-specific patterns of placentation and specific cases of convergent evolution
84                                    Defective placentation and subsequent placental insufficiency lead
85 cells is a requisite process for hemochorial placentation and successful pregnancy.
86 n vivo evidence that IGFBP-1 plays a role in placentation and suggests that IGFBP-1 has a pathologica
87 ioxidant defenses may contribute to abnormal placentation and the later development of pregnancy comp
88   Given the role of imprinted genes in human placentation and the vulnerability of imprinted genes to
89 -induced adaptations critical to hemochorial placentation and thus nutrient flow to extraembryonic an
90 o modulate several processes associated with placentation and to promote maternal tolerance toward fe
91 normal placentation; however, TPbeta impairs placentation, and promotes the development of IUGR, and
92 vels of AM in the processes of implantation, placentation, and subsequent fetal growth.
93 ortant roles in nurturing the embryo, normal placentation, and uterine tissue remodeling.
94 thrombosis (alphaIIbbeta3) and implantation, placentation, angiogenesis, bone remodeling, and tumor p
95                                  Controlling placentation are maternal natural killer (NK) cells that
96 cells (uNK) play a role in the regulation of placentation, but their functions in nonpregnant endomet
97 dds to our understanding of implantation and placentation by reporting the expression and function of
98 ordinates implantation, decidualization, and placentation crucial to pregnancy success.
99 s in mouse are caused by decidualisation and placentation defects that can be rescued by transferring
100 n aged female mice is associated with severe placentation defects, which result from major deficits i
101  to failures in yolk sac and chorioallantoic placentation, die around embryonic day 10.5.
102 stem cells as a discovery platform for human placentation disorders and suggest that LIMK1 activity h
103  causal or pathogenetic model of superficial placentation driven by immune maladaptation, with subseq
104 echanisms and in turn sustaining hemochorial placentation during the long gestation of anthropoid pri
105                                 During human placentation, fetal cytotrophoblast stem cells different
106  of the anchoring villi convert during human placentation from a transporting epithelium to an invasi
107            Partial failure of the process of placentation has been implicated, and recent findings su
108                                     Invasive placentation has further required the maternal immune sy
109 Cyprinodontiformes, in which livebearing and placentation have evolved several times independently.
110 n the cases of placenta previa with abnormal placentation, however statistically insignificant.
111 e that expression of TPalpha mediates normal placentation; however, TPbeta impairs placentation, and
112 n selection coincident with the evolution of placentation in fishes, with particularly strong selecti
113  (KIRs) on the maternal uNK cells--influence placentation in human pregnancy.
114 ve been used for the convergent evolution of placentation in independently evolved and highly distant
115 mals and is likely to be a major effector of placentation in its related clade.
116                                              Placentation in primates is associated with the producti
117 iated with an increased risk of disorders of placentation in subsequent pregnancies, but effects on t
118                  The mechanisms of deficient placentation in the first trimester remain poorly unders
119 esis that they are associated with deficient placentation in the first trimester.
120 n the diagnostics and management of abnormal placentation in women with placenta previa and to compar
121 lar program that is reminiscent of eutherian placentation, including both fetal and maternal signals.
122           Trophoblast differentiation during placentation involves an epithelial-mesenchymal transiti
123                                              Placentation is a process that establishes the maternal-
124 s hypothesis, which is that the evolution of placentation is associated with reduced pre-copulatory f
125  with a noninvasive epitheliochorial type of placentation is critical establishing an adequate uterin
126                             In most mammals, placentation is critical for fetal development and pregn
127                     Although chorioallantoic placentation is initiated appropriately in p38alpha null
128                                       Faulty placentation manifests in the mother as preeclampsia wit
129  of selection pressures on the efficiency of placentation may stem from changes in nutritional demand
130                        In this in vivo human placentation model, human cytotrophoblasts invade the re
131 pears to be an important component of normal placentation, perhaps limiting the proliferative and inv
132 on, and cervical insufficiency) and abnormal placentation (preeclampsia and intrauterine growth restr
133 in endometrial cells, which is essential for placentation/pregnancy in eutherian mammals and is a dir
134 ey play a major role in the implantation and placentation processes.
135 g selection among lineages that have evolved placentation recently.
136 ns the most common cause of IUGR is impaired placentation resulting from poor trophoblast function, w
137 es of rabbit biology, including primate-type placentation, short gestation, and delivery of litters,
138 , leading to decreased oxygen tension at the placentation site, stabilized hypoxia-inducible factor 1
139 g post-natal lactation than during pre-natal placentation, so there may be greater selection for geno
140 ene family known to be involved in mammalian placentation: the prolactins (two clusters), serpins, ca
141  We conclude that NK cells guide hemochorial placentation through controlling a hypoxia-sensitive ada
142 nderstanding the pathophysiology of impaired placentation to establish screening tests for stillbirth
143 icated genes are utilized at later stages of placentation to meet the metabolic needs of a diverse ra
144                         For implantation and placentation to occur, mouse embryo trophoblast cells mu
145                                 Early during placentation, trophoblast cell columns help anchor the d
146 ulating invasive trophoblast and hemochorial placentation was investigated using Rcho-1 trophoblast s
147 ence of histologic features of dysfunctional placentation, was associated with preeclampsia and fetal
148 le effects of the maternal genotype on fetal placentation, we generated transgenic mice that expresse
149        The results of MRI and US in abnormal placentation were compared with post-operative data.
150 tion reflect the pathology of defective deep placentation, where conversion of uterine spiral arterie
151 cipate in implantation, decidualization, and placentation, whether there is a common molecular link t
152 ncomplicated pregnancy and is present during placentation, which occurs under low oxygen tensions.
153            Hectd1 is widely expressed during placentation with enrichment in trophoblast giant cells

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