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1 rus (ZIKV) epidemic is to prevent congenital foetal abnormalities, including microcephaly, following
2                    The phenotype ranges from foetal akinesia resulting in in utero or neonatal mortal
3 itance and degrees of severity (ranging from foetal akinesia, through lethality in the newborn period
4 ystem to adapt and positively respond to the foetal allotype.
5 life with pronounced differences between the foetal and adult human brain.
6 protection assays, the expression in several foetal and adult human tissues of genes encoding FMO1, F
7 s lacZ expression in transgenic mice to most foetal and adult long-term repopulating haematopoietic s
8 e performed a detailed analysis of both late foetal and adult muscle development in the absence of Me
9              In particular, we discover that Foetal and Adult Testis Expressed 1 (FATE1) is a key sur
10  mRNA is present in low abundance in several foetal and adult tissues and thus the corresponding gene
11             Furthermore, comparison of human foetal and adult tissues indicates a developmental splic
12                           Cell types of both foetal and maternal origin are profiled.
13 , which parallel the facilitative effects of foetal and MHP36 grafts in rats with ischaemic CA1 damag
14 placenta and has been shown to have roles in foetal and placental development in animal models.
15    A few genes are known that influence both foetal and placental growth and might therefore coordina
16 rnally-inherited allele and acts to restrict foetal and placental growth.
17 ugh these findings imply that growth in both foetal and postnatal life influences cognitive performan
18 es are developmentally regulated during both foetal and postnatal mammary gland development.
19                      Cultures of dissociated foetal and postnatal mouse gut gave rise to neurosphere-
20 d for BDNF-promoted neurite growth from both foetal and postnatal mouse sensory neurons, there is a d
21            These trials use human embryonic, foetal and umbilical cord tissue-derived stem cells and
22 ry airway malformation (CPAM) is an uncommon foetal anomaly with a very wide range of ultrasound appe
23                                        Since foetal antiepileptic drug exposure is associated with lo
24 igation, we examined dose-related effects of foetal antiepileptic drug exposure on verbal and non-ver
25 d changes in the maternal immune response to foetal antigens.
26                                 However, the foetal blood-brain barrier to plasma proteins remained i
27 cylinders aged in Phosphate Buffered Saline, Foetal Bovine Serum, Dulbecco's - Minimum Essential Medi
28 l) of cells dissected from the CA1 region of foetal brain at embryonic day 94-96, or of conditionally
29                           We also found that foetal brain C3 deposition was associated with cortical
30 ticles bind within the inflamed placenta and foetal brain cortical tissue, causing a shortening of th
31 ion of complement activation in placenta and foetal brain in vivo in utero.
32  transmission, reducing the ZIKV load in the foetal brain more than 20-fold.
33         We screened an array of 27 648 human foetal brain proteins with 12 well-expressed antibody fr
34 ptor null mouse shows extensive apoptosis in foetal brain.
35   Only the shortest 3R isoform is present in foetal brain.
36                            Fluid from normal foetal brains did not have this effect.
37   CSF from the lateral ventricle of affected foetal brains not only inhibited in vitro proliferation
38 odopsin+ rods develop in the presence of 10% foetal calf serum (FCS), large numbers develop in the ab
39 comere integrity, in the context of enabling foetal cardiomyocyte hypertrophy, maintenance of contrac
40 fibrils, and fibrils isolated from adult and foetal cartilage and vitreous humour.
41                                              Foetal cases (n = 25) represent the severe end of the sp
42 cts may reach the placenta and spread to the foetal circulation and amniotic fluid.
43 ical forward planning resulted from maternal-foetal co-adaptation facilitated by co-expression of the
44 regnancies ending in delivery or spontaneous foetal death after 21 October 2009 and starting before 0
45 n was assumed to be transient, the hazard of foetal death during gestational weeks 9 through 12 (HR(u
46                             Hazard ratios of foetal death for vaccinated compared to unvaccinated pre
47 ous abortion, sudden intrauterine unexpected foetal death syndrome and stillbirth.
48                A stillbirth was defined as a foetal death with a gestation period of >/=28 weeks wher
49 ancy does not appear to increase the risk of foetal death.
50 ituation where there is an imbalance between foetal demand and placental supply of nutrients (the ins
51 e is a mismatch between placental supply and foetal demand for nutrients during gestation.
52 ectoderm differentiation leading to abnormal foetal development and premature death.
53 r leptin in gut and immune regulation and in foetal development have been proposed.
54 betacatenin signalling in oocyte biology and foetal development, and provides novel insights into the
55 e effect profile affecting metabolism and/or foetal development.
56 ntial nutrients each have important roles in foetal development.
57 re generated during late embryonic and early foetal development.
58 v-src oncogene was introduced into the human foetal diploid fibroblasts MRC-5 and into MRC-SV1, a sim
59        To address this issue we transplanted foetal dopaminergic neurons from mice lacking the dopami
60 stoma cells were fused with cells from human foetal dorsal root ganglia and several continuously-grow
61 ess various antigens characteristic of human foetal dorsal root ganglion neurons.
62                          We hypothesize that foetal drug exposure may alter normal cerebral lateraliz
63 red increased maternal feeding in advance of foetal energetic demands; the mammary glands are primed
64 morphological features comparable with human foetal epicardial explants and engrafted in the subepica
65 l maturation of foetal organs, yet excessive foetal exposure is detrimental to adult cardiovascular h
66                                              Foetal exposure may also result in tissue damage, increa
67  language may be particularly susceptible to foetal exposure.
68 ype that is induced through abnormalities in foetal fibre formation.
69  in the heart also causing cardiac fibrosis, foetal gene reprogramming, and impaired mitochondrial bi
70                                              Foetal glomerular podocytes expressed Fras1 transcripts
71 cell grafts are as functionally effective as foetal grafts and appear to integrate into the host brai
72                Visualized by Nissl staining, foetal grafts formed clumps of pyramidal-like cells with
73 omparing foetal neural precursor and primary foetal grafts in both allo- and xenograft environments u
74 ts with richer axonal outgrowth than primary foetal grafts, and that this is independent of the immun
75   These maternal biomarkers are important to foetal growth and could be used in prenatal care as an a
76                                     In utero foetal growth has required increased maternal feeding in
77                               The control of foetal growth is poorly understood and yet it is critica
78 there is a genetic link between diabetes and foetal growth.
79 ed placenta was more efficient in supporting foetal growth.
80     They remained neurogenic in vitro and in foetal gut grafts.
81 life, have a minimal or late contribution to foetal haematopoiesis but instead largely proliferate du
82 in both lymphoid and myeloid lineages during foetal haematopoiesis, contributing to the increased ris
83 ast extracellular vesicles (STBEVs) and free foetal haemoglobin (HbF) into the maternal circulation.
84 he human syndrome, hereditary persistence of foetal haemoglobin (HPFH).
85 d group phenotype, hereditary persistence of foetal haemoglobin, borderline HbA(2), and congenital dy
86 reduces haemolysis and anaemia by increasing foetal haemoglobin, which leads to lower hypoxic transcr
87 functional and biochemical maturation of the foetal heart is dependent on glucocorticoid signalling w
88  injections of wild-type CPCs into Speg(-/-) foetal hearts.
89 a, the latter specifically in the setting of foetal hydantoin syndrome.
90 of the deficient cortical development in the foetal hydrocephalic rat brain, we conclude that the con
91 y-life exposures may act upon the developing foetal immune system and include infection, environmenta
92  foeto-placental compartment can stimulate a foetal immune/inflammatory response characterized by the
93 us transplacental infection (TPI)' to define foetal infection from a recrudescent maternal infection
94 ly prenatally) and 'exogenous TPI' to define foetal infection that occurs as a result of an infection
95  such as maternal genotype effects, maternal-foetal interactions and parent-of-origin (imprinting) ef
96  distinct cell types present at the maternal-foetal interface and advance our knowledge of dynamic ge
97  increases in methylation levels relative to foetal kidney and reductions relative to the adult kidne
98 ildhood is more important than growth during foetal life in determining cognitive function.
99 was expressed in the cerebral cortex only in foetal life stages, while in the cerebellum it was also
100 s throughout adult life and are specified in foetal life, have a minimal or late contribution to foet
101 ormation and preservation of the pluripotent foetal lineage.
102 e functionally differentiated progeny to all foetal lineages of chimaeras.
103  numbers of megakaryocytes in the c-myb(-/-) foetal liver also refute early suggestions that megakary
104 ession to haematopoietic progenitors in both foetal liver and adult bone marrow.
105 e of haematopoietic stem cells (HSCs) in the foetal liver at E12.5, the embryo contains only a few de
106                                       During foetal liver colonization, circulating HSCs remained wit
107 e large pool of definitive HSC/RUs in day 12 foetal liver is formed predominantly by recruiting 'read
108 hought that the burst of HSC activity in the foetal liver is underpinned by rapid maturation of immat
109 correlates with an absence in the c-myb(-/-) foetal liver of uni- and multilineage CFUs.
110 y self-renew and can be seeded from yolk sac/foetal liver progenitors with little input from monocyte
111 initive progenitors, initially populated the foetal liver, but are unable to expand like wild type pr
112        By E12.5, in addition to apoptosis in foetal liver, endocardium and myocardium, the erythropoi
113 ortion of CD34+CD45+ cells in the c-myb(-/-) foetal liver.
114 population of definitive HSCs emerges in the foetal liver.
115 s the number of definitive HSCs in the E12.5 foetal liver.
116 sed levels of RUNX1, C-KIT and PU.1 in human foetal livers with T21.
117                      The only association of foetal loss (during gestational weeks 11 to 27) was obse
118                      To evaluate the risk of foetal loss associated with pandemic influenza vaccinati
119     There was no difference in the hazard of foetal loss during weeks 25 to 43 in either model.
120 ether the potential effect of vaccination on foetal loss might be transient (for ~4 weeks post vaccin
121 nated pregnancies also had a lower hazard of foetal loss than unvaccinated pregnancies in gestational
122 ral forms of reproductive suboptimality (viz foetal loss, preterm birth and low birth weight).
123 PCP genes Celsr1 and Vangl2 are required for foetal lung development thereby revealing a novel signal
124 iption start sites are utilized in adult and foetal lungs.
125 rus which emerged in Europe in 2011, causing foetal malformations in ruminants.
126 sorder characterised by raised bile acids in foetal-maternal circulation, which threatens perinatal h
127 ave potential to influence the health of the foetal-maternal unit.
128                                              Foetal membranes possess distinctive properties which ca
129           Intrastriatal transplants of human foetal mesencephalic tissue in Parkinson's patients have
130 A libraries from human embryonic, neural and foetal mesenchymal stem cells.
131 ls harvested from the subventricular zone of foetal mice were preconditioned with interleukin 6 in vi
132 ected on foetal ultrasound, through abnormal foetal movements and a multisystem neonatal disorder, to
133  suggested the existence of adult as well as foetal multipotent progenitor cells with combined B cell
134 o compensation by retained expression of the foetal NaV1.5 isoform was detected.
135 n's and Parkinson's disease who had received foetal neural allografts.
136 e addressed this issue directly by comparing foetal neural precursor and primary foetal grafts in bot
137               We present clear evidence that foetal neural precursors produce grafts with richer axon
138 dicting placental insufficiency and abnormal foetal neurodevelopment that leads to neuropsychiatric d
139                         A key feature of the foetal-onset hydrocephalus in this rat is obstruction in
140                     They can be derived from foetal or adult germinal tissues and continuously propag
141  the structural and functional maturation of foetal organs, yet excessive foetal exposure is detrimen
142                                Although the 'foetal origins of adult disease' hypothesis has signific
143 t common molecular defect found in the human foetal overgrowth syndrome, Beckwith-Wiedemann syndrome
144 expression of Igf2 in endodermal tissues and foetal overgrowth, demonstrating that methylation in viv
145 s but instead largely proliferate during the foetal period.
146 nal hypothalamus is hormonally primed by the foetal placenta for nest building and post-natal care.
147 oorganisms and/or their components reach the foetal-placental unit and one indirect, in which Inflamm
148 lammatory mediators circulate and impact the foetal-placental unit.
149 thotrexate can be injected directly into the foetal pole under transvaginal ultrasound guidance in or
150 are, the origin and biological mechanisms of foetal programming are largely unknown.
151 tory, cautious interpretation of skin tests, foetal Rh genotyping from maternal blood and, in some ca
152 gnature to a genomic bar code of the fate of foetal Sertoli cells.
153 at neural crest-derived cells present within foetal small intestine explants migrate towards an exoge
154  in E17.5 GR(-/-) hearts, they are normal in foetal SMGRKO hearts.
155 d partly or entirely by incorporation of the foetal-specific gamma-subunit into end-plate AChR.
156 nitial reports on phase 1 clinical trials of foetal spinal cord grafts into patients with post-trauma
157 bnormal development of the caudal end of the foetal spine along with many associated anomalies.
158 gest that steroidogenic adrenal cells during foetal stages require Sf1 to give rise to the adult adre
159 is currently being assessed clinically using foetal striatal tissue in Huntington's disease.
160 ggests that neuronal precursors derived from foetal striatum may have a greater capacity than primary
161 tum may have a greater capacity than primary foetal striatum to project to the usual striatal target
162 und chromatin regions from murine and bovine foetal testes with sequencing of RNA samples from mouse
163                                           In foetal testes, SOX9 modulates both transcription and dir
164 re with the presence of SOX9 on chromatin in foetal testes, therefore equating this signature to a ge
165 e identified TRIM28 as a new SOX9 partner in foetal testes.
166 roid pathology, 30 population controls, nine foetal thyroid tissues and nine foetal tissues of non-th
167                      Epigenetic variation in foetal tissue may have a mechanistic role in metabolic d
168 cursor and primary grafts derived from human foetal tissue produced a significantly richer outgrowth
169 ntrols, nine foetal thyroid tissues and nine foetal tissues of non-thyroid origin, either kidney or l
170 women of South Asian origin were studied and foetal tissues sampled at term delivery.
171 e resource that provides human embryonic and foetal tissues to the scientific community, enabling gen
172  were expressed in a wide range of adult and foetal tissues.
173 be ubiquitously expressed in human adult and foetal tissues.
174 d is also present, in low abundance, in some foetal tissues.
175 larized organ comprised of both maternal and foetal tissues.
176  the extent and factors influencing maternal-foetal transfer in low transmission areas co-endemic for
177                                     Maternal-foetal transfer of anti-malarial IgG to Plasmodium spp.
178 acking the donor cells, whereas most primary foetal transplant studies have utilized an allograft par
179 tors presumably influence the development of foetal Tregs.
180 lated to the persistence or re-occurrence of foetal type 2 signalling.
181 y extended from ventriculomegaly detected on foetal ultrasound, through abnormal foetal movements and
182                  We previously reported that foetal valproate exposure impairs intelligence quotient.
183        In this study, we transplanted murine foetal ventral mesencephalic cells into rats rendered he
184 en a surprising side-effect of intrastriatal foetal ventral mesencephalic transplantation in patients
185 fection in these mice precludes the study of foetal (vertical) viral transmission.

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