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1 implantation embryos and a 10 week old whole foetus.
2 gue in the protozoan parasite Tritrichomonas foetus.
3 t-dependent cytotoxicity of host cells by T. foetus.
4 ituents of the lipophosphoglycan (LPG) of T. foetus.
5 ay of the parasitic protozoan Tritrichomonas foetus.
6  gallinae and cattle parasite Tritrichomonas foetus.
7 ation to ensure immune tolerance towards the foetus.
8 specifically in germ cells of the mouse male foetus.
9 that may be pro-arrhythmic in the developing foetus.
10 in order to stop the cardiac activity in the foetus.
11 ly appears only to function in the mammalian foetus.
12 in Drosophila and eyelid fusion in the mouse foetus.
13 city, as are the size and composition of the foetus.
14  the prognostic value of ADC changes in IUGR foetuses.
15 e responses to IUGR in the muscle of porcine foetuses.
16  severity of placental insufficiency in IUGR foetuses.
17  the developmental mechanisms of pig embryos/foetuses.
18  health outcomes in both pregnant people and foetuses.
19 in the rudimentary kidney tissue of SALL1-KO foetuses.
20 e use of an empty developmental niche in pig foetuses.
21 henotypes, including 11 pairs of anencephaly foetuses, 10 pairs of hydrocephalus foetuses and nine pa
22                               Tritrichomonas foetus, a venereal pathogen of cattle, was recently iden
23 derived primary fibroblastic cell lines from foetuses affected by NTDs and subjected them to the dU s
24                  Stillbirth is the loss of a foetus after 22 weeks of gestation, of which almost half
25                               Tritrichomonas foetus, an anaerobic flagellated protozoan, causes uroge
26 transmitted disease caused by Tritrichomonas foetus and characterized by early embryo loss.
27 e and risk factors for feline Tritrichomonas foetus and Giardia infection.
28 aining difference in MPA affinity between T. foetus and human IMPDH.
29 old difference in sensitivity between the T. foetus and human IMPDHs derive from the residues in the
30 nhibitor experiments with the Tritrichomonas foetus and human type 2 IMPDHs using tiazofurin and ADP,
31  the effect of medications on the developing foetus and is a major contributor to loss of asthma cont
32 l messenger of sexual differentiation in the foetus and is an emerging biomarker of postnatal reprodu
33 to intracranial non-traumatic haemorrhage of foetus and newborn (5% increased risk of death per Mb in
34 d the incidence of haemolytic disease of the foetus and newborn previously responsible for one death
35 ike growth factor-2 is expressed in both the foetus and placenta and has been shown to have roles in
36 hree matrilineal generations as one (mother, foetus and post-meiotic oocytes) has provided a maternal
37 the cytopathogenic effects of Tritrichomonas foetus and the role of lipophosphoglycan (LPG)-like cell
38 )CD8(+) (SP8) thymocyte populations from the foetus and young adult mouse.
39 ups of intrauterine growth restricted (IUGR) foetuses and control cases.
40 ncephaly foetuses, 10 pairs of hydrocephalus foetuses and nine pairs of encephalocele foetuses, was i
41 bnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in
42  within the perinatal period, the sex of the foetus, and exposure to maltreatment in childhood.
43 ession in myotome and muscle fibres in human foetuses, and zebrafish embryos and adolescents.
44                                           T. foetus appears to depend on HGXPRTase for its supply of
45 files in the muscle of growth restricted pig foetuses at different gestational days (GD; gestational
46 ly similar to bovine venereal Tritrichomonas foetus but having a unique tropism for the intestinal tr
47  regulation of nutrients and hormones to the foetus, but also activate downstream pathways through in
48 not exist for the ongoing transmission of T. foetus by water, food, or contact with other species.
49 bryos, placenta, uterus, ovary, and brain of foetuses by immunohistochemistry and quantified by real-
50 d AFX stem cells gave rise to cloned porcine foetuses by nuclear transfer.
51 s protozoan, and the costa of Tritrichomonas foetus; c) the flagellulm of trypanosomatids, that in ad
52 enes with critical roles in development in L foetuses can be observed from GD45, whereas for a majori
53 e demonstrated to be largely dependent on T. foetus cell-associated cysteine protease activity.
54      TF2 inhibited the growth of cultured T. foetus cells in a concentration-dependent manner with an
55 und scan showed a single, live, intrauterine foetus corresponding to a gestational age of around 22 w
56                                  Finally, T. foetus cysteine proteases were identified as enabling cy
57 e cytopathogenic effect was a function of T. foetus density.
58                       Patient 1 was a female foetus diagnosed with del(4)(q33) following chorionic vi
59  gestation period of >/=28 weeks wherein the foetus did not show any sign of life.
60  the two native histidine residues in the T. foetus enzyme as monitored by (1)H NMR revealed that H44
61      Unlike IMPDH from other species, the T. foetus enzyme has a single arginine that is largely resp
62  while Monocercomonas sp. and Tritrichomonas foetus formed the other.
63 of brucellosis transmission (through aborted foetuses) from migrant and resident elk to livestock.
64 Likewise, the bovine parasite Tritrichomonas foetus had no cytotoxic effects on hVECs.
65                                          All foetuses had normal foetal structural brain anatomy.
66    HLA class II disparity between mother and foetus has been associated with significantly increased
67 ltransferase (HGXPRTase) from Tritrichomonas foetus has been determined and refined against X-ray dat
68 ltransferase (HGXPRTase) from Tritrichomonas foetus has been proven to be a target for potential anti
69 e include riboflavin status and how well the foetus has been supplied with vitamin B6 by the mother.
70 H from the protozoan parasite Tritrichomonas foetus have been solved: with its substrate IMP, IMP and
71                           Thus, Arg155 in T. foetus HGXPRT and Arg187 in S. mansoni HGPRT will be att
72 aracterized as a competitive inhibitor of T. foetus HGXPRT with respect to guanine with a K(I) of 0.4
73 efforts to use the X-ray structure of the T. foetus HGXPRT-GMP complex to design compounds that bind
74         A comparison of the structures of T. foetus HGXPRTase and human HGPRTase reveals that, while
75                                           T. foetus HGXPRTase crystallizes as an asymmetric dimer, wi
76  the loop and the dynamics of the loop in T. foetus HGXPRTase were investigated using site-directed m
77 as shown to be a competitive inhibitor of T. foetus HGXPRTase with respect to both guanine (in the fo
78        Guided by the crystal structure of T. foetus HGXPRTase, we used structure-based drug design to
79 esponsible for the high Km for PPi in the T. foetus HGXPRTase-catalyzed reaction.
80                    The Kms for PPi in the T. foetus HGXPRTase-catalyzed reactions are unusually high,
81 (m) for PPi (165.5 microM) in Tritrichomonas foetus HGXPRTase-catalyzed reverse reaction.
82 rine cells, we micro-CT imaged a 12-week-old foetus homozygous for the nonsense mutation RFX6 c.1129C
83 e irreversibly inactivate the Tritrichomonas foetus hypoxanthine-guanine-xanthine phosphoribosyltrans
84                      Lys310 and Glu431 of T. foetus IMPDH are replaced by Arg and Gln, respectively,
85 res of the protozoan parasite Tritrichomonas foetus IMPDH complexed with the inhibitor ribavirin mono
86  the catalytic core domain of Tritrichomonas foetus IMPDH in complex with IMP and beta-methylene-TAD
87 An X-ray crystal structure of Tritrichomonas foetus IMPDH with mizoribine monophosphate (MZP) reveals
88                           A comparison of T. foetus IMPDH with the Chinese hamster and Streptococcus
89                                       For T. foetus IMPDH, tiazofurin and ADP are extraordinarily syn
90 cats has been mired by unfamiliarity with T. foetus in cats as well as misdiagnosis of the organisms
91 signed and optimized for the detection of T. foetus in feline feces by using a combination of novel (
92 inity chromatography to purify Tf190 from T. foetus in order to analyze its composition and examine i
93 H from the protozoan parasite Tritrichomonas foetus in the apo form at 2.3 A resolution and the enzym
94 me-editing approach to generate anephrogenic foetuses in a genetically engineered pig model.
95 ssed at sites of chondrogenesis within human foetuses, including the vertebrae.
96 ptosis is involved in the pathogenesis of T. foetus infection in vivo, which may have important impli
97  vitro coculture approach to model feline T. foetus infection of the intestinal epithelium, these stu
98 cells undergoing apoptosis in response to T. foetus infection or incubation with CP30.
99 ific PCR test for the diagnosis of feline T. foetus infection.
100                                           T. foetus infects the mucosal surfaces of the reproductive
101 in-like growth factor-2 in both placenta and foetus (insulin-like growth factor-2-total KO).
102 n China and estimate that 0.14 points of per-foetus intelligence quotient (IQ) decrements and 7,360 d
103 plification of a conserved portion of the T. foetus internal transcribed spacer (ITS) region (ITS1 an
104 mption prevents 0.39 x 10(-2) points for per-foetus IQ decrements and 194 deaths from fatal heart att
105                                           T. foetus is a good organism to study because its purine sa
106 ) from the protozoan parasite Tritrichomonas foetus is a rational target for antiparasitic drug desig
107                               Tritrichomonas foetus is a serious veterinary pathogen, causing bovine
108 tive Adaptive Response), and that the female foetus is better adapted than the male to maternal adver
109         Growth and survival of the mammalian foetus is dependent upon a functional placenta throughou
110 y, the inner cell mass (ICM), from which the foetus is derived and hence of interest in reproductive
111 RTase), a type I PRTase, from Tritrichomonas foetus, is a potential target for antitritrichomonal che
112 d in kidney but not in liver, whereas in the foetus it is expressed in both organs.
113 cle samples were collected from the lightest foetus (L) and the sex-matched foetus with weight closes
114                            Infection with T. foetus leads to apoptotic cell death of bovine vaginal e
115 ngenital defects and neurological lesions in foetuses like haemorrhages, diffuse cerebral edema, necr
116                                           T. foetus LPG inhibited the binding of T. foetus to BVECs;
117 the maternal immune system does not reject a foetus may involve the downregulation of T-cell receptor
118 dynamic changes present in growth-restricted foetuses may persist postnatally.
119                Brain development in affected foetuses might be improved through prenatal treatment.
120 erious deleterious effects on the mother and foetus/neonate.
121 ason is because inhibition of Tritrichomonas foetus ODC results in growth arrest, destruction of hydr
122   Case Report: We present a case of CRS in a foetus of a non-diabetic mother and discuss the role of
123 s the rarity caudal regression syndrome in a foetus of a non-diabetic mother.
124 determine the pathogenic effect of feline T. foetus on porcine intestinal epithelial cells, the depen
125                                        As T. foetus organisms are fastidious and fragile, routine flo
126 arasite is spread efficiently from mother to foetus over several generations, and naturally infected
127 the infection, the cellular mechanisms of T. foetus pathogenicity in the intestinal tract have not be
128 tinal epithelial cells, the dependence of T. foetus pathogenicity on adhesion of T. foetus to the int
129                          The diagnosis of T. foetus presently depends on the demonstration of live or
130 pithelium, these studies demonstrate that T. foetus promotes a direct contact-dependent activation of
131 erase (HGXPRTase), an essential enzyme in T. foetus required for salvaging exogenous purine bases, ha
132            Exposure of BVEC monolayers to T. foetus resulted in extensive damage of monolayers.
133       Metronidazole- or periodate-treated T. foetus showed no damage to BVEC monolayers.
134 of the ribosomal RNA gene from feces with T. foetus-specific primers (34 out of 36).
135 usly characterized IMPDH from Tritrichomonas foetus ( TfIMPDH).
136                            In the APS model, foetuses that showed increased C3 in their brains additi
137 ginalis LPG (but not LPG from Tritrichomonas foetus, the causative agent of bovine trichomoniasis) in
138 s of Tf190 occurs in different strains of T. foetus, the Tf190 adhesion complex is widespread in diff
139 e of the trichomonad parasite Tritrichomonas foetus, this otherwise highly conserved histidine is rep
140 nd interactions mediate the attachment of T. foetus to BVECs.
141    T. foetus LPG inhibited the binding of T. foetus to BVECs; the LPG from T. vaginalis and a variety
142 y, and the vulnerability of the placenta and foetus to invasion are important features.
143  structures, important in the adhesion of T. foetus to mammalian cells, are located in the LPG-like c
144                     Exposure of a developing foetus to maternal gestational diabetes (GDM) has been s
145  forms late in embryogenesis, permitting the foetus to survive a terrestrial environment at birth.
146 of T. foetus pathogenicity on adhesion of T. foetus to the intestinal epithelium, and the identity of
147 topathic effects by promoting adhesion of T. foetus to the intestinal epithelium.
148 ased immunoassays in the frontal cortex from foetuses to adults with Down syndrome and control subjec
149 0,963 images spanning a wide age range (from foetuses to elderly individuals) acquired using a variet
150 e cellular mechanisms of pathogenicity of T. foetus toward the intestinal epithelium and support furt
151 etic mechanism for IMPDH from Tritrichomonas foetus using ligand binding, isotope effect, pre-steady-
152                             Prevalence of T. foetus was 31% among cats (36 out of 117) and catteries
153                        Catteries in which T. foetus was identified were more likely to have had a rec
154 syltransferase (HGXPRTase) of Tritrichomonas foetus was inactivated by the thiol reagents iodoacetate
155 lus foetuses and nine pairs of encephalocele foetuses, was investigated by NanoString nCounter techno
156                                           In foetus we identified less influence of MHC-restriction o
157                                    From this foetus, we derived iPSCs and show that differentiation o
158  and metabolism differences between L and AW foetuses were apparent by GD60 or only at GD90, thus ide
159                                              Foetuses were extracted via C-section on gestational Day
160  to the normal group, the ADC values in IUGR foetuses were significantly lower in cerebellar hemisphe
161 y active females abandon investment in their foetus when conditions are poor, exemplified using an ex
162 em needs to maintain immune tolerance of the foetus while also responding to infection, which can cau
163 ere significantly lower in IUGR than control foetuses, while there was no significant difference amon
164      TF1 inhibited the in vitro growth of T. foetus with an EC50 of approximately 40 microM.
165 ometry experiments on several isolates of T. foetus with Tf190-specific antibodies revealed that Tf19
166  the lightest foetus (L) and the sex-matched foetus with weight closest to the litter average (AW) fr
167 ly upregulated in the brain tissues of human foetuses with anencephaly.
168                               We included 44 foetuses with appropriate weight for gestational age (AG
169                       IUGR cases included 23 foetuses with clinical severity signs (group A) and 15 f
170 iate weight for gestational age (AGA) and 46 foetuses with documented IUGR, defined as the estimated
171 tical primary cultures from second trimester foetuses with Down syndrome (Down syndrome n = 7, contro
172                                A total of 38 foetuses with IUGR and 18 normal control foetuses with s
173  38 foetuses with IUGR and 18 normal control foetuses with similar gestational age were compared usin
174                                              Foetuses with structural brain abnormalities were exclud
175 ith clinical severity signs (group A) and 15 foetuses without clinical severity signs (group B).

 
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