ライフサイエンスコーパス: foetus

1 ly appears only to function in the mammalian foetus.

2 in Drosophila and eyelid fusion in the mouse foetus.

3 in order to stop the cardiac activity in the foetus.

4 city, as are the size and composition of the foetus.

5 implantation embryos and a 10 week old whole foetus.

6 gue in the protozoan parasite Tritrichomonas foetus.

7 t-dependent cytotoxicity of host cells by T. foetus.

8 ituents of the lipophosphoglycan (LPG) of T. foetus.

9 ay of the parasitic protozoan Tritrichomonas foetus.

10 Tritrichomonas foetus, a venereal pathogen of cattle, was recently iden

11 derived primary fibroblastic cell lines from foetuses affected by NTDs and subjected them to the dU s

12 Tritrichomonas foetus, an anaerobic flagellated protozoan, causes uroge

13 transmitted disease caused by Tritrichomonas foetus and characterized by early embryo loss.

14 e and risk factors for feline Tritrichomonas foetus and Giardia infection.

15 aining difference in MPA affinity between T. foetus and human IMPDH.

16 old difference in sensitivity between the T. foetus and human IMPDHs derive from the residues in the

17 nhibitor experiments with the Tritrichomonas foetus and human type 2 IMPDHs using tiazofurin and ADP,

18 l messenger of sexual differentiation in the foetus and is an emerging biomarker of postnatal reprodu

19 d the incidence of haemolytic disease of the foetus and newborn previously responsible for one death

20 ike growth factor-2 is expressed in both the foetus and placenta and has been shown to have roles in

21 hree matrilineal generations as one (mother, foetus and post-meiotic oocytes) has provided a maternal

22 the cytopathogenic effects of Tritrichomonas foetus and the role of lipophosphoglycan (LPG)-like cell

23 bnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in

24 T. foetus appears to depend on HGXPRTase for its supply of

25 ly similar to bovine venereal Tritrichomonas foetus but having a unique tropism for the intestinal tr

26 not exist for the ongoing transmission of T. foetus by water, food, or contact with other species.

27 e demonstrated to be largely dependent on T. foetus cell-associated cysteine protease activity.

28 TF2 inhibited the growth of cultured T. foetus cells in a concentration-dependent manner with an

29 und scan showed a single, live, intrauterine foetus corresponding to a gestational age of around 22 w

30 Finally, T. foetus cysteine proteases were identified as enabling cy

31 e cytopathogenic effect was a function of T. foetus density.

32 Patient 1 was a female foetus diagnosed with del(4)(q33) following chorionic vi

33 gestation period of >/=28 weeks wherein the foetus did not show any sign of life.

34 the two native histidine residues in the T. foetus enzyme as monitored by (1)H NMR revealed that H44

35 Unlike IMPDH from other species, the T. foetus enzyme has a single arginine that is largely resp

36 while Monocercomonas sp. and Tritrichomonas foetus formed the other.

37 Likewise, the bovine parasite Tritrichomonas foetus had no cytotoxic effects on hVECs.

38 HLA class II disparity between mother and foetus has been associated with significantly increased

39 ltransferase (HGXPRTase) from Tritrichomonas foetus has been determined and refined against X-ray dat

40 ltransferase (HGXPRTase) from Tritrichomonas foetus has been proven to be a target for potential anti

41 e include riboflavin status and how well the foetus has been supplied with vitamin B6 by the mother.

42 H from the protozoan parasite Tritrichomonas foetus have been solved: with its substrate IMP, IMP and

43 Thus, Arg155 in T. foetus HGXPRT and Arg187 in S. mansoni HGPRT will be att

44 aracterized as a competitive inhibitor of T. foetus HGXPRT with respect to guanine with a K(I) of 0.4

45 efforts to use the X-ray structure of the T. foetus HGXPRT-GMP complex to design compounds that bind

46 A comparison of the structures of T. foetus HGXPRTase and human HGPRTase reveals that, while

47 T. foetus HGXPRTase crystallizes as an asymmetric dimer, wi

48 the loop and the dynamics of the loop in T. foetus HGXPRTase were investigated using site-directed m

49 as shown to be a competitive inhibitor of T. foetus HGXPRTase with respect to both guanine (in the fo

50 Guided by the crystal structure of T. foetus HGXPRTase, we used structure-based drug design to

51 esponsible for the high Km for PPi in the T. foetus HGXPRTase-catalyzed reaction.

52 The Kms for PPi in the T. foetus HGXPRTase-catalyzed reactions are unusually high,

53 (m) for PPi (165.5 microM) in Tritrichomonas foetus HGXPRTase-catalyzed reverse reaction.

54 e irreversibly inactivate the Tritrichomonas foetus hypoxanthine-guanine-xanthine phosphoribosyltrans

55 Lys310 and Glu431 of T. foetus IMPDH are replaced by Arg and Gln, respectively,

56 res of the protozoan parasite Tritrichomonas foetus IMPDH complexed with the inhibitor ribavirin mono

57 the catalytic core domain of Tritrichomonas foetus IMPDH in complex with IMP and beta-methylene-TAD

58 An X-ray crystal structure of Tritrichomonas foetus IMPDH with mizoribine monophosphate (MZP) reveals

59 A comparison of T. foetus IMPDH with the Chinese hamster and Streptococcus

60 For T. foetus IMPDH, tiazofurin and ADP are extraordinarily syn

61 cats has been mired by unfamiliarity with T. foetus in cats as well as misdiagnosis of the organisms

62 signed and optimized for the detection of T. foetus in feline feces by using a combination of novel (

63 inity chromatography to purify Tf190 from T. foetus in order to analyze its composition and examine i

64 H from the protozoan parasite Tritrichomonas foetus in the apo form at 2.3 A resolution and the enzym

65 ptosis is involved in the pathogenesis of T. foetus infection in vivo, which may have important impli

66 vitro coculture approach to model feline T. foetus infection of the intestinal epithelium, these stu

67 cells undergoing apoptosis in response to T. foetus infection or incubation with CP30.

68 ific PCR test for the diagnosis of feline T. foetus infection.

69 T. foetus infects the mucosal surfaces of the reproductive

70 in-like growth factor-2 in both placenta and foetus (insulin-like growth factor-2-total KO).

71 plification of a conserved portion of the T. foetus internal transcribed spacer (ITS) region (ITS1 an

72 T. foetus is a good organism to study because its purine sa

73 ) from the protozoan parasite Tritrichomonas foetus is a rational target for antiparasitic drug desig

74 Tritrichomonas foetus is a serious veterinary pathogen, causing bovine

75 Growth and survival of the mammalian foetus is dependent upon a functional placenta throughou

76 RTase), a type I PRTase, from Tritrichomonas foetus, is a potential target for antitritrichomonal che

77 d in kidney but not in liver, whereas in the foetus it is expressed in both organs.

78 Infection with T. foetus leads to apoptotic cell death of bovine vaginal e

79 T. foetus LPG inhibited the binding of T. foetus to BVECs;

80 the maternal immune system does not reject a foetus may involve the downregulation of T-cell receptor

81 erious deleterious effects on the mother and foetus/neonate.

82 ason is because inhibition of Tritrichomonas foetus ODC results in growth arrest, destruction of hydr

83 Case Report: We present a case of CRS in a foetus of a non-diabetic mother and discuss the role of

84 s the rarity caudal regression syndrome in a foetus of a non-diabetic mother.

85 determine the pathogenic effect of feline T. foetus on porcine intestinal epithelial cells, the depen

86 As T. foetus organisms are fastidious and fragile, routine flo

87 arasite is spread efficiently from mother to foetus over several generations, and naturally infected

88 the infection, the cellular mechanisms of T. foetus pathogenicity in the intestinal tract have not be

89 tinal epithelial cells, the dependence of T. foetus pathogenicity on adhesion of T. foetus to the int

90 The diagnosis of T. foetus presently depends on the demonstration of live or

91 pithelium, these studies demonstrate that T. foetus promotes a direct contact-dependent activation of

92 erase (HGXPRTase), an essential enzyme in T. foetus required for salvaging exogenous purine bases, ha

93 Exposure of BVEC monolayers to T. foetus resulted in extensive damage of monolayers.

94 Metronidazole- or periodate-treated T. foetus showed no damage to BVEC monolayers.

95 of the ribosomal RNA gene from feces with T. foetus-specific primers (34 out of 36).

96 usly characterized IMPDH from Tritrichomonas foetus ( TfIMPDH).

97 In the APS model, foetuses that showed increased C3 in their brains additi

98 ginalis LPG (but not LPG from Tritrichomonas foetus, the causative agent of bovine trichomoniasis) in

99 s of Tf190 occurs in different strains of T. foetus, the Tf190 adhesion complex is widespread in diff

100 e of the trichomonad parasite Tritrichomonas foetus, this otherwise highly conserved histidine is rep

101 nd interactions mediate the attachment of T. foetus to BVECs.

102 T. foetus LPG inhibited the binding of T. foetus to BVECs; the LPG from T. vaginalis and a variety

103 y, and the vulnerability of the placenta and foetus to invasion are important features.

104 structures, important in the adhesion of T. foetus to mammalian cells, are located in the LPG-like c

105 Exposure of a developing foetus to maternal gestational diabetes (GDM) has been s

106 forms late in embryogenesis, permitting the foetus to survive a terrestrial environment at birth.

107 of T. foetus pathogenicity on adhesion of T. foetus to the intestinal epithelium, and the identity of

108 topathic effects by promoting adhesion of T. foetus to the intestinal epithelium.

109 e cellular mechanisms of pathogenicity of T. foetus toward the intestinal epithelium and support furt

110 etic mechanism for IMPDH from Tritrichomonas foetus using ligand binding, isotope effect, pre-steady-

111 Prevalence of T. foetus was 31% among cats (36 out of 117) and catteries

112 Catteries in which T. foetus was identified were more likely to have had a rec

113 syltransferase (HGXPRTase) of Tritrichomonas foetus was inactivated by the thiol reagents iodoacetate

114 TF1 inhibited the in vitro growth of T. foetus with an EC50 of approximately 40 microM.

115 ometry experiments on several isolates of T. foetus with Tf190-specific antibodies revealed that Tf19