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1 f human microsporidia belonging to the genus Encephalitozoon.
2 Microsporidian organisms within the genus Encephalitozoon are the cause of nephrologic, ophthalmic
4 m Encephalitozoon intestinalis (2.3 Mbp) and Encephalitozoon cuniculi (2.9 Mbp) revealed massive gene
6 e genomes are strikingly similar to those of Encephalitozoon cuniculi and Encephalitozoon intestinali
7 assembly components for the microsporidians Encephalitozoon cuniculi and Trachipleistophora hominis.
8 c acid, a TrpRS from the eukaryotic pathogen Encephalitozoon cuniculi bound to tryptophan, a HisRS fr
9 rystal structure of the N-terminal domain of Encephalitozoon cuniculi Cdc27 (Cdc27(Nterm)), revealing
12 evious mutational and structural analyses of Encephalitozoon cuniculi Ecm1, a prototypal cellular cap
13 Here we show that the intracellular parasite Encephalitozoon cuniculi encodes a complete mRNA capping
14 Notably the genome of the microsporidian Encephalitozoon cuniculi has lost all of its genes for M
16 er animals exhibit greater susceptibility to Encephalitozoon cuniculi infection, and their ability to
24 er (ITS) region of a recently cultured human Encephalitozoon cuniculi isolate was analyzed by gene am
26 primary human macrophages were infected with Encephalitozoon cuniculi or Encephalitozoon intestinalis
27 n to examine the protein interactions of the Encephalitozoon cuniculi polar tube proteins (EcPTPs).
30 testinalis but not Encephalitozoon hellem or Encephalitozoon cuniculi was confirmed in 6 of 8 mammali
33 (delta) T cells during murine infection with Encephalitozoon cuniculi, an intracellular parasite, was
34 al antibody, termed 3B6, strongly recognized Encephalitozoon cuniculi, E. hellem, and E. intestinalis
35 sis with oligonucleotide probes specific for Encephalitozoon cuniculi, E. hellem, and Encephalitozoon
37 In aged animals challenged with the parasite Encephalitozoon cuniculi, effector CD8+ T cell survival
38 osporidian species: Enterocytozoon bieneusi, Encephalitozoon cuniculi, Encephalitozoon hellem, and En
39 t with culture-grown Encephalitozoon hellem, Encephalitozoon cuniculi, or Vittaforma corneae or with
40 , E. intestinalis, and E. hellem, as well as Encephalitozoon cuniculi, spores in fecal samples and is
41 0 also demonstrated in vivo activity against Encephalitozoon cuniculi, with prolonged survival and th
45 o intermediate-sized genomes (2.5 Mbp), from Encephalitozoon hellem and Encephalitozoon romaleae.
49 ve genotyping tool, the genetic diversity of Encephalitozoon hellem was examined at the polar tube pr
50 oon intestinalis, 2 (2.1%) were positive for Encephalitozoon hellem, and 9 samples (9.6%) contained b
51 cytozoon bieneusi, Encephalitozoon cuniculi, Encephalitozoon hellem, and Encephalitozoon intestinalis
53 this serum does not react with culture-grown Encephalitozoon hellem, Encephalitozoon cuniculi, or Vit
58 show that both Encephalitozoon cuniculi and Encephalitozoon intestinalis are preferentially recogniz
59 to cause a gastrointestinal disease whereas Encephalitozoon intestinalis causes both a disseminated
61 lar to those of Encephalitozoon cuniculi and Encephalitozoon intestinalis in both form and content.
65 e in size from 2.3 Mb for the microsporidian Encephalitozoon intestinalis up to 8000 Mb for Entomopha
67 ozoon bieneusi, 43 (45.8%) were positive for Encephalitozoon intestinalis, 2 (2.1%) were positive for
68 re infected with Encephalitozoon cuniculi or Encephalitozoon intestinalis, and the recruitment of nai
72 isseminated microsporidial infection with an Encephalitozoon-like species was diagnosed by electron m
73 2 avian) containing spores detected by anti-Encephalitozoon monoclonal antibody immunofluorescence (
75 microsporidia were amplified by PCR with pan-Encephalitozoon primers, and the PCR DNA products were s
80 ons allowed for the differentiation of three Encephalitozoon species (E. intestinalis, E. cuniculi, a
81 rn blot, and immunoelectron microscopy using Encephalitozoon species from fresh and fixed samples fro
86 clonal antibody 3B6 bound to the exospore of Encephalitozoon species, while in Western blot assays, i
90 rocedure is established for the isolation of Encephalitozoon spores from clinical specimens, identifi
92 the initial inflammatory response induced by Encephalitozoon spp. to TLR2 stimulation in human macrop
93 nofluorescence with E. bieneusi but not with Encephalitozoon spp., Candida albicans, Staphylococcus a
94 y, formalin-treated and nontreated spores of Encephalitozoon were identified to the species level by
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