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1 uated two real-time PCR assays for detecting Brugia DNA in human blood and compared the results of th
6 on passive transfer, led to the clearance of Brugia malayi (Bm) microfilariae (mf) from infected jird
8 nts generated from MF patients, filarial Ag (Brugia malayi adult Ag (BmA))-stimulated supernatants fr
10 Brugian filariasis (caused by the nematodes Brugia malayi and B. timori) is an important cause of di
11 During our investigations into the course of Brugia malayi and Brugia pahangi infections in immunodef
13 e (Mb) genome of the human filarial parasite Brugia malayi and predict approximately 11,500 protein c
14 duals (n = 11) were stimulated in vitro with Brugia malayi antigen (BMA) or mycobacterial purified pr
15 association between ratios of polyclonal to Brugia malayi antigen (BmAg)-specific IgE (range, 14:1 t
16 (-/-) mice were first immunized with soluble Brugia malayi antigens and then inoculated intravenously
17 d secondary murine and human infections with Brugia malayi are characterized by substantial increases
18 s brenneri, using Pristionchus pacificus and Brugia malayi as outgroups, and identified numerous oper
19 chocerca volvulus, Wuchereria bancrofti, and Brugia malayi available, new drug targets have been iden
20 response to live, infective-stage larvae of Brugia malayi but not to microfilariae of this parasite.
21 uble extracts of the human filarial parasite Brugia malayi can induce potent inflammatory responses,
23 sponding genes in Caenorhabditis elegans and Brugia malayi contained a cysteine codon in place of TGA
29 e heme; however, the human filarial parasite Brugia malayi has acquired a bacterial gene encoding fer
30 sponse to the infective-stage larvae (L3) of Brugia malayi has not been well-characterized in vivo (b
31 he genomic environment of a newly identified Brugia malayi Hox6-8 ortholog (Bm-ant-1) revealed that i
33 We have shown that live microfilariae of Brugia malayi induce caspase-dependent apoptosis in huma
34 luated the contributions of T and B cells in Brugia malayi infection by utilizing knockout mice on a
35 after treatment with diethylcarbamazine for Brugia malayi infection, and recorded the severity of an
41 tics and anti-Wolbachia efficacy in a murine Brugia malayi model of minocycline versus doxycycline.
43 del of alternative activation in which adult Brugia malayi nematodes are implanted surgically in the
44 termine, via preclinical infection models of Brugia malayi or Onchocerca ochengi that elevated exposu
45 ells (PEC) from mice transplanted with adult Brugia malayi parasites suppress the proliferation of ly
46 ympahtic filariasis is the nematode parasite Brugia malayi that requires a competent mosquito vector
47 cation of binding protein(s) of the helminth Brugia malayi to CaGC and the ability of binding complex
49 e, C. remanei, C. brenneri, C. japonica, and Brugia malayi using some of the best-performing gene-fin
50 a donovani, Toxoplasma gondii) and helminth (Brugia malayi) parasites were examined, each of which pr
51 ge larvae (L3) or live microfilariae (Mf) of Brugia malayi, a causative agent of human lymphatic fila
52 has been isolated from the filarial nematode Brugia malayi, a causative agent of human lymphatic fila
53 of almost all the major mammalian stages of Brugia malayi, a causative agent of lymphatic filariasis
54 ertaken the first study of heme transport in Brugia malayi, a causative agent of lymphatic filariasis
55 ical to the MIFs from the parasitic nematode Brugia malayi, and 22-35% identical to mammalian MIFs.
56 cells were exposed to microfilariae (mf) of Brugia malayi, and their phenotypic and functional chara
57 enomes to that of another filarial parasite, Brugia malayi, and to those of several other nematodes,
58 rgillus nidulans, Schizosaccharomyces pombe, Brugia malayi, Caenorhabditis elegans, Trypanosoma cruzi
59 bitor of NO synthase abrogated resistance to Brugia malayi, one of the causative agents of human lymp
61 IL4Ralpha(-/-) mice elicited by the nematode Brugia malayi, or via intraperitoneal thioglycollate inj
62 ocheilonema viteae, Onchocerca volvulus, and Brugia malayi, strongly supporting the concept that the
63 pod Drosophila melanogaster and the nematode Brugia malayi, together with the partial genome sequenci
64 e infective-stage larvae or microfilariae of Brugia malayi, we found significant impairment of both T
66 t the filarial nematodes responsible for LF (Brugia malayi, Wuchereria bancrofti) or onchocerciasis (
67 interactions between the infective stage of Brugia malayi--one of the extracellular parasites respon
91 gations into the course of Brugia malayi and Brugia pahangi infections in immunodeficient mouse model
93 lymphocytes in antifilarial immunity, using Brugia pahangi infections in the murine peritoneal cavit
94 cleared a challenge infection with infective Brugia pahangi L3 in an accelerated manner, whereas coho
95 es aimed to define early tissue migration of Brugia pahangi L3 in the gerbil (Meriones unguiculatus)
100 a abortus-killed S19 was inoculated into the Brugia-permissive gerbil host to induce gamma interferon
101 of transmission of Wuchereria bancrofti and Brugia spp. through the application of annual mass drug
103 22 million years ago (Myr ago) involving the Brugia/Wuchereria lineage and >20-17 Myr ago involving t
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