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1 d comparable central nervous system signs or intestinal lesions.
2 eria that cause attaching and effacing (A/E) intestinal lesions.
3 ction with 100 cysts and did not develop the intestinal lesions.
4 ed for its isogenic parent and caused marked intestinal lesions.
5 mpromised patients, is often associated with intestinal lesions.
6 colonized and caused attaching-and-effacing intestinal lesions.
7 ts revealed a marked reduction or absence of intestinal lesions.
8 teria that cause attaching and effacing (AE) intestinal lesions.
9 necessary for causing attaching and effacing intestinal lesions.
11 ve in regressing both early and intermediate intestinal lesions and could be an effective therapeutic
13 tant strain of C. albicans failed to produce intestinal lesions and exhibited poor dissemination, dem
14 A accurately and safely evaluates solid peri-intestinal lesions and improves lymph node staging accur
16 orphology of spiral bacteria associated with intestinal lesions and PCR amplification of a genus-spec
17 necrosis factor alpha (TNF-alpha), in PBMCs, intestinal lesions, and mesenteric lymph nodes of cattle
18 EHEC) O157:H7 that mediate attach and efface intestinal lesions are classified as intimin alpha, beta
19 s in two cases indicate that the gastric and intestinal lesions are derived from different tumour sub
23 calicivirus, the induction of diarrhea, and intestinal lesions in Gn pigs caused by i.v. inoculation
24 s were the absence of attaching and effacing intestinal lesions in pigs inoculated with non-O157:H7 s
29 HEV-infected turkeys strongly suggested that intestinal lesion induced by this virus may be immune sy
30 tation patterns in one case suggest that the intestinal lesion is secondary to the gastric tumor, and
31 aused villous atrophy, more-widespread small intestinal lesions occurred in calves coinfected with WD
32 ive mononuclear cells was higher in skin and intestinal lesions of BD patients than in those of HCs.
33 train caused diarrhea (five/five calves) and intestinal lesions (one/two calves tested) in the proxim
34 an or in addition to bacterial colonization, intestinal lesions, or electrolyte loss contribute to le
35 ive acute-phase sera induced diarrhea, small intestinal lesions, PEC shedding in feces, and seroconve
36 y that in IGB piglets, as in human patients, intestinal lesions provide the mechanism for escape of C
37 ved from the same clone and suggest that the intestinal lesions result from dissemination of gastric
40 however, NB virus elicited only diarrhea and intestinal lesions that were most severe in the upper sm
42 enic rats died within 6 days, only very mild intestinal lesions were seen in nontransgenic rats 10 to
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