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1 unoglobulin G (IgG) antibodies reactive with Rickettsia rickettsii.
2 fe-threatening, tick-borne disease caused by Rickettsia rickettsii.
3 umbilical vein endothelial cells (HUVEC) by Rickettsia rickettsii.
4 om those of several other agents, especially Rickettsia rickettsii.
5 ), Ehrlichia canis, Bartonella henselae, and Rickettsia rickettsii.
6 ct human umbilical vein after infection with Rickettsia rickettsii.
7 d Rickettsia spp.; the other is specific for Rickettsia rickettsii.
8 about the structure and morphogenesis of the Rickettsia rickettsii actin tail relative to Shigella an
9 dothelial cells consequent to infection with Rickettsia rickettsii, an obligate intracellular gram-ne
10 me host cell apoptosis was explored by using Rickettsia rickettsii, an obligate intracellular Gram-ne
11 vein endothelial cells during infection with Rickettsia rickettsii, an obligate, intracellular bacter
13 veloped for the detection and enumeration of Rickettsia rickettsii and other closely related spotted
14 spotted fever and boutonneuse fever, due to Rickettsia rickettsii and R. conorii, respectively, are
15 The type I signal peptidase lepB genes from Rickettsia rickettsii and Rickettsia typhi, the etiologi
17 infections caused by Ehrlichia chaffeensis, Rickettsia rickettsii, and Coxiella burnetti, no signifi
19 ed fever group rickettsiae (SFGR) other than Rickettsia rickettsii are responsible for spotted fever
20 nstrated IgG or IgM antibodies reactive with Rickettsia rickettsii at a diagnostic titer (i.e., >/=64
21 plasma phagocytophilum, Ehrlichia canis, and Rickettsia rickettsii), but the sample was highly positi
22 cognized by reference human antisera against Rickettsia rickettsii, Chlamydia group positive, Trepone
23 ponse to certain pathogenic organisms (e.g., Rickettsia rickettsii), data documenting endothelial cel
25 steria monocytogenes, Shigella flexneri, and Rickettsia rickettsii, exploit the host cytoskeleton by
27 WB-8-2 and two other nonpathogenic isolates (Rickettsia rickettsii Hip2 and Rickettsia montana M5/6)
31 etion of chemokines and prostaglandins after Rickettsia rickettsii infection of human cerebral, derma
34 otted fever, a tick-borne zoonosis caused by Rickettsia rickettsii, is among the most lethal of all i
35 used by the obligate intracellular bacterium Rickettsia rickettsii, is associated with widespread inf
37 e HGE agent and to either Coxiella burnetii, Rickettsia rickettsii, or Rickettsia typhi was infrequen
38 Ehrlichia canis, E. chaffeensis, E. ewingii, Rickettsia rickettsii, R. conorii, and other spotted fev
41 m, Borrelia miyamotoi, Borrelia mayonii, and Rickettsia rickettsii The sensitivity for identification
42 rs of the spotted fever group (SFG), such as Rickettsia rickettsii, the agent of Rocky Mountain spott
44 nse during infection of endothelial cells by Rickettsia rickettsii, the causative agent of Rocky Moun
45 k Amblyomma cooperi in the enzootic cycle of Rickettsia rickettsii, the etiologic agent of Brazilian
46 potentially fatal human infection caused by Rickettsia rickettsii, the etiologic agent of Rocky Moun
47 l (EC) is a primary target of infection with Rickettsia rickettsii, the etiologic agent of Rocky Moun
49 s similar to, but distinct from, isolates of Rickettsia rickettsii, the etiological agent of RMSF.
50 mutant pairs from two independent strains of Rickettsia rickettsii, the virulent R strain and the avi
52 cies of a mariner-based transposon system in Rickettsia rickettsii were determined using a plaque ass