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1 n sacral ganglia from guinea pigs vaccinated intravaginally.
3 fected with HSV-2 intravaginally and treated intravaginally 24 h later with 100 microg DNA encoding I
5 tics of virus spread, we inoculated macaques intravaginally and euthanized them after 2, 4, 7, and 15
7 intravenously or mucosally (intranasally or intravaginally) and then challenged intravaginally with
9 as shown promise as antiherpetics, including intravaginally applied CpG-containing oligodeoxynucleoti
12 cells, was detected in all hCD4/R5/cT1 mice intravaginally challenged with an HIV-1 infectious molec
15 eic dendritic cells did not induce responses intravaginally even in ovariectomized mice in the absenc
16 r of the genital tract, rhesus macaques were intravaginally exposed to cell-free simian immunodeficie
18 onses were compared in female mice immunized intravaginally (i.vag.) or intranasally (i.n.) with a ba
19 , BALB/c or congenic SCID mice were infected intravaginally (i.vag.) with the HSV type 2 (HSV-2) vhs
20 to either peptide Ag or male cells delivered intravaginally in ovariectomized mice, but this response
21 itope (gB(498-505)), and both were delivered intravaginally in the progesterone-induced B6 mouse mode
23 amydia-infected mice, and in initial studies intravaginally infected wild-type, IL-10(-/-), IL-4(-/-)
25 rol of a CD4 promoter (JR-CSF/hu-cycT1) were intravaginally infected with HSV-2 and evaluated for dis
30 ) T cells followed by development of AIDS in intravaginally inoculated macaques and thus provides a h
31 tics of retroviral recombination in vivo, we intravaginally inoculated rhesus macaques, either simult
32 e with pathogenic SIV, all five animals were intravaginally inoculated twice with pathogenic SIV-mac2
33 (-/-), IL-17RA(-/-) and IL-22(-/-) mice were intravaginally inoculated with Candida, and vaginal lava
34 was eventually found in four of six animals intravaginally inoculated with the two SIVmac239 deletio
35 1 (HIV-1) env/rev and gag/pol were delivered intravaginally (IVAG) and intramuscularly (IM) to 2 preg
37 us macaques inoculated intravenously (IV) or intravaginally (IVAG) with a genetically heterogeneous S
38 arious mucosal routes-oral, intrarectal, and intravaginally (ivag)-followed by a systemic or mucosal
40 sis of tissues of rhesus macaques inoculated intravaginally or i.v. with SIV supports the proposed ro
42 HeJ mice were either sham or INP0341 treated intravaginally pre- and postinoculation with 5 x 10(2) i
43 l mucosa, while the same antibodies injected intravaginally significantly reduced Thy-1+ T cells in b
44 in which female rhesus macaques were exposed intravaginally to a high dose of simian immunodeficiency
46 re significantly greater in macaques exposed intravaginally to lower rather than higher inoculum dose
48 served only in macaques that were challenged intravaginally twice within the same day with a high dos
50 nnate immunity-deficient C3H/HeJ female mice intravaginally with a human serovar D urogenital isolate
54 into syngeneic naive animals and challenged intravaginally with Chlamydia, recipients of IM immuniza
55 mia, nonobese diabetic (NOD) mice inoculated intravaginally with clinical C. glabrata isolates were s
56 g from 5 to 14 weeks of age, were inoculated intravaginally with different doses of the Chlamydia tra
57 Chlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2
58 t this hypothesis, we treated rhesus monkeys intravaginally with either the TLR9 agonist, CpG oligode
59 2Rgamma(-/-)) (NSG)-BLT mice were inoculated intravaginally with HIV and were monitored for plasma vi
60 or the licensed HPV vaccines and challenged intravaginally with HPV6, HPV16, HPV26, HPV31, HPV33, HP
61 O 2000 gel protected 100% of mice challenged intravaginally with HSV-2 introduced in PBS, whereas onl
65 rogesterone or estradiol and then inoculated intravaginally with M. genitalium type strain G37 or a c
68 ult female macaques that had been inoculated intravaginally with pathogenic SIVmac251 became transien
71 ciency virus (SHIV) 89.6 and then challenged intravaginally with SIVmac239 controlled viral replicati
72 Four female rhesus macaques were inoculated intravaginally with SIVmac251, and then killed 2, 5, 7,
73 e TNF-alpha response in guinea pigs infected intravaginally with the guinea pig strain of Chlamydia p
74 feron gamma gene-deficient C57 mice infected intravaginally with the mouse pneumonitis agent of Chlam
76 L/6), treated with progesterone and infected intravaginally with the mouse pneumonitis strain of Chla
77 oth B7-1 and B7-2 (B7KO mice), when infected intravaginally with virulent herpes simplex virus type 2
79 reated with 17-beta-estradiol and inoculated intravaginally with wild-type gonococcal strain FA1090 o
80 ceptibility to N. gonorrhoeae and inoculated intravaginally with wild-type gonococci or a catalase (k
82 highly attenuated in wild-type mice infected intravaginally, with reduced mucosal replication, diseas
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