戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 otoacoustic emissions (DPOAEs) in humans and CBA mice.
2 eripheral tolerance induced with mouse Tg in CBA mice.
3 6.6 +/- 0.4 to 9.4 +/- 0.6 mm Hg (n = 10) in CBA mice.
4 nificantly reduced numbers from the feces of CBA mice.
5 d in both young (6 week) and older (8 month) CBA mice.
6 testinal persistence in Salmonella-resistant CBA mice.
7 tches to the depilated midtail of female MC, CBA mice.
8 ng fetuses from maternal immune responses in CBA mice.
9 onducted using spleen MNLs from the tolerant CBA mice.
10  in normal tibial cartilage from STR/ort and CBA mice.
11 ated lesion development in disease-resistant CBA mice.
12 he inferior colliculus (IC) of young and old CBA mice.
13 nsurethrally inoculated into the bladders of CBA mice.
14 lpis markedly enhanced L. major infection in CBA mice.
15 the number of CR+ cells, but only in the old CBA mice.
16 f nonhematopoietic neoplasms were reduced in CBA mice.
17 etically susceptible (BALB/c) and resistant (CBA) mice.
18 ere applied to the right knees of 8-week-old CBA mice, 3 times a week for 2 weeks (and assessed immed
19                                 Importantly, CBA mice, a naturally high pathology strain, also displa
20 ep wake cycles in young, middle-aged and old CBA mice, a strain capable of melatonin biosynthesis, to
21 tand the biological bases of presbycusis, 39 CBA mice, a well-studied animal model of presbycusis, un
22 nted the development of cytotoxic T cells in CBA mice against BALB/c MNLs.
23 xamined learning over the adult life span in CBA mice, along with morphological and electrophysiologi
24 % decrease in the number of CB+ cells in old CBA mice and a 25.1% decrease in old C57 mice.
25 RB6-8C5) decreased the partial resistance of CBA mice and led to severe pathology compared to control
26 ulomas of S. mansoni-infected high-pathology CBA mice and low-pathology C57BL/6 mice.
27 ve indices in the cecum and fecal samples of CBA mice at 30 days after infection, suggesting that the
28 the rate and severity of amebic infection in CBA mice by all measures (cecal culture positivity, para
29 ) were respectively induced in presensitized CBA mice by embolization of beads coupled to purified pr
30                                Compared with CBA mice, C57BL/6 mice develop smaller granulomas compos
31 ificantly higher in spleen and granulomas of CBA mice, compared with C57BL/6 mice.
32 e pyelonephritis in transurethrally infected CBA mice, contains two distinct copies of the pap operon
33           In the mouse model of the disease, CBA mice develop large granulomas, whereas in C57BL/6 (B
34                                       CBA/J (CBA) mice develop severe hepatic granulomatous inflammat
35 nulomas from C57BL/6 mice than in those from CBA mice ex vivo; the apoptosis further increased upon c
36 ngation of CBK cardiac grafts was induced in CBA mice fed with multiple doses of CBK splenocytes (MST
37 rified MR/P fimbriae significantly protected CBA mice from ascending urinary tract infection by P. mi
38 EHV-1 KyA immunization effectively protected CBA mice from pathogenic RacL11 challenge at 1 to 7 days
39 sults showed that KyA immunization protected CBA mice from pathogenic RacL11 challenge at 2 and 4 wee
40       After 96 h, T cells of old C57BL/6 and CBA mice generated up to 20-fold more IL-17 and up to 3-
41 r of MHCII IA(b) genes in the bone marrow of CBA mice (H-2(k)) prior to the grafting of IA(b+) fully
42                                              CBA mice (H-2(k)) were used as transfusion recipients.
43 ded T-cell lines from purified Treg cells of CBA mice (H2k).
44 mice(H2b) were abdominally transplanted into CBA mice (H2k).
45 trophysiology recorded from an additional 48 CBA mice indicated significant deficits in LTD appearing
46 pared the course of respiratory infection of CBA mice infected with either wild-type RacL11, attenuat
47 ononuclear leukocytes (MNLs) in the tolerant CBA mice is responsible for the negative regulatory acti
48 sly reported that overexpression of IL-12 in CBA mice leads to mononuclear infiltration of salivary a
49 lasticity were assessed at different ages in CBA mice: long-term depression (LTD) in both cerebellum
50                                       Hence, CBA mice may provide a convenient model of ES isolation
51 m from fecal samples collected from infected CBA mice over a 30-day time period.
52                   While cells from resistant CBA mice produced more IFN-gamma, IL-10, and nitric oxid
53    However, this also occurred in vivo since CBA mice produced substantial amounts of IL-10 following
54                          Lethally irradiated CBA mice received BMT from allogeneic (B10.BR) or syngen
55  against the egg antigen Sm-p40; conversely, CBA mice responded better to Sm-p40 than to Sm-PEPCK.
56  dendritic cells plus naive CD4 T cells from CBA mice resulted in increased levels of IL-6, IL-23, IL
57 ochlear pathology as they age, whereas aging CBA mice retain good hearing.
58                                   These same CBA mice showed no significant differences in contextual
59        We investigated the kidneys of B6 and CBA mice subjected to UUO and SNX, and the effects of ti
60                                   Forty-four CBA mice tested at one of five ages (4, 8, 12, 18, or 24
61 ndent, with higher serum anti-OprF titers in CBA mice than in BALB/c or C57BL/6 mice.
62                                           In CBA mice that naturally display a severe form of schisto
63 lls after thymectomy and T-cell depletion in CBA mice that received CBK (H2k+Kb) skin grafts, the exp
64                       CD25+CD4+ T cells from CBA mice that were pretreated with C57BL/6 (B.6) blood (
65 st the major egg antigen, Sm-p40, whereas in CBA mice the reverse was true.
66 rogated the partial resistance of C3H/HeJ or CBA mice through an innate, lymphocyte-independent mecha
67 te dendritic cells from high pathology-prone CBA mice to produce IL-12p40, IL-6, and TGF-beta, wherea
68       Second, bladder and kidney tissue from CBA mice transurethrally inoculated with E. coli CFT073
69                                           In CBA mice treated with anti-CD4 (GK1.5, 0.5 mg intraperit
70 ity to OA to examine changes in non-OA-prone CBA mice versus OA-prone STR/Ort mice, which develop dis
71                 To assess virulence in vivo, CBA mice were challenged transurethrally with 10(7) CFU
72 multiple doses of alloantigen was essential, CBA mice were given CBK splenocytes orally on a single o
73  (BMC) and spleen MNL from tolerant or naive CBA mice were transplanted into lethally irradiated BALB
74  nucleus (CN) of C57BL/6J (C57) and CBA/CaJ (CBA) mice were studied by using immunocytochemical and r
75 e (transplanted mice without GVHD and normal CBA mice) were infected intranasally with herpes simplex
76 ith less-severe hearing loss) or in very old CBA mice (which do not exhibit severe hearing loss).
77 n gp120 from HIV strain 89.6 was examined in CBA mice, whose MHC class II protein has one of the most
78         Following transurethral infection of CBA mice with a sat mutant, no reduction of CFU in urine
79   To prevent these infections, we vaccinated CBA mice with formalin-killed bacteria or purified manno
80                                              CBA mice with H-2k phenotype and BALB/c mice with H-2d p
81                   Intranasal immunization of CBA mice with MBP-MrpH (residues 23 to 157) conferred ef
82 l independent challenges and cochallenges of CBA mice with the wild type and each mutant.
83 was assessed by transurethral cochallenge of CBA mice with wild-type and mutant strains.
84 did not anticipate that cells from resistant CBA mice would make more IL-10 in vitro.