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1 t alone was unable to induce any significant hydrosalpinx.
2 LN was detected in plasma from patients with hydrosalpinx.
3 while inducing oviduct fibrotic blockage or hydrosalpinx.
4 oth uterine horn/glandular duct dilation and hydrosalpinx.
5 lammation of the oviduct and fails to induce hydrosalpinx.
6 ) IFU, the CBA/J mice still developed robust hydrosalpinx.
7 ed ascending infection and failed to develop hydrosalpinx.
8 -borne gene pgp3, -4, or -7 for induction of hydrosalpinx.
9 As a result, all mice developed significant hydrosalpinx.
10 tes significantly to chlamydial induction of hydrosalpinx.
11 ained susceptible to chlamydial induction of hydrosalpinx.
12 fection do not always lead to a reduction in hydrosalpinx.
13 ither pgp3 or -4 but not -7 failed to induce hydrosalpinx.
14 but not TLR2 developed significantly reduced hydrosalpinx.
15 on in the oviduct may be necessary to induce hydrosalpinx.
16 se susceptibility to chlamydial induction of hydrosalpinx.
17 fection sooner, and had a lower incidence of hydrosalpinx.
18 se of infection (25 days), but all developed hydrosalpinx.
19 (22 days) and the lowest incidence of severe hydrosalpinx.
20 nfection (38 days), and all developed severe hydrosalpinx.
21 figured to simulate unilateral and bilateral hydrosalpinx.
23 end to the upper genital tract, resulting in hydrosalpinx, a pathological hallmark for tubal infertil
24 er MMPi protected mice from the formation of hydrosalpinx-a surrogate marker of oviduct occlusion and
25 both confirming the role of C5 in promoting hydrosalpinx and indicating that the C5-facilitated hydr
27 ells significantly enhanced the incidence of hydrosalpinx and oviduct dilatation compared to those of
30 m inoculation, wild-type mice develop robust hydrosalpinx, but OT1 mice fail to do so because their T
32 OT1 mice led to the induction of significant hydrosalpinx by Chlamydia, indicating that CD8(+) T cell
34 amydial clearance and decreased frequency of hydrosalpinx compared to wild-type (WT) mice, implying a
36 lamydial clearance but significantly reduced hydrosalpinx, compared to those of wild-type C57BL/6 mic
37 ignificantly reduced chlamydial induction of hydrosalpinx, demonstrating that OT1 CD8(+) T cells are
39 s from OT1 mice also significantly inhibited hydrosalpinx development in wild-type mice following an
41 V inactivation were no longer able to induce hydrosalpinx even when directly delivered into the ovidu
42 free C. muridarum organisms failed to induce hydrosalpinx even when the organisms were directly inocu
44 these mice were still able to develop robust hydrosalpinx following C. muridarum infection, both cont
46 rganisms appeared to directly correlate with hydrosalpinx formation after both primary infection and
48 became infertile and sustained high rates of hydrosalpinx formation regardless of prior infection wit
49 s of RNS in vivo, and sustain lower rates of hydrosalpinx formation than both wild-type (WT) NOS2(+/+
50 isease, as evidenced by an increased rate of hydrosalpinx formation that was comparable to that for N
51 d on fertility rates, number of embryos, and hydrosalpinx formation, vaccinated mice were protected a
55 ridarum readily induces fibrotic blockage or hydrosalpinx in mice and is used for investigating C. tr
56 um, which naturally infects mice, can induce hydrosalpinx in mice, a tubal pathology also seen in wom
58 not plasmid-free Chlamydia muridarum induces hydrosalpinx in mouse upper genital tract, indicating a
59 dial mutants that are attenuated in inducing hydrosalpinx in the genital tract also reduce their colo
60 tis and C. muridarum can induce long-lasting hydrosalpinx in the upper genital tract of women and fem
62 ignificantly reduced chlamydial induction of hydrosalpinx, indicating that CD4(+) T cells became path
64 plasmid-independent factors, which makes the hydrosalpinx induction in CBA/J mice by intrauterine inf
66 e, C5(-/-) mice were still more resistant to hydrosalpinx induction than C5(+/+) mice, even when live
70 two endometriomas); mature teratoma (n = 3); hydrosalpinx (n = 2); fibroma (n = 1); and benign Brenne
71 eficient C. muridarum strains did not induce hydrosalpinx or spread to the GI tract even when deliver
74 sociated antigens) while the 13 mice with no hydrosalpinx preferentially recognized 10 proteins (TC00
76 and chlamydial infection courses between the hydrosalpinx-resistant A/J mice and CBA/J mice known to
77 ase state, we analyzed 17,798 cells from two hydrosalpinx samples and observed shifts in epithelial a
78 nses in chlamydial induction of long-lasting hydrosalpinx, suggesting that a rapid but transient inva
79 significant role in chlamydial induction of hydrosalpinx than those mediated by the pattern recognit
81 topathology revealed the incidence of severe hydrosalpinx to be significantly greater in C3H mice tha
82 +) T cells at the time of challenge restored hydrosalpinx to levels observed in wild-type C57BL/6 mic
86 prise among the most prominent proteins with hydrosalpinx was mesothelin (MSLN), which until now has
87 lpinx and indicating that the C5-facilitated hydrosalpinx was not due to enhancement of ascending inf
89 mid, which is essential for the induction of hydrosalpinx, was not required for the induction of uter
90 To better understand the pathobiology of hydrosalpinx, we compared the proteome of lavages from d
91 gistic regression analysis showed women with hydrosalpinx were 2.11 times more likely to be infertile
92 surgically evaluated adnexal masses, but no hydrosalpinx, were randomly chosen as control subjects.
93 duces upper genital tract pathology, such as hydrosalpinx, which can be modeled with Chlamydia murida
94 ction in the lower genital tract can lead to hydrosalpinx, which is accompanied by activation of both
95 e lacking C5 (C5(-/-)) failed to develop any hydrosalpinx, while approximately 42% of the correspondi
96 ued an attenuated Chlamydia mutant to induce hydrosalpinx, while the chlamydial mutant infection in t
97 etter correlation of chlamydial induction of hydrosalpinx with chlamydial colonization in the gastroi