ライフサイエンスコーパス: hydrosalpinx

1 ed ascending infection and failed to develop hydrosalpinx.

2 -borne gene pgp3, -4, or -7 for induction of hydrosalpinx.

3 tes significantly to chlamydial induction of hydrosalpinx.

4 ained susceptible to chlamydial induction of hydrosalpinx.

5 fection do not always lead to a reduction in hydrosalpinx.

6 ither pgp3 or -4 but not -7 failed to induce hydrosalpinx.

7 but not TLR2 developed significantly reduced hydrosalpinx.

8 on in the oviduct may be necessary to induce hydrosalpinx.

9 se susceptibility to chlamydial induction of hydrosalpinx.

10 oth uterine horn/glandular duct dilation and hydrosalpinx.

11 fection sooner, and had a lower incidence of hydrosalpinx.

12 se of infection (25 days), but all developed hydrosalpinx.

13 (22 days) and the lowest incidence of severe hydrosalpinx.

14 lammation of the oviduct and fails to induce hydrosalpinx.

15 nfection (38 days), and all developed severe hydrosalpinx.

16 figured to simulate unilateral and bilateral hydrosalpinx.

17 ) IFU, the CBA/J mice still developed robust hydrosalpinx.

18 end to the upper genital tract, resulting in hydrosalpinx, a pathological hallmark for tubal infertil

19 er MMPi protected mice from the formation of hydrosalpinx-a surrogate marker of oviduct occlusion and

20 both confirming the role of C5 in promoting hydrosalpinx and indicating that the C5-facilitated hydr

21 ells significantly enhanced the incidence of hydrosalpinx and oviduct dilatation compared to those of

22 dial infection, including the development of hydrosalpinx and oviduct dilatation.

23 Although TLR2-deficient mice developed hydrosalpinx as severe as that of wild-type mice, perito

24 ighly resistant to induction of long-lasting hydrosalpinx by C. muridarum.

25 C5 may contribute to chlamydial induction of hydrosalpinx by enhancing inflammatory responses.

26 amydial clearance and decreased frequency of hydrosalpinx compared to wild-type (WT) mice, implying a

27 but significantly reduced oviduct pathology (hydrosalpinx) compared to that of wild-type mice.

28 lamydial clearance but significantly reduced hydrosalpinx, compared to those of wild-type C57BL/6 mic

29 The hydrosalpinx development in CBA/J mice correlated with i

30 yosalpinx during the acute phase followed by hydrosalpinx during the chronic phase.

31 V inactivation were no longer able to induce hydrosalpinx even when directly delivered into the ovidu

32 free C. muridarum organisms failed to induce hydrosalpinx even when the organisms were directly inocu

33 All 5 strains developed hydrosalpinx following intravaginal inoculation with pla

34 rganisms appeared to directly correlate with hydrosalpinx formation after both primary infection and

35 otects a significant proportion of mice from hydrosalpinx formation and infertility.

36 became infertile and sustained high rates of hydrosalpinx formation regardless of prior infection wit

37 s of RNS in vivo, and sustain lower rates of hydrosalpinx formation than both wild-type (WT) NOS2(+/+

38 isease, as evidenced by an increased rate of hydrosalpinx formation that was comparable to that for N

39 th mouse strain-related innate resistance to hydrosalpinx formation.

40 y increased rates of disease, as assessed by hydrosalpinx formation.

41 was found to improve the differentiation of hydrosalpinx from nonhydrosalpinx mice.

42 um, which naturally infects mice, can induce hydrosalpinx in mice, a tubal pathology also seen in wom

43 ese two receptors to chlamydial induction of hydrosalpinx in mice.

44 not plasmid-free Chlamydia muridarum induces hydrosalpinx in mouse upper genital tract, indicating a

45 tis and C. muridarum can induce long-lasting hydrosalpinx in the upper genital tract of women and fem

46 Although Chlamydia-induced hydrosalpinx in women and mice has been used as a surrog

47 The lack of hydrosalpinx induction by plasmid-free C. muridarum corr

48 plasmid-independent factors, which makes the hydrosalpinx induction in CBA/J mice by intrauterine inf

49 Hydrosalpinx induction in mice by Chlamydia muridarum in

50 e, C5(-/-) mice were still more resistant to hydrosalpinx induction than C5(+/+) mice, even when live

51 ce and CBA/J mice known to be susceptible to hydrosalpinx induction.

52 Hydrosalpinx is a pathological hallmark of tubal inferti

53 two endometriomas); mature teratoma (n = 3); hydrosalpinx (n = 2); fibroma (n = 1); and benign Brenne

54 eficient C. muridarum strains did not induce hydrosalpinx or spread to the GI tract even when deliver

55 to upper genital tract pathologies, such as hydrosalpinx, potentially affecting fertility.

56 sociated antigens) while the 13 mice with no hydrosalpinx preferentially recognized 10 proteins (TC00

57 However, the mechanisms of hydrosalpinx remain unknown.

58 and chlamydial infection courses between the hydrosalpinx-resistant A/J mice and CBA/J mice known to

59 nses in chlamydial induction of long-lasting hydrosalpinx, suggesting that a rapid but transient inva

60 significant role in chlamydial induction of hydrosalpinx than those mediated by the pattern recognit

61 topathology revealed the incidence of severe hydrosalpinx to be significantly greater in C3H mice tha

62 +) T cells at the time of challenge restored hydrosalpinx to levels observed in wild-type C57BL/6 mic

63 Depiction of unilateral and bilateral hydrosalpinx was also reliably demonstrated.

64 lpinx and indicating that the C5-facilitated hydrosalpinx was not due to enhancement of ascending inf

65 Ultimately, gross hydrosalpinx was observed 21 days to 10 weeks p.i. in ap

66 mid, which is essential for the induction of hydrosalpinx, was not required for the induction of uter

67 surgically evaluated adnexal masses, but no hydrosalpinx, were randomly chosen as control subjects.

68 ction in the lower genital tract can lead to hydrosalpinx, which is accompanied by activation of both

69 e lacking C5 (C5(-/-)) failed to develop any hydrosalpinx, while approximately 42% of the correspondi