ライフサイエンスコーパス: endometriotic

1 In contrast to full-length SRC-1, the endometriotic 70-kDa SRC-1 C-terminal fragment prevents

2 bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cell lines.

3 Silencing of TTP in endometriotic and endometrial epithelial cells revealed

4 Using human fluorescent endometriotic cell lines and chimeric mouse model as pre

5 MIF protein secretion and mRNA expression in endometriotic cells in response to E(2).

6 esponse of 12Z immortalized human epithelial endometriotic cells to TNF-alpha.

7 OA neurons are influenced by the presence of endometriotic cysts in the abdominal cavity.

8 The endometriotic cysts were found to be significantly large

9 ecrosis factor (TNF)-alpha is central to the endometriotic disease process.

10 posure to seminal plasma could contribute to endometriotic disease progression in women.

11 NF-alpha-induced signaling pathways in human endometriotic epithelial cells results in decreased expr

12 n of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the pro

13 of all the above endometriotic genes in 12Z endometriotic epithelial cells.

14 epithelial-mesenchymal transition (EMT) from endometriotic epithelial cells.

15 of small molecule kinase inhibitors to block endometriotic gene expression directly.

16 NF-alpha-induced expression of all the above endometriotic genes in 12Z endometriotic epithelial cell

17 dy early angiogenesis in vivo and to monitor endometriotic growth and the efficacy of systemic antian

18 Here, we report that primary human endometriotic H-38 cells express high levels of GPR30 wi

19 is, we now report that Icon largely destroys endometriotic implants by vascular disruption without ap

20 evealed five patients with surgically proved endometriotic implants in the ileum at enteroclysis (thr

21 Barium studies revealed endometriotic implants in the terminal ileum within 10 c

22 Recent evidence indicates that ectopic endometriotic implants recruit their own unique neural a

23 le-contrast barium enema studies, associated endometriotic implants were found in the rectosigmoid co

24 hat host-derived TGFB1 deficiency suppresses endometriotic lesion development and provides proof of p

25 tigated the physiologic function of TGFB1 in endometriotic lesion development, using Tgfb1-null mutan

26 ly is one of the fundamental requirements of endometriotic lesion survival in the peritoneal cavity.

27 ells are a disease-inducing component of the endometriotic lesion, we explored the response of 12Z im

28 y proved endometrioma and no associated deep endometriotic lesions and 317 healthy subjects for a cas

29 ential expression of IL-17A in human ectopic endometriotic lesions and matched eutopic endometrium fr

30 898 will prevent neovascularization of human endometriotic lesions and that ABT-898 treatment will no

31 functional cytokine that is abundant in both endometriotic lesions and the peritoneal fluid in women

32 The oxidative stress conditions found within endometriotic lesions are likely to contribute to the tr

33 positive endothelial cells incorporated into endometriotic lesions but not eutopic endometrium, as re

34 Caplostatin suppressed the growth of endometriotic lesions by 59% compared with controls.

35 that RNABPs TTP and HuR are dysregulated in endometriotic lesions compared to matched eutopic patien

36 Endometriotic lesions from ABT-898-treated mice exhibite

37 Furthermore, endometriotic lesions from IL-33 treated mice were highl

38 m of affected women and secreted products of endometriotic lesions have given insight into the pathog

39 Endometriotic lesions increased circulating endothelial

40 Endometriotic lesions induce a state of chronic peritone

41 ese findings indicate that vasculogenesis in endometriotic lesions is dependent on estrogen, which ad

42 e the first evidence, to our knowledge, that endometriotic lesions produce IL-17A and that the remova

43 We found that endometriotic lesions produce significantly higher level

44 Because endometriotic lesions require new blood supply for survi

45 We demonstrate the establishment of endometriotic lesions that exhibit similarities to those

46 Endometriotic lesions were induced in irradiated FVB/N m

47 ere higher, but numbers of recruited EPCs in endometriotic lesions were significantly lower when comp

48 Endometriotic lesions were surgically induced in irradia

49 the loss of FKBP52 encourages the growth of endometriotic lesions with increased inflammation, cell

50 ABT-898 inhibits neovascularization of human endometriotic lesions without affecting mouse fecundity.

51 romoting factor markedly expressed in active endometriotic lesions, and estradiol (E(2)) in ectopic e

52 red well with the location of the transgenic endometriotic lesions, and lesion size correlated with t

53 nagement, and many aspects of the biology of endometriotic lesions, the pathophysiological mechanisms

54 e euthanized to assess neovascularization of endometriotic lesions, using CD31(+) immunofluorescence.

55 bition of COX-2 suppresses vasculogenesis in endometriotic lesions, which may contribute to an impair

56 essels contributes to the vascularization of endometriotic lesions.

57 f11-/- knockout mice with surgically induced endometriotic lesions.

58 gral part in the establishment and growth of endometriotic lesions.

59 ous expression of TF by endothelial cells in endometriotic lesions.

60 mportant role in the formation and growth of endometriotic lesions.

61 isk reduction was greatest for women who had endometriotic lesions.

62 essels contributes to the vascularization of endometriotic lesions.

63 on of the 70-kDa SRC-1 C-terminal isoform in endometriotic mouse tissue.

64 with surgically induced endometriosis and in endometriotic stromal cells biopsied from patients with

65 ons positively correlated with the amount of endometriotic tissue and peaked 1 to 4 days after induct

66 lytic isoform is highly elevated both in the endometriotic tissue of mice with surgically induced end

67 thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesio

68 ls, enhanced ERbeta activity was detected in endometriotic tissues, and the inhibition of enhanced ER