ライフサイエンスコーパス: SCID-hu mice

1 y given implants of a human fetal bone chip (SCID-hu mice).

2 human fetal thymic and liver tissue (thy/liv-SCID-hu mice).

3 uman fetal thymus and liver tissues (thy/liv-SCID-hu mice).

4 nted with bilateral human fetal bone grafts (SCID-hu mice).

5 ed with human fetal liver and thymus tissue (SCID-hu mice).

6 bserved in the reconstituted human thymus in SCID-hu mice.

7 ignificantly depleted CD4(+) thymocytes from SCID-hu mice.

8 tients depleted human CD4(+) thymocytes from SCID-hu mice.

9 or HIV-1 infection of thymus/liver grafts in SCID-hu mice.

10 ible for human CD4(+) thymocyte depletion in SCID-hu mice.

11 loid, T, and B cells, when transplanted into SCID-hu mice.

12 ere inoculated into human thymic implants in SCID-hu mice.

13 nts readily grew in the human environment of SCID-hu mice.

14 vity of the left bone implants in irradiated SCID-hu mice.

15 lacement by the CTE on HIV-1 expression with SCID-hu mice.

16 th human foreskin fibroblast (HFF) cells and SCID-hu mice.

17 of the allogenic pancreata were observed in SCID-hu mice.

18 e) and AD169 virus were tested for growth in SCID-hu mice.

19 After transplantation into SCID-hu mice, all neural stem cells, regardless of passa

20 The PB of the BM-SCID-hu mice also became populated with human T cells af

21 cted into the human thymic grafts of thy/liv-SCID-hu mice and induced IN#33 expression in most of the

22 reased replication and cytopathic effects in SCID-hu mice and likely contributes to the development o

23 ional human hematopoietic tissue grafts (NOD/SCID-hu mice) and observed that a subset of animals prod

24 icate that human T lymphocytes developing in SCID-hu mice are able to mount in vivo responses against

25 in the left human fetal bone implants within SCID-hu mice as early as 4 weeks after injection of as f

26 ients did not deplete CD4(+) thymocytes from SCID-hu mice as well as later clones.

27 on in severe combined immunodeficient-human (SCID-hu) mice as an in vivo assay for transplantable hum

28 Treatment of SCID-hu mice bearing WM with rituximab induced tumor reg

29 icated that the BM of our BM-SCID-hu and Liv-SCID-hu mice became engrafted with retrovirally transduc

30 INA-6 MM cells engrafted in SCID-hu mice but not in SCID mice that had not been give

31 Likewise, treatment of myelomatous SCID-hu mice, carrying primary disease, with recombinant

32 x vivo infected human lymphoid tissue and in SCID/hu mice, despite similar replication levels.

33 monocytes and T cells, the modified thy/liv-SCID-hu mice developed disseminated HIV infection that w

34 These SCID-hu mice have functional, mature T cells with a poly

35 man insulin was not detected in the serum of SCID-hu mice in which pancreas rejection occurred.

36 icity of the Rev-independent HIV-1 clones in SCID-hu mice, independent of the presence of Nef.

37 Growth curve analysis using MeWo cells and SCID-hu mice indicated that ORF1, ORF2, and ORF3 were di

38 tion of JR-CSF mouse leukocytes into thy/liv-SCID-hu mice, indicating that these cells provide an in

39 EphB4-Fc treatment of myelomatous SCID-hu mice inhibited myeloma growth, osteoclastosis, a

40 sis factor-alpha, were detectable in sera of SCID-hu mice injected with MM cells.

41 plasma viremia and HIV infection in thy/liv-SCID-hu mice inoculated with HIV-1(59) was inhibited by

42 mice implanted with human fetal bone chips (SCID-hu mice) into which WM cells from patient bone marr

43 lymphoproliferative disorders and tumors in SCID/hu mice is dependent on the presence of T cells, in

44 studied the replication and cytopathicity in SCID-hu mice of R5 human immunodeficiency virus type 1 (

45 antation of SCID mice with cultured HFBM (BM-SCID-hu mice) or HFL cells (Liv-SCID-hu mice), significa

46 Thus, thy/liv-SCID-hu mice populated with JR-CSF mouse leukocytes, a p

47 WM cells in SCID-hu mice produced human monoclonal paraprotein (immu

48 ice into which human tissues were implanted (SCID-hu mice) provide an alternative and valuable model

49 able to metabolize thalidomide efficiently, SCID-hu mice received implants of fetal human liver frag

50 Thus, these modified thy/liv-SCID-hu mice should prove to be a useful system for eval

51 Thus, these modified thy/liv-SCID-hu mice should prove to be a valuable in vivo model

52 emical analysis of human bone retrieved from SCID-hu mice showed infiltration with CD20+, IgM+, and m

53 on of human thymus/liver or skin implants in SCID-hu mice showed that ORF47 protein was required for

54 red HFBM (BM-SCID-hu mice) or HFL cells (Liv-SCID-hu mice), significant engraftment of the mouse bone

55 d with human fetal thymus and liver (thy/liv-SCID-hu mice) so that the peripheral blood of the mice c

56 is clone also replicated to higher levels in SCID-hu mice than the two earlier clones, and a signific

57 1 isolate to eliminate CD4(+) human cells in SCID-hu mice to a region of the env gene including the t

58 However, in SCID-hu mice transplanted with graded doses of donor cel

59 detected in the BM of the BM-SCID-hu and Liv-SCID-hu mice up to 8 months after transplantation.

60 rying replication-competent HIV-1 in thy/liv-SCID-hu mice was indicated by the emergence of HIV-1 inf

61 In transplanted SCID-hu mice, we directly compared marking and gene expr

62 mononuclear cells in these modified thy/liv-SCID-hu mice were responsive to in vivo treatment with e

63 Within 12 to 36 wk after construction, SCID-hu mice were transplanted with an HLA-mismatched hu

64 When thy/liv-SCID-hu mice were treated with a combination of zidovudi

65 SCID-hu mice were used to determine the effects of virul

66 unodeficiency virus (HIV)-inoculated thy/liv-SCID-hu mice were used to evaluate the in vivo efficacy

67 d with human fetal thymus and liver tissues (SCID-hu mice) were infected with three primary isolates

68 le or no human CD4(+) thymocyte depletion in SCID-hu mice, while syncytium-inducing (SI), R5X4 or R3R

69 Inoculation of SCID-hu mice with HTLV-1-infected T cells or enriched po

70 analyses of data obtained from infection of SCID-hu mice with patient ACH142 R5 clones revealed that

71 t of severe combined immunodeficiency-human (SCID-hu) mice with established WM using the SGN-70 antib