ライフサイエンスコーパス: Beige mice

1 mised SCID (severe combined immunodeficient)-Beige mice.

2 plantation into the cleared fat pads of SCID/Beige mice.

3 rs of severe combined immunodeficient (SCID)/beige mice.

4 taylorii to cause chronic infection in SCID/BEIGE mice.

5 rm tumors in severe combined immunodeficient-beige mice.

6 erase reporter gene were established in SCID/beige mice.

7 ent severe combined immune deficiency (SCID)-beige mice.

8 al aorta of severe combined immunodeficiency/beige mice.

9 cted SCID (severe combined immunodeficiency)-Beige mice.

10 n into CB.17 severe combined immunodeficient-beige mice.

11 o porcine skin xenografts in human PBMC-SCID/beige mice.

12 sed lethal virulence in immunodeficient SCID-beige mice.

13 hotopically implanted into the lungs of SCID-beige mice.

14 odies and in severe combined immunodeficient/Beige mice.

15 scid or into T, B and NK cell-deficient scid/beige mice.

16 stic human xenografts was maintained in SCID-beige mice.

17 till a 33% inhibition of tumor metastasis in beige mice.

18 zoledronic acid proved highly toxic to SCID Beige mice.

19 ) and in the severe combined immunodeficient-beige mice (117+/-18 in untreated mice, 137+/-19 in mice

20 ouse model of chronic infection, 5 of 6 SCID/beige mice (83.3%) were cured after treatment with a sin

21 d SCID mice, T-cell-receptor-deficient mice, beige mice (a mouse strain deficient in natural killer [

22 ll-defective severe combined immunodeficient/beige mice also failed to abrogate this response.

23 rect feeder contact formed teratomas in SCID/beige mice and differentiated in vitro into cells from a

24 ring severe combined immunodeficiency (SCID)-Beige mice and eradicate disseminated intramedullary tum

25 om C3H/HeJ-Lystbg-2J/+ mice (commonly called beige mice and have selectively impaired NK cell functio

26 the therapeutic effects of AdIFN in scid and beige mice and in inducible NO synthase (iNOS) knockouts

27 rast, B16-FIII.H cells formed more tumors in beige mice and NK cell-depleted C57BL/6 mice than did B1

28 atic progression in syngeneic BALB/c or SCID-beige mice, and in BALB/c or SCID-beige mice treated wit

29 7 infected severe combined immunodeficiency-beige mice, and the parasites did not recur in these imm

30 hances tumour growth in immunodeficient SCID-beige mice; anti-TGF-beta monoclonal antibodies but not

31 on into the tibialis anterior muscle of SCID/Beige mice, as assessed by bioluminescence imaging.

32 id:pDNA treatment of athymic, SCID, and SCID/Beige mice bearing a murine i.p. mesothelioma (AC29) res

33 When C.B-17 SCID/beige mice bearing human skin grafts are injected i.p. w

34 In vivo using SCID/beige mice bearing human skin with adoptively transferre

35 tion was still observed in NK cell-deficient beige mice but not in CD8-/- mice.

36 Inactivation of Mphi in SCID/beige mice by silica treatment abrogated the antitumor e

37 tumor-bearing, immune-deficient (SCID, SCID/beige) mice; (c) detection of high levels of specific an

38 creatic tumors and improved survival of SCID beige mice carrying A549 human lung tumors compared with

39 nts that were infused with spleen cells from beige mice compared with recipients infused with wild-ty

40 10 days, but immunocompromised SCID and SCID/BEIGE mice developed persistent infection in the spleen,

41 s because interferon-gamma knockout and SCID-Beige mice exhibited attenuated iNOS staining in excisio

42 to newborn severe combined immunodeficiency-beige mice exposed to 90% O2 from birth; sham controls r

43 BALB/c mice or defective NK function in C3H beige mice extended transgene expression compared to the

44 and CD8 T cells and use of NK cell-defective beige mice failed to abrogate the response to AdVmIL-12.

45 retards tumor growth in immunodeficient SCID/Beige mice following transplantation of primary tumor B

46 as few as 100 cells) injected s.c. into SCID/Beige mice formed tumors, and in one case, SKNBE(2)C iCS

47 of anti-Bordetella antibodies protected SCID-beige mice from B. bronchiseptica lethal infection.

48 -231 xenograft growth and metastasis in SCID/beige mice, implicating a critical role for macrophages

49 mpared to wt strains in colonization of SCID-beige mice, indicating that the defects were not limited

50 Most (13/14) control SCID/beige mice inoculated intraperitoneally with BCBL-1 cell

51 t murine hosts and could only form tumors in beige mice lacking NK cells.

52 to stimulate NKT cells, but did not occur in beige mice lacking NK cells.

53 to the liver of retrorsine (RS)-treated SCID/beige mice, naive hAECs differentiated into hepatocyte-l

54 ce), but not in those deficient in NK cells (beige mice or NK cell-depleted mice).

55 bstitutes were transplanted onto C.B-17 SCID/beige mice receiving systemic rapamycin or vehicle contr

56 ear skin of C57BL/6 and immunodeficient SCID/Beige mice resulted in tumor formation in only the latte

57 In the SCID-beige mice, T24 human bladder transitional cell carcinom

58 man HLA into severe combined immunodeficient/beige mice that had been transplanted with human skin gr

59 n MHC class I K matching is eliminated in B6 beige mice that lack NK cell function, as well as in wil

60 A cells (MCF10AT) form small nodules in nude/beige mice that persist for at least 1 year and sporadic

61 In streptozotocin-induced diabetic SCID/beige mice, the injection of 750 rat islet equivalents e

62 using severe combined immunodeficient (SCID)/beige mice to study the pathogenesis of HHM.

63 /c or SCID-beige mice, and in BALB/c or SCID-beige mice treated with cyclosporine.

64 Hypothyroidism was generated in SCID-beige mice using an iodine-deficient diet containing 0.1

65 In this study, using Lyst-mutant beige mice, we show that lysosomal trafficking regulator

66 MAC-infected beige mice were given clarithromycin daily; the frequenc

67 ed Myocardium avium complex (MAC) infection, beige mice were infected with MAC strains isolated from

68 SCID/beige mice were inoculated intraperitoneally with a huma

69 C.B.-17 severe combined immunodeficiency-beige mice were transplanted with human artery segments

70 LB/c mice or severe combined immunodeficient-beige mice were treated with 2 or 4 mg/kg of tacrolimus,

71 T and NK cells by Ab treatment, or from scid/beige mice, were still activated by anti-CD40 mAb to med

72 SCID/beige mice with engrafted RV-ATL cells developed lymphom

73 ith PTLD, and prolonged the survival of SCID-beige mice with established lymphoproliferative disease.

74 In beige mice with impaired natural killer cell function, t

75 s infusion of CD19-targeted nTregs into SCID-Beige mice with systemic Raji tumors traffic to sites of

76 Xenotransplantation of SCID/Beige mice with U87 cells and GSDCs gave rise to tumors

77 ficient controls, but did not decrease CS in beige mice, with platelet granules that are defective in