ライフサイエンスコーパス: Lew rat

1 allelic variations between the S rat and the LEW rat.

2 id early T. gondii-killing mechanisms in the LEW rat.

3 1 and F2 offspring of the crossing of SD and LEW rats.

4 A extracted from femurs of COP, DA, F344 and LEW rats.

5 as well as after at least 10 backcrosses to LEW rats.

6 C3Smn.CB17-Prkdc(scid)/J mice, as well as in LEW rats.

7 ll-depleted F344 bone marrow into irradiated LEW rats.

8 re heterotopically transplanted in recipient LEW rats.

9 by the transfusion of F344 whole blood into LEW rats.

10 oups: control Sprague-Dawley (SD) and Lewis (LEW) rats, 3- to 4-month diabetic SD and LEW rats, and 4

11 In diabetic LEW rats, a supernormal (P < 0.05) panretinal DeltaPO2(t

12 It is noteworthy that LEW rats acquire self-administration more rapidly than F

13 nes generated from RT1.Dubeta20-44 immunized LEW rats all expressed TCR Vbeta9.

14 Interestingly, the helical regions of LEW rats (alpha(1h)1) and Wistar Furth (WF; RT1u) rats (

15 Similar to the corticosterone results, LEW rats also had blunted prolactin responses to morphin

16 nonimmune-suppressed streptozotocin-diabetic LEW rats and insulin and porcine proinsulin mRNA-express

17 elerated (< 36 h) rejection in presensitized LEW rats and results in permanent acceptance of LBNF1 ca

18 is (LEW) rats, 3- to 4-month diabetic SD and LEW rats, and 4-month diabetic LEW rats preventatively t

19 tar rats took more drug per session than the LEW rats but did not differ from each other.

20 Using congenic strains containing the LEW rat chromosomal segments on the Dahl salt-sensitive

21 Cyclosporine-A-treated LEW rats chronically rejected F344 SB grafts.

22 In control LEW rats, DeltaPO2(t1-ra) and DeltaPO2(t2-t1) were not s

23 with the exception of stress-hyporesponsive LEW rats, despite all strains displaying similar functio

24 Lewis (LEW) rats did not develop EAE, even after immunization w

25 tion more rapidly than F344 or ACI rats, yet LEW rats display reduced corticosterone responses to str

26 gnificantly across strains, and in this case LEW rats displayed a reduced sensitivity to morphine.

27 Systemic injection of the 2F4 clone to naive LEW rats elicited an antigen-specific delayed-type hyper

28 We found that LEW rats exhibited higher novelty- and AMPH-induced loco

29 ltures of five rat strains, including Lewis (LEW) rats, exhibited a disrupted DG cytoarchitecture, sl

30 king the irradiated LEW donor liver in naive LEW rats for 48 hr before retransplantation to DA recipi

31 ly, despite having higher levels of ROS, the LEW rat had lower transcript levels for antioxidant enzy

32 red to the uninfected BN rat, the uninfected LEW rat has inherently higher transcript levels of cytoc

33 f morphine and cocaine in these two strains, LEW rats have lower basal, and generally higher drug-ind

34 and basal activity were also observed, with LEW rats having less protein and slower in vivo clearanc

35 CI skin and cardiac allografts on 3 of the 9 LEW rats in group 1 are viable to date (skin, > 170 days

36 en together, the lower basal DAT function in LEW rats is consistent with their greater novelty-induce

37 red to the Brown Norway (BN) rat, the Lewis (LEW) rat is extremely resistant to T. gondii infection.

38 Orthotopic syngeneic LEW rat liver transplantation (OLT) was performed after

39 C incompatible DA (RTl(a)) to Lewis (RT1(1), LEW) rat liver allografts are acutely rejected, the reci

40 xidase) than the BN rat, suggesting that the LEW rat maintains cellular oxidative stress that it tole

41 Together, our results indicate that the LEW rat maintains inherent cellular oxidative stress tha

42 An established F344 --> LEW rat model of chronic rejection was used to examine (

43 Using the F334 into LEW rat model of chronic renal allograft rejection, tran

44 irs were performed in three groups of Lewis (LEW) rats: negative controls (n = 4), local MSCs (epineu

45 Similarly, LEW rats neonatally tolerized against either Rhsp65 or B

46 Also, control and diabetic LEW rat panretinal DeltaPO2(t1-ra) were lower (P < 0.05)

47 rin (MnTBAP) decreased the refractoriness of LEW rat peritoneal cells to T. gondii infection, resulti

48 , resulting in proliferation of parasites in LEW rat peritoneal cells which, in turn, led to augmente

49 ection of (LEW x BN)F1 cardiac allografts in LEW rats presensitized with BN skin grafts.

50 rejected in an accelerated manner (<36 h) by LEW rats presensitized with Brown-Norway skin grafts.

51 abetic SD and LEW rats, and 4-month diabetic LEW rats preventatively treated with a chow LPA admix (4

52 usage in splenic IgM-producing B cells from LEW rats rapidly expands from 0.8% in naive animals to 1

53 onal antibodies and splenic lymphocytes from LEW rats rejecting hamster heart xenografts were used to

54 p 1 (n=8)-isotransplantations between Lewis (LEW) rats (RT1)-served as controls.

55 VS in a model of Fisher 344 (F344) to Lewis (LEW) rat SB transplantation.

56 Specifically, LEW rats self-administer morphine and cocaine to a great

57 Similar results were obtained in the ACI --> LEW rat strain combination.

58 cted in an accelerated manner within 36 h by LEW rats that have been sensitized with Brown Norway rat

59 ation between Sprague-Dawley (SD) and Lewis (LEW) rats throughout the lesion.

60 Interestingly, pretreatment of adult LEW rats using either a mixture of peptides 120-134 and

61 we performed RNA sequencing analysis of the LEW rat versus the BN rat, with or without T. gondii inf

62 The LEW rats were brought to term, and groups 1, 3, and 4 we

63 Donor LEW rats were pretreated 24 hr before transplantation wi

64 a secondary immune response, three groups of LEW rats were transfused with ACI blood with no accompan

65 Lewis (LEW) rats were bilaterally nephrectomized and received a

66 , a T cell line from peptide + IFA-immunized LEW rats (which did not develop EAE) failed to secrete t

67 However, Lewis (LEW) rats, which share the same major histocompatibility

68 antigens (ED1) persisted for longer times in LEW rats while expression of MHC class II molecules was

69 We observed that LEW rats with DIA spontaneously raised a vigorous T cell

70 Although treatment of LEW rats with Rapamycin (RPM) prolongs the survival of L

71 Hence, 1) treatment of LEW rats with RIB-5/2, a CD4 nondepleting mAb, produces

72 Most importantly, pretreatment of LEW rats with the dexamethasone-treated DC led to the in