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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 oups: control Sprague-Dawley (SD) and Lewis (LEW) rats, 3- to 4-month diabetic SD and LEW rats, and 4
10                                  In diabetic LEW rats, a supernormal (P < 0.05) panretinal DeltaPO2(t
11                        It is noteworthy that LEW rats acquire self-administration more rapidly than F
12 nes generated from RT1.Dubeta20-44 immunized LEW rats all expressed TCR Vbeta9.
13        Interestingly, the helical regions of LEW rats (alpha(1h)1) and Wistar Furth (WF; RT1u) rats (
14       Similar to the corticosterone results, LEW rats also had blunted prolactin responses to morphin
15 nonimmune-suppressed streptozotocin-diabetic LEW rats and insulin and porcine proinsulin mRNA-express
16 elerated (< 36 h) rejection in presensitized LEW rats and results in permanent acceptance of LBNF1 ca
17 is (LEW) rats, 3- to 4-month diabetic SD and LEW rats, and 4-month diabetic LEW rats preventatively t
18 tar rats took more drug per session than the LEW rats but did not differ from each other.
19        Using congenic strains containing the LEW rat chromosomal segments on the Dahl salt-sensitive
20                       Cyclosporine-A-treated LEW rats chronically rejected F344 SB grafts.
21                                   In control LEW rats, DeltaPO2(t1-ra) and DeltaPO2(t2-t1) were not s
22                                       Lewis (LEW) rats did not develop EAE, even after immunization w
23 tion more rapidly than F344 or ACI rats, yet LEW rats display reduced corticosterone responses to str
24 gnificantly across strains, and in this case LEW rats displayed a reduced sensitivity to morphine.
25 Systemic injection of the 2F4 clone to naive LEW rats elicited an antigen-specific delayed-type hyper
26                                We found that LEW rats exhibited higher novelty- and AMPH-induced loco
27 ltures of five rat strains, including Lewis (LEW) rats, exhibited a disrupted DG cytoarchitecture, sl
28 king the irradiated LEW donor liver in naive LEW rats for 48 hr before retransplantation to DA recipi
29 ly, despite having higher levels of ROS, the LEW rat had lower transcript levels for antioxidant enzy
30 red to the uninfected BN rat, the uninfected LEW rat has inherently higher transcript levels of cytoc
31 f morphine and cocaine in these two strains, LEW rats have lower basal, and generally higher drug-ind
32  and basal activity were also observed, with LEW rats having less protein and slower in vivo clearanc
33 CI skin and cardiac allografts on 3 of the 9 LEW rats in group 1 are viable to date (skin, > 170 days
34 en together, the lower basal DAT function in LEW rats is consistent with their greater novelty-induce
35 red to the Brown Norway (BN) rat, the Lewis (LEW) rat is extremely resistant to T. gondii infection.
36                         Orthotopic syngeneic LEW rat liver transplantation (OLT) was performed after
37 C incompatible DA (RTl(a)) to Lewis (RT1(1), LEW) rat liver allografts are acutely rejected, the reci
38 xidase) than the BN rat, suggesting that the LEW rat maintains cellular oxidative stress that it tole
39      Together, our results indicate that the LEW rat maintains inherent cellular oxidative stress tha
40                      An established F344 --> LEW rat model of chronic rejection was used to examine (
41                          Using the F334 into LEW rat model of chronic renal allograft rejection, tran
42 irs were performed in three groups of Lewis (LEW) rats: negative controls (n = 4), local MSCs (epineu
43                                   Similarly, LEW rats neonatally tolerized against either Rhsp65 or B
44                   Also, control and diabetic LEW rat panretinal DeltaPO2(t1-ra) were lower (P < 0.05)
45 rin (MnTBAP) decreased the refractoriness of LEW rat peritoneal cells to T. gondii infection, resulti
46 , resulting in proliferation of parasites in LEW rat peritoneal cells which, in turn, led to augmente
47 ection of (LEW x BN)F1 cardiac allografts in LEW rats presensitized with BN skin grafts.
48 rejected in an accelerated manner (<36 h) by LEW rats presensitized with Brown-Norway skin grafts.
49 abetic SD and LEW rats, and 4-month diabetic LEW rats preventatively treated with a chow LPA admix (4
50  usage in splenic IgM-producing B cells from LEW rats rapidly expands from 0.8% in naive animals to 1
51 onal antibodies and splenic lymphocytes from LEW rats rejecting hamster heart xenografts were used to
52 p 1 (n=8)-isotransplantations between Lewis (LEW) rats (RT1)-served as controls.
53 VS in a model of Fisher 344 (F344) to Lewis (LEW) rat SB transplantation.
54                                Specifically, LEW rats self-administer morphine and cocaine to a great
55 Similar results were obtained in the ACI --> LEW rat strain combination.
56 cted in an accelerated manner within 36 h by LEW rats that have been sensitized with Brown Norway rat
57 ation between Sprague-Dawley (SD) and Lewis (LEW) rats throughout the lesion.
58         Interestingly, pretreatment of adult LEW rats using either a mixture of peptides 120-134 and
59  we performed RNA sequencing analysis of the LEW rat versus the BN rat, with or without T. gondii inf
60                                          The LEW rats were brought to term, and groups 1, 3, and 4 we
61                                        Donor LEW rats were pretreated 24 hr before transplantation wi
62 a secondary immune response, three groups of LEW rats were transfused with ACI blood with no accompan
63                                       Lewis (LEW) rats were bilaterally nephrectomized and received a
64 , a T cell line from peptide + IFA-immunized LEW rats (which did not develop EAE) failed to secrete t
65                              However, Lewis (LEW) rats, which share the same major histocompatibility
66 antigens (ED1) persisted for longer times in LEW rats while expression of MHC class II molecules was
67                             We observed that LEW rats with DIA spontaneously raised a vigorous T cell
68                        Although treatment of LEW rats with Rapamycin (RPM) prolongs the survival of L
69                       Hence, 1) treatment of LEW rats with RIB-5/2, a CD4 nondepleting mAb, produces
70            Most importantly, pretreatment of LEW rats with the dexamethasone-treated DC led to the in

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