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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
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
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
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.
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
42 irs were performed in three groups of Lewis (LEW) rats: negative controls (n = 4), local MSCs (epineu
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
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
56 cted in an accelerated manner within 36 h by LEW rats that have been sensitized with Brown Norway rat
59 we performed RNA sequencing analysis of the LEW rat versus the BN rat, with or without T. gondii inf
62 a secondary immune response, three groups of LEW rats were transfused with ACI blood with no accompan
64 , a T cell line from peptide + IFA-immunized LEW rats (which did not develop EAE) failed to secrete t
66 antigens (ED1) persisted for longer times in LEW rats while expression of MHC class II molecules was
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