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1 (24 months), but not young (3 months) F344 x BN rats.
2 athways in BN-J rats compared with wild-type BN rats.
3 n adult (3 months) and aged (24 months) F344/BN rats.
4 ectable in the vitreous, lens, and cornea of BN rats.
5 anin-like activity was 100-fold less than in BN rats.
6 oximately 1.5-fold higher in SD rats than in BN rats.
7 in magnitude and of shorter duration than in BN rats.
8 induced retinal neovascularization in SD and BN rats.
9 the F(2) progeny of BB(DR) and CIA-resistant BN rats.
10 it TNF-alpha bioactivity in virus-inoculated BN rats.
11  reversed the renoprotective effects in SS.5(BN) rats.
12  induced by laser treatment in Brown Norway (BN) rats.
13 Dahl Salt-Sensitive (DSS), and Brown Norway (BN) rats.
14  selective COX-2 inhibitor) to Brown Norway (BN) rats.
15 re harvested and purified from Brown-Norway (BN) rats.
16 susceptibility in DA/Bkl (DA) and BN/SsNHsd (BN) rats.
17    Male Wistar-Kyoto (WKY) and Brown Norway (BN) rats (11-12 weeks, n = 184) received an injection of
18 arizes our clinical and biochemical control (bNED) rates after conformal radiotherapy (RT).
19 ular brown adipose tissue (IBAT) from F344 x BN rats ages 3, 12, 18, 24, and 30 months (n = 8/age).
20                                              BN rats also had greater numbers of bronchiolar macropha
21          Given the unique T-helper-2 bias in BN rats, altered sympathetic-immune communication may be
22 e to compare virus-susceptible brown Norway (BN) rats and virus-resistant F344 rats and to determine
23 at) were administered periocularly in SD and BN rats, and celecoxib levels in these eye tissues were
24 r basis of the neuromodulatory deficiency in BN rats, and further suggest an important functional rol
25 peptide levels were significantly reduced in BN rats, and injections of the stable TRH analogue Talti
26 ble Han:SPRD(cy/+) and control Brown Norway (BN) rats, and performed a whole-genome scan in 182 PKD a
27 ive abilities of aging (24-month-old) F344 x BN rats are generally good, but are more vulnerable to t
28 in startle amplitude was seen in CRF-treated BN rats but not in CRF-treated WKY rats.
29 ed significant retinal neovascularization in BN rats but not in SD rats, as demonstrated by fluoresce
30                                              BN rats, but not BN/Ka rats, showed a 56% reduction in c
31 ormalized the ventilatory CO2 chemoreflex in BN rats, but TAL did not affect CO2 sensitivity in contr
32 A and the AT(2)-ant blocked these effects in BN rats, but the B(2)-ant did not.
33  nonreactivity was produced in Brown-Norway (BN) rats by transplantation of Lewis (LEW) liver, bone m
34                                              BN rat carotid bodies have naturally higher CO and lower
35                        Reducing CO levels in BN rat carotid bodies increased H2S generation, restorin
36                               In CRF-treated BN rats, clozapine-enhanced PPI.
37 upnoeic breathing and CO2 sensitivity in the BN rats compared to other rat strains.We measured ventil
38 d a 35% increase in fractional shortening in BN rats compared with a 16% increase in BN/Ka rats.
39                    Celecoxib kinetics in the BN rat cornea can be described by a two-compartment (per
40 bronchiolitis at an early age, Brown Norway (BN) rats develop chronic airway dysfunction consisting o
41         In oxygen-induced retinopathy (OIR), BN rats developed retinal vascular hyperpermeability fro
42                   In contrast, Brown Norway (BN) rats developed severe disease when immunized with RP
43 otocin (STZ)-induced diabetes, Brown Norway (BN) rats developed sustained vascular hyperpermeability
44 ry cancer when treated continuously with E2, BN rats did not develop palpable mammary cancer during t
45                                  Wild-caught BN rats displayed absence-like SWD/immobility events tha
46                                Brown Norway (BN) rats exhibit an inherent and severe ventilatory inse
47 with Sprague-Dawley (SD) rats, Brown-Norway (BN) rats exhibit impaired carotid body O2 sensing and de
48                                Brown Norway (BN) rats exhibit natural PPI deficits under certain para
49               In response to decreased flow, BN rats exhibited the smallest reduction in shear stress
50 ibited a smaller response, and Brown Norway (BN) rats exhibited the smallest response.
51 tuarial survival, disease-free survival, and bNED rates for the entire population were 80.5%, 70.0%,
52 Treg function and protects Themis1-deficient BN rats from spontaneous IBD development.
53 luding 32 that distinguish the Brown Norway (BN) rat from the other strains studied.
54                                              BN rats had increase pulmonary mRNA levels of TGF-beta 1
55                             Virus-inoculated BN rats had increased TNF-alpha pulmonary mRNA levels (P
56                                Brown Norway (BN) rats have a relatively specific deficit in CO2 sensi
57                                Brown Norway (BN) rat heart or kidney allografts were transplanted int
58   Lewis rats transplanted with Brown Norway (BN) rat hearts were treated with different dose levels o
59 CO was examined in a fully allogeneic LEW to BN rat heterotopic heart transplantation (HHTx) model.
60                                           In BN rats, ICF was reduced and LVEF increased by AT(1)-ant
61 y events that were highly similar to outbred BN rats in terms of spike-wave morphology, frequency, di
62 y, AA and W men had similar 5-year actuarial bNED rates in favorable (78% v 79%, P: = .91), intermedi
63             Administration of HgCl2 to naive BN rats induced marked autoantibody production, systemic
64                                              BN rats infected with virus developed increases in respi
65 haloperidol or clozapine to determine if the BN rat is a useful animal model with predictive validity
66  ventilatory insensitivity to hypercapnia in BN rats is due to altered raphe gene expression and the
67 the development of severe acute rejection in BN rat lungs, transplanted into LEW recipients.
68 This drug response profile suggests that the BN rat may be useful for detecting atypical antipsychoti
69 We used genomic DNA from a male BN/NHsdMcwi (BN) rat of the same strain and from the same colony as t
70  formation of 20-HETE from the Brown Norway (BN) rat onto the SS genetic background increased renal 2
71 49163 but not haloperidol facilitated PPI in BN rats (p < .001).
72 s) or morphological changes in Brown Norway (BN) rat pituitaries.
73                                 In contrast, BN rats pretreated with HgCl2-resistant allogeneic Lewis
74                                              BN rats received subcutaneous injections of either salin
75                      They were compared with BN rats receiving either no pretreatment (naive) or FK50
76 odel of allergic lung disease, Brown Norway (BN) rats sensitized to HDM with alum and Bordetella pert
77                                          The BN rat sequence is the third complete mammalian genome t
78                        The hyperoxia-treated BN rats showed a significant reduction in retinal PEDF,
79                                              BN rats showed less PPI than WKY rats, and neither antip
80 e ACI strain and the unrelated Brown Norway (BN) rat strain.
81 ere the genome sequence of the Brown Norway (BN) rat strain.
82 appa 1, and glutathione peroxidase) than the BN rat, suggesting that the LEW rat maintains cellular o
83 P = 0.001) and 2-fold (P = 0.0001) higher in BN rats than in SD rats.
84  shorter duration in wild-caught and outbred BN rats than the outbred Long-Evans and inbred WAG/Rij s
85     We found that compared to the uninfected BN rat, the uninfected LEW rat has inherently higher tra
86       However, compared to the Brown Norway (BN) rat, the Lewis (LEW) rat is extremely resistant to T
87                     Indeed, by contrast with BN rats, Themis1 deficiency in Lewis rats neither impair
88 Treg) function and predisposes Brown-Norway (BN) rats to spontaneous inflammatory bowel disease (IBD)
89 m male and female wild-caught (Brown-Norway [BN]) rats to recordings from laboratory outbred BN, outb
90              In HCC of genetically resistant BN rats, very low changes in the Mat1A:Mat2A ratio, CpG
91 elanin in choroid-RPE, sclera, and retina of BN rats were 200 +/- 30, 12 +/- 4, and 3 +/- 0.2 mug/mg
92                          Higher CO levels in BN rats were associated with higher substrate affinity o
93                                              BN rats were low responders to PII and resistant to CIA
94 body weight and blood glucose, Brown Norway (BN) rats were divided into three groups.
95       BN/Ka rats and wild-type Brown Norway (BN) rats were exposed to local heart irradiation with a
96                                Brown-Norway (BN) rats were pretreated with a syngeneic or allogeneic
97 ognostic risk category, the 5-year actuarial bNED rates were 78.7% for favorable, 57.7% for intermedi
98 ly attenuated laser-induced CNV formation in BN rats when initiated 3 days before or within 1 hour af
99 tional defects were also observed in LEW and BN rats, which are susceptible to induced autoimmunity,
100 pathetic activity/tone in male Brown Norway (BN) rats, which live longer and have a strikingly differ
101                                   We treated BN rats with haloperidol or clozapine to determine if th
102 ies of Sprague Dawley (SD) and Brown Norway (BN) rats with ischemia-induced retinal neovascularizatio
103 equencing analysis of the LEW rat versus the BN rat, with or without T. gondii infection, in order to

 
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