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1 and faster induction of social motivation in SD rats.
2 chemia and 0 to 24 hours reperfusion in male SD rats.
3 iographically in seven urethane anesthetized SD rats.
4 Cl were significantly higher in F344 than in SD rats.
5 imulated GEPR-9s, seizure-naive GEPR-9s, and SD rats.
6 lality and urea concentration (P < 0.001) in SD rats.
7 ture was greater in BHE/cdb rats than in the SD rats.
8 e lower in both SHR and WKY[LJ] rats than in SD rats.
9 rosis or other histopathological findings in SD rats.
10 Dawley (SD) rats and 5/6 nephrectomized (Nx) SD rats.
11 ynaptoneurosomes were prepared from P30 male SD rats.
12  thick ascending limbs (mTALs) isolated from SD rats.
13  liver and kidney after an acute exposure in SD rats.
14 cated in vivo in neonatally infected LEW and SD rats.
15 efore the outset of extinction training than SD rats.
16  detection and compared between WKY, WIS and SD rats.
17  WKY rats consistently had lower levels than SD rats.
18  5-HT turnover when compared to both WKY and SD rats.
19 IC neurons of SN-GEPR-3s compared to control SD rats.
20 -fold (P = 0.0001) higher in BN rats than in SD rats.
21  studies on ageing (F344) by comparison with SD rats.
22 ffects on the other urinary parameters in Nx SD rats.
23 o a dorsal spinal cord transection lesion of SD rats.
24 nephrine (NE) release in BSTL of WKY but not SD rats.
25  and increased nephron number, compared with SD rats.
26  WKY response was not different from that of SD rats.
27 ism on adult female and male Sprague Dawley (SD) rats.
28 tment in Long-Evans (LE) and Sprague-Dawley (SD) rats.
29 ne rats (GEPR-9s) and normal Sprague-Dawley (SD) rats.
30 red normotensive rat strain, Sprague-Dawley (SD) rats.
31  inhibit gastric emptying in Sprague-Dawley (SD) rats.
32 ing from 0.1 to 200 mg/kg in Sprague Dawley (SD) rats.
33  and behavioral responses in Sprague-Dawley (SD) rats.
34 nditions: C57BL/6 J mice and Sprague Dawley (SD) rats.
35 GEPR-3s) compared to control Sprague-Dawley (SD) rats.
36 b data from a prior study in Sprague-Dawley (SD) rats.
37 oyang (GMFS) in healthy male Sprague Dawley (SD) rats.
38 ollowing gonadectomy in male Sprague-Dawley (SD) rats.
39 HR), Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats.
40 ective assessment of baseline craving (mean [SD] rating: 2 days, 26.05 [9.85]; 1 week, 18.70 [11.01];
41 , 3.00 [3.77]) and cue-induced liking (mean [SD] rating: 2 days, 3.06 [2.34]; 1 week, 2.33 [2.87]; 1
42  and 1 year, 1.00 [1.26]) and wanting (mean [SD] rating: 2 days, 3.44 [2.62]; 1 week, 2.72 [2.87]; 1
43 e single remaining kidney of Sprague Dawley (SD) rats (3 days) stimulated the functional marker (pAKT
44 d them more to generate new questions (mean [SD] rating, 7.0 [2.9] vs 5.3 [3.5]; P = .005).
45                           MicroPET images of SD rats after [(18)F]10 administration allowed easy asse
46 tion of T-2 toxin and DON in Sprague-Dawley (SD) rats after a single dose exposure.
47  coincided with the inflammatory response in SD rats and may constitute a neuroprotective mechanism.
48                           MicroPET images of SD rats and nonhuman primates after [18F]27 administrati
49 resistance locus on chromosome (chr) 6q16 in SD rats and, surprisingly, a locus on chr3q21-23 that wa
50 in anesthetized non-diabetic Sprague Dawley (SD) rats and 5/6 nephrectomized (Nx) SD rats.
51 ferred to the right atrium of Spague-Dawley (SD) rats and acetylcholine (ACh) or noradrenaline (NA) r
52 d streptozocin diabetic male Sprague-Dawley (SD) rats and of control and diabetic female Lewis rats w
53 alysis was conducted in both Sprague-Dawley (SD) rats and rhesus macaques over 1.5 and 3 months, resp
54 educed cytokine levels in the hippocampus in SD rats, and increased neurogenesis in the dorsal dentat
55 h intravenous AUC (64.9 muM.h, 2.0 mg/kg) in SD rats, and significant in vivo antitumor activity (T/C
56 ial isolation in non-anxious Sprague Dawley (SD) rats, and a depression model, Wistar-Kyoto (WKY) rat
57 y (BN), Long-Evans (LE), and Sprague-Dawley (SD) rats, and protein expression in the retina was measu
58 y of AMPA receptors in the IC of GEPR-9s and SD rats are similar, our results indicate that altered A
59 d with Long-Evans (LE) rats, Sprague-Dawley (SD) rats are more sensitive to the PPI-disruptive effect
60  We previously reported that Sprague-Dawley (SD) rats are significantly more sensitive than Long Evan
61 nal neovascularization in BN rats but not in SD rats, as demonstrated by fluorescein retinal angiogra
62  molecules was attenuated in LEW compared to SD rats at all times examined.
63                        In a subgroup of male SD rats, blood-retinal barrier (BRB) integrity was also
64                Compared with Sprague-Dawley (SD) rats, Brown-Norway (BN) rats exhibit impaired caroti
65 e shown that CCG was maximal at d 9 of RI in SD rats but did not occur in JCR rats.
66 transient ( approximately 4-fold, d 3 RI) in SD rats but greater and sustained in JCR rats ( approxim
67  it decreased gastric emptying in S5B/P1 and SD rats but not in OM rats.
68  a high-fate diet in Osborne-Mendel (OM) and SD rats but not in S5B/Pl rats, whereas it decreased gas
69 out Rag1, Rag2, and Il2rg in Sprague Dawley (SD) rats by clustered regularly interspaced short palind
70 henotype in drug-dependent and singly housed SD rats, characterized by slowed norepinephrine clearanc
71 n (r = 0.99) with the observed values in the SD rat corneas.
72 dia from uninfected cultures of both LEW and SD rats could prevent BDV-induced DG damage in infected
73                                   In control SD rats, DeltaPO2(t1-ra) > DeltaPO2(t2-t1) (P <0.05) was
74                                DSP-4-treated SD rats demonstrated a dependence-like phenotype, wherea
75  [(18)F]10 administration to Sprague-Dawley (SD) rats demonstrated high uptake of the radiotracer fro
76                      Eleven weeks after A/I, SD rats developed proteinuria, severe kidney damage, dec
77  rat retina are highly strain dependent, and SD rats exhibit low-level inflammation similar to that o
78                                 In addition, SD rats expressed more Fos-LI in the area postrema and m
79 ry bulbs of adult transgenic Sprague Dawley (SD) rats expressing green fluorescent protein (GFP) were
80  excretion rate were increased compared with SD rats fed the 25% protein diet (GFR, 2.66 +/- 0.16 ver
81                                           In SD rats fed the 50% protein diet, GFR, RPF, and kallikre
82 o be significantly greater in LE compared to SD rats for both drugs, with F1 rats intermediate.
83                                We found that SD rats have significantly more duodenal myenteric neuro
84                                       In OIR-SD rats, however, hyperpermeability was observed from P1
85                 In age-matched normal BN and SD rats, however, there was no detectable difference in
86 essure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear
87 f analogues ([18F] 22-28) in Sprague-Dawley (SD) rats identified [18F]27 as the most promising radiot
88 ry (IHC) across a large bank of PhIP-induced SD rat mammary gland carcinomas.
89                                   Therefore, SD rats may be a good model for the study of early infla
90                               In conclusion, SD rats may express more myenteric Fos-LI in response to
91                                           In SD rats, melanin was not detected in all tissues assesse
92 e and miR-224 antagonist using an orthotopic SD rat model.
93                             Similarly, in Nx SD rats (n = 5-6), luseogliflozin significantly increase
94 , HR, RBF, or creatinine clearance (CrCl) in SD rats (n = 7).
95 nically catheterized, awake, Sprague Dawley (SD) rats (n = 78).
96 mal change disease 87% (85 to 89) with mean (SD) rates of eGFR loss -26.5 (34.7), -6.2 (14.3), and -1
97                                        Mean (SD) rates of PDA from baseline to 6-month follow-up were
98                During the same period, mean (SD) rates of PSA testing increased from 20.6 (0.8) to 22
99 R, WKY and standard, outbred Sprague-Dawley (SD) rats on a delay discounting task where the primary m
100 of diabetes), while diabetic Sprague Dawley (SD) rats only showed retinal hyperpermeability from 3 to
101 m male and female embryos of Sprague Dawley (SD) rats or C57BL/6J mice.
102                         Postnatal day 4 (P4) SD rat pups were subjected to bilateral common carotid a
103                   Wistar and Sprague-Dawley (SD) rats received 1 of 3 diets: control (CON); Western (
104 IC neurons of SN-GEPR-3s compared to control SD rats, respectively.
105                            Hyperoxia-treated SD rats showed changes in PEDF and VEGF levels that were
106  protective factors in the disease-resistant SD rat strain.
107 ay respiratory output is similar in F344 and SD rat strains.
108 d eyes were approximately 1.5-fold higher in SD rats than in BN rats.
109               In addition to Sprague-Dawley (SD) rats that have CT responses typical of most rat stra
110 sly, using skin chambers mounted on backs of SD rats, that neutralizing antibodies directed against V
111                                  In diabetic SD rats, the superior, but not the inferior, hemiretina
112                 In 3-month-old diabetic male SD rats, total and postreceptor retinal thickness increa
113           To generate HFrEF, Sprague-Dawley (SD) rats underwent permanent left anterior descending co
114 f the NO system in WF versus Sprague Dawley (SD) rats was examined with the 5/6 renal ablation/infarc
115 rone BHE/cdb rats and normal Sprague Dawley (SD) rats was studied.
116 sing a phenol red gavage technique in fasted SD rats, we showed that insulin administration accelerat
117                          On gestation day 22 SD rats were anesthetized and the uterine horns were ext
118                                   Forty male SD rats were divided into four surgery groups: bilateral
119                   To test this, young female SD rats were either sham implanted or implanted s.c. wit
120           Two days after the injections, the SD rats were exposed to light of 2000 lux for 48 hours.
121                                       Female SD rats were fed a HFD for 8 weeks to induce obesity and
122                                  Normal male SD rats were fed regular powdered diet with or without t
123                                HCR, LCR, and SD rats were grouped by strain and randomly assigned to
124                                         Male SD rats were infused with glucosamine at 0.1 mg x kg(-1)
125                                         Male SD rats were pretreated with alpha-lipoic acid (ALA) and
126                                              SD rats were randomized to AAN and control groups.
127                                              SD rats were randomly divided into 6 groups: Sham, R/I,
128 te matter damage (WMD), postnatal day 4 (P4) SD rats were subjected to bilateral common carotid arter
129                              Sprague-Dawley (SD) rats were exposed to fractionated RTx (6.6 Gy/day fo
130                          Male Spragu-Dawley (SD) rats were subjected to left descending artery occlus
131                     120 male Sprague Dawley (SD) rats were treated with lithium chloride-pilocarpine
132 aturally higher CO and lower H2S levels than SD rat, whereas SH carotid bodies have reduced CO and gr
133 primary rat hepatocytes (PRH) or intact male SD rats with replication-defective recombinant adenoviru
134 ers, LCR), and 3) unselected Sprague-Dawley (SD) rats with or without free access to running wheels f
135 as decreased in the BHE/cdb rats compared to SD rats, with the exception of the comparison made at 37

 
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