ライフサイエンスコーパス: WKY rat

1 40% to 60% lower in the SH rat compared with WKY rat.

2 (Mcs) loci underlying the resistance of the WKy rat.

3 tment had no effect on blood pressure in the WKY rat.

4 SHRSP and the normotensive reference strain, WKY rat.

5 at and in conferring resistance to AA in the WKY rat.

6 uronal firing in cells from the SHR than the WKY rat.

7 l activity in cells from the SHR but not the WKY rat.

8 PVN was significantly lower in SHRs than in WKY rats.

9 2 versus 110 +/- 2 mmHg, saline versus Dex) WKY rats.

10 e in the excitability of PVN neurons only in WKY rats.

11 n CRF-treated BN rats but not in CRF-treated WKY rats.

12 ts were significantly higher in SHRs than in WKY rats.

13 y contribute to the stress susceptibility of WKY rats.

14 ransport in isolated soleus muscle strips of WKY rats.

15 ACTH secretion in control SD but not control WKY rats.

16 did not induce pathology in lungs of normal WKY rats.

17 f the nucleus tractus solitarius of SHRs and WKY rats.

18 sexual dimorphic induction of CYP2B1 gene in WKY rats.

19 areas of the NTS in SHRs versus no effect in WKY rats.

20 catecholaminergic fibers than bladders from WKY rats.

21 these changes toward the levels observed in WKY rats.

22 he elevated arteriolar tone as compared with WKY rats.

23 brovascular membranes from SHR compared with WKY rats.

24 SHRs voided more frequently than WKY rats.

25 LC-terminal-selective toxin DSP-4 to SD and WKY rats.

26 ex, was significantly higher in SHRs than in WKY rats.

27 la were significantly higher in SHRs than in WKY rats.

28 ns were significantly higher in SHRs than in WKY rats.

29 he cytosolic vesicle fraction in SHR than in WKY rats.

30 etion and iNOS mRNA expression compared with WKY rats.

31 nsive SHRs but suppressed these responses in WKY rats.

32 VN were significantly higher in SHRs than in WKY rats.

33 uN2B in the PVN were greater in SHRs than in WKY rats.

34 tumor suppressor genes were induced only in WKY rats.

35 ry gene expression also was apparent only in WKY rats.

36 sympathetic nerve activity in SHR but not in WKY rats.

37 ited currents of PVN neurons in SHRs than in WKY rats.

38 iring activity of PVN neurons in SHR than in WKY rats.

39 n NMDAR-EPSCs of PVN neurons in SHRs than in WKY rats.

40 ex, was significantly higher in SHRs than in WKY rats.

41 g activity of PVN neurons in SHRs but not in WKY rats.

42 led PVN neurons in SHRs but had no effect in WKY rats.

43 l normotensive young SHR compared to control WKY rats.

44 he AAV2-apelin viral vector into the RVLM of WKY rats.

45 cular zone (SVZ) of 6 and 18 week-old GK and WKY rats.

46 spontaneously hypertensive rats (SHR) versus WKY rats.

47 l artery structure or microvessel density in WKY rats.

48 oline receptor) was similar in young SHR and WKY rats.

49 t improvement of depression-like behavior in WKY rats.

50 ascular reactivity to stress in both BHR and WKY rats.

51 sive rat (SHR) compared to the Wistar Kyoto (WKY) rat.

52 ) relative to the normotensive Wistar-Kyoto (WKY) rat.

53 nimal model of depression, the Wistar-Kyoto (WKY) rat.

54 ntic glomerulonephritis in the Wistar Kyoto (WKY) rat.

55 rats, and a depression model, Wistar-Kyoto (WKY) rats.

56 y hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats.

57 on by PB of the CYP2B1 gene in Wistar Kyoto (WKY) rats.

58 o microsomes from normotensive Wistar-Kyoto (WKY) rats.

59 red with those to normotensive Wistar Kyoto (WKY) rats.

60 SHRs), but not in normotensive Wistar-Kyoto (WKY) rats.

61 -matched normotensive control, Wistar Kyoto (WKY) rats.

62 urrent-voltage relationship in Wistar-Kyoto (WKY) rats.

63 pertensive rats (SHRs) than in Wistar-Kyoto (WKY) rats.

64 g PVN neurons in SHRs and male Wistar-Kyoto (WKY) rats.

65 (SHR) compared to normotensive Wistar-Kyoto (WKY) rats.

66 HR) compared with normotensive Wistar-Kyoto (WKY) rats.

67 HR) compared with normotensive Wistar-Kyoto (WKY) rats.

68 and their control normotensive Wistar-Kyoto (WKY) rats.

69 tensive rats (BHR) and control Wistar-Kyoto (WKY) rats.

70 as approximately 25% higher than that of the WKY rats (1.2+/-0.2 ml/g/min), likely due to the hyperte

71 ter peripheral nerve injury in Wistar-Kyoto (WKY) rats, a genetic variation of Wistar rats with demon

72 of depression-like behavior in Wistar-Kyoto (WKY) rats, a genetic variation of Wistar rats.

73 al selective breeding from the Wistar-Kyoto (WKY) rat, an accepted model of major depressive disorder

74 o, we inhibited degradation in MPO-immunized WKY rats and found greater immune responsiveness to MPO

75 ively expressed more RORgammat than those of WKY rats and produced more IL-17F on induction.

76 reased the firing activity of PVN neurons in WKY rats and SHRs.

77 R7/8 and TLR9 activation and similar between WKY rats and SHRs.

78 -regulated kinase (1/2) in neurons from both WKY rats and SHRs; however, the stimulation was 50% grea

79 ession is enhanced in the RVLM of SHR versus WKY rats and that overexpression of this gene in the RVL

80 of an EET agonist increases BP and HR in the WKY rat, and 3) inhibition of NAD(P)H oxidase by gp91ds-

81 ody (Ab) GN, a model of crescentic GN in the WKY rat, and whether the effects of MDC were dependent o

82 oth strains, although to a greater extent in WKY rats, and enhanced stress-induced norepinephrine (NE

83 BN rats showed less PPI than WKY rats, and neither antipsychotic alone enhanced PPI.

84 as approximately 3-fold greater than that of WKY rats, and pretreatment with the tungsten diet elimin

85 brain noradrenergic system was deficient in WKY rats, and they lacked noradrenergic facilitation of

86 ure and lumbar sympathetic nerve activity in WKY rats, and this effect was eliminated by microinjecti

87 Exposure of WKY rat aortas to IL-17F impaired endothelium-dependent

88 assessment of the neurochemical profile for WKY rats as compared to the outbred progenitor controls,

89 In WKY rats, both haloperidol and clozapine attenuated the

90 signal transduction pathway in Wistar Kyoto (WKY) rat brain neurons.

91 s showed that PB induced CYP2B1 mRNA in male WKY rats but not female rats.

92 D elicited locomotor sensitization in SD and WKY rats but not in SHR.

93 SCs and puff NMDA currents in PVN neurons in WKY rats but not in SHRs.

94 only sensitized the release of NE in BSTL of WKY rats, but also restored noradrenergic facilitation o

95 ells survived to 3 weeks in the 18 weeks old WKY rats, but in the GK rats only 16+/-7% of the new cel

96 owing that sera from recovery phase Lewis or WKY rats, but not that of naive rats, afforded protectio

97 e's disease, can be induced in Wistar Kyoto (WKY) rats by a single injection of collagenase-solubiliz

98 e's disease, can be induced in Wistar Kyoto (WKY) rats by a single injection of rat glomerular baseme

99 e's disease, can be induced in Wistar Kyoto (WKY) rats by immunization with either collagenase-solubi

100 e's disease, can be induced in Wistar Kyoto (WKY) rats by immunization with the noncollagenous domain

101 ferating neural progenitor cells compared to WKY rats (by 183+/-16% in SVZ and by 36+/-5% in DG; p<0.

102 senteric vascular beds isolated ex vivo from WKY rats caused dose-dependent vasorelaxation.

103 ensive rat (SHR) compared with Wistar-Kyoto (WKY) rat cerebrovascular smooth muscle cells (n = 18 and

104 T was 2.6-fold higher in the SHR than in the WKY rat, confirming increased EET hydrolysis in the SHR

105 ippocampus and the nucleus accumbens shell), WKY rats consistently had lower levels than SD rats.

106 The results indicated that WKY rats consumed a greater amount of alcohol (P < 0.001

107 gest that altered levels of PPTRH 178-199 in WKY rats could cause, at least in part, the hyper-activi

108 sults show that susceptibility to NTN in the WKY rat depends on both circulating and intrinsic renal

109 ced by a small dose of nephrotoxic globulin, WKY rats developed crescents in 80 +/- 2% of glomeruli a

110 d by the tungsten diet, whereas Wistar Koto (WKY) rats displayed no significant alteration in the pre

111 Wistar-Kyoto (WKY) rats exhibit hyperresponsive neuroendocrine and beh

112 The neuroendocrine results indicate that WKY rats exhibited a sustained corticosterone response t

113 WKY rats exhibited changes in anxiety and autoreceptor f

114 SHRs and normotensive control Wistar-Kyoto (WKY) rats from birth to adulthood.

115 The Fcgr3-rs gene is deleted from the WKY rat genome, and this deletion is associated with enh

116 Similarly, WKY rats had lower monoamine levels compared to WIS, alt

117 WKY rats had significantly greater numbers of immunoreac

118 WKY rats have been shown to possess neuroendocrine abnor

119 ertensive (SHR) or age-matched Wistar-Kyoto (WKY) rat hearts.

120 , by adjusting the immunization regimen, all WKY rats immunized with myeloperoxidase develop experime

121 odel of Goodpasture's disease, Wistar Kyoto (WKY) rats immunized with collagenase-solubilized glomeru

122 re statistically different from those of the WKY rats in all structures analyzed (P<0.05) except for

123 ine and stress-induced monoamine turnover in WKY rats, including alterations to DA and 5-HT turnovers

124 Paraplegia in both the SHR and WKY rats increased heart rates (27 and 22% in SHR and WK

125 and neural protection in both the SHRSP and WKY rats, indicating that SEH inhibition has broad pharm

126 t developed from normoglycemic Wistar-Kyoto (WKY) rat is a model for type-2 diabetes, with insulin re

127 Given that the Wistar-Kyoto (WKY) rat is a putative animal model of depressive behavi

128 The Wistar Kyoto (WKy) rat is resistant to mammary carcinomas induced with

129 The Wistar Kyoto (WKY) rat is uniquely susceptible to experimentally induc

130 from col(V) immune rats were transferred to WKY rat lung isograft recipients followed by assessments

131 tly constricted pial arterioles from SHR and WKY rats (n = 6 to 8).

132 neuroendocrine activation, male, Wistar and WKY rats (N=6/group) were exposed to an acute forced-swi

133 stimulation of NET and TH mRNA levels in the WKY rat neuron, whereas it caused only a 45% decrease in

134 rsistent in the SHR neuron compared with the WKY rat neuron.

135 d longer in the SHR neuron compared with the WKY rat neuron.

136 PI3-kinase had no significant effect in the WKY rat neuron.

137 with 8 SHR and 8 normotensive Wistar-Kyoto (WKY) rats over their life cycle.

138 6 x 10(-12)), with an age-dependent rise for WKY rats (P < 2 x 10(-5)).

139 i(FDG) and Ki(FTHA) were higher in SHRs than WKY rats (P < 3 x 10(-8) and 0.005, respectively) indepe

140 D, was found to be higher in SHR compared to WKY rats (P<0.05).

141 iameter (58+/-3 vs. 49+/-3 mum at 60 mmHg in WKY rats, P<0.05), suggesting inward remodeling that was

142 ) channel expression was assessed in SHR and WKY rat pial arterioles, which were monitored by intravi

143 o increase NMDAR activity in brain slices of WKY rats pretreated with the protein phosphatase 1/2A, c

144 nistration of collagenase-solubilized GBM to WKY rats prevented the development of EAG.

145 In nephrotoxic nephritis in WKY rats, recombinant rat IFN-beta started either at ind

146 Paraplegia in the WKY rats reduced systolic (-4%) and diastolic (-5%) bloo

147 lso protective in normotensive Wistar-Kyoto (WKY) rats, reducing both hemispheric infarct and neurode

148 At 24 h, SHR rats showed no change while the WKY rats showed a 20% decrease in seizure length (P < 0.

149 analyses of the congenic rats, compared with WKY rats, showed that of the top 100 most changed genes,

150 The Wistar-Kyoto (WKY) rat shows marked susceptibility to crescentic glome

151 umption was similar in SHR and Wistar-Kyoto (WKY) rats (SHR: 600 +/- 55 nmol O(2)/min per g, WKY: 611

152 18-wk-old female normotensive Wistar-Kyoto (WKY) rats, spontaneous hypertensive rats (SHRs), and SHR

153 esistant Mcs5a allele from the Wistar-Kyoto (WKy) rat strain consists of two non-protein-coding genet

154 The inbred Wistar Kyoto (WKY) rat strain has been proposed as a model of stress v

155 us studies have shown that the Wistar-Kyoto (WKY) rat strain may be a genetic model of depression whe

156 using the uniquely susceptible Wistar Kyoto (WKY) rat strain, we have identified multiple crescentic

157 Mesangial cells that were derived from WKY rats synthesized significantly more monocyte chemoat

158 xpression in the anterior cingular cortex in WKY rats than in Wistar rats.

159 Separately, WKY rats that received F344 lung allografts were treated

160 However, crescents were also seen in WKY rats that were given Lewis marrow.

161 CRF was assessed in SHR, an inbred strain of WKY rats (the WKY[LJ] rat), and an outbred normotensive

162 In WKY rats, the binding of [3H]-GBR12935 to DAT sites was

163 ly hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats; the number of HSD2 neurons in both of these s

164 Susceptibility of WKY rats to anxiety and depressive behavior may be relat

165 es in the locomotor activity of SD, SHR, and WKY rats to repeated 2.5- and 10-mg/kg MPD treatment.

166 genetic susceptibility of the Wistar-Kyoto (WKY) rat to nephrotoxic nephritis, a rat model of Crgn.

167 s and their progenitor strain, Wistar-Kyoto (WKY) rats, to compare eyeblink conditioning in strains t

168 tes, may be related to the predisposition of WKY rats towards depressive behavior.

169 ody on leukocyte-endothelial interactions in WKY rats via immunization with human myeloperoxidase.

170 In WKY rats, vigorous responses to the BCTD, to which the L

171 In this study, the Wistar-Kyoto (WKy) rat was genetically characterized for loci that mod

172 GHS x WKY rats were backcrossed to breed for congenic rats wit

173 is hypothesis, intact and paraplegic SHR and WKY rats were chronically instrumented for recording BP-

174 istar Kyoto rat recipients (WKY, RT1(l)), or WKY rats were fed col(V) pretransplantation.

175 During phase 1, SHR and WKY rats were not different in their ability to learn th

176 Two differences between SHR and WKY rats were observed for Ang II-mediated MAP kinase ac

177 WKY rats were then treated intraperitoneally with variou

178 losporine (CsA)-mediated immune suppression, WKY rats were treated with low-dose CsA (5 mg/kg), postt

179 strated a dependence-like phenotype, whereas WKY rats were unchanged.

180 Age-matched Wistar Kyoto (WKY) rats were controls.

181 Wistar-Kyoto (WKY) rats were immunised with human myeloperoxidase (MPO

182 suppressed the TLR-mediated IL-6 response in WKY rats, whereas Ang II had no effect.

183 ted after LA exposure in SH and SHHF but not WKY rats, whereas tumor suppressor genes were induced on

184 e and similar FA utilizations (compared with WKY rats), which indicates maladaptation of energy subst

185 ic modulation of the innate immune system in WKY rats, which is reversed in prehypertensive SHRs.

186 kg MPD induced locomotor tolerance in SD and WKY rats, while SHR had variable locomotor responses to

187 A) receptor antagonist, on pain behaviors in WKY rats with chronic constriction sciatic nerve injury

188 Groups of WKY rats with EAG, induced by immunization with recombin

189 rks and BK channel function in Wistar-Kyoto (WKY) rats with borderline hypertension and in spontaneou

190 NE) and dopamine (DA) systems functioning in WKY rats, yet no attempt has been made to provide a comp