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 spontaneously hypertensive rats (SHR) versus WKY rats.

9 l artery structure or microvessel density in WKY rats.

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

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

12 2 versus 110 +/- 2 mmHg, saline versus Dex) WKY rats.

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

14 only evoked bradycardia in conscious SH and WKY rats.

15 sitivity to sympathetic blockade compared to WKY rats.

16 y contribute to the stress susceptibility of WKY rats.

17 ransport in isolated soleus muscle strips of WKY rats.

18 aused similar bradypnoea in conscious SH and WKY rats.

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

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

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

22 sexual dimorphic induction of CYP2B1 gene in WKY rats.

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

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

25 catecholaminergic fibers than bladders from WKY rats.

26 these changes toward the levels observed in WKY rats.

27 he elevated arteriolar tone as compared with WKY rats.

28 brovascular membranes from SHR compared with WKY rats.

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

30 SHRs voided more frequently than WKY rats.

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

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

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

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

35 letal muscle were up-regulated in SHRSP than WKY rats.

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

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

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

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

40 etion and iNOS mRNA expression compared with WKY rats.

41 pathetic nerve discharges in SHRs but not in WKY rats.

42 nsive SHRs but suppressed these responses in WKY rats.

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

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

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

46 tumor suppressor genes were induced only in WKY rats.

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

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

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

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

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

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

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

54 l normotensive young SHR compared to control WKY rats.

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

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

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

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

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

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

61 nsive stroke-prone (SHRSP) and Wistar-Kyoto (WKY) rats.

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

63 nts in labelled PVN neurons in Wistar-Kyoto (WKY) rats.

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

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

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

67 compared with age-matched male Wistar-Kyoto (WKY) rats.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 sympathoexcitatory response in SHRs than in WKY rats, an effect that was blocked by preapplication o

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

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

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

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

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

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

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

90 responses of the normotensive Wistar-Kyoto (WKY) rat and the spontaneously hypertensive (SH) rat to

91 s to irritants in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive (SH) rats.

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

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

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

95 atropine-sensitive bradycardia in conscious WKY rats, and evoked atropine-sensitive bradycardia and

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

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

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

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

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

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

102 In WKY rats, both haloperidol and clozapine attenuated the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 WKY rats exhibited changes in anxiety and autoreceptor f

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

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

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

130 WKY rats had significantly greater numbers of immunoreac

131 WKY rats have been shown to possess neuroendocrine abnor

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

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

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

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

136 ic transport of Gd-DOTA in SHR compared with WKY rats in both age groups, implying that glymphatic tr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 6 x 10(-12)), with an age-dependent rise for WKY rats (P < 2 x 10(-5)).

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

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

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

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

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

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

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

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

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

162 s significantly smaller in SHR compared with WKY rats, regardless of age.

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

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

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

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

167 18-wk-old female normotensive Wistar-Kyoto (WKY) rats, spontaneous hypertensive rats (SHRs), and SHR

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

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

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

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

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

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

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

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

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

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

178 dosis, and hyperleptinemia in both SHRSP and WKY rats, the SHRSP rats weighed less but had comparable

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

180 h atrial-ventricular (AV) block in conscious WKY rats, thus indicating a parasympathetic reflex.

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

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

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

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

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

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

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

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

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

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

191 Male and female WKY rats were exposed to air (0 ppm) or acrolein (3.16 p

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

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

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

195 WKY rats were then treated intraperitoneally with variou

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

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

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

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

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

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

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

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

204 less but had comparable percent adiposity to WKY rats, which supports the use of HFD-fed SHRSP rats a

205 ng depressive-like behavior of Wistar Kyoto (WKY) rats, which are considered as a promising animal mo

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

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

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

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

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