ライフサイエンスコーパス: SHR

1 SHR acquired cocaine self-administration faster than Wis

2 SHR deficiency attenuated H2O2-dependent gene expression

3 SHR is also essential for BS cell-fate specification, bu

4 SHR, SCR and SCL23 homologs are present in many plant sp

5 SHRs exhibited an abnormally large population of CD161(+

6 SHRs have a markedly enhanced potential for RORgammat-dr

7 of SHR in root development, we identified 17 SHR-interacting proteins.

8 Among the 34 patients with >/=20% SHR/T, 32 patients (94%) had a positive OFC with a low t

9 ; 95% CI, 1.1-1.9), CCI score higher than 3 (SHR 2.8; 95% CI, 2.1-3.7), a central venous catheter (SH

10 telet count (<100 x 10(3) vs >/=100 x 10(3): SHR, 1.86; 95% CI, 1.01-3.42; P = .046) and LSM (cirrhos

11 H2 O2 promoted VT in all 30 SHR but none of the NR hearts.

12 .5: SHR, 0.96; P = 0.41; 25 to less than 30: SHR, 1.05; P = 0.01; 30 to less than 35: SHR, 1.15; P =

13 30: SHR, 1.05; P = 0.01; 30 to less than 35: SHR, 1.15; P = <0.001; 35 to less than 40: SHR, 1.21; P

14 : SHR, 1.21; P < 0.001; and greater than 40: SHR, 1.13; P = 0.002.

15 : SHR, 1.15; P = <0.001; 35 to less than 40: SHR, 1.21; P < 0.001; and greater than 40: SHR, 1.13; P

16 ratios (SHRs) for BMI were: less than 18.5: SHR, 0.96; P = 0.41; 25 to less than 30: SHR, 1.05; P =

17 more likely to die before progression to AD (SHR, 1.24; 95% CI, 1.23 to 1.24) or dementia (SHR, 1.26;

18 ation, with an adjusted subhazard ratio (adj SHR) of 1.38 [95% CI 1.06 to 1.80] for major fractures.

19 ulase-negative staphylococci (CoNS; adjusted SHR, 0.91; 95% CI, .50-1.67).

20 4.1%), 38.9% higher than the median adjusted SHR rate of 2.5% (2.0%-3.4%) (P < .001).

21 ibbean versus European age- and sex-adjusted SHR of 0.64 (95% CI: 0.52 to 0.79, p < 0.001) remained s

22 derlie the behavioral deficits in adolescent SHR and enhancing PFC activity could be a treatment stra

23 orated the behavioral deficits of adolescent SHR and restored AMPAR-mediated synaptic function.

24 n both young (postnatal day 30-58) and adult SHRs (4-6 months).

25 augmented CO2 chemoreflex in young and adult SHRs and the high ABP in young SHRs and significantly lo

26 ats (99 +/- 5 mmHg), but lower than in adult SHRs (152 +/- 4 mmHg; P < 0.05).

27 14 +/- 9% increase), but lower than in adult SHRs (226 +/- 10% increase; P < 0.05).

28 nd significantly lower the high ABP in adult SHRs.

29 natal day 30-58) and become greater in adult SHRs.

30 g SHRs and significantly lowers ABP in adult SHRs.

31 a DEPICT revealed that height loci affecting SHR, and especially those affecting leg length, show enr

32 vs. none) (SHR = 5.45, P < 0.001), and age (SHR = 0.98, P = 0.006) were associated with death-censor

33 microbleeds 2.33, 1.38-3.94), and older age (SHR per 10-year increase 1.34, 1.00-1.79) were risk fact

34 nd SHR+V (n=4/4), but not in WKY (n=0/5) and SHR+RLX (n=1/8; P<0.01).

35 on triggered sustained AF in SHR (n=5/5) and SHR+V (n=4/4), but not in WKY (n=0/5) and SHR+RLX (n=1/8

36 The proportion of DHRs vs SHRs, AHR and SHR rates, and excess readmissions.

37 spatio-temporal dynamics of SHR movement and SHR-SCR interaction is currently unavailable.

38 Since SIEL and SHR associate with endosomes, we suggest that KinG serve

39 ring activity of PVN neurons in WKY rats and SHRs.

40 s, spontaneous hypertensive rats (SHRs), and SHRs treated with human relaxin 2 for 14 d (4 mug/h; n=8

41 patients followed by a preemptive approach (SHR, 1.46 [95% CI, 1.01-2.12]; P = .047), especially in

42 Our findings reveal a link between SHR and photorespiratory H2O2 production that has implic

43 5% CI, 1.4 to 6.5) and hepatobiliary cancer (SHR, 5.5; 95% CI, 2.3 to 13.6).

44 2.27-2.98), and posttransplant skin cancer (SHR, 2.92; 95% CI, 2.52-3.39), PTLD (SHR, 1.93; 95% CI,

45 ated but orthogonal phenotypes, in this case SHR with height, as a prism to dissect the biology under

46 95% CI, 2.1-3.7), a central venous catheter (SHR 1.8; 95% CI, 1.4-2.2) and unemployed status (SHR 1.7

47 that in the cytoplasm of root or leaf cells, SHR localizes to endosomes in a SIEL-dependent manner.

48 We identified a conserved SHR-binding motif in 13 BIRD/IDD transcription factors.

49 had only a miniscule (1%) risk of dementia (SHR, 1.01; 95% CI, 1.01 to 1.02); patients treated with

50 HR, 1.24; 95% CI, 1.23 to 1.24) or dementia (SHR, 1.26; 95% CI, 1.25 to 1.26).

51 eceiving an organ from a seropositive donor (SHR, 1.92 [95% CI, 1.30-2.85]; P = .001), but not among

52 Across cocaine doses, SHR earned more cocaine infusions and had higher progres

53 and sex-adjusted South Asian versus European SHR was 1.70 (95% confidence interval [CI]: 1.52 to 1.91

54 ebrovascular event-40% higher than expected (SHR=1.4, 95% confidence interval, 1.3-1.4).

55 to bind directly to SHR and is required for SHR movement.

56 lated, split-open collecting ducts (CD) from SHR-A3 displayed decreased basal intracellular Ca(2+) le

57 lization that requires SOCE in CD cells from SHR-A3.

58 vo rings, aortic and mesenteric vessels from SHR treated with DHI exhibited significantly greater ace

59 otein, little information is known about how SHR trafficking is controlled or how SIEL promotes the m

60 in cancer had increased risk of PTM (sub-HR [SHR], 2.60; 95% CI, 2.27-2.98), and posttransplant skin

61 rons from normal (WKY) and pro-hypertensive (SHR) rats that are sympathetically hyper-responsive and

62 sponsive in both spontaneously hypertensive (SHR) and Goldblatt hypertensive (two kidney one clip; 2K

63 In the hypothalamus, SHRs have more orexin neurons, and a greater proportion

64 f the SHR-SCR binary and JACKDAW (JKD)/IDD10-SHR-SCR ternary complexes.

65 ne ratio) from 6.6 to 1.2 mg/mg (P<0.001) in SHR-A3.

66 SD) reduces arterial blood pressure (ABP) in SHR.

67 antly inhibited renal neprilysin activity in SHR and WKY with HF.

68 d not augment cocaine self-administration in SHR, but acquisition was enhanced in Wistar-Kyoto.

69 rammed stimulation triggered sustained AF in SHR (n=5/5) and SHR+V (n=4/4), but not in WKY (n=0/5) an

70 RLX treatment suppressed AF in SHR hearts by increasing CV from a combination of revers

71 ing impaired sensitivity of the CD to AVP in SHR-A3.

72 the normalization of ADHD-like behaviors in SHR.

73 The proportion of diagnostic codes in SHR that could be verified varied with frequency of diag

74 cantly increased serum kallikrein content in SHR.

75 ne expression consistent with the decline in SHR central Chga expression.

76 rt, to the antihypertensive effect of DHI in SHR.

77 of prefrontal cortex (PFC) was diminished in SHR, which was correlated with the decreased surface exp

78 uaporin 2, further suggesting the effects in SHR-A3 result from the expression of truncated STIM1.

79 Inflammatory cytokines were elevated in SHR kidney and urine after nicotine infusion.

80 genetic determination of Chga expression in SHR, including a cis-quantitative trait loci (QTLs) (i.e

81 MMF treatment also reduced renal fibrosis in SHR-A3 (3.9 versus 2.0; P<0.001).

82 infiltration, and premature hypertension in SHR.

83 uting to the pathogenesis of hypertension in SHR.

84 ulating arginine vasopressin (AVP) levels in SHR-A3 compared with SHR-B2.

85 er DAT kinetic parameters or localization in SHR mPFC.

86 decrease (71 loci) or increase (59 loci) in SHR, suggesting that different height loci disproportion

87 feration of CD161a(+)/CD68(+) macrophages in SHR-derived splenocytes, their renal infiltration, and p

88 but an increase with age was evident only in SHR (P < 7 x 10(-6)).

89 the ligand for CD161a, was overexpressed in SHR kidney, whereas vascular cellular and intracellular

90 ting via PDE3 in control neurons to PDE2A in SHR neurons in the modulation of the Ca(2+) current.

91 dministered MN10021 lowers blood pressure in SHR rats by 10-15% within 1 h suggesting a direct or ind

92 ubules results in a significant reduction in SHR transport.

93 ons to a conductance similar to that seen in SHR neurons, whereas the inhibitor slightly decreased th

94 In SHRs, there was a strong trend towards an increased orex

95 istensibility in SHRs (34+/-2 vs. 10+/-2% in SHRs, P<0.05).

96 augmented CO2 chemoreflex and higher ABP in SHRs are measureable at a young age and increase in adul

97 ented CO2 chemoreflex (breathing and ABP) in SHRs, which indicates an important role for the central

98 ression in abundant CD161(+) immune cells in SHRs represent an abnormal proinflammatory adaptive immu

99 e and lumbar sympathetic nerve discharges in SHRs.

100 Relaxin also increased PA distensibility in SHRs (34+/-2 vs. 10+/-2% in SHRs, P<0.05).

101 lysis not only decreased the basal firing in SHRs, but also eliminated DHPG-induced excitation of spi

102 blood pressure with celiac ganglionectomy in SHRs did not alter the increased level of phosphorylated

103 Insulin plasma concentrations were higher in SHRs than controls (P < 3 x 10(-3)), with an age-depende

104 frontal cortex, was significantly higher in SHRs than in WKY rats.

105 f NMDA currents were significantly higher in SHRs than in WKY rats.

106 led PVN neurons were significantly higher in SHRs than in WKY rats.

107 lateral medulla were significantly higher in SHRs than in WKY rats.

108 Ki(FDG) and Ki(FTHA) were higher in SHRs than WKY rats (P < 3 x 10(-8) and 0.005, respective

109 n of RORgammat can attenuate hypertension in SHRs.

110 ex and in the development of hypertension in SHRs.

111 level in the PVN was significantly lower in SHRs than in WKY rats.

112 corded in spinally projecting PVN neurons in SHRs and male Wistar-Kyoto (WKY) rats.

113 puff NMDA currents in labeled PVN neurons in SHRs but had no effect in WKY rats.

114 ncreases in NMDAR currents of PVN neurons in SHRs.

115 R-mediated miniature EPSCs of PVN neurons in SHRs.

116 rrents in PVN neurons in WKY rats but not in SHRs.

117 The orexin system is overactive in SHRs and contributes to the augmented CO2 chemoreflex an

118 o the pathogenesis of high blood pressure in SHRs and suggests that modulation of the orexin system c

119 digoxin decreased systolic blood pressure in SHRs.

120 f the CD161 surface marker on splenocytes in SHRs and normotensive control Wistar-Kyoto (WKY) rats fr

121 Here, we quantify parameters including SHR mobility, oligomeric state, and association with SCR

122 SHR hearts to VT/VF, patch clamped isolated SHR ventricular myocytes developed EADs and triggered ac

123 confidence interval, 2.2-3.1), and leukemia (SHR=2.5, 95% confidence interval, 1.9-3.1) were at great

124 on rates and anticipated performance, making SHRs an incomplete surrogate for AHRs-particularly for c

125 I, 1.23-1.93), and solid organ malignancies (SHR, 1.54; 95% CI, 1.13-2.11).

126 the risk of posttransplant skin malignancy (SHR, 1.55; 95% CI, 1.07-2.25) but not of posttransplant

127 the risk of posttransplant skin malignancy (SHR, 2.79; 95% CI, 1.82-4.28).

128 ables included venous compression from mass (SHR, 3.1; 95% CI, 1.4 to 6.5) and hepatobiliary cancer (

129 In this report, we measured SHR and Wistar-Kyoto rat (control) Chga expression in ce

130 1), a higher number of cerebral microbleeds (SHR for >5 cerebral microbleeds 2.33, 1.38-3.94), and ol

131 P = 0.009), acute rejection (one vs. none) (SHR = 1.93, P = 0.033), acute rejection (two vs. none) (

132 P = 0.033), acute rejection (two vs. none) (SHR = 5.45, P < 0.001), and age (SHR = 0.98, P = 0.006)

133 We found that SHR-A3, but not SHR-B2, have a novel truncating mutation in the gene enc

134 In 33% of SHR cases, focal VT degenerated to VF within 3 s.

135 mation about the spatio-temporal dynamics of SHR movement and SHR-SCR interaction is currently unavai

136 Examination of SHR and KinG localization and dynamics in live cells sug

137 dermis is spatially limited independently of SHR.

138 hese parameters into a mathematical model of SHR and SCR, which shows that SHR reaches a steady state

139 a decrease in the intercellular movement of SHR and an increase in the sensitivity of SHR movement t

140 trolled or how SIEL promotes the movement of SHR.

141 endosomes disrupts intercellular movement of SHR.

142 In addition, soleus muscles of SHR showed reduced activity of the sarcoplasmic reticulu

143 nmotile kinesin that promotes the pausing of SHR-associated endosomes.

144 Microelectrode recording of SHR hearts showed that VT was initiated by early afterde

145 ream of GA in part through the regulation of SHR and SCR.

146 To elucidate the role of SHR in root development, we identified 17 SHR-interactin

147 of SHR and an increase in the sensitivity of SHR movement to treatment with oryzalin.

148 The alpha/beta core subdomain of SHR forms the BIRD binding groove, which specifically re

149 ver, despite the increased susceptibility of SHR hearts to VT/VF, patch clamped isolated SHR ventricu

150 Our model reveals the timing of SHR and SCR dynamics and allows us to understand how pro

151 cretion, in the intercellular trafficking of SHR.

152 are required for cell-to-cell trafficking of SHR.

153 hat facilitate the cell-to-cell transport of SHR.

154 itable: 26% and 39% of the total variance of SHR can be explained by common variants in European and

155 calcium homeostasis in the soleus muscle of SHRs occurred with changes of some functional outcomes a

156 ensor digitorum longus and soleus muscles of SHRs were differently altered with respect to the relate

157 Sixty 12-week-old SHRs were randomly allocated into 5 groups: BSJYD high d

158 ate pathways) than do loci with no effect on SHR (e.g., embryonic development).

159 We found that only SHR hearts exhibited left ventricular fibrosis and hyper

160 n MP, this MP function is, at least in part, SHR independent.

161 cium optical mapping of Langendorff-perfused SHR hearts revealed that H2 O2 -induced VT/VF arose spon

162 = .046) and LSM (cirrhosis vs precirrhosis: SHR, 5.67; 95% CI, 2.27-14.1; P < .0001).

163 pe CD161a(+) immune cells in prehypertensive SHR after cholinergic activation with nicotine and deter

164 from different ancestors in the injury-prone SHR-A3 and the resistant SHR-B2 lines.

165 ng those who received antiviral prophylaxis (SHR, 1.13 [95% CI, .70-1.83]; P = .6).

166 cancer (SHR, 2.92; 95% CI, 2.52-3.39), PTLD (SHR, 1.93; 95% CI, 1.01-3.66), solid tumor (SHR, 1.44; 9

167 fts with the spontaneously hypertensive rat (SHR) as a model of left ventricular hypertrophy (LVH) an

168 nsion in the spontaneously hypertensive rat (SHR) has not been investigated.

169 Using the spontaneously hypertensive rat (SHR) model of ADHD, we reported that adolescent treatmen

170 The spontaneously hypertensive rat (SHR) strain exists in lines that contrast strongly in su

171 udies in the spontaneously hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent

172 udies in the spontaneously hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent

173 ation in the spontaneously hypertensive rat (SHR/Ola).

174 to derive the subdistribution hazard ratio (SHR) of the associations between VF and patient clinical

175 We studied sitting height ratio (SHR), the ratio of sitting height to total height, to id

176 of the spontaneous histamine release ratio (SHR/T) and low responders in the automated basophil hist

177 ed risk of AD (subdistribution hazard ratio [SHR], 0.98; 95% CI, 0.97 to 0.99) and had only a miniscu

178 V replication (subdistribution hazard ratio [SHR], 1.30 [95% confidence interval {CI}, .97-1.74]; P =

179 rate (adjusted subdistribution hazard ratio [SHR], 2.68; 95% CI, 1.44-4.98).

180 recurrent VTE (subdistribution hazard ratio [SHR], 3.3; 95% CI, 1.7 to 6.4).

181 s, age older than 50 years (subhazard ratio [SHR] 1.4; 95% CI, 1.1-1.9), CCI score higher than 3 (SHR

182 ated superficial siderosis (subhazard ratio [SHR] 7.45, 95% CI 4.27-12.99), cortical atrophy score (S

183 isks model, high Ficolin-3 (subhazard ratio [SHR] = 1.95, P = 0.009), acute rejection (one vs. none)

184 of posttransplant overall (subhazard ratio [SHR], 1.51; 95% confidence interval [95% CI], 1.27-1.81)

185 s fibrosis stage (F4 vs F3, subhazard ratio [SHR], 2.1; 95% CI, 1.07-4.1; P = .032).

186 ative incidence of relapse (subhazard ratio [SHR], 5.83; P < .001) and a shorter overall survival (OS

187 n using standardized hospitalization ratios (SHRs) and absolute excess risks per 10 000 person-years.

188 ate analyses) and shown as subhazard ratios (SHRs) and adjusted subhazard ratios (aSHRs), respectivel

189 or all-cause mortality and subhazard ratios (SHRs) for cause-specific mortality associated with subst

190 25 as the reference, the subhazards ratios (SHRs) for BMI were: less than 18.5: SHR, 0.96; P = 0.41;

191 effects in spontaneously hypertensive rats (SHR) also revealed that oral administration of Val-Glu-L

192 th-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive rats (NR) to VT/VF

193 Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were subje

194 Spontaneously hypertensive rats (SHR) are the most widely used animal model for the study

195 bo- treated Spontaneously Hypertensive Rats (SHR) by both noninvasive and invasive measurements.

196 pressure in spontaneously hypertensive rats (SHR).

197 effects in spontaneously hypertensive rats (SHR).

198 D on LVH in spontaneously hypertensive rats (SHRs) and explore its possible mechanism on regulation o

199 ganglia of spontaneously hypertensive rats (SHRs) and their normotensive controls.

200 neurons in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats.

201 to rats and spontaneously hypertensive rats (SHRs) by cytofluorimetric technique and determined the e

202 o (WKY) rats, spontaneous hypertensive rats (SHRs), and SHRs treated with human relaxin 2 for 14 d (4

203 neurons in spontaneously hypertensive rats (SHRs), but not in normotensive Wistar-Kyoto (WKY) rats.

204 In spontaneously hypertensive rats (SHRs), high ABP is associated with enhanced sympathetic

205 ggerated in spontaneously hypertensive rats (SHRs), resulting in an augmented CO2 chemoreflex that af

206 nistered to spontaneously hypertensive rats (SHRs).

207 ons in male spontaneously hypertensive rats (SHRs).

208 identify 30-day same-hospital readmissions (SHRs), DHRs, and AHRs.

209 elected from the segmental homology regions (SHRs) of 13 QTLs.

210 In the Skane Healthcare Register (SHR), all healthcare consultations are continuously coll

211 At 4 weeks post-reperfusion, SHR and WKY underwent either bilateral RF-RDN or sham-RD

212 in the injury-prone SHR-A3 and the resistant SHR-B2 lines.

213 g a mobile transcription factor, SHORT ROOT (SHR), and mobile microRNA species also determines vascul

214 Two GRAS proteins, SHORT-ROOT (SHR) and SCARECROW (SCR), cooperatively direct asymmetri

215 Here we show that the SHORT-ROOT (SHR) protein, which moves between cells in the root to r

216 l studied example of this is the SHORT-ROOT (SHR) protein, which moves from the stele into the neighb

217 address the question of how the Short-root (SHR) proteins from Arabidopsis thaliana (AtSHR), Brachyp

218 we discovered that a mutation in SHORT-ROOT (SHR) rescued the cell death phenotype of cat2-2 plants u

219 AS family transcription factors, SHORT-ROOT (SHR), SCARECROW (SCR) and SCARECROW-LIKE 23 (SCL23), aff

220 volving around the key regulator SHORT-ROOT (SHR).

221 95% CI 4.27-12.99), cortical atrophy score (SHR per 1-point increase 2.61, 1.70-4.01), a higher numb

222 nt, the intercellular movement of SHORTROOT (SHR) and subsequent interaction with its downstream targ

223 interacts with the SHR-binding protein SIEL (SHR-INTERACING EMBRYONIC LETHAL) and localizes to both m

224 t that KinG serves as a linker between SIEL, SHR, and the plant cytoskeleton.

225 fidence interval [95% CI], 1.27-1.81), skin (SHR, 1.55, 95% CI, 1.23-1.93), and solid organ malignanc

226 1.8; 95% CI, 1.4-2.2) and unemployed status (SHR 1.7; 95% CI, 1.3-2.2) at dialysis entry were signifi

227 er reabsorption, using the inbred rat strain SHR-A3 as an animal model with disrupted SOCE.

228 sion, when challenged with oxidative stress, SHR hearts showed an increased ventricular arrhythmogeni

229 was associated with improved graft survival (SHR = 0.50, P = 0.016).

230 We found that SHR is heritable: 26% and 39% of the total variance of S

231 We found that SHR-A3, but not SHR-B2, have a novel truncating mutation

232 cumulation of glycolate further implied that SHR deficiency impacts the cellular redox homeostasis by

233 Here we show that SHR can move from multiple different cell types in the r

234 While it has been shown that SHR trafficking relies on plasmodesmata (PD), and intera

235 tical model of SHR and SCR, which shows that SHR reaches a steady state in minutes, while SCR and the

236 The present study suggested that SHR/T could be an indicator of basophil activation and h

237 The SHR exhibited alterations in myocardial substrate use at

238 The SHR exhibited higher K1(FDHROL) (P < 5 x 10(-6)) than th

239 The SHR splenocytes constitutively expressed more RORgammat

240 a steady state in minutes, while SCR and the SHR-SCR complex reach a steady-state between 18 and 24 h

241 heritance of haplotype blocks containing the SHR-A3 alleles of these 5 genes correlated with increase

242 However, the SHR protein moves into the BS cells, where it directly r

243 ignaling of neuronal calcium channels in the SHR and that targeting cGMP can restore the channel phen

244 nd found Chga protein to be decreased in the SHR brainstem, yet increased in the adrenal and the plas

245 05,696, arterial pressure was reduced in the SHR compared to the normotensive control and this reduct

246 CP-105,696, reduced arterial pressure in the SHR compared to the normotensive control and this reduct

247 mechanical changes of LVH progression in the SHR model.

248 Here we report in the SHR, increased brainstem infiltration of T cells and mac

249 In the SHR, we observed an increase in T cells and macrophages

250 Instead, the SHR proteins moved multiple cell layers and determined t

251 At 20 mo, the SHR had LVH characterized by decreased LVEF and increase

252 ownstream signalling in the brainstem of the SHR are dynamically regulated during hypertension.

253 ownstream signalling in the brainstem of the SHR are dynamically regulated during hypertension.

254 mobile signals in A. thaliana and all of the SHR homologs physically interact with the AtSHR binding

255 Unlike AtSHR, movement of the SHR homologs was not limited to the endodermis.

256 We find that all of the SHR proteins function as mobile signals in A. thaliana a

257 anism by which the regulated movement of the SHR transcription factor determines the number of cortex

258 ules also results in mis-localization of the SHR-INTERACTING EMBRYONIC LETHAL (SIEL) protein, which h

259 re, we present the crystal structures of the SHR-SCR binary and JACKDAW (JKD)/IDD10-SHR-SCR ternary c

260 Our results demonstrate the utility of the SHR/SST-2 model and the potential of mitochondrially-dir

261 To demonstrate the utility of the SHR/SST-2 model for monitoring both anticancer efficacy

262 type of cat2-2 mutants did not depend on the SHR functional interactor SCARECROW and the sugar signal

263 Elevating cGMP restored the SHR Ca(2+) current to levels seen in normal neurons that

264 tar-Kyoto and Wistar, demonstrating that the SHR phenotype models comorbid ADHD and cocaine abuse.

265 challenge-positive: n=79) in relation to the SHR/T.

266 Strikingly, whereas the SHR network depends on MP, this MP function is, at least

267 plasmodesmata (PD), and interaction with the SHR INTERACTING EMBRYONIC LETHAL (SIEL) protein, little

268 ain kinesin that directly interacts with the SHR-binding protein SIEL (SHR-INTERACING EMBRYONIC LETHA

269 CD161a(+) immune cells are dominant in the (SHR) spontaneously hypertensive rat and expand in respon

270 tween auxin and cytokinin, signaling through SHR, microRNA165/6, and PHABULOSA is required to maintai

271 n vivo administration of miR-22 antagomir to SHR causes substantial ( approximately 18 mmHg) reductio

272 ed RORgammat and IL-17F levels contribute to SHR hypertension and might be therapeutic targets.

273 in, which has been shown to bind directly to SHR and is required for SHR movement.

274 BPs were significantly lower in DHI-treated SHR than controls by both tail-cuff and invasive BP meas

275 ar injury scores were reduced in MMF-treated SHR-A3 from 1.6 to 1.4 (P<0.002).

276 terstitial injury was reduced in MMF-treated SHR-A3 from 2.62 to 2.0 (P=0.001).

277 (SHR, 1.93; 95% CI, 1.01-3.66), solid tumor (SHR, 1.44; 95% CI, 1.04-1.99), death (HR, 1.20; 95% CI,

278 vors of central nervous system (CNS) tumors (SHR=4.6, 95% confidence interval, 4.3-5.0), head and nec

279 ce interval, 4.3-5.0), head and neck tumors (SHR=2.6, 95% confidence interval, 2.2-3.1), and leukemia

280 .25) but not of posttransplant solid tumors (SHR, 1.23; 95% CI, 0.69-2.19).

281 is of ADHD and its potential treatment using SHR.

282 (calculated per the Medicare formula) using SHRs and AHRs to determine what might happen if the fede

283 Excess readmission ratios using SHRs inaccurately anticipated penalties (changed from >1

284 berculosis treatment was associated with VF (SHR, 11.50 [95% confidence interval, 3.92-33.74]; P < .0

285 ent- and hospital-level predictors of DHR vs SHR.

286 The proportion of DHRs vs SHRs, AHR and SHR rates, and excess readmissions.

287 g the myocyte ss-adrenergic phenotype, where SHR cultures elicited heightened myocyte cAMP responses

288 nts are nominally associated (p < 0.05) with SHR, more than expected by chance (p = 5 x 10(-40)).

289 icance (p < 5 x 10(-8)) for association with SHR and overlapped biological candidate genes, including

290 pressin (AVP) levels in SHR-A3 compared with SHR-B2.

291 pean admixture is negatively correlated with SHR in African Americans (r(2) approximately 0.03).

292 st a model in which interaction of KinG with SHR allows for the formation of stable movement complexe

293 acetylcholine receptor) was similar in young SHR and WKY rats.

294 linergic inflammatory effect exists in young SHR, measured by expansion of CD161a(+)/CD68(+) macropha

295 Studies used young SHR and WKY (Wistar-Kyoto) rats.

296 The resting ABP is higher in young SHRs (122 +/- 5 mmHg) than in age-matched Wistar-Kyoto r

297 e to normoxic hypercapnia is higher in young SHRs (mean +/- SEM: 179 +/- 11% increase) than in age-ma

298 ex and the high ABP are measureable in young SHRs (postnatal day 30-58) and become greater in adult S

299 ed CO2 chemoreflex and the high ABP in young SHRs and normalize the augmented CO2 chemoreflex and sig

300 ung and adult SHRs and the high ABP in young SHRs and significantly lowers ABP in adult SHRs.