ライフサイエンスコーパス: SHR

1 SHR capillary density is increased in both ventricles an

2 SHR deficiency attenuated H2O2-dependent gene expression

3 SHRs exhibited an abnormally large population of CD161(+

4 SHRs have a markedly enhanced potential for RORgammat-dr

5 at enrollment (no AKI [SHR, 1] vs. stage 1 [SHR, 3.28; 1.30-8.25] vs. stage 2 [SHR, 4.33; 1.76-10.66

6 The procedure was tolerated well in over 100 SHR and normotensive rats that received unilateral and b

7 stage 1 [SHR, 3.28; 1.30-8.25] vs. stage 2 [SHR, 4.33; 1.76-10.66] vs. stage 3 [SHR, 4.5; 1.59-12.73

8 stage 2 [SHR, 4.33; 1.76-10.66] vs. stage 3 [SHR, 4.5; 1.59-12.73]) were identified as baseline risk

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

10 .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 =

11 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

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

13 : 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

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

15 usted transplantation rates decreased in AC (SHR, 0.6), AIH (SHR, 0.78), and CC (SHR, 0.95).

16 and are necessary and sufficient to activate SHR-mediated divisions and CYCD6;1 expression.

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

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

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

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

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

24 14 +/- 9% increase), but lower than in adult SHRs (226 +/- 10% increase; P < 0.05).

25 g SHRs and significantly lowers ABP in adult SHRs.

26 nd significantly lower the high ABP in adult SHRs.

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

28 CI]: 0.2 [0.0-0.7]), but accounting for age (SHR [95% CI]: 1.0 [0.9-1.0]), insurance (SHR [95% CI]: 5

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

30 r for AC (subhazard ratio [SHR], 1.17), AIH (SHR, 1.17), and CC (SHR, 1.13) when compared with NASH,

31 ation rates decreased in AC (SHR, 0.6), AIH (SHR, 0.78), and CC (SHR, 0.95).

32 1.58; 1.07-2.33), episodes of previous AKI (SHR, 1.26; 1.02-1.56), and AKI stage at enrollment (no A

33 -1.56), and AKI stage at enrollment (no AKI [SHR, 1] vs. stage 1 [SHR, 3.28; 1.30-8.25] vs. stage 2 [

34 (SHR = 0.62; 95% CI 0.54-0.71; P < .001 and SHR = 0.53; 95% CI 0.43-0.64; P < .001).

35 y, genetic analysis reveals that BAM-CLE and SHR converge to regulate additional cell divisions outsi

36 Female 4-week-old Wistar Kyoto and SHR rats were studied after 24-hour systemic AT(1)R (Ang

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

38 ies (ROS) production in normotensive rat and SHR vessels, which suggested eNOS uncoupling.

39 the plasma and brain of male Wistar rats and SHR that had received LPS (1.5 mg kg(-1) ) or saline.

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

41 roximal tubule (RPT) cells from both WKY and SHRs but was greater in the latter than the former group

42 rent fates depending on the feedback between SHR's availability and the state of the regulatory netwo

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

44 nd mesenteric arteries supernatant's of both SHR and normotensive groups.

45 er treatment reduced risk of gastric cancer (SHR, 0.24; 95% CI, 0.15-0.41; P < .001).

46 ill had an increased risk of gastric cancer (SHR, 1.16; 95% CI, 0.74-1.83; P = .51) but confirmed H p

47 5% CI, 1.4 to 6.5) and hepatobiliary cancer (SHR, 5.5; 95% CI, 2.3 to 13.6).

48 ositivity also had a reduced risk of cancer (SHR 0.74; 95% CI, 0.54-1.04; P = .04).

49 2.27-2.98), and posttransplant skin cancer (SHR, 2.92; 95% CI, 2.52-3.39), PTLD (SHR, 1.93; 95% CI,

50 d in AC (SHR, 0.6), AIH (SHR, 0.78), and CC (SHR, 0.95).

51 ratio [SHR], 1.17), AIH (SHR, 1.17), and CC (SHR, 1.13) when compared with NASH, but after 2 months,

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

53 rk suggests that acquisition of the cortical SHR-SCR module enabled cell division coupled to rhizobia

54 The cortical SHR-SCR network is conserved across legume species, resp

55 I episodes (SHR, 1.25; 1.15-1.37), and CysC (SHR, 1.38; 1.01-1.89) predicted CKD development.

56 ence interval (CI)]: 1.8 [1.2-2.8]) or DDKT (SHR [95% CI]: 2.0 [1.3-3.2]) than non-Hispanic white in

57 02), 16% lower subhazard for waitlist death (SHR 0.84; 95% CI 0.73-0.95, P = .07), and 13% increased

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

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

60 CI: 1.403 to 2.818), lack of pre-dilatation (SHR: 1.485; 95% CI: 1.065 to 2.069), and treatment in a

61 [1.1-33.7]), presenting with a living donor (SHR [95% CI]: 4.1 [1.4-12.3]), dialysis duration (SHR [9

62 0.3 [0.2-0.6]), network of potential donors (SHR [95% CI]: 1.0 [1.0-1.1]), self-esteem (SHR [95% CI]:

63 95% CI]: 4.1 [1.4-12.3]), dialysis duration (SHR [95% CI]: 0.3 [0.2-0.6]), network of potential donor

64 R, 1.01; 1.00-1.03), number of AKI episodes (SHR, 1.25; 1.15-1.37), and CysC (SHR, 1.38; 1.01-1.89) p

65 (SHR [95% CI]: 1.0 [1.0-1.1]), self-esteem (SHR [95% CI]: 0.4 [0.2-0.8]), transplant knowledge (SHR

66 001 for race), Hispanic or Latino ethnicity (SHR, 1.59; 95% CI, 1.34-1.87; P < .001), and history of

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

68 tical expression of SCR, and stele-expressed SHR protein accumulates in cortical cells of M. truncatu

69 /2) family receptor kinases are required for SHR-dependent formative divisions and CYCD6;1 expression

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

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

72 (+) -K(+) -ATPase activity in RPT cells from SHR.

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

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

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

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

77 young and adult spontaneously hypertensive (SHR) rats compared with age-matched normotensive Wistar-

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

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

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

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

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

83 the normalization of ADHD-like behaviors in SHR.

84 the AP and NTS, transiently decreased BP in SHR and this effect was attenuated after lesion of NTS D

85 a(+) excretion or renal interstitial cGMP in SHR.

86 s the suppression of glymphatic clearance in SHR rats and thus offers new insight into the coexistenc

87 cantly increased serum kallikrein content in SHR.

88 mal tubule cell AT(2)R natriuretic defect in SHR that may contribute to the development of hypertensi

89 cGMP could bypass the natriuretic defect in SHR, we infused 8-bromo-cGMP.

90 nvestigate caveolae integrity and density in SHR aortas and mesenteric arteries and the role played b

91 be related to decreased caveolae density in SHR vessels.

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

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

94 d impeded glymphatic transport of Gd-DOTA in SHR compared with WKY rats in both age groups, implying

95 We observed ventricular reflux of Gd-DOTA in SHR rats only, indicating abnormal CSF flow dynamics sec

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

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

98 found that an RNA G-quadruplex (GQ) forms in SHR mRNA and is capable of triggering RNA phase separati

99 ean arterial pressure was slightly higher in SHR but within the normotensive range and unaffected by

100 induced drop in blood pressure was higher in SHR than in Wistar rats.

101 nted, whereas oxidative stress was higher in SHR.

102 unteracts the development of hypertension in SHR, accompanied by attenuated sympathetic nerve activit

103 infiltration, and premature hypertension in SHR.

104 lar CMT- 3 infusion was also investigated in SHR (spontaneously hypertensive rats).

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

106 re associated with an increased heat loss in SHR compared to Wistar rats.

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

108 evels in the AVPO in Wistar rats, but not in SHR.

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

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

111 ed heat loss, but not by heat production, in SHR.

112 fect on natriuresis or AT(2)R recruitment in SHR.

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

114 r and brain volumes significantly smaller in SHR compared with WKY rats, regardless of age.

115 the presence of caveolae-like structures in SHR aortas and mesenteric arteries.

116 ry angular dispersion increases with time in SHR.

117 ollowed by fever in Wistar rats, whereas, in SHR, a maintained hypothermia without fever were observe

118 In SHRs, we found significant remodelling of the capillary

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

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

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

122 re and renal sympathetic nerve discharges in SHRs but not in WKY rats.

123 e and lumbar sympathetic nerve discharges in SHRs.

124 ed ETBR-mediated natriuresis and diuresis in SHRs.

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

126 tion in the PVN were significantly higher in SHRs than in WKY rats.

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

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

129 s), renal ETBR phosphorylation was higher in SHRs.

130 n of RORgammat can attenuate hypertension in SHRs.

131 ex and in the development of hypertension in SHRs.

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

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

134 uff NMDA currents of labelled PVN neurons in SHRs.

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

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

137 digoxin decreased systolic blood pressure in SHRs.

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

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

140 In anti-DBH-SAP injected SHR, the antihypertensive effect of repeated LV injectio

141 ge (SHR [95% CI]: 1.0 [0.9-1.0]), insurance (SHR [95% CI]: 5.9 [1.1-33.7]), presenting with a living

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

143 % CI]: 0.4 [0.2-0.8]), transplant knowledge (SHR [95% CI]: 1.3 [1.0-1.7]), and changes to Kidney Allo

144 0.6 [0.4-0.9]), religious objection to LDKT (SHR [95% CI]: 0.6 [0.4-1.0]), and donor preference (SHR

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

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

147 time-varying competing risk analysis, MELD (SHR, 1.01; 1.00-1.03), number of AKI episodes (SHR, 1.25

148 of gastric adenocarcinoma compared with men (SHR, 0.52; 95% CI, 0.40-0.68; P < .001); patients whose

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

150 5% CI 0.58 to 1.96], P = 0.82; multivariable SHR 1.42 [95% CI 0.78 to 2.57], P = 0.26).

151 5% CI 0.68 to 1.38], P = 0.85; multivariable SHR 1.16 [95% CI 0.80 to 1.69], P = 0.43), and although

152 In Wistar Kyoto, but not SHR, C-21 induced AT(2)R translocation to apical plasma

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

154 ve divisions and CYCD6;1 expression, but not SHR-dependent ground tissue specification.

155 Ectopic activation of SHR and SCR in legumes is sufficient to induce root cort

156 ular regulatory network, and the dynamics of SHR intercellular transport as a cell-cell coupling mech

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

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

159 d an ordinary differential equation model of SHR and SCR in the QC and CEI which incorporated the sto

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

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

162 pic reconstructions of the entire network of SHR hearts combining gel-based fluorescent labelling of

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

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

165 ll as upstream transcriptional regulation of SHR and SCR.

166 tein complex stoichiometry and regulation of SHR transcription modulate the division timing of two di

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

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

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

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

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

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

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

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

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

176 changes to Kidney Allocation System policy (SHR [95% CI]: 0.3 [0.2-0.5]) mitigated race differences

177 changes to Kidney Allocation System policy (SHR [95% CI]: 10.3 [2.5-42.1]) in multivariable analysis

178 CB00, after accounting for other predictors (SHR = 0.62; 95% CI 0.54-0.71; P < .001 and SHR = 0.53; 9

179 % CI]: 0.6 [0.4-1.0]), and donor preference (SHR [95% CI]: 2.5 [1.2-5.1]), accounted for some racial

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

181 study aimed to delineate in prehypertensive SHR kidneys the receptor or postreceptor defect causing

182 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

183 .15; P < .001), black/African American race (SHR, 2.00; 95% CI, 1.80-2.22), Asian race (SHR, 2.52; 95

184 (SHR, 2.00; 95% CI, 1.80-2.22), Asian race (SHR, 2.52; 95% CI, 1.64-3.89) (P < .001 for race), Hispa

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

186 in vivo in a spontaneously hypertensive rat (SHR) model of hypertension.

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

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

189 hesized that spontaneously hypertensive rat (SHR) vessels should have a smaller number of caveolae, a

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

191 th an association with sitting height ratio (SHR); the IGFBP5 signal (associated with IGFBP-5 levels)

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

193 >360 miles had a 27% lower subhazard ratio (SHR) for waitlist removal (SHR 0.73, 95% confidence inte

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

195 tatin C (CysC; subdistribution hazard ratio [SHR], 1.58; 1.07-2.33), episodes of previous AKI (SHR, 1

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

197 kidney failure (univariable subhazard ratio [SHR] 0.97 [95% CI 0.68 to 1.38], P = 0.85; multivariable

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

199 V/HCV co-infected patients (subhazard ratio [SHR] = 1.88; 95% confidence interval [CI], 1.15-3.06; P

200 ariate analysis, variables (subhazard ratio [SHR] [95% CI]) associated with developing clinical outco

201 ariate analysis, variables (subhazard ratio [SHR] [95% confidence interval]) associated with developi

202 tion of H pylori infection (subhazard ratio [SHR], 1.13; 95% confidence interval [CI], 1.11-1.15; P <

203 listing was higher for AC (subhazard ratio [SHR], 1.17), AIH (SHR, 1.17), and CC (SHR, 1.13) when co

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

205 Younger age (subhazard ratio [SHR]: 0.969; 95% confidence interval [CI]: 0.944 to 0.99

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

207 25 as the reference, the subhazards ratios (SHRs) for BMI were: less than 18.5: SHR, 0.96; P = 0.41;

208 o get any KT (subdistribution hazard ratios [SHR] [95% confidence interval (CI)]: 1.8 [1.2-2.8]) or D

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

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

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

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

213 We used Spontaneously Hypertensive Rats (SHR) exhibiting many features of the human hypertensive

214 Spontaneously hypertensive rats (SHR) were compared to normotensive rats and were subject

215 Spontaneously hypertensive rats (SHR) were treated with the NK-1R antagonist L732138 (5 m

216 rtension in spontaneously hypertensive rats (SHR).

217 pressure in spontaneously hypertensive rats (SHR).

218 peptides on spontaneously hypertensive rats (SHR).

219 e model) in spontaneously hypertensive rats (SHR).

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

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

222 cohorts of Spontaneously Hypertensive Rats (SHRs) were exposed to 150 or 500 mug/m(3) diesel exhaust

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

224 o (WKY) and spontaneously hypertensive rats (SHRs), renal ETBR phosphorylation was higher in SHRs.

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

226 neurons in spontaneously hypertensive rats (SHRs).

227 ons in male spontaneously hypertensive rats (SHRs).

228 ated with a 38% and 47% subhazard reduction (SHR), respectively, compared to ZCB00, after accounting

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

230 ults show that the transcriptional regulator SHR is critical for the most frequent asymmetric divisio

231 subhazard ratio (SHR) for waitlist removal (SHR 0.73, 95% confidence interval [CI]: 0.60, 0.89, P =

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

233 oratory as opposed to hybrid operating room (SHR: 1.648; 95% CI: 1.187 to 2.287) were independently a

234 -separation-like phenomenon that SHORT ROOT (SHR) RNA undergoes in cells.

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

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

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

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

239 In Arabidopsis, the SHORT-ROOT (SHR)/SCARECROW (SCR) transcription factor dimer activate

240 Here we show that a SHORTROOT-SCARECROW (SHR-SCR) stem cell program in cortical cells of the legu

241 95% CI 4.27-12.99), cortical atrophy score (SHR per 1-point increase 2.61, 1.70-4.01), a higher numb

242 ce interval [CI]: 0.944 to 0.994), male sex (SHR: 1.989; 95% CI: 1.403 to 2.818), lack of pre-dilatat

243 g the mobile transcription factor SHORTROOT (SHR) and its binding partner SCARECROW (SCR).

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

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

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

247 .34-1.87; P < .001), and history of smoking (SHR, 1.38; 95% CI, 1.25-1.52; P < .001).

248 minants of health, including marital status (SHR [95% CI]: 0.6 [0.4-0.9]), religious objection to LDK

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

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

251 Stroked SHRs displayed grey matter atrophy and had a two-fold in

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

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

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

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

256 ing of QC and CEI division and suggests that SHR repression of QC division depends on formation of th

257 Thus, our results support that SHR-SCR protein complex stoichiometry and regulation of

258 The SHR splenocytes constitutively expressed more RORgammat

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

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

261 05,696, arterial pressure was reduced in the SHR compared to the normotensive control and this reduct

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

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

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

265 ypertrophy in Ang II rats, as well as in the SHR.

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

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

268 n of QC division depends on formation of the SHR homodimer.

269 ight be responsible for the formation of the SHR phase-separation-like phenomenon in vivo.

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

271 l validation, showed that high levels of the SHR-SCR complex are associated with more CEI division bu

272 which incorporated the stoichiometry of the SHR-SCR complex as well as upstream transcriptional regu

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

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

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

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

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

278 and 13% increased likelihood for transplant (SHR 1.13, 95% CI: 1.07, 1.20, P < .001).

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

280 (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,

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

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

283 ted with risk of kidney failure (univariable SHR 1.07 [95% CI 0.58 to 1.96], P = 0.82; multivariable

284 allowed us to propose the putative upstream SHR regulators SEUSS and WUSCHEL-RELATED HOMEOBOX 5 and

285 is of ADHD and its potential treatment using SHR.

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

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

288 to receive an LDKT than non-Hispanic white (SHR [95% CI]: 0.2 [0.0-0.7]), but accounting for age (SH

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

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

291 l relationship of measured serum levels with SHR (for IGFBP-3) and birth weight (for IGFBP-5) than wi

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

293 paired during evolving hypertension in young SHR, an effect that worsens in states of chronic hyperte

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.