ライフサイエンスコーパス: overload

1 sive remodeling in response to mild pressure overload.

2 oportin (Fpn), resulting in parenchymal iron overload.

3 after pressure overload but not after volume overload.

4 ry edema was induced in pigs by acute volume overload.

5 of hyper-inflammation rather than bacterial overload.

6 d transfusion therapy contribute to the iron overload.

7 systemic lipolysis during intravenous lipid overload.

8 lls and mice experiencing iron deficiency or overload.

9 ckout (KO) mouse, a model of cellular Ca(2+) overload.

10 m Hg and IV fluids held for concern of fluid overload.

11 pheral inflammatory responses due to caloric overload.

12 regulatory mechanism for prevention of sugar overload.

13 d in the lungs harvested 1 hour after volume overload.

14 into the myocardium in response to pressure overload.

15 lized into the lung immediately after volume overload.

16 by reactive oxygen species (ROS) and calcium overload.

17 reased in an SKO heart, suggesting a glucose overload.

18 pecific deletion leads to fatal cardiac iron overload.

19 disorders characterized by parenchymal iron overload.

20 rly rapid galactose catabolism and metabolic overload.

21 red blood cells) and primary (Hfe(-/-)) iron overload.

22 tibility to mild-to-moderate late-onset iron overload.

23 major and is associated with myocardial iron overload.

24 lammatory processes in response to metabolic overload.

25 ire metabolic network results in information overload.

26 t ventricular dilatation secondary to volume overload.

27 egative for viral hepatitis B and C and iron overload.

28 on of reactive oxygen species, and metabolic overload.

29 relationship between ECV and myocardial iron overload.

30 h as a low skeletal muscle mass and/or fluid overload.

31 se manifestations despite significant copper overload.

32 nical ventilation and the avoidance of fluid overload.

33 ice under situations of copper deficiency or overload.

34 postoperative acute kidney injury and fluid overload.

35 ction, particularly in the setting of Ca(2+) overload.

36 cardiac hypertrophy in response to pressure overload.

37 resulting in right heart pressure or volume overload.

38 mitochondrial functional response to Ca(2+) overload.

39 F model induced by slow-progressive pressure overload.

40 in D2 would be beneficial during hemodynamic overload.

41 t and less than half have evidence of volume overload.

42 2+) from intracellular vesicles after Zn(2+) overload.

43 Only 40% (n=57/142) had signs of volume overload.

44 f surrounding tissue and, sometimes, cardiac overload.

45 lation against lipotoxicity under fatty acid overload.

46 which may contribute to perioperative fluid overloading.

47 ver phantom) to 5 mg Fe/g liver phantom iron overload (100X overdose).

48 se (FBG), 2-hour blood glucose after glucose overload (2h-OGTT), HbA1c, triglyceride (TG) levels and

49 ad higher ECV than did patients without iron overload (31.3% +/- 2.8 vs 28.2% +/- 3.4, P = .030) and

50 n 6 unrelated patients with unexplained iron overload (9% of our cohort).

51 gulated Ca(2+) cycling, mitochondrial Ca(2+) overload activates cellular death pathways.

52 Fluid overload after congenital heart surgery is frequent and

53 on in hepatocytes illustrating the metabolic overload after resection was attenuated.

54 In response to muscle overload after synergist ablation in mice, we show that

55 al and acylcarnitine production during lipid overload, along with muscle insulin sensitivity, improve

56 PTL2-knockdown in mice subjected to pressure overload ameliorates cardiac dysfunction.

57 system was evaluated by analyzing under- and overloaded aminopyrenetrisulfonate (APTS)-labeled oligos

58 However, after the establishment of pressure overload, an increase in leptin levels has protective ca

59 n should be considered in patients with iron overload and a history of GBCA exposure.

60 These data showed high sensitivity to iron overload and a strong relationship between quantitative

61 ermined their association with percent fluid overload and acute organ dysfunction and generated a rec

62 Here we investigated the effects of iron overload and age on cardiac hypertrophy using 1-, 5- and

63 (2+) release results in mitochondrial Ca(2+) overload and consequent apoptosis.

64 ference in ECV between patients without iron overload and control subjects (P = .647).

65 Iron overload and deficiency can adversely affect human healt

66 ivity and disinhibition give rise to frontal overload and disrupt executive control, fuelling and per

67 red cardiac function in response to pressure overload and exacerbated fibrosis by enhancing inflammat

68 mice with either genetic or iatrogenic iron overload and in human plasma.

69 egulated neuronal calcium responses, calcium overload and increased neuronal death.

70 a depletion reduced resistance against lipid overload and increased production of reactive oxygen spe

71 laboratory results in the setting of volume overload and liver dysfunction.

72 lmonella, envelope protection against copper overload and macrophage survival depends on CueP, a majo

73 Mechanical stress due to pressure and volume overload and metabolic dysfunction also induce profound

74 ve metabolic sensor in the liver under lipid overload and metabolic stress.

75 However, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely

76 d dynamics of ribosomal disassembly, calcium overload and mitochondrial fission.

77 receptor 1), leading to mitochondrial Ca(2+) overload and opening of the mitochondrial permeability t

78 production of erythrocytes, anemia, and iron overload and PV by erythrocytosis and thrombosis.

79 tions for fatty liver disease and liver iron overload and their prevalence in a large-scale populatio

80 reased SHub and decreased DHub relate to hub overload and thus poorer/deteriorating cognition.

81 isk in this population, partly due to volume overload and variable visceral adiposity.

82 nockout (KO) mice is characterized by Ca(2+) overloaded and swollen SR and by changes in the properti

83 isms ultimately drives Zn(2+)-induced Ca(2+) overloading and cell death.

84 ckness, which diminishes performance by mass overload, and create a harsh environment, which reduces

85 ed state of oxaloacetate deficiency, acetate overload, and ketoacidosis.

86 The complications of iron overload, arising from transfusions that represent the b

87 were directly associated with percent fluid overload at baseline (rs = 0.18; p = 0.0008) and at 6 ho

88 During pressure overload, both hypertrophic and hypoxic signals can stim

89 angiogenic stimuli occurring during pressure overload bridging both hypertrophic and hypoxia-stimulat

90 ition occurs in pediatric patients with iron overload but normal renal and hepatic function who under

91 al remodeling and dysfunction after pressure overload but not after volume overload.

92 thoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and

93 Mice were subjected to pressure overload by means of angiotensin-II infusion or transver

94 In this study, the impact of iron overload by SPIONs was assessed on a mouse cirrhosis mod

95 the right ventricular volume and/or pressure overload by TPVR will have a beneficial effect on TR, as

96 We induced pressure overload by transthoracic aortic constriction (TAC) or v

97 ce and in mice subjected to chronic pressure-overload by transverse aorta constriction (TAC).

98 ce and in mice subjected to chronic pressure-overload by transverse aorta constriction.

99 Iron overload can increase cellular oxidative stress levels d

100 ical conditions such as ischemia or pressure overload can induce a release of extracellular nucleotid

101 aintain organellar physiology, Ca(2)(+) mito overload can lead to cell death.

102 mulating excessive iron in body organs (iron overload) can damage or even destroy an organ.

103 tly these changes preceded the onset of iron overload cardiomyopathy, providing an early biomarker of

104 sease (WD) is associated with massive copper overload caused by mutations in a liver-specific copper-

105 reduce cellular ferritin expression in iron overloaded cells and regulate intracellular iron levels

106 Fpn C326S mice had systemic iron overload compared to wild type and had the fastest retin

107 yocytes increased significantly under Ca(2+) overload conditions and/or at higher frequency of stimul

108 (gut granules) in the intestine under copper overload conditions for copper detoxification, whereas c

109 s that when an atrial cell is paced under Ca overload conditions, Ca waves can then nucleate on the c

110 rbid obesity and hyperglycemia under dietary overload conditions.

111 thmic events became more severe under Ca(2+) overload conditions.

112 rotect nerve cells from death at the calcium overload conditions.

113 Iron overload damages many organs.

114 LV pressure overload did not upregulate miR-182.

115 dly effective treatments for hereditary iron overload disorders.

116 double knockout mice, a model for bile acid overload, display cardiac hypertrophy, bradycardia, and

117 ngs reveal a novel mechanism by which Ca(2+) overload disrupts myofibril integrity by activating a Ca

118 cardiac pathology was attributed to mCa(2+) overload driving increased generation of superoxide and

119 alpha-syn in exosomes, suggesting that iron overload due to impaired ferritinophagy or other cause(s

120 ndary end points included incidence of fluid overload, duration of mechanical ventilation and intensi

121 In particular, valgus extension overload during the throwing motion can precipitate a ca

122 s, with major complications including volume overload, electrolyte disorders, uremic complications, a

123 Pressure overload enhanced BM-FPC mobilization and homing in IL10

124 nflux of newly synthesized proteins into the overloaded ER.

125 r activated fibroblasts exacerbates pressure overload-evoked fibrosis.

126 ive oxygen species and mitochondrial calcium overload, factors implicated in neuronal and cardiac pat

127 We also disclosed that protein overload first acts on the expression of the cubilin-amn

128 Sustained fluid overload (FO) is considered a major cause of hypertensio

129 In a mouse model of cardiac pressure overload, global genetic deletion of miR-29 or antimiR-2

130 Patients with prior myocardial iron overload had higher ECV than did patients without iron o

131 arison with nontreated cells, whereas copper overload has the opposite effects.

132 by arsenic-induced liver insult and pressure overload heart injury.

133 against excessive remodeling of the pressure-overloaded heart.

134 nd cardiomyocyte hypertrophy in the pressure-overloaded heart.

135 Echocardiographic analysis of pressure overloaded hearts revealed that all LV parameters (LV en

136 dependent cardiac stress exacerbated by iron overload hemochromatosis.

137 2 levels are associated with increased fluid overload, hepatic and coagulation dysfunction, acute kid

138 Volume-overload HF was created in Yorkshire swine by inducing s

139 educes the hypertrophic response to pressure overload; however, knocking out Pmca4 specifically in ca

140 lthy volunteers (P < .001) because of volume overload; however, volume did not correlate with the his

141 on improved the cardiac function in pressure overloaded Hras null hearts in vivo.

142 phy was induced by slow progressive pressure overload in adult cats.

143 histones induced profound calcium influx and overload in cultured cardiomyocytes with dose-dependent

144 embryonic lethality potentially due to iron overload in developing embryos.

145 s reticulo-endothelial macrophages from heme overload in heme-loaded Hx-null mice and reduces product

146 ased susceptibility to mitochondrial calcium overload in LRRK2-driven neurodegeneration, and suggest

147 Pressure overload in mice lacking SRC-2 induces an abrogated hype

148 o pathological hepcidin suppression and iron overload in mice with nontransfused beta-thalassemia.

149 rses cardiac hypertrophy induced by pressure overload in mice.

150 t have been previously shown to prevent iron overload in murine models of hemochromatosis and induce

151 cient mice, resulting in ameliorated calcium overload in neurons and astrocytes.

152 blood cell mass that are features of volume overload in patients with chronic heart failure and help

153 PR2) gene on right ventricular (RV) pressure overload in patients with pulmonary arterial hypertensio

154 nisms for mitochondrial adaptations to lipid overload in postnatal hearts in vivo.

155 /fl) (Bmp2(LSECKO)) mice caused massive iron overload in the liver and increased serum iron levels an

156 sts of Ca(2+) release probably due to Ca(2+) overload in the sarcoplasmic reticulum.

157 tion strategies would reduce myocardial iron overload in TM patients compared with placebo.

158 The most common complications are iron overload in transfused patients and syndrome-specific ma

159 ery hypertension by using pressure or volume overload in vitro or in vivo.

160 lobes ex vivo and reduced edema in a volume overload in vivo pig model of hydrostatic pulmonary edem

161 n levels significantly decreased on pressure overload in wild-type mice, paralleling a decreased oxid

162 Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 prote

163 hondrial Ca(2+) overload or through a Ca(2+) overload-independent pathway that involved reduced activ

164 ion of heart failure in response to pressure overload independently of autoantibodies.

165 le exhibited increased fibrosis after muscle overload, indicating a protective role for normal stem c

166 levels are increased in mouse models of iron overload, indicating that TGF-beta1 may contribute to he

167 model of cardiac fibrosis, cardiac pressure overload induced NETosis and significant platelet recrui

168 ake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown.

169 Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not

170 n on a common form of RyR2 regulation; store overload-induced Ca(2+) release (SOICR).

171 to no aberrant effect on RyR2-mediated store overload-induced Ca(2+) release in HEK293 cells compared

172 arrhythmias, and reduced threshold for store overload-induced Ca(2+)-release events in the CPVT2-hiPS

173 Here, we examined pressure overload-induced cardiac fibrosis in fibroblast- and myo

174 blast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis.

175 at interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the role of

176 lcium channels has been reported in pressure overload-induced cardiac hypertrophy and heart failure.

177 tructural remodeling in response to pressure overload-induced cardiac hypertrophy.

178 Pressure overload-induced cardiac stress induces left ventricular

179 and correlated local contraction in pressure-overload-induced cardiomyopathy.

180 rate, elevated mROS, and enhanced [Ca(2+)]m overload-induced cell death.

181 Overload-induced changes in microRNA levels regulate SIR

182 but not Smad2, markedly reduced the pressure overload-induced fibrotic response as well as fibrosis m

183 To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors wer

184 t GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake.

185 s to determine whether GLUT4 is required for overload-induced glucose uptake.

186 deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting inters

187 Pressure overload-induced heart failure is more severe in the mic

188 break (SSB) in the pathogenesis of pressure overload-induced heart failure.

189 x1 deficiency in the heart promoted pressure overload-induced heart failure.

190 dystrophy-Hippo deficiency protected against overload-induced heart failure.

191 Pressure overload-induced heart hypertrophy and failure are atten

192 ns, we used an established model of pressure overload-induced heart muscle hypertrophy caused by tran

193 In pressure overload-induced HF mice and isolated hypertrophic myoca

194 We created a mouse model of pressure-overload-induced HF with transverse aortic constriction

195 We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart and thei

196 is upregulated in mouse hearts with pressure overload-induced hypertrophy and in human hearts with di

197 lencing prevents the development of pressure overload-induced hypertrophy but also reverses preestabl

198 1 may actually play a crucial causal role in overload-induced hypertrophy of skeletal muscle.

199 s and activity, SIRT1-regulated pathways and overload-induced hypertrophy.

200 c myocytes following development of pressure overload-induced hypertrophy.

201 m cells and observed a complete reduction of overload-induced hypertrophy.

202 ivity and content increased significantly in overload-induced hypertrophy.

203 anonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming

204 Ca(2+) overload-induced mitochondrial permeability transition p

205 reveal a molecular mechanism by which lipid overload-induced mitochondrial ROS generation causes mit

206 Overload-induced muscle glucose uptake and hypertrophic

207 demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic g

208 cell in vitro and in vivo and reestablished overload-induced muscle growth.

209 esis and promotes skeletal muscle growth and overload-induced myofiber hypertrophy in mice.

210 cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate

211 Lipid overload induces insulin resistance in muscle and alters

212 otect pancreatic acinar cells against Ca(2+) overload, intracellular protease activation, and necrosi

213 lence of fatty liver diseases and liver iron overload is 42.2% (1082 of 2561) and 17.4% (447 of 2561)

214 Cardiac damage associated with iron overload is the most common cause of morbidity and morta

215 dualized, appropriate therapy-not all volume overload is the same.

216 s cope with excess Ca(2+) when ER stores are overloaded is unclear.

217 lysis time (isocratic), the effect of volume overload (isocratic), and separations of a limited numbe

218 ons, a consequence of which is systemic iron overload leading to acute heart failure.

219 myocytes under basal conditions, with Ca(2+) overload leading to even greater prolongation.

220 tracellular matrix remodeling after pressure overload, leading to fibrosis and diastolic dysfunction.

221 left ventricle (LV) in response to pressure overload leads to the re-expression of the fetal gene pr

222 ddition, functional readouts such as calcium overload may be a more useful outcome measure to monitor

223 t a cost for increased sensitivity to Ca(2+) overload mediated cell death.

224 In addition, it removes iron from iron overloaded mice, including models of acquired (iron-dext

225 onstriction (TAC) surgery, a pressure-volume overload model of HF.

226 In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by

227 tion of RBFox1 expression in murine pressure overload models substantially attenuated cardiac hypertr

228 ole heart tissue in multiple murine pressure overload models.

229 as treatment with beta-blockers in pressure-overloaded mouse hearts prevented its down-regulation an

230 and exercise) and pathologic (i.e., pressure overload) myocardial hypertrophy.

231 lectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy and fibro

232 on was markedly up-regulated in the pressure-overloaded myocardium.

233 ifferentiation to myofibroblasts in pressure-overloaded myocardium.

234 ing excessive environmental stimulation from overloading neural resources.

235 ing excessive environmental stimulation from overloading neural resources.

236 Fluid overload occurred in 8.3% of protocolized care and 6.3%

237 Fluid overload occurring as a consequence of overly aggressive

238 are poorly retained during injection, volume overload occurs which leads to altered peak shapes, decr

239 up was 3 times more likely to have 10% fluid overload (odds ratio [OR], 3.0; 95% CI, 1.3-6.9), was mo

240 bal (integrative) information processing and overload of local (sensory) information.

241 s parallel computing to reduce computational overload of this analysis, it does not fully automate th

242 r metaflammation is the persistent metabolic overloading of the endoplasmic reticulum (ER), leading t

243 Given the information overload often imparted to human cognitive-processing sy

244 de new insight into the role of carbohydrate overload on mitochondrial function in other hepatic dise

245 (AR) imposes significant volume and pressure overload on the left ventricle (LV), but such patients t

246 In addition, pressure overload or CTCF depletion remodeled long-range interact

247 Pressure overload or CTCF depletion selectively altered boundary

248 target for the treatment of diseases of iron overload or deficiency.

249 aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin (TM) dev

250 P was induced by either mitochondrial Ca(2+) overload or through a Ca(2+) overload-independent pathwa

251 tan causes aquaresis in patients with volume overload, potentially facilitating decongestion and impr

252 iac isoprostane levels, suggesting that iron overload promotes oxidative stress and cardiac hypertrop

253 Exposing human podocytes to albumin overload prompted an increase in CUBILIN, AMNIONLESS and

254 In mice, systemic iron overload protected against renal ischemia-reperfusion in

255 suggest that chronic alterations and calcium overload rather than an induction of transient Ca(2+) pe

256 Cardiac pressure overload resulted in a modest increase in c-kit-derived

257 Cardiac pressure overload resulting from trans-aortic constriction in mic

258 ity, resolution, and peak capacity of volume overloaded samples beyond gradient compression alone.

259 ression and localization also showed calcium overload, sarcofilamental atrophy, and accumulation of c

260 The Hemochromatosis and Iron Overload Screening (HEIRS) Study was a multicenter study

261 ing excessive environmental stimulation from overloading shared neural resources.

262 ing excessive environmental stimulation from overloading shared neural resources.

263 ive day 1, as well as avoidance of 10% fluid overload; shorter duration of mechanical ventilation, in

264 disease severity related to myocardial iron overload states or glycosphingolipid accumulation in And

265 and the methods by which we determine volume overload status.

266 he cardiac hypertrophic response to pressure overload stimulation.

267 hy and heart failure in response to pressure overload stress.

268 Dysmetabolic iron overload syndrome (DIOS) is a common cause of hyperferri

269 lower in patients with prior myocardial iron overload than in control subjects (850.3 +/- 115.1 vs 10

270 This model predicts a connectivity 'overload' that precedes structural and functional declin

271 ng to ectopic lipid accumulation and glucose overload, the exact contribution of these two parameters

272 After pressure overload, the TF genes in Module 1 were up-regulated bef

273 Acute Decompensated Heart Failure and Volume Overload to Assess Treatment Effect on Congestion and Re

274 Acute Decompensated Heart Failure and Volume Overload to Assess Treatment Effect on Congestion and Re

275 cardiac oxidative metabolism under pressure overload to ensure survival.

276 ression in murine CFs after chronic pressure overload to identify CF-enriched lncRNAs and investigate

277 knockout mice and subjected them to pressure overload to induce cardiac hypertrophy and dysfunction.

278 ts (n = 32) were subjected to sham or volume overload to induce HFpEF.

279 r mechanism that limits mitochondrial Ca(2+) overload to prevent cell death.

280 on induced by Ca(2+), and such resistance to overload translated into improved cell survival.

281 -1 was significantly perturbed upon pressure overload, underscored by disorganization of the IDs in M

282 for stroke risk, improved management of iron overload using oral chelators and non-invasive MRI measu

283 mice did not clear existing plaques, calcium overload was ameliorated over time.

284 Prevalence of fatty liver diseases and iron overload was calculated (weighted by probability of part

285 Overload was induced in mouse plantaris muscle by unilat

286 Pressure overload was induced in TNC knockout and wild-type mice

287 Pressure overload was induced in wild-type (WT) and IL10 knockout

288 Iron overload was mediated by decreased hepatic expression of

289 Iron overload was observed in 17.4% (447 of 2561 participants

290 of their perceived risk for iatrogenic fluid overload, we also evaluated patients with a history of h

291 In a rat model of acute exogenous albumin overload, we quantified glomerular sieving coefficients

292 ed ionomycin treatment, as a model of Ca(2+) overload, were lower when cells were cultured long-term

293 d tryptase content in mast cells with copper overload, whereas copper starvation increased tryptase c

294 cardiac hypertrophy after 7 days of pressure overload, whereas female galectin-3 knockouts had delaye

295 ransferrin saturation and massive liver iron overload, whereas Smad1(fl/fl);Smad5(fl/wt);Cre(+) mice

296 which a small group of reputable workers are overloaded while leaving other workers idle.

297 vations in iron absorption, which cause iron overload with associated organ toxicities.

298 HFE(-/-) livers were overloaded with ferritin but had low mitochondrial iron

299 activated long chromatin stretches that were overloaded with transcriptional regulators, known as sup

300 cally stable, the plasma wave can be locally overloaded without compromising the witness bunch normal