ライフサイエンスコーパス: hemolysis

1 3 fibroblast toxicity; HC10 > 400 mug/mL for hemolysis).

2 ty of red blood cells to pneumolysin-induced hemolysis.

3 ravascular hemolysis than with intravascular hemolysis.

4 carboxylic functionalities did not cause any hemolysis.

5 bation of RBCs with Stx2, which also induced hemolysis.

6 t prevents complement-mediated intravascular hemolysis.

7 ed oxidative stress and shear stress-induced hemolysis.

8 hains causing ineffective erythropoiesis and hemolysis.

9 ate dehydrogenase in whole blood, indicating hemolysis.

10 ythrocytes, which enhances cytoadherence and hemolysis.

11 candidate marker to predict post-AS delayed hemolysis.

12 reatment with phenylhydrazine, an inducer of hemolysis.

13 n in these patients occurs via extravascular hemolysis.

14 and IL-1R in the lethality caused by sterile hemolysis.

15 es free hemoglobin following malaria-induced hemolysis.

16 ading to clinically meaningful extravascular hemolysis.

17 d for more than 8 days, 13 (22%) had delayed hemolysis.

18 late-stage erythroid precursors and reducing hemolysis.

19 phocyte syndrome (PLS) is an immune-mediated hemolysis.

20 dothelial damage, thrombosis, and mechanical hemolysis.

21 an increasingly important causative role of hemolysis.

22 ic inflammation, and microcirculation during hemolysis.

23 , hypoxia also causes hemoglobin release via hemolysis.

24 asking screening questions about symptoms of hemolysis.

25 al therapy to prevent complications of acute hemolysis.

26 ssociated with indirect markers of increased hemolysis.

27 ic conditions, leading to vaso-occlusion and hemolysis.

28 cs for patients with excessive intravascular hemolysis.

29 5 patients) including 13 readmissions due to hemolysis.

30 ess is self-terminating to prevent excessive hemolysis.

31 emic inflammation in a rodent model of acute hemolysis.

32 ning normal erythropoiesis and in preventing hemolysis.

33 xygen species (ROS) and cause red blood cell hemolysis.

34 ovel antileukemia treatment without inducing hemolysis.

35 they were capable of killing without causing hemolysis.

36 ed silica had no effect on cell viability or hemolysis.

37 es in trace levels of blood before and after hemolysis.

38 itors correlated with the levels of residual hemolysis.

39 -producing tumors, acute brain diseases, and hemolysis.

40 ated with hepatotoxicity, nephrotoxicity and hemolysis.

41 d to prevent the early onset of SLS-mediated hemolysis.

42 concentrations against hypochlorite-induced hemolysis.

43 ine, asymmetric dimethylarginine (ADMA), and hemolysis.

44 ne oxygenation are bleeding, thrombosis, and hemolysis.

45 nuate disease complications in patients with hemolysis.

46 oglobin alone is not sufficient to determine hemolysis.

47 ns may preserve vascular NO signaling during hemolysis.

48 proteins could preserve NO signaling during hemolysis.

49 oimmune problems, including thyroiditis (3), hemolysis (1), thrombocytopenia (4), and neutropenia (1)

50 ons for closure were heart failure (80%) and hemolysis (16%).

51 and vasculopathy consequent to intravascular hemolysis, (2) chronic pulmonary thromboembolism, or (3)

52 h old but not new blood led to intravascular hemolysis, acute hypertension, vascular injury, and kidn

53 as corroborated by the finding that residual hemolysis after forceful activation of the classical pat

54 e beneficial effects in conditions of severe hemolysis after prolonged hypotension.

55 Low levels of intravascular hemolysis after transfusion of aged stored red cells dis

56 Extravascular hemolysis after transfusion progressively increased with

57 Hemolysis also did not correlate with adherence to or cy

58 The normalized hemoglobin and resolution of hemolysis among engrafted patients were accompanied by s

59 e of significant differences in the rates of hemolysis and associated diseases and because there is c

60 low dose of hemin caused acute intravascular hemolysis and autoamplification of extracellular hemin i

61 ritical role of C5b-9 in complement-mediated hemolysis and but also highlight the critical role of C5

62 ibitors of C3 activation effectively prevent hemolysis and C3 opsonization of PNH erythrocytes, and a

63 Through hemolysis and calcein releasing assays, it is revealed t

64 Detterich et al confirm a role for hemolysis and cell-free plasma hemoglobin (Hb) in pulmon

65 Hemolysis and consequent release of cell-free hemoglobin

66 hemolysin gene clusters responsible for the hemolysis and cytotoxicity of V. anguillarum were identi

67 ed families and its association with chronic hemolysis and dehydrated cells, also referred to as here

68 experimental evidence for such extravascular hemolysis and demonstrate that PNH erythrocytes from ant

69 -Friedenreich antigen exposure can result in hemolysis and direct endothelial injury leading to HUS p

70 increases deoxyHbS polymerization, sickling, hemolysis and disease progression.

71 e of this organism, including cell adhesion, hemolysis and heme utilization genes.

72 MSSA strains with strong blood agar hemolysis and high alpha-hemolysin activity are markers

73 ent correlated significantly with markers of hemolysis and HO-1 induction.

74 stent with the hypothesis that intravascular hemolysis and increased endogenous erythropoiesis damage

75 lica formulations are colloidal instability, hemolysis and inefficient drug loading and release.

76 inuria erythrocytes from complement-mediated hemolysis and inhibited both C3 fragment and C5b-9 depos

77 In addition, hemolysis and macrophage heme/iron accumulation in a mou

78 eratively, donors were closely monitored for hemolysis and medications, which can induce hemolysis, w

79 both beta globin genes, resulting in chronic hemolysis and multiorgan disease that ultimately leads t

80 ulence factors, enhancing phenotypes such as hemolysis and NAD(+) hydrolysis.

81 ificant cause of infection- and drug-induced hemolysis and neonatal jaundice.

82 ism, which may have supported coevolution of hemolysis and normal vascular function.

83 ing form (polyethylene glycol [PEG]-Cp40) on hemolysis and opsonization of PNH erythrocytes in an est

84 lled complement activation that accounts for hemolysis and other PNH manifestations.

85 would benefit from potential treatments for hemolysis and plasma hemoglobin-associated renal dysfunc

86 ns as a substitute for red blood cells after hemolysis and preserves NO signaling in the vasculature.

87 s the red cell "storage lesion" is increased hemolysis and reduced red cell lifespan after infusion.

88 manifested clinically in infancy by chronic hemolysis and relapsing peripheral demyelinating disease

89 f childhood familial chronic Coombs-negative hemolysis and relapsing polyneuropathy presenting as chr

90 y system composed of EepR and EepS regulates hemolysis and swarming motility through transcriptional

91 Yet hemolysis and the export of ESX-1 substrates into the ba

92 red-blood-cell ghosts were made by hypotonic hemolysis and then reconstituted such that they were smo

93 conjugate effectively inhibited LPS-induced hemolysis and tumor necrosis factor alpha (TNFalpha) sec

94 analyze the association between steady-state hemolysis and vascular complications of SCD among sub-Sa

95 This study investigated whether Stx2 induces hemolysis and whether complement is involved in the hemo

96 olonies, reduced pigmentation, and decreased hemolysis and/or coagulase activity are periodically iso

97 levels presaging thrombosis (and associated hemolysis), and outcomes of different management strateg

98 s damage to endothelial cells, intravascular hemolysis, and activation of platelets leading to a proc

99 al conditions, after phenylhydrazine-induced hemolysis, and after induction of cytochromes P450 synth

100 determine whether eculizumab reduces chronic hemolysis, and cumulative doses of steroids and intraven

101 Therefore hemostasis, anticoagulation, hemolysis, and inflammatory parameters were monitored.

102 with regard to hemostasis, anticoagulation, hemolysis, and inflammatory parameters within the first

103 s attributed to improvement in RBC survival, hemolysis, and insufficient erythropoiesis, which is evi

104 dical-scavenging activity, anti-AAPH-induced hemolysis, and ORAC activity.

105 ulting in thrombocytopenia, microangiopathic hemolysis, and organ dysfunction.

106 lipoprotein peroxidation, anti-AAPH-induced hemolysis, and oxygen radical absorbance capacity activi

107 Major bleeding at the vascular access site, hemolysis, and pericardial tamponade occurred in 34 (28.

108 o raise the hemoglobin concentration, reduce hemolysis, and prevent vaso-occlusive events that cause

109 Hb levels </=6 g/dL at onset, intravascular hemolysis, and previous splenectomy.

110 which fixed complement, led to intravascular hemolysis, and resulted in decreased levels of KEL2 anti

111 of hemolysis, the metabolism of products of hemolysis, and the effects of both on recipient biology.

112 on in iron handling, increased extravascular hemolysis, and the formation of circulating non-transfer

113 usion that was inhibited by TAK-242, linking hemolysis- and infection-induced vaso-occlusive crises t

114 rocytes were more resistant to osmosensitive hemolysis as compared to Galphai2(+/+) erythrocytes.

115 and cyto-compatibility testing prior to the hemolysis assay and coagulation assessment.

116 Hemolysis assay further authenticated the biocompatibili

117 reover, in vitro cytotoxicity evaluation and hemolysis assay showed that the nanoparticles possessed

118 In an FH-dependent hemolysis assay, we showed that the hybrid protein cause

119 rane attack complex formation as tested in a hemolysis assay.

120 A series of hemolysis assays at various pHs revealed that increasing

121 and subjected this library to metabolic and hemolysis assays to functionally characterize each EIIC.

122 In hemolysis assays with 2-aminoethylisothiouronium bromide

123 o dose-limiting cytotoxicity at >/=2x MIC or hemolysis at >/=8x MIC was observed.

124 Analogue 17 showed little hemolysis at 32 mug/mL and lysed 11% of red blood cells

125 uM, but the four-Leu peptides induced 40-80% hemolysis at the same concentration range.

126 europathy with conduction block, and chronic hemolysis attributed to p.Cys89Tyr mutation in the CD59

127 less membrane perturbation (vesicle leakage, hemolysis, bacterial lysis) than their linear counterpar

128 emoglobinuria (PNH) cells are susceptible to hemolysis because of a loss of the complement regulatory

129 terized by complement-mediated intravascular hemolysis because of the lack from erythrocyte surface o

130 genomic (dDDH, ANI, and AAI) and phenotypic (hemolysis, biochemical profiles, protein spectra, antibi

131 From 2010 to 2012, clinical data, hemolysis biomarkers, complement assessment, and free ec

132 ocytes from oxidative AAPH- and H2O2-induced hemolysis, but at high concentrations a pro-oxidant effe

133 protein C1s, prevents induction of in vitro hemolysis by cold agglutinins (CA).

134 an quickly characterize a patient's level of hemolysis by measuring the color of blood plasma.

135 ace of red cells, resulting in extravascular hemolysis by the reticuloendothelial system.

136 These analogs also blocked hemolysis by wild-type S. aureus group I-IV strains-a vi

137 We tested the hypothesis that the hemolysis byproduct hemin elicits events that induce ACS

138 with extreme levels or the peaks affected by hemolysis can be discarded from further analysis.

139 Intravascular hemolysis can impair NO bioavailability and cause oxidat

140 d, or neutral) and ten combination forms via hemolysis, cell viability, and AnnexinV-FITC/PI staining

141 fusion of fresh blood, which results in less hemolysis, CFH, and iron release, is less toxic than tra

142 tion of mesoporous silica nanorods (MSNR) on hemolysis, colloidal stability, mitoxantrone (MTX) loadi

143 of a KCNN4 mutation associated with chronic hemolysis constitutes the first report of a human diseas

144 This early onset hemolysis correlated with an increased lesion size and s

145 ckle cell anemia is characterized by chronic hemolysis coupled with extensive vascular inflammation.

146 pment of PH is associated with intravascular hemolysis, cutaneous leg ulceration, renal insufficiency

147 SCD-related endothelial dysfunction include hemolysis, defects in nitric oxide metabolism, ischemia-

148 at sublethal irradiation, unlike bleeding or hemolysis, depletes almost all marrow and splenic erythr

149 We investigated whether hemolysis-derived heme contributes to aHUS pathogenesis.

150 These results strongly suggest that hemolysis-derived heme represents a common secondary hit

151 Intravascular hemolysis describes the relocalization of heme and hemog

152 Hemolysis drives susceptibility to bacterial infections

153 terized by complement-mediated intravascular hemolysis due to the lack of CD55 and CD59 on affected e

154 PTS) exhibited Streptolysin S (SLS)-mediated hemolysis during exponential growth.

155 Erythrocytes undergo hemolysis during storage and after transfusion.

156 d used LMWH); 9 cases of preeclampsia or the hemolysis, elevated liver enzyme level, and low platelet

157 Preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet coun

158 e is a pregnancy-associated disease inducing hemolysis, elevated liver enzymes, and low platelets in

159 discussing these areas, we suggest that the hemolysis-endothelial dysfunction phenotype also reflect

160 Resolution of a primary hemolysis event without CVA or death occurred in 21/24 p

161 Sixty-four hemolysis events occurred in 49/367 patients implanted w

162 of this study was to compare the outcomes of hemolysis events treated with surgical interventions ver

163 Of 49 primary hemolysis events, 24 were treated with surgical interven

164 nges, pump malfunctions, pump thrombosis, or hemolysis events.

165 nt and outcome was noted in the 15 recurrent hemolysis events.

166 confirm a close relationship between ACR and hemolysis evolution in patients with SCD.

167 motic shock and energy depletion, as well as hemolysis following decrease of extracellular osmolarity

168 Patients with delayed hemolysis had higher parasite counts on admission (geome

169 Delayed hemolysis has been described in hyperparasitemic nonimmu

170 r a malaria infection, but in mice, malarial hemolysis impairs resistance to nontyphoid Salmonella by

171 mmatory effects of intravenous water-induced hemolysis in C57BL/6 mice and determined the abilities o

172 Intravenous water induced acute hemolysis in C57BL/6 mice, attaining plasma Hb levels co

173 blood at high concentration due to increased hemolysis in conditions such as erythroblastosis fetalis

174 srS-deficient mutant induced severe systemic hemolysis in mice.

175 lack of clinically significant intravascular hemolysis in patients with IGD.

176 We conclude that intravascular hemolysis in SCD releases heme that activates endothelia

177 P inhibitor that blocked complement-mediated hemolysis in several species.

178 und that PEGylation prevented dose-dependent hemolysis in the concentrations studied (0-10 mg/ml) and

179 complement opsonins that drive extravascular hemolysis in the liver.

180 Management of hemolysis in the setting of suspected device thrombosis

181 from VC-induced oxidative stress and undergo hemolysis in vitro, despite activation of the PPP.

182 tion correlates with platelet activation and hemolysis in vivo and can be recapitulated in vitro by e

183 A high hemolysis index was associated with microalbuminuria in

184 S-induced alternative pathway activation and hemolysis induced by sera from patients with atypical he

185 hand, AMP/betaCD did not alter the degree of hemolysis induced by the pure AMPs.

186 Pathologic hemolysis induced loss of RPM and BMM due to excess heme

187 Almeida et al show in mice that hemolysis induces inflammation that is caused by nitric

188 Hemolysis is a complication in septic infections with St

189 Delayed hemolysis is a frequent and relevant complication in hyp

190 Hemolysis is a fundamental feature of sickle cell anemia

191 treatment anemia in malaria in which delayed hemolysis is a new entity.

192 dy of research indicating that intravascular hemolysis is a pathological mechanism in several human d

193 Acute hemolysis is associated with organ damage, inflammation,

194 is, and describes another mechanism by which hemolysis is connected to thrombotic events.

195 tes is disrupted, only partial inhibition of hemolysis is mediated by TT30 in solution, which is simi

196 We now demonstrate that H. pylori-induced hemolysis is strain specific and is mediated by phosphol

197 sions and increased iron absorption, chronic hemolysis is the major cause of tissue-iron accumulation

198 Hemolysis led to vascular and kidney injury that was med

199 The hemolysis level cannot be controlled tightly as it depen

200 ors affecting peptide intensity were (1) the hemolysis level, (2) stopping trypsin digestion with aci

201 moglobin-derived peptides in the case of the hemolysis level.

202 calibration curve, and reports the patient's hemolysis level: non-hemolyzed, slightly hemolyzed, mild

203 the type of blood collection tube, different hemolysis levels, differences in clotting times, the num

204 Persistent low-level hemolysis (LLH) during continuous-flow mechanical circul

205 the ACR decrease and high baseline levels of hemolysis markers and percentage of dense red blood cell

206 ongly associated with decreases in levels of hemolysis markers, percentage of dense red blood cells,

207 topoietic stem cells that is associated with hemolysis, marrow failure, and thrombophilia.

208 llular heme, released during malaria-induced hemolysis, mediates a number of pathogenic processes ass

209 rbent assay and a red blood cell (RBC)-based hemolysis neutralization assay.

210 Neither hemolysis nor thrombotic events increased the risk of mo

211 rs had biochemical evidence of postoperative hemolysis not needing any specific treatment.

212 Intravascular hemolysis occurred in 5 patients, of which 3 males were

213 Hemolysis occurs in many hematologic and nonhematologic

214 Intravascular hemolysis occurs in patients on extracorporeal membrane

215 The low hemolysis of 2.39% with short prothrombin time (PT) and

216 compared to wild-type FH19-20, at promoting hemolysis of C3b-coated erythrocytes through competition

217 Additional results from HA-mediated hemolysis of chicken red blood cells (cRBCs), competitio

218 ease of calcein from erythrocyte ghosts, and hemolysis of erythrocytes was much slower when membrane-

219 med poorly at preventing complement-mediated hemolysis of ES PspCN, a CFH-binding Streptococcus pneum

220 reatment at different concentrations through hemolysis of horse red blood cells.

221 s of 2.4kDa and low hemolytic activity (<50% hemolysis of human erythrocytes at concentration of 1000

222 improves antibacterial activity and reduces hemolysis of mouse blood cells.

223 intravascular and C3-mediated extravascular hemolysis of PNH erythrocytes and warrants consideration

224 mpletely inhibits in a dose-dependent manner hemolysis of PNH erythrocytes in a modified extended aci

225 w therapeutic strategies for controlling the hemolysis of PNH.

226 he Staphylococcus aureus genome that altered hemolysis on blood agar medium.

227 The primary outcome was incidence of delayed hemolysis on day 14.

228 gated the impact of persistent intravascular hemolysis on liver dysfunction using the mouse malaria m

229 sin activity by semiquantitative analysis of hemolysis on sheep blood agar and quantitative measureme

230 ons for anemia without an apparent source of hemolysis or bleeding.

231 rease of extracellular heme is a hallmark of hemolysis or extensive cell damage.

232 reened, and 9 genes involved specifically in hemolysis or growth on human blood agar were identified

233 ttenuates anti-erythrocyte antibody-mediated hemolysis or LPS-induced acute shock.

234 Diseases that cause hemolysis or myonecrosis lead to the leakage of large am

235 ulating miRNAs selected were not affected by hemolysis or platelets, two pre-analytical factors known

236 xtracellular heme is released as a result of hemolysis or tissue damage; hence the post-translational

237 as not associated with bleeding, thrombosis, hemolysis, or mortality.

238 tors completely blocks the RTX toxin-induced hemolysis over a larger concentration range.

239 The degree of intravascular hemolysis post-transfusion and effects on endothelial-de

240 ge lesion as storage-related posttransfusion hemolysis producing Hb-driven pathophysiology.

241 inated glycoprotein inhibitor of VCC-induced hemolysis, promoted oligomerization of 65-kDa VCC to a s

242 Finally, in vivo, hemolysis promotes an increase in ALIS formation in targ

243 -CFH, R53H-CFH, and LA-CFH and also enhanced hemolysis protection by I62-CFH and LA-CFH.

244 We strongly recommend routine hemolysis quantification.

245 ice, loss of Spi2A worsened anemia caused by hemolysis, radiation, or transplantation.

246 Hemolysis refractory to intensification of antithromboti

247 s were categorized as surgical management if hemolysis refractory to intensification of standard anti

248 Nutritional intervention reduced hemolysis-related renal tubular cell damage, hepatocyte

249 Thus, intravascular hemolysis represents an intrinsic mechanism for human va

250 %), late device embolization (0.4%), and new hemolysis requiring transfusion (1.6%).

251 This hemolysis resulted in significant and rapid systemic inf

252 are characterized by enhanced intravascular hemolysis resulting in heme-catalyzed reactive oxygen sp

253 thy human volunteers increased extravascular hemolysis, saturated serum transferrin, and produced cir

254 Free hemoglobin from ongoing hemolysis scavenges nitric oxide (NO) to create an NO de

255 In 2 patients early transient autoimmune hemolysis settled after treatment and did not recur.

256 roup B antiserum and demonstrating wide beta-hemolysis should be suspected of being S. pseudoporcinus

257 Intravascular hemolysis showed a positive correlation with liver damag

258 When challenged by hemolysis, Spry1-null mice exhibited worsened anemia and

259 microneutralization (MN), and single radial hemolysis (SRH) assays, and the CD4(+) T-helper 1 (Th1)-

260 This finding was mirrored in hemolysis studies in human erythrocytes, where Ala-only

261 reshold for producing laboratory evidence of hemolysis (subclinical PNH), expansion of the clone to a

262 h adverse clinical outcomes in patients with hemolysis, such as acute and chronic vascular disease, i

263 ng in RBCs and WBCs in patients with chronic hemolysis suffering from paroxysmal nocturnal hemoglobin

264 lar antioxidant activity (CAA) assay and the hemolysis test.

265 nificantly higher in 9 patients with delayed hemolysis than in 12 with other patterns of anemia (0.30

266 , resulting in approximately 30-fold reduced hemolysis than Tyrc A.

267 ars to be more associated with extravascular hemolysis than with intravascular hemolysis.

268 and adenine nucleotides are all products of hemolysis that promote vasomotor dysfunction, proliferat

269 been accumulated regarding the mechanisms of hemolysis, the metabolism of products of hemolysis, and

270 croangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kidney failure.

271 indicating better RBC quality, biomarkers of hemolysis, thrombophilia, and inflammation (LDH, bilirub

272 undamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pathogenesis.

273 oxidant stress for the endothelium, linking hemolysis to vascular injury.

274 incomplete understanding of pathways linking hemolysis to vaso-occlusion.

275 In summary, pathophysiological levels of hemolysis trigger an immediate inflammatory response, po

276 ere Ala-only peptides displayed virtually no hemolysis up to 320 muM, but the four-Leu peptides induc

277 Erythrocyte ROS generation, hemolysis, vaso-occlusion, and the inflammatory response

278 We demonstrate that hemolysis was a rare trait, with only 4 of the 26 strain

279 DAT positive hemolysis was confirmed and anti-A antibodies were detec

280 gnificantly enhanced resistance to oxidative hemolysis was confirmed in red blood cells, while no sig

281 The role of complement in Stx2-mediated hemolysis was demonstrated by its occurrence only in the

282 Delayed hemolysis was detected in 5 children (7%), with 1 child

283 No alternative explanation for clinical hemolysis was found.

284 Stx2-induced hemolysis was not demonstrated in the absence of plasma

285 Hemolysis was predictive of subsequent thrombotic events

286 Intravascular hemolysis was simulated by infusion of prelysed erythroc

287 e in hemoglobin >/=2 g/dL (in the absence of hemolysis) was the primary end point.

288 nt or graft loss nor vascular rejection, nor hemolysis, was encountered in the ABO nonidentical patie

289 acute inflammatory effects of water-induced hemolysis were abolished by the simultaneous administrat

290 ss III or class IV G6PDd without evidence of hemolysis were evaluated for donation, if there was no o

291 1 g/dL; P = .0001), markers of intravascular hemolysis were not higher in severe disease.

292 hemolysis and medications, which can induce hemolysis, were avoided.

293 uria (PNH) is characterized by intravascular hemolysis, which is effectively controlled with eculizum

294 Incubation of erythrocytes with VC induced hemolysis, which was exacerbated in erythrocytes from gl

295 protection against AAPH-induced erythrocyte hemolysis while (-)-epicatechin gallate, (-)-epigallocat

296 er liter discriminated patients with delayed hemolysis with 89% sensitivity and 83% specificity.

297 Predictive tests for intravascular hemolysis with crossmatch-incompatible sera indicated co

298 The disease is associated with chronic hemolysis with elevated cell-free hemoglobin and heme.

299 ds demonstrated dose-dependent inhibition of hemolysis with IC50 approximately 4 microM and full inhi

300 potassium release occurred within 5 min and hemolysis within 20 min in human red blood cells (RBC) e