ライフサイエンスコーパス: hemolysis

1 at are retained in the spleen are subject to hemolysis.

2 idative damage, and therefore susceptible to hemolysis.

3 ssociated with indirect markers of increased hemolysis.

4 ovel antileukemia treatment without inducing hemolysis.

5 g lifelong transfusions to fully compensated hemolysis.

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

7 ated with hepatotoxicity, nephrotoxicity and hemolysis.

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

9 concentrations against hypochlorite-induced hemolysis.

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

11 ne oxygenation are bleeding, thrombosis, and hemolysis.

12 nuate disease complications in patients with hemolysis.

13 oglobin alone is not sufficient to determine hemolysis.

14 ns may preserve vascular NO signaling during hemolysis.

15 proteins could preserve NO signaling during hemolysis.

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

17 ravascular hemolysis than with intravascular hemolysis.

18 osited on the cell membranes and can lead to hemolysis.

19 carboxylic functionalities did not cause any hemolysis.

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

21 t prevents complement-mediated intravascular hemolysis.

22 ed oxidative stress and shear stress-induced hemolysis.

23 ate dehydrogenase in whole blood, indicating hemolysis.

24 ythrocytes, which enhances cytoadherence and hemolysis.

25 candidate marker to predict post-AS delayed hemolysis.

26 reatment with phenylhydrazine, an inducer of hemolysis.

27 nkage of the cell and ultimately resulted in hemolysis.

28 n in these patients occurs via extravascular hemolysis.

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

30 ng erythrocyte turnover through induction of hemolysis.

31 es free hemoglobin following malaria-induced hemolysis.

32 ading to clinically meaningful extravascular hemolysis.

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

34 late-stage erythroid precursors and reducing hemolysis.

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

36 (+/+), SCD(bmt) mice consistent with greater hemolysis.

37 o render LukS-PV capable of DARC binding and hemolysis.

38 dy, L&K-NPs effectively inhibit PLA2-induced hemolysis.

39 worsened anemia in SCD mice due to increased hemolysis.

40 study period, with improvement in markers of hemolysis.

41 openia, elevated creatinine, and evidence of hemolysis.

42 re, stroke or transient ischemic attack, and hemolysis.

43 nt, resulting in predominantly extravascular hemolysis.

44 sed hemoglobin levels and reduced markers of hemolysis.

45 itors correlated with the levels of residual hemolysis.

46 hains causing ineffective erythropoiesis and hemolysis.

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

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

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

50 was recently shown to contribute to delayed hemolysis, a frequent adverse event of artesunate.

51 io, 1.81; 95% CI, 1.30-2.52; p < 0.001), and hemolysis (adjusted odds ratio, 1.87; 95% CI, 1.11-3.16;

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

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

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

55 Extravascular hemolysis after transfusion progressively increased with

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

57 Hemolysis and accumulation of cell-free hemoglobin (Hb)

58 emopexin ratio is associated with markers of hemolysis and AKI in both humans and mice with SCD.

59 al in assuaging H(2)O(2) induced erythrocyte hemolysis and antioxidant activity by inhibiting membran

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

61 ymptoms and findings associated with chronic hemolysis and avoid the complications associated with cu

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

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

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

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

66 onstrated an isoform-dependent inhibition of hemolysis and complement deposition at the level of sC5b

67 dose of venomous PLA2, L&K-NPs also inhibit hemolysis and confer a significant survival benefit.

68 Hemolysis and consequent release of cell-free hemoglobin

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

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

71 Both SCD patients had pronounced hemolysis and depleted plasma hemopexin and haptoglobin.

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

73 Gross hemolysis and excess host nucleic acid reduced assay sen

74 Several studies demonstrate that hemolysis and free heme in circulation cause endothelial

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

76 d occurs in many hemorrhagic injuries due to hemolysis and hemoglobin degradation, which not only med

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

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

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

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

81 Hemolysis and iron overload improved upon iron chelation

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

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

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

85 wn-regulation of virulence genes and reduced hemolysis and neutrophil chemotaxis, while exhibiting in

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

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

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

89 ents including increased Hb and reduction in hemolysis and percentage of sickled red cells, supportin

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

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

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

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

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

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

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

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

98 erythrocytic polymerization of Hb S promotes hemolysis and vasoocclusive events in the microvasculatu

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

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

101 biomedical applications, such as RBC damage (hemolysis) and mechanoporation-based drug delivery.

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

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

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

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

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

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

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

109 ilm formation, streptolysin S (SLS)-mediated hemolysis, and localized ulcerative lesion progression d

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

111 observed a drastic reduction in proteolysis, hemolysis, and pigmentation that was fully complementabl

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

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

114 pt by improving clinical measures of anemia, hemolysis, and sickling.

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

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

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

118 of LukE with DARC and the role this plays in hemolysis are incompletely characterized.

119 These data identify hemolysis as a key event in the turnover of senescent er

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

121 ple by quantitation of hemoglobin and report hemolysis as either minimal (<=5%) or undetectable (<=1%

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

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

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

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

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

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

128 In hemolysis assays with 2-aminoethylisothiouronium bromide

129 eries of time-kill studies, cytotoxicity and hemolysis assays, as well as whole-cell uptake and devel

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

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

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

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

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

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

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

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

138 LukE binds to DARC and facilitates hemolysis, but the closely related Panton-Valentine leuk

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

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

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

142 onstrate that small changes in porcine blood hemolysis can be detected through a simple resistance me

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

144 Intravascular hemolysis can impair NO bioavailability and cause oxidat

145 Blood damage (hemolysis) can occur during clinical procedures, e.g. di

146 Hemolysis causes an increase of intravascular heme, oxid

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

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

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

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

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

152 Intravascular hemolysis describes the relocalization of heme and hemog

153 Hemolysis drives susceptibility to bacterial infections

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

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

156 Erythrocytes undergo hemolysis during storage and after transfusion.

157 ith features of TMA (preeclampsia/eclampsia; hemolysis elevated liver enzymes low platelets syndrome;

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

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

160 AALD, of whom nearly half were attributed to hemolysis, elevated liver enzymes, and low platelets (HE

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

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

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

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

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

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

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

168 antibodies that inhibit granadaene-mediated hemolysis ex vivo and diminish GBS infection in vivo.

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

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

171 Delayed hemolysis has been described in hyperparasitemic nonimmu

172 sue of Blood, Ofori-Acquah et al investigate hemolysis, hemopexin deficiency, and kidney function in

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

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

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

176 Finally, lethality caused by sterile hemolysis in mice required TLR4, TNFR1, and mitochondria

177 and rapidly stopped C1s complement-mediated hemolysis in patients with cold agglutinin disease, sign

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

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

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

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

182 complement opsonins that drive extravascular hemolysis in the liver.

183 ltered in abundance in sera, irrespective of hemolysis in the samples.

184 Management of hemolysis in the setting of suspected device thrombosis

185 ions of the eventual failure of RBCs causing hemolysis in various hemolytic pathologies.

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

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

188 h anti-(alpha)-Rh(D) antibodies that mediate hemolysis in vivo was inhibited by a humanized monoclona

189 A high hemolysis index was associated with microalbuminuria in

190 he major dose-limiting toxicity observed was hemolysis, indicating that a narrow therapeutic window e

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

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

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

194 Here we found that intravascular hemolysis, induced by injection of phenylhydrazine, resu

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

196 Hemolysis is a complication in septic infections with St

197 Delayed hemolysis is a frequent and relevant complication in hyp

198 Hemolysis is a fundamental feature of sickle cell anemia

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

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

201 amino acid residues in solving long-standing hemolysis issues of AMPs.

202 Angiopoietin-2 was associated with hemolysis (lactate dehydrogenase, total bilirubin) and i

203 The hemolysis level cannot be controlled tightly as it depen

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

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

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

207 ose a simple technique to monitor changes in hemolysis levels continuously and in real time.

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

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

210 During hemolysis, macrophages in the liver phagocytose damaged

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

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

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

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

215 o regions of LukE's rim domain contribute to hemolysis, namely residues 57-75 (DR1) and residues 182-

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

217 with increased potency and reduced in vitro hemolysis, nonspecific membrane toxicity in vivo continu

218 Neither hemolysis nor thrombotic events increased the risk of mo

219 Sutimlimab rapidly abrogated extravascular hemolysis, normalizing bilirubin levels within 24 hours

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

221 Intravascular hemolysis occurs in patients on extracorporeal membrane

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

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

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

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

226 In addition to the decreased hemolysis of human erythrocytes, CM14 impedes host cell

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

228 and 83.1% for technologist reading for beta-hemolysis on blood agar accompanied by any zone of inhib

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

230 and 97.7% for technologist reading for beta-hemolysis on blood agar, and 39.5% and 83.1% for technol

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

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

233 ting with human blood and plasma revealed no hemolysis or complement activation following incubation

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

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

236 liver endothelium in mice with intravascular hemolysis or injected with heme as well as on cultured h

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

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

239 e peritonitis-sepsis model, without observed hemolysis or renal injury in murine toxicity studies.

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

241 sfusion reactions, medical-device associated hemolysis, or after a subarachnoid hemorrhage.

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

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

244 Post-artesunate delayed hemolysis (PADH) and hyperparasitemia are associated wit

245 volunteers was incubated with TIMP-GLIA, and hemolysis, platelet activation and aggregation, and comp

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

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

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

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

250 We strongly recommend routine hemolysis quantification.

251 Hemolysis refractory to intensification of antithromboti

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

253 of a complement-activating phenotype during hemolysis remain unclear.

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

255 %), late device embolization (0.4%), and new hemolysis requiring transfusion (1.6%).

256 This hemolysis resulted in significant and rapid systemic inf

257 r functions, but release of free heme during hemolysis results in oxidative tissue damage, vascular d

258 With the exception of hemolysis (RR, 2.18 [95% CI, 1.58-3.01]; P<0.00001), ove

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

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

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

262 were developed applying a concentration and hemolysis step before a test for carbapenemase productio

263 uman cancer cells, it showed low toxicity in hemolysis studies and zebrafish, demonstrating the role

264 ge, hC3Nb3 inhibits classical pathway-driven hemolysis, suggesting that the C-terminal domain of C3b

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

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

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

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

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

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

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

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

273 NH) is an acquired disorder characterized by hemolysis, thrombosis, and bone marrow failure caused by

274 Cyt1Aa exerts its insecticidal activity and hemolysis through different mechanisms.

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

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

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

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

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

280 Manaus, the frequency of primaquine-induced hemolysis was 85.2 cases per 100 000 primaquine users.

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

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

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

284 Post-artesunate delayed hemolysis was detected in 7 children (5%) with only mino

285 No alternative explanation for clinical hemolysis was found.

286 Hemolysis was higher in patients who underwent VA-ECMO w

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

288 Hemolysis was predictive of subsequent thrombotic events

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

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

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

292 1 g/dL; P = .0001), markers of intravascular hemolysis were not higher in severe disease.

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

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

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

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

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

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 ent, as well as the absence of posttreatment hemolysis with these drugs.