ライフサイエンスコーパス: heparin

1 ivin and two model polyanion drugs (suramin, heparin).

2 no inhibition is observed in the absence of heparin.

3 agulants, warfarin, and low-molecular-weight heparin.

4 s between human platelet factor 4 (hPF4) and heparin.

5 to complexes of platelet factor 4 (PF4) and heparin.

6 mpared with warfarin or low-molecular-weight heparin.

7 rculating B cells in some patients receiving heparin.

8 positive charge may be the binding site for heparin.

9 coated over copper layer for the sensing of heparin.

10 n situ warm ischemia, without application of heparin.

11 mpared with warfarin or low-molecular-weight heparin.

12 was elevated by infusion of Intralipid plus heparin.

13 which was treated with low-molecular-weight heparin.

14 sed affinity for ADAMTS-5 in the presence of heparin.

15 was cannulated and flushed with 10 000 U of heparin.

16 in receptor, and its activity is reversed by heparin.

17 ffected by anticoagulants such as aspirin or heparin.

18 ence in a high-risk population compared with heparin.

19 hibition of KLK7 by vaspin is accelerated by heparin.

20 deled BIH behave similarly to pharmaceutical heparin.

21 antigenic complexes that were dissociated by heparin.

22 .59-1.36]; factor Xa vs low-molecular-weight heparin 1.02 [0.42-2.70]; and low-molecular-weight hepar

23 , taurolidine-citrate-heparin, compared with heparin 100 IE/mL on CRBSI occurrence.Forty-one high-ris

24 Antithrombin (2.6 muM) plus heparin (4 U/mL) inhibits 72% of the active clot-bound t

25 residues contributing to heparin binding and heparin activation were identified by a selective labeli

26 afforded two remodeled heparins that met USP heparin activity and Mw specifications.

27 In particular, heparin acts as an interacting template that rapidly for

28 rawal in the operating theater and premortem heparin administration improve DCD liver transplant outc

29 Because heparin affects collagen fibril formation, we investigat

30 The heparin affinities of AAV2-based tyrosine-to-phenylalani

31 Heparin also facilitated hIL-12 binding and signaling in

32 roteins, the molecular mechanism(s) by which heparin alters vascular cell physiology is not well unde

33 Heparin, an analog of the heparan sulfate proteoglycans

34 of a uniformly (13)C-labeled octasaccharide heparin analogue enabled magic-angle spinning solid-stat

35 nt complexes formed by intact unfractionated heparin and antithrombin-III, interaction which is centr

36 ogo-A region, named Nogo-A-Delta20, binds to heparin and brain-derived heparan sulfate glycosaminogly

37 Binding of Hic to hTSP-1 is inhibited by heparin and chondroitin sulfate A, indicating binding to

38 nus-derived basic peptides (FS2 and NFS3) to heparin and chondroitin sulfate A.

39 Further, we predict the pose of heparin and chondroitin sulfate derivatives bound to the

40 Heparin and heparan sulfate (HS) by nature contain multi

41 Glycosaminoglycans (GAGs), especially heparin and heparan sulfate (HS), modulate the functions

42 Despite the large number of heparin and heparan sulfate binding proteins, the molecu

43 The complexity of heparin and heparan sulfate saccharides makes their puri

44 .0/1000 CVC days) in the taurolidine-citrate-heparin and heparin arm, respectively, tending to prolon

45 Heparin and HS were found to bind human IL-12 (hIL-12) w

46 n, we report a co-immobilization strategy of heparin and potent anti-neointimal drug (Mitogen Activat

47 The electrostatic attraction between heparin and protamine-stabilized Pt NPs induced nanopart

48 Heparin and related members of the glycosaminoglycan (GA

49 ltimerization is enhanced in the presence of heparin and stabilized by the matrix cross-linking enzym

50 , both of which induce focal adhesions, bind heparin and syndecan-4.

51 after cardiac surgery-as an agent to bind to heparin and thereby reverse its anticlotting activity.

52 CEA) to reverse the anticoagulant effects of heparin and to limit the risk for postoperative bleeding

53 can neutralize the anticoagulant activity of heparins and the prothrombotic activity of polyP.

54 igosaccharides, hyaluronan, heparan sulfate, heparin, and chondroitin sulfate, and collagen-like pept

55 ore than the natural sulfated polysaccharide heparin, and promoted regeneration of bone in the spine

56 neered FN fragments with differing (defined) heparin- and integrin-binding capacities were applied di

57 It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposu

58 chanism that incites such prevalent anti-PF4/heparin antibody production in more than 50% of patients

59 y, studies in mice reveal that UHRA reverses heparin anticoagulant activity without the lung injury s

60 up B; initial treatment using a non-DOAC/non-heparin anticoagulant with transition to a DOAC during H

61 n the taurolidine arm (euro2348) than in the heparin arm (euro6744) owing to fewer admission days rel

62 In the taurolidine-citrate-heparin arm, no CRBSIs occurred, whereas 7 CRBSIs occurr

63 days) in the taurolidine-citrate-heparin and heparin arm, respectively, tending to prolong CVC surviv

64 s occurred, whereas 7 CRBSIs occurred in the heparin arm, with an incidence of 1.0/1000 CVC days (95%

65 Indeed, the polycation used to counteract heparin-associated bleeding in surgical settings, protam

66 ne, and polyanions (pentosan polysulfate and heparin) based on the strong binding reaction of polyani

67 releasing them in a controlled manner via a heparin-based coacervate delivery vehicle to improve wou

68 nlike USP porcine heparin, bovine intestinal heparin (BIH) has a low anticoagulant activity.

69 Pathogenic antibodies to PF4/heparin bind and activate cellular FcgammaRIIA on platel

70 sCT fibrillates without GAGs, but heparin binding accelerates the process by decreasing th

71 sidues of central beta-sheet A contribute to heparin binding and activation of vaspin.

72 Mutation of basic residues decreased heparin binding and activation of vaspin.

73 In addition, basic residues contributing to heparin binding and heparin activation were identified b

74 center loop insertion into sheet A decreased heparin binding because it disturbs the basic cluster.

75 that key markers of implantation, including Heparin binding EGF-like growth factor and Mucin 1, exhi

76 Heparin binding epidermal growth factor-like growth fact

77 Analysis of heparin binding of the main transglutaminases revealed t

78 een TG1 and HS is strong, the conformational heparin binding site of TG2 is not conserved, suggesting

79 tidisciplinary research were to characterize heparin binding to interleukin-12 (IL-12) and determine

80 aracterized monoclonal antibodies that block heparin binding to vascular cells have been found to mim

81 We show that AAV2-based vectors lacking heparin binding transduce retina by subretinal injection

82 During pregnancy, up-regulation of heparin-binding (HB-) EGF and cyclooxygenase-2 (COX-2) i

83 by administration of a mAb that targets the heparin-binding domain of Hpa2, implying that Hpa2 funct

84 igen stimulation increased the expression of heparin-binding EGF-like growth factor (HB-EGF) and acti

85 infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upre

86 d to, basic fibroblast growth factor (FGF2), heparin-binding EGF-like growth factor (HBEGF), vascular

87 electively expressing the EGFR ligand, human heparin-binding EGF-like growth factor (hHB-EGF), in ren

88 Heparin-binding epidermal growth factor (EGF)-like growt

89 Heparin-binding epidermal growth factor-like growth fact

90 Here we identify heparin-binding epidermal growth factor-like growth fact

91 dation in clinical specimens showed that the heparin-binding factor midkine is a systemic inducer of

92 its target protease kallikrein 7 (KLK7) are heparin-binding proteins, and inhibition of KLK7 by vasp

93 est the hypotheses that (i) the matricryptic heparin-binding region of the first type III repeat of f

94 of beta-sheet A and is different from other heparin-binding serpins.

95 Interestingly, all proteins bound at the heparin-binding sites of laminin, including the globular

96 -ray scattering (SAXS) data, and location of heparin-binding sites.

97 Heparin blocks egress by interacting with both the surfa

98 Unlike USP porcine heparin, bovine intestinal heparin (BIH) has a low antic

99 hat the Y-F and T-V AAV2 capsid mutants bind heparin but with slightly reduced affinity relative to t

100 glycosaminoglycans and low molecular weight heparins by microscale thermophoresis and analyzed accel

101 Our analysis indicates that the role of heparin cannot be explained by enhancement of nucleation

102 fe dependent on HPS, the taurolidine-citrate-heparin catheter lock demonstrates a clinically substant

103 stream infections compared with standard and heparin central venous catheters.

104 iometry, the measurements allow the range of heparin chain lengths to be obtained for each complex an

105 (CHC), a compound of multiple unfractionated heparin chains, coats cells with a glycocalyx-like layer

106 ), the representative sequence of helix D of heparin co-factor II, was demonstrated to be potent agai

107 ycan (GAG) sequences that selectively target heparin cofactor II (HCII), a key serpin present in huma

108 -IV, C-I and M, histidine-rich glycoprotein, heparin cofactor II and attractin, which are involved in

109 s of any type of impregnation (antibiotic or heparin) compared with standard central venous catheters

110 catheter lock solution, taurolidine-citrate-heparin, compared with heparin 100 IE/mL on CRBSI occurr

111 In healthy donors, PF4/heparin complexes bind preferentially to B cells (>90% o

112 Binding of PF4/heparin complexes to B cells is mediated through the int

113 to demonstrate complement activation by PF4/heparin complexes, opsonization of PF4/heparin to B cell

114 stic insights into the immunogenicity of PF4/heparin complexes.

115 enabled the determination of the therapeutic heparin concentration in a single drop of blood.

116 Therefore, the lowest detectable heparin concentrations through UV-vis absorption and by

117 rmediate thresholds (ELISA, CLIA), high-dose heparin confirmation step (ELISA), and particle immunofi

118 Corline Heparin Conjugate (CHC), a compound of multiple unfracti

119 h macromolecular heparin conjugates (Corline Heparin Conjugate, CHC).

120 lamine (PAV) and coupled with macromolecular heparin conjugates (Corline Heparin Conjugate, CHC).

121 closed-loop patch is developed for prolonged heparin delivery in a feedback-controlled manner.

122 mmune response is remarkably transient, with heparin-dependent antibodies no longer detectable 40 to

123 derivatives toward different diseases (e.g., heparin derivatives against Alzheimer's disease), there

124 Heparin derivatives counteract this mechanism and, as su

125 Heparan sulfate proteoglycans and heparin derivatives further enhance HBEGF-induced differ

126 earing human prostate cancer xenografts, and heparin derivatives specifically abrogate this effect by

127 We further show that heparin-derived dodecasaccharide is able to induce dimer

128 The approval of fondaparinux, a heparin-derived factor Xa (fXa) inhibitor, provided vali

129 Solid-state NMR reveals that heparin does not alter the sCT fibrillary core around Ly

130 randomly assigned to receive bivalirudin or heparin during PCI, which was performed predominantly wi

131 g to vascular cells have been found to mimic heparin effects.

132 ose with both positive antiplatelet factor 4/heparin enzyme-linked immunosorbent assay (optical densi

133 ytopenia and underwent antiplatelet factor 4/heparin enzyme-linked immunosorbent assay and serotonin

134 If antiplatelet factor 4/heparin enzyme-linked immunosorbent assay is used to con

135 n encouraging a higher antiplatelet factor 4/heparin enzyme-linked immunosorbent assay optical densit

136 patients (81.8%) with antiplatelet factor 4/heparin enzyme-linked immunosorbent assay optical densit

137 135 patients had 4Ts, antiplatelet factor 4/heparin enzyme-linked immunosorbent assay, and serotonin

138 ed including age, sex, antiplatelet factor 4/heparin enzyme-linked immunosorbent assay, serotonin rel

139 patients had positive antiplatelet factor 4/heparin enzyme-linked immunosorbent assay; 10 patients w

140 The results show suramin and heparin exerted multiple concentration-dependent effects

141 days irrespective of the patient's previous heparin exposure status or history of HIT.

142 ver, the minimum interval from an immunizing heparin exposure to the development of HIT is 5 days irr

143 F4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patien

144 m that with warfarin or low-molecular-weight heparin (factor Xa vs warfarin IRR 0.78 [95% CrI 0.47-1.

145 nticoagulation therapy (low-molecular-weight heparin followed by vitamin K antagonists).

146 mpared with warfarin or low-molecular-weight heparin for all indications.

147 olism to receive either low-molecular-weight heparin for at least 5 days followed by oral edoxaban at

148 stive transducer that is functionalized with heparin for low-cost, label-free, ultra-sensitive, and r

149 d that prophylaxis with low-molecular-weight heparin for the 8 days after knee arthroscopy or during

150 y a VKA (LMWH and VKA); or 4) unfractionated heparin for the first trimester, followed by a VKA (UFH

151 ials of edoxaban versus low-molecular-weight heparin for the treatment of venous thromboembolism in p

152 stitution of heparin or low-molecular weight heparin for warfarin (n = 13 [72%]), intravenous sodium

153 a prophylactic dose of low-molecular-weight heparin (for the 8 days after arthroscopy in the POT-KAS

154 rin mimetics with defined structure or short heparin fragments.

155 quire prolonged intermittent dialysis need a heparin-free easy-to-use alternative type of anticoagula

156 y-to-use, efficient, and inexpensive form of heparin-free regional anticoagulation.

157 We assessed the safety and efficiency of heparin-free regional citrate anticoagulation of the dia

158 The hypothesis that unfractionated heparin functions to decrease inflammatory signal transd

159 0 days) ST were similar with bivalirudin and heparin+/-GPI (1.0% versus 1.4%, P=0.24).

160 ients treated with bivalirudin compared with heparin+/-GPI because of increased ST within 4 hours aft

161 ated patients compared with 16 of 40 (40.0%) heparin+/-GPI-treated patients (adjusted hazard ratio, 0

162 in the bivalirudin group and in 2.4% in the heparin group (hazard ratio, 0.84; 95% CI, 0.60 to 1.19;

163 udin group and in 12.8% (383 of 3002) in the heparin group (hazard ratio, 0.96; 95% confidence interv

164 3), protamine (group 4), and protamine plus heparin (group 5).

165 n MRI did not differ between bivalirudin and heparin groups (65.5% vs. 58.1%; p = 0.55).

166 AGs) with affinities in the following order: heparin > heparan sulfate > chondroitin sulfate = dermat

167 y indicates that the host glycosaminoglycans heparin (Hep) and heparan sulfate (HS) are high-priority

168 atographic isolation and purification of two heparin hexasaccharide isomers that interact with the ol

169 minoglycans-hyaluronan (HA), heparan sulfate/heparin (HS/HP), chondroitin/dermatan sulfate (CS/DS), a

170 /=4 points; positive platelet factor 4 [PF4]/heparin immunoassay, positive serotonin-release assay).

171 nts have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clin

172 and antibiotic-impregnated catheters versus heparin-impregnated catheters (-1.98%, -3.90 to -0.06, N

173 c-impregnated group, and 17 (3%) assigned to heparin-impregnated catheters.

174 he widely used lifesaving anticoagulant drug heparin in 2007 has drawn renewed attention to the chall

175 lts of this study demonstrate a new role for heparin in modulating the biological activity of IL-12.

176 n mimetics including Roneparstat, a modified heparin in phase I trials in myeloma patients, significa

177 tion in more than 50% of patients exposed to heparin in some clinical settings is poorly understood.

178 ally to B cells (>90% of B cells bind to PF4/heparin in vitro) relative to neutrophils, monocytes, or

179 4A eliminated the physiological responses to heparin, including effects on ERK pathway activity and B

180 Flow cytometry studies revealed that heparin increased the amount of hIL-12 bound to cell sur

181 h inversely parallel waning of serum-induced heparin-independent serotonin release) with successful o

182 ngle X-ray scattering studies indicated that heparin induced dimerization of hIL-12.

183 Biophysical studies demonstrated that heparin induced only minor conformational changes while

184 nsduction in endothelial cells (ECs) through heparin-induced expression of DUSP1 was tested.

185 184A (TMEM184A) confirmed its involvement in heparin-induced signaling as seen in VSMCs.

186 of ApoC-III had no effect on VLDL secretion, heparin-induced TG reduction, or uptake of lipids into h

187 Heparin-induced thrombocytopenia (HIT) is a prothromboti

188 Heparin-induced thrombocytopenia (HIT) is an adverse dru

189 Heparin-induced thrombocytopenia (HIT) is an immune comp

190 Heparin-induced thrombocytopenia (HIT) is characterized

191 Life-threatening heparin-induced thrombocytopenia (HIT) is treated with t

192 nheparin anticoagulants for the treatment of heparin-induced thrombocytopenia (HIT), few data are ava

193 ACs) are attractive options for treatment of heparin-induced thrombocytopenia (HIT).

194 the diagnostic accuracy of immunoassays for heparin-induced thrombocytopenia (HIT).

195 Prevalence of heparin-induced thrombocytopenia and heparin-induced thr

196 al and cardiac ICU who were presumed to have heparin-induced thrombocytopenia and underwent antiplate

197 reveal a high occurrence of overdiagnosis of heparin-induced thrombocytopenia in surgical patients wi

198 Overtreatment of heparin-induced thrombocytopenia in the surgical ICU con

199 There was no difference in mortality between heparin-induced thrombocytopenia positive and negative p

200 orbent assay; 10 patients were identified as heparin-induced thrombocytopenia positive.

201 The optimal criteria for diagnosis of heparin-induced thrombocytopenia remain unclear, contrib

202 itted to surgical ICUs and were suspected of heparin-induced thrombocytopenia to identify how often p

203 etrospective Registry of Patients With Acute Heparin-induced Thrombocytopenia Type II; NCT01304238).

204 tive patients (100%) compared with 19 of 125 heparin-induced thrombocytopenia-negative patients (15%)

205 troban, lepirudin, or fondaparinux: 10 of 10 heparin-induced thrombocytopenia-positive patients (100%

206 Heparin-induced thrombocytopenia-positive patients were

207 ence of heparin-induced thrombocytopenia and heparin-induced thrombocytopenia-related thrombosis amon

208 -12) and determine the mechanism(s) by which heparin influences IL-12 bioactivity.

209 The Avoid-Heparin Initiative, implemented at a tertiary care hospi

210 Moreover, we found that heparin is a strong inhibitor of AKAV and SBV infections

211 rone tau as induced by the complexation with heparin is accompanied by large changes in local tau con

212 but not the 2-O-sulfate of iduronate within heparin is required for 3Q binding, indicating selectivi

213 Low-molecular-weight heparin is the standard treatment for cancer-associated

214 ciated with: hypocoagulable TEG profile with heparin-like effect; falls in thrombin generation, Facto

215 previously that the GAG low-molecular-weight heparin (LMWH) binds to Abeta40 fibrils with a three-fol

216 lved replacing UFH with low-molecular-weight heparin (LMWH) for prophylactic and therapeutic indicati

217 The potential of low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempe

218 We hypothesized that low molecular weight heparin (LMWH) is superior to unfractionated heparin (UH

219 above a threshold where low-molecular-weight heparin (LMWH) prophylaxis is clearly indicated or below

220 hroughout pregnancy; 2) low-molecular-weight heparin (LMWH) throughout pregnancy; 3) LMWH for the fir

221 rolled trials comparing low-molecular-weight heparin (LMWH) vs no LMWH in women with inherited thromb

222 ty patients received the taurolidine-citrate-heparin lock and 21 received the heparin lock, with 9622

223 ine-citrate-heparin lock and 21 received the heparin lock, with 9622 and 6956 treatment days, respect

224 erapy (initial treatment with unfractionated heparin, low-molecular-weight heparin, or fondaparinux,

225 metry of the oligosaccharides obtained after heparin lyase III digestion of the polysaccharide indica

226 Additionally, administration of heparin may be useful, and restoration of physiological

227 We apply these methods to the problem of heparin-mediated tau polymerization, which displays comp

228 Heparin or heparin mimetics including Roneparstat, a modified hepar

229 s client proteins use synthetically produced heparin mimetics with defined structure or short heparin

230 Heparin modestly protected hIL-12 from proteolytic degra

231 e form of silica glass beads and polyanionic heparin molecules potently seeds the amyloid conversion

232 ed bivalirudin than among those who received heparin monotherapy.

233 re randomized to bivalirudin (n = 29) versus heparin (n = 31).

234 Labeled heparin neither bound to nor translocated through the in

235 Finally, heparin non-specifically binds at the YKL-40 surface, as

236 characterized the interaction of a panel of heparin oligosaccharides to CXCL5 using solution NMR, is

237 ed this by characterizing the binding of GAG heparin oligosaccharides to hCXCL1 using NMR spectroscop

238 Here, we present the CTA-SAX purification of heparin oligosaccharides using volatile salt (VS) buffer

239 act of a hospital-wide strategy for avoiding heparin on the incidence of HIT, HIT with thrombosis (HI

240 infections were inhibited by the addition of heparin or enzymatic removal of cell surface heparan sul

241 Heparin or heparin mimetics including Roneparstat, a mod

242 t common treatments included substitution of heparin or low-molecular weight heparin for warfarin (n

243 effects of anticoagulant therapy (low-weight heparin or warfarin vs no therapy) in patients with cirr

244 As a result, the vast majority of studies of heparin (or related GAGs) interactions with its client p

245 , a central venous catheter impregnated with heparin, or a standard central venous catheter with comp

246 unfractionated heparin, low-molecular-weight heparin, or fondaparinux, usually overlapping with and f

247 ients whose DCD donors were given antemortem heparin (P = 0.62).

248 This "smart" heparin patch can be transcutaneously inserted into skin

249 NSTEMI and CAG scheduled within 72 hours to heparin plus eptifibatide versus otamixaban.

250 e duration on AST when either bivalirudin or heparin plus glycoprotein IIb/IIIa receptor inhibitor (G

251 87; 95% CI, 1.01-8.17; P = .04) but not with heparin plus GPI (0 vs 3 [0.3%]; P = .30).

252 th bivalirudin but not patients treated with heparin plus GPI, possibly because of the rapid offset o

253 286 receiving bivalirudin and 1412 receiving heparin plus GPI.

254 ts and were randomized 1:1 to bivalirudin or heparin plus GPI.

255 py vs unfractionated or low-molecular-weight heparin plus optional GPIs (control group).

256 with unfractionated or low-molecular-weight heparin plus optional GPIs on 1-year mortality.

257 Here, using a library of short heparin polysaccharides modified at specific sites, we s

258 ) the crystal structure poses for four known heparin-protein structures.

259 etries are observed ranging from 1:1 to 1:3 (heparin/protein ratio).

260 Since this action of heparin recapitulates that of neutralizing antibodies, m

261 developed a synthetic polycation, Universal Heparin Reversal Agent (UHRA), which is nontoxic and can

262 effects, such as the risk of bleeding due to heparin's anticoagulant activity.

263 Heparin's template effect highlights its role in amyloid

264 hods have enabled exact mass measurements of heparin saccharides roughly up to degree-of-polymerizati

265 Using heparin-Sepharose-enriched fractions that hybridized to

266 re, 2-O-, and 6-O-, but not N-desulfation of heparin, significantly increased the inhibitory effect o

267 ophil CD203c in samples collected in EDTA or heparin, stored at 4 degrees C, and analyzed 24 hours af

268 ikely to cause clotting compared with use of heparin strategies (hazards ratio, 1.62; p = 0.003).

269 ), a known tumor suppressor which attenuates heparin sulfate binding growth factor signaling, also re

270 STD NMR experiments using a heparin sulfate decasaccharide confirmed that H3 binds h

271 lfate decasaccharide confirmed that H3 binds heparin sulfate.

272 ia acquired basic mutations interacting with heparin sulphate (HS); this virus is attenuated in natur

273 The natural glycosaminoglycan heparin surprisingly inhibited malaria parasite egress,

274 1, -3, and/or 3-OST-1 afforded two remodeled heparins that met USP heparin activity and Mw specificat

275 cytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of pla

276 borated to redefine quality expectations for heparin, thus making an important natural product better

277 y PF4/heparin complexes, opsonization of PF4/heparin to B cells via CD21, and the presence of complem

278 activated thrombin and subsequently releases heparin to prevent coagulation in the blood flow.

279 ine antagonist activity is fully reversed by heparin treatment both in vitro and in vivo Thus, our re

280 Baseline characteristics, duration of heparin treatment, and rates of bleeding leading to stud

281 linical characteristics, duration of initial heparin treatment, bleeding rates, or quality of warfari

282 tion can be conducted with blood obtained in heparin tubes and stored at 4 degrees C for 24 hours.

283 By contrast, blood samples collected in heparin tubes were adequate for quantification of upregu

284 th peanut allergy was collected into EDTA or heparin tubes, and samples were stored at 4 degrees C or

285 The binding of heparin-tyramine polymer (HT) onto the polycarprolactone

286 comes between bivalirudin and unfractionated heparin (UFH) have not been well described.

287 to 5% of patients exposed to unfractionated heparin (UFH).

288 heparin (LMWH) is superior to unfractionated heparin (UH) for venous thromboembolism (VTE) prophylaxi

289 eter removal with impregnated (antibiotic or heparin) versus standard central venous catheters, asses

290 ultaneous estimation of vitamin K1 (VK1) and heparin via cascaded channel multianalyte sensing probe

291 n 1.02 [0.42-2.70]; and low-molecular-weight heparin vs dabigatran 0.67 [0.20-1.82]).

292 nergy was used for ablation in all cases and heparin was administered with goal-activated clotting ti

293 se-like activity and protamine can recognize heparin, we prepared the protamine-modified Pt NPs throu

294 se both anti-Mac-1 function-blocking mAb and heparin were required to block adhesion.

295 Heparin, which binds ligands including PDGF and SCF, and

296 d is resistant to inhibition by antithrombin/heparin while still susceptible to small, active-site in

297 Together, these data show that vaspin binds heparin with high affinity (KD = 21 +/- 2 nm) and that b

298 rvention, treatment with bivalirudin or with heparin with optional use of GPI resulted in similar 1-y

299 rvival benefits of bivalirudin compared with heparin with routine or optional use of glycoprotein IIb

300 Suramin and heparin yielded qualitatively and quantitatively differe