ライフサイエンスコーパス: heparin

1 tional units bid or therapeutic unfractioned heparin).

2 te propagation similarly to standard porcine heparin.

3 hyperglycemic stress, which was inhibited by heparin.

4 G1 - vehicle, G2 - rhC1INH+heparin, and G3 - heparin.

5 in vitro in the absence of additives such as heparin.

6 e a cellulose-based photoacoustic sensor for heparin.

7 ce were resistant to thromboprophylaxis with heparin.

8 ompared to "state-of-the art" treatment with heparin.

9 in decreased binding affinity of SCR6-8 for heparin.

10 conformation that promotes association with heparin.

11 (89%) were treated with low-molecular-weight heparin.

12 d in WT mice, and restored responsiveness to heparin.

13 ructure of EEEV complexed with the HS analog heparin.

14 isorder affecting 1-5% of patients receiving heparin.

15 onstrating the need for alternate sources of heparin.

16 that all tested TcAs bind negatively charged heparins.

17 (8 kDa) has a higher affinity for PCV2 than heparin (12 kDa), chondroitin sulfate B (41 kDa), hyalur

18 th vitamin K antagonists (48.4%), parenteral heparins (27.7%), and direct oral anticoagulants (22.6%)

19 iduals that could be restored by addition of heparin, a GAG similar to heparan sulfate.

20 latively small subset of GAGs - particularly heparin, a readily available, promiscuously-binding GAG.

21 This interaction is blocked by heparin, a sulfated glycosaminoglycan.

22 om hourly activated clotting time to anti-Xa heparin activity assay every 6 hours with an associated

23 tivated clotting time assay with the anti-Xa heparin activity assay for heparin monitoring during ext

24 Minimum anti-Xa heparin activity assay levels of 0.25 U/mL were associat

25 tion from activated clotting time to anti-Xa heparin activity assay monitoring and the associated cli

26 iation with reduced circuit changes, anti-Xa heparin activity assay monitoring was also associated wi

27 he 4 years, patients with an average anti-Xa heparin activity assay of at least 0.25 U/mL showed a 59

28 are needed to determine the optimum anti-Xa heparin activity assay therapeutic range during extracor

29 on using activated clotting times to anti-Xa heparin activity assays.

30 Heparin administration for venous thromboembolism (VTE)

31 Cytokine-profiling analyses revealed that heparin affected the level, but not the type, of cytokin

32 in the absence of denaturation and fixation, heparin-affinity chromatography, and high-resolution LC-

33 grafts containing VEGF and those containing heparin alone.

34 Heparin also significantly reduced the EC(50) value of h

35 the interaction between the PCV2 capsid and heparin, an analog of heparan sulfate, to better than 3.

36 first example where the interaction between heparin and an icosahedral capsid does not follow the sy

37 While all strains directly bound to heparin and chondroitin sulfate in enzyme-linked immunos

38 -083 in vitro revealed its high affinity for heparin and extracellular matrix while surface plasmon r

39 Heparin and heparan sulfate antagonize the binding of th

40 binds most strongly to longer GAG chains of heparin and heparan sulfate.

41 A series of applications for heavy heparin and its heavy biosynthetic intermediates are dem

42 ivity was previously shown to be enhanced by heparin and other sulfated glycosaminoglycans.

43 ng of Vn to IsdB was specifically blocked by heparin and reduced at high ionic strength.

44 e of fibril formation in the presence of LMW-heparin and slowing the rate at higher concentrations.

45 cantly impairs binding of y+z+ agrin to both heparin and the low-density lipoprotein receptor-related

46 nally, we visualized the interaction between heparin and the PCV2 capsid using cryo-electron microsco

47 intestinal submucosa (SIS) immobilized with heparin and vascular endothelial growth factor (VEGF) co

48 ate implantability of submillimeter diameter heparin and VEGF-decorated A-TEVs in a mouse model and d

49 ticoagulants, primarily low-molecular-weight heparin and warfarin, are used to treat children with sy

50 m) or high glucose (25.6 mm) with or without heparin, and analyzed for glucose uptake.

51 nylaspartate diglyceride) (PEAD) polycation, heparin, and cargo insulin-like growth factor-1 (IGF-1),

52 treatment groups: G1 - vehicle, G2 - rhC1INH+heparin, and G3 - heparin.

53 olved in imparting anticoagulant activity to heparin, and HS3ST3A1, another glucosaminyl 3-O-sulfotra

54 ole in binding to several glycans, including heparin, and identify interactions of NHBA with both gon

55 cs, neurotoxins, the pesticide paraquat, and heparin anti-coagulants by the PK approach.

56 t- and second-line immunoassays for anti-PF4/heparin antibodies is accurate for ruling in or out HIT

57 ssays detecting anti-platelet factor 4 (PF4)/heparin antibodies, derived a diagnostic algorithm with

58 d PF4/heparin binding to platelets, anti-PF4/heparin antibody binding to PF4/heparin complexes, and a

59 nding to PF4/heparin complexes, and anti-PF4/heparin antibody-induced platelet activation as a result

60 ring with PF4/heparin complexes and anti-PF4/heparin antibody-platelet interaction, thus explaining d

61 cium level of 1.0 to 1.40 mg/dL, or systemic heparin anticoagulation (n = 296), which consisted of a

62 ith regional citrate, compared with systemic heparin anticoagulation, resulted in significantly longe

63 When applied to a paradigmatic heparin/antithrombin system, the new method generates a

64 Heparan sulfate and heparin are highly acidic polysaccharides with a linear

65 itamin K antagonists or low molecular weight heparins are still alternatives to DOACs for the treatme

66 and a ternary complex can be generated using heparin as a scaffold.

67 th IL-12 family cytokines and for the use of heparin as an immunomodulatory agent.

68 gulation strategy with either bivalirudin or heparin as monotherapy in this patient group.

69 approach could have applications in bed-side heparin assays for continuous heparin monitoring.

70 uine, azithromycin, and low-molecular-weight heparin at anticoagulant dose.

71 orming even stronger attraction with PRM(5), heparin at low concentrations partitioned heavily into t

72 This manuscript reports the use of a heparin-based complex coacervate to deliver IL-12, in wh

73 nding protein [fHbp]-GNA2091, and Neisserial heparin binding antigen [NHBA]-GNA1030).

74 ial reduction in gelatinolytic and TNF-alpha/heparin binding epithelial growth factor shedding activi

75 We further show that IL-37 is a heparin binding protein that modulates this self-associa

76 Heparin binding stabilizes LPL helices, and the presence

77 Fibronectin also inhibited PF4/heparin binding to platelets, anti-PF4/heparin antibody

78 current study, we investigate the neisserial heparin-binding antigen (NHBA) of N. gonorrhoeae and con

79 ctor H-binding protein (fHbp) and Neisserial Heparin-Binding Antigen (NHBA), two major antigens inclu

80 ssembles into a nonamer in its high-affinity heparin-binding conformation.

81 Human interleukin-12 (hIL-12) is a heparin-binding cytokine whose activity was previously s

82 ndothelial growth factor (VEGF)(165) and its heparin-binding domain (HBD) with the signaling receptor

83 owth factor-BB (PDGF-BB), mainly through the heparin-binding domain (HBD) within the VWF A1 domain.

84 he C-terminal domain of the alpha-chain, the heparin-binding domain on the beta-chain, and other func

85 ts identified a binding site in FN's primary heparin-binding domain.

86 he NTHi interactome mainly targeted multiple heparin-binding domains of laminin.

87 e method also facilitated the mapping of the heparin-binding domains, making it possible to predict t

88 idermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pat

89 was to determine the role of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) in the b

90 Overexpression of one such ligand, soluble heparin-binding EGF-like growth factor (sHB-EGF), also s

91 s the substrate selectivity of ADAM17 toward Heparin-binding epidermal growth factor like growth fact

92 tigated the efficacy of locally administered heparin-binding epidermal growth factor-like growth fact

93 growth factor receptor (EGFR) ligand HBEGF (heparin-binding epidermal growth factor-like growth fact

94 Midkine is a heparin-binding growth factor, originally reported as th

95 The mycobacterial heparin-binding hemagglutinin (HBHA) is a protein Ag wit

96 Heparin-binding hemagglutinin (HBHA), a surface protein

97 omplex coacervate to deliver IL-12, in which heparin-binding motifs on IL-12 allow for its effective

98 Unlike the heparin-binding paracrine FGFs, eFGFs require a unique K

99 that are capable of antagonizing binding of heparin-binding pathogens to HSPGs.

100 Heparin-binding peptides (HBPs) are suitable nonanticoag

101 ssity, and therapeutic interventions such as heparin-binding peptides (HBPs), which are used for othe

102 The neutrophil heparin-binding protein (HBP) is an inflammatory mediato

103 we characterized one of the newly-discovered heparin-binding proteins, C-type lectin 14a (CLEC14A), a

104 eins, including many previously unidentified heparin-binding proteins.

105 ular modeling and mutagenesis, we mapped its heparin-binding site.

106 g it possible to predict the location of the heparin-binding site.

107 with different laminin isoforms via multiple heparin-binding sites.

108 While the enzymes involved in heparin biosynthesis are identical to those for heparan

109 preserve the chemical diversity displayed by heparin by allowing the longer and structurally diverse

110 not on ATP concentration and is inhibited by heparin, caffeine, and 2-aminomethoxydiphenyl borate (2-

111 Both ACE2 and heparin can bind independently to spike protein in vitro

112 igate PF4 interactions with relatively short heparin chains (up to decasaccharides).

113 Enzymatic lysis of the protein-bound heparin chains followed by the product analysis using si

114 Here we construct heparin-coated 3D-printed hydrogel scaffolds seeded with

115 0, TNFalpha, and decreased levels of leptin, heparin cofactor 2, and serum paraoxonase were associate

116 NA-positive and protein-rich fractions after heparin column separation, still had immune-inducing cap

117 needed to verify the safety and efficacy of heparin compared with other methods for VTE prevention.

118 PF4/heparin-specific IgG production upon PF4/heparin complex challenge.

119 tatically driven LLPS represented by tau-RNA/heparin complex coacervation (LLPS-ED).

120 duced platelet activation as a result of PF4/heparin complex disruption.

121 dentify a plasma factor interfering with PF4/heparin complexes and anti-PF4/heparin antibody-platelet

122 ts, anti-PF4/heparin antibody binding to PF4/heparin complexes, and anti-PF4/heparin antibody-induced

123 This sensor is an excellent to detect low heparin concentration (from 25 ng/ml to 3 mug/ml) using

124 s and 3 min for plasma samples regardless of heparin concentration.

125 otein-heparin interactions vary at different heparin concentrations.

126 Perfusion of porcine kidneys with heparin conjugate during HMP reduces preservation injury

127 the renal arteries in porcine kidneys with a heparin conjugate during hypothermic machine perfusion (

128 cleavage of anti-PF4/H IgG by IdeS abolishes heparin-dependent cellular activation induced by HIT ant

129 titration calorimetry assays, we found that heparin-dependent modulation of hIL-12 function correlat

130 reduced, and sc5B9 was also unable to induce heparin-dependent platelet activation.

131 which fully abolished the ability to induce heparin-dependent platelet aggregation and tissue factor

132 ether the benefits and harms associated with heparin differ by cancer type is unclear.

133 served that the interaction between PCV2 and heparin does not adhere to the icosahedral symmetry of t

134 lementation of antithrombin did not decrease heparin dose (13.5 international units/kg/hr [9.6-17.9 i

135 rom 11 +/- 4 to 2 +/- 1 (p < 0.001), smaller heparin dose changes (less variation in dose), and reduc

136 monitoring was also associated with reduced heparin dose changes per day from 11 +/- 4 to 2 +/- 1 (p

137 brane oxygenation for respiratory failure on heparin dose, adequacy of anticoagulation, and safety.

138 , whereas platelet count, coagulation tests, heparin dose, and thrombotic events were not.

139 om 2015 to 2018, we switched from monitoring heparin during extracorporeal membrane oxygenation using

140 Indeed, addition of heparin enhanced the rate of procollagen cleavage by mat

141 n micrographs of spike protein suggests that heparin enhances the open conformation of the RBD that b

142 was variable, holding warfarin and starting heparin/enoxaparin/bivalirudin bridge was most common (6

143 Moreover, heparin-exposed patients vary considerably with respect

144 However, in vitro heparin-fibrillized 2N4R tau, which contains all four mi

145 previously treated with low-molecular weight heparin, fondaparinux, or a vitamin K antagonist for at

146 es of anticoagulants: vitamin K antagonists, heparins, fondaparinux, thrombin inhibitors and factor X

147 recently compared with low-molecular-weight heparin for the management of acute cancer-associated th

148 al anticoagulant versus low-molecular-weight heparin for treatment of venous thromboembolism in cance

149 3 groin hematomas (1 of them due to needing heparin for venous thrombosis, none required interventio

150 nt COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat

151 s; 4139 included in the low-molecular-weight heparin group and 4139 in the control group).

152 h available data in the low-molecular-weight heparin group compared with 279 (7.1%) of 3957 in the co

153 on and 88 (2.1%) in the low-molecular-weight heparin group, and minor bleeding events in 478 (12.1%)

154 In the regional citrate group vs systemic heparin group, median filter life span was 47 hours (int

155 Compared with the systemic heparin group, the regional citrate group had significan

156 of 3937 patients in the low-molecular-weight heparin group.

157 es compared with the no post-PCI infusion or heparin groups.

158 eric, oppositely charged protein constructs; heparin (H), an anionic polymer; and lysozyme (L), a cat

159 he promoter regions of all genes involved in heparin/heparan sulfate assembly uncovered a transcripti

160 High-affinity binding of heparin/heparan sulfate to the Ig-like domain may procee

161 Docking studies suggest a heparin/heparan sulfate-binding site adjacent to the ACE

162 Here, we identify heparins/heparan sulfates and Lewis antigens as receptor

163 nd Xenorhabdus nematophila XptA1 reveal that heparins/heparan sulfates unexpectedly bind to different

164 Unfractionated heparin, non-anticoagulant heparin, heparin lyases, and lung heparan sulfate potent

165 ic granules) and mediator content (including heparin, histamine, and neutral proteases), test cells a

166 To investigate a modulating risk for PF4/heparin immunization and breakthrough of HIT, we also te

167 considerably with respect to the risk of PF4/heparin immunization and, among antibody-positive patien

168 isk of thrombosis extends beyond exposure to heparin implicating other PF4 partners.

169 possibility of bioengineering anticoagulant heparin in cultured cells.

170 h molecular modeling also allows the role of heparin in destabilizing the ACE2/RBD association to be

171 ALIDATE-SWEDEHEART trial (Bivalirudin Versus Heparin in ST-Segment and Non-ST-Segment Elevation Myoca

172 ed anticoagulant, low-molecular-weight (LMW) heparin, in the initiation and subsequent aggregation ph

173 Of note, heparin increased the anti-inflammatory markers arginase

174 t study investigated the mechanisms by which heparin increases hIL-12 activity.

175 n protein secondary structure during pH- and heparin-induced fibril formation of apolipoprotein A-I (

176 The Kappa coefficient between heparin-induced multiple electrode aggregometry and the

177 ced thrombocytopenia diagnosis as reference, heparin-induced multiple electrode aggregometry showed a

178 Heparin-induced multiple electrode aggregometry was asse

179 rbent assay, the serotonin release assay and heparin-induced multiple electrode aggregometry.

180 topenia diagnosis in ICU patients, known as "heparin-induced multiple electrode aggregometry." DESIGN

181 as recently shown that zinc ions accelerated heparin-induced oligomerization of Tau constructs.

182 r a positive gold standard functional assay (heparin-induced platelet activation [HIPA]).

183 The heparin-induced tau filaments differ from those of Alzhe

184 al describe a novel diagnostic algorithm for heparin-induced thrombocytopenia (HIT) based on the 4Ts

185 Heparin-induced thrombocytopenia (HIT) is a prothromboti

186 Prompt diagnostic evaluation of suspected heparin-induced thrombocytopenia (HIT) is critical for g

187 ermine spectral markers for the diagnosis of heparin-induced thrombocytopenia (HIT), a difficult-to-d

188 aggregates implicated in the development of heparin-induced thrombocytopenia (HIT), a potentially fa

189 odies to platelet factor 4 (PF4) involved in heparin-induced thrombocytopenia (HIT), beta-2-glycoprot

190 electrode aggregometry was assessed against heparin-induced thrombocytopenia diagnosis (clinical pic

191 Using heparin-induced thrombocytopenia diagnosis as reference,

192 pid and easy to perform functional assay for heparin-induced thrombocytopenia diagnosis in ICU patien

193 Heparin-induced thrombocytopenia had no effect on mortal

194 The frequency of heparin-induced thrombocytopenia in extracorporeal membr

195 al density threshold less than 1 to rule out heparin-induced thrombocytopenia in patients on extracor

196 ith (6/19, 31.6%) or without (89/279, 32.2%) heparin-induced thrombocytopenia in patients on extracor

197 There was no difference in prevalence of heparin-induced thrombocytopenia in patients on venoveno

198 the Pretest Probability Score in identifying heparin-induced thrombocytopenia in patients post cardio

199 Heparin-induced thrombocytopenia is a recognized concern

200 Heparin-induced thrombocytopenia is more frequent in bot

201 unosorbent assay optical density thresholds, heparin-induced thrombocytopenia negative was defined as

202 ined as an optical density less than 1.0 and heparin-induced thrombocytopenia positive as an optical

203 Pretest Probability Score and heparin-induced thrombocytopenia testing results were co

204 of Pretest Probability Score in identifying heparin-induced thrombocytopenia was lower in extracorpo

205 may aid clinicians in objectively ruling out heparin-induced thrombocytopenia without sending a confi

206 ee patients (23.1%) had laboratory-confirmed heparin-induced thrombocytopenia, and all of them develo

207 The glycosaminoglycan heparin inhibits mesangial cell growth, but the molecula

208 ia also accumulate intracellular HA and that heparin inhibits the HA accumulation.

209 w numbers, lending support to a model of PF4/heparin interaction in which the latter wraps around the

210 an sulfate moieties, indicating that protein-heparin interactions vary at different heparin concentra

211 transitions and simultaneously characterize heparin interactions.

212 bout the specific molecular mechanism of PF4-heparin interactions.

213 Association of platelet factor 4 (PF4) with heparin is a first step in formation of aggregates impli

214 Heparin is a fractionated form of heparan sulfate derive

215 The destabilizing effect of heparin is more pronounced in the case of the longer cha

216 However, heparin is not ideal for managing chronic neurodegenerat

217 Heparin is the most widely prescribed biopharmaceutical

218 Indeed, heparin-like molecules, or heparinoids, have previously

219 bleeding compared with low-molecular-weight heparin (LMWH) in patients with GI and potentially genit

220 Low molecular weight heparin (LMWH) in therapeutic doses is the treatment of

221 be good alternatives to low molecular weight heparin (LMWH) or vitamin K antagonists (VKA) for treatm

222 Low molecular weight heparin (LMWH; standard prophylactic dose, 28-35 days) r

223 and safety of DOACs and low-molecular-weight heparins (LMWHs) in these patients.

224 hance of being cost-effective, compared with heparin locks in the hemodialysis setting, an 88.00% cha

225 tionated heparin, non-anticoagulant heparin, heparin lyases, and lung heparan sulfate potently block

226 In contrast, in grafts containing only heparin, MCs converted primarily into M1-M s, and the en

227 ed by relatively short polyanions (synthetic heparin-mimetic pentasaccharide), with the majority of t

228 veral allosteric plasmin inhibitors based on heparin mimetics have been developed.

229 red with no or low-dose post-PCI infusion or heparin (Minimizing Adverse Haemorrhagic Events by TRans

230 Specifically, only heparin molecules longer than eight saccharide units enh

231 From 2015 to 2018, heparin monitoring during extracorporeal membrane oxygen

232 with the anti-Xa heparin activity assay for heparin monitoring during extracorporeal membrane oxygen

233 exists on the optimal method or targets for heparin monitoring.

234 ns in bed-side heparin assays for continuous heparin monitoring.

235 nts were randomized to either bivalirudin or heparin monotherapy during percutaneous coronary interve

236 Therefore, we compared bivalirudin to heparin monotherapy in a contemporary cohort of such pat

237 found in the elderly between bivalirudin and heparin monotherapy regarding the primary end point (180

238 s were equal between bivalirudin (n=799) and heparin (n=793) treated patients >=75 years.

239 of antithrombin might decrease the amount of heparin needed to achieve a given anticoagulation target

240 Unfractionated heparin, non-anticoagulant heparin, heparin lyases, and

241 ave not been explored without confounding by heparin nor has their relationship to myocardial protein

242 n with longer and structurally heterogeneous heparin oligomers (decamers).

243 ride) and relatively long (eicosasaccharide) heparin oligomers form 1:1 complexes with RBD, indicatin

244 pitopes" within the limited subsets of short heparin oligomers produced either enzymatically or synth

245 explained by a stimulatory effect of plasma heparin on antithrombin.

246 sed controlled trials examines the effect of heparin on survival, venous thromboembolism, and bleedin

247 rst example of an asymmetric distribution of heparin on the surface of an icosahedral virus capsid.

248 ameworks for the chemoenzymatic synthesis of heparin or HS analogs.

249 omplexes between platelet factor 4 (PF4) and heparin or other polyanions, but the risk of thrombosis

250 equivalent dose or standard anticoagulants (heparin or switched to vitamin K antagonist).

251 a fully O-sulfated alpha-methyl glycoside of heparin pentasaccharide motif known to interact with the

252 inflammation, liver failure, anticoagulants (heparins, phenprocoumon, apixaban), and antiplatelet med

253 or inhibition of viral adhesion by exogenous heparin presents new therapeutic opportunities.

254 NF263 in mast cells compared with other (non-heparin-producing) immune cells.

255 Heparin prophylaxis was associated with an increased ris

256 Furthermore, electrostatics may rescue the heparin/protein interaction in the absence of the canoni

257 G(1) phase in normal glucose with or without heparin rapidly cease glucose uptake.

258 Low-molecular-weight heparin reduces risk of venous thromboembolism without i

259 nalyses provide high-certainty evidence that heparin reduces the risk of symptomatic venous thromboem

260 Anticoagulation with unfractionated heparin remains the most common therapy used to prevent

261 The primary outcome was the total amount of heparin required to maintain activated partial thrombopl

262 ntithrombin supplementation may not decrease heparin requirement nor diminish the incidence of bleedi

263 f hIL-12 function correlates with several of heparin's biophysical characteristics, including chain l

264 de a foundation for further investigation of heparin's interactions with IL-12 family cytokines and f

265 ic repulsion between the low-pI ACE2 and the heparin segments not accommodated on the RBD surface.

266 ytosis patients, DAO is likely released from heparin-sensitive gastrointestinal storage sites.

267 ose a model of hIL-12 stabilization in which heparin serves as a co-receptor enhancing the interactio

268 -observed platelet-recruitment reduction and heparin-size modulation, upon establishment of DNA-vWF i

269 Rag1-deficient recipients also produced PF4/heparin-specific Abs spontaneously.

270 tional Treg cells spontaneously produced PF4/heparin-specific Abs.

271 ell-specific deletion of IL-10 increased PF4/heparin-specific IgG production upon PF4/heparin complex

272 This approach was validated with heparin-spiked whole human blood and had a linear correl

273 Our results revealed that LMW-heparin strongly promotes WT-hbeta(2)m fibrillogenesis d

274 bind to C4S, but not chondroitin-6-sulfate, heparin sulfate or dermatan sulfate, in a concentration-

275 llularly in an isoform-dependent manner by a heparin sulfate proteoglycan-dependent mechanism.

276 adulterated material was introduced into the heparin supply chain, resulting in several hundred death

277 Therapeutic anticoagulation with heparin (target activated partial thromboplastin time be

278 and systemic treatment with either LMW-DS or heparin, targeting an activated partial thromboplastin t

279 In the presence of heparin, the monovalent Fab shows essentially no inhibit

280 n attenuation of the ACE2/RBD association by heparin, the study demonstrates the yet untapped potenti

281 Higher doses of heparin to achieve therapeutic activated clotting times

282 sis, and proteinurea, which are inhibited in heparin-treated diabetic rats.

283 ype identified the most certain benefit from heparin treatment in patients with lung cancer (RR 0.59

284 We conclude that heparin treatment of high glucose-exposed dividing BMDMs

285 up) or blood cultures first and then lithium heparin tube (control group).

286 up) or blood cultures first and then lithium-heparin tube (control group).

287 was either aspirated into a sterile lithium heparin tube before blood culture bottles (diversion gro

288 was either aspirated into a sterile lithium-heparin tube before blood culture bottles (diversion gro

289 lood obtained at venipuncture into a lithium heparin tube prior to aspiration of blood culture reduce

290 Use of lithium-heparin tubes for diversion prior to obtaining blood cul

291 Use of lithium heparin tubes for diversion prior to obtaining blood cul

292 Standard of care (low-molecular-weight heparins, unfractionated heparin, vitamin K antagonists

293 stin time between 50 and 70 s) or lower dose heparin (up to 12,000 U/24 hr aiming for activated parti

294 of N-MADD-4B with NLG-1 is also disrupted by heparin, used as a surrogate for the extracellular matri

295 ow-molecular-weight heparins, unfractionated heparin, vitamin K antagonists or fondaparinux) was comp

296 Therapy with low-molecular-weight heparin, vitamin K antagonists, and direct-acting antico

297 ion and fibrin formation induced by 5B9 with heparin was strongly reduced after IdeS treatment.

298 lectin domain of CLEC14A binds one-to-one to heparin with nanomolar affinity, and using molecular mod

299 interactions of glycosaminoglycans (such as heparin) with proteins remains challenging due to their

300 oral Xa inhibitors over low-molecular-weight heparin, with gastrointestinal lesions being a relative