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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

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