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2 proximately twice normal clotting times in a platelet factor 3 availability assay and, in a prothromb
7 two positively acting sequences in the human platelet factor 4 (hPF4) gene promoter that synergized t
8 ed a panel of HDPs and determined that human platelet factor 4 (hPF4) kills malaria parasites inside
10 antimicrobial peptides from human platelets: platelet factor 4 (PF-4), RANTES, connective tissue acti
12 APC) improves survival in severe sepsis, and platelet factor 4 (PF4) accelerates APC generation in a
13 that monocytes complexed with surface-bound platelet factor 4 (PF4) activated by HIT antibodies cont
15 mediated by antibodies to complexes between platelet factor 4 (PF4) and heparin or cellular glycosam
16 antibodies that recognize complexes between platelet factor 4 (PF4) and heparin or glycosaminoglycan
19 oss-linking of Fc gamma RIIA by anti-heparin/platelet factor 4 (PF4) antibodies is central to the pat
23 uires detection of antibodies to the heparin/platelet factor 4 (PF4) complexes via enzyme-linked immu
32 e estrogen receptor under the control of the platelet factor 4 (PF4) megakaryocyte-specific promoter.
35 xes between unfractionated heparin (UFH) and platelet factor 4 (PF4) that form over a narrow molar ra
36 tight electrostatic binding of the chemokine platelet factor 4 (PF4) to polyanions induces heparin-in
38 fic for complexes formed between heparin and platelet factor 4 (PF4), a basic protein found normally
44 we used the megakaryocyte-specific promoters platelet factor 4 (PF4), and glycoprotein IIb (GPIIb) as
46 sorder caused by immune complexes containing platelet factor 4 (PF4), antibodies to PF4 and heparin o
47 exes of platelet activation: platelet count, platelet factor 4 (PF4), beta-thromboglobulin (beta-TG),
50 by four essential components--heparin (Hep), platelet factor 4 (PF4), IgG antibodies against the Hep-
51 neutrophils and have a structure similar to platelet factor 4 (PF4), in which the first two cysteine
57 ients with HIT develop autoantibodies to the platelet factor 4 (PF4)/heparin complex, which is termed
60 h patients tested strongly positive for anti-platelet factor 4 (PF4)/heparin immunoglobulin (Ig)G in
63 ility that immune complexes formed following platelet factor 4 (PF4/CXCL4) binding to anti-PF4 antibo
64 onstrate that the platelet-derived chemokine platelet factor 4 (PF4/CXCL4) stimulates VSMC injury res
65 and effectiveness of intravenous recombinant platelet factor 4 (rPF4) as an alternative to protamine
67 s overexpression in transgenic mice (via the platelet factor 4 [PF4] promoter) on megakaryocyte devel
68 ting (IL-3) and growth-inhibitory (MIP-1 and platelet factor 4 [PF4]) cytokines, and extracellular ma
69 ration (glycoprotein [GP] Ibalpha, GPIX, and platelet factor 4 [PF4]), whereas GABPalpha-deficient me
70 iomarkers (fractalkine, platelet P-selectin, platelet factor 4 [PF4], and tumor necrosis factor-alpha
71 nfirmed HIT (4Ts score >/=4 points; positive platelet factor 4 [PF4]/heparin immunoassay, positive se
72 rollary of these concepts is that disrupting platelet factor 4 and beta(2)GPI conformation (or ultral
73 and analyzed for sCD40L, interleukin-6, and platelet factor 4 and beta-thromboglobulin (markers of p
76 re more cognitively impaired, and had higher platelet factor 4 and beta-thromboglobulin levels; cardi
77 gin as other markers of platelet activation, platelet factor 4 and beta-thromboglobulin, were not inc
79 th antibodies to complexes that form between platelet factor 4 and glycosaminoglycan (GAG) side chain
81 Platelet-transported inflammatory mediators platelet factor 4 and serotonin accumulated in the graft
83 ts demonstrated that P-selectin, fibrinogen, platelet factor 4 and vascular endothelial growth factor
86 n has improved in recent years, with heparin-platelet factor 4 complex as the culprit antigen in most
87 shown that antibodies reactive with heparin-platelet factor 4 complexes lead to FcgammaRIIA-mediated
89 7082, or TPCA-1) or by genetic manipulation (platelet factor 4 Cre:IKK-beta(flox/flox)), blocked SNAP
92 lasmic maturation (ie, glycoprotein GPIb and platelet factor 4 expression) and reduced the ability of
95 in the absence of clinical disease, such as platelet factor 4 in heparin-induced thrombocytopenia an
96 by determination of beta-thromboglobulin and platelet factor 4 in the supernatants, platelets bound t
97 0, monokine induced by gamma interferon, and platelet factor 4 inhibit epidermal growth factor (EGF)-
100 (MIP-1beta), MIP-2, and KC (a member of the platelet factor 4 neutrophil chemoattractant family), as
101 kine C-X-C motif ligand 4 (CXCL4, also named platelet factor 4 or PF4) in the bone marrow, and we fou
106 neration, platelet-derived growth factor and platelet factor 4 release, incorporation of thrombin int
107 hemokines, monokine induced by IFN-gamma and platelet factor 4 that also generate cAMP, inhibited EGF
109 n PEDF and TSP-1 but did contain IGFBP-1 and platelet factor 4 while significantly suppressing neovas
111 l expressed and secreted, RANTES) and CXCL4 (platelet factor 4) to the monocyte surface and endotheli
112 CL4L1, is a homologue of CXCL4 chemokine (or platelet factor 4) with potent anti-angiogenic activity
113 kines, PBP (platelet basic protein) and PF4 (platelet factor 4), are within 5.3 kilobases (kb) of eac
114 subjects with severe asthma, whereas plasma platelet factor 4, a second platelet activation marker,
115 correlated with plasma levels of P-selectin, platelet factor 4, and platelet basic protein in the pop
116 ble factors serotonin (5-hydroxytryptamine), platelet factor 4, and platelet-activating factor, which
118 e Western blotting of factor V, prothrombin, platelet factor 4, antithrombin III, and fibrinogen.
121 role for platelets and their products (e.g., platelet factor 4, beta-thromboglobulin, RANTES, thrombo
122 0, monokine induced by interferon gamma, and platelet factor 4, limit fibroblast responsiveness to gr
123 osaccharides also exhibit low binding toward platelet factor 4, raising the possibility of preparing
124 well as platelet-derived molecules including platelet factor 4, serotonin, P-selectin, and CD154 (CD4
126 tibodies show several similarities with anti-platelet factor 4-heparin antibodies and are a potential
131 t is for GAG, its binding is not competed by platelet factor 4/CXCL4, and it is present on cells that
132 ted with a high incidence of IgG Abs against platelet factor 4/heparin (PF4/H) complexes by day 6 aft
133 a 4Ts score, rapid particle gel immunoassay (platelet factor 4/heparin [PF4/H]-PaGIA), and serotonin-
137 due primarily to IgG antibodies specific to platelet factor 4/heparin complexes (PF4/Hs) that activa
138 PRT/H Abs showed no cross-reactivity to platelet factor 4/heparin complexes, but were cross-reac
140 P483H contains the heparin-binding region of platelet factor-4 (PF-4) and a lysine-rich sequence for
141 evidence that changes in platelet-associated platelet factor-4 (PF-4) detect malignant growth across
142 rostate specific membrane antigen (PSMA) and platelet factor-4 (PF-4) in serum were captured on the a
143 , prostate specific membrane antigen (PSMA), platelet factor-4 (PF-4), and interleukin-6 (IL-6) simul
145 g to provide direct evidence that tetrameric platelet factor-4 (PF4) and dimeric interleukin-8 (IL8),
146 -10, macrophage-derived chemokine [MDC], and platelet factor-4 [PF-4]) to be expressed by CD34(+) cel
148 , including neutrophil-activating protein-2, platelet factor-4, RANTES, and macrophage chemotactic pr
149 tment with rhMIP-1 beta or rhRANTES, but not platelet factor-4, resulted in improved thymic homing of
150 otein convertase subtilisin/kexin type 9 and platelet factor-4, whereas they had a minimal inhibitory
151 wth-related protein-alpha (Gro-alpha) and to platelet factor-4-M2 (PF4-M2), an N-terminal chimera of
153 secretion of [3H]-5HT (dense core granules), platelet factor IV (alpha granules), or hexosaminidase (
155 crophage inflammatory protein (MIP)-1 alpha, platelet factor (PF) 4, interferon inducible protein (IP
156 kDa proteins were subsequently identified as platelet factor (PF)4 and connective tissue activating p
162 sts may in addition be the result of reduced platelet factor Va expression and modulation of the plat
165 y led to platelet aggregation and release of platelet factors which would trigger the proliferation o
166 r collagen at various concentrations exposed platelet factor XI and PAC1 antibody binding in parallel
175 he outer surface of growing thrombi, such as platelet factor XI or blood-borne TF, appears essential
177 B subunit of factor XIII since placental or platelet factor XIII (A2), which does not contain B subu
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