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1  PAI-1-deficient mice (PAI-1 -/-; n=11) with ferric chloride.
2 iron source, but retained the ability to use ferric chloride.
3 ith LDA followed by oxidation with anhydrous ferric chloride.
4 y oxidation with dilute aqueous solutions of ferric chloride.
5 al over a 24-h period following injection of ferric chloride.
6 wing mesenteric arteriolar injury induced by ferric chloride.
7 the growth medium was amended with 25 microM ferric chloride.
8 ts investigated were: (1) 10% citric acid/3% ferric chloride, (2) 10% maleic acid, (3) 2.5% nitric ac
9 ere compared to particles formed from dosing ferric chloride, a common water treatment coagulant.
10 asein fractions, even at the lowest level of ferric chloride addition (5mM).
11 sulting solutions from Fe(VI) self-decay and ferric chloride addition in borate- and phosphate-buffer
12 ed to a carotid artery injury assay in which ferric chloride administration induces de-endothelializa
13   Reaction of carbaporphyrin 4a with aqueous ferric chloride afforded the corresponding 21-chloro der
14 e exteriorized mesentery was superfused with ferric chloride and the accumulation of fluorescently la
15 d acenaphthylene ring was also oxidized with ferric chloride and this produced a ketal derivative wit
16 erated, but animal growth was stunted in the ferric chloride animals compared with the control group.
17  either intra-arterial thrombin injection or ferric chloride application followed by measurement of c
18        Sprague-Dawley rats (n = 7) underwent ferric chloride application on the femoral vein to trigg
19 travenous infusion and induced thrombosis by ferric chloride application to the carotid artery (high
20 sein-iron precipitates were formed by adding ferric chloride at >/=10mM to sodium caseinate solutions
21                               The effects of ferric chloride, at two concentration levels (100 and 50
22  HBC is achieved in a one-pot reaction using ferric chloride both as a Lewis acid catalyst and as an
23  demonstrated antithrombotic effects in both ferric chloride carotid artery and laser-induced microva
24 (n=10) formed stable occlusive thrombi after ferric chloride carotid artery injury, whereas the major
25  isomeric purities by two catalytic methods, ferric chloride-catalyzed addition of acid anhydrides to
26                                   Up to 20mM ferric chloride could be added to sodium caseinate solut
27 to the iron chelator 2,2'-dipyridyl, but not ferric chloride, demonstrated an increase in fumarase ac
28 n few-layer graphene (FLG) intercalated with ferric chloride (FeCl(3)) have an outstandingly low shee
29 e necessity to use powerful oxidants such as ferric chloride (FeCl(3)) or DDQ/H(+) for Scholl reactio
30                               Application of ferric chloride (FeCl(3)) to exposed blood vessels is wi
31 K mice were protected from occlusion with 4% ferric chloride (FeCl3) challenges compared with wild-ty
32                                              Ferric chloride (FeCl3) injury was used to induce platel
33 chanism of action of the widely used in vivo ferric chloride (FeCl3) thrombosis model remains poorly
34 et al demonstrate that thrombus formation in ferric chloride (FeCl3) thrombosis models relies on phys
35                                   By using a ferric chloride (FeCl3)-induced carotid artery injury th
36  Furthermore, using intravital microscopy to ferric chloride (FeCl3)-injured mesenteric arterioles an
37 sensitive and heat labile, and could utilize ferric chloride, ferric citrate, and human holotransferr
38 strains acquired iron from ferrous chloride, ferric chloride, ferrous sulfate, ferric ammonium citrat
39 H(2)Cl(2), followed by oxidation with DDQ or ferric chloride, gave excellent yields of corannulenopor
40 lic acid, followed by oxidation with aqueous ferric chloride, gave the targeted porphyrinoid system.
41 , and subsequent oxidation with 0.2% aqueous ferric chloride generated a series of fully conjugated n
42                              The presence of ferric chloride generated both doubly protonated and Fe(
43 e oxidation of bacteriopyropheophorbide with ferric chloride hexahydrate or its anhydrous form produc
44 roxide was less effective than freshly dosed ferric chloride in accelerating Fe(VI) decomposition.
45 nd to undergo regioselective oxidations with ferric chloride in methanol, ethanol, isopropyl alcohol,
46 y occlusion compared with WT control using a ferric chloride in vivo thrombosis model, indicating tha
47 ere investigated by ultrasound in a model of ferric chloride induced non-occlusive carotid artery thr
48     Further evaluation of mutant mice by the ferric chloride-induced arterial injury model suggests t
49                             However, using a ferric chloride-induced arterial thrombosis model, the f
50         fXII-deficient mice are resistant to ferric chloride-induced arterial thrombosis, and this re
51 ) mice but not TFPI(LysM) mice had increased ferric chloride-induced arterial thrombosis.
52 mers and offered systemic protection against ferric chloride-induced arterial thrombosis.
53                                We found that ferric chloride-induced arterial thrombus formation was
54 owed severely impaired thrombus formation on ferric chloride-induced carotid artery injury.
55  of NAC on larger vessels, we also performed ferric chloride-induced carotid artery thrombosis.
56 ced injury (0.3-3 mg/kg, iv), and guinea pig ferric chloride-induced injury (0.3-1 mg/kg, iv).
57 llular PAD4 on platelet-plug formation after ferric chloride-induced injury of mesenteric venules.
58 red the time to vessel occlusion (TTO) after ferric chloride-induced injury.
59  F8-/-/PN-1-/- mice than in F8-/-mice in the ferric chloride-induced mesenteric vessel injury model.
60                                              Ferric chloride-induced mouse mesenteric arteriolar thro
61                   Furthermore, 3F8 prevented ferric chloride-induced occlusive arterial thrombogenesi
62 il-vein bleeding test and the carotid artery ferric chloride-induced thrombosis model.
63 ndent protection from carotid occlusion in a ferric chloride-induced thrombosis model.
64 t that Par3(-/-) mice were protected against ferric chloride-induced thrombosis of mesenteric arterio
65 ling in mouse platelets and protects against ferric chloride-induced thrombosis of mouse mesenteric a
66 ant to both pulmonary thromboembolism and to ferric chloride-induced thrombosis of the carotid artery
67 y, arrestin2(-/-) mice are less sensitive to ferric chloride-induced thrombosis than WT mice, suggest
68 in a mouse hemophilia model, when assayed as ferric chloride-induced thrombosis.
69                     We found that it reduces ferric-chloride-induced experimental thrombosis in mice
70 % less seizure activity than vehicle-treated ferric chloride-injected animals, suggesting that lipoic
71 o observe the formation of platelet plugs in ferric chloride-injured arterioles of live mice.
72    Using gene-targeted mice, we show that in ferric chloride-injured veins platelet adhesion to suben
73 elets form in occluding murine thrombi after ferric chloride injury and are attenuated with megakaryo
74 ht) prevented carotid artery occlusion after ferric chloride injury in a plasminogen-dependent proces
75 e to thrombus formation determined using the ferric chloride injury model was reduced.
76 on relative to FVIII-WT in the tail clip and ferric chloride injury models in hemophilia A (HA) mice.
77 ombus-mediated flow reduction in response to ferric chloride injury of the carotid arteries was signi
78 rpin prevents thrombus formation provoked by ferric chloride injury of the carotid artery and increas
79                                              Ferric chloride injury of the midportion of the common c
80 n carotid arteries of C57Bl6 mice in vivo by ferric chloride injury were then assessed with ultrasoun
81                             At 21 days after ferric chloride injury, neointima formation in P2Y(12)(-
82 ls of arterial injury, namely ballooning and ferric chloride injury.
83 ombus formation in an in vivo carotid artery ferric chloride-injury model is significantly impaired.
84 thrombus formation was almost abolished in a ferric chloride-injury model, with only a thin layer of
85 itrile-functionalized ionic precursors and a ferric chloride mediator.
86                                            A ferric chloride model of thrombosis was used to investig
87 in VI (GPVI) and integrin alpha2beta1 in our ferric chloride murine thrombosis model.
88 y bioavailable to Trichodesmium, relative to ferric chloride or citrate-associated iron.
89        Iron, supplied as ferrous sulfate, as ferric chloride, or as holo-transferrin, was able to neg
90 dase-mediated reduction of iron in ferritin, ferric chloride, or ferric ADP.
91 hthalaldehyde in the absence and presence of ferric chloride, respectively.
92                              The addition of ferric chloride restore HER formation.
93 degrees C, followed by addition of anhydrous ferric chloride, resulted in an efficient tandem halogen
94 zed materials synthesized in the presence of ferric chloride showed higher activity and stability in
95                              The presence of ferric chloride significantly (P<0.05) affected the oxid
96 method involves an extraction with an acidic ferric chloride solution, to quantitatively convert EDTA
97  give, following oxidation with 0.1% aqueous ferric chloride solutions, a series of tropiporphyrins 9
98 ipyrrane, followed by oxidation with aqueous ferric chloride solutions, afforded moderate yields of a
99 ntadiene, followed by oxidation with aqueous ferric chloride solutions, gave 23-alkyl-21-carbaporphyr
100 f freshly precipitated ferric hydroxide from ferric chloride solutions.
101 he reaction mixture was stirred with aqueous ferric chloride solutions.
102                                    Exogenous ferric chloride suppressed these deficiencies in the apb
103 stable brown color in the presence of acidic ferric chloride that can be quantitated spectrophotometr
104      Compound 30d showed efficacy in the rat ferric chloride thrombosis model when administered intra
105      When Cbl-b(-/-) mice were tested in the ferric chloride thrombosis model, occlusion time was inc
106 rtery occlusion times on the rose bengal and ferric chloride thrombosis models.
107 onbiomimetic polyene cyclization mediated by ferric chloride to generate the generic celastroid penta
108                               As adding >5mM ferric chloride to sodium caseinate solutions results in
109                               By addition of ferric chloride to the reaction mixture, a selective aro
110  presence of HCl, followed by oxidation with ferric chloride, to give a modest yield of an azuliporph
111  presence of TFA, followed by oxidation with ferric chloride, to give a tropone-fused carbaporphyrin
112 ted group (P = 0.057), and 62.5 mg/d for the ferric chloride-treated group (P < 0.002).
113                         Platelet adhesion to ferric chloride-treated mesenteric arterioles in IL4Ralp
114 rmed in vivo by characterizing blood flow in ferric chloride-treated mouse carotid arteries.
115         Here we demonstrate that exposure to ferric chloride triggers rugose biofilm formation by the
116                                       In the ferric-chloride vasculature injury model, Abcc4 KO mice
117                                              Ferric chloride was used to induce carotid artery injury
118                   In the large-vessel model, ferric chloride was used to injure the carotid artery, a
119 hesia, unilateral intracortical infusions of ferric chloride were performed stereotaxically.
120 oncentration was overcome by the addition of ferric chloride which also contributed to the color stab

 
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