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Intraperitoneal sepsis was induced by using the infected fibrin thrombin clot model.
Intraperitoneal sepsis was induced with the infected fibrin thrombin clot model described by Mathiak and colleagues [ 8].
The study demonstrated that after incubation, different concentrations of CAPE led to fibrinolytic activity in the human blood clot model.
The present study aims at comparing mono- and bifrequency excitations both in terms of thrombolytic efficiency for an in vitro blood clot model and in terms of heating of tissue in the focal region.
The thrombolysis efficiency of a bifrequency excitation consisting in two high neighbouring frequency components has been tested on an in vitro blood clot model and compared to the thrombolysis efficiency of a monofrequency excitation of the same ultrasound intensity.
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To better understand the regulatory role of the PGC family in the complex process of mitochondrial biogenesis during the acute inflammatory response, we used an established fibrin-clot model of S. aureus sepsis to test the hypothesis that TLR signaling leads to downstream regulation of the PGC family of genes.
In addition, in the tail-clot model described above, RACPPNleTPRSFL (25) gave a Cy5/Cy7 ratio increase from 0.75 ±0.11) at one minute to 3.1 ±0.45) at five minutes post injury (n = 3, p = 0.01; Figure 4 b) compared to no significant change in Cy5/Cy7 ratio for RACPPPPRSFL over the same time interval.
The purpose of this study was to evaluate the efficacy of antiplatelet loading and the effects of endogenous estrogen on stroke outcome in female subjects in the rabbit small clot embolic model (RSCEM).
The purpose of this proof-of-concept study was to evaluate the medicating effects of estrogen in the efficacy of acute antiplatelet loading therapy on stroke outcome in the rabbit small clot embolic model.
Therefore, without a pressure-driving factor, tissue-plasminogen activator (t-PA) encapsulated in PLGA NPs with chitosan (CS) and CS-GRGD coating and their thrombolysis capabilities in a blood clot-occluded tube model were evaluated by determining clot lysis times and the masses of the digested clots.
The picture reminds me of a paper I read a couple of weeks ago, using similar techniques to model clot trajectories in the case of atrial fibrillation and ischaemic stroke.
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Justyna Jupowicz-Kozak
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