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Pribush A.,Experimental Hematology Laboratory | Pribush A.,Ben - Gurion University of the Negev | Meyerstein D.,Ben - Gurion University of the Negev | Meyerstein D.,Ariel University | Meyerstein N.,Experimental Hematology Laboratory
Colloids and Surfaces B: Biointerfaces | Year: 2010

Results reported in the companion paper showed that erythrocytes in quiescent blood are combined into a network followed by the formation of plasma channels within it. This study is focused on structural changes in the settling dispersed phase subsequent to the channeling and the effect of the structural organization on the sedimentation rate. It is suggested that the initial, slow stage of erythrocyte sedimentation is mainly controlled by the gravitational compactness of the collapsed network. The lifetime of RBC network and hence the duration of the slow regime of erythrocyte sedimentation decrease with an increase in the intercellular pair potential and with a decrease in Hct. The gravitational compactness of the collapsed network causes its rupture into individual fragments. The catastrophic collapse of the network transforms erythrocyte sedimentation from slow to fast regime. The size of RBC network fragment is insignificantly affected by Hct and is mainly determined by the intensity of intercellular attractive interactions. When cells were suspended in the weak aggregating medium, the Stokes radius of fragments does not differ measurably from that of individual RBCs. The proposed mechanism provides a reasonable explanation of the effects of RBC aggregation, Hct and the initial height of the blood column on the delayed erythrocyte sedimentation. © 2009 Elsevier B.V. All rights reserved. Source


Pribush A.,Experimental Hematology Laboratory | Pribush A.,Ben - Gurion University of the Negev | Meyerstein D.,Ben - Gurion University of the Negev | Meyerstein D.,Ariel University | Meyerstein N.,Experimental Hematology Laboratory
Colloids and Surfaces B: Biointerfaces | Year: 2010

Despite extensive efforts to elucidate the mechanism of erythrocyte sedimentation, the understanding of this mechanism still remains obscure. In attempt to clarify this issue, we studied the effect of hematocrit (Hct) on the complex admittance of quiescent blood measured at different axial positions of the 2 mm × 2 mm cross-section chambers. It was found that after the aggregation process is completed, the admittance reveals delayed changes caused by the formation of cell-free zones within the settling dispersed phase. The delay time (τd) correlates positively with Hct and the distance between the axial position where measurements were performed and the bottom and is unaffected by the gravitational load. These findings and literature reports for colloidal gels suggest that erythrocytes in aggregating media form a network followed by the formation of plasma channels within it. The cell-free zones form initially near the bottom and then propagate toward the top until they reach the plasma/blood interface. These channels increase the permeability of a network and, as a result, accelerate the sedimentation velocity. The energy of the flow field in channels is sufficiently strong to erode their walls. The upward movement of network fragments in channels is manifested by erratic fluctuations of the conductivity. The main conclusion, which may be drawn from the results of this study, is that the phase separation of blood is associated with the formation of plasma channels within the sedimenting dispersed phase. © 2009 Elsevier B.V. All rights reserved. Source


Li B.-N.,Experimental Hematology Laboratory | Li B.-N.,Shenzhen Institute of Xiangya Biomedicine | Li Z.-Y.,Experimental Hematology Laboratory | Li Z.-Y.,Shenzhen Institute of Xiangya Biomedicine | And 6 more authors.
Progress in Biochemistry and Biophysics | Year: 2011

The adeno-associated virus (AAV) has many safety features that favor its use in the treatment of arteriosclerosis; however, the conventional, adeno-associated virus (AAV) mediated single-gene delivery is inefficient for arteriosclerosis. This has been attributed that the incidence of atherosclerosis is caused by a variety of genetic defects but not a particular gene. To overcome this, double-gene delivery was evaluated for the treatment of atherosclerosis. Four experimental groups were administered the following AAV vector constructs: rAAV-apoAI-IRES-SR-BI, rAAV-apoAI-GFP, rAAV-IRES-GFP, and PBS. ApoAIand SR-BIgene expression was detected using RT-PCR. The apoAIand SR-BIprotein expression was determined by Western blotting and ELISA. Diet-induced hypercholesterolemia and atherosclerosis in rats was adopted and rAAV was administered through the tail vein injection. HepG2 cells were cultured and infected with the three viral vectors. The apoAIand SR-BIsecreted from HepG2 cells in the AAV- apoAI/SR-BIgroup enhanced cholesterol efflux and resulted in a stronger RCT ability, respectively. In the rats' model with diet-induced hypercholesterolemia and atherosclerosis, GFP expression could be detected at 8 weeks post-injection. The rAAV vector had superior gene expressing activity. Eight weeks after gene transfer, plasma total cholesterol and LDL-cholesterol concentrations were significantly reduced (P < 0.05) compared to control for rAAV-IRES-GFP (AAV-GFP) treated group. No effect on HDL-cholesterol concentrations occurred. Ultrasound determined intima-media thickness also has been significantly reduced compared to control. Serum hs-CRP and SOD levels increased significantly (P< 0.01). Serum MDA levels decreased significantly. Gene mRNA expression was detected in atherosclerosis rats' model. The results show that rAAV-hapoAI-IRES-hSR-BIvector can anti-inflammatory, reduce atherosclerotic macrophage content and increases lesion stability of pre-existing plaques through quenching of NF- κB activity and reducing plasma cholesterol. Simultaneous over-expression of apoAIand SR-BIby AAV-mediated gene transfer may have a favorable effect on diet-induced hypercholesterolemia and arteriosclerosis in rats. These results may provide a new method for gene therapy of arteriosclerosis. Source

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