Low-Density Polybutylene Terephthalate Foams with Enhanced Compressive Strength via a Reactive-Extrusion Process

Due to their appealing properties such as high-temperature dimensional stability, chemical resistance, compressive strength and recyclability, new-generation foams based on engineering thermoplastics such as polyethylene terephthalate (PET) and polybutylene terephthalate (PBT) have been gaining significant attention. Achieving low-density foams without sacrificing the mechanical properties is of vital importance for applications in the field of transportation and construction, where sufficient compressive strength is desired. In contrast to numerous research studies on PET foams, only a limited number of studies on PBT foams and in particular, on extruded PBT foams are known. Here we present a novel route to extruded PBT foams with densities as low as 80 kg/m3 and simultaneously with improved compressive properties manufactured by a tandem reactive-extrusion process. Improved rheological properties and therefore process stability were achieved using two selected 1,3,5-benzene-trisamides (BTA1 and BTA2), which are able to form supramolecular nanofibers in the PBT melt upon cooling. With only 0.08 wt % of BTA1 and 0.02 wt % of BTA2 the normalized compressive strength was increased by 28% and 15%, respectively. This improvement is assigned to the intrinsic reinforcing effect of BTA fibers in the cell walls and struts

In Vivo Serial MR Imaging of Magnetically Labeled Endothelial Progenitor Cells Homing to the Endothelium Injured Artery in Mice

Background: Emerging evidence of histopathological analyses suggests that endothelial progenitor cells (EPCs) play an important role in vascular diseases. Neointimal hyperplasia can be reduced by intravenous transfusion of EPCs after vascular injury in mice. Therefore, it would be advantageous to develop an in vivo technique that can explore the temporal and spatial migration of EPCs homing to the damaged endothelium noninvasively. Methodology/Principal Findings: The left carotid common artery (LCCA) was injured by removal of endothelium with a flexible wire in Kunming mice. EPCs were collected by in vitro culture of spleen-derived mouse mononuclear cells (MNCs). EPCs labeling was carried out in vitro using Fe2O3-poly-L-lysine (Fe2O3-PLL). In vivo serial MR imaging was performed to follow-up the injured artery at different time points after intravenous transfusion of EPCs. Vessel wall areas of injured artery were computed on T2WI. Larger MR signal voids of vessel wall on T2WI was revealed in all 6 mice of the labeled EPC transfusion group 15 days after LCCA injury, and it was found only in 1 mouse in the unlabeled EPC transfusion group (p = 0.015). Quantitative analyses of vessel wall areas on T2WI showed that the vessel wall areas of labeled EPC transfusion group were less than those of unlabeled EPC transfusion group and control group fifteen days after artery injury (p,0.05). Histopathological analyses confirmed accumulation and distribution of transfused EPCs at the injury site of LCCA. Conclusions/Significance: These data indicate that MR imaging might be used as an in vivo method for the tracking of EPC

Lack of influence of the COX inhibitors metamizol and diclofenac on platelet GPIIb/IIIa and P-selectin expression in vitro

BACKGROUND: The effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A(2 )synthesis has been well documented. However, the influence on platelet function is not fully explained. Aim of this study was to examine the influence of the COX-1 inhibiting NSAIDs, diclofenac and metamizol on platelet activation and leukocyte-platelet complexes, in vitro. Surface expression of GPIIb/IIIa and P-selectin on platelets, and the percentage of platelet-leukocyte complexes were investigated. METHODS: Whole blood was incubated with three different concentrations of diclofenac and metamizol for 5 and 30 minutes, followed by activation with TRAP-6 and ADP. Rates of GPIIb/IIIa and P-selectin expression, and the percentage of platelet-leukocyte complexes were analyzed by a flow-cytometric assay. RESULTS: There were no significant differences in the expression of GPIIb/IIIa and P-selectin, and in the formation of platelet-leukocyte complexes after activation with ADP and TRAP-6, regarding both the time of incubation and the concentrations of diclofenac and metamizol. CONCLUSIONS: Accordingly, the inhibitory effect of diclofenac and metamizol on platelet aggregation is not related to a reduced surface expression of P-selectin and GPIIb/IIIa on platelets