At 6 months, most of the SES were covered with thin neointima, but few showed full coverage.

In 56 patients with angina, 126 plaques identified by IVUS findings were analysed using both VH-IVUS and OCT. IVUS-derived TCFA was defined as an abundant necrotic core (>10% of the cross-sectional area) in contact with the lumen (NCCL) and %plaque-volume >40%. OCT-derived TCFA was defined as a fibrous cap thickness of <65 microm overlying a low-intensity area with an unclear border. Plaque meeting both TCFA criteria was defined as definite-TCFA. Sixty-one plaques were diagnosed as IVUS-derived TCFA and 36 plaques as OCT-derived TCFA. Twenty-eight plaques were diagnosed as definite-TCFA; the remaining 33 IVUS-derived TCFA had a non-thin-cap and eight OCT-derived TCFA had a non-NCCL (in discord with NCCL visualized by VH-IVUS, mainly due to misreading caused by dense calcium). Based on IVUS findings, definite-TCFA showed a larger plaque and vessel volume, %plaque-volume, higher vessel remodelling index, and greater angle occupied by the NCCL in the lumen circumference than non-thin-cap IVUS-derived TCFA. Conclusion Neither modality alone is sufficient for detecting TCFA. The combined use of OCT and VH-IVUS might be a feasible approach for evaluating TCFA.

The Eph family of receptors is the largest family of RTKs. Eph receptors are stimulated by a family of membrane-linked ligands designated ephrins (6, 7). Both biochemical and genetic studies have established the central role that ephrins have in the control of cell contact repulsion, boundary formation, cell migration, and repulsive axon guidance (6). Repulsive axon guidance appears to be caused by modulation of cytoskeletal organization leading to regulation of neural growth-cone development (8). Eph-receptors also regulate cell-matrix interaction and cell proliferation by affecting signaling by integrins (9-11) and by modulation of MAPK response (12)(13)(14).In this article, we demonstrate that EphA4 binds directly and specifically via the N-terminal portion of its protein tyrosine kinase core to the juxtamembrane (JM) region of FGFRs. In cells that express EphA4 and FGFRs, the interactions between the cytoplasmic domains of EphA4 and FGFRs can lead to transreceptor activation, resulting in tyrosine phosphorylation of FRS2␣ and MAPK activation. The synergistic effect of ephrin-A1 stimulation on FGF2-induced cellular responses may influence the biological outcome of the activation of these two families of RTKs. Materials and MethodsYeast Two-Hybrid Experiments. The yeast two-hybrid system was used as described (15). The bait used for screening was 81 aa (amino acids 398-478), derived from the JM domain of human FGFR3. A human brain cDNA library in a pJG4-5 vector consisting of 3.5 ϫ 10 6 primary transformants (Clontech) was used for screening for proteins that interact with the JM domain of FGFR3. Fig. 1A shows the constructs used to detect interactions between the cytoplasmic domain of EphA4 and the JM domain of FGFR3.Cells. HEK293 cells were maintained in DMEM supplemented with 10% calf serum. For neural differentiation, P19 cells were maintained in ␣-MEM supplemented with 10% FBS containing 0.5 M retinoic acid for 3 days. Rat L6 myoblasts were maintained in DMEM supplemented with 10% FBS.Preparation of Ephrin-A1. Ephrin-A1 fused to human IgG-Fc was purchased from Sigma-Aldrich. Before application to the cells, 5 g of ephrin-A1-Fc was oligomerized by mixing with 12 g of rabbit anti-human IgG-Fc (Jackson ImmunoResearch) in 1 ml of PBS at 4°C for at least 1 h. As a control, a human IgG-Fc fragment (Jackson ImmunoResearch) was also applied after oligomerization.Expression Plasmids. Full-length cDNA of human EphA4 was prepared by RT-PCR using total RNA from a human brain extract (Clontech) as the template. The cDNA of human FGFR4 was prepared by RT-PCR using K562 cell-derived RNA as the template. The cDNAs for FGFR1 and FGFR2 were provided by W. McKeehan (Texas A&M University, College Station, TX). The cDNA for FGFR3 was provided by D. E. Johnson (University of Pittsburgh, Pittsburgh). Receptor mutants were prepared by applyConflict of interest statement: No conflicts declared.

Longer stents and greater asymmetric stent expansion may be important determinants of thrombus formation after SES implantation. In this small cohort, the presence of thrombus did not increase the risk of major adverse cardiac events.