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.

BackgroundRecent experimental studies have revealed that n-3 fatty acids, such as eicosapentaenoic acid (EPA) regulate postprandial insulin secretion, and correct postprandial glucose and lipid abnormalities. However, the effects of 6-month EPA treatment on postprandial hyperglycemia and hyperlipidemia, insulin secretion, and concomitant endothelial dysfunction remain unknown in patients with impaired glucose metabolism (IGM) and coronary artery disease (CAD).Methods and resultsWe randomized 107 newly diagnosed IGM patients with CAD to receive either 1800 mg/day of EPA (EPA group, n = 53) or no EPA (n = 54). Cookie meal testing (carbohydrates: 75 g, fat: 28.5 g) and endothelial function testing using fasting-state flow-mediated dilatation (FMD) were performed before and after 6 months of treatment. The primary outcome of this study was changes in postprandial glycemic and triglyceridemic control and secondary outcomes were improvement of insulin secretion and endothelial dysfunction. After 6 months, the EPA group exhibited significant improvements in EPA/arachidonic acid, fasting triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C). The EPA group also exhibited significant decreases in the incremental TG peak, area under the curve (AUC) for postprandial TG, incremental glucose peak, AUC for postprandial glucose, and improvements in glycometabolism categorization. No significant changes were observed for hemoglobin A1c and fasting plasma glucose levels. The EPA group exhibited a significant increase in AUC-immune reactive insulin/AUC-plasma glucose ratio (which indicates postprandial insulin secretory ability) and significant improvements in FMD. Multiple regression analysis revealed that decreases in the TG/HDL-C ratio and incremental TG peak were independent predictors of FMD improvement in the EPA group.ConclusionsEPA corrected postprandial hypertriglyceridemia, hyperglycemia and insulin secretion ability. This amelioration of several metabolic abnormalities was accompanied by recovery of concomitant endothelial dysfunction in newly diagnosed IGM patients with CAD.Clinical Trial Registration UMIN Registry number: UMIN000011265 (https://www.upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000013200&language=E)Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0437-y) contains supplementary material, which is available to authorized users.

The present study investigated the relation between plasma high-sensitivity C-reactive protein (hs-CRP) and adiponectin and coronary plaque components in patients with acute coronary syndrome (ACS). Previous studies showed a pivotal role of inflammation in the progression of atherosclerosis and the prognostic value of several biomarkers. However, relations among inflammatory biomarkers and plaque characteristics were unknown. Ninety-three culprit plaques (ACS n = 50, non-ACS n = 43) and 56 nonculprit plaques (ACS n = 28, non-ACS n = 28) were analyzed using Virtual Histology intravascular ultrasound to examine relations among plasma hs-CRP, adiponectin, and ratios of each coronary plaque component. Plasma adiponectin was significantly lower and plasma hs-CRP was significantly higher in patients with than without ACS. Culprit plaques in patients with ACS had greater amounts of necrotic core plaque than those in patients without ACS. There was an inverse relation between serum hs-CRP and adiponectin with regard to necrotic core ratio in both culprit and nonculprit lesions in patients with ACS, but not those without ACS. In conclusion, increased plasma hs-CRP and hypoadiponectinemia might be related to the progression of ACS.

Trigeminal trophic syndrome is a rare complication of trigeminal nerve injury that causes facial ulceration, anesthesia and paresthesia in the same trigeminal dermatomes. We present a case of a 65-year-old woman with a history of meningioma resection 18 years prior who presented 16 years later with an intractable ulceration around her left nasolabial sulcus. Pain and light-touch sensations around the ulcer were decreased. She admitted to frequent manipulation due to a crawling sensation. A skin biopsy showed acanthotic changes and a decreased number of peripheral nerve fibers. Trigeminal trophic syndrome was diagnosed. Carbamazepine was not effective, and the ulcer persisted at 7 months after the initial presentation. We reviewed 36 English-language publications from 2003 to 2012, and analyzed 61 cases of trigeminal trophic syndrome, including this patient. The mean age was 53.3 ± 19.7 years (range, 6-91). The right side of the face was more commonly affected (57%) than the left side. The ala nasi were involved in 48 cases (79%), followed by the cheek in 17 cases (28%). A corneal lesion was observed in 11 cases (18%), suggesting the importance of ophthalmologic consultations. The two major etiologies were trigeminal nerve ablation (18 cases; 30%) and cerebrovascular accidents (18 cases; 30%). The latent period ranged from days to 30 years. Gabapentin and carbamazepine were frequently administrated with variable efficacy. Application of thermoplastic dressings or negative pressure wound therapy demonstrated favorable outcomes. Surgery was an option with a high recurrence rate. Trigeminal trophic syndrome remains a clinical challenge.

Most EES struts were covered with uniform and thin neointima. The frequency of low-intensity neointima was very low, which may be a result of promoted vessel healing. These results may support improved clinical outcomes with EES in clinical trials.