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An optimal marine propeller design method is proposed, which integrates the lifting line and surface panel method and is characterized by the use of the surface panel method to take the hub effect into consideration. By developing an integrated approach instead of an iterative method for the calculation of the interaction between the hub and the designed blades, the hub effects on the optimal circulation can be accounted for throughout the theoretical design procedure. This new integrated method provides a fast and accurate enough method to model the straight forward hub surface, in the optimal propeller design. A systematic design procedure from the basic design inputs to the blade geometry determination is performed and the designed propellers are validated by the surface panel method and the RANS method. The design and analysis cases are considered by different approaches with comparison and validation. And a comparative study including different hub geometries is also performed to reveal the mechanism of the hub effect on the distributions of the propeller optimal loads.

Levosimendan is a calcium sensitizer that enhances myocardial contractility without increasing myocardial oxygen use. Limited data are available on its renal-protective effect, and no statistically significant effects have been found. A meta-analysis was conducted for randomized studies to show whether perioperative levosimendan use could reduce acute kidney injury (AKI) in patients undergoing cardiac surgery.BioMed Central, PubMed EMBASE, and the Cochrane Central Register of Controlled Trials were searched for pertinent studies.Randomized trials that compared levosimendan versus placebo or any other control in cardiac surgery with data on AKI were included. Exclusion criteria were duplicate publications, nonadult studies, oral administration of levosimendan, and studies with no data on AKI.Study endpoints, study design, population, clinical setting, levosimendan dosage, and treatment duration were extracted.Data from 529 patients in 5 randomized trials were analyzed. The analysis showed that levosimendan decreased postoperative incidence of AKI in the levosimendan group.This analysis suggests that levosimendan might reduce renal injury in adult patients undergoing cardiac surgery. More prospective randomized studies are needed to further demonstrate the benefits of levosimendan on renal protection in cardiac surgery.

Defensins are important components in host defense systems. The therapeutic use of β-defensins is limited by their innate toxicity and high cost due to the size and complex disulfide pairing. In this study, we used linear avian β- defensin-4 (RL38) without disulfide bonds as model peptide to derive two peptides by the truncation. GL23 is the C-terminal truncated sequence of RL38, and GLI23 is the derivative of GL23 by the replacement of cysteines with isoleucines. Results showed that these peptides exhibited strong antibacterial activity against gram-negative and gram-positive bacteria. An exception was that GL23 showed weak antimicrobial activity against gallinaceous pathogenic bacteria Salmonella Pullorum C79-13. Two truncated peptides GL23 and GLI23 displayed no or weak hemolysis, which was in accordance with little blue shifts of the peptides in the presence of synthetic eukaryotic membranes. CD spectroscopy demonstrated that these peptides appeared to be unfolded in aqueous solution but acquire structure in the presence of membrane- mimicking phospholipids. GLI23 kept the antibacterial activity at high concentrations of NaCl or low concentration of divalent cations (Mg2+ and Ca2+). The peptides preferentially bound to negatively charged phospholipids over zwitterionic phospholipids, which led to greater cell selectivity. The outer and inner membranes assay displayed that GLI23 killed bacteria by targeting the cell membrane. These results suggest the peptides derived by truncation of linear β-defensins may be a promising candidate for future antibacterial agent.

Antimicrobial peptides are major components of the innate self-defence system and a large number of peptides have been designed to study the mechanism of action. In the present study, a small combinatorial library was designed to study whether the biological activity of Val/Arg-rich peptides is associated with targeted cell membranes. The peptides were produced by segregating hydrophilic residues on the polar side and hydrophobic residues on the opposite side. The peptides displayed strong antimicrobial activity against Gram-negative and Gram-positive bacteria, but weak haemolysis even at a concentration of 256 µM. CD spectra showed that the peptides formed α-helical-rich structure in the presence of negatively charged membranes. The tryptophan fluorescence and quenching experiments indicated that the peptides bound preferentially to negatively charged phospholipids over zwitterionic phospholipids, which corresponds well with the biological activity data. In the in vivo experiment, the peptide G6 decreased the bacterial counts in the mouse peritoneum and increased survival after 7 days. Overall, a high binding affinity with negatively charged phospholipids correlated closely with the cell selectivity of the peptides and some peptides in this study may be likely candidates for the development of antibacterial agents.

Increasing evidence indicates that inflammation plays an important role in intimal hyperplasia (IH) induced by autologous vein grafts. The proteasome inhibitor bortezomib shows anti-inflammatory effects, so we used an autologous vein transplantation model to test whether bortezomib inhibits neointimal formation in transplant-induced vasculopathy.We subjected 88 rats to autologous external jugular vein grafting surgery randomly assigned to be treated with bortezomib or vehicle. After 24 or 72 hours, rats were humanely killed and vein grafts processed for real-time RT-PCR (24 and 72 hours), ELISA (24 hours), or neutrophil chemotaxis assay (24 hours). Subsequently, rats were humanely killed at 1 and 2 weeks after grafting with samples processed for morphometric analysis.Bortezomib significantly inhibited IH at 2 weeks compared with untreated controls (P.05). Expression of mRNA for vascular cell adhesion molecule-1, intercellular adhesion molecule-1, cytokine-induced neutrophil chemoattractant 2beta, monocyte chemoattractant-1, interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha markedly increased in injured vessels during the first day after surgery declining over the following 3 days. Bortezomib significantly attenuated gene expression and protein levels of most inflammatory mediators (P.05), simultaneously inhibiting neutrophil chemotactic activity of vessel homogenates.Bortezomib inhibited neointimal formation at least partially by attenuating the inflammatory response in transplant-induced vasculopathy. It may become a novel vasoprotective agent in the clinical field.

Strain rate (SR) provides a quantitative segmental analysis of myocardial function. However, the use of SR with stress echocardiography to determine the ischemic myocardium has not been completely investigated. The present study aimed to determine the changes in systolic function of the ischemic myocardium by strain-rate imaging (SRI) with adenosine stress echocardiography.Stenosis and complete occlusion of coronary arteries were produced in 11 canine models by constricting the left anterior descending coronary artery (LAD). Myocardial longitudinal strain with adenosine was measured at baseline and during ischemia and infarction.Strain and SR did not differ during ischemia and infarction as compared with that at baseline in non-LAD segments or after adenosine treatment. As compared with baseline, during ischemia, LAD segments showed significantly decreased peak systolic SR (SR(peak sys)) (P0.05) and significantly increased ratio of postsystolic strain (epsilon(ps)) to strain during ejection time (epsilon(et)) (epsilon(ps)/epsilon(et)) (P0.05); epsilon(max) and epsilon(et) were reduced slightly, epsilon(ps) and the ratio of epsilon(ps) to maximal systolic strain (epsilon(max))(epsilon(ps)/epsilon(max)) were increased minimally, but had no significance(P0.05). During infarction, the epsilon(ps) and the ratios of epsilon(ps)/epsilon(max) and epsilon(ps)/epsilon(et) were increased markedly (P0.01) and epsilon(et) and SR(peak sys) decreased as compared with that at baseline and during ischemia, whereas epsilon(max) was reduced only with at baseline (P0.01). After adenosine treatment, in the non-LAD segments, the values of strain and SR did not change at baseline or during ischemia and infarction and in LAD segments, values did not change at baseline and during infarction. However, during ischemia, SR(peak sys) and epsilon(et) were significantly reduced (P0.05), whereas epsilon(ps), epsilon(ps)/epsilon(max) and epsilon(ps)/epsilon(et) were increased (P0.05 and0.01, respectively).Combined with adenosine stress echocardiography, SRI can quantitatively differentiate the ischemic from non-ischemic myocardium. epsilon(ps)/epsilon(max) and epsilon(ps)/epsilon(et) can be used as objective indices to identify the ischemic myocardium.

The pathophysiology of coronary atherosclerotic plaques is a complex process. Early detection of coronary atherosclerotic plaques is critical in the prevention, prognostic and therapeutic intervention of cardiovascular disease. MicroRNAs (miRNAs), endogenous short non-coding RNAs, have been reported to play an important role in cardiovascular diseases and are also used as disease markers. However, the miRNA expression profile in early coronary atherosclerotic plaques has yet been reported. We hypothesize that miRNAs can be used as effective disease markers for detection of early coronary atherosclerotic plaques. In this analysis, coronary artery samples from three patients with early coronary atherosclerosis were harvested and miRNA expression profile determined using microarray analysis. Compared with healthy controls, a total of 44 miRNAs were upregulated and 57 miRNAs were downregulated. Among the dysregulated miRNAs, eight were significantly upregulated while five miRNAs were significantly downregulated, as determined by t-test (P < 0.05). Four of the significantly dysregulated miRNAs, including miR-221, miR-155, miR-100 and hsa-miR-1273, were selected and verified by real-time PCR. The real-time PCR results were consistent with the microarray data that miR-221, miR-155 and miR-100 were significantly downregulated in plaques, whereas miR-1273 was significantly upregulated. These results indicate that miRNAs expression level can be used as potential markers for early coronary atherosclerotic plaque formation.

The photophysics and conformation of single long-chain 2,5-dioctyloxy-p-phenylenevinylene (DOO-PPV) polymers are investigated. The fluorescence intensity−time trace of an individual polymer contains abrupt quantized intensity changes superimposed on small gradual changes. Under the same processing conditions, the size of abrupt changes varies from individual to individual, varying between 0 and 100% of the total intensity. Polarization modulation indicates considerable orientation of absorption dipoles within the polymer. Time-dependent measurements indicate that, in the majority of polymers, absorption dipoles in those regions of the polymer responsible for abrupt intensity changes are arranged less anisotropically than in regions responsible for the gradual changes. Spectroscopic measurements show a greater spectral variation accompanying jumps than that accompanying gradual decay. This can be explained by the coexistence of extended regions and a core region. The first is characterized by a relatively ...

Quenchers, such as oxygen, play an important role influencing the transient fluorescence behavior of conjugated polymers. It is important to reduce these quenching effects in order to study a polymer's intrinsic fluorescence behaviors. The fluorescent transient of a single DOO-PPV polymer embedded in a polystyrene matrix is found to be qualitatively dependent on the sealing method used to protect the thin film from contact with oxygen. The results show that the preparation process affects single polymer fluorescence.

Conventional robot control schemes are basically model-based methods. However, exact modeling of robot dynamics poses considerable problems and faces various uncertainties in task execution. This paper proposes a reinforcement learning control approach for overcoming such drawbacks. An artificial neural network (ANN) serves as the learning structure, and an applied stochastic real-valued (SRV) unit as the learning method. Initially, force tracking control of a two-link robot arm is simulated to verify the control design. The simulation results confirm that even without information related to the robot dynamic model and environment states, operation rules for simultaneous controlling force and velocity are achievable by repetitive exploration. Hitherto, however, an acceptable performance has demanded many learning iterations and the learning speed proved too slow for practical applications. The approach herein, therefore, improves the tracking performance by combining a conventional controller with a reinforcement learning strategy. Experimental results demonstrate improved trajectory tracking performance of a two-link direct-drive robot manipulator using the proposed method.

OBJECTIVES: Internal mammary arteries graft failure in coronary artery bypass grafting (CABG) is mostly considered to be a result of competitive flow (CF) from the native coronary artery, which significantly limits future revascularization options. METHODS: With the left internal mammary artery (LIMA) anastomosed to the left anterior descending (LAD) coronary artery using an off-pump technique, CABG was performed on 15 Chinese swine. Then we produced varying degrees of stenosis in the proximal LAD coronary artery with an adjustable flow occluder, measured the mean flow of the LIMA and LAD coronary artery and detected the plasma concentrations of nitric oxide (NO) and endothelin (ET) in the LIMA graft. RESULTS: When stenosis of the proximal LAD artery was decreased, the CF of the native LAD coronary artery showed an increasing trend, while the mean flow of the LIMA revealed a decreasing trend. Distal LAD coronary artery flow remained nearly constant, despite the varying proximal LAD artery or LIMA flow rates. An oscillating flow pattern (retrograde/antegrade) was noted in the LIMA graft when the proximal LAD coronary artery was not fully occluded. The plasma concentration of ET in the LIMA graft was significantly higher than that before grafting (P< 0.05), and the plasma concentration of NO was significantly lower (P< 0.05). The concentration of NO was positively related to the mean flow in the LIMA (r= 0.872, P< 0.05). CONCLUSIONS: CF from the native LAD coronary artery can decrease the blood flow in the LIMA graft and even change the direction of the flow. These changes may impair the function of the LIMA graft and affect ET or NO production, which in turn may lead to early LIMA graft failure.

A novel α-helical antimicrobial peptide G6 rich in Val/Arg residues has been screened previously. In this study, we further evaluated the biochemical stability, interaction with whole bacteria, and in vivo therapeutic or prophylactic role of the peptide in Salmonella typhimurium-infected mice. The results showed that G6 exhibited strong resistance to pH, heat, and salts. But G6 lost the antimicrobial activity when treated with proteolytic enzymes. G6 had no toxicity on mammalian cell. An intraperitoneal model of sepsis caused by Salmonella typhimurium was established in mice. G6 was administered intraperitoneally 1 h before or after mice were infected with Salmonella typhimurium. For the mice given peptide post-bacterial infection, the mortality of the mice and the peritoneal bacterial counts were significantly lower in the groups that were administered 2.5 mg/kg BW and 5.0 mg/kg BW of G6 (P < 0.05) compared to the PBS-treated group. Similar trend was obtained when G6 was given 1 h prior to Salmonella typhimurium infection. Peptide-membrane experiments showed that G6 was effective in permeabilizing the outer and inner membrane in a dose dependent manner, indicating that the peptide targets the cell membrane. Taken together, the results revealed that the peptide G6 may provide a useful alternative to antibiotic agents to treat or prevent bacterial infections.

The increasing power and rapid advance of mobile devices has changed the way people access information. According to the International Telecommunication Union [18], the number of mobile cellular subscribers worldwide is estimated to reach 5.3 billion, including 940 million subscriptions to 3G services in the end of 2010. Commercialized 3G services are widespread in many countries and users have been rapidly switching to the 3G platform. The development of mobile devices and mobile applications has created great potential market for mobile data services. The objective of this research is to investigate the critical factors that affect consumers' intention to using mobile data service. We build a theoretical framework that considers both the technology acceptance and economics perspectives. We conducted a survey research among the consumers of mobile data services and collected 310 valid questionnaires in late 2010. Our findings are as follows. First, consumers' perceived service availability has a positive impact on perceived ease of use and perceived usefulness of mobile data services. Second, switching benefits and perceived ease of use have positive effects on consumers' perceived usefulness of mobile data services. Third, perceived usefulness has a positive effect on the intention to use mobile data services. Overall, our research provides both theoretical and practical insights into the determinants of consumers' intention to use mobile data services.

Reconstructive surgery is the primary goal in pediatric patients with valve disease. However, in cases with irreparable valve lesions, valve replacement is the only option. This study aimed to retrospectively analyze the clinical experience of heart valve prosthesis replacement in children.Between January 1990 and July 2009, 35 pediatric patients (16 boys, 19 girls) underwent mechanical valve replacement in Shandong University Qilu Hospital. The ages ranged from 2.5 to 14 years (mean, (8.8 ± 3.8) years) and body weight varied from 11 to 37 kg (mean, (22.1 ± 5.2) kg). Mechanical valve replacement was performed because of congenital heart disease in 23 patients, rheumatic disease in ten patients and infective endocarditis in two patients. St. Jude bileaflet mechanical valves were implanted in all the 35 patients including mitral valve replacement (MVR) in 18, aortic valve replacement (AVR) in 12, tricuspid valve replacement (TVR) in two, AVR and MVR in two and MVR and TVR in one. The size of the prostheses ranged between 19 and 27 mm. All patients received long-term anticoagulation treatment with sodium warfarin, aiming to maintain an international normalized ratio between 1.5 to 2.0. Follow-up was performed in all the patients with a total follow-up of 119.4 patient-years.The operative mortality was 8.57% (3/35). One patient, who underwent cardiac debridement and AVR, died 2 hours after being admitted to the intensive care unit because of severe low cardiac output syndrome and ventricular fibrillation. Two patients died of cardiogenic shock and renal failure during initial hospitalization after the operation. One patient who received replacement of a tricuspid valve developed complete heart block requiring temporary pacing and recovered sinus rhythm 4 days later. Thirty-two patients survived and their cardiac function was in New York Heart Association (NYHA) class I to class II when discharged. Late events included hemorrhage and endocarditis. Two patients required reoperation. No late deaths occurred during the follow-up.Mechanical valve replacement remains an acceptable treatment option in children when the valve reparation is impossible or unsuccessful. The operative mortality and incidence of any valve-related events such as endocarditis, reoperation, thromboembolism or anticoagulation-related bleeding are acceptable.

Because of the anergy of CD25+CD4+ regulatory T cells, it is unclear how the number of these regulatory T cells is sustained and expanded in normal physiologic circumstances. In the present study, we examined the effect of natural allogeneic mature dendritic cells (DCs) on the proliferation and function of CD25+CD4+ T cells. Our data showed that natural allogeneic mature DCs stimulated CD25+CD4+ T-cell growth vigorously, whereas immature DCs had little effect on the proliferation of CD25+CD4+ T cells. After expansion by mature DCs, CD25+CD4+ T cells maintained their expression of Foxp3 and suppressed the proliferation of CD25- CD4+ T cells similar to freshly isolated CD25+CD4+ T cells. Our results introduce a potentially critical role played by natural allogeneic mature DCs, which exist in normal physiologic circumstances, in controlling CD25+CD4+ regulatory T-cell expansion and function.

We aimed to investigate whether tolerogenic dendritic cells (DCs) were induced in the tolerant recipients with the blockade of CD40-CD40L costimulation. Mouse heterotopic heart transplantation was performed. DCs were sorted from rejected and tolerant recipients using magnetic-activated cell sorting. Their expression of CD40, CD80, and CD86 was examined using fluorescence-activated cell sorting. DCs were stimulated with lipopolysaccharide in vitro, and interleukin 10 (IL-10) and IL-12 levels in the supernatants were evaluated using enzyme-linked immunosorbent assay. By using mixed leukocyte reaction, we investigated the stimulatory capacities and tolerogenic capability of DCs. DCs from tolerant recipients expressed lower level of costimulatory molecules, including CD40, CD80, and CD86 and released higher levels of IL-10 and lower levels of IL-12. In addition, DCs from tolerant recipients were weak stimulators of the mixed leukocyte reaction and inhibited the proliferation of splenocytes. IL-10(high)IL-12(low) DCs with immature phenotype were induced in the tolerant recipients with the blockade of CD40-CD40L costimulation, and they obtained the tolerogenic function.

To study the roles of serum inflammatory factors IL-6 and TNF-alpha and allograft adventitial inflammation in the pathogenesis of allograft arteriosclerosis in rats.Thirty-six allogeneic allograft rats and 16 syngeneic allograft rats were randomly divided into 4 groups (9 rats in each experimental group and 4 in each control group): A, harvested at Week 1 post-operation; B, harvested at Week 2 post-operation; C, harvested at Week 3 post-operation; D, harvested at Week 4 post-operation. Blood samples were collected before transplantation and after harvest. The method of ELISA was used for testing serum inflammatory factors including interleukin-6 (IL-6), tumor necrosis factor-alpha(TNF-alpha), HE staining for pathologic changes of aortic allograft and immunohistochemical method for expression of alpha-actin, cyclin dependent kinase-1 (CDK(1)) and proliferating cell nuclear antigen (PCNA). Compare the inflammatory factors and other observations between groups and preoperative.At Week 1 post-operation, a large amount of inflammatory cell infiltration in adventitia was observed; at Week 2 post-operation, slight collagen fibers hyperplasia with inflammatory infiltration; at Week 4 post-operation, obvious adventitia thickening with a large number of smooth muscle cells, collagen fibers and inflammatory cells, smooth muscle cells migration from adventitia to intima. Expressions of alpha-actin, CDK(1) and PCNA kept increasing with time in adventitia (P0.05). There was a significant increase in serum TNF-alpha level in Groups A, B, C and D, as compared with pre-operative basal level (P0.01). There was no difference between controls and pre-operative basal level. IL-6 level slightly declined in the middle stage, but finally increased in experimental group B (P0.05) while it significantly increased in Groups A, C, D (P0.01). In the control groups A, B, C, it was higher than pre-operative level (P0.05). In experimental groups A, C, D, it had a significant increase as compared with controls (P0.01).In abdominal aortic allograft models, obvious angiosclerosis was found in adventitia and intima in accordance with the severity of adventitial inflammation. Thus the inflammatory factors and inflammatory cell infiltration in adventitia are both involved in the pathogenesis of early allograft arteriosclerosis.

To transduce the new hepatocellular carcinoma (HCC) specific antigen gene glypican3 (GPC3) into dendritic cells (DCs) and to observe the in vitro cytotoxic effect induced by the genetically modified DCs against the hepatocellular carcinoma cell line (HepG2).This study was performed in China Medical University Shenyang, China from September 2007-February 2008. The design of the study was to modify DCs with GPC3 and to be used to activate human T cells and elicit a cell-mediated immune response against HepG2 in vitro. The GPC3 gene expression was identified by western blot and immunocytochemistry. The proliferation of responder cells and cytotoxicity against HepG2 were examined by water-soluble tetrazolium salt -1 and lactate dehydrogenase assay respectively. The interferon-y (IFN-y) secreted was detected by ELISA assay.Both Western blot and immunocytochemical analysis assured the validity of GPC3 transfection. Glypican3 modified DCs were potent in inducing responder cells proliferation and IFN-y production. The cytotoxicity in the group of GPC3 transfected DCs were (38.90+/-0.95%) at the ratio of effector cells/target cells E/T:100:1, 30.83+/-1.24% at the ratio of E/T:50:1, and 23.84+/-0.65% at the ratio of E/T:10:1, respectively (which is significant compared with other groups, p0.001). And the GPC3 modified DCs showed ability to induce high specific cytotoxicity against HepG2 in vitro.The effector cells stimulated with DCs that were transfected with pEF-hGPC3 plasmid could effectively lyse GPC3 expressing HepG2 cells, which suggested that those genetically engineered DCs have the potential to serve as novel vaccine for HCC.

Autologous vein grafts is still commonly used for arterial reconstructive procedures. Their success is limited by the development of neointimal hyperplasia. Clinical and experimental evidence suggest that the bone marrow derived mesenchymal stem cells (MSCs) participate in the neovascularization. The current study used a direct approach to test the hypothesis that, after vein grafting in a rat model, MSCs have potential effects on reendothelialization and neointimal formation. MSCs were isolated by bone marrow cell adherence. Autologously interpositioning left external jugular vein (LEJV) to left common carotid artery-induced vein grafting model of r at w as utilized. Vascular lesion formation after transplantation of MSCs labeled with 4',6-diamidino-2-phenylindole (DAPI) was investigated. Two weeks after implantation, immunofluorescence studies revealed that engrafted cells acquired an endothelial phenotype, and some expressed endothelial nitric oxide synthase (eNOS). Furthermore, proliferation of cells and neointimal formation decreased significantly after MSC implantation. Real-time reverse transcription-PCR and western blotting analysis showed a rise of eNOS expression in the MSC group compared with the vein grafting group. Therefore, engrafted MSCs appeared to differentiate into endothelial cells, diminish the neointima formation and contribute to the improvement on endothelial function, which indicates that MSCs may exert an important function as repair mechanism in vascular injury after vein grafting.

To detect the nitric oxide (NO) production and energy metabolism of the interleukin (IL)-1beta-treated residual hepatocytes from rats after partial hepatectomy.Forty rats were equally divided into partial hepatectomies (PH) group and control group. In the control group the rats were otherwise matched and underwent sham surgeries. The residual hepatocytes were separated by the collagenase perfusion method. The hepatocytes were cultured with cytokines such as IL-1beta. The production of NO in the two groups were measured with Griess reagent method, the production of inducible nitric oxide synthase (iNOS) protein detected with Western blot, the content of the nucleotide in the hepatocytes detected with high-performance liquid chromatography, and the content of the ketone body in the hepatocytes of the two groups determined with the enzymatic method. Afterwards the ketone body ratio (acetoacetate/beta-hydroxy butyrate, KBR) was calculated.The production of NO in the PH group was twice as much as that in the Sham group. IL-1beta decreased the content of ATP and the KBR in the hepatocytes of both groups, and the decrease magni tude in the PH group was significantly larger than that in the Sham group. After the injection of L-arginine, the production of NO in the hepatocytes in the PH group increased, and the level of ATP and KBR decreased. N(G)-methyl-L-arginine (L-NMMA), the inhibitor of NO synthase, inhibited the production of NO and reversed the decrease of ATP and KBR.After partial hepatectomy, increased NO production in the hepatocytes after the treatment of interleukin-1beta may disturb the function of mitochondria by inhibiting the synthesis of ATP.

[Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4][![Graphic][5] ][5][![Graphic][6] ][6] A 45-year-old man with significant ST-segment changes in anterolateral derivations underwent cardiac catheterization. A coronary angiogram revealed severe stenosis and ectasia of