Radiation shielding effects of lead equivalent thickness of a radiation protective apron and distance during C-arm fluoroscopy-guided pain interventions: A randomized trial.

BACKGROUND: The present study aimed to evaluate the degree of radiation shielding effects according to lead equivalent thickness and distance during C-arm fluoroscopy-guided lumbar interventions. METHODS: The exposure time and air kerma were recorded using a fluoroscope. The effective dose (ED) was measured with and without the shielding material of the lead apron using 2 dosimeters at 2 positions. According to the lead equivalent thickness of the shielding material and distance from the side of the table, the groups were divided into 4 groups: group 1 (lead equivalent thickness 0.6 mm, distance 0 cm), group 2 (lead equivalent thickness 0.6 mm, distance 5 cm), group 3 (lead equivalent thickness 0.3 mm, distance 0 cm), and group 4 (lead equivalent thickness 0.3 mm, distance 5 cm). Mean differences such as air kerma, exposure time, ED, and ratio of EDs (ED with protector/ED without protector) were analyzed. RESULTS: A total of 400 cases (100 cases in each group) were collected. The ratio of ED was significantly lower in groups 1 and 2 (9.18 ±â€…2.78% and 9.56 ±â€…3.29%, respectively) when compared to that of groups 3 and 4 (21.93 ±â€…4.19% and 21.53 ±â€…4.30%, respectively). The reductive effect of a 5-cm distance was 33.3% to 36.1% when comparing the ED between groups 1 and 2 and groups 3 and 4. CONCLUSIONS: The 0.3- and 0.6-mm lead equivalent thickness protectors have a radiation attenuation effect of 78.1% to 78.5% and 90.4% to 90.8%, respectively. The 5-cm distance from the side of the table reduces radiation exposure by 33.3% to 36.1%.

General anesthesia, using remimazolam, for the patient with myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD): A case report.

RATIONALE: Myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) is one of auto-immune demyelinating diseases of nervous system. Although both regional anesthesia and general anesthesia has been successfully performed in the patient with demyelinating diseases of nervous system, it has been controversial which one is better. PATIENT CONCERNS: Forty-four male patient was admitted for arthroscopic elbow surgery due to limitation of range of motion. The patient was diagnosed as MOGAD with anti-N-methyl-D-aspartate (NMDA) receptor encephalitis, and steroid was used to prevent and treat symptoms and signs. DIAGNOSIS: He was diagnosed as MOGAD with anti-NMDA receptor encephalitis, 1 year ago. The patient complaint of dizziness, diplopia, nausea, vomiting, seizure, general weakness and so on when he was confirmed as MOGAD with anti-NMDA receptor encephalitis. The diagnosis of MOGAD was confirmed with positive anti-myelin oligodendrocyte glycoprotein (MOG) Immunoglobulin (Ig)G and negative anti-aquaporin 4 (AQP4) IgG in the blood. INTERVENTIONS AND OUTCOMES: After steroid cover, total intravenous anesthesia (TIVA) with remimazolam and remifentanil was established for the patients. Rocuronium was administered under monitoring of neuromuscular blockade, using train of 4 (TOF). The operation was performed without any event under right lateral decubitus position. The patient was uneventfully recovered from anesthesia. LESSONS: The case report showed total intravenous anesthesia with remimazolam and remifentanil under proper monitoring was successfully performed in the patient with MOGAD.

The Neutrophil-to-Lymphocyte Ratio and Preoperative Pulmonary Function Test Results as Predictors of In-Hospital Postoperative Complications after Hip Fracture Surgery in Older Adults.

Purpose: This study retrospectively evaluated the usefulness of the neutrophil-to-lymphocyte ratio (NLR), prognostic nutritional index (PNI), and pulmonary function test (PFT) results as objective predictors of in-hospital postoperative complications after hip fracture surgery in older adults. Methods: The patients aged >65 years who underwent hip fracture surgery under general anaesthesia were enrolled. In-hospital postoperative complications with preoperative NLR, PNI and PFT results were evaluated. The NLR was calculated as the preoperative neutrophil count/lymphocyte count in peripheral blood. The PNI was calculated as the serum albumin (g/dL) × 10 + total lymphocyte count × 0.005 (/mm3). Results: One hundred ninety nine patients were analysed. The most common postoperative complications were respiratory complications. Compared with patients who did not have postoperative complications, patients with postoperative complications had a significantly higher NLR (8.01 ± 4.70 vs. 5.12 ± 4.34, p < 0.001), whereas they had a significantly lower PNI (38.33 ± 6.80 vs. 42.67 ± 6.47, p < 0.001), preoperative functional vital capacity (FVC; 2.04 ± 0.76 vs. 2.45 ± 0.71 L, p < 0.001), and forced expiratory volume at 1 s (FEV1; 1.43 ± 0.53 vs. 1.78 ± 0.58 L, p < 0.001). Multiple logistic regression analysis identified NLR (odds ratio [OR], 1.142; 95% confidence interval [CI], 1.060−1.230; p < 0.001) and FEV1 (OR, 0.340; 95% CI, 0.191−0.603; p < 0.001) as risk factors for postoperative complications after hip fracture surgery. Conclusion: Preoperative NLR and FEV1 are objective predictors of in-hospital postoperative complications after hip fracture surgery in older patients.

Superior nanopatterns via adjustable nanoimprint lithography on aluminum oxide in high-K thin films with ultraviolet curable polymer.

The present study substantiate that ultraviolet-nanoimprint lithography (UV-NIL) can be used to transfer a one-dimensional nano-pattern onto a high-k thin film of aluminum oxide mixed with a UV photocuring agent. Polydimethylsiloxane (PDMS) molds fabricated on silicon wafers were made using deep ultraviolet laser interference lithography in order to investigate one-dimension nanopatterns. These imprinted nano-patterns induce geometric deformations in the liquid crystal (LC), creating collective and elastic properties, which act as a guide for homogeneous alignment. The nanoimprint method can process a large area, so it can be processed much easier, faster, and more accurately than the conventional rubbing method. Moreover, the optical properties of the nano-imprinted aluminum oxide (AlO) thin-film are about 1.5p% superior to that of conventional commercialized cells, so it has a high effect on the luminance and color gamut of the display. After pattern imprinting, atomic force microscope (AFM) was performed to confirm the result. We can compared the cycle of AlO mixed with UV photocuring agent PDMS pattern cycle, the period is 776 and 750 nm, the width is 468 and 450 nm, the spacing is 292 and 300 nm, and the height is 40 and 30 nm. The nano-imprinted film appears to replicate the width, amplitude, and spacing of the PDMS template. In addition, X-ray photoelectron spectroscopy was performed to determine the chemical properties of the thin film and it was confirmed that UV irradiation induces oxidation, thus increases the intensity significantly. The binding energies of Al 2p and C-O spectra were situated at 74.27 ± 0.5 eV and 531.78 ± 0.5 eV, respectively.

Physicochemical Modification Effect on Homogeneously Aligned Liquid Crystals Based on the Nickel Oxide Thin Film.

We demonstrated homogeneous liquid crystal (LC) alignment on Nickel Oxide (NiO) films subjected to ion beam (IB) irradiation. Uniform LC alignment was achieved at high IB intensity values of 1200 and 1800 eV. To determine the mechanism of LC alignment following IB irradiation, physicochemical analysis was performed using atomic force microscopy and X-ray photoelectron spectroscopy. IB irradiation with high intensity increases uniformity of the surface, and IB irradiation induces the formation of oxygen vacancies and increases the NiO (Ni2+) phase components. Hence, both of the smooth surface and the strong van der Waals interactions between the NiO film and the LC molecules provides the LC molecules with a stable anchor on the surface, leading to uniform LC alignment on NiO films after IB irradiation. IB-irradiated NiO exhibited a high transparency of 85% in the visible light range as compared with the 83% average transmittance of conventional polyimide, which makes the IB-irradiated NiO alignment layer attractive in display devices.

Formyl Peptide Receptor 2 Is Involved in Cardiac Repair After Myocardial Infarction Through Mobilization of Circulating Angiogenic Cells.

Increasing evidence suggests that circulating angiogenic cells (CACs) promote repair of ischemic tissues. Activation of formyl peptide receptor 2 (Fpr2) has been reported to stimulate repair of ischemic heart. This study was conducted to investigate the role of Fpr2 on CAC mobilization and cardiac protection in myocardial infarction (MI). WKYMVm, a strong agonist for Fpr2, was administered in a murine model of acute MI, and mobilization of CACs including endothelial progenitor cells (CD34+ Flk1+ or Sca1+ Flk1+ cells) in peripheral blood was monitored. CAC mobilization by daily injection of WKYMVm for the first 4 days after MI was as efficient as granulocyte colony-stimulating factor and provided myocardial protection from apoptosis with increased vascular density and preservation of cardiac function. Transplantation of bone marrow (BM) from green fluorescent protein mice showed that BM-derived cells homed to ischemic heart after WKYMVm treatment and contributed to tissue protection. Transplantation of BM from Fpr2 knockout mice showed that Fpr2 in BM cells is critical in mediation of WKYMVm-stimulated myocardial protection and neovascularization after MI. These results suggest that activation of Fpr2 in BM after WKYMVm treatment provides cardiac protection through mobilization of CACs after MI, which may lead to the development of a new clinical protocol for treating patients with ischemic heart conditions. Stem Cells 2017;35:654-665.

5-Azacytidine modulates interferon regulatory factor 1 in macrophages to exert a cardioprotective effect.

Macrophages are actively involved in inflammatory responses during the progression of cardiac injury, including myocardial infarction (MI). A previous study showed that 5-azacytidine (5AZ), a DNA methylation inhibitor, can ameliorate cardiac injury by shifting macrophages toward an anti-inflammatory phenotype via iNOS inhibition. Here, we show that the beneficial effect of 5AZ is associated with sumoylation of interferon regulatory factor-1 (IRF1) in macrophages. IRF1 is a critical transcription factor for iNOS induction and is antagonized by IRF2. In the stimulated macrophages, IRF1 accumulated in the nucleus without degradation by 5AZ treatment. In animal study, 5AZ administration resulted in significant improvements in cardiac function and fibrosis. IRF1-expressing macrophages were more abundant in the 5AZ-treated MI group than in the PBS-treated MI group. Because sumoylated IRF1 is known to mimic IRF2, we examined the IRF1 sumoylation. Sumoylated IRF1 was resistant to degradation and significantly increased in the 5AZ-treated MI group. Collectively, 5AZ had a protective effect after MI by potentiation of IRF1 sumoylation and is suggested as a novel therapeutic intervention for cardiac repair.

Involvement of miR-34c in high glucose-insulted mesenchymal stem cells leads to inefficient therapeutic effect on myocardial infarction.

High glucose-insulted bone marrow-derived mesenchymal stem cells (BMCs) showed impaired angiogenesis along with downregulation of stem cell factor (SCF). This study was designed to determine the involvement of microRNAs (miR), which are actively involved in the physiological function of stem cells. We observed that miR-34c was significantly induced by high glucose treatment and blunted tube formation of BMCs. Stem cell factor (SCF) was confirmed as a target of miR-34c by 3'-UTR promoter analysis and Western blot. SCF knockdown by siRNA induced Krüppel-like factor 4 (KLF4) and resulted in the blockade of angiogenesis of BMCs. Sequentially, KLF4 overexpression completely blocked tube formation through inducing PAI-1 (plasminogen activator inhibitor-1). To study the action of miR-34c in terms of the therapeutic potential of BMCs, myocardial infarction (MI) was induced by ligation of the coronary artery in nude mice, BMCs transfected with miR-control or miR-34c were injected into the infarcted myocardium 7 days later, and histological studies were performed 2 weeks later. Cardiac fibrosis was 18.24±4.7% in the miR-34c-BMC group and 10.01±0.2% in the miR-control-BMC group (p<0.05). Cardiac function and vessel density were decreased in the miR-34c-BMC group compared with the miR-con-BMC group. Particularly, miR-34c-BMCs failed to incorporate into vessels. Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.

Pik3ip1 modulates cardiac hypertrophy by inhibiting PI3K pathway.

Cardiac hypertrophy is an adaptive response to various physiological and pathological stimuli. Phosphoinositide-3 kinase (PI3K) is a highly conserved lipid kinase involved in physiological cardiac hypertrophy (PHH). PI3K interacting protein1 (Pik3ip1) shares homology with the p85 regulatory subunit of PI3K and is known to interact with the p110 catalytic subunit of PI3K, leading to attenuation of PI3K activity in liver and immune cells. However, the role of Pik3ip1 in the heart remains unknown. In the present study, the effects of Pik3ip1 on cardiac hypertrophy were examined. We found that the expression level of Pik3ip1 was markedly higher in cardiomyocytes than in fibroblasts. The interaction of Pik3ip1 with the p110a subunit of PI3K in the heart was identified by immunoprecipitation using neonatal rat cardiomyocytes (NRCM). Approximately 35% knockdown of Pik3ip1 was sufficient to induce myocardial hypertrophy. Pik3ip1 deficiency was shown to lead to activation of PI3K/protein kinase B (AKT)/ mammalian target of rapamycin (mTOR) signaling pathway, increasing protein synthesis and cell size. However, adenovirus-mediated overexpression of Pik3ip1 attenuated PI3K-mediated cardiac hypertrophy. Pik3ip1 was upregulated by PHH due to swimming training, but not by pathological cardiac hypertrophy (PAH) due to pressure-overload, suggesting that Pik3ip1 plays a compensatory negative role for PHH. Collectively, our results elucidate the mechanisms for the roles of Pik3ip1 in PI3K/AKT signaling pathway.

Impact of smoking on clinical outcomes in female patients with acute myocardial infarction.

BACKGROUND AND OBJECTIVES: Cigarette smoking has been recognized as a prominent threat to women's health. We investigated the impact of smoking on clinical outcomes in Korean female patients after acute myocardial infarction (AMI). SUBJECTS AND METHODS: Out of the AMI patients who enrolled in the Korea AMI Registry, 4444 female patients were included in this study. Patients were divided into two groups-non-smoker and smoker-according to their current smoking status. We compared in-hospital mortality and major adverse cardiac events (MACE), including cardiac death, myocardial infarction, repeated percutaneous coronary intervention (PCI), or coronary artery bypass grafting during the one-year clinical follow-up period between two groups. RESULTS: The non-smoker group had more hypertension (HTN) and diabetes mellitus. The levels of total cholesterol, triglyceride, and low-density lipoprotein cholesterol were higher in the non-smoker group. However, in-hospital mortality was significantly higher in the smoker group (1.0% vs. 2.4%, p=0.002), and cardiac death during the 12-month clinical follow-up was significantly more frequent in the smoker group (2.2% vs. 4.5%, p=0.003). Total MACEs during the 12 months were higher in the smoker group (4.9% vs. 6.8%, p=0.014). Smoking and HTN were independent predictors of MACE {odds ratio (OR): 1.742, 95% confidence interval (CI): 1.010-3.000, p=0.046; OR: 1.573, 95% CI: 1.003-2.466, p=0.049, respectively}. CONCLUSION: Female smokers with AMI showed significantly higher in-hospital mortality and MACE rates during the one-year clinical follow-up period.

Nickel Oxide Nanoparticles Doped Liquid Crystal System for Superior Electro-Optical Properties.

We examined the properties of nematic liquid crystal (N-LC) systems with dispersed nickel oxide nanoparticles (NPs). Uniform LC alignments with regular pretilt angles were achieved on rubbed polymer surface regardless of NiO nanoparticles concentration. We confirmed the electro-optical characteristics of twisted nematic (TN) cells containing NiO nanoparticles on rubbed polymer surface, which exhibited lower threshold voltages and faster response times with less capacitance hysteresis than pure LC cells. It is clear that the response time of TN cells on rubbed polymer surfaces decreases with increasing the NiO nanoparticles concentration. These results demonstrate the relationship between NP doping concentration and trapping of impurity ions, and were confirmed by a software simulation of electric flux and field density. NiO nanoparticles in the LC cells focused the electric field flux and strengthened the electric field. Further, NiO nanoparticles in LC medium trapped charged ionic impurities and suppressed the screen effect, leading to a stronger electric field and the van der Waals interactions between LC molecules and the alignment layers.

Genistein promotes endothelial colony-forming cell (ECFC) bioactivities and cardiac regeneration in myocardial infarction.

UNLABELLED: Although stem cell-mediated treatment of ischemic diseases offers significant therapeutic promise, the limitation in the therapeutic efficacy of transplanted stem cells in vivo because of poor engraftment remains a challenge. Several strategies aimed at improving survival and engraftment of stem cells in the ischemic myocardium have been developed, such as cell transplantation in combination with growth factor delivery, genetic modification of stem cells, and/or cell therapy using scaffolds. To improve therapeutic efficacy, we investigated the effects of genistein on the engraftment of transplanted ECFCs in an acute myocardial ischemia model. RESULTS: We found that genistein treatment enhanced ECFCs' migration and proliferation, which was accompanied by increases in the expression of ILK, α-parvin, F-actin, and phospholylation of ERK 1/2 signaling. Transplantation of genistein-stimulates ECFCs (GS-ECFCs) into myocardial ischemic sites in vivo induced cellular proliferation and secretion of angiogenic cytokines at the ischemic sites and thereby enhanced neovascularization and decreased myocardial fibrosis as well as improved cardiac function, as shown by echocardiography. Taken together, these data suggest that pretreatment of ECFCs with genistein prior to transplantation can improve the regenerative potential in ischemic tissues, providing a novel strategy in adult stem cell therapy for ischemic diseases.

Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.

We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary artery in rats, and the rats were divided into two groups; a saline-injection group and a 5AZ-injection group (2.5 mg/kg/day, intraperitoneal injection). LV function was evaluated and immunohistochemical analyses were performed 2 weeks after MI. Cardiac fibrosis was induced by angiotensin II (AngII) infusion with or without 5AZ (5 mg/kg/day) in mice. Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment. Both induction of inducible nitric oxide synthase (iNOS) and iNOS promoter activity by PGN were inhibited by 5AZ. Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration. Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05). Arginase-1(+)CD68(+) macrophages with anti-inflammatory phenotype were predominant in the infarct border zone of the MI+5AZ group, in comparison with the MI group. AngII-induced cardiac fibrosis was also attenuated after 5AZ administration. In cardiac fibroblasts, pro-fibrotic mediators and cell proliferation were increased by AngII, and these increases were attenuated after 5AZ treatment. 5AZ exerts its cardiac protective role through modulation of macrophages and cardiac fibroblasts.

Mesenchymal stem cells reciprocally regulate the M1/M2 balance in mouse bone marrow-derived macrophages.

Mesenchymal stem cells (MSCs) have been widely studied for their applications in stem cell-based regeneration. During myocardial infarction (MI), infiltrated macrophages have pivotal roles in inflammation, angiogenesis and cardiac remodeling. We hypothesized that MSCs may modulate the immunologic environment to accelerate regeneration. This study was designed to assess the functional relationship between the macrophage phenotype and MSCs. MSCs isolated from bone marrow and bone marrow-derived macrophages (BMDMs) underwent differentiation induced by macrophage colony-stimulating factor. To determine the macrophage phenotype, classical M1 markers and alternative M2 markers were analyzed with or without co-culturing with MSCs in a transwell system. For animal studies, MI was induced by the ligation of the rat coronary artery. MSCs were injected within the infarct myocardium, and we analyzed the phenotype of the infiltrated macrophages by immunostaining. In the MSC-injected myocardium, the macrophages adjacent to the MSCs showed strong expression of arginase-1 (Arg1), an M2 marker. In BMDMs co-cultured with MSCs, the M1 markers such as interleukin-6 (IL-6), IL-1ß, monocyte chemoattractant protein-1 and inducible nitric oxide synthase (iNOS) were significantly reduced. In contrast, the M2 markers such as IL-10, IL-4, CD206 and Arg1 were markedly increased by co-culturing with MSCs. Specifically, the ratio of iNOS to Arg1 in BMDMs was notably downregulated by co-culturing with MSCs. These results suggest that the preferential shift of the macrophage phenotype from M1 to M2 may be related to the immune-modulating characteristics of MSCs that contribute to cardiac repair.

Enhanced switching behavior of iron oxide nanoparticle-doped liquid-crystal display.

It is well known that doping nanoparticles (NPs) in liquid crystals (LCs) can easily change the physical and electro-optical properties of LC mixture. In this paper, we demonstrate homogeneous, aligned nematic LC (N-LC) system dispersed in iron oxide (Fe2O3) NPs. The prepared Fe2O3 NPs have an average particle size of 50 nm. By changing the doping concentration of Fe2O3 NPs, we observed the characteristics of LC systems. Electrooptical (EO) characteristics included faster rising and falling times (2.14 ms and 10.24 ms, respectively) and lower driving voltage (1.45 V) compared with a pure N-LC cell. We demonstrated these results via the relationship between dielectric con- stant and LC device properties. The results were verified by software simulation based on general physical properties. Moreover, we observed that LC system with Fe2O3 NPs could be accomplished without capacitance hysteresis by capturing charged impurities. Superior performance of LC cell with Fe2O3 NPs indicates that the proposed LC system have strong potential for use in the production of advanced LC displays.

Comparative assessment of angiotensin II type 1 receptor blockers in the treatment of acute myocardial infarction: surmountable vs. insurmountable antagonist.

BACKGROUND: The mechanisms of antagonism vary between the angiotensin II type 1 receptor blockers (ARBs): insurmountable antagonism and surmountable antagonism. Recent retrospective observational studies suggest that ARBs may not have equivalent benefits in various clinical situations. The aim of this study was to compare the effect of two categories of ARBs on the long-term clinical outcomes of patients with acute myocardial infarction (AMI). METHODS: We analyzed the large-scale, prospective, observational Korea Acute Myocardial Infarction Registry study, which enrolled 2740 AMI patients. They divided by the prescription of surmountable ARBs or insurmountable ARBs at discharge. Primary outcome was major adverse cardiac events (MACEs), defined as a composite of cardiac death, nonfatal MI, and re-percutaneous coronary intervention, coronary artery bypass graft surgery. RESULTS: In the overall population, the MACEs rate in 1 year was significantly higher in the surmountable ARB group (14.3% vs. 11.2%, p=0.025), which was mainly due to increased cardiac death (3.3% vs. 1.9%, p=0.031). Matching by propensity-score showed consistent results (MACEs rate: 14.9% vs. 11.4%, p=0.037). In subgroup analysis, the insurmountable ARB treatment significantly reduced the incidence of MACEs in patients with left ventricular ejection fraction greater than 40%, with a low killip class, with ST segment elevation MI, and with normal renal function. CONCLUSIONS: In our study, insurmountable ARBs were more effective on long-term clinical outcomes than surmountable ARBs in patients with AMI.

Characteristics of patients with a significant stenosis in a conventional coronary angiogram with a normal multi-detector computed tomographic coronary angiogram.

Multi-detector computed tomography (MDCT) has high diagnostic value for detecting or excluding coronary artery stenosis. However, conventional coronary angiograms (CCA) are occasionally required in patients having persistent chest pain with normal MDCT. We retrospectively analyzed 90 patients who underwent CCA due to persistent chest pain with normal MDCT. The patients were classified into patients having more than 50% diameter stenosis in CCA (false negative, group I: n = 14, 62.6 +/- 7.5 years, 7 males) and those having less than 50% diameter stenosis (true negative, group II: n = 76, 52.1 +/- 12.0 years, 42 males). Significant stenosis was observed in 9 patients at the left anterior descending artery, 4 at the right coronary artery, and 1 at the left circumflex artery in group I. Group I patients were older than group II patients (63 +/- 8 versus 52 +/- 12 years, P < 0.001). There were more patients with hypertension and smoking in group I (64.3% versus 7.9%, 35.7% versus 3.9%, P < 0.001, P < 0.001, respectively). The levels of uric acid and homocysteine were higher in group I than in group II (5.7 +/- 1.5 versus 4.6 +/- 1.2 mg/dL, 9.6 +/- 3.1 versus 7.4 +/- 2.5 mol/L, P = 0.008, P = 0.010, respectively). There were more ST or T changes in the electrocardiograms in group I (35.7% versus 1.3%) (P < 0.001). In multivariate analysis, a history of hypertension, uric acid levels, and ischemic evidence in the electrocardiogram were independent factors for a false negative of MDCT (odds ratio 11.11, 4.76, 1.81, 95% confidence interval 4.67 to 10.00, 1.41 to 1.61, 1.05 to 3.33, P = 0.009, P = 0.012, P = 0.046, respectively). In certain situations, the findings of coronary stenosis by MDCT do not always correlate with that of CCA.

Acute dermatomyositis associated with generalized subcutaneous edema.

Generalized subcutaneous edema is an uncommon manifestation of inflammatory myopathy. We report a 48-year-old female patient who presented with severe generalized edema, an erythematous skin rash, dysphagia and proximal muscle weakness. She was diagnosed with dermatomyositis from the clinical signs, increased muscle enzymes, electromyographic findings and a muscle biopsy. Magnetic resonance imaging revealed increased signal intensity in the muscular and subcutaneous layers. The conditions causing generalized edema were excluded. It was concluded that the generalized edema was secondary to dermatomyositis. Aggressive treatments with high-dose glucocorticoids and immunosuppressive agents were used to control the severe subcutaneous edema.