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Effects of oil brand, temperature and atmosphere conditions on copper sulfide deposition on insulating paper were investigated by thermal aging test. Copper sulfide deposition occurred in a certain oil brand and dibenzyi disulfide (DBDS) was found in the oil. There was an incubation period observed before copper sulfide deposition occurred. Copper sulfide deposition was accelerated by temperature. The deposition rate after the incubation period became twice when the heating temperature was increased by approximately 10 [degrees]C. The incubation period and the deposition rate were the same at 140 [degrees]C whether the thermal aging test was done in air or nitrogen atmosphere. On the other hand, the incubation period in air was shorter than that in nitrogen at 120 [degrees]C. The deposition rate was not affected by atmosphere condition at 120 [degrees]C. Intermediate substances due to copper dissolution into oil are introduced to explain the incubation period and the atmosphere dependence of incubation period observed at 120 [degrees]C. Index Terms--Copper, copper compounds, oil insulation, paper insulation, sulfur, sulfur compounds, transformers.

Background: Although oxidative stress mediated by reactive oxygen species plays an important role in the pathogenesis of heart failure (HF), good clinical markers for reactive oxygen species in patients with HF have not been established. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) is formed from deoxyguanosine in DNA by hydroxyl free radicals and might serve as a sensitive biomarker of intracellular oxidative stress in vivo. Thioredoxin (TRX) is known to be induced in cells as a radical scavenger against oxidative stress. The aim of this study is to evaluate the clinical significance of the serum 8-OHdG and TRX of patients with chronic HF with idiopathic dilated cardiomyopathy (DCM). Methods and Results: We estimated serum 8-OHdG and TRX levels using enzyme-linked immunosorbent assay in 32 patients with DCM and investigated the impact of these markers to the clinical characteristics of these patients. Serum levels of 8-OHdG, but not TRX were significantly correlated with New York Heart Association functional class, left atrial diameters, left ventricular end-diastolic diameters, left ventricular end-systolic diameters, and plasma levels of brain natriuretic peptide. Conclusion: These data suggest oxidative DNA damage is increased in patients with DCM according to the severity of HF. Serum levels of 8-OHdG may represent clinically useful markers of left ventricular remodeling. [ABSTRACT FROM AUTHOR]

Background: It remains unclear whether end-stage hypertrophic cardiomyopathy (HCM) is associated with as high a rate of sudden death as occurs among HCM patients with preserved left ventricular (LV) systolic function. The purpose of this study was to evaluate the incidence of sudden death among patients with end-stage HCM and to identify high-risk end-stage patients., Methods and Results: A total of 490 consecutive patients with HCM, who were diagnosed and followed-up at our hospital, were analyzed retrospectively. End-stage HCM was defined by an LV ejection fraction <50% on echocardiography during follow-up. Among the 490 HCM patients, 43 patients (8.8%) were diagnosed as having end-stage HCM during a mean follow-up period of 12 ± 7 years after the initial diagnosis. During a mean follow-up period of 5 ± 3 years after progression to end-stage HCM, sudden death occurred in 21 of 43 patients (47%). Cox proportional hazards analysis identified syncope as an independent predictor of sudden death (hazard ratio = 6.15; 95% confidence interval, 2.40-15.75; P < .001)., Conclusions: This study demonstrated that patients with end-stage HCM have a high incidence of sudden death. Therefore, it is suggested that an aggressive therapeutic strategy to counter sudden death should be considered for patients with end-stage HCM., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Purpose: In patients with acute decompensated heart failure (ADHF) and left ventricular systolic dysfunction (LVSD), the role of initial vasodilator therapy remains uncertain. The present study aimed to evaluate the acute efficacy of initial carperitide therapy and to predict its response in ADHF patients with LVSD., Methods: Twenty-four consecutive patients with ADHF and LVSD were enrolled. Inclusion criteria were a left ventricular ejection fraction < 40%, systolic blood pressure (BP) > 90 mm Hg, and pulmonary capillary wedge pressure >or=18 mm Hg at baseline. Hemodynamic parameters were evaluated by right heart catheterization before and after carperitide infusion. Responders were defined as a >or=30% reduction of pulmonary capillary wedge pressure (PCWP) or a decrease to < 16 mm Hg within 6 h after carperitide infusion., Results: Seventeen (71%) of the 24 patients were responders for initial carperitide therapy. The responders had significantly higher systolic BP and cardiac index at baseline compared with nonresponders. The area under the curve (AUC) for systolic BP was 0.93 and a cut-off value of 120 mm Hg had a sensitivity of 94% and specificity of 86% for predicting the efficacy of carperitide. The AUC for the cardiac index was 0.88 and a cut-off value of 2.30 L/min/m(2) had a sensitivity of 65% and a specificity of 100% for predicting the response to carperitide., Conclusions: The initial use of carperitide therapy safely reduces PCWP in ADHF patients with LVSD and baseline systolic BP may be useful for predicting the response to initial carperitide therapy for ADHF with LVSD.

A procedure of continuous-wave ultrasound (US)-induced hemolysis and reseal in solution containing water soluble protein was applied to a method for encapsulating concentrated protein solutions into resealed rat erythrocyte ghosts. To find a condition yielding a higher mean corpuscular concentration of encapsulated protein (MCC), we investigated the value of MCCs for various conditions. Additions of a small amount of plasma, Ca(2+) and Mg(2+) significantly increased MCC, whereas these additives did not alter the degree of hemolysis. It was suggested that plasma protect the molecular damages by the US, and that Ca(2+) and Mg(2+) physically stabilized the lipids of the erythrocyte membrane to fuse and reseal the pore induced by US. A maximal MCC of approximately 50 mg/mL, which is 2.5 times the reported maximum amount encapsulated by the osmotic dialysis method, was obtained without a blood-washing procedure.

Chronic renal failure (CRF) is one of the risk factors of a worse outcome for patients with coronary artery disease. However, few studies have assessed the outcome in such patients. This study investigated the clinical characteristics, treatment modalities, and prognosis for patients with angina pectoris accompanied by CRF and evaluated the validity of current treatment strategy for these patients. A total of 593 patients (248 with stable angina and 345 with unstable angina) admitted to our institution were studied. Renal failure was defined as serum creatinine of > or = 2.0 mg/dl. Patients were divided into 2 groups, with renal failure (46 patients) and without renal failure (547 patients), and the former group was further divided into 2 groups with hemodialysis (26 patients) and without hemodialysis (20 patients). The mean follow-up period was 2.5 +/- 1.2 years and the follow-up rate was 99%. The prevalences of congestive heart failure (26% vs 3%, p < 0.001), hypertension (72% vs 45%, p < 0.005), and multivessel coronary artery disease (65% vs 33%, p < 0.001) were higher in patients with CRF. The left ventricular end-diastolic volume was greater in patients with CRF than in patients without CRF (114 +/- 36 vs 85 +/- 24 ml/m2, p < 0.001). The calcification score of both coronary arteries and abdominal aorta evaluated by electron-beam computed tomography was higher in patients with CRF (2,187 +/- 2,727 vs 631 +/- 841, p = 0.03; 4,091 +/- 3,068 vs 2,191 +/- 2,249, p = 0.02, respectively). In-hospital cardiac mortality was higher in patients with CRF than in patients without CRF (8.7% vs 0.7%, p < 0.001). The cumulative survival was 88% at 1 year and 65% at 3 years in patients with CRF and 99% and 97% in patients without CRF, respectively (p < 0.001). The incidence of re-hospitalization due to congestive heart failure was higher in patients with CRF (19% vs 1.3%, p < 0.0001). The cumulative survival in CRF was 93% at 1 year, 57% at 3 years in the medical treatment group and 87% and 75% in the invasive therapy group, respectively (p = 0.1). Patients with angina pectoris and CRF had a poor prognosis under the current treatment strategy. Newly developed therapeutic strategies, such as rotational atherectomy, minimally invasive direct coronary artery bypass surgery and combinations, will be necessary to improve the long-term prognosis for these patients.

Auditory Brainstem Response (ABR) is the most reliable and most frequently used procedure to evaluate audiological conditions in early infancy. However, several reports have demonstrated that developmental change in the central nervous system may affect the results of ABR in audiological evaluations. We examined statistically the reliability of ABR for the diagnosis of profound deafness in early childhood according to our experience over the past 12 years of follow-up in our facility. Subjects included 371 children among 1,041 children who were admitted to Kanariya-Gakuen (institute for pre-school deaf children) from April 1985 to March 1997. These children were examined with ABR to determine their hearing levels. In five cases with an abnormal hearing threshold determined by ABR and other audiological tests, repeated examinations carried out during a 5- to 6-month follow-up period revealed that they had normal hearing. Three of these children had been diagnosed previously with mental retardation and the remaining two were infants < 5 months old. The specificity and sensitivity of ABR were calculated as 97.3% and 100%, respectively. The predictive value of a positive result was 94.7%. There remains the possibility of a false negative for such cases, although the rate seems to be very low (< 0.2%).

Using two models of acute lung inflammatory injury in rats (intrapulmonary deposition of immunoglobulin G immune complexes and systemic activation of complement after infusion of purified cobra venom factor), we have analyzed the requirements and patterns for upregulation of lung vascular P-selectin. In the immune complex model, upregulation of P-selectin was defined by Northern and Western blot analysis of lung homogenates, by immunostaining of lung tissue, and by vascular fixation of 125I-labeled anti-P-selectin. P-selectin protein was detected by 1 hour (long before detection of mRNA) and expression was sustained for the next 7 hours, in striking contrast to the pattern of P-selectin expression in the cobra venom factor model, in which upregulation was very transient (within the 1st hour). In the immune complex model, injury and neutrophil accumulation were P-selectin dependent. Upregulation of P-selectin was dependent on an intact complement system, and the presence of blood neutrophils was susceptible to the antioxidant dimethyl sulfoxide and required C5a but not tumor necrosis factor alpha. In contrast, in the cobra venom factor model, upregulation of P-selectin, which is C5a dependent, was also dimethyl sulfoxide sensitive but neutrophil independent. Different mechanisms that may explain why upregulation of lung vascular P-selectin is either transient or sustained are discussed.