An 80-year-old Japanese man was admitted with orthopnea and pitting edema of both lower legs. We diagnosed congestive heart failure (CHF) on the basis of a chest X-ray and an echocardiogram. An ...electrocardiogram showed a heart rate of 120 beats/min with atrial fibrillation rhythm (Af). The patient developed aortic valve failure and destruction of the base of right coronary artery (RCA) due to infectious endocarditis at 71 years of age. The patient underwent aortic valve replacement and coronary artery bypass grafting with an interposed graft with polyester vascular graft to RCA. The patient recovered from CHF after the 6 days of treatment with diuretics and verapamil. We confirmed the patency of coronary arteries and bypass grafts using a 64-slice cardiac computed tomography scan (CT) and diagnosed CHF due to Af. Here we describe the estimation of the prosthetic coronary artery graft patency with the interposition procedure using 64-slice cardiac CT.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK, VSZLJ
Recent studies suggest that granulocyte colony-stimulating factor (G-CSF) may be beneficial in the treatment of myocardial infarction (MI). However, the effects of G-CSF on MI are still controversial ...and the molecular mechanism of G-CSF treatment for repair of the infarcted heart is not fully understood.
Mice were divided into three groups: Control, MI and MI treated with G-CSF. Four weeks after MI, we examined cardiac function by Doppler echocardiography and measured non-infarcted myocardial mRNA expression by northern blot analysis.
Cardiac function decreased significantly in the MI groups compared with the sham-operated groups. Additionally, the ratios of E wave to A wave peak velocity (E/A) in the MI groups were higher than in the control group. E/A in G-CSF MI mice was significantly lower than in control MI mice (p<0.01). Matrix metalloproteinase-2 (MMP-2) mRNA expression was significantly increased in the MI groups compared with the control group (p<0.01). Furthermore, mRNA expression in the G-CSF MI group was significantly higher than in the Control MI group (p<0.05).
G-CSF can prevent the LV remodeling process after MI that accompanies progressive cardiac dysfunction. One of the mechanisms of G-CSF treatment for cardiac remodeling after MI may be overexpression of MMP-2 in non-infarcted myocardium.
Aortoesophageal fistula (AEF) is a rare but life-threatening pathology. We report a case of a primary AEF that was successfully managed with temporary thoracic endovascular aortic repair (TEVAR) and ...esophagectomy with video-assisted thoracoscopic surgery. A 73-year-old man was transferred to the emergency department with a complaint of hematemesis. A computed tomography scan identified an AEF due to aortic aneurysm. We placed a stent using TEVAR for the purpose of hemodynamic stasis, and the operation was performed 23 h after admission. Right video-assisted thoracoscopic esophagectomy (VATS-E) was chosen, and a cervical esophagostomy and a feeding gastrostomy tube was constructed. Infection had been effectively controlled postoperatively. Four months after the first operation, we performed esophageal reconstruction. At the 70-month follow-up examination, the patient had no signs of mediastinitis. VATS-E immediately after hemostabilization by TEVAR is useful management for primary AEF.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The toxic interaction between disopyramide and propranolol were studied in chick embryos. Fertilized eggs of White Leghorns were incubated and investigated. Disopyramide with and without propranolol ...was injected into the air sac of a fertilized egg on the 16th day of incubation. Electrocardiograms (ECGs) were recorded 0 to 60 min after the injection. After each drug injection alone, the heart rate was not different compared with control. However, the heart rate was significantly decreased by combination with disopyramide and propranolol. In addition, arrhythmia was produced by disopyramide 1.0 mg/egg alone and in combination with propranolol. These findings indicate that the interaction between disopyramide and propranolol has a marked influence on the heart rate in chick embryos.
The purpose of this study was to determine the effects of resin hydrophilicity on dentin bonds. The study examined the microtensile bond strength of six experimental self-etching primers and two ...experimental bonds (50wt% ethanol/50wt% comonomers) of various degrees of hydrophilicity, that is various degrees of HEMA, to intact dentin. Following composite buildup, hourglass-shaped slabs were prepared from the bonded teeth for microtensile testing after24hours or6months. Higher bond strengths were achieved with increased resin hydrophilicity after 24hours, while the lowest bond strengths were achieved with increased resin hydrophilicity after6months. Measurements of water sorption/solubility of the polymers that were previously described showed high correlations between water sorption and the degree of HEMA, and between polymer solubility and the degree of HEMA. These results indicated that higher resin hydrophilicity was effective for short-term microtensile strength, while increased resin hydrophilicity may cause lower bond strength due to the weakness of polymers that have absorbed water after 6 months.
In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca2+ transport protein, such as ...sarcoplasmic reticulum Ca2+(SR-Ca2+)-ATPase, Na+-Ca2+ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca2+ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ratio of E wave to A wave velocity. Expression of myocardial alpha-skeletal actin, beta-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca2+-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na+-Ca2+ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Strength of compression members in a steel truss bridge are generally calculated as that of a pin-connected member by considering their effective buckling length. But the strength of the members is ...to be figured out by considering rotational restriction by gusset plates through FEM analysis of the truss bridge. Then, effects of the gusset plates on the ultimate strength and deformation of the compression members are discussed in this paper. It is concluded that the compression members can be classified into 3 types depending on bending moment distributions and deformation modes at their ultimate state and the ultimate strength of the compressive members in truss bridge can be obtained by those of the single column with different boundary conditions with the member positions.
T. Omura, M. Yoshiyama, K. Takeuchi, S. Kim, H. Iwao, H. Yamagishi, I. Toda, M. Teragaki, K. Akioka and J. Yoshikawa. Angiotensin Blockade Inhibits SIF DNA Binding Activities via STAT3 after ...Myocardial Infarction. Journal of Molecular and Cellular Cardiology (2000) 32, 23–33. The in vivo activation of transcription factors, which is important for cell regulation by gene expression, has not been well examined in myocardial infarcted heart. The purpose of this study was to determine whether myocardial signal transducer and activator of transcription (STAT) pathway is activated as sis-inducing factor (SIF) in infarcted heart, and to assess the angiotensin blockade on SIF activity in ischemic and non-ischemic myocardium of rat. Myocardial infarction was made by ligation of the coronary artery in Wistar rats. In electrophoretic mobility shift assay, myocardial SIF DNA binding activities gradually increased and reached to peak at 1 week in infarcted and non-infarcted regions after myocardial infarction. Imidapril and candesartan cilexitil significantly prevented the increase in SIF DNA binding activity in infarcted and non-infarcted regions. This increased SIF DNA complex was supershifted by specific anti-STAT3 antibody, indicating that increased SIF complex at least contained activated STAT3 proteins in myocardial infarcted heart. Furthermore, immunoprecipitation-Western blot analysis revealed that STAT3 of infarcted and non-infarcted regions were tyrosine-phosphorylated at 1 week after myocardial infarction. Imidapril and candesartan cilexitil prevented the increase in phosphorylated STAT3. Thus, the transcriptional activation of STAT3 through AT1 receptor may be partially involved in cardiac remodeling after myocardial infarction.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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