Vectorcardiogram in persistent common atrioventricular canal.
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Biomedical subjects
Publications and source records attributed to A Furuse.
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The sural nerves of 2 siblings, 7 and 6 years of age with Group A xeroderma pigmentosum, were biopsied. The densities of myelinated fibers, 5,808/mm2 and 5,163/mm2, respectively, were strikingly decreased in comparison to control data. Both large and small myelinated fibers were reduced. Electron microscopy demonstrated many collagen fibers in the endoneurium and some collagen pockets. The loss of myelinated fibers was less severe than in previously reported patients. This discrepancy may be due to age differences at biopsy; our patients were biopsied at the ages of 7 and 6 years, while those patients reported previously were 10 years of age or older. The incidence of neurologic manifestations in xeroderma pigmentosum may increase after 6 years of age.
This study was conducted to test a three-layered artificial neural network analysis of phonocardiogram recordings to diagnose, automatically and objectively, the condition of the heart in patients with heart murmurs. The data were recorded simultaneously in each of 49 patients with a heart murmur through eight microphones attached to the skin surface with adhesive tape, and were analysed by computer. The diagnosis was automated using a three-layered neural network technique. The neural network generated correct answers in over 70% of cases. Furthermore, about 80% of cases of two concurrent diseases were identified correctly. However, ventricular septal defects were incorrectly classified as aortic stenosis or aortic regurgitation, and patent ductus arteriosus was not diagnosed correctly. Accurate diagnoses can frequently be obtained using a neural network, but accuracy can be improved with further data accumulation.
A new biodegradable tracheal prosthesis was developed using hydroxyapatite rings as the artificial tracheal cartilage, a carbon fiber tube as the tracheal tube; it was then implanted into the cervical trachea in dogs. Morphologic examination revealed that the hydroxyapatite ring was anchored firmly to the tracheal cartilage by ingrowth of cartilaginous tissue into the macropores of the hydroxyapatite.
A multicomparative study to establish adequate anticoagulation therapy for left ventricular assist devices was undertaken by administrating various anticoagulants: heparin, a prostacyclin analogue combined with a protease inhibitor; thromboxane A2 synthetase inhibitor; or a protease inhibitor alone. Our investigation suggested that combined administration of prostacyclin analogue and protease inhibitor (FUT-175) is ideal anticoagulation therapy from the point of blood coagulation and fibrinolysis. Currently, however, sole administration of FUT-175 is adequate anticoagulation therapy during clinical use of left ventricular assist devices.
To establish ideal anticoagulation therapy for use with a left ventricular assist device, a study was done administering various anticoagulants: heparin, argatroban, a prostacyclin analogue combined with a protease inhibitor, or a protease inhibitor alone. Cardiac asisting by LVAD without any anticoagulants results in marked activation of blood coagulation or fibrinolysis. Administration of argatroban, as well as heparin, produces a bleeding tendency. Administration of a protease inhibitor (nafamostat mesilate, FUT-175) as a sole anticoagulant induces activation of the blood coagulation system to some extent, but it is within acceptable limits. Combined administration of a prostacyclin analogue (PG) and FUT-175 is most effective in maintaining balanced blood coagulation and fibrinolysis.
The sole administration of urokinase causes no initial prolongation of activated partial thromboplastin time (A-PTT), but thereafter produces serious progressive prolongation of A-PTT; it also causes a progressive, severe decrease in fibrinogen levels and alpha 2-plasmin inhibitor activity by depletion. The antithrombogenicity of urokinase is not caused by prevention of blood coagulation system activation by antithrombin effect, but by secondary fibrinolysis by plasmin. Consequently, the administration of urokinase as a sole anticoagulant results in activation of coagulation and fibrinolysis, and, as a result, induces disseminated intravascular coagulation. Therefore, it is concluded that administration of urokinase is an inadequate anticoagulation therapy unless it is combined with other antithrombin agents.
A new ventricular assist device (VAD) pneumatic driver with a servomatic left atrial pressure (LAP) control mechanism was developed for easy and safe control of left ventricular assist devices. The negative driving pressure (NP) can be automatically varied to control the assisted circulatory flow (AF), comparing the patient's LAP with prescheduled LAP (s-LAP). Animal experiments revealed this servomatic control system to be useful.
To establish ideal anticoagulant therapy for left ventricular assist devices (LVADs), a comparative study was made of a thromboxane A2 synthetase inhibitor, a protease inhibitor, and combined administration of the two. Results of the investigation indicate that combined administration of a thromboxane A2 synthetase inhibitor (OKY-046) and a protease inhibitor (nafamostat mesilate, FUT-175) provides ideal anticoagulant therapy during cardiac support using LVADs from the point of blood coagulation and fibrinolysis. Artificial hearts have come into practical use as left ventricular assist devices, and have contributed to the saving of many patients with severe postoperative low cardiac output syndrome, but they sometimes encounter severe complications, i.e. cerebrovascular bleeding, thromboembolism, infection, or multiple organ failure. It is very important, therefore, to control coagulation and fibrinolysis adequately during cardiac support by an LVAD.
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Total unilateral anomalous pulmonary venous connection with intact atrial septum is a rare form of congenital heart disease. Operative method to correct this anomaly varies according to the site of drainage of the anomalous pulmonary veins. Surgical experience in four patients are described.
We report a dramatic response of the nephrotic syndrome to prednisolone therapy (2 mg per kg per day) in a 6-year-old boy with IgA nephropathy. He had developed massive proteinuria (22.1 gm per day) and microscopic hematuria shortly after an episode of tonsillitis. Renal biopsy two months after onset showed mild mesangial hypercellularity with typical mesangial deposition of IgA. Corticosteroid therapy resulted in a sharp cessation of proteinuria and complete resolution of the urinary abnormalities. We suggest that massive proteinuria associated with IgA nephropathy may be responsive to corticosteroid therapy when there are minimal glomerular changes.