Complete nucleotide sequence of an infectious clone of human T-cell leukemia virus type II: an open reading frame for the protease gene.

The entire nucleotide sequence of an infectious clone of human T-cell leukemia virus type II provirus was determined. This provirus consists of 8952 nucleotides. In addition to long terminal repeats and gag, pol, env, and X, a protease gene that is responsible for processing the gag precursor protein was found. The protease gene is encoded in a different frame from gag and pol and was located between the gag and pol open reading frames. The 5' region of the protease gene overlaps the 3' gag region. Coding regions of the provirus show about 60% homology with those of human T-cell leukemia virus type I at the nucleotide level. The evolutionary relationship between human T-cell leukemia virus types I and II is discussed.     

Mechanism of antiarrhythmic action of beta-blocking agents

We investigated the antiarrhythmic effect of beta-blocking agents. Using 35 anesthetized dogs, the chest was opened and the left anterior descending coronary artery (LAD) was ligated for 30 min and the ventricular multiple response threshold (VMRT) was observed in the time course. The dogs were divided into five groups premedicated intravenously ten min before LAD ligation with either isotonic saline (the control group), D,L-propranolol (0.5 mg/kg), D-propranolol (0.5 mg/kg), D,L-pindolol (0.1 mg/kg), or D,L-acebutolol (2.5 mg/kg). Thirty min after ligation, myocardial mitochondria were prepared from the ischemic and the non-ischemic areas, and then the content of mitochondrial long-chain acyl-CoA and Ca++-binding activity were measured. The value of VMRT 1.59 +/- 0.21 mA before ligation decreased to 0.99 +/- 0.13 mA 30 min after ligation. Content of acyl-CoA in mitochondria from the ischemic area increased significantly compared to those from the non-ischemic area. Mitochondrial Ca++-binding activity in the ischemic area decreased significantly compared to that in the non-ischemic area. Each administration of three beta-blocking agents prevented the decreases in VMRT and Ca++-binding activity and excessive accumulation of acyl-CoA; D-propranolol had no effect. These results suggest that the antiarrhythmic action of beta-blocking agents is based, at least in part, on the protection from decrease in Ca++-binding activity due to mitochondrial dysfunction induced by the excessive accumulation of long-chain acyl-CoA in mitochondria.     

The effect of Coenzyme Q10 on reperfusion injury in canine myocardium

The mechanism of mitochondrial damage during reperfusion injury of ischemic myocardium was studied using mongrel dogs in vivo and isolated mitochondria in vitro. Seventy-seven adult dogs were divided into three groups: the control group (n = 38), the Coenzyme Q10 (CoQ10)-5 mg group (n = 24), and the CoQ10-15 mg group (n = 15). In the control group, the left anterior descending coronary artery (LAD) of the dog was occluded for 15 min followed by 5 min of reperfusion after 40 min of premedication with physiological saline. In both CoQ10 groups, 5 mg/kg or 15 mg/kg of CoQ10 was infused intravenously for 20 min and then physiological saline was administered for 20 min before 15 min occlusion of the LAD. Subsequently, reperfusion was allowed for 5 min. Each group was further divided into two subgroups depending on the presence (arrhythmia group) or the absence (non-arrhythmia group) of ventricular arrhythmias. Immediately after 15 min occlusion, myocardial samples were taken from the normal and reperfused areas to measure CoQ10 content of myocardium. Heart mitochondria were prepared after 5 min of reperfusion from both areas. Arrhythmias appeared in 12 of 38 dogs in the control group (32%), two of 24 dogs in the CoQ10-5 mg group (8%) and none of 15 dogs in the CoQ10-15 mg group (0%). Premedication with CoQ10 increased tissue CoQ10 content in a dose-dependent manner. In the CoQ10-5 mg group, the increase in CoQ10 content of dogs with reperfusion arrhythmias was relatively less than that of dogs without reperfusion arrhythmias. In each group, mitochondrial function was decreased in the arrhythmia group compared to that of the non-arrhythmia group. The increase in free fatty acid (FFA) content and the decrease in phospholipid content were also observed in mitochondria from the reperfused area of each arrhythmia group. The increase in FFA and mitochondrial dysfunction were induced by the incubation of mitochondria in vitro with phospholipase (PLase) A2 or PLase C, and protected by the addition of CoQ10. These results suggest that PLase plays an important role in the development of mitochondrial damage associated with reperfusion.     

Adenosine deaminase (ADA) in leukemia: clinical value of plasma ADA activity and characterization of leukemic cell ADA

Adenosine deaminase (ADA) activity was measured in plasma, erythrocytes, and mononuclear cells from 18 patients with acute and chronic leukemia. High levels of ADA activities were found in plasma, erythrocytes, and mononuclear cells from patients with acute leukemia, especially acute lymphoblastic leukemia, and blastic crisis of chronic myeloid leukemia. Serial determination of plasma ADA activities was done in 9 patients with acute leukemia. All patients untreated or in relapse had an elevation of plasma ADA activity, which decreased to normal or subnormal levels during complete remission. On starch gel electrophoresis, plasma ADA in leukemic patients separated into two bands. The major band showed a mobility identical to that of normal red cells and mononuclear cells, and the minor band corresponded to that of normal plasma ADA. Enzymatic and immunological studies were performed on ADA from leukemic cells of acute myeloid and lymphoblastic leukemia. There were no differences in Michaelis constant for adenosine, thermostability, electrophoretic mobility, immunological reactivity, and specific activity between ADA of leukemic cells and normal mononuclear cells. These results strongly suggest that the increased ADA activity in leukemic cells is caused by an increased synthesis of a structurally normal enzyme and that increased plasma ADA activity in leukemic patients reflects an increment of leukemic cells in bone marrow. Therefore, serial determination of plasma ADA activities seems to provide a good indicator of the total mass of leukemic cells in bone marrow.     

Reoperation of tetralogy of Fallot for the transannular patch neo-intimal stenosis: a case report]

A 3-year-old male patient underwent right ventricular outflow tract reconstruction with a glutaraldehyde-preserved equine pericardium for tetralogy of Fallot. Because of progressive severe pulmonary restenosis with over systemic right ventricular pressure, tricuspid regurgitation, and abnormal high echoic shadow in the distal main pulmonary artery on echocardiogram, he required reoperation a year after the first correction. In the reoperative findings, the pseudointima was thickened heavily and detached from glutaraldehyde-preserved equine pericardial patch. The patch was removed and the right ventricular outflow was reconstructed widely to the pulmonary bifurcation with porcine pericardial patch again. Patho-histological findings showed foreign body giant cells and macrophages in the pseudointima. Four years after the reoperation, echocardiogram shows 41 mmHg for the right ventricular pressure and 22 mmHg for the pressure gradient of right ventricular outflow tract, and the patient is doing well now.     

Bilateral distal anterior cerebral artery aneurysm associated with supreme anterior cerebral artery: case report]

A 67-year-old woman presented with bilateral distal anterior cerebral artery aneurysms manifesting as consciousness disturbance. Computed tomography revealed subarachnoid hemorrhage in the interhemispheric fissure, right sylvian fissure, and a hematoma in the right frontal lobe and lateral ventricles. Angiography showed bilateral symmetrical aneurysms located on the pericallosal artery at the bifurcation of the callosomarginal artery. The operation was performed on the day the patient was admitted. The aneurysms were clipped via the interhemispheric approach, and the hematoma was aspirated. Operative view demonstrated rupture of the left aneurysm, and supreme anterior cerebral aneurysm. Postoperative angiography showed disappearance of the aneurysms and an intact bilateral anterior cerebral artery. The patient was discharged with mild organic mental syndrome. However, a few days later, she was admitted again with a high fever and died of complications due to sepsis. Pathological view showed clipped aneurysms and the connection of the bilateral distal anterior cerebral artery with the so-called supreme anterior communicating artery.     

Tricuspid valve replacement in a patient with idiopathic tricuspid regurgitation]

Tricuspid regurgitation is often seen but is rarely categorized as "idiopathic". A 66-year-old man suspected of idiopathic tricuspid regurgitation underwent tricuspid valve replacement. With right heart failure over twenty years, his CTR increased to eighty six (86) per cent. During operation, no abnormal findings were observed except for the dilated tricuspid valve ring. Then a stented porcine xenograft (Carpentier-Edwards 33 mm) was inserted in the tricuspid valve annulus. Seven years after replacement, he died. Autopsy demonstrated myocardial hypertrophy of the right ventricle and dilatation of the right heart, supporting the diagnosis of idiopathic tricuspid regurgitation.     

Superior biocompatibility of heparin-bonded circuits in pediatric cardiopulmonary bypass.

BACKGROUND: Heparin bonding of pediatric cardiopulmonary bypass circuits may decrease activation of blood compartments as inflammatory responses. We studied the biocompatibility of heparin-bonded circuits in infant cardiac surgery. METHODS: Twenty-four infants undergoing elective cardiac surgery were randomly assigned to either a nonheparin-bonded control circuit (n = 12) or a fully heparin-bonded circuit (n = 12) including membrane oxygenator, reservoir, and all tubing. Blood samples were used to identify differences in complement activation and cytokine release between groups during and after cardiopulmonary bypass. The postbypass oxygenation index was also compared. RESULTS: The C3 activation product in the heparin-bonded group was significantly lower during (p < 0.01) and just after (p < 0.05) cardiopulmonary bypass. No statistically significant difference in C4 activation products was observed. Lower interleukin-6 and tumor necrosis factor-alpha were found immediately after cardiopulmonary bypass (p < 0.05) and a higher mean postbypass oxygenation index was also seen (p < 0.05) in the heparin-bonded group. CONCLUSION: We found that a heparin-bonded cardiopulmonary bypass circuit reduced inflammatory response and improved oxygenation in pediatric cardiac surgery. These results suggest that the superior biocompatibility of the bonded circuit may reduce pulmonary complications.