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Biomedical subjects

B Akikusa

Publications and source records attributed to B Akikusa.

46 records · Page 3Linked to original sources

Lipid metabolism in arteriosclerotic arterial wall of rats.

Arteriosclerotic lesions were formed in rat aorta by the administration of vitamin D2, a high-fat diet and a thyroid suppressing agent. This treatment increased the serum total cholesterol level to 12 times the control level. In the arteriosclerotic lesions that were induced the activities of lysosomal enzymes, such as acid phosphatase and acid lipase, were higher than in controls, that of acid cholesterol esterase was decreased, those of microsomal lipid-synthesizing enzymes--such as acyl-CoA synthetase and cholesterol ester synthesizing activity--were increased and that of neutral cholesterol esterase was decreased. These data suggest that lipid metabolism in arteriosclerotic lesions was changed, resulting in the accumulation of cholesterol esters in the aorta. Administration of high-fat diet and thyroid suppressing agent also increased the serum cholesterol levels to 12-fold the control level, but did not induce arteriosclerotic lesions. After this treatment the activities of hydrolyzing enzymes, such as acid and neutral cholesterol esterase and lipase, in the aorta increased, but the activities of lipid synthesizing enzymes also increased. These data suggest that lipid metabolism in the aorta in this condition changed to compensate for the large influx of serum lipids and to prevent arteriosclerosis. The roles of the serum lipid level, cell injury and lipid metabolism in the aorta in forming arteriosclerotic lesions are discussed on the basis of these results.

Animals↗

Nephrotic syndrome developed in the healing stage of necrotizing angiitis.

A case of necrotizing angiitis is reported. After acute inflammatory changes had subsided, the patient developed the nephrotic syndrome. Postmortem examination disclosed a unique sclerotic glomerular lesion with deposition of eosinophilic material which contained IgM, IgA, C1, and C3. The lesion was distributed in rather selective areas perfused by some of the arcuate arteries.

Adult↗

Chronic Masugi nephritis in the rat. An electron microscopic study on evolution and consequences of glomerular capsular adhesions.

Chronic focal glomerulonephritis was induced in the rat by using goat nephrotoxic IgG. In the later stage (6 to 15 months) a number of glomeruli were found to be attached to Bowman's capsule with variable segmental sclerosis and/or hyalinosis. The morphogenesis of the changes was studied by electron microscopy. It was found that partial cytoplasmic necrosis of podocytes was an initiating event of the capsular adhesion. When this occurred in the peripheral tufts, the denuded portion of the glomerular basement membrane (GBM) became attached to the parietal epithelium, resulting in progressive thickening of the mesangium and GBM, deposition of hyaline or proteinaceous material, and desquamation of the endothelial sheet, the features being compatible with segmental glomerular sclerosis and/or hyalinosis. It seemed that these changes, in turn, accelerated podocyte desquamation and extension of the capsular adhesion, producing a progressive cycle that terminated in global glomerular hyalinosis. Such a sequence of events most often occurred in rats with massive proteinuria, suggesting that persistent, severe proteinuria caused the podocyte lesion which led to the development of segmental glomerular sclerosis and/or hyalinosis.

Animals↗

Aortic insufficiency caused by Takayasu's arteritis without usual clinical features.

A 30-year-old woman with rapidly progressive, fatal aortic insufficiency was studied. Pathologic studies revealed that the aortic insufficiency was caused by dilation of the aortic root due to Takayasu's arteritis that, unusually, was confined to the ascending aorta and aortic arch. When other diseases that bring about aortic insufficiency can be excluded, Takayasu's arteritis should be considered, even if most of its manifestations are absent.

Adult↗

Arthus-type nephritis. II. Glomerular clearing system against poorly soluble and insoluble immune complexes.

The uptake and transport of immune complexes (IC) in glomeruli were studied in Arthus-type nephritis induced by ferritin anti-ferritin IC. This experimental nephritis was transient in nature, forming electron dense aggregates and deposits in glomeruli, and was considered to be suitable for the analysis of the glomerular defence against immune complex injury. The IC were taken up and removed from the glomerular circulation first by polymorphonuclear leukocytes and later by macrophages. The IC in the glomerular capillary walls and mesangium were seen to shift slowly from the peripheral part of the glomeruli to the more central and juxtaglomerular area. It is speculated that the glomerular integrity is maintained from the immune complex induced tissue injury through the handling and removal of phlogogenic IC by the blood derived phagocytic system and intrinsic glomerular clearing system.

Animals↗

Cellular aspects of rabbit Masugi nephritis. IV. Cell quantitation of proliferative glomerulonephritis.

Diffuse proliferative glomerulonephritis was induced in the rabbit with injection of goat nephrotoxic serum, and cell dynamics in the glomerulus were quantitatively investigated. The mean total cell number of a normal glomerulus in cross-section was 54.8, consisting of 24.1 endothelial cells, 16.0 podocytes, and 14.3 mesangial cells. In 5 selected nephritic rabbits, the mean total cell number of a glomerulus at the florid stage (7 to 12 experimental days) was 2.4 times as great as the control. It was revealed that the cells consisted of 27.9 endothelial cells, 14.9 podocytes, 21.1 mesangial cells, and 57.8 monocytic cells, indicating that about 76 per cent of the increased cells were of monocytic origin. Mesangial cells showed moderate increase in number (1.5 times) which persisted until 100 days, whereas endothelial cells increased only slightly. The monocytic cells promptly disappeared at 40 days correlating well with resolution of the proliferative change. Although the cellular compositions varied in each case, it was concluded that monocytes were essential in producing proliferative glomerular changes in the reversible type of Masugi nephritis.

Animals↗

Accelerated serum sickness in the rabbit. IV. Characteristic endarteritis in the pulmonary artery.

A unique angiitis developing in acute serum sickness in the rabbit was studied by immunofluorescence and light microscopy and by transmission and scanning electron microscopy. The angiitis occurred predominantly in the pulmonary artery and was characterized by a prominent accumulation of monocytes in the subendothelial space. During the early stage, scanning electron microscopy revealed the occurrence of various endothelial alterations, especially the formation of many endothelial holes leading to a subendothelial emigration of monocytes. There was neither emigration of polymorphs nor significant thrombotic lesion, and it is possible that this was due to a paucity in the amount of immune complexes deposited. The monocytes ingested platelets and fibrin, suggesting their preventive role in the development of thrombotic changes. The intimal change resolved within several days, leaving only slight fibrosis. A distinct resemblance in the disease process between this type of angiitis and acute serum sickness nephritis is emphasized.

Animals↗

Effects of anticonvulsant agents on halothane-induced liver injury in human subjects and experimental animals.

In order to evaluate the clinical implication of experimental studies on halothane-induced liver damage in phenobarbital-treated rats, we studied the clinical records of 315 consecutive patients who underwent brain surgery with halothane anesthesia. After exclusion of subjects with a history of alcoholism or antecedent chronic liver disease, clinical data of 279 patients with normal preoperative transaminase activities were analyzed. The incidence of halothane-induced liver injury was significantly higher in the subjects given phenobarbital than in those with no phenobarbital medication (7/100 vs. 1/179, p less than 0.01). To determine if other anticonvulsant compounds can influence halothane-induced liver injury, rats were pretreated with diphenylhydantoin or valproic acid prior to exposure to halothane under hypoxic conditions for comparison with phenobarbital. The degree of halothane hepatotoxicity assessed from ALT activities and morphological alterations was of the decreasing order of phenobarbital greater than controls = diphenylhydantoin greater than valproic acid, and a similar order was observed in the extent of reductive metabolism of halothane. These results indicate that patients pretreated with phenobarbital may be at a greater risk of halothane-induced liver damage, and that treatment with valproic acid and diphenylhydantoin lead to the production of toxic intermediates of halothane to a lesser extent than treatment with phenobarbital does.

Adult↗

Granular cell ameloblastoma of the mandible with metastasis to the third thoracic vertebra. A case report.

A 62-year-old housewife had a metastasis of granular cell ameloblastoma to the third thoracic vertebra. She had suffered at least four local recurrences during the 38-year duration of the right mandibular tumor and was treated by posterior decompression of the spinal cord with instrumentation. Histologically, the granular cells appeared to be of epithelial origin. Ultrastructurally, the granules were identified as lysosomes, including some that were autophagic. Of 45 reported cases of granular cell ameloblastoma, there have been only three cases with pathologically confirmed metastasis. Their characteristics are long duration of the tumor, multiple local recurrences, and predominance in blacks.

Ameloblastoma↗