Fatty-meal sonography for diagnosis of obstruction of common bile duct.
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Biomedical subjects
Publications and source records attributed to E Pascual.
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A 59-year-old man with ischemic pancreatic disease, polyarthritis, and cutaneous nodules has shown histopathologic findings indicative of disseminated fat necrosis in a percutaneous biopsy specimen from the right knee. The histopathologic findings in the synovium included necrotic fat cells, distorted fat cells and adjacent lymphocytes, lipid laden histiocytes, and giant cells. In prior histopathologic studies of the joint involvement associated with this disorder, fat cell necrosis has been found only in the periarticular tissues, and the synovium has appeared normal or showed nonspecific inflammation. However, the present study shows that the synovial membrane may also be the site of fat necrosis and an associated inflammatory reaction; thus patients with this disorder may manifest arthritis in addition to periarthritis.
Detailed study of four patients with BD, four controls with recurrent aphthous stomatitis, and 12 healthy controls has demonstrated markedly decreased levels of salivary SC in both its free and bound forms, and normal total protein concentration in BD salivas. In two BD patients, SC deficiency was also found in jejunal fluids. Depressed in vitro response of blood T cells to mitogens was also noted in BD. Levels of IgA in serum were normal, as well as total numbers of T cells and IgA-carrying B cells in blood. A fluid phase abnormality of the fibrinolytic system as tested by the clot lysis assay was demonstrated in the blood from BD patients. Studies of BD SF and synovial membrane by light and electron microscopy showed inclusions composed of degenerated neutrophils inside monocytes. Abnormalities of host defense mechanisms at the mucous membrane level due to SC deficiency, together with a systemic T cell functional defect and fibrinolytic abnormality, could be important mechanisms in the pathogenesis of recurrent mucosal ulcers and thrombosis in BD.
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The catalytic activity of phosvitin in Fe(II) oxidation and the addition of iron to transferrin were studied under various conditions. It was concluded that the Fe(II) oxidized by phosvitin would bind to apotransferrin, although an appreciable fraction of Fe(III) remained bound to phosvitin. Fe(III) also migrated from phosvitin to apotransferrin. This reaction was first-order with respect to Fe(III)-phosvitin concentration with a half-time (t1/2) of 10 min, and a first-order rate constant, k=0.069min-1, in 700 muM-phosphate buffer, pH 7.2, at 30 degrees C. The catalysis of the oxidation of Fe(III) by phosvitin was proportional to O2 concentration, and is quite different from the relative O2 independence of Fe(II) oxidation as catalysed by ferroxidase. A scheme for the mobilization and transfer of iron in the chicken, including the role of ferroxidase, phosyitin and transferrin, is presented.
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A patient with a history of alcoholism and pancreatic calcification, developed subcutaneous fat necrosis and an arthropathy, associated with a pancreatic pseudocyst and accompanied by an elevation of serum lipase and amylase. The illness was complicated by bacteremia and destructive bone lesions. A clinical distinction between osteomyelitis and medullary fat necrosis proved difficult. Infection of bone was demonstrated at one site but did not exclude medullary fat necrosis elsewhere.
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A simple method was developed to identify large mononuclear (LMN) cells in human synovial fluid based on morphology and staining with Sudan black B. All cells were classified as monocyte-derived macrophages (MDM), lymphoblasts (LB), or synovial lining cells (SLC). Lymphoblasts were seen in 58 of 60 rheumatoid fluids (mean: 69 +/- 18% LB per LMN cells). However lymphoblasts were rarely seen in synovial fluids from patients with crystal-induced synovitis or bacterial infections.
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