Biomedical subjects
Publications and source records attributed to E Ueda.
We reported a case of interstitial pneumonia immediately after hepatic arterial infusion of Lipiodol anticancer drug emulsion for hepatocellular carcinoma. The reason was considered that Lipiodol-anticancer drug emulsion ran through an A-V shunt to alveolar septum resulting in alveolitis.
In order to clarify the cause of arterial changes after intra-arterial infusion of anti-cancer drugs (AI-AD) experiments were made on the arteries of rabbits. Histopathologic sections, 7 days after AI-AD revealed endothelial damage characterized by pyknosis, hyalinization with edematous change of the intimal layer. Proliferation of the endothelial cells was also observed. The cause of narrowing or occlusion of the arteries was considered to occur with thrombus formation surrounded by the proliferated endothelial cells and this suggested that thrombolytic agents would be effective to prevent these arterial changes.
Hepatic arterial embolization was performed on VX2 liver tumor of rabbit with subsequent induction heating to the tumor. Prior to the heating, iron particle suspension was injected into tumor tissue as a target of induction heating (500 KHZ, 9 KW). The temperatures of the tumor and liver parenchyma were measured with fluoroptic thermometer. Elevation of the tumor temperature during initial heating for 6 minutes were well correlated to the dose of iron particles injected; 1.4 degrees C with 1 g, 3.0 degrees C with 2 g, and 4.9 degrees C with 3 g. The temperature of liver parenchyma were below 39 degrees C even with 3 g injection.
Fc gamma RIII (CD16), the type three receptor for the Fc portion of IgG, is expressed on neutrophils, killer (K)/NK lymphocytes and macrophages. K/NK lymphocyte Fc gamma RIII, which plays a role in antibody-dependent cellular cytotoxicity, is an efficient signal transducing molecule, whereas neutrophil Fc gamma RIII, which plays a role in immune-complex clearance, seems less efficient in signal transduction. Neutrophil Fc gamma RIII has been reported to be a glycan-phosphatidylinositol-anchored membrane protein. Our studies suggest that K/NK lymphocyte Fc gamma RIII is protein-anchored rather than glycan-phosphatidylinositol-anchored. That is, K/NK lymphocyte Fc gamma RIII was resistant to phosphatidylinositol-specific phospholipase C and surface expression of Fc gamma RIII was not affected on K/NK lymphocytes from patients with paroxysmal nocturnal hemoglobinuria, a disorder of hemopoietic stem cells resulting in deficient expression of glycan-phosphatidylinositol-anchored proteins. Different membrane anchoring mechanisms of the Fc gamma RIII may account for different consequences of the ligand binding to two cell types.
Fourteen untreated patients with essential hypertension (EH) were subjected to mild aerobic exercise with the intensity at 50% of the maximum oxygen uptake (VO2max) twice a week for 12 weeks, as compared with 14 normotensive subjects (NT). Blood pressure and norepinephrine (NE) in plasma, platelet and urine were measured as the indices of sympathetic activity. In EH, a significant fall in both systolic and diastolic blood pressure was observed. In addition, exercise training produced a significant decrease both urinary and platelet NE, but not in plasma NE. Neither significant changes in blood pressure nor NE in plasma, platelet and urine were observed in NT. These results suggest that an inhibition of the sympathetic nervous system might be related to the blood pressure fall in physical exercise training.
Three cases of hepatocellular carcinoma with remarkable fatty metamorphosis were reported. When we encounter lipomatous tumor with liver cirrhosis on CT and MRI, further examination is necessary because of its high possibility of hepatocellular carcinoma.
UNLABELLED: Cor pulmonale is an important cause of death in patients with pulmonary tuberculosis. However, the treatment of cor pulmonale is difficult and its result is usually miserable. Many factors are considered to be responsible for the development of cor pulmonale. We intended to clarify the factors promoting progress of cor pulmonale. MATERIALS AND METHODS: Diagnosis of cor pulmonale was done using echocardiogram and ECG. Patients with cor pulmonale who have been examined with right side catheterization were analyzed. Patients were divided into two groups according to their survival periods. a) surviving group: patients who survived more than 18 month after right side catheterization. b) non-surviving group: patients who died within 18 month after right side catheterization. Analyzed items were as follows; grade of Hugh-Jones dyspnea criteria, grade of obesity, arterial blood O2 and CO2, pulmonary function, echocardiogram and right side catheterization finding. RESULTS AND DISCUSSION: Grade of obesity, PaO2, Stroke volume index were significantly higher in surviving group than in non-surviving group. Hugh-Jones grade, RPEP/RET and Pcw were significantly higher in non-surviving group than in surviving group. PaCO2, %FVC, FEV1.0%, RVth, %FS, PPA and PVR showed no difference between the two groups. Multifactorial analysis was performed and the following discrimination function was obtained: Z = 3.34 (H-J degrees) + (-0.44) (obesity %) + (-0.57) (PaO2 torr) + 0.04 (%VC) + 67.95 (RPEP/RET) + (-0.8) (PAP) + 0.61 (SVl) + 0.9 (PCW) + 0.03 (PVR) + (-0.9) (LVDdi) + 24.83.(ABSTRACT TRUNCATED AT 250 WORDS)
An anti-Gc antiserum (anti-Gc) was prepared by immunizing rabbits with purified Gc, a major vitamin D-binding protein in human serum. Gc is expressed on the surfaces of a small proportion of resting T cells and almost all B cells are natural killer (NK) cells. We investigated the effects of anti-Gc on NK activity of normal peripheral blood lymphocytes. Both anti-Gc and purified IgG isolated from anti-Gc prominently inhibited human NK activity in vitro. Inhibition of anti-Gc was dependent on the concentration of the antiserum employed. Competition assay showed that purified Gc significantly blocked the inhibitory effect of anti-Gc. The inhibition of NK activity in the cells treated with anti-Gc was restored time-dependently by being cultured in anti-Gc free medium. Anti-Gc-treated NK cells retained their capacity to bind to target cells. These findings suggest that mGc is associated with the process of the NK cytolysis on the post-binding cytolytic phase.
It is not clear whether cells from various chronic B cell leukemias including B-chronic lymphocytic leukemia (CLL), CLL in prolymphocytoid transformation (CLL-PLT), B-prolymphocytic leukemia (PLL), and hairy cell leukemia (HCL) simply represent different stages of a single B cell differentiation pathway. Furthermore, it is not known whether cells from any given B cell leukemia are characterized by the same population during the differentiation process. Differentiation of various B cell leukemic cells was induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), and the resulting changes in their morphology, cytoplasmic immunoglobulin (clg), and cytochemistry were evaluated. With respect to peculiar morphological change, i.e. extending long thin processes (spreading) and the appearance of clg, each sample showed different responses. According to these two indices samples were classified into three groups; spread+ clg- samples (one case of CLL-PLT, all HCL), spread+ clg+ samples (one of CLL, one of CLL-PLT), and spread- clg+ samples (a majority of CLL, one of CLL-PLT, and all PLL). Unexpectedly, both CLL and CLL-PLT consisted of heterogenous populations as to the reactivity to TPA. In the process of TPA-induced differentiation in CLL cells, features similar to those of HCL cells were not found. Since three different TPA-induced response patterns were observed in each chronic B cell leukemia type, it was not possible to sequentially assign each of these leukemias along a single B cell differentiation pathway. In order to explain this result, we introduced the hypothesis that these groups might be divided into different lineages in B cell differentiation. Since TPA-induced spreading cells were present in the B cell fraction of normal peripheral blood mononuclear cells, this morphological change should not be associated with malignant transformation.
Echocardiography and cardiac catheterization were performed in 30 patients of chronic pulmonary disease and cor pulmonale. We studied the relation of echo-cardiographic data and pulmonary hemodynamics to prognosis in these patients. In the nonsurvival group (12 patients) the extent of dyspnea was worse significantly (p less than 0.05), PaO2 was decreased significantly (p less than 0.05, 7 +/- 8.2 Torr), right ventricular preejection period (RPEP)/right ventricular ejection time (RVET) ratio increased significantly (p less than 0.05, 0.51 +/- 0.07), left ventricular diastolic diameter index (LVDdI) was shortened significantly (p less than 0.05, 23.5 +/- 3.1 mm/m2), and pulmonary capillary wedge mean pressure (PCWm) rose significantly (p less than 0.05, 11.9 +/- 6.9 mmHg) in comparison with the survival group (12 patients). In the survival group PaO2, RPEP/RVET ratio, LVDdI and PCWm averaged 60.9 +/- 12.8 Torr, 0.41 +/- 0.09, 27.5 +/- 5.1 mm/m2, 6.2 +/- 3.3 mmHg, respectively. The rate of survival was decreased significantly (p less than 0.05) in pulmonary vascular resistance (PVR) of greater than 400 dyne.sec.cm-1 or stroke volume index (SVI) of less than 35 ml/m2. These factors and 3 factors of obesity, %VC and pulmonary artery mean pressure (PAPm) differentiated nonsurvivors from survivors with linear discriminant function.
A hairy-cell leukemia (HCL) line, BNBH-I, was established from the peripheral blood of a 40-year-old male patient with HCL in a relatively stable clinical phase after splenectomy. The cells have since been growing continuously for more than 2 years. Their cell surface immunoglobulin (sIg) was identical with that found on the surface of freshly isolated leukemic cells, consisting of IgG-kappa. The BNBH-I cells were more mature than the original hairy cells in their degree of B-cell differentiation, as reflected by a decrease in sIg expression together with the appearance of some cytoplasmic Ig (cIg)+ cells, loss of EA gamma-rosette formation and reactivity with monoclonal antibody (MAb) FMC7, and an increase in the proportion of MAb PCA-I+ cells. The BNBH-I cells possessed the antigen recognized by Leu-M5, a highly specific MAb for HCL. Epstein-Barr virus nuclear antigen (EBNA) was present. Both the freshly isolated leukemic cells and the cell line had the 14q+ involving q32 chromosomal abnormality, and their Ig gene rearrangements were also identical. Following exposure to 12-O-tetradecanoylphorbol-13-acetate (TPA), both the freshly isolated leukemic cells and the BNBH-I cells adhered to culture dishes and extended long, thin processes, a phenomenon characteristic of HCL. These results indicate that the BNBH-I line was derived from the leukemic hairy cells.
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This report describes a case of B cell lymphoma, the clinicopathological features of which are quite similar to those of malignant histiocytosis. The clinical features included fever, anemia, and marked hepatosplenomegaly without lymphadenopathy. Histological findings revealed diffuse and noncohesive proliferation of cytologically atypical cells and benign-appearing histiocytes in the splenic red pulp, where the erythrophagocytosis was frequently found. Immunological studies, however, revealed a B cell nature of proliferating atypical cells. Accordingly, the histology of this patient was interpreted as a neoplastic proliferation of B cells accompanied by marked proliferation and activation of the histiocytes.
Deficiency of decay-accelerating factor (DAF) occurs in blood cells in paroxysmal nocturnal hemoglobinuria (PNH), characterized by an unusual susceptibility to hemolysis by complement activation. This study examined DAF expression on hematopoietic progenitors from normal individuals and PNH patients using a fluorescence-activated cell sorter (FACS) with monoclonal antibodies to DAF. Nonphagocytic mononuclear marrow cells expressing different density distributions of DAF were sorted into DAF-, DAF+/-, DAF+, and DAF++ fractions. The cells from each fraction were cultured in methylcellulose and assayed for CFU-E, BFU-E, CFU-GM, and CFU-Mix. The percentages of distribution of DAF-negative normal progenitors increased in the order of CFU-E, CFU-GM, BFU-E, and CFU-Mix, whereas those of DAF-positive cells inversely decreased in this order. These results indicate that DAF expression may accompany differentiation from CFU-Mix to CFU-E. On the other hand, most progenitors in PNH patients had little, if any, expression of DAF on their cell surfaces. These findings were supported by another approach using a complement-dependent cytotoxicity method with the anti-DAF monoclonal antibodies. Abnormal expression of DAF was found on the progenitors in the bone marrow as well as on mature cells circulating in the blood in PNH.
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