Experimental clonorchiasis sinensis. I. Gross anatomy, liver function and serum protein.
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Biomedical subjects
Publications and source records attributed to H Iida.
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The growth of subcutaneously transplanted Lewis lung carcinoma in BDF1 mice was inhibited by an inorganic dye, Ruthenium Red. The mean volume of the tumors of the mice which were given Ruthenium Red by daily ip injection of 5 mg/kg on days 1 approximately 10 was 28 and 39% of that of the controls at days 18 and 23 after transplantation, respectively. The median survival time (MST) of the treated mice was 27.8 days while that of the control was 23.0 days. The higher MST (32.5 days) was obtained when the dye was given at 2.5 mg/kg for 1 approximately 20 days, although the tumor volume in this group of mice was 51% of that of the control at day 18.
The red blood cells from rats with intra- and extrahepatic cholestasis obtained by feeding of alpha-naphthylisothiocyanate (ANIT) and ligation of bile duct, respectively, were analysed from biochemical as well as ultrastructural point of view. A significant increase of cholesterol content was observed in the red cell membrane from bile duct-ligated rat. An increment of absolute lecithin content without accompanied increase in phospholipid content was observed in both groups. The fatty acyl chain composition of lecithin remained unchanged except a small increase in stearic acid (13.0% leads to 18.1%) in the bile duct-ligated rat. Despite a small change in the lipid composition, scanning electron microscopic observation revealed a profound alteration in red cell ultrastructure; most of cells were in spur type in ANIT-fed group while variations in red cell shape were observed in bile duct-ligated group.
Mouse P388 leukemic cells inoculated into the right forefootpad metastasized primarily to the right axillary lymph node. No significant metastasis to other lymph nodes or organs was detected on Day 12 after the inoculation of 10(6) P388 cells in the forefootpad, except that a lesser extent of metastasis was observed in some cases in the right inguinal lymph node, liver, and spleen. A quantitative estimation of metastasis in the axillary lymph node was accomplished by transferring the lymph node i.p. to the recipient mice (bioassay method). The metastasis of P388 cells to the axillary lymph node occurred linearly depending on the elapse of time after inoculation. In studying the chemotherapeutic effect on lymph node metastasis, two experimental models were established. Model 1, 10(6) P388 cells were inoculated into the right forefootpad, and drug was administered thereafter. The right axillary lymph node was removed on Day 8, and the extent of inhibition of lymph node metastasis was estimated by the bioassay method. In Model 2, P388 cells were inoculated, and the right forelimb including original tumor was amputated on Day 6 when the metastasis had already been established. The drug was given thereafter, and the extent of inhibition of metastasis was estimated on Day 12 by the bioassay method. In this experimental system, a lipophilic derivative N4-behenoyl-1-beta-D-arabinofuranosylcytosine was more effective than its parent compound 1-beta-D-arabinofuranosylcytosine; however, 5-fluorouracil was found to be more potent than its lipophilic derivative ftorafur for the inhibition of lymph node metastasis, suggesting an existence of various pharmacokinetic factors for the inhibition of lymph node metastasis.
Biochemical and ultrastructural studies of red blood cell membranes from seven patients with congenital biliary atresia have been performed. Scanning electron microscopic observations revealed that more than half of these cells were of abnormal shapes, such as target, spur and cup-formed cells. By freeze-fracture electron microscopy, membrane particle-free smooth areas were noted in the fracture faces. In addition, the number of membrane-associated particles was 20% less than those in control subjects. The lipid analysis of red blood cells showed a significant increase in phospholipid and a marked increase in cholesterol content. The increase of phospholipid content was primarily caused by the increase of lecithin. The acyl chain analysis of erythrocyte lecithin demonstrated an increase in palmitic, palmitoleic and oleic acid, and a decrease in stearic and linoleic acid. These observations are similar to those of acquired biliary obstruction. The fluidity of erythrocyte membrane lipid, studied by a fluorescence technique using fluorescent probe 1,6-diphenyl-1,3,5-hexatriene (DPH), was found to be less in an individual with congenital biliary atresia than in the control subject.
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Toxin production in Clostridium botulinum types C and D is governed by specific bacteriophages. Prior passages of a phage controlling type C toxin production caused subsequently lysogenized bacteria to become variably toxigenic. This appears to be one of the causes of the decrease in toxigenicity which is common in some type C and D strains. The morphology of bacteria was also changed from rod-shaped to filamentous by infection with a successively propagated phage.
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Formation of the lateral flagella by Vibrio parahaemolyticus was inhibited under an alkaline condition of the medium. However, flagellation of the polar monotrichous flagellum was not affected in the same condition. Flagellation of the lateral flagella depended on the pH of the medium.
Lipid peroxidation of adrenocortical mitochondria and microsomes was greatly stimulated by addition of 1.0 mM or less ferric ions. In the presence of NADPH-yielding system, the formation of corticosterone from endogeneous cholesterol and exogeneous deoxycorticosterone was inhibited as the concentrations of iron increased. Of interest is the fact that 0.5 mM ferric ion-mediated lipid peroxidation was completely abroagated upon addition of 2 mM calcium ions. Accordingly, protected from the peroxidative damage.
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The lipid compositions of erythrocyte membranes, plasma and bile of 16 patients with biliary obstruction were analysed to obtain information regarding the origin of excess lecithin which is usually found in the erythrocyte membranes in obstructive jaundice. Phospholipids and free cholesterol were found to be increased proportionally to the degree of biliary obstruction with an elevation in the free cholesterol/phospholipid ratio in the red cell membranes. The increase in phospholipid content is primarily due to lecithin. There was a highly significant alteration in the fatty acid composition of lecithin of erythrocyte membranes, plasma and bile from patients with severe jaundice. Red cell membrane lecithin amounted to more than 40% of the total phospholipid in these patients. Interestingly, the fatty acid composition of lecithin showed a similar pattern in erythrocyte membranes, plasma and bile. In addition, the fatty acyl chain composition of lecithin in lipoprotein-X was very similar to that of the red cell membrane. Freeze-fracture electron microscopy showed an alteration in membrane morphology and a reduced number of membrane-associated particles in the fractured faces. From these findings, we suggest that the lecithin of lipoprotein-X is derived from abnormal bile lecithin, which is incorporated into erythrocyte membranes by fusion with lipoprotein-X. On the other hand, the fatty acid composition of bile lecithin from patients with mild jaundice, whose erythrocyte membrane lecithin amounted to less than 31% of total phospholipid, was not different from that of normal individuals. However, in sharp contrast to the bile content, the fatty acid composition of erythrocyte membranes and plasma in these same patients showed a similar but small change compared to that of patients with severe biliary obstruction. The red cells of patients with mild jaundice were almost normal, biconcave disc-shaped, as observed by scanning electron microscopy and no abnormalities in the distribution or number of membrane particles were detected by freeze-fracturing. We propose that the abnormal lecithin content of erythrocyte membranes in patients with mild jaundice can be explained by the gradual exchange of lecithin between red blood cells and plasma lipoprotein.
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