Post-translational modification from methionine to aspartic acid-residue on a variant hemoglobin, Hb Bristol, a proof by ESI-MS-MS.
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Amino Acid Sequence↗
Biomedical subjects
A Miyazaki
Publications and source records attributed to A Miyazaki.
Ethanol retards gastric epithelial restoration in monolayer cultures.
The purpose of this study was to clarify the effect of ethanol on confluent monolayer gastric epithelial cells that had a round cell-free area in the center of the culture dish. Restoration of such "wounding" was evaluated quantitatively every 12 hr using a computer image analyzer with and without ethanol. Without ethanol, restoration was achieved within 48 hr. Exposure to ethanol retarded cellular restoration significantly. Staining for actin and myosin in the control group revealed the presence of lamellipodia and stress fibers. However, in the ethanol group narrowed lamellipodia and few stress fibers were observed. In conclusion, ethanol retarded the migration and proliferation of cultured gastric mucosal cells after in vitro wounding, possibly by damaging the cytoskeletal system.
Actins↗
The heparin-bound fraction of human lipoprotein-deficient serum inhibits endocytic uptake of oxidized low density lipoprotein by macrophages.
We recently demonstrated that bovine lactoferrin, a cationic whey protein from bovine milk, interacts with the negative charges of modified low density lipoproteins (modified LDL) such as acetylated LDL (acLDL) and oxidized LDL (oxLDL), which markedly interferes with their endocytic uptake by rat peritoneal macrophages (Kajikawa M, Ohta T, Takase M, Kawase K, Shimamura S, Matsuda I. Biochim Biophys Acta 1994;1213:82-90). In the present study, we examined whether human lipoprotein-deficient serum (LPDS) might contain protein(s) that could inhibit the endocytic uptake of oxLDL by mouse macrophages. We fractionated LPDS by heparin affinity chromatography and found that the cellular binding of oxLDL to mouse macrophages and subsequent endocytic uptake were inhibited by 50%-60% with the heparin-bound fraction, whereas the heparin-unbound fraction had no effect. Similar results were obtained in the experiments with acetylated LDL. Sephacryl S-300 gel-filtration chromatography of a mixture of oxLDL and the heparin-bound fraction revealed that a 150-kDa protein was associated with oxLDL. These results indicate that the electrostatic interaction of oxLDL with some component(s) of the heparin-bound fraction might interfere with the endocytic uptake of oxLDL by the macrophage scavenger receptor.
Animals↗
Effects of rebamipide on bile acid-induced inhibition of gastric epithelial repair in a rabbit cell culture model.
BACKGROUND: Anti-ulcer agents exert various functional effects on gastric epithelial cells. AIM: The effects of a novel gastro-cytoprotective agent (rebamipide) on epithelial restoration following bile acid damage were assessed using primary cultured rabbit gastric epithelial cells. METHODS: Rebamipide was added to complete confluent cell sheets with deoxycholic acid just after creating a cell-free wound (2 mm2). The restoration was monitored and analysed by phase contrast microscopy and an image analyser for 48 h. The migration speed was measured during the initial 3 h after wounding. Cell proliferation was detected by staining for bromodeoxyuridine (BrdU) at 12-h intervals. The labelling index was calculated per unit area. The major cytoskeletal protein actin was detected by immunohistochemical staining. RESULTS: In the controls, restoration was completed 48 h following wounding. Deoxycholic acid retarded this process. The addition of rebamipide to deoxycholic acid abolished the bile acid-induced retardation. The migration speed was 26 microns/h in the controls. 15 microns/h in the deoxycholic acid group and 27 microns/h in the deoxycholic acid plus rebamipide group. In the controls, BrdU-positive cells, which were rarely detected in the initial 24 h, were maximal at 36 h (labelling index 1.7%). In the deoxycholic acid group, proliferation was inhibited (peak labeling index; 0.5% at 48 h). Actin-containing stress fibres were detected throughout the cells and the periphery of the lamellipodia in the controls, and were disrupted in the deoxycholic acid-treated group. Rebamipide prevented these effects. CONCLUSIONS: Deoxycholic acid significantly retarded restoration by the inhibition of both cell migration and proliferation, potentially through an effect on the cytoskeleton. Rebamipide protected the mucosal cells from bile acid mediated injury.
Actins↗
Platelet-derived growth factor accelerates gastric epithelial restoration in a rabbit cultured cell model.
BACKGROUND & AIMS: Growth factors play an important role in gastric wo und repair. The aim of this study was to assess the role of platelet-derived growth factor (PDGF) in gastric epithelial restoration. METHODS: PDGF-BB (1-50 ng/mL) was added to confluent cultures of rabbit gastric epithelial cells after wounding. Regrowth of the epithelial cells was monitored for 48 hours. The speed of cell migration was measured, and cell proliferation was detected by using a 5-bromodeoxyuridine (BrdU) staining technique. The labeling index was calculated for a 0.05-mm(2) area around the wound. RESULTS: After wounding, cells at the wound edge formed lamellipodia and showed ruffling movements. The addition of PDGF-BB significantly accelerated cell migration and proliferation as well as gastric restoration. Migration speed was 21 microm/h in control cultures and 32 microm/h and 40 microm/h in cultures containing 10 ng/mL and 50 ng/mL of PDGF-BB, respectively. In control cultures, BrdU-positive cells were rarely detected in the initial 24 hours after wounding, and maximum labeling occurred at 36 hours (labeling index, 3.4%). Cultures containing PDGF-BB showed maximum labeling at 24 hours (labeling index, 6.9%). CONCLUSIONS: PDGF-BB dose-dependently accelerated the migration rate and proliferation of cultured gastric epithelial cells after wounding. Therefore, PDGF-BB may play a role in gastric epithelial cell restoration during healing of gastric mucosal lesions.
Animals↗
Infarct size reduction with coronary venous retroinfusion of diltiazem in the acute occlusion/reperfusion porcine heart model.
Calcium channel blockers are commonly used for the treatment of ischemic heart disease, but their effects on myocardial infarct size (IS) after reperfusion are not well known. Enflurane-anesthetized open-chest pigs subjected to 60-min left anterior descending coronary artery (LAD) occlusion followed by 3-h reperfusion were referred to one of the four experimental groups. Beginning 10 min before the onset of reperfusion, pigs in group A received diltiazem (7.5 micrograms/kg/min) retrogradely infused into the coronary vein for 30 min. In group B, the same amount of diltiazem was infused into the right atrium. A corresponding volume of saline was infused into the coronary vein in group C or into the right atrium in group D. IS expressed as a percentage of the myocardium at risk was significantly smaller (p < 0.01) in group A (33 +/- 14%; mean +/- SD) than in groups B (58 +/- 11%), C (58 +/- 11%), and D(63 +/- 10%). After reperfusion, functional recovery of the ischemic myocardium, determined by ultrasound crystals, was significantly more improved (p < 0.05) in group A as compared with other groups. The ischemic and nonischemic regional myocardial blood flow (RMBF), determined by radioactive microspheres, did not differ between four groups. Coronary venous retroinfusion of diltiazem had a myocardial protective effect in the porcine experimental model of acute coronary occlusion/reperfusion, whereas intravenous drug administration was not effective. The protective effect could not be attributed to washout of toxic metabolites from the ischemic area or to improved microcirculation. It was probably related to a pronounced accumulation of the calcium-channel blocker diltiazem in the ischemic myocardium achieved by the coronary venous route of delivery.
Animals↗
Malignant fibrous histiocytoma of the esophagus.
A 78-year-old man presented with an esophageal polyp that was confirmed by immunohistochemistry and electron microscopy to be malignant fibrous histiocytoma. The tumor was comprised of a proliferation of spindle-shaped cells admixed with bizarre giant cells. These tumor cells were immunoreactive for smooth muscle actin, vimentin, alpha-1-anti-chymotrypsin and CD68. Electron microscopic examination revealed the myofibroblastic and histiocytic features of the tumor cells. No elements of epithelial or myogenic differentiation were found in the tumor. Malignant fibrous histiocytoma of the esophagus is extremely rare, with 10 cases being documented so far in the literature. The differential diagnosis of pleomorphic tumors of the esophagus is discussed.
Aged↗
Evaluation of ethanol on gastric epithelial restoration in vitro.
Ethanol exerts damaging effects on gastric mucosa and delays ulcer healing. To investigate the effect of ethanol on the wound repairing process, we used a wound repair model using primary cultured gastric mucosal cells. A confluent monolayer gastric mucosal cell sheet consisting mainly of mucous cells was wounded to make a cell-free area of constant size. Cell-free area was restored with time after wounding and monitored every 12 hr using a computer image analyzer to observe epithelial cell restoration quantitatively in the presence and absence of ethanol (2.0%). It was found that, although the control wound was completely repaired in 36 to 48 hr, the group treated with 2.0% ethanol showed a significant delay of repair. In the control, 5-bromodeoxyuridine-positive cells appeared around the wound in 24 to 36 hr. In contrast, the group treated with 2.0% ethanol showed no 5-bromodeoxyuridine-positive cells during the experiment. In conclusion, 2.0% ethanol retarded the repair of gastric mucosal restoration by inhibiting the initial gastric cell migration, followed by inhibition of proliferation of cells.
Animals↗
Lysophosphatidylcholine potentiates the mitogenic activity of modified LDL for human monocyte-derived macrophages.
The growth of murine peritoneal macrophages is induced by oxidized LDL (Ox-LDL), and lysophosphatidylcholine (lysoPC) plays an important role in its mitogenic activity. In the present++ study, Ox-LDL-induced macrophage growth was examined with human monocyte-derived macrophages. The cell growth of human macrophages was significantly induced by Ox-LDL but not by acetylated LDL (acetyl-LDL). The treatment of acetyl-LDL with phospholipase A2, however, led to a marked increase in its mitogenic activity, with a concomitant conversion of 75% of its phospholipids to lysoPC. The growth-stimulating activity became positive only when both acetyl-LDL and lysoPC were coincubated, although neither of them exhibited cell growth-promoting activity. These results suggest that Ox-LDL could stimulate the growth of human monocyte-derived macrophages, and lysoPC may play an essential role in the mitogenic activity of Ox-LDL.
Cell Division↗
Quantitative analyses of lesion areas of coronary atherosclerosis in cholesterol-fed rabbits.
A simple method to quantitatively evaluate atherosclerosis in the rabbit coronary arteries by measuring macroscopic lesion areas (%) was attempted in the present study. Sixteen rabbits were fed a 0.5% cholesterol diet for 15 weeks and then 9 rabbits were sacrificed whereas the remaining 7 rabbits were maintained for further 9 weeks on a normal chow (at week 24). The left circumflex coronary arteries (LCX) were excised from the rabbit hearts under stereoscopic observation. The prepared arterial strips of LCX were 38.7 +/- 7.1 mm long and all of them reached the cardiac apex from the orifice. At week 15, the lesion area in LCX was negligible (3.2 +/- 0.4%) whereas the aortic lesions significantly developed (50.0 +/- 7.6%). At week 24, atherosclerotic lesions in both LCX and aortas increased to 32.8 +/- 9.2% and 85.9 +/- 5.6%, respectively. This is the first report that determined the luminal surface areas of atherosclerotic lesions in rabbit coronary arteries. This method may be more practical and useful for quantitative evaluation of coronary atherosclerosis in a large number of rabbits than histological observations of serial sections of rabbit hearts.
Animals↗
Implementing public policies and services in rural Japan: issues and problems.
While the sharply increased services for the elderly in the revised Gold Plan--announced in 1994--are noteworthy, implementation of the revised Plan is expected to present numerous issues and problems, particularly in the rural areas of Japan, because of unique circumstances such as depopulation and the presence of a disproportionately large number of elderly; geographical and physical isolation; a conservative and tradition-bound political climate; and conservative attitudes of the elderly. This article examines the current state of policy implementation, identifying issues and problems that are being encountered in the rural areas of Japan. Such issues as economic and family life, health care, and service delivery for the elderly are examined.
Aged↗
Endocytic uptake of lysophosphatidylcholine mediated by macrophage scavenger receptor plays a major role in oxidized low density lipoprotein-induced macrophage growth.
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Animals↗
[A case of giant hepatocellular carcinoma successfully treated by arterial administration of SMANCS].
A 68-year-old male was referred to our hospital for the precise examination of a giant hepatic tumor detected in a mass survey. The lesion occupied most of the right hepatic lobe, further advancing to the medial segment of the left lobe. However, hepatic functions were well preserved (ICG K = 0.141). Considering the characteristic images of the lesion with positive anti-HCV and high titer of PIVKA II (0.860 AU/ml), the diagnosis was hepatocellular carcinoma. First arterial administration of SMANCS was performed on May in 1994, followed by 6 successive procedures with an interval of about 2 months (total dosage 36 mg), resulting in remarkable tumor shrinkage and tumor marker normalization. On January in 1995, a metastatic lesion to the right rib was controlled by 2 mg of SMANCS administered to the intercostal artery combined with radiation therapy (60 Gray). Frequent administrations of SMANCS caused no serious complications, and tumor feeders were well preserved. Therefore, arterial administration of SMANCS is thought to be one choice for the therapy of giant HCC with good functional reserve.
Aged↗
Hepatocyte growth factor inhibits intercellular communication via gap junctions in rat hepatocytes.
We demonstrated that HGF reduces gap junctional intercellular communication of rat hepatocyte doublets and increases cell spreading. Intercellular communication via gap junctions was markedly reduced in hepatocyte doublets with HGF (20 ng/ml) 3-12 hr after inoculation. Immunocytochemistry revealed spotty localization of connexin 32 on the plasma membrane of 3-hr cultured control hepatocyte doublets, whereas HGF-treated doublets showed significantly less connexin 32 staining. Genistein maintained intercellular communication in the presence of HGF, indicating that HGF reduces intercellular communication by down regulation of connexin 32 through the c-met/HGF receptor-tyrosine-kinase-mediated pathway. Furthermore, TGF-beta 1 maintained intercellular communication in the presence of HGF. Regulation of intercellular communication in hepatocytes by HGF and TGF-beta 1 might play an important role during liver regeneration.
Analysis of Variance↗
Differential effects of an acyl-coenzyme A:cholesterol acyltransferase inhibitor on HDL-induced cholesterol efflux from rat macrophage foam cells.
When rat macrophages were converted to foam cells with acetylated low density lipoprotein (acetyl-LDL) and then reacted with high density lipoprotein (HDL) and an inhibitor of acyl-coenzyme A:cholesterol acyltransferase (58-035) (sequential incubation system), 58-035 did not enhance HDL-induced cholesterol efflux. In contrast, when macrophages were exposed to acetyl-LDL in the presence of both HDL and 58-035 (simultaneous incubation system), HDL-induced cholesterol efflux was enhanced 1.6-fold by 58-035. Cholesterol efflux with HDL alone was 2-fold greater in simultaneous incubation than in sequential incubation. These results suggest the presence of an efficient cholesterol efflux pathway in simultaneous incubation which is not available in sequential incubation. This pathway, which we refer to as the neutral cholesterol ester hydrolase-independent pathway, is characterized by the efflux of lysosome-derived cholesterol without re-esterification.
Animals↗
[Differences in clinical findings between drug-induced and viral liver diseases].
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Chemical and Drug Induced Liver Injury↗
Tissue-selective inhibition of sterol synthesis in mice by pravastatin sodium after a single or repeated oral administrations.
Pravastatin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, exhibits liver-selectivity in inhibiting sterol synthesis, when administered as a single oral dose to mice or rats, whereas lovastatin and simvastatin do not. This may be due to the fact that pravastatin is distributed intracellularly, to a large extent, in the liver and extracellularly in nonhepatic tissues. In the present study, we examined whether the difference in liver-selectivity among these three HMG-CoA reductase inhibitors observed in single-dose studies was preserved after repeated oral administrations of drugs to mice. De novo sterol synthesis in different tissues of mice was examined in vivo three hours after the last dose of drug by measuring incorporation of intraperitoneally injected [14C]acetate into total sterols. Pravastatin administered orally for 11 consecutive days at 5 and 10 mg/kg exhibited a greater liver-selectivity than lovastatin and simvastatin: sterol synthesis was inhibited more than 60% in the liver by all three drugs, whereas that in nonhepatic tissues was inhibited less than 10% by pravastatin and more than 30% by lovastatin and simvastatinin in most of the nonhepatic tissues examined. Pravastatin administered orally for 11 consecutive days at 10 mg/kg caused more selective inhibition of sterol synthesis in liver ex vivo than two other inhibitors at the same dose. Pravastatin inhibited de novo sterol synthesis from [14C]acetate into sterol fraction in the liver slices in vitro, but minimally in those of the spleen and testis, whereas lovastatin and simvastatin inhibited in those of all three tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Incidental detection of breast cancer during T1-201 myocardial SPECT study.
A case of left breast cancer which was detected incidentally by T1-201 SPECT performed to evaluate the status of myocardial perfusion, is reported. Both stress and redistribution T1-201 SPECT clearly delineated the tumor. It was confirmed later as scirrhous carcinoma of the breast.
Adenocarcinoma, Scirrhous↗