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Biomedical subjects

N Morisaki

Publications and source records attributed to N Morisaki.

At least 73 records · Page 4Linked to original sources
PubMed1996

Slow beta-migrating lipoprotein: an atherogenic subclass of low density lipoproteins.

OBJECTIVE: To clarify the possibility that midband Lp in LDL fractions might act as an atherogenic lipoprotein in their interaction with macrophages. DESIGN AND METHODS: Low density lipoproteins (LDL) isolated by zonal ultracentrifugation from midband lipoprotein-positive serum in type lib hyperlipidemics were subjected to polyacrylamide gel disc electrophoresis. RESULTS: A part of midband lipoprotein was observed between pre beta-and beta-band, in addition to the main beta-band. We named this midband lipoprotein "slow beta-migrating Lp (slow beta-Lp)." The larger LDL subfraction from midband-lipoprotein positive serum on Sepharose 2B column chromatography contained much slow beta-Lp, named slow beta-Lp-rich LDL. The smaller LDL subfraction contained a little slow beta-Lp, named slow beta-Lp-poor LDL. Slow beta-Lp-rich LDL had similar composition to the control LDL except for apolipoprotein E. The uptake of [3H]cholesteryl linoleate-labeled slow beta-Lp-rich LDL by J774 macrophages was higher than that of control LDL. The cholesterol ester content of J774 macrophages incubated with slow beta-Lp-rich LDL increased significantly compared with slow beta-Lp-poor LDL, beta-VLDL, and control LDL. CONCLUSION: These results suggest that slow beta-Lp in type llb might generate foam cells from macrophages in atherosclerotic lesions.

Animals↗
PubMed1996

Different rifampicin inactivation mechanisms in Nocardia and related taxa.

Mycolic acid-containing bacteria inactivate rifampicin in a variety of ways such as glucosylation, ribosylation, phosphorylation and decolorization. These inactivations were found to be a species-specific phenomena in Nocardia and related taxa. Gordona, Tsukamurella and fast-growing Mycobacterium modified rifampicin by ribosylation of the 23-OH group of the antibiotic. Such ribosylation was not observed in Rhodococcus and Corynebacterium, but phosphorylation of the 21-OH group of rifampicin was observed in one strain of Rhodococcus. Nocardia modified the antibiotic by glucosylation (23-OH group) and phosphorylation, but ribosylation was not observed.

Actinomycetales↗
PubMed1996

Dose-dependent effect of niceritrol on plasma lipoprotein-a.

Lipoprotein-a, Lp(a), is a variant form of low density lipoprotein (LDL) that contains apolipoprotein-a, whose structure has 75-85% homology with plasminogen. Elevated plasma levels of Lp(a) are considered to be one of the independent risk factors for cardiovascular disease. We studied the effects of niceritrol, a nicotinic acid derivative, on plasma Lp(a) levels in 72 patients with hypercholesterolaemia. The dose of niceritrol was increased every 4 weeks, from 750 to 1500 and then to 2250 mg day-1. The final dose was adjusted to obtain a plasma cholesterol level less than 5.69 mmol l-1. Niceritrol led to significant decreases in plasma levels of median Lp(a), from 16.1 mg dl-1 (interquartile intervals, 8.7 to 32.8) to 11.1 mg dl-1 (interquartile intervals, 6.6 to 21), the mean reduction rate being 17.6%. In the group with pretreatment Lp(a) levels of over 20 mg dl-1, Lp(a) decreased by 10.0, 22.0 and 31.8% at the doses of 750, 1500, and 2250 mg day-1, respectively. In the group with levels less than 20 mg dl-1, only the dose of 2250 mg day-1 was effective in the reduction of Lp(a). The results suggest that the reduction of Lp(a) was dependent on the dose of niceritrol and on the pretreatment level of Lp(a). In conclusion, niceritrol is effective, in a dose-dependent manner, for reducing Lp(a) levels.

Aged↗
PubMed1995

Ligand-activated platelet-derived growth factor beta-receptor is degraded through proteasome-dependent proteolytic pathway.

The platelet-derived growth factor beta-receptor undergoes polyubiquitination as a consequence of ligand binding. Ubiquitin conjugation to protein is implicated in proteasome-dependent proteolytic pathway for short-lived proteins. In the present study, we have examined effects of different kinds of cell-penetrating proteasome inhibitors, including N-benzyloxycarbonyl-L-isoleucyl-gamma-t-butyl-L-glutamyl-L-alanyl-L-l eucinal (PSI) and a Streptomyces metabolite lactacystin, on ligand-stimulated degradation of the beta-receptor. These proteasome inhibitors were found to considerably inhibit the degradation of autophosphorylated and polyubiquitinated receptors, suggesting the possible involvement of proteasomes in the degradation process of the ligand-activated beta-receptor.

Acetylcysteine↗
PubMed1995

Identification of a major cytokinin in coconut milk.

A major cytokinin found in coconut milk was isolated by using the tobacco callus growth-promoting assay as a guide during purification. The structure of the factor was determined to be 14-O-(3-O-[beta-D-galactopyranosyl-(1-->2)-alpha-D-galactopyranosyl-(1-- >3)- alpha-L-arabinofuranosyl]-4-O-(alpha-L-arabinofuranosyl)-beta-D- galactopyranosyl)-trans-zeatin riboside [G3A2-ZR] by various NMR techniques, including heteronuclear multiple bond connectivity by 2D multiple quantum NMR (HMBC), as well as mass spectroscopy and sugar analysis. The optimum concentration of G3A2-ZR for cytokinin activity in the tobacco callus assay was estimated to be 5 x 10(-6) M, so that G3A2-ZR is one order of magnitude more potent than 1,3-diphenylurea and one order less potent than zeatin riboside. At least 20% of the cytokinin activity of coconut milk could be attributed to G3A2-ZR.

Carbohydrate Conformation↗
PubMed1995

Specific inhibition of vascular cell adhesion molecule-1 expression by type IV collagen in endothelial cells.

The effects of matrices on the expression of adhesion molecules were studied in cultured human umbilical cord vein endothelial cells(HUVEC). The expression of vascular cell adhesion molecule-1 (VCAM-1) but not of intercellular adhesion molecule-1 stimulated with various substances was remarkably low in HUVEC cultured on type IV collagen, the major component of the basement membrane, compared with that on type I collagen. This inhibition was observed not only at the protein level but also at the mRNA level. These data suggested that VCAM-1 expression in endothelial cells is strictly regulated by the underlying basement membrane.

Basement Membrane↗
PubMed1995

Treatment of obesity by personality classification-oriented program.

It is apparent that personality is related to the pathogenesis of obesity, and that understanding the personality of the patient may be a key to successful treatment of the disease. Using the Rorschach test and interviews by a psychiatrist, the types of personality were classified into four groups according to the healthiness of personalities. The judgment of healthiness was based mainly on the scores obtained from the Rorschach test. This classification revealed that the occurrence of mental and physical symptoms during therapy with a very low calorie diet (VLCD) and subsequent rebound of bodyweight were more frequently observed in patients with relatively less healthy personalities. We used this classification to adapt our program to treat obese patients. In this program, severe diet restrictions were applied to patients with relatively healthy personalities. These restrictions were applied with modifications to patients with less healthy personality, because severe restrictions would be possibly very stressful for them and would bring about an undesirable reaction. For strengthening the patients' motivation for therapy, the significance of body weight reduction was explained in different ways to patients with different types of personality. The target of bodyweight reduction, reward for patients with successful weight reduction, and the duration of therapy were set up differently for patients with different personalities types. The results showed that bodyweight rebound one or two years after treatment was reduced with the personality-oriented therapy program compared to that observed with the previous conventional therapies. Also, the incidence of psychological problems was remarkably decreased.

Adult↗
PubMed1995

Mechanism of angiogenic effects of saponin from ginseng Radix rubra in human umbilical vein endothelial cells.

1. The effects of saponin from Ginseng Radix rubra on angiogenesis (tube formation) and its key steps (protease secretion, proliferation and migration) in human umbilical vein endothelial cells (HUVEC) were examined to elucidate the mechanism of the tissue repairing effects of Ginseng Radix rubra. The effect on a wound healing model was also studied. 2. Tube formation was measured by an in vitro system. The activity and immunoreactivity of tissue-type plasminogen activator (tPA) as a protease for angiogenesis and the immunoreactivity of its inhibitor, plasminogen activator inhibitor-1 (PAI-1), were measured in conditioned medium of HUVEC stimulated for 24 h with saponin. Cell proliferation was measured by counting the cell numbers at 2-7 days after seeding. Migration was measured by Boyden's chamber method. The effect on wound healing was studied in the skin of diabetic rats. 3. Saponin at 10-100 micrograms ml-1 significantly stimulated tube formation by HUVEC in a dose-dependent manner. Saponin in a similar concentration-range increased the secretion of tPA from HUVEC as estimated by immunoreactivity and enzyme activity. On the other hand, PAI-1 immunoreactivity was slightly increased at 10 micrograms ml-1 of saponin, but then was significantly decreased at 50 and 100 micrograms ml-1. Cell proliferation was only slightly enhanced by 1-100 micrograms ml-1 of saponin, but migration was significantly enhanced by 10-100 micrograms ml-1 in a dose-dependent manner. Moreover, saponin stimulated wound healing with enhanced angiogenesis in vivo. 4. These results indicate that saponin stimulates tube formation mainly by modifying the balance of protease/protease inhibitor secretion from HUVEC and enhancing the migration of HUVEC, and that it is effective in vivo.

Animals↗
PubMed1995

Ribosylation by mycobacterial strains as a new mechanism of rifampin inactivation.

Several fast-growing Mycobacterium strains were found to inactivate rifampin. Two inactivated compounds (RIP-Ma and RIP-Mb) produced by these organisms were different from previously reported derivatives, i.e., phosphorylated or glucosylated derivatives, of the antibiotic. The structures of RIP-Ma and RIP-Mb were determined to be those of 3-formyl-23-[O-(alpha-D-ribofuranosyl)]rifamycin SV and 23-[O-(alpha-D-ribofuranosyl)]rifampin, respectively. To our knowledge, this is the first known example of ribosylation as a mechanism of antibiotic inactivation.

Inactivation, Metabolic↗
PubMed1995

In vivo effect of TGF- beta 1. Enhanced intimal thickening by administration of TGF- beta 1 in rabbit arteries injured with a balloon catheter.

The in vivo effect of transforming growth factor-beta 1 (TGF-beta 1) was studied in a model system in which arterial intimal thickening was induced by injury of rabbit arteries with a balloon catheter (BCI). Intimal area and its ratio to medial area in carotid arteries after BCI were significantly higher in rabbits treated with 10 micrograms/kg TGF-beta 1 and 10 mg/kg aspirin i.v. QD (TGF-beta 1 group) than in those treated with 10 mg/kg aspirin i.v. QD only (control group). Intimal cell numbers in the TGF-beta 1 and control groups were not significantly different from each other, but matrix volume in the intimal layer was significantly higher in the TGF-beta 1 group. By immunohistochemical and Northern blot analyses, the fibronectin content in carotid intimal and medial layers was greater in the TGF-beta 1 group compared with that in the control group. Thus, in intimal thickenings induced by BCI. TGF-beta 1 mainly enhanced the formation of matrix containing fibronectin. Moreover, the mRNAs of TGF-beta 1 and type II receptors were detected in carotid arteries 7 and 14 days after, but not before, BCI. Thus, TGF-beta 1 influences the process of intimal thickening induced by BCI through a receptor-mediated mechanism in vivo. The significance of this fact is discussed in relation to the development of atherosclerosis.

Animals↗
PubMed1995

Genetic differences of lipid metabolism in macrophages from C57BL/6J and C3H/HeN mice.

Cholesterol metabolism in macrophages from atherosclerosis-prone C57BL/6J mice was compared with that in macrophages from atherosclerosis-resistant C3H/HeN mice. Plasma total cholesterol levels of both types of mice were significantly increased, but HDL cholesterol level was increased only in C3H/HeN mice when a high-cholesterol diet (1% cholesterol) was fed for 5 weeks. After incubation of macrophages from male and female mice on the high-cholesterol diet with beta-VLDL for 24 hours, cholesterol content in macrophages from C57BL/6J was approximately 1.5- to 2.0-fold higher than in those from C3H/HeN mice. [3H]Cholesterol oleate-beta-VLDL incorporation into macrophages from C57BL/6J mice on the high-cholesterol diet was greater than incorporation into those from C3H/HeN mice. The release of [3H]cholesterol from macrophages from C57BL/6J mice on the high-cholesterol diet was one seventh that from macrophages from C57BL/6J mice on the basal diet or that from macrophages from C3H/HeN mice on the basal or high-cholesterol diet. Acid cholesterol esterase activity was almost the same in macrophages from any group. Acyl CoA:cholesterol acyltransferase activity in macrophages from C57BL/6J mice on the high-cholesterol diet increased compared with that from macrophages from C57BL/6J mice on the normal diet. Neutral cholesterol esterase activity in macrophages from C57BL/6J mice was about half of that in macrophages from C3H/HeN mice independent of the type of diet. There were no sex differences in these metabolisms. Considered with our previous data, these results suggested that a high-cholesterol diet may cause metabolic changes to accumulate cholesterol ester in macrophages from C57BL/6J mice in accordance with genetic abnormalities.

Animals↗
PubMed1995

Isolation and structures of an antifungal antibiotic, fusarielin A, and related compounds produced by a Fusarium sp.

A new antifungal antibiotic, fusarielin A, and three related compounds, fusarielins B, C and D, were obtained from a culture of a Fusarium sp. The skeletal structure and the relative stereochemistry of fusarielin A were determined mainly on the basis of its NMR data, and the absolute structure was elucidated by using the exciton chirality method and the modified Mosher method. The structures of the other homologues were determined by comparison of their spectral data with those of fusarielin A.

Animals↗
PubMed1995

Rifampicin inactivation by Bacillus species.

The ability of strains of Bacillus, Staphylococcus, Pseudomonas, and Escherichia coli to inactivate rifampicin was tested. Most Bacillus strains were found to inactivate rifampicin. Two modes of inactivation were identified; one was phosphorylation and the other involved decolorization. Presence or absence of either mechanism appeared unrelated to the phylogenetic relatedness of strains. None of the other organisms could inactivate this antibiotic.

Bacillus↗
PubMed1995

Regulation of neutral cholesterol esterase activity by phospholipids containing negative charges in substrate liposome.

The effect of phospholipids on cholesteryl ester hydrolysis by neutral cholesterol esterase in alveolar macrophages was studied. Among the phospholipids used as emulsifiers, those with a negative charge, such as phosphatidylserine, phosphatidic acid, phosphatidylinositol, and cardiolipin, gave a higher level of hydrolysis by neutral cholesterol esterase than other less negatively charged phospholipids, such as phosphatidylcholine, lysophosphatidylcholine, phosphatidylethanolamine, and sphingomyelin. Phospholipase D treatment of liposomes emulsified with phosphatidylcholine produced phosphatidic acid and enhanced cholesteryl ester hydrolysis. Phospholipase A2 treatment produced lysophosphatidylcholine and decreased the hydrolysis. The hydrolysis of cholesteryl ester in lipid droplets obtained from cholesterol-laden macrophages elicited by thioglycollate in the rat peritoneal cavity was low compared to artificial liposomes emulsified with phosphatidylcholine. The reason for this was speculated to be that lipid droplets were low in total phospholipids and poor in phospholipids with strong negative charges but rich in phosphatidylethanolamine and sphingomyelin. These results suggest that the polar heads of phospholipids may play an important role in cholesteryl ester hydrolysis by neutral cholesterolesterase.

Animals↗