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M Cho

Publications and source records attributed to M Cho.

At least 109 records · Page 6Linked to original sources
PubMed1993

Regulation of apolipoprotein B production and secretion in response to the change of intracellular cholesteryl ester contents in rabbit hepatocytes.

In the present study, we investigated the mechanisms that regulate apolipoprotein B-100 (apoB) secretion in response to the change of intracellular cholesteryl ester contents by adding low density lipoprotein (LDL) and an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase (pravastatin) in rabbit hepatocyte culture system. LDL caused a significant dose-dependent increase in apoB secretion. On the other hand, the addition of pravastatin decreased apoB secretion significantly. LDL caused a dose-dependent increase in cellular cholesteryl ester, while cellular cholesteryl ester was decreased by pravastatin significantly. Therefore, these results indicate that the change of apoB secretion was in parallel with the change of cellular cholesteryl ester contents. Cellular contents of free cholesterol, triglyceride, and phospholipid did not change. To investigate intracellular degradation of apoB prior to secretion, pulse-chase experiments were performed. It was shown that the addition of pravastatin accelerated intracellular degradation of apoB, while LDL slowed the apoB intracellular degradation rate. We also investigated whether the change of cellular cholesteryl ester could affect the apoB mRNA level. Northern blot analysis and solution hybridization RNase protection assay demonstrated that neither LDL nor pravastatin caused a significant change in cellular apoB mRNA level. We conclude that intracellular cholesteryl ester contents play a critical role in apoB secretion, and the intracellular apoB degradation rate could be the main mechanism that regulates apoB secretion in response to the change of intracellular cholesteryl ester level.

Acetates↗
PubMed1993

Three slow myosin heavy chains sequentially expressed in developing mammalian skeletal muscle.

Myosin heavy chain (MyHC) isoforms show a striking diversity of expression patterns during mammalian development. Using a set of monoclonal antibodies that recognize different epitopes on myosin heavy chain isoforms we show that there exist in human and rat skeletal muscle at least three isoforms of slow twitch myosin heavy chain. To facilitate a comparison of our results to others obtained using different antibodies or species, we have identified cDNAs encoding the epitopes recognized by the three slow antibodies. Using these reagents, we show that the onset of expression of three slow MyHC isoforms is temporally distinct during early gestation. This result suggests that a sequence of MyHC transitions plays an important role in determining muscle fiber function at fetal, neonatal, and adult stages.

Animals↗
PubMed1993

Different expression of modified low density lipoprotein receptors in rabbit peritoneal macrophages and Kupffer cells.

We have previously reported that mouse peritoneal macrophages have three types of modified low density lipoprotein (LDL) receptors. One is specific for acetylated LDL (Ac-LDL), the second is for oxidized LDL (Ox-LDL), and the third recognizes both (Arai, H. et al. (1989) Biochem. Biophys. Res. Commun. 159, 1375-1382). In the current study, the characteristics of modified LDL receptors in rabbit peritoneal macrophages and Kupffer cells from rabbits were investigated. Cross-competition studies of the degradation assay between Ox-LDL and Ac-LDL in rabbit peritoneal macrophages showed that the degradation of 125I-labeled Ox-LDL was almost completely inhibited by an excess amount of unlabeled Ac-LDL. On the other hand, an excess amount of unlabeled Ox-LDL suppressed 125I-labeled Ac-LDL degradation only partially. In contrast, in Kupffer cells an excess amount of unlabeled Ox-LDL inhibited the degradation of 125I-labeled Ac-LDL almost completely, whereas the degradation of 125I-labeled Ox-LDL was inhibited only partially by Ac-LDL. Scatchard analysis of binding assay showed that rabbit peritoneal macrophages have a single class of receptor for Ox-LDL, which binds maximally 0.31 microgram/mg cellular protein (Bmax) with an apparent dissociation constant (Kd) of 19.3 micrograms/ml, and two classes of receptors for Ac-LDL; one with high affinity (Bmax 0.025 microgram/mg cellular protein, Kd 0.040 micrograms/ml) and the other with low affinity (Bmax 0.08 microgram/mg cellular protein, Kd 11.31 micrograms/ml). On the other hand, Kupffer cells have two classes for Ox-LDL; one is a high affinity receptor (Bmax 0.53 microgram/mg cellular protein, Kd 0.99 microgram/ml) and the other is a low affinity receptor (Bmax 3.71 micrograms/mg cellular protein, Kd 16.2 micrograms/ml) and a single class for Ac-LDL (Bmax 0.60 microgram/mg cellular protein, Kd 7.24 micrograms/ml). These results indicate that rabbit peritoneal macrophages have two kinds of modified LDL receptors; one is specific for Ac-LDL, and the other recognizes both Ox-LDL and Ac-LDL.

Acetylation↗
PubMed1993

Evidence for myoblast-extrinsic regulation of slow myosin heavy chain expression during muscle fiber formation in embryonic development.

Vertebrate muscles are composed of an array of diverse fast and slow fiber types with different contractile properties. Differences among fibers in fast and slow MyHC expression could be due to extrinsic factors that act on the differentiated myofibers. Alternatively, the mononucleate myoblasts that fuse to form multinucleated muscle fibers could differ intrinsically due to lineage. To distinguish between these possibilities, we determined whether the changes in proportion of slow fibers were attributable to inherent differences in myoblasts. The proportion of fibers expressing slow myosin heavy chain (MyHC) was found to change markedly with time during embryonic and fetal human limb development. During the first trimester, a maximum of 75% of fibers expressed slow MyHC. Thereafter, new fibers formed which did not express this MyHC, so that the proportion of fibers expressing slow MyHC dropped to approximately 3% of the total by midgestation. Several weeks later, a subset of the new fibers began to express slow MyHC and from week 30 of gestation through adulthood, approximately 50% of fibers were slow. However, each myoblast clone (n = 2,119) derived from muscle tissues at six stages of human development (weeks 7, 9, 16, and 22 of gestation, 2 mo after birth and adult) expressed slow MyHC upon differentiation. We conclude from these results that the control of slow MyHC expression in vivo during muscle fiber formation in embryonic development is largely extrinsic to the myoblast. By contrast, human myoblast clones from the same samples differed in their expression of embryonic and neonatal MyHCs, in agreement with studies in other species, and this difference was shown to be stably heritable. Even after 25 population doublings in tissue culture, embryonic stage myoblasts did not give rise to myoblasts capable of expressing MyHCs typical of neonatal stages, indicating that stage-specific differences are not under the control of a division dependent mechanism, or intrinsic "clock." Taken together, these results suggest that, unlike embryonic and neonatal MyHCs, the expression of slow MyHC in vivo at different developmental stages during gestation is not the result of commitment to a distinct myoblast lineage, but is largely determined by the environment.

Cell Differentiation↗
PubMed1993

Multiple factors underlying the maximum motility of Escherichia coli as cultures enter post-exponential growth.

Motility and chemotaxis allow cells to move away from stressful microenvironments. Motility of Escherichia coli in batch cultures, as measured by cell swimming speed, was low in early-exponential-phase cells, peaked as the cells entered post-exponential phase, and declined into early stationary phase. Transcription from the flhB operon and synthesis of flagellin protein similarly peaked in late exponential and early post-exponential phases, respectively. The increase in swimming speed between early-exponential and post-exponential phases was correlated with twofold increases in both flagellar length and flagellar density per cell volume. This increased investment in flagella probably reflects the increased adaptive value of motility in less favorable environments. The decrease in speed between post-exponential and stationary phases was correlated with a threefold decrease in torque produced by the flagellar motors and presumably reflects decreased proton motive force available to stationary-phase cells.

Cell Movement↗
PubMed1992

Beta-enolase is a marker of human myoblast heterogeneity prior to differentiation.

In this report, we define a muscle-specific marker, beta-enolase, that distinguishes proliferating myoblasts from different stages of development. Enolase exists as multiple isoforms and in the course of cardiac and skeletal muscle development the beta isoform progressively replaces the alpha isoform. In skeletal muscle, this change in gene expression, unlike most developmental changes in myogenic gene expression, is evident in undifferentiated myoblasts. Whereas myoblasts from fetal tissues express alpha-enolase mRNA, beta-enolase is the predominant mRNA expressed by myoblasts from postnatal tissues. Our results are consistent with the idea that distinct precursor myoblasts contribute to the diversity of fiber types characteristic of muscle tissue at different stages of development.

Animals↗
PubMed1992

Probucol and atherosclerosis in the Watanabe heritable hyperlipidemic rabbit--long-term antiatherogenic effect and effects on established plaques.

We performed two studies to investigate the effect of probucol on atherogenesis in vivo in the Watanabe heritable hyperlipidemic (WHHL) rabbit. In the first study (Study A), probucol was administered to 2-month-old WHHL rabbits, to evaluate its long-term effect. When killed at about 1.5 years of age, the percentage area of aorta covered with atherosclerotic plaque in probucol-treated rabbits was markedly less than that seen in non-treated rabbits (23.0 +/- 11.4% vs. 87.7 +/- 8.1%, M +/- S.D., P less than 0.001). In the second study (study B), administration of probucol was commenced with 8-month-old WHHL rabbits to investigate whether the drug was effective for limiting atherosclerosis in rabbits in which plaques had already developed. When killed after 6 months of treatment, the percentage area of aorta covered with plaque was 38.1 +/- 12.1% in treated rabbits and 82.7 +/- 22.6% in non-treated rabbits (P less than 0.02). Microscopic observations of lesions also supported the effect of probucol. Probucol treatment resulted in a change not only in the size but also the composition of lesions. Thus, probucol was effective in preventing atherosclerosis in long-term studies at both early and late stages.

Animals↗
PubMed1992

Inhibition of production of monocyte/macrophage-derived angiogenic activity by oxygen free-radical scavengers.

We showed previously that thiol-containing compounds inhibited the production of macrophage-mediated angiogenic activity. Since thiol-containing compounds may act on macrophages by affecting activation and inhibiting the production of oxygen free-radicals, we studied the effects of oxygen free-radical scavengers on production of angiogenic activity by elicited mouse peritoneal macrophages and lipopolysaccharide stimulated normal human monocytes. Monocyte/macrophage conditioned media were potently angiogenic when assayed in rat corneas, while conditioned media, from oxygen free-radical scavenger-treated cells were not. The inhibitory effect of oxygen free-radical scavengers was due to a direct effect on monocyte/macrophage production of angiogenic activity but was not due solely to a decrease in the production of the macrophage-derived angiogenic cytokine tumor necrosis factor-alpha. We conclude that oxygen free-radical scavengers are potent inhibitors of the production of macrophage-mediated angiogenic activity.

Angiogenesis Inducing Agents↗
PubMed1991

A linkage map of distal mouse chromosome 12.

To refine the linkage map of distal mouse Chromosome 12, we have identified DNA restriction fragment variants associated with a creatine kinase gene (Ck-3), the Akt proto-oncogene, an Abelson proviral integration site (D12N1), and the immunoglobulin heavy chain VH3609 variable region family (Igh-V36). The patterns of inheritance of these markers in backcross progeny and recombinant inbred mouse strains allowed their localization with respect to previously mapped genes to yield the linkage map: Aat-15.8 cM-Ck-3-0.9 cM-(Crip, Akt, Igh-C)-0.3 cM-(D12N1, Igh-V). This map confirms genetically the localization of the Igh-V gene complex distal to Igh-C on the chromosome. It differs from previous maps in placing D12N1 distal to Igh-C, and in suggesting that the Igh-V gene complex spans less than one centiMorgan (cM). Other DNA sequence variants detected with the creatine kinase probe allowed definition of four additional genetic loci: Ck-1 near Lmyc-1 on Chromosome 4; Ck-2 between Upg-1 and Hprt-ps1 (D17Rp10) on distal Chromosome 17; Ck-4 near Mpmv-17 and Mls-3 on Chromosome 16; and Ck-5 near Hba on Chromosome 11.

Animals↗
PubMed1991

Thiol-containing compounds inhibit the production of monocyte/macrophage-derived angiogenic activity.

Macrophage (M phi)-mediated angiogenesis is believed to play an important role in the pathogenesis of rheumatoid arthritis. Gold sodium thiomalate, which is used in the treatment of rheumatoid arthritis, is a potent inhibitor of the production of m phi-derived angiogenic activity. To determine the mechanism of this inhibition, we studied the effects of thiol containing compounds (TCCs) on elicited mouse peritoneal m phi and lipopolysaccharide stimulated normal human monocytes. Monocyte/m phi conditioned media were potently angiogenic when assayed in rat corneas, while conditioned media from viable monocyte/m phi s treated with TCCs (at concentrations of 8.3-16.6 x 10(-5) M) were not. TCCs inhibited production of angiogenic activity by the m phi s rather than affecting other components of the angiogenic response such as the angiogenic factors or the target microvasculature of the rat cornea. Levels of the angiogenic mediator tumor necrosis factor-alpha (TNF-alpha) were not decreased in conditioned media of monocyte/m phi s treated with TCCs. We conclude that TCCs are potent inhibitors of the production of m phi-mediated angiogenic activity. This action of TCCs on m phi s may be in part responsible for the mechanism of action of therapeutic gold compounds in rheumatoid arthritis.

Animals↗
PubMed1989

In vitro effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on muscarinic cholinergic receptors in mouse striatum.

1. MPTP significantly lowered Kd of the binding of [3H]QNB to muscarine receptor without affecting Bmax values compared with those of control. Hill coefficients (nH) of control and MPTP (250 microM) added group were 1.15 +/- 0.127 and 0.56 +/- 0.202, respectively. 2. Prior addition of pargyline to MPTP did not prevent the decrease of [3H]QNB binding. The patterns of displacement of [3H]QNB by MPTP and MPP+ were similar to those by some muscarinic agonists, such as acetylcholine, carbamyl choline and methacholine. 3. These results suggest that MPTP might be muscarinic agonist and might play a role to produce Parkinsonism through directly affecting the muscarinic cholinergic receptors in vivo.

Animals↗
PubMed1989

[Neoadjuvant chemoradiotherapy in locally invasive transitional cell carcinoma of the urinary bladder: early results of PVB and CAP therapy].

A total of 22 patients with locally invasive transitional cell carcinoma of the urinary bladder were treated with neoadjuvant cis-diamminedichloroplatinum (CDDP), vincristine, peplomycin (PVB) or cyclophosphamide, doxorubicin, CDDP (CAP) combined with radiation therapy in our institutes between June, 1982 and May, 1988. Twelve patients were entered into the PVB regimen and the remaining 10 patients into the CAP regimen. In the PVB treated group, clinical response was obtained in 2 complete response (CR) and 6 partial response (PR), 8 out of 12 patients (66.7%). Downstaging was noted in 8 out of 12 patients (66.7%). In the CAP treated group, a clinical response was obtained in 1 of CR and in 2 of PR out of the 9 patients with evaluable lesions (33.3%). Downstaging was noted in 6 out of 9 patients (66.7%). There were no significant side effects in either the PVB or CAP treated groups, and these neoadjuvant therapies were well-tolerated. These results indicated that neoadjuvant PVB or CAP combined with radiation therapy would be useful in the management of invasive bladder cancer.

Aged↗
PubMed1989

[Infectious cysts of a müllerian duct: a case report].

We report a case of infectious cysts of Müllerian duct. A 48-year-old male patient was referred to our department complaining of terminal miction pain on July 19, 1985. The excretory urogram showed right lateral displacement of bladder and pelvic CT-scan demonstrated a large mass containing multiple cysts. A total of 5 percutaneous punctures was performed, but without success. The cysts were removed completely on November 26, 1985. A large volume of pus subsequently yielded a pure culture of Serratia marcescens and multilobular cysts were observed in the incised tumor. Wound healing was delayed because of severe infection. We discussed the difficulty of the management for infectious cysts of the Müllerian duct.

Cysts↗
PubMed1989

[Penile and urethral metastases from superficial bladder tumor after TUR: a case report].

A case of metastasis to the penis and the urethra from superficial bladder tumor of transitional cell carcinoma (TCC), grade 3 is reported. A 52-year-old male patient was diagnosed to have TCC of the urinary bladder (grade 3, stage pT1a) in May, 1985 and was treated initially with transurethral resection followed by adriamycin (ADR) instillation. In February, 1986, urethroscopy showed a papillary tumor in the cavernosal urethra and a metastatic tumor was noted in the corpus spongiosum penis. Biopsy of urethral tumor revealed TCC, grade 3. Therefore partial urethrectomy with resection of penile tumor was performed. Although the patient underwent combination chemotherapy involving CAP (cisplatin + ADR + cyclophosphamide) and M-VAC (methotrexate + vincristine + ADR + cisplatin) regimens, local lesion and metastatic lesions progressed, and he died in June 1986, 20 days after emasculation. The management of superficial bladder tumor with TCC, grade 3 was reviewed and discussed here.

Carcinoma, Transitional Cell↗
PubMed1988

Inhibition of production of macrophage-derived angiogenic activity by the anti-rheumatic agents gold sodium thiomalate and auranofin.

We have investigated the effect of gold sodium thiomalate and auranofin, gold compounds employed in the treatment of rheumatoid arthritis, on production of macrophage-derived angiogenic activity. Elicited mouse peritoneal macrophages were cultured in the presence or absence of gold compounds or thiomalic acid, and the macrophages or their conditioned media were then assayed for their angiogenic activity in rat corneas. Control macrophage conditioned medium was potently angiogenic. In contrast, conditioned medium from gold or thiomalic acid treated macrophages was not. Addition of gold compounds or thiomalic acid to control macrophage conditioned medium did not inhibit its angiogenic activity. Drug treatments did not significantly affect macrophage lactate dehydrogenase release, lysozyme release, or protein synthesis. We conclude that gold sodium thiomalate and auranofin potently reduce the detectable angiogenic activity produced by macrophages.

Animals↗
PubMed1988

Horizontal and vertical vergence training and its effect on vergences and fixation disparity curves: I. Horizontal data.

The purpose of this study was to assess the effects of horizontal and vertical vergence training on fusional vergences and the fixation disparity (FD) curve. Thirty-four subjects were divided into three groups. One-third served as controls and the other two-thirds underwent 5 h of supervised horizontal and vertical vergence training, respectively. Before and after the 4 week training period, vergences and FD curves were measured by a single individual who was intentionally uninformed of each subject's group. We hypothesized that the subjects in the horizontal training group would have increased vergence amplitudes and flatter FD slopes. Our analysis revealed that the positive vergences increased significantly for those in the horizontal group. No evidence was found to suggest changes in any variables related to the FD curve. Because type II errors were likely to be unacceptably large, further work is necessary to determine the relation between fusional vergence training and variables derived from the FD curve.

Adult↗