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Biomedical subjects

H M Kim

Publications and source records attributed to H M Kim.

At least 217 records · Page 12Linked to original sources
PubMed1998

Specific inhibition of immunoglobulin E-mediated allergic reaction using antisense Fc epsilon RI alpha oligodeoxynucleotides.

We have investigated the ability of an antisense immunoglobulin E (IgE) receptor alpha-subunit oligodeoxynucleotide (Fc epsilon RI alpha ODN) specifically to inhibit IgE-mediated allergic reactions in the mouse. Synthetic antisense Fc epsilon RI alpha ODN dose-dependently inhibited passive cutaneous anaphylaxis and histamine release from the mouse peritoneal mast cells (MPMC) activated by anti-dinitrophenyl (DNP) IgE. Northern blot analysis showed that the mast cells treated with antisense Fc epsilon RI alpha ODN exhibited no detectable levels of L-histidine decarboxylase mRNA after anti-DNP IgE stimulation, whereas the cells treated with sense Fc epsilon RI alpha ODN possessed significant amounts of this mRNA. Examination of the elevation of cAMP levels in MPMC following the activation with anti-DNP IgE demonstrated a significant rise in activated cells, but not in the antisense Fc epsilon RI alpha ODN-treated cells. Moreover, antisense Fc epsilon RI alpha ODN had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha production. Our results demonstrated that antisense Fc epsilon RI alpha ODN inhibited the IgE-mediated allergic reaction in vivo and in vitro.

Animals↗
PubMed1998

Morphological alterations in rat peritoneal mast cells by stem cell factor.

Stem cell factor (SCF) stimulates mast cell adhesion and, because SCF is produced normally in tissues, it may be a major factor responsible for the adhesion of mast cells to connective tissue matrix. We found that the morphology of rat peritoneal mast cells (RPMC) altered after the addition of recombinant murine SCF (rmSCF) in vitro. The ability of rmSCF to enhance morphological alteration was dose dependent and completely abolished by anti-c-kit ACK2 monoclonal antibody. Exposure of RPMC to transforming growth factor-beta 1, wortmannin, genistein, herbimycin A, staurosporine, indomethacin and cytochalasin D before the addition of rmSCF antagonized rmSCF-induced morphological alteration. However, nordihydroguiaretic acid had no effect. Many RPMC appeared to respond also to nerve growth factor (NGF) but the total number of cells with altered morphology was much greater when the culture was stimulated by rmSCF than by NGF. We suggest that morphological alterations of mast cells by rmSCF is an important step for the participation in adhesion to tissue under resident physiological conditions.

Animals↗
PubMed1998

Efficient in vitro model for immunotoxicologic assessment of mammary silicone implants.

In clinical and experimental studies, silicone gel has been assumed to cause immune alterations that may be related to macrophage activation of silicone implants. However, it has not been proven that the immunotoxicities are caused by the direct contact of macrophages and silicone gel because there has not been an adequate experimental model. In the present study, silicone gel was loaded directly onto Petri dishes and was distributed uniformly to the bottom by centrifugation. Peritoneal macrophages and splenic lymphocytes were cultured either on the silicone-coated plates or on the conventional, normal plates, and their functions were compared with each other. The experiments were repeated three times. The cytotoxic activities of peritoneal macrophages on cancer cells were markedly augmented by cultivation on silicone gel, and the primary T-dependent immunoglobulin M response in which macrophages participated as antigen presenting cells was also enhanced by incubation on silicone gel. However, macrophage-unrelated functions mediated by B and T lymphocytes were not affected by the silicone gel treatment. It was proven that the direct contact of macrophages with silicone gel was a primary cause of acute immune activation that was related to foreign body reaction. In addition, the present in vitro model exhibited similar silicone-induced immunotoxicities in previous animal and clinical studies.

Animals↗
PubMed1998

Inhibition of anaphylaxis by sulfasalazine in rats.

We studied the effect of sulfasalazine on anaphylaxis. Sulfasalazine dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. Sulfasalazine also inhibited local anaphylaxis activated by anti-dinitrophenyl (anti-DNP) IgE. Moreover, sulfasalazine dose-dependently inhibited histamine release in the peritoneal mast cells activated by compound 48/80 or anti-DNP IgE. All of these effects were comparable to those of the disodium cromoglycate (reference drug) tested. When sulfasalazine was added, the level of cAMP in rat peritoneal mast cells transiently and significantly increased about 6-fold compared with that of basal cells. Our studies provide evidence that sulfasalazine may be beneficial in the treatment of anaphylaxis.

Anaphylaxis↗
PubMed1998

Inhibitory effect of anaphylactic reaction of Sosiho-Tang.

Mast cells synthesize and secrete chemical mediators which play an central role in anaphylactic reactions. Compound 48/80 is a condensation product of formaldehyde with paramethoxyphenylethylamine that reliably induces the release of chemical mediators in the mast cell granules. Aggregation of the high-affinity Fc receptor also stimulates the mast cells. The objective of the current study was to determine the effect of Sosiho-Tang (SS-Tang) on mast cell-mediated anaphylactic reaction. SS-Tang completely inhibited systemic anaphylaxis induced by compound 48/80 in mice. SS-Tang inhibited local anaphylaxis induced by anti-dinitrophenyl (DNP) IgE. In addition SS-Tang concentration-dependently inhibited histamine release in mast cells induced by compound 48/80 or anti-DNP IgE. These results indicate that SS-Tang may contain compounds with actions that inhibit mast cell degranulation.

Animals↗
PubMed1998

Solanum lyratum inhibits anaphylactic reaction and suppresses the expression of L-histidine decarboxylase mRNA.

We investigated the effect of aqueous extract of Soloanum lyratum THUNB. (Solanaceae) (SLAE) on anaphylactic reaction. The mast cell is widely thought to contribute to the acute changes associated with anaphylaxis. SLAE inhibited skin mast cells-mediated anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. SLAE dose-dependently inhibited histamine release in mouse peritoneal mast cells activated by anti-DNP IgE or substance P. Substance P increased steady state levels of L-histidine decarboxylase (HDC) mRNA in mouse mastocytoma P-815 cells. Northern-blot analysis demonstrated that significantly reduced level of the mRNA of HDC was expressed in mast cells treated with SLAE, compared to that without SLAE. We conclude that SLAE directly affect IgE-mediated anaphylactic reaction and substance P-induced HDC mRNA over-expression.

Anaphylaxis↗
PubMed1998

Taraxacum officinale restores inhibition of nitric oxide production by cadmium in mouse peritoneal macrophages.

Nitric oxide (NO) produced at high concentrations by the inducible NO synthase is an important effector molecule involved in immune regulation and defense. The involvement of NO in the toxicity of cadmium (Cd) has been proposed. We have established that Cd inhibits the production of NO by recombinant IFN-gamma (rIFN-gamma) and lipopolysaccharide-stimulated mouse peritoneal macrophages. In the present study, we searched restoration drug against the inhibition of NO production by Cd in Oriental medicine. An aqueous extract of Taraxacum officinale (Compositae) (TOAE) restored the inhibition of NO production by mouse peritoneal macrophages pretreated with Cd in a dose-dependent manner. The effect of TOAE was mainly dependent on TOAE-induced tumor necrosis factor-alpha (TNF-alpha) secretion. These results suggest that the capacity of TOAE to restore NO production from interferon-gamma (IFN-gamma)-primed mouse peritoneal macrophages is the result of TOAE-induced TNF-alpha secretion.

Animals↗
PubMed1998

Streptococcal keratitis after myopic laser in situ keratomileusis.

A 24-year-old healthy male underwent uncomplicated laser in situ keratomileusis (LASIK) in left eye. One day after the surgery, he complained of ocular pain and multiple corneal stromal infiltrates had developed in left eye. Immediately, the corneal interface and stromal bed were cleared, and maximal antibiotic treatments with fortified tobramycin (1.2%) and cefazolin (5%) were given topically. The causative organism was identified as 'Streptococcus viridans' both on smear and culture. Two days after antibiotic therapy was initiated, the ocular inflammation and corneal infiltrates had regressed and ocular pain was relieved. One month later, the patient's best corrected visual acuity had returned to 20/20 with -0.75 -1.00 x 10 degrees, however minimal stromal scarring still remained. This case demonstrates that microbial keratitis after LASIK, if treated promptly, does not lead to a permanent reduction in visual acuity.

Adult↗
PubMed1997

Activation of inducible nitric oxide synthase by human choriogonadotropin in RAW 264.7 cells.

Although human choriogonadotropin (hCG) plays a crucial role in the regulation of the menstrual cycle and maintenance of pregnancy, little is known about the other functions. However, recently hCG receptors have been identified in nongonadal cells. The objective of the current study was to determine the effect of hCG on the production of nitric oxide (NO). Stimulation of RAW 264.7 cells with hCG after treatment with recombinant interferon-gamma (rIFNgamma) resulted in increased NO synthesis. hCG had no effect on NO synthesis itself. NO production was inhibited by N(G)-monomethyl-L-arginine. rIFNgamma in combination with hCG showed marked increase of the expression of the inducible nitric oxide synthase (iNOS) gene. In addition, synergy between rIFNgamma and hCG was mainly dependent on hCG-induced tumor necrosis factor-alpha (TNF-alpha) secretion. All the preparations of hCG were endotoxin free. These results suggest that the capacity of hCG to increase NO production from rIFNgamma-primed RAW 264.7 cells is the result of hCG-induced TNF-alpha secretion.

Animals↗
PubMed1997

Abnormal expression of mouse mast cell protease 5 gene in cultured mast cells derived from mutant mi/mi mice.

Mast cells contain a lot of mast cell-specific proteases. We have reported that the expression of mouse mast cell protease 6 (MMCP-6) is remarkably reduced in both cultured mast cells (CMCs) and skin mast cells of mi/mi mutant mice. In the present study, we found that the expression of MMCP-5 was reduced in CMCs but not in skin mast cells of mi/mi mice, and we compared the regulation mechanisms of MMCP-5 with those of MMCP-6. The mi locus encodes a member of the basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF). The consensus sequence recognized and bound by bHLH-Zip transcription factors is CANNTG. The overexpression of the normal (+) MITF but not of mi-MITF normalized the poor expression of the MMCP-5 gene in mi/mi CMCs, indicating the involvement of +-MITF in transactivation of the MMCP-5 gene. Although +-MITF directly bound CANNTG motifs in the promoter region of the MMCP-6 gene and transactivated it, the binding of +-MITF to the CAGTTG motif in the promoter region of the MMCP-5 gene was not detectable. The +-MITF appeared to regulate the transactivation of the MMCP-5 gene indirectly. Moreover, addition of stem cell factor to the medium normalized the expression of the MMCP-5 but not of the MMCP-6 gene in mi/mi CMCs. Despite the significant reduction of both MMCP-5 and MMCP-6 expressions in mi/mi CMCs, their regulation mechanisms appeared to be different.

Animals↗
PubMed1997

Involvement of transcription factor encoded by the mouse mi locus (MITF) in expression of p75 receptor of nerve growth factor in cultured mast cells of mice.

The mi locus of mice encodes a member of the basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF). Cultured mast cells (CMCs) of mi/mi genotype showed a poor response to nerve growth factor (NGF). Addition of NGF to the suboptimal dose of interleukin-3 (IL-3) increased the plating efficiency of normal (+/+) CMCs but not mi/mi CMCs. Although +/+ CMCs were berberine sulfate-negative when cultured with IL-3, +/+ CMCs became berberine sulfate-positive when cultured in the presence of both IL-3 and NGF, which suggested increased heparin content. In contrast, NGF did not influence the phenotype of mi/mi CMCs. The poor response of mi/mi CMCs to NGF was attributed to the deficient expression of p75 NGF receptor. The purpose of the present study is to examine the effect of MITF on p75 gene transcription. Overexpression of +-MITF or mi-MITF was observed in mi/mi CMCs to which cDNA encoding each type of MITF had been introduced using the retroviral vector. Overexpression of +-MITF but not of mi-MITF normalized the expression of p75 and the above-mentioned poor responses of mi/mi CMCs to NGF, indicating the involvement of +-MITF in p75 gene transactivation. Then, we analyzed the promoter of the p75 gene. Two CANNTG motifs recognized by bHLH-Zip-type transcription factors were conserved between the mouse and rat p75 promoters. One of these two CANNTG motifs was specifically bound by +-MITF. When the luciferase gene under the control of the p75 promoter was cotransfected into NIH/3T3 fibroblasts with cDNA encoding +-MITF or mi-MITF, luciferase activity increased significantly only when +-MITF cDNA was cotransfected. The mutation of this CANNTG motif abolished the transactivation effect of +-MITF, indicating that +-MITF transactivated the p75 gene, at least in part, through direct binding.

3T3 Cells↗
PubMed1997

MDR-1 gene expression is a minor factor in determining the multidrug resistance phenotype of MCF7/ADR and KB-V1 cells.

The relevance of MDR-1 gene expression to the multidrug resistance phenotype was investigated. Drug-resistant cells, KB-V1 and MCF7/ADR, constantly expressed mRNA of the MDR-1 gene and were more resistant to vinblastine and adriamycin than drug-sensitive cells, KB-3-1 and MCF7. The drug efflux rate of KB-V1 was the same as KB-3-1 although the MDR-1 gene was expressed in only the resistant cell. The higher intracellular drug concentration of KB-3-1 than KB-V1 was due to the large drug influx. In the case of MCF7 and MCF7/ADR, the influx and efflux of the drug had nearly the same pattern and drug efflux was not affected by verapamil. The amount of ATP, cofactor of drug pumping activity of P-glycoprotein, was not changed by the resistance. These observations suggested that drug efflux mediated by MDR-1 gene expression was not a major determining factor of drug resistance in the present cell systems, and that the drug resistance could be derived from the change in drug uptake and other mechanisms.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Thromboxane A2 synthase inhibition and thromboxane A2 receptor blockade by 2-[(4-cyanophenyl)amino]-3-chloro-1,4-naphthalenedione (NQ-Y15) in rat platelets.

The effects of 2-[(4-acetylphenyl)amino]-3-chloro-1,4-naphthalenedione (NQ-Y15), a synthetic 1,4-naphthoquinone derivative, on platelet activity and its mechanism of action were investigated. NQ-Y15 caused a concentration-dependent inhibition of the aggregation induced by thrombin, collagen, arachidonic acid (AA), and A23187. The IC50 values of NQ-Y15 on thrombin (0.1 U/mL)-, collagen (10 microg/mL)-, AA (50 microM)-, and A23187 (2 microM)-induced aggregation were 36.2 +/- 1.5, 6.7 +/- 0.7, 35.4 +/- 1.7, and 93.1 +/- 1.4 microM, respectively. NQ-Y15 also inhibited thrombin-, collagen-, AA-, and A23187-stimulated serotonin secretion in a concentration-dependent manner. However, a high concentration (100 microM) of NQ-Y15 showed no significant inhibitory effect on ADP-induced primary aggregation, which is independent of thromboxane A2 (TXA2) production in rat platelets. In fura-2-loaded platelets, the elevation of intracellular free calcium concentration stimulated by AA, thrombin, and 4-bromo-A23187 was inhibited by NQ-Y15 in a concentration-dependent manner. The formation of TXA2 caused by AA, thrombin, and collagen was inhibited significantly by NQ-Y15. NQ-Y15 inhibited TXA2 synthase in intact rat platelets, since this agent reduced the conversion of prostaglandin (PG) H2 to TXA2. Similarly, NQ-Y15 selectively inhibited the TXA2 synthase activity in human platelet microsomes, whereas it had no effect on activity of phospholipase A2, cyclooxygenase, and PGI2 synthase in vitro. NQ-Y15 inhibited platelet aggregation induced by the endoperoxide analogue U46619 in human platelets, indicating TXA2 receptor antagonism, possibly of a competitive nature. These results suggest that the antiplatelet effect of NQ-Y15 is due to a combination of TXA2 synthase inhibition with TXA2 receptor blockade, and that it may be useful as an antithrombotic agent.

Animals↗
PubMed1997

Apoptosis-mediated immunotoxicity of polychlorinated biphenyls (PCBs) in murine splenocytes.

Polychlorinated biphenyls (PCBs) exhibited immunotoxicity on antibody forming response to T-dependent antigen of sheep red blood cells, primary activation of T cells by mixed lymphocyte response, and lymphocyte proliferation induced by various mitogens. These immunosuppressions were related with the loss of lymphocyte viability which was determined by the propidium iodide method, and this death was proven to be linked with apoptosis which showed DNA fragmentation detected by the diphenylamine method and agarose gel electrophoresis. The degree of DNA fragmentation was increased in a dose- and time-dependent manner in PCB-treated splenocytes. In conclusion, it was assumed that apoptosis was attributable to the immunotoxicity of PCBs in murine splenocytes.

Animals↗
PubMed1997

Suppression of L-histidine decarboxylase mRNA expression by methyleugenol.

We investigated the effect of methyleugenol on anaphylaxis. Methyleugenol completely inhibited systemic anaphylaxis induced by compound 48/80 in mice. Methyleugenol also inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) IgE. Moreover, methyleugenol dose-dependently inhibited histamine release in mast cells activated by compound 48/80 or anti-DNP IgE. Northern-blot analysis demonstrated that significantly reduced level of the mRNA of L-histidine decarboxylase (HDC) was expressed in mast cells treated with methyleugenol, compared to that without methyleugenol. We conclude that methyleugenol directly affect histamine release and HDC gene over-expression in mast cells.

Animals↗
PubMed1997

Bonding of chemically treated titanium implants to bone.

A study was undertaken in rabbit tibiae to determine the effects of chemical treatments and/or surface-induced bonelike apatite on the bone-bonding ability of titanium (Ti) implants. Smooth-surfaced plates (10 x 10 x 2 mm) of pure Ti, alkalil- and heat-treated Ti, and bonelike apatite-formed Ti after the treatments were implanted into the tibial metaphyses of mature rabbits. The tibiae containing the implants were harvested at 4, 8, and 16 weeks after implantation and subjected to a tensile testing and histologic evaluation. Biomechanical results showed that both treated implants exhibited significantly higher failure loads compared with untreated Ti implants at all time periods. Histologic examination by Giemsa surface staining, contact microradiography (CMR), and scanning electron microscopy (SEM) in backscatter mode revealed that both treated Ti implants directly bonded to bone tissue during the early postimplantation period, whereas untreated Ti implants formed direct contact with the bone only at 16 weeks. SEM-electron-probe microanalysis (EPMA) examination showed a Ca-P-rich layer at the interface between the treated implants and bone, although the Ca-P-rich layer was not detected on the surface of untreated implants during observation periods. The results of this study suggest that chemical treatments may accelerate the bone-bonding behavior of titanium implants and enhance the strength of bone-implant bonding by inducing a bioactive surface layer on Ti implants.

Animals↗
PubMed1997

Bonding strength of bonelike apatite layer to Ti metal substrate.

Our previous study showed that titanium metal forms a bonelike apatite layer on its surface in simulated body fluid when it was subjected to NaOH and heat treatments to form a sodium titanate hydrogel or amorphous sodium titanate surface layer. In the present study, bonding strength of the apatite layer formed on the titanium metals to the substrates were examined under tensile stress, in comparison with those of the apatite layers formed on Bioglass 45S5-type glass, dense sintered hydroxyapatite, and glass-ceramic A-W, which are already clinically used. The NaOH-treated titanium metals showed higher bonding strength of the apatite layer to the substrates, which was maximized by heat treatments at 500 and 600 degrees C, than all the examined bioactive ceramics. It is believed that bioactive metals thus obtained are useful as bone substitutes, even under load-bearing conditions.

Apatites↗