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K S Hong

Publications and source records attributed to K S Hong.

16 recordsLinked to original sources
PubMed1994

Phosphorylation and activation of mitogen-activated protein kinase by kainic acid-induced seizure in rat hippocampus.

Injection of kainic acid into rat induced a limbic seizure and increased the activities of two protein kinases with Mrs of 42 kDa and 44 kDa in the hippocampus. These two protein kinases were identified as MAP kinases by an anti-MAP kinase antibody. These MAP kinases were phosphorylated at least at a tyrosine residue. The time course of the MAP kinase activation was roughly parallel with that of the seizure. These results indicate that the kainic acid-induced seizure induces MAP kinase activation in rat hippocampus.

Animals↗
PubMed1994

Activation and tyrosine phosphorylation of 44-kDa mitogen-activated protein kinase (MAPK) induced by electroconvulsive shock in rat hippocampus.

Electroconvulsive shock (ECS) has been reported to induce the phosphorylation and activation of 42-kDa, but not 44-kDa, mitogen-activated protein kinase (MAPK) in rat hippocampus. We studied the activation and tyrosine phosphorylation of MAPKs in rat brain after ECS. We observed the increase of the activities of both 42- and 44-kDa MAPKs in rat hippocampus after ECS. The activities reached peak at 2 min and returned to basal levels by 15 min after ECS. We also observed the increased phosphorylation on the tyrosine residue of 42-kDa MAPK in rat hippocampus after ECS, but not on that of 44-kDa MAPK. However, when we examined the immunoprecipitated 44-kDa MAPK, we could demonstrate that the tyrosine phosphorylation of 44-kDa MAPK at 2 min after ECS was markedly increased, in accordance with the increase of kinase activity. These results indicate that ECS induces the transient activation and tyrosine phosphorylation of 44-kDa MAPK, as well as 42-kDa MAPK, in rat hippocampus, although the amount of tyrosine phosphorylation is far less and the kinase activity is lower in 44-kDa MAPK than in 42-kDa MAPK.

Animals↗
PubMed1993

Complex duplications in maize lines.

Rp1 is a disease resistance complex and is the terminal morphological marker on the short arm of maize chromosome 10. Several restriction fragment length polymorphisms (RFLPs), which map within 5 map units of Rp1, were examined to determine if they are also complex in structure. Two RFLP loci, which mapped distally to Rp1, BNL3.04 and PIO200075, existed in a single copy in all maize lines examined. These two loci cosegregated perfectly in 130 test cross progeny. Two RFLP loci that map proximally to Rp1 had unusual structures, which have not yet been reported for maize RFLPs; the loci were complex, with variable numbers of copies in different maize lines. One of the loci, NP1285, occasionally recombined in meiosis to yield changes in the number of copies of sequences homologous to the probe. The other proximal locus, detected by the probes NPI422, KSU3, and KSU4, was relatively stable in meiosis and no changes in the number of restriction fragments were observed. The similarity in map position between Rp1 and the complex RFLP loci indicate there may be genomic areas where variable numbers of repeated sequences are common. The structure of these complex loci may provide insight into the structure and evolution of Rp1.

Chromosome Mapping↗
PubMed1992

Role of TraT protein, an anticomplementary protein produced in Escherichia coli by R100 factor, in serum resistance.

Escherichia coli K12 strain W3110/SM bearing a plasmid containing the traT gene (traT+ strain) was more resistant to the bactericidal activity of guinea pig serum than the same strain bearing this plasmid without the traT gene (traT- strain). A murine mAb was generated against synthetic TraT peptide (86-99). This antibody reacted only with denatured TraT protein, but it was used for monitoring TraT protein by immunoblotting during purification of the protein. Six mAb were then generated against partially purified traT protein from the solubilized membrane fraction of the traT+ strain. These mAb reacted with the native protein even on living cells, and their F(ab) fragments were found to suppress the inhibitory effect of the TraT protein on the bactericidal activity of serum. TraT protein was purified from solubilized membranes of the traT+ strain by ion exchange and gel filtration chromatographies. The purified TraT protein inhibited the lysis of sensitized erythrocytes by serum complement. Its inhibitory action was mainly on the C6 step. It strongly inhibited the reaction of C6 with EAC14b2a3b and excess C5, C7, C8, and C9. TraT protein also inhibited the reaction of C7-deficient human serum with guinea pig erythrocytes when it was activated by cobra venom factor. It did not inhibit the reaction of preformed C5b6 complexes. However, TraT did not have any effect on the cleavage of 125I[C5] to 125I[C5b] in similar conditions. It also partially inhibited the reaction steps of C4, C5, and factor B and limited guinea pig complement serum in 0.1% gelatin veronal buffered saline, pH 7.4, containing 10 mM EDTA with their respective preceding intermediate cells. It had no effect on either the binding of C3 to EAC14b2a or the cleavage of C3b by factors H and I. TraT protein probably inhibits the formation of C5b6 complex or causes structural alteration of the complex to a nonfunctional form.

Amino Acid Sequence↗
PubMed1992

Bactericidal activity of C9-deficient human serum.

Escherichia coli B/SM, strain 1-1, was killed dose dependently by human hereditary C9-deficient serum (C9DHS), which was shown to contain no C9 Ag by an ELISA method. On the other hand, human hereditary C7-deficient serum did not kill the bacteria under similar conditions. The bactericidal activity of C9DHS was inhibited by rabbit anti-C5 antibody but not by murine anti-C9 mAb. The anti-C9 antibody decreased the bactericidal activity of normal human serum (NHS) to the level of that with C9DHS. Sheep anti-human lysozyme antibody did not affect the bactericidal activity of C9DHS or NHS even when added at more than twice the concentration required to block the serum lysozyme activity on Micrococcus luteus. After treatment with C9DHS and washing, surviving Escherichia coli were killed by C9, but not by lysozyme, transferrin, or both. Other strains of E. coli (K12 W3110, C600, and NIHJ) and Salmonella typhimurium (strain NCTC 74), all maintained in the laboratory, were also killed by C9DHS. However, pathogenic strains recently isolated from patients with traveler's diarrhea and some strains of S. typhimurium were resistant to both C9DHS and NHS, at least at the serum concentration tested. A concentration of 0.1 M Tris did not increase the susceptibility of serum-resistant strains of bacteria to C9DHS, but made one strain of S. typhimurium tested susceptible to NHS, but not to C9DHS. These results clearly showed that C9DHS kills bacteria that are sensitive to NHS through activation of C up to the step of C8 in the same way that C9-deficient C serum lyzed sensitized erythrocytes.

Blood Bactericidal Activity↗
PubMed1991

Preferential inactivation of the C5 convertase of the alternative complement pathway by factor I and membrane cofactor protein (MCP).

Human C3b bound to the ghost of sheep erythrocytes (E*) via activation of the alternative complement pathway (E*AC3b) consists of four major constituents on SDS-PAGE of 350, 260, 210 and 180 kDa. 350 kDa C3b is a dimeric form of C3b in which the alpha' chain of one C3b binds covalently to that of the other C3b. This complex is presumed to serve as a core for the alternative pathway C5 convertase. The other C3b populations are monomers complexed with membrane proteins or sugars. Using E*AC3b (C3b labeled) as a substrate, we have investigated functional properties of membrane cofactor protein (MCP), which is an integral membrane protein with C3b-binding and factor I-dependent cofactor activities. In conjunction with factor I, MCP was found to degrade the protein-bound C3b preferentially including the 350 kDa dimer. There was a similar but lesser tendency of this selective cleavage of C3b-dimer by CR1 but not by factor H or C4bp. In contrast to CR1 and factor H, detergent solubilization of EAC3b was required for MCP to fully express its cofactor activity for this selective degradation of C3b. We next separated the C3b dimer from the monomers and assessed their ability to assemble the alternative C5 convertase. The C3b dimer but not the monomers expressed C5 convertase activity following the addition of factors B and D, C5 and Ni2+. Kinetic analysis of the degradation of the C3b dimer by MCP and factor I suggested that only one C3b was efficiently converted to C3bi and this occurred concomitant with a decrease in C5 convertase activity. These results suggest that MCP has the ability to more efficiently interact with protein-bound C3b and that this may relate as well to its preferential ability to irreversibly inactivate the C5 convertase.

Antigens, CD↗
PubMed1990

Oriental cholangiohepatitis: sonographic findings in 48 cases.

Oriental cholangiohepatitis is characterized by recurrent attacks of abdominal pain, fever, chill, and jaundice and grossly dilated extrahepatic and intrahepatic ducts containing soft, pigmented stone and pus. Sonograms were studied in 48 patients in whom the diagnosis was later proved during surgery (n = 34) or on the basis of clinical and laboratory findings and endoscopic retrograde cholangiography (n = 14). The sonographic findings included intrahepatic and/or extrahepatic bile duct stones (n = 47); moderate to severe dilatation of the extrahepatic ducts with relatively mild or no dilatation of intrahepatic bile ducts (n = 41); localized dilatation of the lobar or segmental bile ducts, especially the left hepatic lobe (n = 16); and gallstones (n = 22). Our experience suggests that the preoperative diagnosis of oriental cholangiohepatitis can be strongly suggested by sonographic findings.

Adult↗
PubMed1989

Red cell sodium and ionic fluxes in patients with hyper- and hypothyroidism.

To investigate the status of the Na+ concentrations [Na+]i, K+ concentrations [K+]i and ionic fluxes in red cells of human subjects with abnormal thyroid function, we measured the Na(+)-K+ pump activity as well as Na(+)-K+ cotransport (CoT), Na(+)-Li+ countertransport (CTT) and Na+ passive permeability in erythrocytes of 37 normal subjects, 19 untreated hyperthyroid patients, 12 treated hyperthyroid patients and 9 hypothyroid patients with T4 replacement. The mean [Na+]i value in the untreated hyperthyroidism group was significantly higher than that in the normal subjects (p less than .05), but not significantly different from that in the treated hyperthyroidism group. The mean [Na+]i value in the hypothyroidism with T4 replacement group, however, was significantly lower than that in the normal group (p less than .01). We did not find any significant difference of [K+]i in comparing each group. It was found that the Na(+)-K+ pump activity in erythrocytes was significantly increased in untreated hyperthyroidism (mean; 23.4% above control, p less than 10(-5], but there was no significant difference in treated hyperthyroidism and hypothyroid patients with T4 replacement. The rate constant for ouabain-sensitive Na+ efflux in the hypothyroidism with T4 replacement group was markedly higher than that in normal subjects (p less than .01), but not significantly different in the untreated hyperthyroidism group. We observed a significant increase of the Na+ CoT value in the patients with untreated hyperthyroidism as compared with that of the normal subjects (p less than .05), but there was no significant difference in the patients treated for hyperthyroidism and the hypothyroidism with T4 replacement group. However, the rate constant for Na(+)-CoT in the patients with hypothyroidism with T4 replacement was significantly higher than that in normal subjects (p less than .05). We observed a marked decrease of Na(+)-Li+CTT value in the patients with untreated hyperthyroidism versus that in the normal group (p less than .01). Passive Na+ permeability in the patients with untreated hyperthyroidism was markedly increased (p less than .05), and was markedly decreased in the patients with hypothyroidism with T4 replacement compared to normal subjects (p less than .01). It can be concluded from these studies that an increase in Na(+)-K+ pump activity in the patients untreated for hyperthyroidism might then be regarded as a secondary adaptive cellular response to higher [Na+]i values due to enhanced passive Na+ permeability, rather than a direct effect of the thyroid hormone.

Adult↗
PubMed1989

Effects of cyclosporin A on insulin binding and action in isolated fat cells of rat.

To study the effect of cyclosporin A (CsA) on glucose metabolism in peripheral insulin target cells, we studied the intraperitoneal glucose tolerance test (i.p. GTT), insulin binding, glucose transport and lipogenesis in isolated adipocytes of CsA-treated male Wistar rats. The rats were treated for 7 days with an intramuscular injection of vehicle (control group), or 5 (group I) or 50 mg/kg body weight (group II) of CsA dissolved in ethanol. The results of i.p. GTT in group II showed markedly impaired glucose tolerance with significantly decreased basal and glucose-stimulated serum insulin levels. In isolated adipocytes of CsA-treated rats, the insulin bindings were decreased by 26% in group I and 32% in group II. The maximum insulin-stimulated glucose transports were decreased by 34% in group I and 41% in group II. The maximum insulin-stimulated lipogenesis was decreased by 33% in group I and 37% in group II. There was a right shift of the dose response curves for insulin of glucose transport and lipogenesis of both CsA-treated groups. In conclusion, these results suggest that CsA produces significant functional changes of pancreatic B cells and also induces insulin resistance in adipocytes due to combined receptor and postreceptor defects in insulin action.

Adipose Tissue↗
PubMed1988

C5 convertase of the alternative complement pathway: covalent linkage between two C3b molecules within the trimolecular complex enzyme.

C5 convertase of the alternative C pathway is a complex enzyme consisting of three C fragments--one molecule of a major fragment of factor B (Bb) and two molecules of a major fragment of C3 (C3b). Within this C3bBbC3b complex, the first C3b binds covalently to the target surface, and Bb, which bears a catalytic site, binds noncovalently to the first C3b. In the present investigation, we studied the nature of the convertase that is assembled on E surfaces and obtained evidence that the second C3b binds directly to the alpha'-chain of the first through an ester bond rather than to the target surface. Thus, the alternative pathway C5 convertase could be described as a trimolecular complex in which Bb binds noncovalently to a covalently linked C3b dimer. We also obtained evidence that not only the second C3b but also the first C3b participates in binding C5, that is, covalently-linked C3b dimer acts as a substrate-binding site. Because of this two-site binding, the convertase has a much higher affinity for C5 than the surrounding monomeric C3b molecules. Based on this evidence, a new model of the alternative pathway C5 convertase is proposed. Covalent association of two subunits and the bivalent binding of the substrate are then common properties of the alternative and classical pathway C5 convertases.

Animals↗
PubMed1988

Developmentally regulated, phospholipase C-mediated release of the major surface glycoprotein of amastigotes of Trypanosoma cruzi.

The surface of amastigotes of Trypanosoma cruzi is covered by Ssp-4, a major stage-specific glycoprotein. Ssp-4 is anchored to the cell membrane by GPI. It can be metabolically labeled with [3H]myristic acid, and is converted into a hydrophilic form by treatment with the glycan-specific phospholipase C of T. brucei, or after lysis of the parasites in non-ionic detergents. The hydrophilic form of Ssp-4 is recognized by antibodies to the cross-reactive determinant of the variant surface glycoprotein of African trypanosomes. Ssp-4 is progressively shed during the intra- or extracellular development of amastigotes preceding their transformation into epi- and trypomastigotes. We show here that T. cruzi contains a phospholipase C and that most shed Ssp-4 is hydrophilic, does not contain myristic acid, and reacts with anti-CRD. These observations provide strong evidence that phospholipase C mediates the release of this glycosyl-phosphatidylinositol-anchored protein under physiological conditions, as the parasite undergoes differentiation.

Animals↗
PubMed1987

Stage-specific surface antigens expressed during the morphogenesis of vertebrate forms of Trypanosoma cruzi.

The origin of Trypanosoma cruzi slender and broad forms found in the circulation of the mammalian host has remained obscure and, unlike what has been proposed for African trypanosomes, no precise form-function relationship has been ascribed to them. We show here that parasites circulating in the blood of infected animals display a high degree of polymorphism. Around 10% of the forms found circulating in mice during the acute phase of infection were amastigotes, and the other 90% included slender and broad trypomastigotes and intermediate forms between amastigotes and trypomastigotes. Slender trypomastigotes, from blood or cell culture, undergo extracellularly morphological rearrangements in which the parasites become gradually broader and transform into amastigotes. By scanning electron microscopy a progressive internalization of the flagellum and reorganization of the cell shape in a helical fashion were observed in parasites undergoing transformation. After 48 hr of extracellular incubation the parasite population consisted exclusively of amastigotes with a short protruding flagellum. The morphological changes were associated with the expression of different surface antigens defined by monoclonal antibodies: the trypomastigote-specific antigens Ssp-1 (a 100-120-150-Mr glycoprotein), Ssp-2 (a 70-Mr glycoprotein), Ssp-3 (undefined), and Ssp-4, an amastigote-specific surface antigen. Ssp-4 was also detected on intracellular amastigotes (in vitro and in vivo). We conclude that trypomastigotes are programmed to develop into amastigotes whether or not they enter cells, and that the differentiation can occur in the blood of the vertebrate host. These findings raise some questions regarding conventional views on the life cycle of T. cruzi.

Animals↗
PubMed1985

Complement anaphylatoxins activity in middle ear effusion.

There are various theories on the causes of otitis media with effusion. The exact pathogenesis, however, still remains unknown, while the causes have been so far elucidated and studied by many researchers. This disease occurs frequently in children, showing an increasing trend, often causes subsequent deafness, and its treatment takes a long time causing social hardships. Therefore it is urgent to elucidate the pathogenesis of this disease. In this study the C3a and C5a fragments of complements from middle ear fluids, most closely related to the inflammatory reaction, were measured. The subjects were patients with otitis media with effusion consisting of 5 children and 9 adults. All cases showed retraction in the tympanic membrane findings, B type in the tympanogram classification, and serous type in the properties of middle ear fluids. CRP, alpha-1, alpha-2, beta-, gamma-globulin, neutrocytes, and lymphocytes in serum were normal when examined, and C3, C4, C3a, C5a, and CH50 were normal as well. Extremely high values of C3a and C5a in middle ear fluids were observed. The values of C3a were 18,000 ng/ml at maximum, 5,800 ng/ml at minimum, and 9,293 ng/ml on average. The values of C5a were 86, 20, and 55 ng/ml, respectively. No difference between childhood and adult cases was observed, in spite of differences in the underlying diseases among them. The above results revealed that an extremely intensive inflammatory reaction may take place in the middle ear, and that anaphylatoxin might play an important role as a delayed factor in otitis media with effusion.

Adult↗
PubMed1984

Wedge-shaped BGO scintillation crystal for positron emission tomography: concise communication.

In order to increase the detection efficiency and also reduce the interdetector spillage, a new wedge-shaped BGO scintillation detector array is proposed. By shaping the front part of a detector as a wedge, the absorption path becomes longer, particularly for obliquely incident photons, thereby improving the uniformity in the sensitivity for the incident photons of different angles. To demonstrate the effectiveness of the proposed detector shape, a Monte Carlo simulation was performed and the results are presented.

Bismuth↗
PubMed1983

High-resolution circular ring positron tomograph with dichotomic sampling: Dichotom-I.

The circular ring transaxial positron camera developed earlier was refitted with a new dichotomic sampling scheme and aperture collimators on the detector array to improve the sampling and the overall system resolution. The z-axis slice thickness collimators were also limited to 1 cm, which corresponds to a slice thickness of 0.5 cm FWHM. Two different types of aperture collimators were adopted for high resolution (HR) and very high resolution (VHR) imaging, respectively. In HR mode a resolution of 6.5 mm FWHM was obtained without appreciable degradation of overall sensitivity, which represents a threefold improvement in resolution over the original system. In phantom studies with HR mode a sensitivity of 4500 counts s-1 muCi-1 cm-3 was obtained for a 20 cm diameter uniform phantom filled with water. A VHR mode experiment was also conducted to observe the ultimate resolution capability of the Dichotom-I system, and a resolution of 4.2 mm FWHM was obtained at the expense of sensitivity which was reduced by a factor of four from the HR mode experiment. The experience gained with Dichotom-I suggests a relatively simple and inexpensive modification of the existing NaI(T1) ring positron cameras, most of which suffer from low resolution due to poor sampling and poor intrinsic detector resolution.

Animals↗