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K Yun

Publications and source records attributed to K Yun.

At least 37 records · Page 2Linked to original sources
PubMed1998

Use of a quartz crystal microbalance to monitor immunoliposome--antigen interaction.

We have used quartz crystal microbalance (QCM)-based real-time biospecific interaction measurement to analyze the binding of immunoliposomes to antigen and examined the use of liposomes as signal-enhancing reagents in competitive QCM immunoassay. For the preparation of immunoliposomes, various amounts of bacterially produced lipid-tagged single-chain antibody against 2-phenyloxazolone were incorporated in phosphatidylcholine liposomes. The immunoliposomes bound specifically to immobilized hapten, and this binding was inhibited by soluble hapten in a concentration-dependent manner. In this competitive assay, antigen could be measured in the concentration range from 10(-5) to 10(-8) M.

Antibodies↗
PubMed1998

Promoter-specific insulin-like growth factor 2 gene imprinting in human fetal liver and hepatoblastoma.

Insulin-like growth factor 2 (IGF2) gene imprinting has been demonstrated to be promoter-specific, in that expression from the P1 promoter is biallelic whereas that from the P2-P4 promoters is monoallelic. In the present study, in order to investigate IGF2 gene imprinting status at the cellular level, allelic analysis was performed of IGF2 gene expression transcribed from the P1 and P3 promoters, using reverse transcription polymerase chain reaction (RT-PCR) on human fetal liver and hepatoblastoma. In situ hybridization was also undertaken, to obtain information about the cellular localization of transcripts expressed from the P1 and P3 promoters. The results indicated that transcripts expressed from the P1 and P3 promoters co-localized in the same fetal or neoplastic hepatocytes. These data should provide information regarding the molecular basis of genomic imprinting, suggesting that an imprint recognized for the differential expression may be strictly local and localized downstream of the IGF2 P1 promoter.

Alleles↗
PubMed1998

In situ detection of insulin-like growth factor II (IGF2) and H19 gene expression in hepatocellular carcinoma.

To assess the relationship between insulin-like growth factor II (IGF2) and H19 gene expression at the cellular level, we have examined the distribution of IGF2 and H19 mRNA by means of an situ hybridization in hepatic malignancies consisting of hepatocellular carcinoma (HCC), cholangiocellular carcinoma (CCC), and metastatic liver cancer (MLC). In HCC, 15 of 27 tumors (56%) and 11 of 27 tumors (41%) demonstrated increased IGF2 and H19 gene expression, respectively. Of 16 HCCs with increased expression of either IGF2 or H19, 10 tumors coexpressed both transcripts at comparable levels. Moreover, the spatiotemporal distribution and the cellular localization of the two gene transcripts were almost identical, suggesting the presence of a reciprocal relation between IGF2 and H19. In addition, 5 HCCs showed increased IGF2 expression without concomitant H19 expression, whereas 1 HCC showed increased H19 expression without IGF2 transcripts. However, 11 HCCs showed no IGF2 or H19 expression. On the other hand, neither IGF2 transcripts nor H19 transcripts were detected in 2 CCCs or 10 MLCs studied. The data suggest that IGF2 and/or H19 gene expression may be characteristic of some HCCs.

Adolescent↗
PubMed1998

A SacII polymorphism in the human ASCL2 (HASH2) gene region.

The mouse achaete-scute homolog-2 gene (Ascl2 or Mash2) encodes a transcription factor playing a role in the development of the trophoblast. The Ascl2 gene is paternally imprinted in the mouse, but whether this applies to its human homolog is unknown. In the present study, we found a SacII polymorphism in the possible 3' untranslated region (UTR) of the gene. It would be very useful to determine definitively whether the gene is imprinted, as well as to analyze the allelic methylation status of the gene.

Alleles↗
PubMed1998

Selective MT2 melatonin receptor antagonists block melatonin-mediated phase advances of circadian rhythms.

This study demonstrates the involvement of the MT2 (Mel1b) melatonin receptor in mediating phase advances of circadian activity rhythms by melatonin. In situ hybridization histochemistry with digoxigenin-labeled oligonucleotide probes revealed for the first time the expression of mt1 and MT2 melatonin receptor mRNA within the suprachiasmatic nucleus of the C3H/HeN mouse. Melatonin (0.9 to 30 microg/mouse, s.c.) administration during 3 days at the end of the subjective day (CT 10) to C3H/HeN mice kept in constant dark phase advanced circadian rhythms of wheel running activity in a dose-dependent manner [EC50=0.72 microg/mouse; 0.98+/-0.08 h (n=15) maximal advance at 9 microg/mouse]. Neither the selective MT2 melatonin receptor antagonists 4P-ADOT and 4P-PDOT (90 microg/mouse, s.c.) nor luzindole (300 microg/mouse, s.c.), which shows 25-fold higher affinity for the MT2 than the mt1 subtype, affected the phase of circadian activity rhythms when given alone at CT 10. All three antagonists, however, shifted to the right the dose-response curve to melatonin, as they significantly reduced the phase shifting effects of 0.9 and 3 microg melatonin. This is the first study to demonstrate that melatonin phase advances circadian rhythms by activation of a membrane-bound melatonin receptor and strongly suggests that this effect is mediated through the MT2 melatonin receptor subtype within the circadian timing system. We conclude that the MT2 melatonin receptor subtype is a novel therapeutic target for the development of subtype-selective analogs for the treatment of circadian sleep and mood-related disorders.

Animals↗
PubMed1998

Genomic imprinting and carcinogenesis.

The Mendelian inheritance is based on the fundamental rule in which mammalian genes are expressed equally from two homologous biparental alleles. Recently a small number of genes have been identified to show an exception to this rule in that homologous alleles can function differently in somatic cells depending on whether they come from the mother or the father. This intriguing biological phenomenon is called as genomic imprinting which does not conform classical Mendelian inheritance and has potentially far reaching implications for genetics, evolution, developmental biology and pathology including cancer. The gene encoding insulin-like growth factor 2 (IGF2) harbors at 11p15.5 and serves as paradigm for an imprinted gene. The IGF2 gene has been demonstrated to be imprinted with the paternal allele expressed and the maternal being silent which is evolutionally conserved between mice and human. Loss of imprinting (LOI) of IGF2 has been demonstrated in a dozen of tumor types including Wilms tumor (WT) with a promise of many more to come. The LOI of IGF2 may induce increased or deregulated IGF2 expression which could initiate the onset of WT. Thus the LOI of IGF2 may provide a novel mechanism of gene activation and play a role in the development of a wide range of tumors. This review also discusses other imprinted genes on 11p15 which may have a role in WT or other diseases. Finally molecular mechanisms of genomic imprinting are discussed.

Alleles↗
PubMed1998

Comparative reverse transcription-polymerase chain reaction and in situ hybridization analyses of human imprinted p57KIP2 and insulin-like growth factor 2 gene transcripts in fetal kidney and Wilms' tumors using archival tissue.

p57KIP2 (KIP2) is a cyclin-dependent kinase inhibitor that arrests cells in G1 and an imprinted gene mapped on chromosome 11p15.5. To investigate the role of KIP2 in Wilms' tumor (WT), DNA and RNA were extracted from archival tissue sections of WT. KIP2 expression was investigated by reverse transcription-polymerase chain reaction and in situ mRNA hybridization. Thirteen of 39 WT were informative for length polymorphism of KIP2 and subjected to reverse transcription-polymerase chain reaction. KIP2 was expressed predominantly from one allele, although a low level of expression was also detected from the other. Three WT with loss of heterozygosity at the KIP2 locus demonstrated that the remaining KIP2 allele was still active, which was also confirmed by in situ hybridization. Furthermore, among 13 KIP2-informative WT, 2 were heterozygous for insulin-like growth factor II (IGF2). Allele-specific analysis demonstrated that one showed monoallelic IGF2 expression, whereas the other showed biallelic expression. In situ hybridization of fetal kidney showed that KIP2 transcripts were detected in a variety of cell types, among which differentiated epithelial structures showed higher expression than undifferentiated mesenchyme, whereas IGF2 was expressed predominantly in undifferentiated mesenchyme and renal vesicles of an early phase. WT demonstrated KIP2 and IGF2 hybridization patterns similar to fetal kidney in that KIP2 transcripts were detected in epithelial structures and blastema, whereas IGF2 transcripts were seen in blastema and immature epithelial structures. Hybridization results indicated that KIP2 expression in WT did not appear to be significantly reduced compared with that in fetal kidney and that WT demonstrated a significant amount of KIP2 transcripts regardless of retention or loss of heterozygosity at the KIP2 locus. These data suggest that although KIP2 may play a role in differentiation of the fetal kidney, it is not likely as a tumor suppressor gene, which is implicated as the cause of the development of a majority of WT.

Alleles↗
PubMed1997

Self-assembling of glutathione S-transferase/calmodulin fusion protein on chemically modified gold surface.

The fusion protein technique was used to prepare an artificial polyfunctional protein from calmodulin (CaM) and glutathione S-transferase (GST). The fusion protein was designed, expressed, and then assembled to the glutathione self-assembled gold surface. The protein assembly was confirmed through enzyme binding assay and enzyme immunoassay. Specific binding of the fusion protein to glutathione self-assembled on the gold surface was assessed via a quartz crystal microbalance (QCM). The fusion protein was reversibly adsorbed and desorbed by the competitive binding of glutathione present in a solution, thus showing that the binding of the fusion protein was specific and had a highly oriented molecular configuration.

Calmodulin↗
PubMed1997

Insulin-like growth factor 2 gene imprinting in clear cell sarcoma of the kidney.

We examined the expression of insulin-like growth factor 2 (IGF2) transcripts and allelic-specificity in four cases of clear cell sarcoma of the kidney (CCSK). All cases contained abundant IGF2 transcripts in the cytoplasm of tumor cells detected by in situ mRNA hybridization. The level of IGF2 expression was comparable with that of Wilms tumor. The IGF2 gene imprinting status was analysed by using DNA/RNA extracted from one frozen tumor tissue and three archival tumor and kidney tissue. The allele-specific analysis using Apa1 polymorphism in the 5'-untranslated region of the IGF2 gene showed that two out of four tumors were heterozygous at the IGF2 locus. The result showed that one of two informative heterozygous tumors showed biallelic IGF2 expression whereas the other showed monoallelic expression. The data show that disruption of IGF2 gene imprinting occurs in CCSK.

Child↗
PubMed1997

Co-localisation of insulin-like growth factor II and the proliferation marker MIB1 in hepatocellular carcinoma cells.

AIM: To assess the effect of insulin-like growth factor II (IGF-II) on proliferation of hepatocellular carcinoma (HCC) cells. METHODS: Expression of IGF-II mRNA and protein was detected in 10 archival HCC specimens using in situ hybridisation and immunohistochemistry, respectively. Expression of the Ki-67 antigen, a proliferation marker, was determined immunohistochemically on the same sections. RESULTS: Increased expression of IGF-II mRNA and protein was detected in five of the 10 HCCs in cells located at the periphery of tumour nests. The pattern of localisation of IGF-II was almost identical with that of Ki-67 antigen. CONCLUSIONS: Most of the Ki-67 antigen positive cells co-expressed IGF-II, suggesting that IGF-II may act as an autocrine or paracrine growth factor, and may play an important role in the development of HCC.

Carcinoma, Hepatocellular↗
PubMed1997

[Determination of fluoroacetatamide and fluoroacetic acid by capillary gas chromatography].

A rapid qualitative and quantitative analysis of fluoroacetatamide and fluoroacetic acid in rodenticides by capillary gaschromatography was described in this paper. Isoamyl alcohol was used as the internal standard. The determination curves of fluoroacetatamide and fluoroacetic acid in rodenticides were linear in the ranges of 0.0625-4 mg/ml and 0.625-20 mg/ml. The detection limits of fluoroacetatamide and fluoroacetic acid were 31.25 micrograms/ml (32.5 ng) and 625 micrograms/ml (625 ng), 87.5% and 30% of rodenticides sold in Taiyuan ground market from May, 1995 to May, 1996 contain fluoroacetatamide and fluoroacetic acid.

Chromatography, Gas↗
PubMed1997

[Enhancement pattern of hepatic metastases from colorectal cancer on CT arteriography].

The enhancement pattern of hepatic metastases from colorectal cancer on CT arteriography (CTA) was evaluated in 79 cases with 405 lesions. Sixty-two percent of overall lesions irrespective of size showed ring-like enhancement, and 33% of lesions less than 1 cm in diameter showed homogeneous enhancement. In pathological examination of 59 resected lesions, the enhancement pattern on CTA had a good correlation with the extent of tumor cellularity, necrosis or fibrosis in the lesions. And in 8.5% of resected lesions, the extent of enhancement on CTA was larger than that of perfusion defect on CT arterial portography, which was almost equal to the size in the resected specimen. In such lesions, the enhancement on CTA might include enhancement of normal hepatic parenchyma around the lesion.

Adenocarcinoma↗
PubMed1997

[Distribution of clozapine in poisoned rabbits].

The distribution of clozapine in the body of rabbits died of poison was studied by the method of TLC. The concentration of clozapine in blood, urine, bile, livers, kidneys, spleen, lungs, hearts and brains were 19.4 +/- 6.9, 50.2 +/- 12.6, 75.9 +/- 12.5, 25.9 +/- 4.0, 34.0 +/- 4.7, 13.3 +/- 2.2, 20.0 +/- 4.3, 5.0 +/- 2.3 and 43.6 +/- 43.4 ug/ml or ug/g.respectively. It is concluded that the Clozapine be not well-distributed in poisoned rabbits, Blood, bile, urine, liver and spleen are better samples for the analysis of clozapine than others.

Animals↗