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Biomedical subjects

J D Kim

Publications and source records attributed to J D Kim.

At least 37 records · Page 2Linked to original sources
PubMed2000

Activation of telomerase by silica in rat lung.

By measuring the activity of telomerase in a silica-instilled rat lung, the study found a significant increase in telomerase activity compared to that of the control. Pneumoconiosis displays the characteristics of fibroblast-proliferation and accumulation of collagen, which finally causes the pathologic changes of irreversible and progressive fibrosis of the lung. On the basis of the hypothesis that cellular proliferation may trigger telomerase-activity, the experiment was carried out with telomerase-activation in silicosis. Silica-instilled rat lungs showed increased activity of telomerase, which was measured by TRAP (telomeric repeat amplification protocol) assay, at the time of the 1st, 5th and 8th week after intratracheal instillation of silica in vivo. However, no activity was shown in silica-co-cultured fibroblast in vitro. By summarizing these results, the activity of telomerase is thought to be a very sensitive marker for the evaluation of pathogenicity, showing cellular immortalization in an experimental silicosis model.

Animals↗
PubMed2000

Platelet activating factor acetylhydrolase decreases lung reperfusion injury.

BACKGROUND: Ischemia-reperfusion injury involves free radical production, polymorphonuclear neutrophil chemotaxis/degranulation, and production of proteolytic enzymes, complement components, coagulation factors, and cytokines. Activated polymorphonuclear neutrophils, endothelial cells, and macrophages produce platelet activating factor, which further promotes these inflammatory reactions. The recently cloned plasma form of platelet activating factor-acetylhydrolase (PAF-AH) demonstrates antiinflammatory effects by degrading platelet activating factor. We evaluated the effects of PAF-AH in an isolated perfused rat lung model by adding it to the flush solutions or to the reperfusion blood. METHODS: Rat lungs were isolated, flushed with EuroCollins (EC) or University of Wisconsin (UW) solution, stored at 4 degrees C for 6 or 12 hours, and reperfused using a cross-circulating syngeneic support rat. During reperfusion, oxygenation, compliance, and capillary filtration coefficient were calculated. There were four groups in the study; group I (control) had no PAF-AH added, group II had PAF-AH added to the flush solution, group III had PAF-AH added to reperfusion blood, and group IV had PAF-AH added to both flush solution and reperfusion blood. RESULTS: After 6 hours of storage, oxygenation, compliance, and capillary filtration coefficient significantly improved for EC in group IV. For UW, oxygenation improved in group IV whereas compliance improved in groups II, III, and IV. After 12 hours of storage, compliance improved for EC in group IV and capillary filtration coefficient improved in groups III and IV. For UW, oxygenation and compliance improved in groups II and IV, whereas capillary filtration coefficient improved in group IV. CONCLUSIONS: Addition of PAF-AH to intracellular organ preservation solutions and to the blood reperfusate significantly improves postreperfusion oxygenation and compliance, and reduces lung capillary permeability.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2000

Hemostatic ligature for operative laparoscopy.

BACKGROUND: We introduce a safe and convenient method for ligature of vascular pedicles at laparoscopic surgery in which one laparoscopic and two auxillary ports are used. TECHNIQUE: The first two-turn wrap around the loop is made extracorporeally with the hand and is locked by an intracorporeal tie with manipulation of the target tissue. Knot typing is finished with the second and third nontension tie of one-turn throws. EXPERIENCE: We have used this method for laparoscopic surgery for more than 2.5 years and have not observed a failure or late hemorrhage. CONCLUSION: Two-turn throw incomplete loop ligature is a useful and convenient technique for hemostasis in three-port pelviscopic operations.

Gynecologic Surgical Procedures↗
PubMed2000

Variable numbers of TTC repeats in Mycobacterium leprae DNA from leprosy patients and use in strain differentiation.

Strain differentiation of Mycobacterium leprae would be of great value for epidemiological investigation to identify the infectious sources of leprosy, to understand transmission patterns, and to distinguish between relapse and reinfection. From the M. leprae genome sequence database, TTC DNA repeats were identified. Primer sets designed to amplify the region flanking TTC repeats revealed PCR products of different sizes, indicating that the number of repeats at each locus may be variable among M. leprae strains. The TTC repeats were not found in Mycobacterium tuberculosis, Mycobacterium avium, Mycobacterium marinum, or human tissues, which indicated their specificity to M. leprae. Sequence analysis of the TTC repeat region in each of the M. leprae strains showed a variation of 10 to 37 repeats. In the M. leprae strains of 34 multibacillary patients at Cebu, Philippines, M. leprae with 24 and 25 TTC repeats was most common, and this was followed by strains with 14, 15, 20, 21, and 28 repeats. This study thus indicates that there are variable numbers of TTC repeats in a noncoding region of M. leprae strains and that the TTC region may be useful for strain differentiation for epidemiological investigations of leprosy.

Autoradiography↗
PubMed2000

Exclusive mutations related to isoniazid and ethionamide resistance among Mycobacterium tuberculosis isolates from Korea.

SETTING: The single base change at the 94th codon of inhA has been referred to as the event that confers resistance on the drugs isoniazid (INH) and ethionamide (ETH) in Mycobacterium smegmatis and M. bovis. From this observation, it has been anticipated that some of the INH-resistant clinical isolates of M. tuberculosis would carry missense mutations in the same region of the gene. However, few polymorphisms have been identified in this region among INH-resistant isolates. OBJECTIVE: To understand the molecular basis for M. tuberculosis resistance to INH and ETH. DESIGN: The sequence polymorphism at the 94th codon of inhA among M. tuberculosis isolates from Korea was analyzed by polymerase chain reaction (PCR) cloning and sequence analysis. RESULTS: No nucleotide change at the 94th codon of inhA was detected in any of the 24 INH-resistant isolates analyzed in this study. On the other hand, a point mutation was found exclusively at the regulatory region flanking a putative ribosome-binding site of the inhA locus in 14 isolates. Interestingly, all the mutations were of the same kind, which substitutes C to T. Among 14 isolates, 12 were resistant to INH as well as to ETH, while two were resistant to INH only. DISCUSSION: It seems that mutations previously found at the 94th codon of inhA have no particular relationship with the mechanism involved in the resistance of M. tuberculosis to INH and/or ETH. On the other hand, the resistance mechanism of M. tuberculosis to INH/ETH may involve an altered level of InhA, an expression which may have been influenced by the sequence change in the regulatory region of the inhA locus.

Antitubercular Agents↗
PubMed1999

Effects of capsaicin on induction of c-jun proto-oncogene expression in Fisher-344 rats by N-methyl-N'-nitro-N-nitrosoguanidine.

N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a potent inducer of cellular stress leading to chromosomal aberrations, point mutations, and cell death. To study the effect of capsaicin on c-jun expression when given with MNNG to rats, Fisher-344 rats that had been administered MNNG were treated with capsaicin in their diet and organs were removed for measuring c-jun transcripts. We show that pre- or post-treatment of capsaicin relative to MNNG administration up- or down-regulates (depending on the organ) c-jun expression in a consistent pattern in most organs. In fact, we found in this study that capsaicin inhibits c-jun induction, stimulated by MNNG, in the spleen, heart, stomach and lung. Since MNNG, a methylating agent, is a powerful carcinogen that is very effective in the induction of c-jun mRNA, the results suggest that capsaicin uptake in the diet could play a role in inhibition of tumorigenesis induced by MNNG.

Animals↗
PubMed1999

Fas ligand and Fas are expressed constitutively in human astrocytes and the expression increases with IL-1, IL-6, TNF-alpha, or IFN-gamma.

Fas ligand (FasL) and Fas are mediators of apoptosis, which are implicated in the peripheral deletion of autoimmune cells, activation-induced T cell death, and cytotoxicity mediated by CD8+ T cells. Fas is also believed to be involved in several central nervous system diseases, but until now, the effector cells expressing FasL in the brain have not been identified. We investigated the expression levels of Fas and FasL with the stimulation of cytokines and the possible effector cells targeting Fas-bearing cells. Our data demonstrated that: 1) FasL is expressed constitutively on astrocytes taken from a fetus or an adult and that its expression increases when these cells are treated with IL-1, IL-6, or TNF-alpha in which the pretreatment of IFN-gamma triggers astrocytes to express more FasL; 2) astrocytes induce apoptosis in MOLT-4 cells through FasL; 3) Fas is also expressed constitutively and is up-regulated by IL-1, IL-6, or TNF-alpha in which the pretreatment of IFN-gamma triggers astrocytes to express more Fas; 4) apoptosis occurs when fetal astrocytes are treated with agonistic anti-Fas IgM Ab after culture with IFN-gamma and TNF-alpha; and 5) TNF-related apoptosis inducing ligand is up-regulated in fetal astrocytes with stimuli of IL-1 or TNF-alpha. These findings suggest a possible role of astrocytes in the induction of apoptosis in central nervous system diseases.

Adult↗
PubMed1999

Effects of ChunDoSunBup Qi-training on growth hormone, insulin-like growth factor-I, and testosterone in young and elderly subjects.

We observed the response of plasma growth hormone (GH), insulin-like growth factor-I (IGF-I) and testosterone (T) to an acute period of ChunDoSunBup (CDSB) Qi-training. Although the basal level of GH was not different between the two groups, after the portion of the training in which the subjects were physically active (the mid-training point), plasma GH levels increased by 7.26 fold (p < 0.05) in the elderly trainees and by 1.66 fold (p < 0.05) in the young. In response to CDSB Qi-training, IGF-I levels in the young increased significantly at mid-training point, but there were no increase in the elderly. Significant correlations existed between GH and IGF-I levels in the young subjects, but not in the elderly. The T level at the mid-training point increased significantly in elderly subjects but not in the young. These results suggest that CDSB Qi-training is a potential method for modulating of the secretion of growth factor in the young and the elderly, but that the elderly IGF-I response does not equal that of the young. In addition, our study suggests CDSB Qi-training may be one mode of therapy applicable to growth factor related disorders such as GH deficiency in children and osteoporosis in the elderly, especially women.

Aged↗
PubMed1999

Apoptotic cell death induced by taxol is inhibited by nitric oxide in human leukemia HL-60 cells.

Taxol, an antineoplastic drug, increases the fraction of cells in G2/M phases of cell cycle, induces apoptosis of leukemic cells, and activates macrophages to produce nitric oxide (NO) in response to interferon-gamma. NO has been found to play roles as pro-apoptotic or anti-apoptotic effector molecules. In this study, we investigate effects of NO on taxol-induced apoptosis in human myeloid leukemia cell, HL-60. Incubation of the cells with taxol for 24 hr induced marked DNA fragmentation of HL-60 cells. Treatment of the cells with S-nitrosogluthathione (GSNO), a NO-generating agent, protected the cells against taxol-induced apoptosis. Cell cycle analysis showed that treatment of the cells with 100 nM taxol for 12 hr rendered the cells to be accumulated in G2/M phase, but the cotreatment of the cells with taxol and 0.1 mM GSNO decreased the accumulation of the cell in G2/M phases, suggesting that NO might interfere entering of taxol-treated cells into G2/M phases. Deferoxamine or mimosine, which can arrest cells mainly at G1/S phases, also decreased taxol-induced apoptosis and reduced the number of the taxol-treated cells arresting in G2/M phases. Thus, we conclude that a protective effect of NO on taxol-treated cells from apoptosis may be partially caused by interfering entering of the taxol-treated cells into G2/M phases.

Antineoplastic Agents, Phytogenic↗
PubMed1999

Wide-angle fluorescein angiographic scanning with high resolution using a scanning laser ophthalmoscope through a mirror image fixation target.

Internal and moving targets of scanning laser ophthalmoscopes are not capable of observing the fundus beyond a field of more than 80 degrees with high resolution. The authors enabled wide-angle fundus examination with high resolution through a modification of the target. Mirror image fixation targets(MIFT), which fixated the opposite side of the examined eye onto the mirror image of five lamps placed 1.5 m away from the patient, were used to observe the fundus during fluorescein angiography in five diabetic retinopathy patients. In three of them, the ranges of the fundus examinations were measured using conventional internal fixation targets. The mean ranges of the fundus examinations when using MIFT (77.2 +/- 2.5 degrees horizontally, 67.9 +/- 2.1 degrees vertically) were significantly wider than when using internal fixation targets (65.5 +/- 2.6 degrees horizontally, 44.4 +/- 2.8 degrees vertically). MIFT provided a wide angle fundus view with high resolution equal to that of 40 degrees angle images using a scanning laser ophthalmoscope.

Diabetic Retinopathy↗
PubMed1999

Erdheim-Chester disease: a case report.

A 42-year-old man with Erdheim-Chester disease (EC) is presented. This is the first case of this disease reported in Korea. The patient complained of knee pain and plain roentgenogram of the bilateral legs revealed diffusely increased density, coarsened trabecular pattern, and cortical thickening in the diaphysis, and metaphysis as well as epiphysis. Magnetic resonance imaging revealed that the lesions showed low signal intensity on T1-weighted images and heterogeneously low and high signal intensity on T2-weighted images. Histological examination of the biopsy specimen showed a xanthogranulomatous lesion consisting aggregations of foamy histiocytes and Touton-type giant cells. Immunohistochemical staining showed positive reaction to anti-S-100 and lysozyme in the cytoplasm of the giant cells.

Adult↗
PubMed1999

Monophosphoryl lipid A (MPL) upregulates major histocompatibility complex (MHC) class I expression by increasing interferon-gamma (IFN-gamma).

Tumor immunity is primarily mediated by cells as CD8+ cytotoxic T lymphocytes (CTL) recognize tumor antigen by MHC class I molecules. But most tumors are associated with a decreased expression of MHC class I to escape the antitumor immunity of the host. Our previous data have demonstrated that MPL has an antitumor effect on metastatic lung cancer of B16 melanoma with enhancing cytotoxicity due to increase of IFN-gamma and IL-2, and decrease of IL-4, which indicates the stimulation of type 1 helper T cells (Th1). To determine the effects of MPL, IFN-gamma, TNF-alpha, and IL-1 alpha on MHC class I expression of B16 melanoma cells, we evaluated the expression of MHC class I molecules with treatments of MPL, IFN-gamma, TNF-alpha, and IL-1 alpha by flow cytometry. The supernatant of MPL-treated spleen cells in vitro upregulated the expression of MHC class I molecules of B16 melanoma cells compared to the control supernatant of spleen cells. The MHC class I expression of B16 melanoma cells treated with IFN-gamma, but not TNF-alpha or IL-1 alpha, increased in a time-dependent manner. In conclusion, MPL upregulated MHC class I expression of B16 melanoma cells by activating spleen cells via IFN-gamma. These data suggest that increased IFN-gamma by MPL is responsible for the upregulation of MHC class I expression to augment cytotoxicity. Therefore, we suggest that MPL could play an important role in immunotherapy.

Adjuvants, Immunologic↗
PubMed1999

Molecular analysis of HLA-DR gene expression induced by IFN-gamma in malignant melanoma cell lines.

Human leukocyte antigen (HLA) class II molecules are polymorphic cell surface glycoproteins that are crucial for the cellular interaction in immune response. The expression of class II molecules is regulated in a tissue-specific and cytokine-inducible manner, and is mainly restricted to the antigen presenting cells. However, some tumor cells also express class II molecules, and in some class-II-negative tumor cells, class II expression is inducible by interferon (IFN)-gamma. However, their expression varies, even though the tumor cells originate from the same histological origin; some tumor cells show strong expression, others show weak or no expression. To determine whether this differential expression of class II molecules on tumor cells is transcriptionally regulated, FACS analysis and Northern hybridization were performed using a panel of melanoma cell lines, IGR3, Malme-3M, SK-Mel-24, and SK-Mel-28 to analyze the cell surface expression and mRNA transcription rate of HLA-DR before and after treatment with IFN-gamma. FACS analysis showed that before IFN-gamma treatment, IGR3 and Malme-3M cells barely expressed HLA-DR. On the contrary, almost all of the SK-Mel-24 cells (> 90%) and a relatively high rate (> 50%) of SK-Mel-28 cells expressed HLA-DR. After IFN-gamma treatment, HLA-DR expression was induced in Malme-3M cells and SK-Mel-28 cells which displayed elevated levels of HLA-DR expression in a time-dependent manner. However, IGR3 cells never responded to IFN-gamma. Northern analysis showed that treatment with IFN-gamma led to the steady-state mRNA augmentation of the HLA-DR gene in Malme-3M and SK-Mel-28, whereas in IGR3, IFN-gamma did not augment the transcriptional rate of the HLA-DR gene. To further clarify this differential modulation, sequencing analysis of PCR product of the HLA-DR proximal promoter region was done, since the transcription rate of the class II gene is controlled by the well-conserved proximal promoter region. Six independent clones from PCR products of the HLA-DRA proximal promoter region and 16 clones from PCR products of the HLA-DRB proximal promoter region were isolated from the above cell lines and sequenced. Comparison of the nucleotide sequences of all 6 clones of DRA promoter showed that the sequences are extremely similar in both regulatory sequences and their intervening sequences. Sixteen clones of HLA-DRB promoter showed sequence variations such as substitution and insertion/deletion, and these 16 clones could be further grouped into 6 homologues with sequence homology. These data established that the melanoma cell lines studied here showed a differential susceptibility to IFN-gamma on the modulation of HLA-DR molecules, that this modulation is transcriptionally regulated, and that the difference in promoter activity by sequence variation might contribute to such a differential transcriptional regulation at the promoter level.

Base Sequence↗
PubMed1998

Genome characterization of a Korean isolate of cymbidium mosaic virus.

The complete nucleotide sequence of the genomic RNA of a Korean isolate of cymbidium mosaic virus (CymMV-K2) was determined. The genomic RNA is 6227 nucleotides in length, excluding the poly(A) tail. It contains a 5'-noncoding region (NCR) of 73 nucleotides, five open reading frames (ORFs 1 to 5) which encode proteins with M(r) 160 kDa RNA-dependent RNA polymerase (ORF1), 26 kDa movement protein 1 (ORF2), 13 kDa movement protein 2 (ORF3), 10 kDa movement protein 3 (ORF4), 24 kDa coat protein (OFR5), and a 3' NCR of 76 nucleotides. The 5'-end of the CymMV-K2 genome initiates with GGAAAA which contrasts to GAAAA at the 5'-ends of other potexviruses, including a Singapore isolate of CymMV (CymMV-S2). When compared with CymMV-S2, 171 base substitutions were observed in the CymMV-K2 genome. Substitutions in the overlapping ORFs (ORFs 2 to 4) occurred more frequently than those in 5' NCR, ORF1, and 3' NCR. In addition to substitutions, two single-base deletions, one in the intercistronic region between ORF1 and ORF2 and the other in the ORF2, were found on the CymMV-K2 genome. The deletion in the ORF2 induced a frameshift which altered the C-terminal domain of movement protein 1. ORF3 and ORF4 of the CymMV-K2 genome are partially different from those of another Singapore CymMV genome (CymMV-S1) which has four frameshifts due to nucleotide deletions within these ORFs. Interestingly, the frameshifts resulted in no change in the conserved sequences of the movement proteins but reconstructed their transmembrane domains.

Amino Acid Sequence↗
PubMed1998

Overproduction of beta-glucosidase in active form by an Escherichia coli system coexpressing the chaperonin GroEL/ES.

beta-Glucosidase from Cellvibrio gilvus was successfully overproduced in soluble form in Escherichia coli, with the coexpression of GroEL/ES. Without the GroEL/ES protein, the beta-glucosidase overexpressed in E. coli constituted a huge amount (80%) of the total cellular protein, but was localized in the insoluble fraction, and little activity was detected in the soluble fraction. Coexpression of the E. coli GroEL/ES had a drastic impact on the proper folding of the beta-glucosidase; 20% of the overexpressed enzyme was recovered in the soluble fraction in active form. In addition, the synergistic effect of GroEL/ES and the low induction temperature led to 70% solubilization of the total expressed target protein and more than a 20-fold increase in activity. Similar effects of GroEL/ES were also observed on the overexpressed beta-glucosidase from Agrobacterium tumefaciens.

Chaperonin 60↗
PubMed1998

Addition of aprotinin to organ preservation solutions decreases lung reperfusion injury.

BACKGROUND: Organ preservation injury is associated with endothelial cell damage, destabilization of mitochondrial and cell membranes, and the release of proteolytic enzymes. In addition to its well-known clinical effect of reducing perioperative blood loss, aprotinin has antiproteolytic and membrane-stabilizing properties. We hypothesized that adding aprotinin to Euro-Collins (EC) and University of Wisconsin (UW) solutions would decrease preservation injury in cultured endothelial cells and a whole organ rat lung model. METHODS: Bovine aortic endothelial cells were cultured and stored in the respective solution at 4 degrees C for 12 or 48 hours. Endothelial cell viability after storage was assessed by dimethylthiazole tetrazolium cytotoxicity assay. In the whole organ model, rat lungs were isolated, flushed with the respective solution, and stored at 4 degrees C for 6 or 12 hours. The lungs were ventilated with 100% O2 and reperfused with fresh blood. Alveolar-arterial O2 difference, O2 tension, capillary filtration coefficient, and compliance were determined. RESULTS: Endothelial cell viability was optimized with the addition of aprotinin to EC and UW at a dose of 150 KIU/mL (0.02 mg/mL). In the isolated perfused lung model, after 6 hours of ischemic storage, aprotinin-enhanced (100 KIU/mL [0.014 mg/mL]) EC and UW decreased alveolar-arterial O2 difference, increased O2 tension, and decreased capillary filtration coefficient compared with EC and UW alone. After 12 hours of ischemic storage, aprotinin-enhanced EC and UW decreased alveolar-arterial O2 difference, increased O2 tension, decreased capillary filtration coefficient, and increased compliance compared with EC and UW alone. CONCLUSIONS: The addition of aprotinin to EC and UW solutions increases endothelial cell viability in hypoxic cold storage conditions. In terms of whole organ function, aprotinin improves lung preservation as demonstrated by increased oxygenation and compliance, and decreased capillary permeability. This study is clinically applicable as there is already extensive experience with the use of aprotinin in heart and lung transplant recipients, in addition to its routine use in conventional cardiac operations.

Adenosine↗
PubMed1998

Clonal expansion of T-cells in measles.

Some autoimmune complications such as postinfectious encephalomyelitis are associated with immunologic abnormalities induced by measles virus infection. To address the superantigenic stimulation in measles which might be related with autoimmune complications, T-cells bearing the TCRBV5S2 or TCRBV8 chains and the expression of activation markers were analyzed by monoclonal antibodies. To estimate clonal expansions, the CDR3 length profile in T-cells bearing the TCRBV5S2 or TCRBV8 chains was analyzed by two-stage PCR. Results showed that the expression of DR molecules in CD3+ cells was increased significantly in measles patients (19.6 +/- 20.7%) compared to healthy children (2.9 +/- 1.4%). The mean percentage (7.1 +/- 4.4%) of T-cells bearing the TCRBV8 chain was increased in measles patients compared to healthy children (5.6 +/- 3.1%). The percentage of T-cells bearing the TCRBV5S2 chain in measles patients (3.0 +/- 1.2%) was similar to that in healthy children (2.7 +/- 0.6%). By analysis of the CDR3 length we found that there was no evidence of clonal expansions in T-cells bearing the TCRBV8 chain and that there were clonal expansions in T-cells bearing the TCRBV5S2 chain. These data suggest a conventional antigenic stimulation with T-cells bearing the TCRBV5S2 chain and a superantigenic stimulation with T-cells bearing the TCRBV8 chain may occur in the acute stage of measles infection.

Antibodies, Monoclonal↗