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Biomedical subjects

C S Kim

Publications and source records attributed to C S Kim.

At least 145 records · Page 8Linked to original sources
PubMed1998

A relapsed case of imported tertian malaria after a standard course of hydroxychloroquine and primaquine therapy.

Resistance of Plasmodium species to antimalarial agents has become increasingly challenging to the management and prevention of malaria. We experienced an imported case of tertian malaria due to Plasmodium vivax relapsed after a seemingly successful treatment with conventional course of hydroxychloroquine and primaquine. A 35-year-old man developed fever three days after return from India and mainland China. After his illness was diagnosed as tertian malaria, he was managed with hydroxychloroquine and then primaquine (primaquine base 15 mg/day for 14 days). Thereafter peripheral blood smears showed no malarial parasites, and there was no relapse of symptom until the 55th post-treatment day, however, six months after the above treatment tertian malaria relapsed. He was managed with the same medications again and malaria did not relapse for 10 months.

Adult↗
PubMed1998

Detection of soluble Fas mRNA using in situ reverse transcription-polymerase chain reaction.

Fas protein (Fas) is known to induce cell death by apoptosis in susceptible cells. Alternative splicing of the Fas gene produces soluble Fas protein (sFas), which is considered to block the function of Fas. The serum level of sFas is elevated in patients with various malignancies in a manner reflective of disease stage and tumor burden, but the precise cellular origin of sFas in vivo has not yet been clarified. To identify the cells that synthesize sFas mRNA on histologic specimens, we applied in situ reverse transcription-polymerase chain reaction (in situ RT-PCR) in 11 cases of gastric adenocarcinoma/metastatic lymph node. Furthermore, we studied the distribution of Fas using immunohistochemistry and Fas mRNA using in situ RT-PCR. In all primary tumors and 10 of 11 metastatic tumors, tumor cells expressed both Fas- and sFas mRNA. Lymphocytes infiltrated in the tumor tissues and the lymph nodes also revealed both mRNA signals. A clear correlation between the tissue distribution for Fas and its mRNA was also observed. These observations demonstrated that solid tumors in vivo can synthesize sFas mRNA and suggest that tumor cells are responsible in part for elevated sFas in human malignancies. However, the additional expression of sFas mRNA in tissue lymphocytes indicates the complex regulatory mechanisms of Fas-mediated apoptosis pathway in tumor pathogenesis and host defense. We also demonstrated that in situ RT-PCR can be a suitable method for in situ detection of alternatively spliced mRNA.

Alternative Splicing↗
PubMed1998

Platelet endothelial cell adhesion molecule-1 expression modulates endothelial cell migration in vitro.

Endothelial cell migration is an important process that occurs during embryonic vasculogenesis and angiogenesis, wound healing, and tumor growth and metastasis, and after denudation injury following angioplasty and bypass grafting. Mechanisms regulating this process involve a complex interplay of cytoskeletal reorganization, cell-cell adhesion, and cell-extracellular matrix interactions. Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is constitutively expressed in endothelial cells, leukocytes, monocytes, lymphocytes, and platelets. PECAM-1 undergoes dynamic dephosphorylation during endothelial cell migration in vitro and during vasculogenesis in the murine conceptus. In transfected 3T3 cells, in cultured endothelial cells, and in the murine conceptus undergoing vasculogenesis, the tyrosine phosphorylation state of PECAM-1 Y686 correlates with the migratory state of the cells. In the present study, we investigate the role of PECAM-1 in modulating endothelial cell migration in vitro using retroviral transduction of c-myc epitope-tagged, wild-type, Y686 to F-mutated PECAM-1 and extracellular domain-deleted PECAM-1 constructs in endothelial cells devoid of endogenous PECAM-1 (ECV304 cells) and in endothelial cells expressing high levels of endogenous PECAM-1 (bovine aortic endothelial cells, BAEC). In ECV304 cells, the expression of wild-type PECAM-1 inhibited migration rates, whereas in BAEC, overexpression of wild-type PECAM-1 had no effect. Expression of Y686 to F-mutated PECAM-1 or extracellular domain-deleted PECAM-1 in BAEC increased migration rates. These data support the concept that endothelial cell migration is modulated, in part, by a balance between PECAM-1 cytoplasmic domain-mediated "inside-out" and "outside-out" signaling resulting from PECAM-1-mediated cell-cell interactions and integrin-extracellular matrix interactions.

Animals↗
PubMed1998

CDK4 down-regulation induced by paclitaxel is associated with G1 arrest in gastric cancer cells.

Paclitaxel induces a cell cycle block at G2-M phase by preventing the depolymerization of microtubules and induces p53-independent apoptosis in many cancer cells. We observed that gastric cancer cells treated with paclitaxel have shown a cyclin-dependent kinase (CDK)4 down-regulation. This paclitaxel-induced CDK4 down-regulation resulted in a cell cycle arrest at G1-S phase. To confirm this observation, we prepared stable transfectants that overexpressed CDK4 and analyzed the cell cycle progression. Ectopic expression of CDK4 in SNU cells resulted in a release of paclitaxel-induced G1 arrest. The release of G1 arrest by enforced expression of CDK4 seems to make the cells more sensitive to paclitaxel-induced apoptosis. From this finding, we could then suggest that paclitaxel treatment induces both G1-S and G2-M blocks in the cell cycle progression of gastric cancer cells.

Antineoplastic Agents, Phytogenic↗
PubMed1997

Panhandle polymerase chain reaction amplifies MLL genomic translocation breakpoint involving unknown partner gene.

We used a new approach called panhandle polymerase chain reaction (PCR) to clone an MLL genomic translocation breakpoint in a case of acute lymphoblastic leukemia of infancy in which karyotype analysis was technically unsuccessful and did not show the translocation partner. Panhandle PCR amplified known MLL sequence 5' of the breakpoint and 3' sequence from the unknown partner gene from a DNA template with an intrastrand loop schematically shaped like a pan with a handle. The 7-kb panhandle PCR product contained the translocation breakpoint in MLL intron 8. The partner DNA included unique nonrepetitive sequences, Alu and mammalian apparent LTR-retrotransposon (MaLR) repetitive sequences, and a region of homology to expressed sequence tags. MaLR sequences have not been found before near leukemia-associated translocation breakpoints. The nonrepetitive sequences were not homologous to known partner genes of MLL. Screening of somatic cell hybrid and radiation hybrid lines by PCR and fluorescence in situ hybridization analysis of normal metaphase chromosomes mapped the partner DNA to chromosome band 4q21. Reverse transcriptase-PCR identified an MLL-AF-4 chimeric mRNA, indicating that panhandle PCR identified a fusion of MLL with a previously uncharacterized AF-4 intronic sequence. Panhandle PCR facilitates cloning translocation breakpoints and identifying unknown partner genes.

Base Sequence↗
PubMed1997

Depressed Langerhans cell migration and reduced contact hypersensitivity response in mice lacking TNF receptor p75.

Epidermal Langerhans cells (LC) belong to the dendritic cell family and represent the major APC within the skin. LC capture epicutaneous Ag, migrate into regional lymph nodes, and present Ag to T cells, thereby initiating primary immune response. The migratory properties of LC are an essential component of their function. The molecular mechanisms responsible for LC migration are far less defined. However, evidence has been accumulating to suggest that TNF-alpha, a major proinflammatory cytokine, plays an important role in promoting DC migration. To confirm the role of TNF-alpha in LC migration and to examine which type of TNF receptor signaling is involved in such an event, we utilized gene-targeted knockout mice lacking TNF receptor p55 or p75. The migration of LC was assessed by examining the frequency of hapten-bearing cells in draining lymph nodes following hapten FITC painting, and the accumulation of dendritic cells in draining lymph nodes after intradermal injection of TNF-alpha. While LC migration was normal in p55-deficient mice, the migration was markedly depressed in p75-deficient mice. Receptor p75-deficient mice also demonstrated a hyporesponsiveness in allergen-induced contact dermatitis, but a normal responsiveness in irritant-induced contact dermatitis. These results suggest that p75-dependent signaling plays a crucial role in the migration of LC and in the initiation of cutaneous immune responses.

Administration, Cutaneous↗
PubMed1997

An alternative pathway for expression of p56lck from type I promoter transcripts in colon carcinoma.

The lymphoid-specific protein tyrosine kinase, p56lck which is essential for both T cell development and function, is aberrantly expressed in colon and small lung carcinoma lines. In this paper, we demonstrate p56lck is also expressed in colon tumour biopsies due predominantly or exclusively to the use of the lck type I promoter. In T leukaemia lines, the lck type I promoter requires binding sites for both Ets- and Myb-related transcription factors. In contrast, in colon tumour lines the activation of the lck type I promoter requires the Ets but not the Myb binding site. In these lines, a consensus binding site for HMG-related transcription factors, AACAAAG, is required for efficient lck type I promoter activity. Sox-4 is a candidate transcription factor for binding and activating the lck type l promoter in colon carcinoma cells. Co-expression of Ets-1 and Sox-4, but neither protein alone, was sufficient to activate the lck type l promoter in HeLa cells which do not normally express lck transcripts. These results suggest that aberrant expression of p56lck from the lck type l promoter in colon carcinoma arises from transcriptional activation mediated by Ets- and HMG-related transcription factors.

Alternative Splicing↗
PubMed1997

Panhandle PCR strategy to amplify MLL genomic breakpoints in treatment-related leukemias.

Panhandle PCR amplifies genomic DNA with known 5' and unknown 3' sequences from a template with an intrastrand loop schematically shaped like a pan with a handle. We used panhandle PCR to clone MLL genomic breakpoints in two pediatric treatment-related leukemias. The karyotype in a case of treatment-related acute lymphoblastic leukemia showed the t(4;11)(q21;q23). Panhandle PCR amplified the translocation breakpoint at position 2158 in intron 6 in the 5' MLL breakpoint cluster region (bcr). The karyotype in a case of treatment-related acute myeloid leukemia was normal, but Southern blot analysis showed a single MLL gene rearrangement. Panhandle PCR amplified the breakpoint at position 1493 in MLL intron 6. Screening of somatic cell hybrid and radiation hybrid DNAs by PCR and reverse transcriptase-PCR analysis of the leukemic cells indicated that panhandle PCR identified a fusion of MLL intron 6 with a previously uncharacterized sequence in MLL intron 1, consistent with a partial duplication. In both cases, the breakpoints in the MLL bcr were in Alu repeats, and there were Alu repeats in proximity to the breakpoints in the partner DNAs, suggesting that Alu sequences were relevant to these rearrangements. This study shows that panhandle PCR is an effective method for cloning MLL genomic breakpoints in treatment-related leukemias. Analysis of additional pediatric cases will determine whether breakpoint distribution deviates from the predilection for 3' distribution in the bcr that has been found in adult cases.

Adult↗
PubMed1997

Genetic alterations of p16INK4a and p53 genes in sporadic dysplastic nevus.

It is still unclear whether the sporadic form of dysplastic nevi (SDN) represents a premalignant lesion of malignant melanoma and whether genetic alterations are involved in the development of SDN. To determine whether p16INK4a and p53 genetic abnormalities could be associated with development of SDN, nevus cell nests were procured selectively from H & E-stained slide sections by using a modified microdissection technique and were screened for the presence of mutations and loss of heterozygosity (LOH) of p16INK4a and p53 genes using a polymerase chain reaction-based LOH, single-strand conformation polymorphism, and direct DNA sequencing analyses. Hemizygous deletion was detected in 9 of 12 informative cases (75%) for 9p21-22 (p16INK4a) at one or more loci and 60% (6/10) for 17p13 (p53). As for mutation, we found 3 missense mutations and 1 mutation in the first intron in p16INK4a and 2 missense mutations in p53. Among these mutations in p16INK4a and p53, 5 of 6 mutations were of the C:G to T:A transitional type; this is known to be related to ultraviolet radiation as previously confirmed in other skin cancers. This indicates that p16INK4a and p53 genetic alterations may play an important role in the evolution of SDN and may represent an early event in the development of malignant melanoma. Furthermore, ultraviolet radiation might be the predominant etiologic agent in the development of SDN.

Amino Acid Sequence↗
PubMed1997

Increase in levels of total free fatty acids in rat brain regions following 3-nitropropionic acid administration.

Acute exposure to a neurotoxin, 3-nitropropionic acid (3-NPA), in rats results in an increase in total free fatty acid (FFA) concentration in selective brain regions. We investigated the effect of 3-NPA administration on the cerebral concentrations of FFA used as a marker of oxidative stress. Rats (n = 3/group) were dosed subcutaneously (s.c.) either with a vehicle (phosphate buffer) or 3-NPA in phosphate buffer at 30 mg/kg body weight. Animals were sacrificed after 1, 2, 3, and 6 h of injection. Brains were then dissected into frontal cortex (FC), caudate nucleus (CN), and hippocampus (HIP). The concentration of total FFA increased from 130 to 300% within 1-2 h after 3-NPA injection in all brain regions when compared with the baseline level obtained from the control rats and taken as 100%. In CN, FFA returned to the baseline level within 3 h of treatment. However, in FC and HIP the concentration of FFA remained significantly elevated above the baseline until 6 h. The released FFA provide a substrate for free radicals formation. The results of this study suggest a role of oxidative stress in the mechanism of 3-NPA toxicity.

Animals↗
PubMed1997

A simple and rapid method for isolation of high quality genomic DNA from fruit trees and conifers using PVP.

Because DNA degradation is mediated by secondary plant products such as phenolic terpenoids, the isolation of high quality DNA from plants containing a high content of polyphenolics has been a difficult problem. We demonstrate an easy extraction process by modifying several existing ones. Using this process we have found it possible to isolate DNAs from four fruit trees, grape (Vitis spp.), apple (Malus spp.), pear (Pyrus spp.) and persimmon (Diospyros spp.) and four species of conifer, Pinus densiflora, Pinus koraiensis,Taxus cuspidata and Juniperus chinensis within a few hours. Compared with the existing method, we have isolated high quality intact DNAs (260/280 = 1.8-2.0) routinely yielding 250-500 ng/microl (total 7.5-15 microg DNA from four to five tissue discs).

DNA, Plant↗
PubMed1997

Creating auxotrophic mutants in Methylophilus methylotrophus AS1 by combining electroporation and chemical mutagenesis.

Stable auxotrophic mutants of the methylotroph Methylophilus methylotrophus AS1 were obtained by a novel mutagenesis technique in which electroporation is used to transport the chemical mutagen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) across the cell membrane. By combining chemical mutagenesis with electroporation and screening single colonies for auxotrophy in 36 different amino acids and growth factors, 3 auxotrophs per 156 colonies screened were obtained, whereas no auxotrophs were found with chemical mutagenesis alone. MNNG mutagen toxicity was also increased in the methylotroph with this novel mutagenesis technique (death rate 96% compared to 79%). This technique did not increase the mutation rate for strain Escherichia coli BK6 which responds well to simple exposure to the mutagen.

Amino Acids↗
PubMed1997

Variations in preferred living arrangements among Korean elderly parents.

Guided by the assumption that the preferences for a particular type of living arrangement are influenced by values of privacy and the level of needs/resources among the elderly, this study investigates how the socioeconomic and demographic characteristics of the Korean elderly are associated with their preferences for independent living over coresidence with their children. A logit model analysis is conducted based on data from the 1994 Survey on the Living Status of Korean Elderly. The major findings are: (1) contrary to common belief, the rural elderly are more likely to prefer independent living than the urban elderly, (2) provided that elderly parents have financial resources, those in poor health are more likely than those in fair health to prefer separate residence from their children, and (3) the absence of a son increases the likelihood of preferring independent living over coresidence. The implications of these findings for current Korean policy promoting coresidence and for studies of living arrangements of the elderly are discussed.

Journal Article↗
PubMed1997

Induction of the differentiation of HL-60 promyelocytic leukemia cells by vitamin E and other antioxidants in combination with low levels of vitamin D3: possible relationship to NF-kappaB.

Epidemiological studies have provided evidence that diets rich in antioxidant nutrients may reduce the risk of cancer. To evaluate the possibility that dietary phytochemicals with antioxidant potential would create an environment capable of affecting the differentiation of HL-60 leukemia cells, we measured the effects of vitamin E and other dietary antioxidants on the differentiation produced by low levels of vitamin D3 and analogs thereof. Vitamin E succinate and other antioxidant compounds (ie butylated hydroxyanisole, beta-carotene and lipoic acid) used alone had no significant effect on the differentiation of HL-60 cells; however, these agents markedly increased the differentiation produced by vitamin D3. Previous studies from this laboratory have shown that a sequence-specific antisense phosphorothioate oligonucleotide to the Rel A subunit of NF-kappaB enhanced the differentiation of HL-60 cells produced by several inducing agents. Consistent with these observations, vitamin E succinate caused a marked reduction in the nuclear content of NF-kappaB both in the presence and absence of vitamin D3. These findings suggest that NF-kappaB may be a factor in regulating the differentiation of myeloid leukemia cells. The results also indicate that combinations of vitamin D3 and analogs thereof with dietary antioxidants may be useful in overcoming the differentiation block present in acute promyelocytic leukemia cells.

Antioxidants↗
PubMed1997

Combining the hok/sok, parDE, and pnd postsegregational killer loci to enhance plasmid stability.

To enhance plasmid segregational stability in bacterial cells, two pairs of independent postsegregational killing loci (genes which induce host killing upon plasmid loss) isolated from plasmids R1, R483, or RP4 (hok+/sok+ pnd+ or hok+/sok+ parDE+) were cloned into a common site of the beta-galactosidase expression vector pMJR1750 (ptac::lacZ+) to form a series of plasmids in which the effect of one or two stability loci on segregational plasmid stability could be discerned. Adding two antisense killer loci (hok+/sok+ pnd+) decreased the specific growth rate by 50% though they were more effective at reducing segregational instability than hok+/sok+ alone. With the ptac promoter induced fully (2.0 mM isopropyl-beta-D-thiogalactopyranoside) and no antibiotic selection pressure, the combination of a proteic killer locus (parDE+) with antisense killer loci (hok+/sok+) had a negligible impact on specific growth rate, maintained high beta-galactosidase expression, and led to a 30 and 190% increase in segregational stability (based on stable generations) as compared to plasmids containing either hok+/sok+ or parDE+ alone, respectively. Use of hok+/sok+ or parDE+ alone with high cloned-gene expression led to ninefold and fourfold increases in the number of stable generations, respectively. Two convenient cloning cassettes have been constructed to facilitate cloning the dual hok+/sok+ parDE+ and hok+/sok+ pnd+ killer systems.

Antisense Elements (Genetics)↗
PubMed1997

Renal angiomyolipoma: selective arterial embolization--effectiveness and changes in angiomyogenic components in long-term follow-up.

PURPOSE: To evaluate the efficacy of selective arterial embolization in symptomatic renal angiomyolipoma (AML) and the change in angiomyogenic components during long-term follow-up after embolization. MATERIALS AND METHODS: Fourteen adult patients with symptomatic AMLs underwent 16 selective arterial embolizations. The embolic materials used were absolute alcohol with (n = 5) or without (n = 3) iodized oil, Gianturco coils (n = 4), and polyvinyl alcohol foam powder with gelatin sponge (n = 2). Follow-up ultrasonography and computed tomography (CT) were performed in six and 14 patients, respectively. The effectiveness of selective arterial embolization was evaluated on the basis of the area of the angiomyogenic components in the AML on initial and follow-up images and clinical improvement. RESULTS: All patients showed devascularization of the tumor on the postembolization angiograms. In 13 patients, clinical symptoms disappeared. The follow-up period was 7-72 months (mean, 33 months). One patient underwent nephrectomy at 7 months after embolization because of a large cystic lesion found at 1 month. In long-term CT follow-up (> or =12 months) in 12 patients, nearly all angiomyogenic components disappeared, but fatty components partially shrank with liquefactive necrosis in tumors. CONCLUSION: Selective arterial embolization is an effective and safe treatment of AML. The angiomyomatous components crucial for the prevention of bleeding were very sensitive to the embolization.

Adult↗