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Jae-Woo Kim

Publications and source records attributed to Jae-Woo Kim.

17 recordsLinked to original sources
PubMed2006

Electrochemistry of conductive polymers 38. Electrodeposited poly(3,4-ethylenedioxy-thiophene) studied by current sensing atomic force microscopy.

Electrical and morphological properties of poly(3,4-ethylenedioxythiophene) (PEDOT) thin films electrodeposited on gold-on-silicon electrodes by galvanostatic, potentiostatic, and potentiodynamic methods have been determined using current sensing atomic force microscopic experiments. Surface morphologies and vertical conductivities of PEDOT films were affected by the experimental parameters including the preparation method, the current density, the potential, and the potentiodynamic cyclic number. Band gaps obtained from current-voltage curves of dedoped PEDOT were in excellent agreement with those obtained from absorption spectra. When the film thickness was increased on the gold-on-silicon electrode, the topographic images were not very well defined due to the high roughness but conductivities increased significantly in all the galvanostatically, potetiostatically, and potentiodynamically grown PEDOT films.

Journal Article↗
PubMed2006

Electron exchange between Fe(II)-horse spleen ferritin and Co(III)/Mn(III) reconstituted horse spleen and Azotobacter vinelandii ferritins.

Azotobacter vinelandii bacterioferritin (AvBF) containing 800-1500 Co or Mn atoms as Co(III) and Mn(III) oxyhydroxide cores (Co-AvBF, Mn-AvBF) was synthesized by the same procedure used previously for horse spleen ferritin (HoSF). The kinetics of reduction of Co-AvBF and Mn-AvBF by ascorbic acid are first-order in each reactant. The rate constant for the reduction of Mn-AvBF (8.52 M(-1) min(-1)) is approximately 12 times larger than that for Co-AvBF (0.72 M(-1) min(-1)), which is consistent with a previous observation that Mn-HoSF is reduced approximately 10-fold faster than Co-HoSF [Zhang, B. et al. (2005) Inorg. Chem. 44, 3738-3745]. The rates of reduction of M-AvBF (M = Co and Mn) are more than twice that for the reduction of the corresponding M-HoSF. HoSF containing reduced Fe(II) cores (Fe(II)-HoSF), prepared by methyl viologen and CO, also reduces M-HoSF and M-AvBF species, with both cores remaining within ferritin, suggesting that electrons transfer through the ferritin shell. Electron transfer from Fe(II)-HoSF to Co-AvBF occurs at a rate approximately 3 times faster than that to Co-HoSF, indicating that the Co cores in AvBF are more accessible to reduction than the Co cores in HoSF. The presence of nonconductive (SiO2) or conductive (gold) surfaces known to bind ferritins enhances the rate of electron transfer. A more than approximately 4-fold increase in the apparent reaction rate is observed in the presence of gold. Although both surfaces (SiO2 and gold) enhance reaction by providing binding sites for molecular interaction, results show that ferritins with different mineral cores bound to a gold surface transfer electrons through the gold substrate so that direct contact of the reacting molecules is not required.

Animals↗
PubMed2006

Characterization of beta-ketoadipate pathway from multi-drug resistance bacterium, Acinetobacter baumannii DU202 by proteomic approach.

In this study, the biodegradative activities of monocyclic aromatic compounds were determined from the multi-drug resistant (MDR) Acinetobacter baumannii, which were studied in the form of clinical isolates from a hospital in Korea. These bacteria were capable of biodegrading monocyclic aromatic compounds, such as benzoate and p-hydroxybenzoate. In order to determine which pathways are available for biodegradation in these stains, we conducted proteome analyses of benzoate and p-hydroxybenzoate-cultured A. baumannii DU202, using 2-DE/MS analysis. As genome DB of A. baumannii was not yet available, MS/MS analysis or de novo sequencing methods were employed in the identification of induced proteins. Benzoate branch enzymes [catechol 1,2-dioxygenase (CatA) and benzoate dioxygenase alpha subunit (BenA)] of the beta-ketoadipate pathway were identified under benzoate culture condition and p-hydroxybenzoate branch enzymes [protocatechuate 3,4-dioxygenase alpha subunit (PcaG) and 3-carboxy-cis,cis-muconate cycloisomerase (PcaB)] of the beta-ketoadipate pathway were identified under p-hydroxybenzoate culture condition, respectively, thereby suggesting that strain DU202 utilized the beta-ketoadipate pathway for the biodegradation of monocyclic aromatic compounds. The sequence analysis of two purified dioxygenases (CatA and PcaGH) indicated that CatA is closely associated with the CatA of Acinetobacter radiresistance, but PcaGH is only moderately associated with the PcaGH of Acinetobacter sp. ADP1. Interestingly, the fused form of PcaD and PcaC, carboxymuconolactone decarboxylase (PcaCD), was detected on benzoate-cultured A. baumannii DU202. These results indicate that A. baumannii DU202 exploits a different beta-ketoadipate pathway from other Acinetobacter species.

Acinetobacter baumannii↗
PubMed2005

Sequential phosphorylation of CCAAT enhancer-binding protein beta by MAPK and glycogen synthase kinase 3beta is required for adipogenesis.

CCAAT enhancer-binding protein (C/EBP)beta, C/EBPalpha, and peroxisome proliferator activated receptor (PPAR)gamma act in a cascade where C/EBPbeta activates expression of C/EBPalpha and PPARgamma, which then function as pleiotropic activators of genes that produce the adipocyte phenotype. When growth-arrested 3T3-L1 preadipocytes are induced to differentiate, C/EBPbeta is rapidly expressed but still lacks DNA-binding activity. After a long (14-hour) lag, glycogen synthase kinase 3beta enters the nucleus, which correlates with hyperphosphorylation of C/EBPbeta and acquisition of DNA-binding activity. Concurrently, 3T3-L1 preadipocytes synchronously enter S phase and undergo mitotic clonal expansion, a prerequisite for terminal differentiation. Ex vivo and in vitro experiments with C/EBPbeta show that phosphorylation of Thr-188 by mitogen-activating protein kinase "primes" C/EBPbeta for subsequent phosphorylation on Ser-184 and Thr-179 by glycogen synthase kinase 3beta, acquisition of DNA-binding function, and transactivation of the C/EBPalpha and PPARgamma genes. The delayed transactivation of the C/EBPalpha and PPARgamma genes by C/EBPbeta appears necessary to allow mitotic clonal expansion, which would otherwise be prevented, because C/EBPalpha and PPARgamma are antimitotic.

3T3-L1 Cells↗
PubMed2005

Kinetic and thermodynamic characterization of the cobalt and manganese oxyhydroxide cores formed in horse spleen ferritin.

Horse spleen ferritin (HoSF) containing 800-1500 cobalt or 250-1200 manganese atoms as Co(O)OH and Mn(O)OH mineral cores within the HoSF interior (Co-HoSF and Mn-HoSF) was synthesized, and the chemical reactivity, kinetics of reduction, and the reduction potentials were measured. Microcoulometric and chemical reduction of HoSF containing the M(O)OH mineral core (M = Co or Mn) was rapid and quantitative with a reduction stoichiometry of 1.05 +/- 0.10 e/M forming a stable M(OH)(2) mineral core. At pH 9.0, ascorbic acid (AH(2)), a two-electron reductant, effectively reduced the mineral cores; however, the reaction was incomplete and rapidly reached equilibrium. The addition of excess AH(2) shifted the reaction to completion with a M(3+)/AH(2) stoichiometry of 1.9-2.1, consistent with a single electron per metal atom reduction. The rate of reaction between M(O)OH and excess AH(2) was measured by monitoring the decrease in mineral core absorbance with time. The reaction was first order in each reactant with second-order rate constants of 0.53 and 4.74 M(-1) min(-1), respectively, for Co- and Mn-HoSF at pH 9.0. From the variation of absorbance with increasing AH(2) concentration, equilibrium constants at pH 9.0 of 5.0 +/- 1.9 for Co-HoSF and 2.9 +/- 0.9 for Mn-HoSF were calculated for 2M(O)OH + AH(2) = 2M(OH)(2) + D, where AH(2) and D are ascorbic acid and dehydroascorbic acid, respectively. Consistent with these equilibrium constants, the standard potential for the reduction of Co(III)-HoSF is 42 mV more positive than that of the ascorbic acid reaction, while the standard potential of Mn(III)-HoSF is 27 mV positive relative to AH(2). Fe(2+) in solution with Co- and Mn-HoSF under anaerobic conditions was oxidized to form Fe(O)OH within the HoSF interior, resulting in partial displacement of the Co or Mn by iron.

Animals↗
PubMed2005

Identification and characterization of peroxisome proliferator response element in the mouse GLUT2 promoter.

In the present study, we show that the expression of type 2 glucose transporter isoform (GLUT2) could be regulated by PPAR-gamma in the liver. Rosiglitazone, PPAR-gamma agonist, activated the GLUT2 mRNA level in the primary cultured hepatocytes and Alexander cells, when these cells were transfected with PPAR-gamma/RXR-alpha. We have localized the peroxisome proliferator response element in the mouse GLUT2 promoter by serial deletion studies and site-directed mutagenesis. Chromatin immunoprecipitation assay using ob/ob mice also showed that PPAR-gamma rather than PPAR-alpha binds to the -197/-184 region of GLUT2 promoter. Taken together, liver GLUT2 may be a direct target of PPAR-gamma ligand contributing to glucose transport into liver in a condition when PAPR-gamma expression is increased as in type 2 diabetes or in severe obesity.

Animals↗
PubMed2005

Glucose-stimulated upregulation of GLUT2 gene is mediated by sterol response element-binding protein-1c in the hepatocytes.

GLUT2 is mainly expressed in the liver, beta-cells of the pancreas, and the basolateral membrane of kidney proximal tubules and plays an important role in glucose homeostasis in living organisms. The transcription of the GLUT2 gene is known to be upregulated in the liver during postprandial hyperglycemic states or in type 2 diabetes. However, a molecular mechanism by which glucose activates GLUT2 gene expression is not known. In this study, we report evidence that sterol response element-binding protein (SREBP)-1c plays a key role in glucose-stimulated GLUT2 gene expression. The GLUT2 promoter reporter is activated by SREBP-1c, and the activation is inhibited by a dominant-negative form of SREBP-1c (SREBP-1c DN). Adenoviral expression of SREBP-1c DN suppressed glucose-stimulated GLUT2 mRNA level in primary hepatocytes. An electrophoretic mobility shift assay and mutational analysis of the GLUT2 promoter revealed that SREBP-1c binds to the -84/-76 region of the GLUT2 promoter. Chromatin immunoprecipitation revealed that the binding of SREBP-1c to the -84/-76 region was increased by glucose concentration in a dose-dependent manner. These results indicate that SREBP-1c mediates glucose-stimulated GLUT2 gene expression in hepatocytes.

Animals↗
PubMed2004

Effects of organic additives on zinc electrodeposition at iron electrodes studied by EQCM and in situ STM.

Effects of organic additives, such as benzoic acid (BA) and poly(ethylene glycol)s (PEGs), on the initial stage of the zinc electrodeposition have been investigated at iron electrodes using cyclic voltammetry, electrochemical quartz crystal microbalance measurements and in situ electrochemical scanning tunneling microscopy in an acidic zinc chloride solution in efforts to gain a molecular-level understanding of their roles. BA is adsorbed strongly at the sites of more negative potentials on the electrode, although it is randomly adsorbed on the iron surface at around an open circuit potential. Its role seems to control the deposition rate at the dendritic sites by blocking the active surface via adsorption. On the contrary, PEGs are adsorbed more or less evenly with a well-ordered structure on the iron surface and appear to desorb in the underpotential deposition region of zinc ions, which helps inhibit proton reduction by effectively blocking the electrode surface.

Journal Article↗
PubMed2004

DNA marker mining of ILSTS035 microsatellite locus on chromosome 6 of Hanwoo cattle.

We describe tests for detecting and locating quantitative trait loci (QTL) for traits in Hanwoo cattle. From results of a permutation test to detect QTL for marbling, we selected the microsatellite locus ILSTS035 on chromosome 6 for further analysis. K-means clustering analysis applied to five traits and nine DNA markers in ILSTS035 resulted in three cluster groups. Finally we employed the bootstrap test method to calculate confidence intervals using the resampling method to find major DNA markers. We conclude that the major markers of ILSTS035 locus on chromosome 6 of Hanwoo cattle are markers 235 bp and 266 bp.

Animals↗
PubMed2004

CDNA array analysis of gene expression profiles in brain of mice exposed to manganese.

This study is performed to detect changes of gene expression in substantia nigra (SN) and striatum in manganese (Mn)-exposed mice brain. The cDNA array is a recently developed molecular biological method that can detect the differential expression of several hundreds of genes simultaneously and is therefore advantageous in the study of trace metal intoxication effect at the genetic level. Using this technology, we discovered 5 genes in the mouse striatum and 9 genes in SN changed by more than 50% following Mn exposure. Depression were observed in two genes (neural cell adhesion protein BIG2, heavy neurofilament subunit genes) in striatum and three genes (light neurofilament subunit, brain acyl-CoA synthetase II, heavy neurofilament subunit genes) in the SN. However three genes (N-acetylglucosaminyltransferase I, S100beta, and synaptonemal complex protein I genes) in striatum and six genes (noggin, striatin, Ost oncogene, S100beta, calcium/calmodulin-dependent protein kinase kinase beta, and N-acetylglucosaminyltransferase I genes) in SN were elevated following Mn exposure. Immunohistochemical study revealed that protein levels of S100beta also increased following Mn treatment. Activated astrocytes overexpressing S100beta are invariably and intimately associated with decreased expression of heavy and light neurofilament subunits which is a distinguishing feature of neurodegeneration by Mn exposure. All our findings suggested that neuronal degenerations occur in SN as well as striatum of mice exposed to Mn.

Animals↗
PubMed2004

Occupations and Parkinson's disease: a case-control study in South Korea.

We performed a hospital based case-control study in the southeast region of Korea to clarify the role of occupational exposure, especially manganese (Mn), in the etiology of Parkinson's disease (PD) and to discover the association between any occupation and PD. 105 outpatients with PD and 129 neurological disease controls and 101 healthy controls were interviewed. We employed occupational and industrial categories as defined by Section (the most broad category) and Division (sub-category) of the Korea Standard Industry Code and the Korea Standard Classification of Occupations. There was not a significant association between exposure to hazardous materials, especially Mn and PD. There were not any occupations listed under the Section of Industry Classification as a significant risk factor or protective factor for PD. However, the 'clerk' occupation [Section] was positively associated with PD. There is a decreased risk for PD with a subject ever having worked in the 'agriculture, forestry and fishery' occupational group. Ever having worked in 'sales' also was negatively associated with PD. There were not any Divisions of Industry found as a significant risk factor or protective factor for PD. However, ever having worked in an 'agriculture' Division of Occupation was negatively associated with PD.

Case-Control Studies↗
PubMed2003

Acetyl-CoA carboxylase beta gene is regulated by sterol regulatory element-binding protein-1 in liver.

Acetyl-CoA carboxylase (ACC) exists as two major isoforms originated from separate genes: ACCalpha (or ACC1) and ACCbeta (or ACC2). Previous data revealed that ACCbeta has two forms of mRNA with different 5'-untranslated regions derived by different usage of promoters, I and II, in human. In this study, we revealed that ACCbeta expression in liver is markedly stimulated by food intake at the transcriptional level. In the process of this induction in rat liver, promoter II plays the major role in regulating the expression of ACCbeta gene. The transient transfection with promoter II-luciferase reporters elucidated that the region from -93 to -38 nucleotides is important for the responsiveness to sterol regulatory element-binding protein-1 (SREBP-1), which is known to be the principle mediator for the stimulation of gene transcriptions by insulin and diet. The Sp1-binding site (-71 to -66) and neighboring two conserved SREs (-62 to -44) play a critical role in the stimulation of ACCbeta gene expression by SREBP-1. In vivo chromatin immunoprecipitation assay revealed that SREBP-1 directly bound to ACCbeta promoter II in liver, and its binding was regulated by the diet. This study provides evidence that ACCbeta expression in liver is regulated at the transcriptional level by the direct interaction of SREBP-1 with promoter II.

Acetyl-CoA Carboxylase↗
PubMed2003

Effect of manganese exposure on MPTP neurotoxicities.

We used a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice model to evaluate whether manganese (Mn) exposure can affect MPTP-induced neurotoxicity. We randomly assigned adult male C57BL/6 mice (n=5-7 per group) the following treatments: SO, Mn(-) x MPTP(-); MO, Mn(+) x MPTP(-); SM, Mn(-) x MPTP(+); MM, Mn(+) x MPTP(+). Mn (MnCl(2).4H(2)O) was administered intraperitoneally at a dose of 2 mg/kg daily for 3 weeks. MPTP was then administered intraperitoneally at a dose of 30 mg/kg daily for 5 days in the SM and MM groups. Seven days after the last MPTP injection, the animals were sacrificed. Blood Mn levels were elevated in the Mn-exposed groups. Striatal Mn levels were not influenced by Mn treatment alone, however, they were decreased following MPTP. Tyrosine hydroxylase (TH)-immunoreactive (ir) neurons in the substantia nigra pars compacta (SNpc) were decreased significantly in the MPTP-exposed groups. Densities of TH- and dopamine transporter (DAT)-ir axon terminals in the caudate-putamen (CPU) were also decreased in the MPTP-treated groups. Furthermore, glial fibrillary acidic protein (GFAP)-ir astrocytes increased in the CPU with MPTP treatment. However, no effects were observed with Mn exposure. Concentrations of dopamine (DA), 3,4-dihydrophenyl acetic acid (DOPAC) and homovanillic acid (HVA) in the corpus striatum were also decreased significantly with MPTP treatment alone, but Mn had no effect. Thus, decreased dopaminergic activities with MPTP led to decreased DA and its metabolites. Significant hypertrophies of GFAP-ir astrocytes in the globus pallidus (GP) were observed in Mn-exposed groups, especially in the MM group. MPTP targeted dopaminergic systems whereas Mn neurotoxicities occurred in the GP. In conclusion, our data suggest that Mn does not potentiate the neurotoxicity of MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2003

A multicenter randomized crossover multiple-dose comparison study of arotinolol and propranolol in essential tremor.

BACKGROUND: A new medication is needed to treat essential tremor. Preliminary evidence suggests that arotinolol may be effective in the treatment of this disorder. OBJECTIVE: To study the effect of arotinolol and propranolol in a crossover, multiple dose comparative trial of patients with essential tremor. PATIENTS AND METHODS: One hundred and seventy-five outpatients, with essential tremor were included in the study; 161 patients completed the study. Patients were identically evaluated at eight consecutive visits. The study consisted of two treatments, which were arranged according to a crossover design that evaluated the dose of each (arotinolol 10 mg per day and propranolol 40 mg per day, arotinolol 20 mg per day and propranolol 80 mg per day, arotinolol 30 mg per day and propranolol 160 mg per day). Each course of treatment lasted 6 weeks. Major outcome evaluations consisted of a self-reported disability scale, and motor performance score obtained before drug intake and 14 days after each treatment. The treatment effects were evaluated by analysis of variance using the Hills-Armitage test. RESULTS: Arotinolol was found to be as effective as propranolol at reducing tremor. Drug effects as evaluated using motor-task performance scores revealed that arotinolol had a more significant effect than propranolol. CONCLUSIONS: Arotinolol may be more useful than propranolol for the treatment of essential tremor.

Adrenergic beta-Antagonists↗
PubMed2002

C/EBP binding activity to site F of the rat GLUT2 glucose transporter gene promoter is attenuated by c-Jun in vitro.

The expression of the GLUT2 glucose transporter gene in liver is suppressed in cultured hepatoma cell lines and primary cultured hepatocytes. Earlier report showed that CCAAT/enhancer binding protein (C/EBP) regulates the promoter activity of the rat GLUT2 glucose transporter gene in liver cells. C/EBPalpha and C/EBPbeta activated the promoter activity by binding to at least two regions of the promoter and one of the C/EBP binding sites, named as site F, also has the AP-1 binding consensus. In this study, we investigated whether the AP-1 can influence on C/EBP binding to this site. The addition of recombinant c-Jun protein with liver extract caused the attenuation of C/EBP binding to site F with the appearance of a new shifted band. The shifted band was competed out with the addition of unlabeled AP-1 consensus oligonucleotide, indicating that c-Jun also can bind to site F. Another C/EBP site on GLUT2 promoter, site H, did not bind AP-1. Analysis of the DNA-protein complex revealed that C/EBP and c-Jun bind to site F in mutually exclusive manner rather than form heterodimeric complex with each other. From these results, it is suggested that the transcriptional activation of C/EBP may be influenced by c-Jun protein in certain status of the liver cells, such as acute phase response, as well as hepatocarcinogenesis.

Animals↗
PubMed2002

Analysis of polymorphism of the GLUT2 promoter in NIDDM patients and its functional consequence to the promoter activity.

Glucose transporter type 2 (GLUT2), along with glucokinase, has been implicated to participate in glucose-induced insulin secretion in pancreatic beta-cells. Recently, several sequence variations in the promoter of GLUT2 have been identified in patients with non-insulin dependent diabetes mellitus (NIDDM), but the functional effects of these polymorphisms on promoter activity have not previously been studied. We compared the incidence of sequence variations in the GLUT2 promoter in 100 normal subjects and 100 NIDDM patients. Sequencing of the promoter region (-294 to +301) revealed that an A --> G variant at position -44 was found in 45 of 100 NIDDM patients, but only in 23 of 100 normal subjects. In addition, -269 A --> C and + 103 A --> G mutations were identified in a single diabetic patient. Electrophoretic mobility shift assays using double-stranded oligonucleotide containing -44A as a probe showed a clearly shifted band of DNA-protein. To examine whether the sequence variation at position -44 affects the promoter activity, we carried out in vitro transfection experiments. Site-specific mutagenesis at position -44 region from A to C, T, or G resulted in reductions of CAT activity by 52.3%, 63.8%, and 63.6%, respectively. The -269 A --> C and + 103 A --> G mutations also decreased the promoter activity. These results suggest that polymorphisms at positions -269, -44, or + 103 may affect GLUT2 gene transcription, possibly associated with reduced expression of the GLUT2 gene in NIDDM patients.

Cell Line↗