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K T Kim

Publications and source records attributed to K T Kim.

At least 19 recordsLinked to original sources
PubMed2004

A preclinical cadaver fitting study of implantable biventricular assist device-- AnyHeart.

A multifunctional, Korean-made artificial heart (AnyHeart) was developed, and prior to its clinical application, a cadaver-fitting study was performed. The study proposed to determine the optimal cannulation approach, implantation technique and route of the cannula to minimize the organ compression of AnyHeart. The anatomical feasibility and a variety of surgical techniques were evaluated using ten preserved, human cadavers. Implanting AnyHeart with ease is possible using various approaches, including a median sternotomy, and a right or left lateral thoracotomy. The lateral thoracotomy approach is shown to be safe and reproducible, especially in patients who have already undergone an operation that used a median sternotomy. The results of this study will guide improvements in the designs of cannulae and AnyHeart for future clinical applications.

Adolescent↗
PubMed2003

Endothelial nitric oxide synthase gene polymorphisms in Behçet's disease and rheumatic diseases with vasculitis.

OBJECTIVE: To assess potential associations between Korean Behçet's disease (BD) or other rheumatic diseases with vasculitis and two polymorphisms of the endothelial nitric oxide synthase (eNOS) gene, which include the Glu298Asp polymorphism in exon 7 and a variable number of tandem repeats (VNTR) polymorphism in intron 4. METHODS: 65 patients with BD, 27 with rheumatic diseases with vasculitis, and 80 controls were studied. Analyses of the Glu298Asp polymorphism in exon 7 and VNTR polymorphism in intron 4 of the eNOS gene were made by the polymerase chain reaction (PCR)-restriction fragment length polymorphism technique and PCR genotyping, respectively. Additionally, HLA-B51 typing was performed in the BD group and controls by a two step PCR sequence-specific primers method. RESULTS: Significant differences in Glu298Asp genotype frequencies were found between the BD or vasculitis groups and the controls (BD group v controls: p(corr)=0.006; vasculitis group v controls: p<0.001). The Asp298 frequency was much higher in the BD and vasculitis groups than in the controls. Even after stratification of the BD group based on the results of HLA-B51 testing, a significant association of the Glu298Asp polymorphism was still found (p=0.002, Mantel-Haenszel weighted odds ratio 4.3, 95% confidence interval 1.7 to 10.9). Distribution of the genotype frequencies in two eNOS gene polymorphisms was similar in connective tissue diseases-associated vasculitis and primary vasculitic syndromes. In contrast, distribution of alleles and genotypes of VNTR polymorphism did not differ between BD or vasculitis groups and the controls. CONCLUSION: The Glu298Asp polymorphism in exon 7 of the eNOS gene seems to be a susceptibility gene for Korean BD and other rheumatic diseases.

Adult↗
PubMed2001

Blocking of acidosis-mediated apoptosis by a reduction of lactate dehydrogenase activity through antisense mRNA expression.

Lactic acid produced from the cells is a potential cause of extra- and intracellular acidification. Due to scarce technical tools, lactic acid that leads to acidification could not be reduced and direct evidence of the relationship between metabolic lactate and apoptosis has not yet been elucidated. In this study, we designed a cellular pH regulation system in CHO cells by a reduction of lactate dehydrogenase (LDH) activity through LDH antisense mRNA expression. This inhibited lactate production and, therefore, acidification of the cytosol. Under HCO3(-)-buffered growth conditions, both the parent CHO cells and the engineered CHO cells maintained their extracellular pH and intracellular pH fairly well. However, upon acidification of the cytosol, only the parent CHO cells underwent apoptosis under HCO3(-)-free conditions. In fact, we observed a number of apoptosis-related events only in control cells, including mitochondrial dysfunction, cytochrome c release, and an increase in caspase-3 enzymatic activity.

Acidosis, Lactic↗
PubMed2001

Inhibition of H2 histamine receptor-mediated cation channel opening by protein kinase C in human promyelocytic cells.

Histamine, through H(2) receptors, triggers a prominent rise in intracellular free Ca(2+) concentration ([Ca(2+)](i)) in addition to an elevation of cAMP level in HL-60 promyelocytes. Here we show that the histamine-induced [Ca(2+)](i) rise was due to influx of Ca(2+) from the extracellular space, probably through nonselective cation channels, as incubation of the cells with SKF 96365 abolished the histamine-induced [Ca(2+)](i) rise, Na(+) influx, and membrane depolarization. The Ca(2+) influx was specifically inhibited by pretreatment of the cells with PMA or extracellular ATP with 50% inhibitory concentrations of 0.12 +/- 0.03 nM and 185 +/- 17 microM, respectively. Western blot analysis of protein kinase C (PKC) isoforms revealed that PMA (< or =1 nM) and ATP (300 microM) caused selective translocation of PKC-delta to the particulate/membrane fraction. Costimulation of the cells with histamine and SKF 96365 partially reduced histamine-induced granulocytic differentiation, which was evaluated by looking at the extent of fMet-Leu-Phe-induced [Ca(2+)](i) rise and superoxide generation. In conclusion, nonselective cation channels are opened by stimulation of the H(2) receptor, and the channels are at least in part involved in the induction of histamine-mediated differentiation processes. Both effects of histamine were selectively inhibited probably by the delta isoform of PKC in HL-60 cells.

Adenosine Triphosphate↗
PubMed2001

P2X7 nucleotide receptor mediation of membrane pore formation and superoxide generation in human promyelocytes and neutrophils.

The P2X(7) receptor, which induces cation channel opening imparting significant permeability to Ca2+ and pore formation with changes in the plasma membrane potential, has been known to be rather restrictedly expressed in cells of the macrophage lineage including dendrites, mature macrophages, and microglial cells. However, we show here that the P2X(7) receptor is also expressed in cells of granulocytic lineage such as HL-60 promyelocytes, granulocytic differentiated cells, and neutrophils. Exposure of these cells to 2',3'-O-(4-benzoyl)benzoyl-ATP (BzATP) triggered intracellular Ca2+ rise through the mediation of phospholipase C-independent and suramin-sensitive pathways. BzATP also induced depolarization of the plasma membrane in the absence of extracellular Ca2+, whereas it hyperpolarized the cells in the presence of external Ca2+, probably in part through the activation of Ca2+-activated K(+) channels. However, the hyperpolarization phenomenon was markedly attenuated in differentiated HL-60 cells and neutrophils. RT-PCR and Northern blot analysis revealed the presence of P2X(7) receptors on both HL-60 and neutrophil-like cells. This was further confirmed by pore formation through which the uptake of Lucifer yellow and YO-PRO1 occurred on BzATP treatment. BzATP stimulated in a concentration-dependent manner the production of superoxide in differentiated HL-60 cells via a pathway partially dependent on extracellular Ca2+. Moreover, in human neutrophils, BzATP was a more effective inducer of superoxide generation than PMA. Taken together, this is a first demonstration of the expression of P2X(7) receptors on neutrophils, which shows that the receptor is functionally involved in the defense mechanism by activation of the respiratory burst pathway.

Adenosine Triphosphate↗
PubMed2001

Noncompetitive inhibition by camphor of nicotinic acetylcholine receptors.

The effect of camphor, a monoterpenoid, on catecholamine secretion was investigated in bovine adrenal chromaffin cells. Camphor inhibited [3H]norepinephrine ([3H]NE) secretion induced by a nicotinic acetylcholine receptor (nAChR) agonist, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), with a half-maximal inhibitory concentration (IC50) of 70 +/- 12 microM. In addition, camphor inhibited the rise in cytosolic calcium ([Ca2+]i) and sodium ([Na+]i) induced by DMPP with IC50 values of 88 +/- 32 and 19 +/- 2 microM, respectively, suggesting that the activity of nAChRs is also inhibited by camphor. On the other hand, binding of [3H]nicotine to nAChRs was not affected by camphor. [Ca2+]i increases induced by high K+, veratridine, and bradykinin were not affected by camphor. The data suggest that camphor specifically inhibits catecholamine secretion by blocking nAChRs without affecting agonist binding.

Animals↗
PubMed2001

Regulation of macrophage migration inhibitory factor and thiol-specific antioxidant protein PAG by direct interaction.

Macrophage migration inhibitory factor (MIF) is an important mediator that plays a central role in the control of the host immune and inflammatory response. To investigate the molecular mechanism of MIF action, we have used the yeast two-hybrid system and identified PAG, a thiol-specific antioxidant protein, as an interacting partner of MIF. Association of MIF with PAG was found in 293T cells transiently expressing MIF and PAG. The use of PAG mutants (C52S, C71S, and C173S) revealed that this association was significantly affected by C173S, but not C52S and C71S, indicating that a disulfide involving Cys(173) of PAG is responsible for the formation of MIF-PAG complex. In addition, the interaction was highly dependent on the reducing conditions such as dithiothreitol or beta-mercaptoethanol but not in the presence of H2O2. Analysis of the activities of the interacting proteins showed that the D-dopachrome tautomerase activity of MIF was decreased in a dose-dependent manner by coexpression of wild-type PAG, C52S, and C71S, whereas C173S was almost ineffective, suggesting that the direct interaction may be involved in the control of D-dopachrome tautomerase activity of MIF. Moreover, MIF has been shown to bind to PAG and it also inhibits the antioxidant activity of PAG.

Cell Line↗
PubMed2001

Fine-needle aspiration cytology of pleuropulmonary blastoma: a case report with unusual features.

Pleuropulmonary blastoma (PPB) is a rare and aggressive intrathoracic neoplasm of childhood, typically presenting as a pulmonary and/or pleural-based mass with cystic, solid, or combined features. Histologically, the tumor is well characterized with a mixture of primitive mesenchymal and variably differentiated sarcomatous components, and the cytologic features described in the three previous reports are also compatible to the histologic ones. Now, we present another case of PPB showing unusual features. A 3-yr-old boy presented with a pleural- or chest wall-based tumor. The fine-needle aspiration cytologic smears were highly cellular with poorly differentiated cells showing variable size and shape rather than those of typical blastemal cells. The histologic findings were also distinctive, exhibiting diffuse sheets of poorly differentiated cells without typical blastemal cell component. Diagnosis was confirmed by the support of immunohistochemical and ultrastructural features. The patient underwent a typical aggressive clinical course to death within 8 mo after diagnosis.

Biomarkers, Tumor↗
PubMed2001

Sonographic evaluation of gallbladder-wall thickening in hemorrhagic fever with renal syndrome: prediction of disease severity.

PURPOSE: Gallbladder-wall thickening (GBWT) frequently occurs in patients with hemorrhagic fever with renal syndrome (HFRS), an acute infectious disease caused by hantaviruses. HFRS is manifested by fever, hemorrhage, renal failure, and in many cases gastrointestinal symptoms, such as abdominal pain and tenderness. The clinical significance of GBWT in HFRS has not been reported. The purpose of this study was to investigate the incidence of GBWT and the relationship between GBWT and the severity of HFRS. METHODS: We retrospectively reviewed the medical records and sonograms of 68 patients with HFRS (47 males and 21 females, with an age range of 10-76 years) who underwent abdominal sonography in the acute stage of the disease. We measured the gallbladder-wall thickness on the sonograms and reviewed other sonographic and radiographic findings. Clinical factors that reflect the severity of HFRS were compared between the patients with GBWT (defined as thickness of 4 mm or more) and those without GBWT. RESULTS: Of the 68 patients, 29 (43%) had GBWT, which was even and diffuse in all cases. The patients with GBWT had a significantly lower mean platelet count and serum albumin level and significantly higher serum aspartate aminotransferase and serum lactate dehydrogenase levels than did the patients without GBWT. In addition, the incidence of renal failure requiring hemodialysis and the incidences of ascites and pleural effusion were higher in the patients with GBWT than in those without GBWT. Five patients died of HFRS; all 5 had GBWT (p = 0.011 for comparison with patients without GBWT). CONCLUSIONS: Our results suggest that the sonographic measurement of gallbladder-wall thickness during the acute stage of HFRS is useful for determining the severity of HFRS.

Adolescent↗
PubMed2001

Ten-year survival of patients with locally advanced, stage ib-iib cervical cancer after neoadjuvant chemotherapy and radical hysterectomy.

OBJECTIVE(S): The aim of this study was to evaluate the effects of neoadjuvant chemotherapy and radical hysterectomy on long-term survival in stage IB-IIB locally advanced cervical cancer by conducting a 10-year follow-up. METHODS: Between August 1983 and May 1990, 80 locally advanced, stage IB-IIB cervical cancer patients with tumor diameter greater than or equal to 4 cm were treated with neoadjuvant VBP chemotherapy (cisplatin, vinblastine, and bleomycin) followed by radical hysterectomy with pelvic lymphadenectomy. After this therapeutic modality, patients were followed for more than 10 years. Ten-year survival rates and factors affecting recurrence after this therapy were evaluated. RESULTS: Of 80 patients, 75 (93.7%) showed a reduction in tumor size after neoadjuvant chemotherapy. At pathologic examination, stage reduction was noted in 53 (66.2%) patients and 20 patients (25%) showed no residual or microinvasive cervical tumor. Pelvic lymph node metastases were found in 17 patients (21.3%). During the 10-year follow up, 2 patients were lost and 16 patients recurred. Overall 5-year and 10-year disease-free actual survival rates were 82.0 (64/78) and 79.4% (62/78), respectively. Clinical stage, initial tumor size, clinical response, and residual tumor size were not risk factors for recurrence after this therapy. However, pelvic lymph node metastasis was a significant risk factor for recurrence. CONCLUSION(S): Neoadjuvant VBP chemotherapy followed by radical hysterectomy in locally advanced, stage IB-IIB cervical cancer patients seemed to improve the long-term survival rate for these patients compared to that of conventional therapy. However, randomized controlled trials are needed to confirm this result.

Adenocarcinoma↗
PubMed2001

A simple and secure technique for tracheal T-tube insertion.

We describe a simple and secure technique for the insertion of a long Montgomery type T-tube in patients with tracheal stenosis. An endotracheal tube is placed into the lumen of the T-tube and by maintaining the airway during insertion, the technique has been found to be safe and it can prevent the kind of tracheal damage occurring with blind techniques.

Humans↗
PubMed2001

Chlorpromazine inhibits store-operated calcium entry and subsequent noradrenaline secretion in PC12 cells.

1. The effect of chlorpromazine on the store-operated Ca2+ entry activated via the phospholipase C signalling pathway was investigated in PC12 cells. 2. Chlorpromazine inhibited the sustained increase after the initial peak in the intracellular Ca2+ concentration produced by bradykinin while having no effect on the initial transient response. The inhibition was lowered by the removal of extracellular free Ca2+. However, chlorpromazine did not inhibit bradykinin-induced inositol 1,4,5-trisphosphate production. 3. Chlorpromazine inhibited the bradykinin-induced noradrenaline secretion in a concentration-dependent manner (IC(50): 24+/-5 microM, n=3). 4. To test for a direct effect of chlorpromazine on store-operated Ca2+ entry, thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, was used to induce store-operated Ca2+ entry in PC12 cells. Chlorpromazine reduced the thapsigargin-induced sustained Ca2+ level (IC(50): 24+/-2 microM, n=3), and the inhibition also occluded the inhibitory action of 1-[-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenyl]-1H-imidazole hydrochloride (SK&F96365). 5. The results suggest that chlorpromazine negatively modulates the store-operated Ca2+ entry activated subsequent to PLC activation.

Algorithms↗
PubMed2001

Pharmacological characterization of adenosine receptors in PGT-beta mouse pineal gland tumour cells.

1. The adenosine receptor in mouse pinealocytes was identified and characterized using pharmacological and physiological approaches. 2. Expression of the two adenosine receptor subtypes A2B and A3 was detected in mouse pineal glands and PGT-beta cells by polymerase chain reaction and nucleotide sequencing. 3. Adenosine and 5'-N-ethylcarboxamidoadenosine (NECA) evoked cyclic AMP generation but the A2)-selective agonist 2-(4-(2-carboxyethyl)phenylethylamino)adenosine-5'-N-ethylcarboxamideadenosine (CGS 21680) and the A1-specific agonists R-N(6)-(2-phenylisopropyl)adenosine (R-PIA) and N(6)-cyclopentyladenosine (CPA) had little effect on intracellular cyclic AMP levels. The A2B receptor selective antagonists alloxazine and enprofylline completely blocked NECA-mediated cyclic AMP accumulation. 4. Treatment of cells with the A3-selective agonist N(6)-(3-iodobenzyl)-5'-(N-methylcarbamoyl)adenosine (IB-MECA) inhibited the elevation of the cyclic AMP level induced by NECA or isoproterenol in a concentration-dependent manner with maximal inhibition of 40 - 50%. These responses were blocked by the specific A3 adenosine receptor antagonist MRS 1191. Pretreatment of the cells with pertussis toxin attenuated the IB-MECA-induced responses, suggesting that this effect occurred via the pertussis toxin-sensitive inhibitory G proteins. 5. IB-MECA also caused a concentration-dependent elevation in [Ca(2+)]i and IP3 content. Both the responses induced by IB-MECA were attenuated by treatment with U73122 or phorbol 12-myristate 13-acetate. 6. These data suggest the presence of both A2B and A3 adenosine receptors in mouse pineal tumour cells and that the A2B receptor is positively coupled to adenylyl cyclase whereas the A3 receptor is negatively coupled to adenylyl cyclase and also coupled to phospholipase C.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2001

Selective inhibition of beta(2)-adrenergic receptor-mediated cAMP generation by activation of the P2Y(2) receptor in mouse pineal gland tumor cells.

Rhythmic noradrenergic signaling from the hypothalamic clock in the suprachiasmatic nucleus to the pineal gland causes an increase in intracellular cAMP which regulates the circadian fluctuation of melatonin synthesis. The activation of phospholipase C (PLC)-coupled P2Y(2) receptors upon treatment with ATP and UTP exclusively inhibited the isoproterenol-stimulated cAMP production in mouse pineal gland tumor cells. However, the activation of other PLC-coupled receptors including P2Y(1) and bombesin receptors had little or no effect on the isoproterenol-stimulated cAMP production. Also, ATP did not inhibit cAMP production caused by forskolin, prostaglandin E(2), or the adenosine analog NECA. These results suggest a selective coupling between signalings of P2Y(2) and beta(2)-adrenergic receptors. The binding of [(3)H]CGP12177 to beta(2)-adrenergic receptors was not effected by the presence of ATP or UTP. Ionomycin decreased the isoproterenol-stimulated cAMP production, whereas phorbol 12-myristate 13-acetate slightly potentiated the isoproterenol response. Chelation of intracellular Ca(2+), however, had little effect on the ATP-induced inhibition of cAMP production, while it completely reversed the ionomycin-induced inhibition. Treatment of cells with pertussis toxin almost completely blocked the inhibitory effect of nucleotides. Pertussis toxin also inhibited the nucleotide-induced increase in intracellular Ca(2+) and inositol 1,4,5-trisphosphate production by 30-40%, suggesting that the ATP-mediated inhibition of the cAMP generation and the partial activation of PLC are mediated by pertussis toxin-sensitive G(i)-protein. We conclude that one of the functions of P2Y(2) receptors on the pineal gland is the selective inhibition of beta-adrenergic receptor-mediated signaling pathways via the inhibitory G-proteins.

1-Methyl-3-isobutylxanthine↗
PubMed2001

Potentiation of PGE(2)-mediated cAMP production during neuronal differentiation of human neuroblastoma SK-N-BE(2)C cells.

The prostaglandin-evoked cAMP production was studied in human neuroblastoma SK-N-BE(2)C cells during neuronal differentiation induced by all-trans retinoic acid. The incubation with 5 microM all-trans retinoic acid for 4-6 days promoted neurite outgrowth of cells. After differentiation, prostaglandin E(2) (PGE(2))-induced cAMP production was dramatically increased, whereas forskolin- and AlF-induced cAMP productions were not changed. The increase reached maximum after 4-days of incubation with all-trans retinoic acid. The differentiation caused an increase in the maximal response and a decrease in the half-maximal effective concentration of the PGE(2)-induced cAMP production. In addition, the binding of [(3)H]PGE(2) to membrane receptors was enhanced in differentiated cells. However, the order of potency of the various prostaglandins (PGE(1) = PGE(2) > PGD(2) = PGF(2alpha) = PGI(2)) in cAMP production did not change during the differentiation, suggesting that mainly E-prostanoid (EP) receptors were involved. Butaprost, an EP(2) receptor specific agonist, increased the cAMP level in a concentration dependent manner and had a similar potentiating effect on cAMP production as PGE(2) upon differentiation. Northern blot analysis using the human cDNA probes shows that the EP(2) mRNA level was about seven times higher in differentiated cells, while the dopamine beta-hydroxylase (DBH) mRNA completely disappeared. Our results, thus, suggest that elevated gene expression of the prostanoid EP(2) receptor results in an increase in the PGE(2)-evoked cAMP production in SK-N-BE(2)C cells during neuronal differentiation.

Alprostadil↗
PubMed2001

Low-dose levalbuterol in children with asthma: safety and efficacy in comparison with placebo and racemic albuterol.

BACKGROUND: Racemic albuterol (RAC) is an equal mixture of (R)-albuterol and (S)-albuterol. Only the (R)-isomer, levalbuterol (LEV), is therapeutically active. Lower doses of LEV, devoid of (S)-albuterol, have demonstrated efficacy comparable to that of higher doses of the (R)-isomer administered as a component of RAC. OBJECTIVE: The purpose of this study was to determine whether LEV results in improved safety and efficacy in children. METHODS: Asthmatic children aged 4 to 11 years (n = 338; FEV(1), 40% to 85% of predicted) participated in this multicenter, randomized, double-blinded study and received 21 days of 3-times-a-day treatment with nebulized LEV (0.31 or 0.63 mg), RAC (1.25 or 2.5 mg), or placebo. The primary endpoint was FEV(1) (peak percent change). Adverse events, clinical laboratory test results, vital signs, and electrocardiograms were evaluated for safety. RESULTS: All active treatments significantly improved the primary endpoint in comparison with placebo (P < .001). Significant differences in FEV(1) were noted immediately after nebulization (median change, 2.0%, 19.0%, 18.1%, 12.4%, and 15.6% for placebo, LEV 0.31 and 0.63, RAC 1.25 and 2.5 mg, respectively; P < .05 vs placebo; P < .05 for LEV 0.31 and 0.63 vs RAC 1.25 mg). LEV 0.31 mg was the only treatment not different from placebo for changes in ventricular heart rate, QT(c) interval, and glucose (P > .05). All active treatments decreased serum potassium (range, -0.3 to -0.6; P < .002 vs placebo), and RAC 2.5 mg caused the greatest change (P < .005 vs other actives). In a patient subset with severe asthma, a dose-response relationship was observed for levalbuterol, indicating that higher doses were more effective. CONCLUSION: LEV was clinically comparable to 4- to 8-fold higher doses of RAC, and it demonstrated a more favorable safety profile. LEV 0.31 mg should be used as the starting dose in 4-11 year old children with mild to moderate persistent asthma. Patients with severe disease might benefit from higher doses.

Adrenergic beta-Agonists↗
PubMed2001

Effects of polychlorinated biphenyl 19 (2,2',6-trichlorobiphenyl) on contraction, Ca2+ transient, and Ca2+ current of cardiac myocytes.

Polychlorinated biphenyls (PCBs) have been known as serious environmental pollutants, causing developmental delays, motor dysfunction, and decrease in brain dopamine level in humans and animals. We have investigated the effects of a PCB congener, 2,2',6-trichlorobiphenyl (PCB 19) on contractile force, Ca2+ transient, and L-type Ca2+ current (I(Ca,L)) in guinea pig ventricular myocytes stimulated at a rate of 0.25-0.33 Hz. PCB 19 decreased contractile force in a concentration-dependent manner. During the negative inotropic response, the action potential duration at 20% (APD20), 90% of repolarization (APD90), and the action potential amplitude (APA) were decreased concentration dependently: 30 microM PCB 19 reduced APD20, APD90 and APA by 36.7 +/- 3.5%, 22.6 +/- 3.9%, and 2.4 +/- 0.6%, respectively (n = 11, p < 0.01). PCB 19 30 microM decreased the Ca2+ transient and the I(Ca,L) by 46.8 +/- 1.8% (n = 9, p < 0.01) and 47.1 +/- 3.1% (n = 9, p < 0.01), respectively. The results suggest that PCB 19 decreased the Ca2+ transient through inhibition of L-type Ca2+ channels and that the decreased Ca2+ transient consequently caused a negative inotropic effect in cardiac myocytes.

Animals↗