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W Y Kim

Publications and source records attributed to W Y Kim.

At least 55 records · Page 3Linked to original sources
PubMed2000

Motion correction for the quantification of mitral regurgitation using the control volume method.

Quantifying mitral regurgitation is difficult because of the complexity of the flow, geometry and motion of the mitral valve. In this paper a MRI compatible phantom was built incorporating a left ventricle and mitral valve motion. Valve motion was obtained using a pneumatic piston. The mitral valve was made regurgitant and the regurgitant volume quantified using a modified control volume method. The modification to the method was the addition of mitral motion correction. This was attained by moving the control volume in unison with the mitral valve and by correcting for this motion in the integration of velocity. This correction was found to be simple, in that it represented the volume swept out by the moving control surface. The measured regurgitant volume was compared to a second MR measurement using a single slice technique, made possible by the tubular construction of the phantom's left atrium. Regression analysis between these two methods produced a regression line of y = 0 + 1.02 x; R = 0.97; standard error of the estimate = 3.47 ml.

Blood Flow Velocity↗
PubMed2000

Unbiased and efficient estimation of left ventricular volumes by three-dimensional echocardiography with coaxial sections. Validation with magnetic resonance imaging.

The objective of this study was to investigate the degree of bias with coaxial three-dimensional echocardiography in an experimental animal setup and to establish the minimum number of sections needed for estimation of left ventricular (LV) volume. Epicardial coaxial echocardiography and magnetic resonance imaging (MRI) was used to measure LV volume in 14 pigs, with chronic remodeled left ventricles induced by repeated intracoronary microembolizations. In addition, six animals underwent serial MRI at baseline, immediately after intracoronary microembolization, and after 119-165 days (mean 129 days). Coaxial echocardiography was performed by rotational acquisition of long-axis sections starting from an arbitrary angle. Planimetered MRI contours of LV endocardial borders were analyzed to investigate the relationship between the number of coaxial sections, and the precision of volume estimates. The mean +/- 2SD of the differences between coaxial epicardial echocardiography with six sections and MRI were -2.5 +/- 16.4 ml, 0.8 +/- 13.1 ml, and 2% +/- 14% for end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF), respectively. Numerical analysis conducted on MRI contours of LV endocardial borders showed that with six coaxial sections the average coefficient of error was < 1% for the EDV and ESV. Three-dimensional echocardiography with six coaxial sections provides unbiased LV volume estimation with minimal geometric error.

Algorithms↗
PubMed2000

Operational characteristics of an antibody-immobilized QCM system detecting Salmonella spp.

A quartz crystal microbalance (QCM) system detecting Salmonella spp. was developed by an anti-Salmonella antibody immobilization onto one gold surface of a piezoelectric quartz crystal surface with sulfosuccinimidyl 6-[3-(2-pyridyldithio)propionamido]hexanoate (sulfo-LC-SPDP) thiolation. The optimum temperature and pH for the antibody-immobilized sensor were 35 degrees C and 7.2, respectively. The frequency shifts obtained were correlated with the Salmonella concentrations in the range 3.2 x 10(6)-4.8 x 10(8) CFU per ml. The system was quite specific to Salmonella spp. and applicable for repetitive use after a regeneration step employing 1.2 M NaOH. A model sample measurement was done for a market milk spiked with Salmonella typhimurium.

Animals↗
PubMed2000

Steaming of ginseng at high temperature enhances biological activity.

The present study was performed to evaluate the effect of steaming ginseng at a temperature over 100 degrees C on its chemical constituents and biological activities. Raw ginseng was steamed at 100, 110, and 120 degrees C for 2 h using an autoclave. The ginseng steamed at 120 degrees C was more potent in its ability to induce endothelium-dependent relaxation. Steaming the raw ginseng at 120 degrees C also remarkably increased the radical-scavenging activity. Ginsenosides F(4), Rg(3), and Rg(5), which were not present in raw ginseng, were produced after steaming. Ginsenosides Rg(3) and Rg(5) were the most abundant ginsenosides in the ginseng steamed at 120 degrees C, accounting for 39% and 19% of all ginsenosides, respectively.

Chromatography, High Pressure Liquid↗
PubMed1999

Interaction and functional cooperation of PEBP2/CBF with Smads. Synergistic induction of the immunoglobulin germline Calpha promoter.

Smads are signal transducers for members of the transforming growth factor-beta (TGF-beta) superfamily. Upon ligand stimulation, receptor-regulated Smads (R-Smads) are phosphorylated by serine/threonine kinase receptors, form complexes with common-partner Smad, and translocate into the nucleus, where they regulate the transcription of target genes together with other transcription factors. Polyomavirus enhancer binding protein 2/core binding factor (PEBP2/CBF) is a transcription factor complex composed of alpha and beta subunits. The alpha subunits of PEBP2/CBF, which contain the highly conserved Runt domain, play essential roles in hematopoiesis and osteogenesis. Here we show that three mammalian alpha subunits of PEBP2/CBF form complexes with R-Smads that act in TGF-beta/activin pathways as well as those acting in bone morphogenetic protein (BMP) pathways. Among them, PEBP2alphaC/CBFA3/AML2 forms a complex with Smad3 and stimulates transcription of the germline Ig Calpha promoter in a cooperative manner, for which binding of both factors to their specific binding sites is essential. PEBP2 may thus be a nuclear target of TGF-beta/BMP signaling.

Activin Receptors, Type I↗
PubMed1999

Synergy of PEBP2/CBF with mi transcription factor (MITF) for transactivation of mouse mast cell protease 6 gene.

The mi locus encodes a member of the basic - helix - loop - helix - leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF). Although the bHLH-Zip family transcription factors generally recognize and bind CANNTG motifs, the expression of mouse mast cell protease 6 (MMCP-6) gene is regulated by MITF through the GACCTG motif in the promoter region. The GACCTG motif was partly overlapped the TGTGGTC sequence, which was bound by polyomavirus enhancer binding protein 2 (PEBP2). In the present study, the effect of PEBP2 on the expression of MMCP-6 gene was examined. PEBP2 that is composed of alpha and beta subunits was expressed by mast cell lines and cultured mast cells derived from spleen. The overexpression of dominant negative PEBP2 cDNA reduced the expression of MMCP-6. Moreover, the simultaneous transfection of the plasmid containing MITF cDNA and the plasmid containing PEBP2 cDNA increased the MMCP-6 promoter activity. For the synergistic action of PEBP2 and MITF, the intact GACCTG and TGTGGTC motifs were prerequisite. The PEBP2alphaB1 mutant which lacked the region downstream from the Runt domain did not bind MITF and lost the synergistic function. These results indicated that PEBP2 and MITF synergistically transactivated the MMCP-6 gene and that the region downstream from the Runt domain of PEBP2alphaB1 was essential for the physical and functional interactions with MITF.

Animals↗
PubMed1999

Mutual activation of Ets-1 and AML1 DNA binding by direct interaction of their autoinhibitory domains.

The transcription factors Ets-1 and AML1 (the alphaBl subunit of PEBP2/CBF) play critical roles in hematopoiesis and leukemogenesis, and cooperate in the transactivation of the T cell receptor (TCR) beta chain enhancer. The DNA binding capacity of both factors is blocked intramolecularly but can be activated by the removal of negative regulatory domains. These include the exon VII domain for Ets-1 and the negative regulatory domain for DNA binding (NRDB) for alphaB1. Here we report that the direct interaction between the two factors leads to a reciprocal stimulation of their DNA binding activity and activation of their transactivation function. Detailed mapping revealed two independent contact points involving the exon VII and NRDB regions as well as the two DNA binding domains. Using deletion variants and dominant interfering mutants, we demonstrate that the interaction between exon VII and NRDB is necessary and sufficient for cooperative DNA binding. The exon VII and NRDB motifs are highly conserved in evolution yet deleted in natural variants, suggesting that the mechanism described is of biological relevance. The mutual activation of DNA binding of Ets and AML1 through the intermolecular interaction of autoinhibitory domains may represent a novel principle for the regulation of transcription factor function.

Amino Acid Sequence↗
PubMed1999

Characterization of two fungal-elicitor-induced rice cDNAs encoding functional homologues of the rab-specific GDP-dissociation inhibitor.

By using the mRNA differential display approach to isolate defense signaling genes active at the early stage of fungal infection two cDNA fragments with high sequence homology to rab-specific GDP-dissociation inhibitors (GDIs) were identified in rice (Oryza sativa L.) suspension cells. Using polymerase-chain-reaction products as probes, two full-length cDNA clones were isolated from a cDNA library of fungal-elicitor-treated rice, and designated as OsGDI1 and OsGDI2. The deduced amino acid sequences of the isolated cDNAs exhibited substantial homology to Arabidopsis rab-GDIs. Northern analysis revealed that transcripts detected with the 3'-gene-specific DNA probes accumulated to high levels within 30 min after treatment with a fungal elicitor derived from Magnaporthe grisea. The functionality of the OsGDIs was demonstrated by their ability to rescue the Sec19 mutant of Saccharomyces cerevisiae which is defective in vesicle transport. The proteins, expressed in Escherchia coli, cross-reacted with a polyclonal antibody prepared against bovine rab-GDI. Like bovine rab-GDI, the OsGDI proteins efficiently dissociated rab3A from bovine synaptic membranes. Using the two-hybrid system, it was shown that the OsGDIs specifically interact with the small GTP-binding proteins belonging to the rab subfamily. The specific interaction was also demonstrated in vitro by glutathione S-transferase resin pull-down assay.

Animals↗
PubMed1999

Molecular cloning, expression, and functional characterization of a 2Cys-peroxiredoxin in Chinese cabbage.

A cDNA (C2C-Prx) corresponding to a 2Cys-peroxiredoxin (2Cys-Prx) was isolated from a leaf cDNA library of Chinese cabbage. The predicted amino acid sequence of C2C-Prx has 2 conserved cysteines and several peptide domains present in most of the 2Cys-Prx subfamily members. It shows the highest sequence homology to the 2Cys-Prx enzymes of spinach (88%) and Arabidopsis (86%). Southern analysis using the cDNA insert of C2C-Prx revealed that it consists of a small multigene family in Chinese cabbage genome. RNA blot analysis showed that the gene was predominantly expressed in the leaf tissue of Chinese cabbage seedlings, but the mRNA was generally expressed in most tissues of mature plant, except roots. The expression of C2C-Prx was slightly induced by treatment with H2O2 (100 microM) or Fe3+/O2/DTT oxidation system, but not by ABA (50 microM) or GA3 (10 microM). The C2C-Prx is encoded as a preprotein of 273 amino acids containing a putative chloroplast-targeting signal of 65 amino acids at its N-terminus. The N-terminally truncated recombinant protein (deltaC2C-Prx) migrates as a dimer in a non-reducing SDS-polyacrylamide gel and as a monomer in a reducing condition. The deltaC2C-Prx shows no immuno cross-reactivity to antiserum of the yeast thiol-specific antioxidant protein, and vice versa. The deltaC2C-Prx prevents the inactivation of glutamine synthetase and the DNA cleavage in the metal-catalyzed oxidation system. In the yeast thioredoxin system containing thioredoxin reductase, thioredoxin, and NADPH, the deltaC2C-Prx exhibits peroxidase activity on H2O2.

Amino Acid Sequence↗
PubMed1999

Immunoglobulin motif DNA recognition and heterodimerization of the PEBP2/CBF Runt domain.

The polyomavirus enhancer binding protein 2 (PEBP2) or core binding factor (CBF) is a heterodimeric enhancer binding protein that is associated with genetic regulation of hematopoiesis and osteogenesis. Aberrant forms of PEBP2/CBF are implicated in the cause of the acute human leukemias and in a disorder of bone development known as cleidocranial dysplasia. The common denominator in the natural and mutant forms of this protein is a highly conserved domain of PEBP2/CBF alpha, termed the Runt domain (RD), which is responsible for both DNA binding and heterodimerization with the beta subunit of PEBP2/CBF. The three-dimensional structure of the RD bound to DNA has been determined to be an S-type immunoglobulin fold, establishing a structural relationship between the RD and the core DNA binding domains of NF-kappaB, NFAT1, p53 and the STAT proteins. NMR spectroscopy of a 43.6 kD RD-beta-DNA ternary complex identified the surface of the RD in contact with the beta subunit, suggesting a mechanism for the enhancement of RD DNA binding by beta. Analysis of leukemogenic mutants within the RD provides molecular insights into the role of this factor in leukemogenesis and cleidocranial dysplasia.

Cleidocranial Dysplasia↗
PubMed1999

Molecular insights into PEBP2/CBF beta-SMMHC associated acute leukemia revealed from the structure of PEBP2/CBF beta.

PEBP2/CBF is a heterodimeric transcription factor essential for genetic regulation of hematopoiesis and osteogenesis. DNA binding by PEBP2/CBF alpha is accomplished by a highly conserved DNA binding domain, the Runt domain (RD), whose structure adopts an S-type immunoglobulin fold when bound to DNA. The supplementary subunit beta enhances DNA binding by the RD in vitro, but its role in the control of gene expression has remained largely unknown in vivo. Chromosome 16 inversion creates a chimeric gene product fusing PEBP2/CBF beta to a portion of the smooth muscle myosin heavy chain (PEBP2/CBF beta-SMMHC) that is causally associated with the onset of acute myeloid leukemia in humans. The three-dimensional structure of PEBP2/CBF beta has been determined in solution and is shown to adopt a fold related to the beta-barrel oligomer binding motif. Direct analysis of a 43.6 kD ternary RD-beta-DNA complex identifies the likely surface of beta in contact with the RD. The structure of PEBP2/CBF beta enables a molecular understanding of the capacity of PEBP2/CBF beta-SMMHC to sequester PEBP2/CBF alpha in the cytoplasm and therefore provides a molecular basis for understanding leukemogenic transformation.

Binding Sites↗
PubMed1999

Functional remodelling and left ventricular dysfunction after repeated ischaemic episodes. A chronic experimental porcine model.

This experimental study was set up to investigate left ventricular function and remodelling after repeated ischaemic episodes using magnetic resonance imaging (MRI). A significant reduction in mortality due to coronary heart disease (CHD) has been explained by both a decline in the incidence of acute myocardial infarction (AMI) and an improved post-AMI survival rate, suggesting a change in the natural history of CHD. Experimental intracoronary microembolization can induce different ischaemic patterns and the functional impact of repeated ischaemic episodes different from occlusion of central epicardial arteries can be studied. In this study repeated intracoronary microembolizations were performed in 20 domestic pigs. After 129 d, MRI was performed for assessment of left ventricular volume, mass and wall stress. Six pigs underwent serial MRI at baseline, immediately after embolization and at the end of the observation period. Microembolizations induced acute myocardial infarct expansion and increased left ventricular wall stress preceding chronic remodelling. End systolic and end diastolic volumes increased from 15.1 +/- 2.7 cm3 to 41.3 +/- 11.5 cm 3 (p < 0.002), and from 52.0 +/- 6.7 cm3 to 81.1 +/- 9.2 cm3 (p < 0.0007), respectively. End systolic wall stress increased from and 17.5 +/- 2.7 to 29.7 +/- 6.2 N/m2 (p < 0.001). Left ventricular filling pressures and cardiac index were unchanged. Histological examination revealed a diffuse pattern of perivascular fibrosis covering 12 +/- 3% of the left ventricular wall. This study demonstrates that repeated ischaemic episodes different from confined regional myocardial infarctions induce acute infarct expansion and chronic left ventricular remodelling in pigs. Serial assessment of absolute left ventricular volumes and mass is important during acute/chronic remodelling.

Animals↗
PubMed1999

Development of velocity profiles and retrograde flow in the porcine abdominal aorta under different haemodynamic conditions.

Low and/or oscillating wall shear stresses are related to the development of atherosclerosis and this oscillation is influenced by changes in basic haemodynamics (exercise). The objective of this study was to provide in vivo data on the development of velocity profiles and oscillating blood velocities in the abdominal aorta under varying haemodynamic conditions. Six anaesthetized, 90-kg pigs were used in the study. Abdominal aortic velocity profiles across the anterior-posterior diameter were acquired at different axial positions using 10 MHz pulsed Doppler ultrasound. Measurements were obtained under normal conditions and during cardiac pacing up to 170 beats/min. Velocity profiles were obtained during heart rates ranging between 58 and 169 beats/min, and during flow rates ranging between 0.57 and 2.89 l/min. Main outcome measures included minimum velocities, frequency index, shape of velocity profiles (velocity distribution index), Reynolds' numbers, and Womersley's frequency parameter. Velocity profiles were blunted, with lowest velocities at the distal posterior vessel wall. Multiple regression analysis showed the development of velocity profiles to be inversely correlated with the pulsatility index, Womersley's frequency parameter and the mean Reynolds' number (r = 0.89, p < 0.0005). Minimum velocities were negatively correlated with the PI, Womersley's frequency parameter and positively with the mean Reynolds' number (r = 0.94, p < 10(-8)). Retrograde velocities (and hence oscillating wall shear stresses) were present at mean Reynolds' number < 1000. The oscillation of blood velocities at the wall in the porcine abdominal aorta was highly dependent on general haemodynamics (i.e. flow, heart rate and vessel diameter as expressed in the Reynolds' numbers and Womersley's frequency parameters). The velocity profiles in the abdominal aorta were found to be far from parabolic. These findings have important implications for the understanding and future modelling of the complex haemodynamics in the abdominal aorta and their relation to the development of atherosclerotic disease.

Animals↗
PubMed1999

Effect of pin location on stability of pelvic external fixation.

Pelvic external fixators allow two locations of pin purchase: anterosuperior (into the iliac crest) and anteroinferior (into the supraacetabular dense bone, between the anterior superior and anterior inferior iliac spine). The purpose of this study was to compare the stability of these two methods of fixation on Tile Type B1 (open book) and C (unstable) pelvic injuries. Five unembalmed cadaveric pelves (mean age, 68 years; four males and one female) were loaded vertically in a servohydraulic testing machine in a standing posture. The AO tubular system and Orthofix were used. On each pelvis, a Type B1 injury was simulated. Each external fixator was applied in each location in random order. Cyclic loads were applied through the sacral body to a maximum of approximately 200 N while force and displacement of the pelvic ring were recorded digitally. Sacroiliac joint motion was quantified tridimensionally with displacement transducers, mounted on the sacrum and contacting a target fixed to the posterior superior iliac spine. A Type C injury was created and augmented with two iliosacral lag screws, and the tests were repeated. For the Type B1 injuries with anteroinferior pin purchase, the mean stiffness was 201.2 N/mm for the AO frame and 203.2 N/mm for the Orthofix. For the anterosuperior frames the mean stiffness was 143.9 N/mm for the AO frame and 163.3 N/mm for the Orthofix. For Type B1 and Type C injuries, the anteroinferior location of pin purchase resulted in significantly reduced sacroiliac joint separation. There were no significant differences between the frame types. Dissection of the preinserted anatomic specimen revealed no evidence of injury to the lateral femoral cutaneous nerve after blunt dissection and drilling with protective drill sleeves. It is concluded that the anteroinferior location of external fixation pins is a safe technique with the potential for increased stability of fixation.

Acetabulum↗
PubMed1999

Developmental expression of aquaporin 1 in the rat renal vasculature.

Aquaporin 1 (AQP-1) is a water channel protein that is constitutively expressed in renal proximal tubule and descending thin limb cells as well as in endothelial cells of the descending vasa recta. Studies in the developing rat kidney have demonstrated that AQP-1 is expressed in renal tubules before birth. However, nothing is known about the expression of AQP-1 in the renal vasculature during kidney development. The purpose of this study was to establish the distribution of AQP-1 in the renal vasculature of the developing rat kidney and follow the differentiation of the vascular system during kidney development. Kidneys from 16-, 17-, 18-, and 20-day-old fetuses and 1-, 4-, 7-, 14-, 21-, and 28-day-old pups were preserved and processed for immunohistochemical studies using a preembedding immunoperoxidase procedure. AQP-1 immunoreactivity was detected using affinity-purified rabbit polyclonal antibodies to AQP-1. AQP-1 was expressed throughout the arterial portion of the renal vasculature of the fetal and neonatal kidney from gestational age 17 days to 1 wk after birth. AQP-1 immunoreactivity gradually disappeared from the renal vasculature between 1 and 2 wk of age and remained only in the descending vasa recta. In contrast, AQP-1 immunoreactivity was not observed in lymphatic vessels until 3 wk of age and persisted in the adult kidney. AQP-1 was also expressed in a population of interstitial cells in the terminal part of the renal papilla at 3 wk of age as well as in the adult kidney. The transient expression of AQP-1 in the arterial portion of the renal vasculature in the developing rat kidney suggests that AQP-1 is important for fluid equilibrium and/or drainage in the developing kidney or, alternatively, plays a role in the regulation of growth and/or branching of the vascular tree during kidney development.

Aging↗
PubMed1998

Negative regulation of granulocytic differentiation in the myeloid precursor cell line 32Dcl3 by ear-2, a mammalian homolog of Drosophila seven-up, and a chimeric leukemogenic gene, AML1/ETO.

The polyomavirus enhancer binding protein 2alphaB (AML1/PEBP2alphaB/Cbfa2) plays a pivotal role in granulocyte colony-stimulating factor (G-CSF)-mediated differentiation of a myeloid progenitor cell line, 32Dc13. In this article, we report the identification of a PEBP2alphaB interacting protein, Ear-2, an orphan member of the nuclear hormone receptor superfamily that directly binds to and can inhibit the function of PEBP2alphaB. Ear-2 is expressed in proliferating 32Dc13 cells in presence of interleukin 3 but is down-regulated during differentiation induced by G-CSF. Interestingly, AML1/ETO(MTG8), a leukemogenic chimeric protein can block the differentiation of 32Dc13 cells, which is accompanied by the sustained expression of ear-2. Overexpression of Ear-2 can prevent G-CSF-induced differentiation, strongly suggesting that ear-2 is a key negative regulator of granulocytic differentiation. Our results indicate that a dynamic balance existing between PEBP2alphaB and Ear-2 appears to determine the choice between growth or differentiation for myeloid cells.

Animals↗
PubMed1998

The hemodynamic impact of diffuse myocardial ischemic lesions: an animal experimental model based on intracoronary microembolization.

In ischemic heart disease, left ventricular function is affected by a diffuse and segmental loss of myocardium. The decline in the incidence of myocardial infarction and improved early revascularization in acute transmural ischemia predict a change in the natural history of ischemic heart disease. It is now believed that, minor ischemic episodes, which are known to induce multifocal myocardial degeneration, will predominate in the near future. The objective of the present study was to develop a clinically relevant experimental model for investigation of the pathophysiological significance of diffuse ischemic myocardial lesions. Cardiac performance was gradually depressed by selective intracoronary microembolization in 13 pigs. Left ventricular function was quantitated by ejection fraction (EF), pulmonary pressure, cardiac output, and derivatives of left ventricular pressure. Left ventricular volume was estimated by epicardial echocardiography, using a new, unbiased stereological volume estimator. A chronic substudy was performed in order to characterize the histological changes and to evaluate the feasibility of establishing a chronic preparation of the model. Embolization induced acute left ventricular dysfunction; left ventricular pressure change decreased from 966+/-274 to 637+/-146 mmHg/s, and early diastolic relaxation from 1403+/-515 to 824+/-344 mmHg/s, respectively. Ejection fraction decreased by 45%+/-5% and cardiac output by 29%+/-11%. End-diastolic volume increased significantly, from 66.1+/-13.2 to 77.0+/-19.4 cm3, and end-systolic volume increased from 35.9+/-13.9 to 52.3+/-7.6 cm3. No change in heart rate or left ventricular filling pressure was observed. Diffuse ischemic myocardial injury was identified after a mean follow-up of 40 days. Intracoronary microembolization induces acute left ventricular dysfunction due to microinfarcts. Increased left ventricular end-diastolic volume is the initial compensatory response to the acute impairment of cardiac performance in nontransmural myocardial ischemia. This model is suitable for the evaluation of the hemodynamic changes secondary to acute and chronic diffuse loss of functional myocardium.

Animals↗