Search PubMed⌕ Search

Biomedical subjects

K M Kim

Publications and source records attributed to K M Kim.

At least 19 recordsLinked to original sources

Dimensional changes of dental impression materials by thermal changes.

Dental impression materials for prosthodontic treatment must be easy to use, precisely replicate of oral tissue, be dimensionally stable, and be compatible with gypsum materials. The dimensional accuracy of all materials is affected by thermal changes; impression materials shrink during cooling from mouth temperature (37 degrees C) to room temperature (23 degrees C). Five kinds of light body addition-reaction silicone impression materials [Contrast (CT), Voco Co., Germany; Examix (EM), GC Co., Japan; Extrude (EX), Kerr Co., USA; Imprint II (IM), 3M Co., USA; Perfect (PF), Handae Chemical, Korea] were tested by making cylindrical specimens (6 mm diameter and 12 mm height). The thermal expansion of the impression materials was measured with a thermomechanical analyzer (TMA 2940, TA Instruments, USA) between 23-37 degrees C. Data were analyzed via the Mann-Whitney Usage Test. To simulate actual dental impressions, tooth and tray shapes were modeled to measure the linear shrinkage of impression materials at anterior and posterior locations. The thermal expansion of impression materials tested decreased as follows: CT >or= PF >or= EM >or= EX >or= IM (p < 0.05). The anterior region changed more than the posterior region for the same impression materials. The dimensional changes averaged more than 40 microm in the anterior region, but less than 40 microm in the posterior region for all materials. Thermal expansion coefficients of some impression materials were significantly different from each other (p < 0.05), and the anterior region had more dimensional change than the posterior region for the same impression materials.

Dental Impression Materials↗

Biophysical characterization of recombinant human Bcl-2 and its interactions with an inhibitory ligand, antimycin A.

Apoptosis is an essential physiological process, regulated by the family of Bcl-2-related proteins. However, the molecular mechanism by which Bcl-2 regulates apoptosis still remains elusive. Here we report the functional studies of recombinant human Bcl-2 with the deletion of 22 residues at the C-terminal membrane-anchoring region (rhBcl-2Delta22). Characterization of rhBcl-2Delta22 showed that the recombinant protein is homogeneous and monodisperse in nondenaturing solutions, stable at room temperature in the presence of a metal chelator, and an alpha-helical protein with unfolding of secondary structure at a T(m) of 62.8 degrees C. Optimal membrane pore formation by rhBcl-2Delta22 required negatively charged phospholipids. The existence of a hydrophobic groove in rhBcl-2Delta22 was demonstrated by the fluorescence enhancement of the hydrophobic ANS probe with which a pro-apoptotic Bak BH3 peptide competed. The respiratory inhibitor antimycin A also bound to the hydrophobic groove of rhBcl-2Delta22 with a K(d) of 0.82 microM. The optimal binding conformation of antimycin A was predicted from molecular docking of antimycin A with the hBcl-2 model created by homology modeling. Antimycin A selectively induces apoptosis in cells overexpressing Bcl-2, suggesting that hydrophobic groove-binding compounds may act as selective apoptotic triggers in tumor cells.

Amino Acid Sequence↗

Post-translational modification of the N-terminal His tag interferes with the crystallization of the wild-type and mutant SH3 domains from chicken src tyrosine kinase.

Structural studies of the wild type and mutants of the src SH3 domain were initiated to elucidate the correlation of the native-state topology with protein thermostability and folding kinetics. An extra mass of 178 Da arising from the post-translational modification at the N-terminal His tag was observed. The spontaneous alpha-N-6 gluconoylation at the amino group of the His-tagged SH3 domain contributed to the observed extra mass. The partial modification of the N-terminal His-tag produced heterogeneity, both in size and in charge, in the Escherichia coli expressed SH3 domain. The removal of the His tag from the SH3 domain was essential for the crystallization of both wild-type and mutant src SH3. Both the wild type and the W43I mutant were crystallized by hanging-drop vapor diffusion and are in the hexagonal space group P6(5)22 with one molecule in the asymmetric unit. Data sets were collected to 1.8 and 1.95 A resolution for the the wild type and the W43I mutant, respectively.

Amino Acid Sequence↗

Differential regulation of NO availability from macrophages and endothelial cells by the garlic component S-allyl cysteine.

Garlic has been used as a traditional medicine for prevention and treatment of cardiovascular diseases. However, the molecular mechanism of garlic's pharmacological action has not been clearly elucidated. We examined here the effect of garlic extract and its major component, S-allyl cysteine (SAC), on nitric oxide (NO) production by macrophages and endothelial cells. The present study demonstrates that these reagents inhibited NO production through the suppression of iNOS mRNA and protein expression in the murine macrophage cell line RAW264.7, which had been stimulated with LPS and IFNgamma. The garlic extract also inhibited NO production in peritoneal macrophages, rat hepatocytes, and rat aortic smooth muscle cells stimulated with LPS plus cytokines, but it did not inhibit NO production in iNOS-transfected AKN-1 cells or iNOS enzyme activity. These reagents suppressed NF-kappaB activation and murine iNOS promoter activity in LPS and IFNgamma-stimulated RAW264.7 cells. In contrast, these reagents significantly increased cGMP production by eNOS in HUVEC without changes in activity, protein levels, and cellular distribution of eNOS. Finally, garlic extract and SAC both suppressed the production of hydroxyl radical, confirming their antioxidant activity. These data demonstrate that garlic extract and SAC, due to their antioxidant activity, differentially regulate NO production by inhibiting iNOS expression in macrophages while increasing NO in endothelial cells. Thus, this selective regulation may contribute to the anti-inflammatory effect and prevention of atherosclerosis by these reagents.

Animals↗

Quantitative trait loci mapping associated with plant regeneration ability from seed derived calli in rice (Oryza sativa L.).

Quantitative trait loci (QTLs), which are associated with the ability of plant regeneration from seed derived calli, were detected using a recombinant inbred (RI) population from a cross between 'Milyang 23 (toingil)' and 'Gihobyeo (japonica)' in rice (Oryza sativa L.). A tongil type cultivar, 'Milyang 23', has a lower frequency of callus induction and plant regeneration than those of japonica 'Gihobyeo'. Transgressive segregations were observed for the callus induction rate and plant regeneration ability from seed derived calli of the RI population. An interval mapping analysis was used to identify the QTL controlling the plant regeneration ability. Two QTLs for the callus induction rate were detected on chromosomes 1 and 2, explaining the 10.9% total phenotypic variation. Four QTLs that are associated with the plant regeneration ability were located on chromosomes 2, 3, and 11, accounting for 25.7% of the total phenotypic variation.

Chromosome Mapping↗

Somatic mutations of TRAIL-receptor 1 and TRAIL-receptor 2 genes in non-Hodgkin's lymphoma.

Tumor necrosis factor-related apoptosis-inducing ligand-receptor 1 (TRAIL-R1) and tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) are cell-surface receptors involved in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell-death signaling. TRAIL-R1 and TRAIL-R2 genes have recently been mapped to chromosome 8p21-22, which is a frequent site of allelic deletions in many types of human tumors, including non-Hodgkin's lymphoma (NHL). Because TRAIL/TRAIL receptor system plays an important role in lymphocyte homeostasis, we hypothesized that the mutations of TRAIL-R1 and TRAIL-R2 may be involved in the development of NHL and that such mutations may be responsible for the allelic losses of 8p21-22 in NHL. In this study, we analysed the entire coding region of TRAIL-R2 gene and the death domain region of TRAIL-R1 gene for the detection of the somatic mutations in a series of 117 human NHLs using polymerase chain reaction (PCR)-based single strand conformation polymorphism (SSCP) analysis. Overall, eight tumors (6.8%) were found to have two TRAIL-R1 gene mutations or six TRAIL-R2 gene mutations. Interestingly, of the eight mutations, six missense mutations (two TRAIL-R1 and four TRAIL-R2) were detected in the death domains and one nonsense mutation of TRAIL-R2 was detected just before the death domain. Our data suggest that somatic mutations of TRAIL-R1 and TRAIL-R2 genes may play a role in the pathogenesis of some NHLs and that TRAIL-R1 and TRAIL-R2 genes might be the relevant genes to the frequent loss of chromosome 8p21-22 in human NHL.

Humans↗

Evidence for two modes of allelic loss: multifocal analysis on both early and advanced gastric carcinomas.

To assess the extent and the timing of allelic loss required for the progression of gastric carcinoma, the intratumoral distribution of loss of heterozygosity (LOH) was compared in early and advanced tumors: early loss is uniformly observed in all tumor areas and late loss is localized in parts of tumor tissue. Tumor sites (167 sites) obtained from 42 gastric carcinoma tissues (26 advanced cancers and 16 early cancers) were examined for LOH on chromosomes 5q, 9p, 13q, 17p, and 18q. By using two or three microsatellite markers for each chromosome arm, it was shown that of 29 tumors showing LOH in at least one tumor site, 15 (51.7%, 12 advanced and three early cancers) harbored multiple losses on three or more chromosome arms, and 89.4% (84 of 94) of these losses was uniformly found in all tumor sites tested. In the remaining 14 tumors (48.3%, eight advanced and six early tumors) with sporadic losses on one or two chromosome arms, 44% (11 of 25) of the losses were commonly shared among the sites tested. Such marked difference (P<0.001, Fisher's exact test) in the intratumoral distribution of multiple and sporadic LOH patterns proposes two distinct LOH subtypes: multiple losses (high LOH), occurring at an early stage with a few additional losses, and sporadic losses (low LOH), taking place relatively late during tumor progression. The multifocal LOH findings imply that, rather than being gradual, the allelic losses take place in two manners that are already determined at an early stage.

Alleles↗

Functional interaction between monoamine plasma membrane transporters and the synaptic PDZ domain-containing protein PICK1.

PDZ domain-containing proteins play an important role in the targeting and localization of synaptic membrane proteins. Here, we report an interaction between the PDZ domain-containing protein PICK1 and monoamine neurotransmitter transporters in vitro and in vivo. In dopaminergic neurons, PICK1 colocalizes with the dopamine transporter (DAT) and forms a stable protein complex. Coexpression of PICK1 with DAT in mammalian cells and neurons in culture results in colocalization of the two proteins in a cluster pattern and an enhancement of DAT uptake activity through an increase in the number of plasma membrane DAT. Deletion of the PDZ binding site at the carboxyl terminus of DAT abolishes its association with PICK1 and impairs the localization of the transporter in neurons. These findings indicate a role for PDZ-mediated protein interactions in the localization, expression, and function of monoamine transporters.

Animals↗

Design of a PC-based multimedia telemedicine system for brain function teleconsultation.

During time-critical brain surgery, the detection of developing cerebral ischemia is particularly important because early therapeutic intervention may reduce the mortality of the patient. The purpose of this system is to provide an efficient means of remote teleconsultation for the early detection of ischemia, particularly when subspecialists are unavailable. The hardware and software design architecture for the multimedia brain function teleconsultation system including the dedicated brain function monitoring system is described. In order to comprehensively support remote teleconsultation, multi-media resources needed for ischemia interpretation were included: EEG signals, CSA, CD-CSA, radiological images, surgical microscope video images and video conferencing. PC-based system integration with standard interfaces and the operability over the Ethernet meet the cost-effectiveness while the modular software was customized with a diverse range of data manipulations and control functions necessary for shared workspace and standard interfaces.

Brain Ischemia↗

Antimycin A mimics a cell-death-inducing Bcl-2 homology domain 3.

The Bcl-2-related survival proteins confer cellular resistance to a wide range of agents. Bcl-xL-expressing hepatocyte cell lines are resistant to tumour necrosis factor and anti-cancer drugs, but are more sensitive than isogenic control cells to antimycin A, an inhibitor of mitochondrial electron transfer. Computational molecular docking analysis predicted that antimycin A interacts with the Bcl-2 homology domain 3 (BH3)-binding hydrophobic groove of Bcl-xL. We demonstrate that antimycin A and a Bak BH3 peptide bind competitively to recombinant Bcl-2. Antimycin A and BH3 peptide both induce mitochondrial swelling and loss of DeltaPsim on addition to mitochondria expressing Bcl-xL. The 2-methoxy derivative of antimycin A3 is inactive as an inhibitor of cellular respiration but still retains toxicity for Bcl-xL+ cells and mitochondria. Finally, antimycin A inhibits the pore-forming activity of Bcl-x L in synthetic liposomes, demonstrating that a small non-peptide ligand can directly inhibit the function of Bcl-2-related proteins.

Adenosine Triphosphate↗

Cnidicin, a coumarin, from the root of Angelica koreana, inhibits the degranulation of mast cell and the NO generation in RAW 264.7 cells.

Cnidicin (1) and five related coumarins were isolated from the root extract of Angelica koreana (Umbelliferae) as active principles responsible for the inhibitory effect on the degranulation process of cultured mast cells. Cnidicin (1) demonstrated a significant inhibition upon the release of beta-hexosaminidase from the cultured RBL-2H3 cells in a dose dependent manner (IC50 value, 25 microM) and upon the nitric oxide production from the activated RAW264.7 cells (IC50 value, 7.5 microM). In agreement with this, cnidicin inhibited the expression of nitric oxide synthase in RAW264.7 cells.

Animals↗

Cephalic spreading levels after volumetric caudal epidural injections in chronic low back pain.

The volumetric caudal epidural steroid injection has been advocated to facilitate the delivery of medications to the lesion site. This study was aimed to examine the actual spreading patterns of this technique, using epidurogram. A total of 32 patients with chronic low back pain accompanied by radiculopathy of various causes (degenerative spondylosis, herniated nucleus pulposus, spondylolisthesis, and spinal stenosis) were included. The volumetric caudal epidural injection of the 10 mL mixture of contrast medium 5 mL, 0.5% bupivacaine 1 mL, triamcinolone 1.5 mL (60 mg) and normal saline 25 mL was performed. Immediately after the cessation of the first spread, the subsequent solution of another 10 mL of contrast medium 5 mL, 0.5% bupivacaine 1 mL and normal saline 4 mL was injected. This procedure was repeated serially until the total volume to be 50 mL. Continuous fluoroscopic imaging was obtained after each injection. Average time taken to complete the study was 37 sec per every 10 mL. The spreading levels of the mixture were distributed mainly at mid to lower lumbar area in the majority of the patients. During the subsequent injections, the levels were not changed significantly. This was thought to be due to the minimal resistance in cephalad direction, anatomic variations and Starling effect of epidural space.

Adult↗

Fas-mediated apoptosis and expression of related genes in human malignant hematopoietic cells.

Fas transduces apoptotic signals upon cross-linking with the Fas ligand (FasL), which is experimentally replaced by agonistic anti-Fas monoclonal antibodies (mAb). Of eight human malignant hematopoietic cell lines (HL-60, KG-1, THP-1, K562, U937, Jurkat, IM-9, RPMI-8226) examined by flow cytometric analysis, all, except K562, were found to be positive for surface Fas antigen. However, despite surface Fas expression, the agonistic anti-Fas mAb (7C11) induced apoptosis in only three of seven Fas-expressing cell lines (KG-1, Jurkat and IM-9). This Fas-resistance did not correlated with high levels of mRNA either for DcR3, a decoy receptor for FasL, or for FAP-1, a Fas-associated phosphatase that can block the apoptotic function of Fas. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis did not show consistent differences in the expression of Bcl-2 and Bax between Fas-sensitive and Fas-resistant cell lines examined. These findings indicated that the presence or absence of mRNA expression of DcR3, FAP-1, Bcl-2 and Bax did not always correlate with relative sensitivity to Fas-mediated apoptosis. Treatment of cells with cycloheximide converted the phenotype of resistant cell lines from Fas-resistant to Fas-sensitive, and enhanced the sensitivity of Fas-sensitive cell lines. These results suggest that the Fas-resistance is dependent on the presence of labile proteins that determine resistance to Fas-mediated apoptosis and the apoptotic machinery is already in place in Fas-resistant cell lines.

Apoptosis↗

Sphingosine 1-phosphate protects human umbilical vein endothelial cells from serum-deprived apoptosis by nitric oxide production.

Sphingosine 1-phosphate (S1P) can prevent endothelial cell apoptosis. We investigated the molecular mechanisms and signaling pathways by which S1P protects endothelial cells from serum deprivation-induced apoptosis. We show here that human umbilical vein endothelial cells (HUVECs) undergo apoptosis associated with increased DEVDase activity, caspase-3 activation, cytochrome c release, and DNA fragmentation after 24 h of serum deprivation. These apoptotic markers were suppressed by the addition of S1P, the NO donor S-nitroso-N-acetylpenicillamine (100 micrometer), or caspase-3 inhibitor z-VAD-fmk. The protective effects of S1P were reversed by the nitric-oxide synthase (NOS) inhibitor N-monomethyl-l-arginine, but not by the soluble guanylyl cyclase inhibitor 1H-(1,2,4)oxadiazolo[4,3-a]-quanoxaline-1-one, suggesting that NO, but not cGMP, is responsible for S1P protection from apoptosis. Furthermore, S1P increased NO production by enhancing Ca(2+)-sensitive NOS activity without changes in the eNOS protein level. S1P-mediated cell survival and NO production were suppressed significantly by pretreatment with antisense oligonucleotide of EDG-1 and partially by EDG-3 antisense. S1P-mediated NO production was suppressed by the addition of pertussis toxin, an inhibitor of G(i) proteins, the specific inhibitor of phospholipase C (PLC), and the Ca(2+) chelator BAPTA-AM. These findings indicate that S1P protects HUVECs from apoptosis through the activation of eNOS activity mainly through an EDG-1 and -3/G(i)/PLC/Ca(2+) signaling pathway.

Apoptosis↗

Intraoperative thermal regulation in patients undergoing laparoscopic vs open surgical procedures.

BACKGROUND: Although perioperative hypothermia is a well-known consequence of general anesthesia, it has been hypothesized that laparoscopic surgery exacerbates hypothermia to a greater extent than open surgery. The aim of this study was to demonstrate that laparoscopic surgery does not represent an increased risk for hypothermia. METHODS: A case-controlled retrospective study was conducted on 45 patients, 25 undergoing laparoscopic cholecystectomy and 20 undergoing parathyroid surgery under endotracheal general anesthesia. Data were collected regarding age, sex, weight, height, American Society of Anesthesiologists (ASA) status, length of surgery, and anesthesia. In addition, we analyzed the type of intraoperative intravenous fluids, anesthetics and perioperative drugs, and temperature, blood pressure, and heart rate recordings during anesthesia. RESULTS: There was no significant difference between the two groups with respect to age, sex, body mass index (BMI), ASA status, type or amount of intravenous fluids infused, length of anesthesia or surgery, changes in mean blood pressure, or heart rate. Core body temperatures in both groups decreased significantly over time (p 0.05). There was no difference between the groups in terms of maximum drop in temperature (lowest temperature recorded vs baseline temperature) (1.1 +/- 0.7 vs 1.0 +/- 0.7 degrees C, p > 0.05). CONCLUSION: This study demonstrates that patients who undergo laparoscopic and open procedures of similar duration under endotracheal general anesthesia have similar profiles in terms of perioperative hypothermia.

Anesthesia, General↗

Analysis of OPT8511 RAPD fragments closely linked with cold sensitivity at seedling stage in rice (Oryza sativa L.).

OPT8(511) was confirmed to be strongly associated with cold sensitivity of rice by random amplified polymorphic DNA (RAPD) analysis for the cold tolerance with 94 F2 population crossed with 'Dular' (cold sensitive cultivar) and 'Toyohatamochi' (cold resistant cultivar). A DNA marker from the RAPD fragment, OPT8(511), has been cloned with genomic DNA from rice cultivar ('Dular') and the nucleotide sequence has been determined. The nucleotide sequence revealed that the putative open reading frame was 511 base pairs and contained 169 amino acid residues. It is 79% and 57% identical to the rice cDNA (C26347) in DataBank at the nucleotide and amino acid sequence levels, respectively. The clone OPT8(511) specifically amplified a 511 bp band from the DNA of cold sensitive cultivars. Use of this marker could facilitate early selection of character associated with cold tolerance in rice.

Amino Acid Sequence↗

Prognostic implications of microsatellite genotypes in gastric carcinoma.

Microsatellite alterations such as loss of heterozygosity (LOH) and microsatellite instability (MSI) are observed in most (70% to 80%) gastric carcinomas. To determine whether the microsatellite genotypes are correlated with clinicopathological features, 118 patients with gastric carcinomas were examined by using polymorphic microsatellite markers for LOH on 5 gastric cancer-associated chromosome arms and non-polymorphic BAT markers for MSI. Microsatellite genotypes were categorized as high-frequency MSI (MSI-H), high-level LOH (LOH-H), low-level LOH (LOH-L) and LOH non-detectable (LOH-N). A significant fraction of the MSI-H, LOH-H and LOH-L types was observed in intestinal-type gastric carcinomas, whereas the LOH-N type was highly associated with diffuse-type tumors (p = 0.00162). There was a close relationship between microsatellite genotype and TNM (tumor-node-metastasis) stage (p = 0. 001). Univariate analysis showed that patients of LOH-H or LOH-N types and those of MSI-H or LOH-L types correlated with poor and favorable survival, respectively, not only in all tumor stages (p = 0.0001) but also in stages II and III (p = 0.0271). It is likely that the major genotypes of gastric carcinomas can be placed into at least 4 microsatellite categories, thus allowing the construction of a comprehensive genetic classification useful for the prediction of diverse clinical courses.

Adult↗

A phase Ib/II trial of granulocyte-macrophage-colony stimulating factor and interleukin-2 for renal cell carcinoma patients with pulmonary metastases: a case of fatal central nervous system thrombosis.

BACKGROUND: Interleukin-2 (IL-2) and granulocyte-macrophage-colony stimulating factor (GM-CSF) are cytokines with nonoverlapping pleiotropic effects. In a prior Phase Ib study, this combination of agents exhibited antitumor effects in the lungs of four of eight patients with renal cell carcinoma and pulmonary metastases. We conducted this Phase Ib/II trial to determine the response rate of renal cell carcinoma patients with pulmonary metastases treated with continuous infusion IL-2 plus GM-CSF. METHODS: Patients with renal cell carcinoma and pulmonary metastases were treated with 1.5, 2.25, or 4.5 x 10(6) IU/m(2)/day 96-hour continuous infusion IL-2 on Days 1-4, 8-11, and 15-18, and 1.25, 2.25, or 2.5 microg/kg/day GM-CSF on Days 8-19. RESULTS: Sixteen patients were treated per protocol, 14 of whom could be evaluated for disease progression. None of these 14 patients had >50% shrinkage of either total tumor burden or pulmonary metastasis. One patient developed Grade 5 neurotoxicity. Autopsy revealed acute multifocal cerebral venous thrombosis as well as acute subdural and subarachnoid hemorrhage. CONCLUSIONS: The combination of IL-2 and GM-CSF may be associated with marked morbidity and, as in one case in this study, mortality. No significant antitumor activity was appreciated. Thus, the combination of IL-2 and GM-CSF, when administered at this dose and according to this schedule, does not appear to be active in renal cell carcinoma and is associated with significant toxicities. Further studies using this combination of agents should only be undertaken with extreme caution and particular attention to neurotoxicity.

Adult↗