PURPOSE: The purpose of this study was to compare the effect of 3 chairside polishing methods and laboratory polishing methods on surface roughness and C. albicans adhesion of polyamide denture base. MATERIALS AND METHODS: Using contact profilometer, the surface of polyamide specimens (25x15x2 mm) was studied after conventional polishing without finishing and after chiarside polishing with 2 chiarside polishing kits and chairside-pumice polishing following finishing with tungsten carbide bur. To evaluate the adhesion of C. albicans, C. albicans suspension was overlayed on the test specimen. And the specimens were incubated for 2 hours. Imprint culture method was achieved and counted the colony on the agar plate. Polished polyamide were evaluated using a scanning electron microscope. The statistics were conducted using one-way ANOVA and in case of difference, Scheffe test and Tamhane's T2 test were used. RESULTS: Surface roughness (Ra) of surfaces polished with 2 chairside polishing kits had higher than conventional polishing and pumice polishing. The highest roughness value was 0.32 +/- 0.10 microm, and the lowest was 0.02 +/- 0.00 microm. The adhesion of C. albicans on the specimens polished with chairside polishing group and pumice polishing group were increased than conventional polishing group (P<.01). CONCLUSION: Conventional laboratory polishing was found to produce the smoothest surface and the lowest adhesion of C. albicans. Two groups polished with Chairside polishing kits were similar with respect to surface roughness. Surface of the specimen polished with pumice is significantly smoother than 2 chairside polishing groups, but the result of C. albicans adhesion is that group polished with pumice was similar with 2 chairside polishing groups (P>.01).
Agar ; Candida ; Candida albicans ; Denture Bases ; Dentures ; Electrons ; Nylons ; Silicates ; Tungsten ; Tungsten Compounds

Routine protein assays are usually affected with various compounds, and we need to use different protein quantification protocol to deal with different interference. In order to simplify the procedure, we developed a new method, in which the components and concentrations of the reagents were modified mainly based on classic Folin-Ciocalteu's reagent for reducing the susceptibility to interfering substances. Standard curves of the new method were established with different levels of bovine serum albumin, and then, we assessed and evaluated the detectable wavelengths and stability. In particular, the tolerability to several interfering substances was analyzed by using cytolysis solutions containing different chemicals. Our data in this study show that the new method could be applied to detecting protein concentrations accurately, even in the presence of surfactants such as 10% sodium dodecyl sulfate (SDS), 2% NP-40, or 1% TrintonX-100, chelators of 25 mmol/L EDTA or 1 mmol/L Ethylene glycol bis (2-aminoethyl) tetraacetic acid (EGTA), reductants of 1 mmol/L Dithiothretol (DTT) orbeta-Mercaptoethanol (ME), or nitrogen-containing compounds of 0.5 mol/L ammonium sulphate or 4 mol/L urea. Taken together, these results indicate that the new approach significantly improves the tolerance to the interfering substances, which could be potentially useful in measuring the contents of proteins interfered with such substances.
Animals ; Edetic Acid ; chemistry ; Egtazic Acid ; chemistry ; Indicators and Reagents ; chemistry ; Molybdenum ; chemistry ; Proteins ; analysis ; Serum Albumin, Bovine ; analysis ; Surface-Active Agents ; chemistry ; Tungsten Compounds ; chemistry

OBJECTIVE: To explore the effect of sodium tungstate on glucose metabolism in adipocytes and its mechanism. METHODS: After 3T3-L1 preadipocytes were differentiated into adipocytes, these adipocytes were incubated with sodium tungstate (0, 150, 300, 500, and 700 micromol/L) for 48 h, and then glucose consumption of the adipocytes was detected by glucose-oxidase assay. Glucose transport was determined by the uptake of 2-deoxy-[3H]-D-glucose, and the expression of glucose transport-4 (GLUT-4) mRNA was identified by semi-quantitative RT-PCR. RESULTS: Sodium tungstate (150 approximately 700 micromol/L) could significantly increase the glucose consumption and glucose transport with a concentration dependent-effect. Sodium tungstate could increase GLUT-4 mRNA expression. CONCLUSION Sodium tungstate can enhance the glucose metabolism of adipocytes by up-regulating the expression of GLUT-4 mRNA.
3T3-L1 Cells ; Adipocytes ; metabolism ; Animals ; Glucose ; metabolism ; Glucose Transporter Type 4 ; biosynthesis ; genetics ; Hypoglycemic Agents ; pharmacology ; Mice ; RNA, Messenger ; biosynthesis ; genetics ; Tungsten Compounds ; pharmacology ; Up-Regulation

Protein-tyrosine phosphatases (PTPs) constitute a family of receptor-like, and cytoplasmic enzymes, which catalyze the dephosphorylation of phosphotyrosine residues in a variety of receptors and signaling molecules. Together with protein tyrosine kinases (PTKs), PTPs are critically involved in regulating many cellular signaling processes. In this study, diverse compounds were screened for PTP inhibition and selectively screened for inhibitors with the end product inhibition properties. Among phosphate analogues and their derivatives for PTP inhibition, Keggin compounds phosphomolybdate (PM) and phosphotungstate (PT) strongly inhibited both PTP-1B and SHP-1, with K(i) values of 0.06-1.2 micromM in the presence of EDTA. Unlike the vanadium compounds, inhibition potencies of PM and PT were not significantly affected by EDTA. PM and PT were potent, competitive inhibitors for PTPs, but relatively poor inhibitors of Ser/Thr phosphatase. Interestingly, PM and PT did not inhibit alkaline phosphatase at all. The crystal structure of PTP-1B in complex with PM, at 2.0 A resolution, reveals that MoO(3), derived from PM by hydrolysis, binds at the active site. The molybdenium atom of the inhibitor is coordinated with six ligands: three oxo-ligands, two apical water molecules and a S atom of the catalytic cysteine residue. In support of the crystallographic finding, we observed that molybdenium oxides (MoO(3), MoO(2), and MoO(2)Cl(2)) inhibited PTP-1B with IC(50) in the range 5-15 micromM.
Binding, Competitive ; Catalytic Domain ; Crystallography, X-Ray ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Edetic Acid/pharmacology ; Enzyme Inhibitors/*pharmacology ; Human ; Inhibitory Concentration 50 ; Kinetics ; Models, Molecular ; Molybdenum/*pharmacology ; Phosphoric Acids/*pharmacology ; Protein Structure, Tertiary ; Protein-Tyrosine-Phosphatase/*antagonists & inhibitors/*chemistry/isolation & purification ; Substrate Specificity ; Tungsten Compounds/*pharmacology

BACKGROUND: Although cardiac hypertrophy contributes to cardiac failure, the underlying mechanism has not yet been precisely determined. This study was planned in order to determine the pathogenesis of heart failure following cardiac hypertrophy induced by -adrenergic stimulation. METHODS: The extent of cardiac hypertrophy was assessed after administrating isoproterenol (ISO, 5 mg/kg) intraperitoneally for 6 hours, 1, 3, 5, 7 and 10 days. The hematoxylin-eosin, Masson's trichrome and phosphotungstic acid hematoxylin stains along with immunohistochemical stainings for proliferating cell nuclear antigen and Ki-67 were performed in the paraffin-embedded left ventricle sections. Apoptosis was assessed by DNA laddering and terminal deoxynucleotidyl transferase TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay. TUNEL positive myocytes and some nonmyocytes appeared in the subepicardium at 6 hours after ISO administration. The localization of these cells was shifted to the subendocardium within 24 hours, and the TUNEL positive cells were seen throughout the myocardium on the 5th day after ISO treatment. Necrotic myocyte death occurred on the 3rd day of ISO administration in the subendocardium, and initial pericellular fibrosis was followed and increased thereafter, with replacement fibrosis accompanied by further necrotic myocyte cell death. CONCLUSIONS: Our data showed that ISO treatment induced apoptotic myocyte death and superimposed necrotic myocyte death with subsequent fibrosis. The observed cardiac myocyte death may reflect myocardial dysfunction.
Animals ; Apoptosis ; Cardiomegaly* ; Cell Death* ; Coloring Agents ; DNA ; DNA Nucleotidylexotransferase ; Fibrosis ; Heart Failure ; Heart Ventricles ; Hematoxylin ; Hypertrophy ; In Situ Nick-End Labeling ; Isoproterenol ; Muscle Cells ; Myocardium ; Myocytes, Cardiac* ; Phosphotungstic Acid ; Proliferating Cell Nuclear Antigen ; Rats*

Brain ischemia leads to overstimulation of N-methyl-D-aspartate (NMDA) receptors, referred as excitotoxicity, which mediates neuronal cell death. However, less attention has been paid to changes in synaptic activity and morphology that could have an important impact on cell function and survival following ischemic insult. In this study, we investigated the effects of reperfusion after oxygen/glucose deprivation (OGD) not only upon neuronal cell death, but also on ultrastructural and biochemical characteristics of postsynaptic density (PSD) protein, in the stratum lucidum of the CA3 area in organotypic hippocampal slice cultures. After OGD/reperfusion, neurons were found to be damaged; the organelles such as mitochondria, endoplasmic reticulum, dendrites, and synaptic terminals were swollen; and the PSD became thicker and irregular. Ethanolic phosphotungstic acid staining showed that the density of PSD was significantly decreased, and the thickness and length of the PSD were significantly increased in the OGD/reperfusion group compared to the control. The levels of PSD proteins, including PSD-95, NMDA receptor 1, NMDA receptor 2B, and calcium/calmodulin-dependent protein kinase II, were significantly decreased following OGD/reperfusion. These results suggest that OGD/reperfusion induces significant modifications to PSDs in the CA3 area of organotypic hippocampal slice cultures, both morphologically and biochemically, and this may contribute to neuronal cell death and synaptic dysfunction after OGD/reperfusion.
Brain Ischemia ; Cell Death ; Dendrites ; Endoplasmic Reticulum ; Ethanol ; Mitochondria ; N-Methylaspartate ; Neurons ; Organelles ; Phosphotungstic Acid ; Post-Synaptic Density ; Presynaptic Terminals ; Protein Kinases ; Proteins ; Receptors, N-Methyl-D-Aspartate ; Reperfusion

Eighteen cases of osteonecrosis of the femoral head associated with macromolecular polyvinylpyrrolidone (PVP) deposition were analysed on the basis of clinical, radiologic and pathologic features. The cases were observed during 8 years period from January, 1974 to December, 1981. The pathogenesis of the osteonecrosis of the femoral head due to PVP storage in reticuloendothelial system were discussed in detail. Parenteral administration of high-molecular PVP in repeated, long duration led to osteonecrosis of the femoral head. Storage of PVP in the histiocytes of the bone marrow resulted in osteonecrosis of the femoral head followed by microciculation disturbance. PVP-induced osteonecrosis were manifested as multiple foci of necrosis involving not only the femoral head, other long bones around joints, but also the visceral reticuloendo-thelial system characterized by infiltrates of histiocytes laden with PVP. The patients with PVP induced osteonecrosis complianed multiple joint pain in their early course of the disease. On roentgenogram, osteonecrosis were often noted in the hip, shoulder, knee, and ankle in order or frequency. Foamy histiocytes laden with PVP were characteristic on hematoxylin-eosin stain diagnostic on Weigert's elastica, phosphotungstic acid hematoxylin, and Congo red stains. As far as rationale of the treatment concerning a number of staging systems for Osteonecrosis, the choice of surgical procedures were similar to those given by W.F. Enneking et al. In the series, we have performed two hips in total surface replacement, 26 hips in total hip replacement mostly for 3rd generation-configuration of Charnley prosthesis. In addition, one case for free vascularized fibula graft and trans-trochanteric rotational osteotomy after Sugioka were also included for this study. The result of treatment was rather optimistic. However, complications have occured in 4 hips of 3 patients which required removal of whole prosthetic components. Therefore, we underwent revisional surgery in three out of four hips subsequently during the short post-poerative follow-up. These will be published in the future.
Ankle ; Arthralgia ; Arthroplasty, Replacement, Hip ; Bone Marrow ; Coloring Agents ; Congo Red ; Fibula ; Follow-Up Studies ; Head ; Hematoxylin ; Hip ; Histiocytes ; Humans ; Joints ; Knee ; Mononuclear Phagocyte System ; Necrosis ; Osteonecrosis ; Osteotomy ; Phosphotungstic Acid ; Povidone ; Prostheses and Implants ; Rubber ; Shoulder ; Transplants