This study was performed to evaluate clinical practicality of the rebonding method with flowable resin without the removal of the residual resin on the debonded teeth and debonded bracket base after debonding. The samples of the control group (group I) were rebonded with Transbond XT(R) using the usual rebonding method after the residual resin was removed. At experimental group, the brackets were rebonded with Transbond XT(R) (group II) and CharmFil Flow(R) (group III) without removal of residual resin which is the possibility becoming the index for rebonding to similar position with initial bonding. The shear bond strength of the each group was measured. Patterns of bonding failure were evaluated with modified ARI score, and the shear bond strength according to patterns of bonding failure at experimental group was compared. Between the control group (6.51 +/- 1.21 MPa) and the group II rebonded with Transbond XT(R) (6.30 +/- 1.01 MPa) did not have significantly difference in the shear bond strength (p = 0.534), and the shear bond strength of group II was significantly lower than the group III rebonded with CharmFil Flow(R) (7.29 +/- 1.54 MPa) (p = 0.009). At control group, there was not large difference in distribution of bonding failure pattern. But at experimental group, bond failure did not occur in interface between the resin-enamel. and bond failure between the resin-bracket, within the resin was distributed similarly. There was not significantly difference in the shear bond strength according to patterns of bonding failure at experimental group (p > 0.05). The result of this study showed that the method suggested in this study and flowable resin as rebonding adhesive could be useful in clinically.
Adhesives ; Orthodontic Brackets* ; Tooth

We cultured the rabbit inner medullary collecting duct (IMCD) cells as monolayers on collagen-coated membrane filters, and investigated distribution of the P2Y receptors by analyzing nucleotide-induced short circuit current (Isc) responses. Exposure to different nucleotides of either the apical or basolateral surface of cell monolayers stimulated Isc. Dose-response relationship and cross-desensitization studies suggested that at least 3 distinct P2Y receptors are expressed asymmetrically on the apical and basolateral membranes. A P2Y2-like receptor, which responds to UTP and ATP, is expressed on both the apical and basolateral membranes. In addition, a uracil nucleotide receptor, which responds to UDP and UTP, but not ATP, is expressed predominantly on the apical membrane. In contrast, a P2Y1-like receptor, which responds to ADP and 2-methylthio-ATP, is expressed predominantly on the basolateral membrane. These nucleotides stimulated intracellular cAMP production with an asymmetrical profile, which was comparable to that in the stimulation of Isc. Our results suggest that the adenine and uracil nucleotides can interact with different P2Y nucleotide receptors that are expressed asymmetrically on the apical and basolateral membranes of the rabbit IMCD cells, and that both cAMP- and Ca2+-dependent signaling mechanisms underlie the stimulation of Isc.
Adenine ; Adenosine Diphosphate ; Adenosine Triphosphate ; Membranes ; Nucleotides ; Uracil ; Uracil Nucleotides ; Uridine Diphosphate ; Uridine Triphosphate

Vitamin C, one of essential micronutrients, has been reported to modulate the humoral immune responses in some mammals. We investigated whether vitamin C might modulate this response in mice by directly affecting B cells. Splenic B cells were isolated and activated by CD40- and B cell receptor-ligation in vitro. The cells were cultured with a pretreatment of vitamin C from 0 to 1 mM of concentrations. Vitamin C slightly increased apoptosis of B cells dose-dependently and behaved as an antioxidant. We found that in vivo administration of vitamin C by intraperitoneal injection affected isotype switching as previously reported: the titer of antigen-specific IgG1 antibody was decreased, while that of IgG2a was unaffected. Somewhat different from those observed in vivo, in vitro exposure to vitamin C slightly decreased isotype switching to IgG1 and increased isotype switching to IgG2a. Pretreatment with vitamin C in the safe range did not affect either proliferation of cultured B cells or the expression of CD80 and CD86 in those cells. Taken together, in vivo results suggest that vitamin C acts to modulate isotype switching in the mouse. However, because of our in vitro results, we suggest that the modulation exerted by vitamin C in vivo is by indirectly affecting B cells, perhaps by directly influencing other immune cells such as dendritic cells.
Animals ; Apoptosis ; Ascorbic Acid ; B-Lymphocytes ; Dendritic Cells ; Immunity, Humoral ; Immunoglobulin Class Switching ; Immunoglobulin G ; Injections, Intraperitoneal ; Mammals ; Mice ; Micronutrients ; Reactive Oxygen Species ; Vitamins

BACKGROUND: Based on outstanding progresses in animal experiments, vaccines for some human tumors have been developed. However, clinical effects of these vaccines have been far below than expected. This discrepancy might come from differences between animal models and human patients with respect to immunocompetency. The immune status of mice after tumor inoculation has not been well studied, which make us cautious in interpreting and applying the results from mice to human. We evaluated cell-mediated immune responses in mice after tumor cell inoculation. METHODS: Mice were inoculated with TA3Ha, CT26, or 4T1. Delayed-type hypersensitivity (DTH) responses were induced 2-4 weeks after inoculation using 2,4-dinitro-1-fluorobenzene as an antigen. The relationships between the severity of DTH responses and the duration of tumor inoculation or the size of tumor mass were analyzed. RESULTS: In TA3Ha groups, DTH response was elevated 2 weeks after inoculation, but depressed after 4 weeks, compared to the control group. When analyzed based on the sizes of tumor masses elicited, DTH responses were inversely related to the mass size, especially in those greater than 10 mm in diameter. In CT26 groups, while the duration after inoculation did not affect the severity of DTH responses, those with large mass showed depressed responses regardless the duration of inoculation. 4T1 cells grew so slowly that the size of tumor mass was small even 4 weeks after inoculation, and this group showed much higher DTH responses compared to that of tumor-free group. CONCLUSION: At least in an experimental setting where tumor model was induced by inoculating tumor cell lines into immunologically competent mice, the host immune response was elevated in early stage, and then depressed in late stage when the mass grew over a critical size.
Animal Experimentation ; Animals ; Cell Line, Tumor ; Humans ; Hypersensitivity* ; Mice* ; Models, Animal ; Vaccines

It has been reported that activation of sphingomyelin pathway and nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the promotion of colon carcinoma. Ceramide, a metabolite of sphingomyelin, and indomethacin were shown to induce apoptosis in colon carcinoma cells. However, the mechanisms of ceramide- and indomethacin-induced apoptosis in the colon carcinoma cells are not clearly elucidated. Recent studys showed that indomethacin-induced apoptosis in colon cancer cells through the cyclooxygenase-independent pathways, and that may be mediated by generation of ceramide. In this study, we compared effects of ceramide and indomethacin on important modulators of apoptotic processes in HT29 cells, a human colon cancer cell line. Ceramide and indomethacin induced apoptosis dose- and time-dependently. Ceramide and indomethacin increased stress-activated protein kinase (SAPK) activity, and decreased mitogen-activated protein kinase (MAPK) activity. The expression of Bak was increased by the treatment of ceramide and indomethacin. The expression of other Bcl-2 related proteins (Mcl-1, Bcl-XL, Bax) which were known to be expressed in colon epithelial cells was not changed during the ceramide- and indomethacin-induced apoptosis. Our results suggest that ceramide and indomethacin share common mechanisms for induction of apoptosis in HT29 cells.
Apoptosis* ; Cell Line ; Colon ; Colonic Neoplasms ; Epithelial Cells ; HT29 Cells* ; Humans ; Indomethacin ; Protein Kinases

The characteristics of Na+/-dependent cycloleucine uptake was investigated in OK cells with regard to substrate specificity and regulation by protein kinase C (PKC). Inhibition studies with different synthetic and natural amino acids showed a broad spectrum affinity to neutral amino acids regardless of their different side chains including branched or aromatic, indicating that the Na+/-dependent cycloleucine uptake in OK cells is mediated by System B-o or System B degree -like transporter rather than the classical System A or ASC. Phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate, but not 4 alpha-PMA elicited a time-dependent biphasic stimulation of Na+/-dependent cycloleucine uptake, which produced early transient peak at 30 min and late sustained peak at 180 min. Both the early and late stimulations by PMA were due to an increase in Vmax and not due to a change in Km. PKC inhibitors blocked both the early and late stimulation by PMA, while protein synthesis inhibitors blocked the late stimulation only. These results suggest the existence and regulation by PKC of System B degree or System B degree -like broad spectrum transport system for neutral amino acids in OK cells.
Amino Acid Transport Systems* ; Amino Acids ; Amino Acids, Neutral ; Cycloleucine ; Kidney* ; Opossums* ; Phorbol 12,13-Dibutyrate ; Protein Kinase C ; Protein Synthesis Inhibitors ; Substrate Specificity

An important property of the intestine is the ability to secrete fluid. The intestinal secretion is regulated by a number of substances including vasoactive intestinal peptide (VIP), ATP and different inflammatory mediators. One of the most important secretagogues is adenosine during inflammation. However, the controversy concerning the underlying mechanism of adenosine-stimulated Cl- secretion in intestinal epithelial cells still continues. To investigate the effect of adenosine on Cl- secretion and its underlying mechanism in the rabbit colon mucosa, we measured short circuit current (ISC) under automatic voltage clamp with DVC-1000 in a modified Ussing chamber. Adenosine, when added to the basolateral side of the mucosa, increased ISC in a dose-dependent manner. The adenosine-stimulated ISC response was abolished when Cl- in the bath solution was replaced completely with gluconate. In addition, the ISC response was inhibited by a basolateral Na-K-Cl cotransporter blocker, bumetanide, and by apical Clchannel blockers, dephenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), glibenclamide. Amiloride, an epithelial Na+ channel blocker, and 4,4-diisothiocyanato-stilbene-2,2-disulphonate (DIDS), a Ca2+-activated Cl- channel blocker, had no effect. In the mucosa pre-stimulated with forskolin, adenosine did not show any additive effect, whereas carbachol resulted in a synergistic potentiation of the ISC response. The adenosine response was inhibited by 10 micrometer H-89, an inhibitor of protein kinase A. These results suggest that the adenosine-stimulated ISC response is mediated by basolateral to apical Cl- secretion through a cAMP-dependent Cl- channel. The rank order of potencies of adenosine receptor agonists was 5'-(N-ethylcarboxamino)adenosine(NECA) > N6-(R-phenylisopropyl)adenosine(R-PIA)>2-(p-(2-carbonylethyl)-phenyl-et hylamino)-5'-N-ethylcarboxaminoadenosine(CGS21680). From the above results, it can be concluded that adenosine interacts with the A2b adenosine receptor in the rabbit colon mucosa and a cAMP-dependent signalling mechanism underlies the stimulation of Cl- secretion.
Adenosine ; Adenosine Triphosphate ; Amiloride ; Baths ; Bumetanide ; Carbachol ; Colforsin ; Colon* ; Cyclic AMP-Dependent Protein Kinases ; Epithelial Cells ; Glyburide ; Inflammation ; Intestinal Secretions ; Intestines ; Mucous Membrane* ; Purinergic P1 Receptor Agonists ; Receptors, Purinergic P1 ; Vasoactive Intestinal Peptide

A number of substances involved in the proliferation and differentiation of the tracheobronchial epithelium have been identified. The defects in the control of the proliferation and differentiation of tracheobronchial epithelial cells appear to constitute crucial steps in the transition of normal cells to neoplastic ones. Endothelin-1 is produced by tracheal epithelial cells, and its receptors are present in tracheal epithelial cells. However, the effect of endothelin-1 on the proliferation and differentiation of tracheal epithelial cells has not been clearly elucidated. This study was undertaken to investigate these actions of endothelin-1 in primary cultured cells of rat tracheal epithelia. Endothelin-1 stimulated proliferation of tracheal epithelial cells 1.5-fold when compared with that of control cells. Endothelin-1 increased mitogen-activated protein kinase (MAPK) activity. Herbimycin A, a tyrosine kinase inhibitor, inhibited endothelin-1-induced proliferation of epithelial cells. The treatment of endothelin-1 during the primary culture of tracheal epithelial cells increased AB-PAS-stained cell population and ciliated cell population 6.5 fold and 1.5 fold, respectively, when compared with those in control cells. The responsiveness to carbachol and forskolin in the Cl- secretion was increased 1.7 and 1.9 fold, respectively, in the endothelin-treated epithelial cells. These results indicated that endothelin-1 increases proliferation via MAPK pathway and stimulates differentiation to secretory and ciliated cells in rat tracheal epithelial cells.
Animals ; Carbachol ; Cells, Cultured ; Colforsin ; Endothelin-1* ; Epithelial Cells* ; Epithelium ; Protein Kinases ; Protein-Tyrosine Kinases ; Rats*

OBJECTIVE: The aim of this study was to evaluate under target rates of low-density lipoprotein-cholesterol (LDL-C) in Korean patients with stable coronary artery disease (CAD) or an acute coronary syndrome (ACS) in real world practice. METHODS: Dyslipidemia International Study II was an international observational study of patients with stable CAD or an ACS. Lipid profiles and use of lipid-lowering therapy (LLT) were documented at enrollment, and for the ACS cohort, 4 months follow-up was recommended. Rates of under target LDL-C as per European guidelines, were evaluated, and multivariate regression was performed to identify predictive factors of patients presenting under the target. RESULTS: A total of 808 patients were enrolled in Korea, 500 with stable CAD and 308 with ACS. Of these, 90.6% and 52.6% were being treated with LLT, respectively. In the stable CAD group, 40.0% were under target LDL-C, while in ACS group, the rate was 23.7%. A higher statin dose was independently associated with under target LDL-C in both groups (OR, 1.03; p=0.046 [stable CAD] and OR, 1.05; p=0.01 [ACS]). The mean statin dosage (atorvastatin equivalent) was 17 mg/day. In the 79 ACS patients who underwent the follow-up examination, the LDL-C under target rate rose to 59.5%. CONCLUSION: Only a minority of patients with stable CAD or ACS were under their target LDL-C level at enrollment. The statin dose was not sufficient in the majority of patients. These results indicate a considerable LLT gap in Korean patients with established CAD.
Acute Coronary Syndrome ; Cholesterol ; Cohort Studies ; Coronary Artery Disease ; Coronary Vessels ; Dyslipidemias ; Follow-Up Studies ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Korea ; Observational Study